Browse result page of ThPDB2
This is the result page of the browse module of ThPDB2. This page gives the information about the query submitted by the user as per the browse category. Further details of the entries can be seen by clicking on the ID or THPP_ID. Further the user can sort the entries on the basis of various fields by clicking on the respective headers. The user can also download the results in various formats.
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| ID | THPP_ID | Therapeutic Name | Sequence | Molecular Weight | Chemical Formula | Isoelectric Point | Hydrophobicity | Melting Point | Half Life | Description | Disease/Indication | Pharmacodynamics | Mechanism of Action | Toxicity | Metabolism | Absorption | Volume of Distribution | Clearance | Categories | Patent Number | Date of Issue | Date of Expiry | Drug Interaction | Target | Brand Name | Company | Brand Description | Prescribed for | Chemical Name | Formulation | Physical Appearance | Route of Administation | Recommended Dosage | Contraindication | Side Effects | Useful Links 1 | Useful Links 2 | Remarks |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 10028 | Th1005 | Etanercept | >Th1005_Etanercept LPAQVAFTPYAPEPGSTCRLREYYDQTAQMCCSKCSPGQHAKVFCTKTSDTVCDSCEDSTYTQLWNWVPECLSCGSRCSSDQVETQACTREQNRICTCRPGWYCALSKQEGCRLCAPLRKCRPGFGVARPGTETSDVVCKPCAPGTFSNTTSSTDICRPHQICNVVAIPGNASMDAVCTSTSPTRSMAPGAVHLPQPVSTRSQHTQPTPEPSTAPSTSFLLPMGPSPPAEGSTGDEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 51234.9 | C2224H3475N621O698S36 | 7.89 | -0.529 | 71 | 102 hours in RA patients | It is a dimeric fusion protein (934 amino acids) consisting of extracellular ligand-binding portion of the human 75 kilodalton (p75) tumor necrosis factor receptor (TNFR) linked to Fc portion of human IgG1 produced by recombinant DNA technology in a Chinese hamster ovary (CHO) mammalian cell expression system.. The Fc component of etanercept contains the CH2 domain, the CH3 domain and hinge region, but not the CH1 domain of IgG1. | Used to treat severe rheumatoid arthritis in adults, severe juvenile idiopathic arthritis, ankylosing spondylitis, and severe plaque psoriasis. | TNF, a naturally occurring cytokine is involved in normal inflammatory and immune responses. Elevated levels of TNF are found in tissues and fluids of patients suffering from rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis (AS), and plaque psoriasis. Etanercept binds specifically to tumor necrosis factor (TNF) and blocks its interaction with cell surface TNF receptors. | There are two distinct receptors for TNF (TNFRs), a 55 kilodalton (p55) and a 75 kilodalton receptor (p75). The biological activity of TNF is dependent upon binding to either of the cell surface receptors p75 or p55. Etanercept is a dimeric soluble form of the p75 TNF receptor that can bind to two TNF molecules, thereby effectively removing them from circulation. | NA | NA | NA | NA | 160 ± 80 mL/hr [RA patients] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Dermatologicals, Disease-modifying Antirheumatic Agents, Immunoglobulin Constant Regions, Immunoglobulin Fc Fragments, Immunoglobulin Fragments, Immunoglobulin Isotypes, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Membrane Proteins, Peptides, Proteins, Tumor Necrosis Factor Blockers | CA2476934 | 16-Jun-2009 | 27-Feb-2023 | Rilonacept results in increased immunosuppressive effects; increases the risk of infection. | Tumor necrosis factor,Tumor necrosis factor receptor superfamily member 1B,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c,Lymphotoxin-alpha,Low affinity immunoglobulin gamma Fc region receptor III-B | Enbrel | Immunex Corp | Immunex Corp | Used to treat rheumatoid arthritis, psoriatic arthritis, or ankylosing spondylitis, and prevent joint damage caused by these conditions. Enbrel is also used to treat plaque psoriasis in adults and polyarticular juvenile idiopathic arthritis (in children a | NA | Supplied in a multiple-use vial as a sterile, white, preservative-free, lyophilized powder. Reconstitution with 1 mL of the supplied Sterile Bacteriostatic Water for Injection, USP (containing 0.9% benzyl alcohol) yields a multiple-use, clear, and colorle | Lyophilized powder. | Subcutaneous Injection | NA | NA | Signs of infection (fever, chills, sore throat, body aches, confusion, neck stiffness, flu symptoms); shortness of breath with swelling, rapid weight gain; chest pain, ongoing cough, coughing up mucus or blood; signs of skin infection such as itching, sw | Link | NA | NA |
| 10029 | Th1005 | Etanercept | >Th1005_Etanercept LPAQVAFTPYAPEPGSTCRLREYYDQTAQMCCSKCSPGQHAKVFCTKTSDTVCDSCEDSTYTQLWNWVPECLSCGSRCSSDQVETQACTREQNRICTCRPGWYCALSKQEGCRLCAPLRKCRPGFGVARPGTETSDVVCKPCAPGTFSNTTSSTDICRPHQICNVVAIPGNASMDAVCTSTSPTRSMAPGAVHLPQPVSTRSQHTQPTPEPSTAPSTSFLLPMGPSPPAEGSTGDEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 51234.9 | C2224H3475N621O698S36 | 7.89 | -0.529 | 71 | 68 hours in healthy adults | It is a dimeric fusion protein (934 amino acids) consisting of extracellular ligand-binding portion of the human 75 kilodalton (p75) tumor necrosis factor receptor (TNFR) linked to Fc portion of human IgG1 produced by recombinant DNA technology in a Chinese hamster ovary (CHO) mammalian cell expression system.. The Fc component of etanercept contains the CH2 domain, the CH3 domain and hinge region, but not the CH1 domain of IgG1. | Used to treat severe rheumatoid arthritis in adults, severe juvenile idiopathic arthritis, ankylosing spondylitis, and severe plaque psoriasis. | TNF, a naturally occurring cytokine is involved in normal inflammatory and immune responses. Elevated levels of TNF are found in tissues and fluids of patients suffering from rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis (AS), and plaque psoriasis. Etanercept binds specifically to tumor necrosis factor (TNF) and blocks its interaction with cell surface TNF receptors. | There are two distinct receptors for TNF (TNFRs), a 55 kilodalton (p55) and a 75 kilodalton receptor (p75). The biological activity of TNF is dependent upon binding to either of the cell surface receptors p75 or p55. Etanercept is a dimeric soluble form of the p75 TNF receptor that can bind to two TNF molecules, thereby effectively removing them from circulation. | NA | NA | NA | NA | 160 ± 80 mL/hr [RA patients] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Dermatologicals, Disease-modifying Antirheumatic Agents, Immunoglobulin Constant Regions, Immunoglobulin Fc Fragments, Immunoglobulin Fragments, Immunoglobulin Isotypes, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Membrane Proteins, Peptides, Proteins, Tumor Necrosis Factor Blockers | CA2123593 | 14-Mar-2000 | 14-Sep-2013 | Tofacitinib increases the risk of added immunosuppression. It is recommended to avoid concurrent therapy. | NA | Enbrel Sureclick | Amgen Inc. , Boehringer Ingelheim Ltd. | Amgen Inc. , Boehringer Ingelheim Ltd. | NA | NA | NA | Solution | Subcutaneous Injection | NA | Allergy or severe infection as sepsis. | NA | Link | NA | NA |
| 10038 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty. | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | Gonadotropin-releasing hormone receptor | Eligard | Atrix Labs/QLT In | Atrix Labs/QLT In | Eligard is used to treat the symptoms of prostate cancer in men. | 5-oxo-L-prolyl-L-histidyl-L-tryptophyl-L-seryl-L-tyrosyl-D-leucyl-L-arginyl-N-ethyl-L-prolinamide acetate | ELIGARD is prefilled and supplied in two separate, sterile syringes whose contents are mixed immediately prior to administration. The two syringes are joined and the single dose product is mixed until it is homogenous. One syringe contains the ATRIGEL De | Suspension | Subcutaneous Injection | 7.5mg-1 injection/month, 22.5mg-1 injection per 3 month, 30mg-1 injection per 4 month, 45 mg- 1 injection every 6 month. | Hypersensitivity and pregnancy | Rare pain or unusual sensations in your back; numbness, weakness, or tingly feeling in your legs or feet; muscle weakness or loss of use; loss of bowel or bladder control; or liver problems - nausea, upper stomach pain, itching, tired feeling, loss of apetite. | Link | NA | NA |
| 10049 | Th1008 | Peginterferon alfa-2a | >Th1008_Peginterferon_alfa-2a CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 60000 | NA | 5.99 | NA | 61 | Terminal half life is 164 hours (range 84 to 353 hours). | Human interferon 2a, is a covalent conjugate of recombinant interferon alfa-2a with a single branched bis-mono-methoxy polyethylene glycol (PEG) chain. The PEG moiety is linked at a single site to the interferon alfa moiety via a stable amide bond to lysine. Peginterferon alfa-2a has an approximate molecular weight of 60,000 daltons. Interferon alfa-2a is produced using recombinant DNA technology in which a cloned human leukocyte interferon gene is inserted and expressed in Escherichia coli. The resultant protein is 165 amino acids. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | To treat hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma. | Upregulates the expression of MHC I proteins which increases presentation of peptides derived from viral antigens. Thus enhancing the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and make the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. | Interferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which upon dimerization activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | Peginterferon alfa-2a may manifest neuropsychiatric complications include suicide, suicidal ideation, homicidal ideation, depression, relapse of drug addiction, and drug overdose Label. Hypertension, supraventricular arrhythmias, chest pain, and myocardial infarction have been observed in patients using Peginterferon alfa-2a. | NA | NA | NA | 94 milliliters per hour | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cardiotoxic antineoplastic agents, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatotoxic Agents, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferons, Macromolecular Substances, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | CA2203480 | 30-Jun-2009 | 23-Apr-2017 | Interferon increases the effect and toxicity of theophylline called Aminophylline | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | Pegasys | Hoffman-La Roche Inc | Hoffman-La Roche Inc | Pegasys is used to treat chronic hepatitis B or C (adults), and to treat chronic hepatitis C (children 5 or more years of age). It is mostly used with ribavirin | NA | Each vial of 180 mcg/mL peginterferon alfa-2a (expressed as the amount of interferon alfa-2a) also contains acetic acid (0.05 mg), benzyl alcohol (10 mg), polysorbate 80 (0.05 mg), sodium acetate trihydrate (2.62 mg), and sodium chloride (8 mg) at pH 6 ± | Sterile, preservative-free, colorless to light yellow injectable solution | Subcutaneous Injection | Pegasys is usually given once a week. | Allergic | Nausea, vomiting, loss of appetite; headache, muscle pain, feeling weak or tired; sleep problems (insomnia); temporary hair loss; or itching, redness, dryness, or swelling where the medicine was injected. | Link | NA | NA |
| 10064 | Th1011 | Darbepoetin alfa | >Th1011_Darbepoetin_alfa MGVHECPAWLWLLLSLLSLPLGLPVLGAPPRLICDSRVLERYLLEAKEAENITTGCNETCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQVNETLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | -0.188 | 53 | NA | Human erythropoietin with 2 amino acid substitutions to enhance glycosylation (5 N-linked chains), 165 residues (MW 37kD) produced in CHO cells by recombinant DNA technology. | For treating anemia (from renal transplants or certain HIV treatment). | Darbepoetin alfa is used in treating anemia. It is involved in the regulation of erythrocyte differentiation and maintenance of a physiological level of circulating erythrocyte mass. | Darbepoetin alfa stimulates erythropoiesis by the same mechanism as endogenous erythropoietin, it interacts with progenitor stem cells to increase red cell production. Binding of erythropoietin to the erythropoietin receptor leads to receptor dimerization. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antianemic Preparations, Blood and Blood Forming Organs, Colony-Stimulating Factors, Erythropoiesis-Stimulating Agents, Glycoproteins, Hematinics, Hematologic Agents, Hematopoietic Cell Growth Factors, Increased Erythroid Cell Production, Proteins | CA2165694 | 18-Mar-2003 | 15-Oct-2010 | NA | Erythropoietin receptor | Aranesp | Amgen Inc | Amgen Inc | Used to treat anemia. | NA | Each 1 mL contains polysorbate 80 (0.05 mg), sodium chloride (8.18 mg), sodium phosphate dibasic anhydrous (0.66 mg), and sodium phosphate monobasic monohydrate (2.12 mg) in Water for Injection, USP (pH 6.2 ± 0.2). | Sterile, colorless, preservative-free solution containing polysorbate | Intravenous or Subcutaneous administration | NA | Allergic | Fever, chills, body aches, flu symptoms; feeling like you might pass out; easy bruising, unusual bleeding (nose, mouth, vagina, or rectum), purple or red pinpoint spots under your skin; seizure (black-out or convulsions); or dangerously high blood pressure. | Link | NA | NA |
| 10071 | Th1013 | Epoetin alfa | >Th1013_Epoetin_alfa APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 | 4 hours in healthy volunteers receiving an intravenous injection | It is recombinant human erythropoietin which is produced by CHO cells. | For treatment of anemia (from renal transplants or certain HIV treatment). | Used in the treatment of anemia and involved in the regulation of erythrocyte differentiation and maintenance of a physiological level of circulating erythrocyte mass. | Binding of erythropoietin to the erythropoietin receptor leads to receptor dimerization which facilitates activation of JAK-STAT signaling pathways within the cytosol. Activated STAT (signal transducers and activators of transcription) proteins are then translocated to the nucleus where they serve as transcription factors which regulate the activation of specific genes involved in cell division or differentiation. | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system | Bioavailability is 20-40% | 40–63.80 mL/kg | 20.2 ± 15.9 mL/h/kg [150 Units/kg SC TIW, Week 1 when anemic cancer patients were receiving chemotherapy] | Amino Acids, Peptides, and Proteins, Antianemic Preparations, Biological Factors, Blood and Blood Forming Organs, Colony-Stimulating Factors, Cytokines, Erythropoiesis-Stimulating Agents, Erythropoietin, genetics, Glycoproteins, Hematinics, Hematologic Agents, Hematopoietic Cell Growth Factors, Increased Erythroid Cell Production, Intercellular Signaling Peptides and Proteins, Peptides, Proteins | CA1339047 | 27-May-1997 | 27-May-2014 | NA | Erythropoietin receptor | Binocrit | Sandoz | Sandoz | Treatment of symptomatic anaemia associated with chronic renal failure (CRF) in adult and paediatric patients | NA | 1000 IU/0.5 ml means that each ml of solution contains 2000 IU of epoetin alfa corresponding to 16.8 micrograms per ml. One pre-filled syringe of 0.5 ml contains 1000 international units (IU) corresponding to 8.4 micrograms epoetin alfa | Clear colourless solution | Subcutaneous and Intravenous infusion | For less than 10 kg of weight usual maintainence dose is 75-150 (IU/kg given 3x/week). For 10-30 kg weight usual maintainence dose is 60-150 (IU/kg given 3x/week). For more than 30 kg weight usual maintainence dose is 30-100 (IU/kg given 3x/week). | Hypersensitivity, uncontrooled hypertension, Patients who develop Pure Red Cell Aplasia (PRCA) following treatment with any erythropoietin should not receive Binocrit, Patients who develop Pure Red Cell Aplasia (PRCA) following treatment with any erythropoetin. | The most frequent adverse reaction during treatment with epoetin alfa is a dose-dependent increase in blood pressure or aggravation of existing hypertension in cancer patients and in chronic renal failure patients. | Link | NA | NA |
| 10076 | Th1013 | Epoetin alfa | >Th1013_Epoetin_alfa APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 | NA | It is recombinant human erythropoietin which is produced by CHO cells. | For treatment of anemia (from renal transplants or certain HIV treatment). | Used in the treatment of anemia and involved in the regulation of erythrocyte differentiation and maintenance of a physiological level of circulating erythrocyte mass. | Binding of erythropoietin to the erythropoietin receptor leads to receptor dimerization which facilitates activation of JAK-STAT signaling pathways within the cytosol. Activated STAT (signal transducers and activators of transcription) proteins are then translocated to the nucleus where they serve as transcription factors which regulate the activation of specific genes involved in cell division or differentiation. | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system | Bioavailability is 20-40% | 40–63.80 mL/kg | NA | Amino Acids, Peptides, and Proteins, Antianemic Preparations, Biological Factors, Blood and Blood Forming Organs, Colony-Stimulating Factors, Cytokines, Erythropoiesis-Stimulating Agents, Erythropoietin, genetics, Glycoproteins, Hematinics, Hematologic Agents, Hematopoietic Cell Growth Factors, Increased Erythroid Cell Production, Intercellular Signaling Peptides and Proteins, Peptides, Proteins | NA | NA | NA | NA | NA | Epogen | Amgen Inc. | Amgen Inc. | Epogen is used to treat anemia in patients with chronic kidney disease. Epogen is also used in HIV patients who have anemia due to treatment with zidovudine and in cancer patients who have anemia due to chemotherapy. | NA | Each 1 mL vial contains 2000, 3000, 4000, or 10,000 Units of epoetin alfa, Albumin (Human) (2.5 mg), citric acid (0.06 mg), sodium chloride (5.9 mg), and sodium citrate (5.8 mg) in Water for Injection, USP (pH 6.9 ± 0.3). Single-dose 1 mL vials formulated | Sterile, colorless liquid | Subcutaneous Injection | NA | Allergic, untreated or uncontrolled high blood pressure; or if you have ever had pure red cell aplasia (PRCA, a type of anemia) caused by using darbepoetin alfa or epoetin alfa. | Feeling light-headed, fainting; fever, chills, body aches, flu symptoms, sores in your mouth and throat; pale skin, feeling short of breath, rapid heart rate, trouble concentrating; easy bruising, unusual bleeding (nose, mouth, vagina, or rectum), purple | Link | NA | NA |
| 10079 | Th1013 | Epoetin alfa | >Th1013_Epoetin_alfa APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 | NA | It is recombinant human erythropoietin which is produced by CHO cells. | For treatment of anemia (from renal transplants or certain HIV treatment). | Used in the treatment of anemia and involved in the regulation of erythrocyte differentiation and maintenance of a physiological level of circulating erythrocyte mass. | Binding of erythropoietin to the erythropoietin receptor leads to receptor dimerization which facilitates activation of JAK-STAT signaling pathways within the cytosol. Activated STAT (signal transducers and activators of transcription) proteins are then translocated to the nucleus where they serve as transcription factors which regulate the activation of specific genes involved in cell division or differentiation. | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system | Bioavailability is 20-40% | 40–63.80 mL/kg | NA | Amino Acids, Peptides, and Proteins, Antianemic Preparations, Biological Factors, Blood and Blood Forming Organs, Colony-Stimulating Factors, Cytokines, Erythropoiesis-Stimulating Agents, Erythropoietin, genetics, Glycoproteins, Hematinics, Hematologic Agents, Hematopoietic Cell Growth Factors, Increased Erythroid Cell Production, Intercellular Signaling Peptides and Proteins, Peptides, Proteins | NA | NA | NA | NA | NA | Epogin | Chugai | Chugai | EPOGIN Injection (EPOGIN Injection Syringe, EPOGIN Injection Ampule) has been widely used in the clinical settings for its approved indications of renal anemia under dialysis and before dialysis, immature infant anemia, and the autologous blood transfusio | NA | NA | NA | Subcutaneous and Intravenous infusion | The autologous blood transfusion, the intravenous administration of Epogin at 6000 units/per time for three times a week on alternative days has been already approved for three forms of “Epogin Injection 1500, 3000 and 6000. | NA | Nausea, fatigue, and vomiting. | Link | NA | NA |
| 10082 | Th1013 | Epoetin alfa | >Th1013_Epoetin_alfa APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 | NA | It is recombinant human erythropoietin which is produced by CHO cells. | For treatment of anemia (from renal transplants or certain HIV treatment). | Used in the treatment of anemia and involved in the regulation of erythrocyte differentiation and maintenance of a physiological level of circulating erythrocyte mass. | Binding of erythropoietin to the erythropoietin receptor leads to receptor dimerization which facilitates activation of JAK-STAT signaling pathways within the cytosol. Activated STAT (signal transducers and activators of transcription) proteins are then translocated to the nucleus where they serve as transcription factors which regulate the activation of specific genes involved in cell division or differentiation. | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system | Bioavailability is 20-40% | 40–63.80 mL/kg | NA | Amino Acids, Peptides, and Proteins, Antianemic Preparations, Biological Factors, Blood and Blood Forming Organs, Colony-Stimulating Factors, Cytokines, Erythropoiesis-Stimulating Agents, Erythropoietin, genetics, Glycoproteins, Hematinics, Hematologic Agents, Hematopoietic Cell Growth Factors, Increased Erythroid Cell Production, Intercellular Signaling Peptides and Proteins, Peptides, Proteins | NA | NA | NA | NA | NA | Eprex | Janssen-Cilag. Ortho Biologics LLC | Janssen-Cilag. Ortho Biologics LLC | To treat patients with symptomatic or transfusion requiring anaemia associated with chronic renal failure to improve their quality of life. | NA | Each mL of sterile solution contains epoetin alfa 1,000 IU, 2,000 IU, 4,000 IU, 10,000 IU, or 40,000 IU. Nonmedicinal ingredients include glycine and polysorbate 80 as stabilizers, sodium chloride, sodium phosphate dibasic dihydrate, sodium phosphate mono | Solution | Subcutaneous and Intravenous infusion | For children with chronic renal failure, the starting dose for anemia is 50 units (IU) per kilogram body weight, given 3 times a week. For adults with chronic renal failure, the starting dose for anemia is 50 to 100 units per kilogram of body weight. | Uncontrolled hypertension | Clotting of the vascular access site (for people on hemodialysis), dehydration, diarrhea, edema (swelling of the face, fingers, ankles, feet, or lower legs), headache, increased or decreased blood pressure, dizziness, or feeling faint, muscle aches and weakness. | Link | NA | NA |
| 10095 | Th1013 | Epoetin alfa | >Th1013_Epoetin_alfa APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 | NA | It is recombinant human erythropoietin which is produced by CHO cells. | For treatment of anemia (from renal transplants or certain HIV treatment). | Used in the treatment of anemia and involved in the regulation of erythrocyte differentiation and maintenance of a physiological level of circulating erythrocyte mass. | Binding of erythropoietin to the erythropoietin receptor leads to receptor dimerization which facilitates activation of JAK-STAT signaling pathways within the cytosol. Activated STAT (signal transducers and activators of transcription) proteins are then translocated to the nucleus where they serve as transcription factors which regulate the activation of specific genes involved in cell division or differentiation. | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system | Bioavailability is 20-40% | 40–63.80 mL/kg | NA | Amino Acids, Peptides, and Proteins, Antianemic Preparations, Biological Factors, Blood and Blood Forming Organs, Colony-Stimulating Factors, Cytokines, Erythropoiesis-Stimulating Agents, Erythropoietin, genetics, Glycoproteins, Hematinics, Hematologic Agents, Hematopoietic Cell Growth Factors, Increased Erythroid Cell Production, Intercellular Signaling Peptides and Proteins, Peptides, Proteins | NA | NA | NA | NA | NA | Procrit | Ortho Biotech | Ortho Biotech | Used to treat anemia in patients with Chronic Kidney Disease (CKD). Procrit is also used to treat anemia caused by zidovudine in HIV-infected patients and in certain patients receiving chemotherapy. | NA | Each 1 mL of solution contains 2000, 3000, 4000 or 10,000 Units of Epoetin alfa, 2.5 mg Albumin (Human), 5.8 mg sodium citrate, 5.8 mg sodium chloride, and 0.06 mg citric acid in Water for Injection, USP (pH 6.9 ± 0.3). This formulation contains no preser | Sterile, colorless liquid in an isotonic sodium chloride/sodium citrate buffered solution or a sodium chloride/sodium phosphate buffered solution | Intravenous (Intravenous) or Subcutaneous (Subcuta | 100 units/kg subcutaneously or IV 3 times a week. | Allergic | Feeling light-headed, fainting, fever, chills, body aches, flu symptoms, sores in your mouth and throat, pale skin, feeling short of breath, rapid heart rate, trouble concentrating, easy bruising, unusual bleeding (nose, mouth, vagina, or rectum), purple or red pinpoint spots under your skin. | Link | NA | NA |
| 10098 | Th1014 | Salmon Calcitonin | >Th1014_Salmon_Calcitonin CSNLSTCVLGKLSQELHKLQTYPRTNTGSGTP | 3431.853 | C145H240N44O48S2 | 8.86 | -0.537 | NA | 0.83-1.33 hours | Synthetic peptide of 32 residues, formulated as a nasal spray. | Used for the treatment of post-menopausal osteoporosis. | Calcitonin inhibits bone removal by osteoclasts and promotes bone formation by osteoblasts, leading to a net increase in bone mass. Calcitonin also reduces plasma calcium levels and enhances secretion of ions in the kidney. | Calcitonin binds to the calcitonin receptor, found mainly in osteoclasts which then enhances the production of vitamin D producing enzymes (25-hydroxyvitamine D-24-hydroxylase), leading to greater calcium retention and enhanced bone density. Binding of calcitonin to its receptor also activates adenylyl cyclase and the phosphatidyl-inositol-calcium pathway. | It is devoid of embryotoxic, teratogenic and mutagenic potential. | Primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule. | Rapidly absorbed and eliminated. Bioavailability is high following subcutaneous and intramuscular injection in humans and similar for the two routes of administration (71% and 66%, respectively). | 0.15 to 0.3 L/kg | Studies with injectable calcitonin show increase in the excretion of filtered calcium, phosphate, and sodium by decreasing their tubular reabsorption in the kidney. | Amino Acids, Peptides, and Proteins, Bone Density Conservation Agents, Bone Density, drug effects, Calcitonin Preparations, Calcium Homeostasis, Calcium-Regulating Hormones and Agents, Drugs that are Mainly Renally Excreted, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Parathyroid and Antiparathyroid Agents, Parathyroid Hormones and Analogues, Peptide Hormones, Peptides, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | US6440392 | 27-Aug-2002 | 2-Feb-2021 | Eskalith (lithium) | Calcitonin receptor | Calcimar | Sanofi Aventis | Sanofi Aventis | To treat Paget's disease of bone | NA | Each mL of sterile solution contains calcitonin salmon 200 IU. Nonmedicinal ingredients include acetic acid, phenol, sodium acetate, sodium chloride, sodium hydroxide and water for injection. | Solution | Subcutaneous or intramuSubcutaneousular Injection | Based on body weight and injected every 12 hours | Allergy | Feeling light-headed, fainting; or muscle stiffness. | Link | NA | NA |
| 10106 | Th1014 | Salmon Calcitonin | >Th1014_Salmon_Calcitonin CSNLSTCVLGKLSQELHKLQTYPRTNTGSGTP | 3431.853 | C145H240N44O48S2 | 8.86 | -0.537 | NA | 0.83-1.33 hours | Synthetic peptide of 32 residues, formulated as a nasal spray. | Used for the treatment of post-menopausal osteoporosis. | Calcitonin inhibits bone removal by osteoclasts and promotes bone formation by osteoblasts, leading to a net increase in bone mass. Calcitonin also reduces plasma calcium levels and enhances secretion of ions in the kidney. | Calcitonin binds to the calcitonin receptor, found mainly in osteoclasts which then enhances the production of vitamin D producing enzymes (25-hydroxyvitamine D-24-hydroxylase), leading to greater calcium retention and enhanced bone density. Binding of calcitonin to its receptor also activates adenylyl cyclase and the phosphatidyl-inositol-calcium pathway. | It is devoid of embryotoxic, teratogenic and mutagenic potential. | Primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule. | Rapidly absorbed and eliminated. Bioavailability is high following subcutaneous and intramuscular injection in humans and similar for the two routes of administration (71% and 66%, respectively). | 0.15 to 0.3 L/kg | Studies with injectable calcitonin show increase in the excretion of filtered calcium, phosphate, and sodium by decreasing their tubular reabsorption in the kidney. | Amino Acids, Peptides, and Proteins, Bone Density Conservation Agents, Bone Density, drug effects, Calcitonin Preparations, Calcium Homeostasis, Calcium-Regulating Hormones and Agents, Drugs that are Mainly Renally Excreted, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Parathyroid and Antiparathyroid Agents, Parathyroid Hormones and Analogues, Peptide Hormones, Peptides, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | NA | NA | NA | NA | NA | Miacalcin | Novartis, Mylan Institutional LLC, Physicians Total Care, Inc., Sebela Pharmaceuticals Inc. | Novartis, Mylan Institutional LLC, Physicians Total Care, Inc., Sebela Pharmaceuticals Inc. | Miacalcin Nasal Spray is used to treat osteoporosis in women who have been in menopause for at least 5 years. To be supplemented with adequate calcium and vitamin D intake. | NA | Each milliliter contains calcitonin-salmon 200 I.U., acetic acid, USP, 2.25 mg; phenol, USP, 5.0 mg; sodium acetate trihydrate, USP, 2.0 mg; sodium chloride, USP, 7.5 mg; water for injection, USP, qs to 1.0 mL | Solution | Subcutaneous or intramuSubcutaneousular Injection | For treatment of symptomatic Paget's disease of bone, 100 International Units (0.5 mL) per day administered subcutaneously or intramuscularly and for early treatment of hypercalcemia, 4 International Units/kg body weight every 12 hours by subcutaneous or | Allergic, nasal or sinus problem such as nasal deformities, a chronic infection, or nasal pain. | Tremors or shaking, feeling like you might pass out, severe nasal irritation. | Link | NA | NA |
| 10117 | Th1016 | Pegfilgrastim | >Th1016_Pegfilgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 39000 | C845H1343N223O243S9 | 5.65 | 0.209 | 60 | 15-80 hours | PEGylated(at N terminus) form of human G-CSF (Granulocyte colony stimulating factor), 175 residues, produced from E. coli via bacterial fermentation. | Increases leukocyte production, for treatment in non-myeloid cancer, neutropenia and bone marrow transplant | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Pegfilgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment and end cell functional activation. Pegfilgrastim has reduced renal clearance and prolonged persistence in vivo as compared to Filgrastim. | Pegfilgrastim binds to the G-CSF receptor. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Pegfilgrastim also stimulates the release of neutrophils from bone marrowstorage pools and reduces their maturation time. Pegfilgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, pegfilgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | Overdosage of pegfilgrastim may result in leukocytosis and bone pain. Events of edema, dyspnea, and pleural effusion have been reported in a single patient who self-administered pegfilgrastim on 8 consecutive days in error. | It is not know whether pegfilgrastim is metabolized into major metabolites.13 Once it binds to the therapeutic target, pegfilgrastim is internalized by the neutrophil and undergoes nonspecific degradation | lower absolute bioavailability | approximately 170L | 14 mL/h/kg | Adjuvants, Immunologic, Alcohols, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Carbohydrates, Colony-Stimulating Factors, Compounds used in a research, industrial, or household setting, Cytokines, Ethylene Glycols, Glycoconjugates, Glycols, Glycoproteins, Granulocyte Colony-Stimulating Factors, Hematinics, Hematopoietic Cell Growth Factors, Increased Myeloid Cell Production, Intercellular Signaling Peptides and Proteins, Leukocyte Growth Factor, Macromolecular Substances, Pegylated agents, Peptides, Polymers, Proteins | CA1341537 | 31-Jul-2007 | 31-Jul-2024 | NA | Granulocyte colony-stimulating factor receptor,Neutrophil elastase | Neulasta | Amgen Inc. | Amgen Inc. | Neulasta is used to prevent neutropenia(lack of certain white blood cells caused by receiving chemotherapy). | NA | Supplied in 0.6 mL prefilled syringes. Each syringe contains 6 mg pegfilgrastim (based on protein weight) in a sterile, clear, colorless, preservative-free solution (pH 4.0) containing acetate (0.35 mg), polysorbate 20 (0.02 mg), sodium (0.02 mg), and sor | Solution | Subcutaneous Injection | Single subcutaneous injection of 6 mg administered once per chemotherapy cycle in adults. Do not administer Neulasta between 14 days before and 24 hours after administration of cytotoxic chemotherapy. | Allergy, or having sickle cell disorder; chronic myeloid leukemia; myelodysplasia (also called preleukemia); or if you are allergic to latex. | Bone pain; pain in your arms or legs; or bruising, swelling, pain, redness, or a hard lump where the injection was given. | Link | NA | NA |
| 10119 | Th1016 | Pegfilgrastim | >Th1016_Pegfilgrastim MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 39000 | C845H1343N223O243S9 | 5.65 | 0.209 | 60 | 15-80 hours | PEGylated(at N terminus) form of human G-CSF (Granulocyte colony stimulating factor), 175 residues, produced from E. coli via bacterial fermentation. | Increases leukocyte production, for treatment in non-myeloid cancer, neutropenia and bone marrow transplant | Used in the treatment of chemotherapy-induced neutropenia by enhancing the production of neutrophils. Pegfilgrastim acts on hematopoietic cells by binding to specific cell surface receptors thereby stimulating proliferation, differentiation, commitment and end cell functional activation. Pegfilgrastim has reduced renal clearance and prolonged persistence in vivo as compared to Filgrastim. | Pegfilgrastim binds to the G-CSF receptor. As a G-CSF analog, it controls proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Pegfilgrastim also stimulates the release of neutrophils from bone marrowstorage pools and reduces their maturation time. Pegfilgrastim acts to increase the phagocytic activity of mature neutrophils. In patients receiving cytotoxic chemotherapy, pegfilgrastim can accelerate neutrophil recovery, leading to a reduction in duration of the neutropenic phase | Overdosage of pegfilgrastim may result in leukocytosis and bone pain. Events of edema, dyspnea, and pleural effusion have been reported in a single patient who self-administered pegfilgrastim on 8 consecutive days in error. | It is not know whether pegfilgrastim is metabolized into major metabolites.13 Once it binds to the therapeutic target, pegfilgrastim is internalized by the neutrophil and undergoes nonspecific degradation | lower absolute bioavailability | approximately 170L | 14 mL/h/kg | Adjuvants, Immunologic, Alcohols, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Carbohydrates, Colony-Stimulating Factors, Compounds used in a research, industrial, or household setting, Cytokines, Ethylene Glycols, Glycoconjugates, Glycols, Glycoproteins, Granulocyte Colony-Stimulating Factors, Hematinics, Hematopoietic Cell Growth Factors, Increased Myeloid Cell Production, Intercellular Signaling Peptides and Proteins, Leukocyte Growth Factor, Macromolecular Substances, Pegylated agents, Peptides, Polymers, Proteins | NA | NA | NA | NA | NA | Fulphila | Mylan S.A.S, Viatris Limited | Mylan S.A.S, Viatris Limited | decrease the incidence of infection, as manifested by febrile neutropenia, in patients with non-myeloid malignancies receiving myelosuppressive anti-cancer drugs associated with a clinically significant incidence of febrile neutropenia | NA | Fulphila (pegfilgrastim-jmdb) injection is intended for subcutaneous use only and is supplied in a single-dose prefilled syringe with a 29 gauge needle, with UltraSafe Passive Plus ™ Needle Guard. The prefilled syringe does not bear graduation marks and is designed to deliver the entire contents of the syringe (6 mg/0.6 mL). | clear, colorless solution | Fulphila is administered subcutaneously via a single-dose prefilled syringe for manual use. | The recommended dosage of Fulphila is a single subcutaneous injection of 6 mg administered once per chemotherapy cycle. For dosing in pediatric patients weighing less than 45 kg, refer to Table 1. Do not administer Fulphila between 14 days before and 24 hours after administration of cytotoxic chemotherapy. | Fulphila is contraindicated in patients with a history of serious allergic reactions to pegfilgrastim products or filgrastim products. Reactions have included anaphylaxis | Splenic Rupture Acute Respiratory Distress Syndrome Serious Allergic Reactions Use in Patients with Sickle Cell Disorders Glomerulonephritis Leukocytosis Thrombocytopenia Capillary Leak Syndrome Potential for Tumor Growth Stimulatory Effects on Malignant Cells Myelodysplastic syndrome Acute myeloid leukemia Aortitis | Link | NA | NA |
| 10120 | Th1017 | Sargramostim | >Th1017_Sargramostim APARSPSPSTQPWEHVNAIQEALRLLNLSRDTAAEMNETVEVISEMFDLQEPTCLQTRLELYKQGLRGSLTKLKGPLTMMASHYKQHCPPTPETSCATQIITFESFKENLKDFLLVIPFDCWEPVQE | 14434.5 | C639H1006N168O196S8 | 5.05 | NA | NA | NA | Sargramostim (127 residue glycoprotein) is a human recombinant granulocyte macrophage colony-stimulating factor expressed in yeast system. Substitution of Leu23 leads to a difference from native protein. | Used to treat cancer and in bone marrow transplant | Sargramostim is used in the treatment of bone marrow transplant recipients or those exposed to chemotherapy and recovering from acute myelogenous leukemia, Leukine or GM-CSF is a hematopoietic growth factor which stimulates the survival, clonal expansion (proliferation) and differentiation of hematopoietic progenitor cells. GM-CSF is also capable of activating mature granulocytes and macrophages. After a bone marrow transplant or chemotherapy, patients have a reduced capacity to produce red and white blood cells. Supplementing them with external sources of GM-CSF helps bring the level of neutrophils back to normal so that they can better fight infections. | Sargramostim binds to the Granulocyte-macrophage colony stimulating factor receptor which stimulates a JAK2 STAT1/STAT3 signal transduction pathway which leads to the production of hemopoietic cells and neutrophils | NA | NA | NA | NA | 420 mL/min/m2 [Normal people with liquid LEUKINE (IV)] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Colony-Stimulating Factors, Cytokines, Glycoproteins, Granulocyte-Macrophage Colony-Stimulating Factor, Hematopoietic Cell Growth Factors, Immunologic Factors, Increased Myeloid Cell Production, Intercellular Signaling Peptides and Proteins, Leukocyte Growth Factor, Peptides, Proteins | CA1341150 | 5-Dec-2000 | 5-Dec-2017 | NA | Granulocyte-macrophage colony-stimulating factor receptor subunit alpha,Interleukin-3 receptor subunit alpha,Cytokine receptor common subunit beta,Syndecan-2,Bone marrow proteoglycan | Leucomax | Novartis | Novartis | Used for reducing severe, life-threatening, or fatal infections after chemotherapy for acute myelogenous leukemia. It is also used to help increase the success of autologous bone marrow transplant and to help increase survival in patients who have bone ma | NA | NA | Solution | Subcutaneous and Intravenous infusion | In case of Intravenous Chemotherapy-induced neutropenia in adultS, 250 mcg/m2 daily for up to 42 days as required, to be given as IV infusion over 4 hr and in case of Intravenous Treatment and prevention of neutropenia in patients receiving myelosuppressivec chemotherapy. | NA | It is common to have aching bones and joints for 2-3 days starting 1-2 days after the start of the injections. This is usually mild and is caused by the bone marrow working harder to make white cells. Occasionally it is more troublesome and pain killers are required. | Link | NA | NA |
| 10125 | Th1017 | Sargramostim | >Th1017_Sargramostim APARSPSPSTQPWEHVNAIQEALRLLNLSRDTAAEMNETVEVISEMFDLQEPTCLQTRLELYKQGLRGSLTKLKGPLTMMASHYKQHCPPTPETSCATQIITFESFKENLKDFLLVIPFDCWEPVQE | 14434.5 | C639H1006N168O196S8 | 5.05 | NA | NA | NA | Sargramostim (127 residue glycoprotein) is a human recombinant granulocyte macrophage colony-stimulating factor expressed in yeast system. Substitution of Leu23 leads to a difference from native protein. | Used to treat cancer and in bone marrow transplant | Sargramostim is used in the treatment of bone marrow transplant recipients or those exposed to chemotherapy and recovering from acute myelogenous leukemia, Leukine or GM-CSF is a hematopoietic growth factor which stimulates the survival, clonal expansion (proliferation) and differentiation of hematopoietic progenitor cells. GM-CSF is also capable of activating mature granulocytes and macrophages. After a bone marrow transplant or chemotherapy, patients have a reduced capacity to produce red and white blood cells. Supplementing them with external sources of GM-CSF helps bring the level of neutrophils back to normal so that they can better fight infections. | Sargramostim binds to the Granulocyte-macrophage colony stimulating factor receptor which stimulates a JAK2 STAT1/STAT3 signal transduction pathway which leads to the production of hemopoietic cells and neutrophils | NA | NA | NA | NA | NA | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Colony-Stimulating Factors, Cytokines, Glycoproteins, Granulocyte-Macrophage Colony-Stimulating Factor, Hematopoietic Cell Growth Factors, Immunologic Factors, Increased Myeloid Cell Production, Intercellular Signaling Peptides and Proteins, Leukocyte Growth Factor, Peptides, Proteins | NA | NA | NA | NA | NA | Leukine | Berlex Laboratories Inc | Berlex Laboratories Inc | Leukine is used to increase white blood cells and help prevent serious infection in conditions such as leukemia, bone marrow transplant, and pre-chemotherapy blood cell collection. Leukine is used for adults who are at least 55 years old. | NA | The liquid vial and reconstituted lyophilized vial both contain 40 mg/mL mannitol, USP; 10 mg/mL sucrose, NF; and 1.2 mg/mL tromethamine, USP, as excipients | Sterile, preserved (1.1% benzyl alcohol), injectable solution (500 mcg/mL) and also as sterile, white, preservative free lyophilized powder (250 mcg) that requires reconstitution with 1 mL Sterile water for Injection | Subcutaneous Injection (Subcutaneous) or Intraveno | In Neutrophil Recovery, Chemotherapy in Acute Myelogenous Leukemia, the recommended dose is 250 mcg/m2/day, administered intravenously over a 4 hour period starting approximately on day 11 or four days following the completion of induction chemotherapy, if the day 10 bone marrow is hypoplastic with <5% blasts. | Allergy | High fever, chills, sore throat, stuffy nose, flu symptoms; white patches or sores inside your mouth or on your lips; easy bruising, unusual bleeding (nose, mouth, vagina, or rectum), purple or red pinpoint spots under your skin; swelling, rapid weight gain, chest pain, fast or uneven heart rate, weakness or fainting, black-bloody or tarry stools, coughing up blood, painful urination, clay-colored stools, jaundice, breathing problems and problems with vision, speech, balance or memory. | Link | NA | NA |
| 10135 | Th1019 | Peginterferon alfa-2b | >Th1019_Peginterferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 31000 | C130H219N43O42 | 5.99 | NA | 61 | Approximately 40 hours (range 22 to 60 hours) in patients with HCV infection | Peginterferon alfa-2b is a covalent conjugate of recombinant alfa-2b interferon with monomethoxy polyethylene glycol (PEG). The average molecular weight of the PEG portion of the molecule is 12,000 daltons. The average molecular weight of the PEG-Intron molecule is approximately 31,000 daltons. The specific activity of peginterferon alfa-2b is approximately 0.7 x 108 IU/mg protein. Interferon alfa-2b is a water-soluble protein with a molecular weight of 19,271 daltons produced by recombinant DNA techniques. It is obtained from the bacterial fermentation of a strain of Escherichia coli bearing a genetically engineered plasmid containing an interferon gene from human leukocytes. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | Used for the treatment of chronic hepatitis C in patients not previously treated with interferon alpha who have compensated liver disease and are at least 18 years of age. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds to type I interferon receptors IFNAR1 and IFNAR2c which upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | NA | NA | After a single subcutaneous dose of peginterferon alfa-2b, the mean absorption half-life was 4.6 hours. | NA | Oral cl=22 mL/hr/kg [patients with HCV infection], Renal elimination accounts for 30% of the clearance. | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 CYP2C9 Inducers, Cytochrome P-450 CYP2C9 Inducers (weak), Cytochrome P-450 CYP2D6 Inhibitors, Cytochrome P-450 CYP2D6 Inhibitors (weak), Cytochrome P-450 Enzyme Inducers, Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatitis C, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Macromolecular Substances, Myelosuppressive Agents, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | CA1341567 | 19-Feb-2008 | 19-Feb-2025 | Aminophylline. Interferon increases the effect and toxicity of theophylline | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | PEG-Intron | Schering Corp | Schering Corp | Used to treat chronic hepatitis C in adults. Peginterferon alfa-2b is often used in combination with another medication called ribavirin (Rebetol, Ribasphere) to treat hepatitis C in adults and children who are at least 3 years old. It may be used in comb | NA | Provided in both vials and the REDIPEN. Each vial contains either 74 mcg, 118.4 mcg, 177.6 mcg, or 222 mcg of PegIntron as a white to off-white tablet-like solid that is whole/in pieces or as a loose powder, and 1.11 mg dibasic sodium phosphate anhydrous, | Powder | Subcutaneous Injection | 1.5 mcg/kg/week. The volume of PegIntron to be injected depends on the strength of PegIntron and patient's body weight | Allergic or in case of having autoimmune hepatitis, liver failure, severe kidney disease, a hemoglobin blood cell disorder | Vision problems; fast heart rate, feeling like you might pass out; unusual weakness; high fever with severe stomach pain and bloody diarrhea; pain or burning when you urinate; severe pain in your upper stomach spreading to your back, nausea and vomiting and new or worsening liver symptoms. | Link | NA | NA |
| 10136 | Th1019 | Peginterferon alfa-2b | >Th1019_Peginterferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 31000 | C130H219N43O42 | 5.99 | NA | 61 | Approximately 40 hours (range 22 to 60 hours) in patients with HCV infection | Peginterferon alfa-2b is a covalent conjugate of recombinant alfa-2b interferon with monomethoxy polyethylene glycol (PEG). The average molecular weight of the PEG portion of the molecule is 12,000 daltons. The average molecular weight of the PEG-Intron molecule is approximately 31,000 daltons. The specific activity of peginterferon alfa-2b is approximately 0.7 x 108 IU/mg protein. Interferon alfa-2b is a water-soluble protein with a molecular weight of 19,271 daltons produced by recombinant DNA techniques. It is obtained from the bacterial fermentation of a strain of Escherichia coli bearing a genetically engineered plasmid containing an interferon gene from human leukocytes. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | Used for the treatment of chronic hepatitis C in patients not previously treated with interferon alpha who have compensated liver disease and are at least 18 years of age. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds to type I interferon receptors IFNAR1 and IFNAR2c which upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | NA | NA | After a single subcutaneous dose of peginterferon alfa-2b, the mean absorption half-life was 4.6 hours. | NA | Oral cl=22 mL/hr/kg [patients with HCV infection], Renal elimination accounts for 30% of the clearance. | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 CYP2C9 Inducers, Cytochrome P-450 CYP2C9 Inducers (weak), Cytochrome P-450 CYP2D6 Inhibitors, Cytochrome P-450 CYP2D6 Inhibitors (weak), Cytochrome P-450 Enzyme Inducers, Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatitis C, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Macromolecular Substances, Myelosuppressive Agents, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | CA2329474 | 26-Feb-2002 | 31-Oct-2016 | Dyphylline.Interferon increases the effect and toxicity of theophylline | NA | Sylatron | Merck Sharp & Dohme Corp. | Merck Sharp & Dohme Corp. | SYLATRON™ is an alpha interferon indicated for the adjuvant treatment of melanoma with microscopic or gross nodal involvement within 84 days of definitive surgical resection including complete lymphadenect | NA | NA | sterile, white to off-white lyophilized powder | Subcutaneous Injection | The recommended starting dose is 6 mcg/kg/week subcutaneously for 8 doses, followed by 3 mcg/kg/week subcutaneously for up to 5 years. Premedicate with acetaminophen 500 to 1000 mg orally 30 minutes prior to the first dose of SYLATRON and as needed for subsequent doses. The recommended starting doses of SYLATRON in patients with moderate or severe renal impairment or end-stage renal disease (ESRD) are listed in Table 1 [see Use In Specific Populations]. No dose adjustment is needed for patients with a creatinine clearance (CLcr) > 50 mL/min/1.73m². | SYLATRON is contraindicated in patients with: A history of anaphylaxis to peginterferon alfa-2b or interferon alfa-2b autoimmune hepatitis hepatic decompensation (Child-Pugh score >6 [class B and C]) | Headache, joint or muscle pain; nausea, dry mouth, loss of appetite, weight loss; dizziness, sleep problems (insomnia), feeling mildly anxious, depressed, or irritable; or pain, redness, swelling, or irritation where the medicine was injected. | Link | NA | NA |
| 10139 | Th1019 | Peginterferon alfa-2b | >Th1019_Peginterferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 31000 | C130H219N43O42 | 5.99 | NA | 61 | Approximately 40 hours (range 22 to 60 hours) in patients with HCV infection | Peginterferon alfa-2b is a covalent conjugate of recombinant alfa-2b interferon with monomethoxy polyethylene glycol (PEG). The average molecular weight of the PEG portion of the molecule is 12,000 daltons. The average molecular weight of the PEG-Intron molecule is approximately 31,000 daltons. The specific activity of peginterferon alfa-2b is approximately 0.7 x 108 IU/mg protein. Interferon alfa-2b is a water-soluble protein with a molecular weight of 19,271 daltons produced by recombinant DNA techniques. It is obtained from the bacterial fermentation of a strain of Escherichia coli bearing a genetically engineered plasmid containing an interferon gene from human leukocytes. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | Used for the treatment of chronic hepatitis C in patients not previously treated with interferon alpha who have compensated liver disease and are at least 18 years of age. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds to type I interferon receptors IFNAR1 and IFNAR2c which upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | NA | NA | After a single subcutaneous dose of peginterferon alfa-2b, the mean absorption half-life was 4.6 hours. | NA | Oral cl=22 mL/hr/kg [patients with HCV infection], Renal elimination accounts for 30% of the clearance. | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 CYP2C9 Inducers, Cytochrome P-450 CYP2C9 Inducers (weak), Cytochrome P-450 CYP2D6 Inhibitors, Cytochrome P-450 CYP2D6 Inhibitors (weak), Cytochrome P-450 Enzyme Inducers, Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatitis C, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Macromolecular Substances, Myelosuppressive Agents, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | NA | NA | NA | Aldesleukin | NA | Unitron PEG | Merck Ltd. | Merck Ltd. | It is used to treat chronic hepatitis C (a disease of the liver) for people who cannot tolerate or use the antiviral medication, ribavirin. The most effective treatment of chronic hepatitis C is the combination of an interferon and ribavirin. Unitron Peg | NA | NA | Lyophilized powder | Subcutaneous Injection | Its Subcutaneous injection once a week on the same day of the week for 48 weeks. Dosing is based on body weight. Treatment with this medication should be stopped if no response is noticed after 6 months. | Allergic | Abdominal pain or swelling, anemia (paleness, tiredness, shortness of breath), changes in mood (e.g., irritability, depression, anxiety, aggression), confusion, dizziness, eye pain or swelling of the eye, high blood sugar (increased thirst, hunger, weakness, irritability, trouble concentrating, signs of infection (e.g., chills, fever, cough, sore throat, difficulty or painful urination, difficulty breathing), burning sensation in arms or legs, ulcers in mouth or sore throats. | Link | NA | NA |
| 10142 | Th1020 | Asparaginase | >Th1020_Asparaginase MEFFKKTALAALVMGFSGAALALPNITILATGGTIAGGGDSATKSNYTVGKVGVENLVNAVPQLKDIANVKGEQVVNIGSQDMNDNVWLTLAKKINTDCDKTDGFVITHGTDTMEETAYFLDLTVKCDKPVVMVGAMRPSTSMSADGPFNLYNAVVTAADKASANRGVLVVMNDTVLDGRDVTKTNTTDVATFKSVNYGPLGYIHNGKIDYQRTPARKHTSDTPFDVSKLNELPKVGIVYNYANASDLPAKALVDAGYDGIVSAGVGNGNLYKSVFDTLATAAKTGTAVVRSSRVPTGATTQDAEVDDAKYGFVASGTLNPQKARVLLQLALTQTKDPQQIQQIFNQY | 31731.9 | C1377H2208N382O442S17 | 4.67 | 0.059 | NA | 8-30 hours | L-asparagine amidohydrolase from E. coli | To treat acute lympocytic leukemia and non-Hodgkins lymphoma | In most patients with acute leukemia, the malignant cells are dependent on an exogenous source of asparagine for survival. Normal cells, however, are able to synthesize asparagine and thus are affected less by the rapid depletion produced by treatment with the enzyme asparaginase. Elspar exploits a metabolic defect in asparagine synthesis of some malignant cells. | Asparaginase converts asparagine to aspartic acid and ammonia. It facilitates production of oxalo-acetate which is needed for general cellular metabolism. Some malignant cells lose the ability to produce asparagine and thus the loss of exogenous sources of asparagine leads to cell death. | NA | NA | NA | Apparent volume of distribution was slightly greater than the plasma volume. Asparaginase levels in cerebrospinal fluid were less than 1% of concurrent plasma levels | NA | Amidohydrolases, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Asparaginase, Asparagine-specific Enzyme, Enzymes, Enzymes and Coenzymes, Hydrolases, Narrow Therapeutic Index Drugs, Thyroxine-binding globulin inhibitors | NA | NA | NA | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | L-asparagine | Elspar | Lundbeck Inc. | Lundbeck Inc. | To treat acute lymphocytic leukemia. It is used along with other cancer medicines. Elspar is an antineoplastic agent that works by decreasing the amount of asparagine in the body, which kills certain leukemia cells | NA | Each vial contains 10,000 International Units of asparaginase and 80 mg of mannitol. | Lyophilized plug or powder | Intravenous or intramuSubcutaneousular. Intravenou | The recommended dose of Elspar is 6,000 International Units/m_ intramuscularly (IM) or intravenously (IV) three times a week. | Allergic | Fever, chills (see flu like symptoms), Nausea and vomiting, Allergic reaction, (sudden onset of wheezing, itching, rash, face swelling, agitation, low blood pressure). You will be monitored closely for this reaction, Poor appetite, Stomach cramping | Link | NA | NA |
| 10145 | Th1021 | Thyrotropin Alfa | >Th1021_Thyrotropin_Alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 | 25 ± 10 hours | Thyrotropin alfa is a recombinant form of thyroid stimulating hormone used in performing certain tests in patients who have or have had thyroid cancer. It is also used along with a radioactive agent to destroy remaining thyroid tissue in certain patients. | For detection of residueal or recurrent thyroid cancer | Binding of thyrotropin alfa to TSH receptors on normal thyroid epithelial cells or on well-differentiated thyroid cancer tissue stimulates iodine uptake and organification. Thyrogen is an exogenous source of human TSH that offers an additional diagnostic tool in the follow-up of patients with a history of well-differentiated thyroid cancer. | Binding of thyrotropin Alfa to the thyrotropin receptors found on any residual thyroid cells or tissues stimulates radioactive iodine uptake for better radiodiagnostic imaging. | NA | NA | Time to peak: Median: 10 hours (range: 3-24 hours) After a single intramuscular injection of 0.9 mg of thyrotropin alfa: Cmax= 116+38mU/L, Tmax=22+8.5 hours. AUC=5088+1728 mU·hr/L. | NA | Through kidney and liver | Agents used to treat hypothyroidism, Anterior Pituitary Lobe Hormones and Analogues, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Pituitary and Hypothalamic Hormones and Analogues, Pituitary Hormones, Pituitary Hormones, Anterior, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | US5840566 | 24-Nov-1998 | 24-Nov-2015 | NA | Thyrotropin receptor | Thyrogen | Genzyme Corporation , Genzyme Europe Bv | Genzyme Corporation , Genzyme Europe Bv | It is used in performing certain tests in patients who have or have had thyroid cancer. It is also used along with a radioactive agent to destroy remaining thyroid tissue in certain patients who have had their thyroid gland removed because of thyroid canc | NA | Each vial of THYROGEN contains 1.1 mg thyrotropin alfa, 36 mg Mannitol, 5.1 mg Sodium Phosphate, and 2.4 mg Sodium Chloride. | Lyophilized powder | IntramuSubcutaneousular preferably the buttocks | A 0.9 mg intramuscular injection to the buttock followed by a second 0.9 mg intramuscular injection to the buttock 24 hours later. | Allergic | Rash; hives; itching; difficulty breathing; tightness in the chest | Link | NA | NA |
| 10180 | Th1023 | Anakinra | >Th1023_Anakinra MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVVPIEPHALFLGIHGGKMCLSCVKSGDETRLQLEAVNITDLSENRKQDKRFAFIRSDSGPTTSFESAACPGWFLCTAMEADQPVSLTNMPDEGVMVTKFYFQEDE | 17257.6 | C759H1186N208O232S10 | 5.46 | -0.412 | NA | Healthy subjects = 4 - 6 hours | Anakinra is a recombinant, nonglycosylated human interleukin-1 receptor antagonist (IL-1Ra). The difference between anakinra and the native human IL-1Ra is that anakinra has an extra methionine residue at the amino terminus. It is manufactured by using the E. coli expression system. Anakinra is composed of 153 amino acid residues. FDA approved on November 14, 2001. | To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID). | Anakinra blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. IL-1 production is induced in response to inflammatory stimuli and mediates various physiologic responses including inflammatory and immunological responses. Patients with rheumatoid arthritis have elevated levels of IL-1. The levels of the naturally occurring IL-1Ra in synovium and synovial fluid from rheumatoid arthritis (RA) patients are not sufficient to compete with the elevated amount of locally produced IL-1. Increasing the levels of IL-1Ra by artificial means reduces the negative effects (cartilage degradation, bone resorption) of IL-1. | Anakinra binds competitively to the Interleukin-1 type I receptor (IL-1RI), thereby inhibiting the action of elevated levels IL-1 which normally can lead to cartilage degradation and bone resorption. | Most common adverse reactions (incidence 5%) are injection site reaction, worsening of rheumatoid arthritis, upper respiratory tract infection, headache, nausea, diarrhea, sinusitis, arthralgia, flu like-symptoms, and abdominal pain when anakinra is used | As a protein-based therapy, anakinra is expected to be metabolized by proteases throughout the body. | When a 70 mg subcutaneous bolus injection is given to healthy subjects, the absolute bioavailability is 95%. Accumulation does not occur following daily subcutaneous doses. Tmax, SubQ, 1-2 mg/kg, healthy subjects = 3-7 hours; Cmax, SubQ, 3 mg/kg once dail | 18.5 L | Clearance is variable and increases with increasing creatinine clearance and body weight. | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Factors, Biologics for Rheumatoid Arthritis Treatment, Cytokines, Disease-modifying Antirheumatic Agents, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interleukin Inhibitors, Interleukin-1 Receptor Antagonist, Peptides, Proteins | CA2141953 | 8-Apr-2008 | 17-Sep-2013 | Canakinumab results in increased immunosuppressive effects; increases the risk of infection. | Interleukin-1 receptor type 1 | Kineret | Amgen Inc | Amgen Inc | To treat the symptoms of moderate to severe rheumatoid arthritis in adults. Anakinra may also help slow the progress of the disease. | NA | The solution may contain trace amounts of small, translucent-to-white amorphous proteinaceous particles. Each prefilled glass syringe contains: 0.67 mL (100 mg) of anakinra in a solution (pH 6.5) containing disodium EDTA (0.12 mg), sodium chloride (5.48 m | Sterile, clear, colorless-to-white, preservative free solution | Subcutaneous (Subcutaneous) administration | 100 mg/day administered daily | Contraindicated in patients with known hypersensitivity to E coli-derived proteins, Kineret, or any components of the product | Nausea, diarrhea, stomach pain; headache; cold symptoms such as stuffy nose, sneezing, sore throat; or redness, bruising, pain, or swelling where the injection was given. | Link | NA | NA |
| 10205 | Th1027 | Insulin Regular | >Th1027_Insulin_Regular GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | 5.39 | 0.218 | 81 | 2-3.4 hours | Insulin regular is a 51 residue peptide hormone, composed of two amino acid chains covalently linked by disulfide bonds. The structure is identical to native human insulin. Recombinant insulin is synthesized by recombinant DNA techncology. Inserting the human insulin gene into the Escherichia coli bacteria or Saccharomyces cerevisiae produces insulin for human use. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults and children with type 1 and type 2 diabetes mellitus. | Insulin regular is a short-acting insulin. When subcutaneously administered, the onset of action (as evidenced by a decrease in glucose level) occurs 30 minutes post-dose. Maximal effect occurs between 1.5 and 3.5 hours post-dose. The glucose-lowering effect occurs 8 hours post-dose. Compared to other rapid-acting insulin analogs, insulin regular has a slower onset of action and longer duration of action. | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | Hypoglycemia is caused due to insulin toxicity. | Predominantly cleared by metabolic degradation via a receptor-mediated process. | Generally well absorbed. | 0.15 L/kg | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Insulin, Insulin, metabolism, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides | NA | NA | NA | Liraglutide's coadministration may increase the risk of hypoglycemia. A lower dose of the antidiabetic agent may be needed. | Insulin receptor,Insulin-like growth factor 1 receptor,Retinoblastoma-associated protein,Cathepsin D,Insulin-degrading enzyme,Neuroendocrine convertase 2,Carboxypeptidase E,Neuroendocrine convertase 1,Protein NOV homolog,Low-density lipoprotein receptor-r | Humulin R | Eli Lilly and Company | Eli Lilly and Company | Treating diabetes mellitus. | NA | It contains human insulin (rDNA origin) 100 units/mL, glycerin 16 mg/mL and metacresol 2.5 mg/mL, endogenous zinc (approximately 0.015 mg/100 units) and water for injection. The pH is 7.0 to 7.8. Sodiumhydroxide and/or hydrochloric acid may be added durin | Sterile, clear, aqueous, and colorless solution | Subcutaneous Injection in the abdominal wall, the | Humulin R (insulin (human recombinant)) U-100, when used subcutaneously, is usually given three or more times daily before meals. The average range of total daily insulin requirement for maintenance therapy in insulin-treated patients without severe insulin resistance lies between 0.5 and 1 unit/kg/day. | During episodes of hypoglycemia and in patients hypersensitive to humulin R. | Rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue; wheezing; muscle pain; changes in vision; chills; confusion; dizziness; drowsiness; fainting; fast or irregular heartbeat; headache; loss of apetite. | Link | NA | NA |
| 10208 | Th1027 | Insulin Regular | >Th1027_Insulin_Regular GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | 5.39 | 0.218 | 81 | 2-3.4 hours | Insulin regular is a 51 residue peptide hormone, composed of two amino acid chains covalently linked by disulfide bonds. The structure is identical to native human insulin. Recombinant insulin is synthesized by recombinant DNA techncology. Inserting the human insulin gene into the Escherichia coli bacteria or Saccharomyces cerevisiae produces insulin for human use. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults and children with type 1 and type 2 diabetes mellitus. | Insulin regular is a short-acting insulin. When subcutaneously administered, the onset of action (as evidenced by a decrease in glucose level) occurs 30 minutes post-dose. Maximal effect occurs between 1.5 and 3.5 hours post-dose. The glucose-lowering effect occurs 8 hours post-dose. Compared to other rapid-acting insulin analogs, insulin regular has a slower onset of action and longer duration of action. | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | Hypoglycemia is caused due to insulin toxicity. | Predominantly cleared by metabolic degradation via a receptor-mediated process. | Generally well absorbed. | 0.15 L/kg | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Insulin, Insulin, metabolism, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides | NA | NA | NA | NA | NA | Novolin R | Novo Nordisk | Novo Nordisk | Used for the treatment of patients with diabetes mellitus, for the control of hyperglycemia | NA | It contains human insulin (rDNA origin) 100 units/mL, glycerol 16 mg/mL, metacresol 3 mg/mL, zinc chloride approximately 7 mcg/mL and water for injection. The pH is adjusted to 7.4. Hydrochloric acid 2N or sodium hydroxide 2N may be added to adjust pH. No | Sterile, clear, aqueous, and colorless solution | Subcutaneous and Intravenous infusion | The injection of Novolin R (recombinant dna origin) should be followed by a meal within approximately 30 minutes of administration The average range of total daily insulin requirement for maintenance therapy in insulin-treated patients lies between 0.5 and 1.0 IU/kg. | During episodes of hypoglycemia and in patients with hypersensitivity to Novolin R | Hypoglycemia, or low blood sugar, is the most common side effect. Symptoms include headache, hunger, dizziness, sweating, irritability, trouble concentrating, rapid breathing, fast heartbeat, fainting, or seizure (severe hypoglycemia can be fatal). | Link | NA | NA |
| 10215 | Th1029 | Menotropins | >Th1029_Menotropins APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 23390.3 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | NA | Menotropins contains follicle stimulating hormone and luteinizing hormone purified from the urine of postmenopausal women. It is used as a fertility medication that is injected either subcutaneously or intramuscularly. It is composed of LH with 2 subunit alpha = 92 residues, beta = 121 residues and FSH with 2 subunits, alpha = 92 residues, beta=111 residues. | For the treatment of female infertility | Menotropins is used to treat female infertility, stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Menotropins bind to the LH/hCG/FSH receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Menotropins is a combination drug which binds to the Follicle stimulating hormone receptor (which results in ovulation in the absence of sufficient endogenous Luteinizing hormone)and it also binds to the LH receptor, thereby stimulating proper hormone release. The drug contains both FSH and LH,therefore, it induces ovarian follicular growth and development as well as gonadal steroid production in women who do not have ovarian failure.FSH is the primary driver of follicular recruitment and growth in early folliculogenesis, while LH is important for ovarian steroidogenesis and is involved in the physiological events leading to development of a competent pre-ovulatory follicle. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Products, Complex Mixtures, Fertility Agents, Fertility Agents, Female, Genito Urinary System and Sex Hormones, Gonadotropins, Gonadotropins and Antigonadotropins, Gonadotropins, Pituitary, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Peptides, Pituitary Hormones, Pituitary Hormones, Anterior, Reproductive Control Agents, Sex Hormones and Modulators of the Genital System | NA | NA | NA | Antagon (ganirelix) | Follicle-stimulating hormone receptor,Lutropin-choriogonadotropic hormone receptor | Menopur | Ferring Pharmaceuticals | Ferring Pharmaceuticals | Menotropins are used to stimulate ovulation (the release of an egg) when a woman's ovaries can produce a follicle but hormonal stimulation is deficient. Menotropins are also used to stimulate the development of multiple eggs for in vitro fertilization. Li | NA | Each vial of MENOPUR contains 75 International Units of follicle-stimulating hormone (FSH) activity and 75 International Units of luteinizing hormone (LH) activity, plus 21 mg lactose monohydrate and 0.005 mg Polysorbate 20 and Sodium Phosphate Buffer (So | Sterile, lyophilized powder which is reconstitution with Sterile 0.9% Sodium Chloride Injection. | Subcutaneous Injection | The dosing scheme for patients undergoing IVF follows a stepwise approach and is individualized for each woman. The recommended initial dose of MENOPUR for women who have received a GnRH agonist for pituitary suppression is 225 International Units. MENOPU | Hypersensitivity, high level of FSH indicating primary ovarian failure, cause fetal harm when administerd to prergnant woman, ex hormone dependent tumors of the reproductive tract and accessory organs. | Less than 2% of female patients treated with menotropins develop ovarian hyperstimulation syndrome (OHSS), especially after the first cycle of therapy. Symptoms of OHSS include swelling of the hands or legs, abdominal pain and swelling, shortness of breathing. | Link | NA | NA |
| 10218 | Th1029 | Menotropins | >Th1029_Menotropins APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 23390.3 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | NA | Menotropins contains follicle stimulating hormone and luteinizing hormone purified from the urine of postmenopausal women. It is used as a fertility medication that is injected either subcutaneously or intramuscularly. It is composed of LH with 2 subunit alpha = 92 residues, beta = 121 residues and FSH with 2 subunits, alpha = 92 residues, beta=111 residues. | For the treatment of female infertility | Menotropins is used to treat female infertility, stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Menotropins bind to the LH/hCG/FSH receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Menotropins is a combination drug which binds to the Follicle stimulating hormone receptor (which results in ovulation in the absence of sufficient endogenous Luteinizing hormone)and it also binds to the LH receptor, thereby stimulating proper hormone release. The drug contains both FSH and LH,therefore, it induces ovarian follicular growth and development as well as gonadal steroid production in women who do not have ovarian failure.FSH is the primary driver of follicular recruitment and growth in early folliculogenesis, while LH is important for ovarian steroidogenesis and is involved in the physiological events leading to development of a competent pre-ovulatory follicle. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Products, Complex Mixtures, Fertility Agents, Fertility Agents, Female, Genito Urinary System and Sex Hormones, Gonadotropins, Gonadotropins and Antigonadotropins, Gonadotropins, Pituitary, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Peptides, Pituitary Hormones, Pituitary Hormones, Anterior, Reproductive Control Agents, Sex Hormones and Modulators of the Genital System | NA | NA | NA | NA | NA | Repronex | Ferring Pharmaceuticals | Ferring Pharmaceuticals | Repronex is generally used as part of an assisted reproductive technology (ART) program to treat infertility in women. | NA | Each vial of Repronex (menotropins for injection) contains 75 International Units (IU) or 150 IU of follicle-stimulating hormone (FSH) activity and 75 IU or 150 IU of luteinizing hormone (LH) activity, respectively, plus 20 mg lactose monohydrate in a ste | Sterile, lyophilized form | Subcutaneous or intramuSubcutaneousular Injection. | The initial dose of Repronex (menotropins for injection) for patients who have received GnRH agonist or antagonist pituitary suppression is 150 IU daily for the first 5 days of treatment. Based on clinical monitoring (including serum estradiol levels and | A high FSH level indicating primary ovarian failure. | Rash; hives; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); breast pain or enlarged breasts; calf, leg, or arm pain, swelling, redness, or tenderness; change in balance | Link | NA | NA |
| 10226 | Th1030 | Interferon gamma-1b | >Th1030_Interferon_gamma-1b CYCQDPYVKEAENLKKYFNAGHSDVADNGTLFLGILKNWKEESDRKIMQSQIVSFYFKLFKNFKDDQSIQKSVETIKEDMNVKFFNSNKKKRDDFEKLTNYSVTDLNVQRKAIHELIQVMAELSPAAKTGKRKRSQMLFRGRRASQ | 17145.6 | C761H1206N214O225S6 | 9.54 | -0.823 | 61 | NA | Human Interferon gamma-1b (140 residues), produced from E. coli. Production of Actimmune is achieved by fermentation of a genetically engineered Escherichia coli bacterium containing the DNA which encodes for the human protein. Purification of the product is achieved by conventional column chromatography. The sequence displayed is a cDNA sequence which codes for human interferon gamma, as described by Gray et. al. and not specifically interferon gamma 1b. | To treat Chronic granulomatous disease and Osteopetrosis. | IFN gamma stimulates expression of the immunoglobulin heavy chain C gamma 3 and C gamma 2a germline transcripts in B cells. Many components of the antigen presentation pathways are also up-regulated by interferon gamma. It is also a potent activator of macrophages, it has antiproliferative effects on transformed cells and it can potentiate the antiviral and antitumor effects of type I interferons. Interferon gamma may also help the body regulate the activity of fibroblasts. By directly blocking the multiplication of fibroblasts and inhibiting the production and action of TGF-b, a potent scar-inducing molecule, Interferon gamma-1b may prevent excessive scarring. | It binds directly to the type II interferon gamma receptor IFNGR1, leading to a complex of IFNGR1 and IFNGR2. This activates JAK1 and JAK2 kinases which form a STAT1 docking site. This leads to STAT1 phosphorylation, nuclear translocation and initiation of gene transcription of multiple immune-related genes. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon gamma, Interferons, Lymphokines, Macrophage-Activating Factors, Myelosuppressive Agents, Peptides, Proteins | US6936695 | 30-Aug-2005 | 30-Aug-2022 | NA | Interferon gamma receptor 1,Interferon gamma receptor 2 | Actimmune | InterMune Inc, Hznp Usa, Inc., Horizon Therapeutics USA, Inc. | InterMune Inc, Hznp Usa, Inc., Horizon Therapeutics USA, Inc. | Used for reducing the number and severity of infections associated with chronic granulomatous disease. It is also used to delay the progression of severe, life-threatening bone density disease | NA | Each 0.5 mL of ACTIMMUNE contains 100 mcg (2 million IU) of Interferon gamma-1 b formulated in 20 mg mannitol, 0.36 mg sodium succinate, 0.05 mg polysorbate 20 and Sterile Water for Injection. | Sterile, clear, colorless solution | Subcutaneous Injection | Dose for the treatment of patients with Chronic Granulomatous Disease and severe, malignant osteopetrosis is 50 mcg/m2(1 million IU/m2) for patients whose body surface area is greater than 0.5 m2 and 1.5 mcg/kg/dose for patients whose body surface area is equal to or less than 0.5 m2. | Hypersensitivity | Diarrhea; fatigue; flu-like symptoms (eg, low-grade fever, chills, general body discomfort); headache; joint pain; muscle pain; nausea; pain, redness, or swelling at the injection site; tiredness; vomiting; weakness. Severe side efects include Severe dizziness and troubled breathing. | Link | NA | NA |
| 10229 | Th1031 | Interferon Alfa-2a, Recombinant | >Th1031_Interferon_Alfa-2a,_Recombinant CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 19241.1 | C860H1353N227O255S9 | 5.99 | -0.336 | NA | IM half-life of interferon alfa-2a is 6 hours to 8 hours | Its a type I interferon consisting of 165 amino acid residues with lysine in position 23. This protein is produced by recombinant DNA technology and resembles interferon secreted by leukocytes. It is used extensively as an antiviral or antineoplastic agent. An oral form is being developed by Amarillo Biosciences. | For the treatment of chronic hepatitis C, hairy cell leukemia, AIDS-related Kaposi's sarcoma, and chronic myelogenous leukemia. Also for the treatment of oral warts arising from HIV infection. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a bbetter target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds directly to the type II interferon gamma receptor IFNGR1, leading to a complex of IFNGR1 and IFNGR2. This activates JAK1 and JAK2 kinases which form a STAT1 docking site. This leads to STAT1 phosphorylation, nuclear translocation and initiation of gene transcription of multiple immune-related genes. | Interferon alfa-2 may cause serious adverse effects such as anemia; autoimmune diseases, including vasculitis, arthritis, hemolytic anemia, and erythematosus syndrome; cardiotoxicity; hepatotoxicity; hyperthyroidism or hypothyroidism; transient ischemic a | NA | Absorption is high (greater than 80%) when administered intramuscularly or subcutaneously. | 0.223 to 0.748 L/kg [healthy people] | 2.14 - 3.62 mL/min/kg [healthy] | Adjuvants, Immunologic, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Myelosuppressive Agents, Peptides, Proteins | CA2172664 | 3-Oct-2000 | 26-Mar-2016 | Interferon increases the effect and toxicity of theophylline | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | Roferon A | Hoffmann-La Roche Inc | Hoffmann-La Roche Inc | To treat chronic hepatitis C and hairy cell leukemia in patients 18 years of age or older. In addition, it is indicated for chronic phase, Philadelphia chromosome (Ph) positive chronic myelogenous leukemia (CML) patients who are minimally pretreated (with | NA | 3 million IU (11.1 mcg/0.5 mL) Roferon-A (interferon alfa-2a, recombinant) per syringe  The solution is colorless and each 0.5 mL contains 3 MIU of Interferon alfa-2a, recombinant, 3.605 mg sodium chloride, 0.1 mg polysorbate 80, 5 mg benzyl alcohol as a | Solution | Subcutaneous Injection | Dosage for the treatment of chronic hepatitis C is 3 MIU three times a week (tiw) administered subcutaneously for 12 months (48-52 weeks). As an alternative, patients may be treated with an induction dose of 6 MIU tiw for the first 3 months (12 weeks) followed by 3 MIU tiw for 9 months (36 weeks). | Hypersensitivity to Roferon-A (interferon alfa-2a, recombinant) or any of its components | Injection site reactions (pain/swelling/redness), headache, tiredness, diarrhea, upset stomach, loss of appetite, back pain, dizziness, dry mouth, taste changes, nausea, or vomiting may occur. Tooth and gum problems may sometimes occur during treatment. | Link | NA | NA |
| 10242 | Th1033 | Oprelvekin | >Th1033_Oprelvekin GPPPGPPRVSPDPRAELDSTVLLTRSLLADTRQLAAQLRDKFPADGDHNLDSLPTLAMSAGALGALQLPGVLTRLRADLLSYLRHVQWLRRAGGSSLKTLEPELGTLQARLDRLLRRLQLLMSRLALPQPPPDPPAPPLAPPSSAWGGIRAAHAILGGLHLTLDWAVRGLLLLKTRL | 19047.2 | C854H1411N253O235S2 | 11.16 | -0.07 | NA | 6.9 ± 1.7 hours | Oprelvekin, the active ingredient in Neumega is recombinant Interleukin eleven, which is produced in Escherichia coli by recombinant DNA technology. The protein has a molecular mass of approximately 19,000 daltons, and is non-glycosylated. The polypeptide is 177 amino acids in length (the natural IL-11 has 178). This alteration has not resulted in measurable differences in bioactivity either in vitro or in vivo. The primary hematopoietic activity of Neumega is stimulation of megakaryocytopoiesis and thrombopoiesis. In mice and nonhuman primate studies Neumega has shown potent thrombopoietic activity in compromised hematopoiesis, including moderately to severely myelosuppressed animals. In these studies, Neumega improved platelet nadirs and accelerated platelet recoveries compared to controls. In animal studies Oprelvekin also has non-hematopoetic activities. This includes the regulation of intestinal epithelium growth (enhanced healing of gastrointestinal lesions), the inhibition of adipogenesis, the induction of acute phase protein synthesis (e.g., fibrinogen), and inhibition of macrophageal released pro-inflammatory cytokines. | Increases reduced platelet levels due to chemotherapy. | Oprelvekin is indicated for the prevention of severe thrombocytopenia and the reduction of the need for platelet transfusions following myelosuppressive chemotherapy in adult patients with nonmyeloid malignancies who are at high risk of severe thrombocytopenia. The primary hematopoietic activity of Oprelvekin is stimulation of megakaryocytopoiesis and thrombopoiesis. Oprelvekin has shown potent thrombopoietic activity in individuals with compromised hematopoiesis | Oprelvekin binds to the interleukin 11 receptor which leads to a cascade of signal transduction events. IL-11 is a thrombopoietic growth factor that directly stimulates the proliferation of hematopoietic stem cells and megakaryocyte progenitor cells and induces megakaryocyte maturation resulting in increased platelet production. | NA | NA | Absolute bioavailability is over 80%. | NA | NA | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Cytokines, Intercellular Signaling Peptides and Proteins, Interleukins, Megakaryocyte Growth Factor, Peptides, Proteins | NA | NA | NA | Dihydrocodeine may increase the serum levels of opioid analgesics. It is recommended to monitor therapy for the signs and symptoms of respiratory depression and enhanced sedation. | Interleukin-11 receptor subunit alpha | Neumega | Wyeth Pharmaceuticals | Wyeth Pharmaceuticals | Prevention of severe reductions in the number of blood clotting cells (platelets) caused by some chemotherapy | NA | Neumega is formulated in single-use vials containing 5 mg of oprelvekin (specific activity approximately 8 x 106 Units/mg) as a sterile, lyophilized powder with 23 mg Glycine, USP, 1.6 mg Dibasic Sodium Phosphate Heptahydrate, USP, and 0.55 mg Monobasic S | Sterile, lyophilized powder | It must be Subcutaneous Injection not in the muSub | The recommended dose of Neumega in adults with severe renal impairment(creatinine clearance<30 mL/min) is 25 µg/kg. An estimate of the patient's creatinine clearance(CLcr) in mL/min is required. CLcr in mL/min may be estimated from a spot serum creatinine determination. | In patients with a history of hypersensitivity to Neumega or any component of the product. | Chills; constipation; cough; diarrhea; dizziness; fever; flushing; hair loss; headache; increased cough; indigestion; inflammation or sores of the mouth or lips; joint pain; loss of appetite; mild swelling of the arms and legs; muscle pain; nausea; nervousness. | Link | NA | NA |
| 10252 | Th1035 | Glucagon recombinant | >Th1035_Glucagon_recombinant HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | -1.197 | NA | 0.43 hours for an intramuscular dose | Glucagon is a 29 residue peptide hormone, synthesized in a special non- pathogenic laboratory strain of Escherichia coli bacteria that has been genetically altered by the addition of the gene for glucagons. | Used to treat severe hypoglycemia, also used in gastrointestinal imaging. | Used in the treatment of hypoglycemia and in gastric imaging, glucagon increases blood glucose concentration and is used in the treatment of hypoglycemia. Glucagon acts only on liver glycogen, converting it to glucose through the release of insulin. It also relaxes the smooth muscles of the gastrointestinal tract. | Glucagon binds the glucagon receptor(G protein-coupled receptor located in the plasma membrane) which then initiates a dual signaling pathway using both adenylate cyclase activation and increased intracellular calcium. Adenylate cyclase manufactures cAMP (cyclic AMP), which activates protein kinase A (cAMP-dependent protein kinase). This enzyme, in turn, activates phosphorylase kinase, which, in turn, phosphorylates glycogen phosphorylase, converting into the active form called phosphorylase A. Phosphorylase A is the enzyme responsible for the release of glucose-1-phosphate from glycogen polymers. This yields glucose molecules to be released into the blood. Glucagon receptors are found in the liver, kidney, brain and pancreatic islet cells. The glucagon mediated signals lead to an increase in insulin excretion | atients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium. Phentolamine may be given to control blood pressure. Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia. | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma. | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes. A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes | 0.25 L/kg | 13.5 mL/min/kg [Adults with IV 1 mg] | Amino Acids, Peptides, and Proteins, Antihypoglycemic Agent, Decreased GI Motility, Decreased GI Smooth Muscle Tone, Decreased Glycolysis, Gastrointestinal Agents, Gastrointestinal Hormones, Gastrointestinal Motility Inhibitor, Glucagon, antagonists & inhibitors, Glycogenolytic Agents, Glycogenolytic Hormones, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Increased Gluconeogenesis, Increased Glycogenolysis, Pancreatic Hormones, Peptide Hormones, Peptides, Proglucagon, Protein Precursors, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | NA | NA | NA | NA | Glucagon receptor,Glucagon-like peptide 2 receptor,Glucagon-like peptide 1 receptor | GlucaGen | Novo Nordisk, Boehringer Ingelheim Pharmaceuticals, Inc. | Novo Nordisk, Boehringer Ingelheim Pharmaceuticals, Inc. | GlucaGen is used to treat severe hypoglycemic (low blood sugar) reactions which may occur in patients with diabetes mellitus treated with insulin. It is also used as a diagniostic aid. GlucaGen is indicated for use during radiologic examinations to tempor | NA | The reconstituted solution contains glucagon as hydrochloride 1 mg/mL (1 unit/mL) and lactose monohydrate (107 mg). GlucaGen is supplied at pH 2.5-3.5 and is soluble in water. | Sterile, lyophilized white powder | Subcutaneous, intramuSubcutaneousular, or Intraven | Inject 1 mL (adults and children, weighing more than 55 lbs (25 kg)) or 0.5 mL (children weighing less than 55 lbs (25 kg)) subcutaneously, intramuscularly, or intravenously. If the weight is not known: children younger than 6 years should be given a 0.5 | Hypersensitivity | Severe side effects are very rare, although nausea and vomiting may occur occasionally especially with doses above 1 mg or with rapid injection (less than 1 minute). You may also have rapid heart beat for a short while. | Link | NA | NA |
| 10254 | Th1035 | Glucagon recombinant | >Th1035_Glucagon_recombinant HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | -1.197 | NA | 0.53 hours for subcutaneous auto-injector or pre-filled syringe | Glucagon is a 29 residue peptide hormone, synthesized in a special non- pathogenic laboratory strain of Escherichia coli bacteria that has been genetically altered by the addition of the gene for glucagons. | Used to treat severe hypoglycemia, also used in gastrointestinal imaging. | Used in the treatment of hypoglycemia and in gastric imaging, glucagon increases blood glucose concentration and is used in the treatment of hypoglycemia. Glucagon acts only on liver glycogen, converting it to glucose through the release of insulin. It also relaxes the smooth muscles of the gastrointestinal tract. | Glucagon binds the glucagon receptor(G protein-coupled receptor located in the plasma membrane) which then initiates a dual signaling pathway using both adenylate cyclase activation and increased intracellular calcium. Adenylate cyclase manufactures cAMP (cyclic AMP), which activates protein kinase A (cAMP-dependent protein kinase). This enzyme, in turn, activates phosphorylase kinase, which, in turn, phosphorylates glycogen phosphorylase, converting into the active form called phosphorylase A. Phosphorylase A is the enzyme responsible for the release of glucose-1-phosphate from glycogen polymers. This yields glucose molecules to be released into the blood. Glucagon receptors are found in the liver, kidney, brain and pancreatic islet cells. The glucagon mediated signals lead to an increase in insulin excretion | atients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium. Phentolamine may be given to control blood pressure. Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia. | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma. | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes. A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes | 0.25 L/kg | 13.5 mL/min/kg [Adults with IV 1 mg] | Amino Acids, Peptides, and Proteins, Antihypoglycemic Agent, Decreased GI Motility, Decreased GI Smooth Muscle Tone, Decreased Glycolysis, Gastrointestinal Agents, Gastrointestinal Hormones, Gastrointestinal Motility Inhibitor, Glucagon, antagonists & inhibitors, Glycogenolytic Agents, Glycogenolytic Hormones, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Increased Gluconeogenesis, Increased Glycogenolysis, Pancreatic Hormones, Peptide Hormones, Peptides, Proglucagon, Protein Precursors, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | NA | NA | NA | NA | NA | Gvoke | Xeris Pharmaceuticals, Inc. | Xeris Pharmaceuticals, Inc. | symptoms of severe Hypoglycemia. | C153H225N43O49S | Glucagon is a single chain containing 29 amino acid residues and has a molecular weight of 3483 and is identical to human glucagon. Glucagon is produced by solid phase synthesis with subsequent purification. | clear, colorless to pale yellow, sterile solution | subcutaneous injection | Adults and Pediatric Patients Aged 12 and Older: The recommended dose of GVOKE is 1 mg administered by subcutaneous injection into lower abdomen, outer thigh, or outer upper arm. If there has been no response after 15 minutes, an additional 1 mg dose of GVOKE from a new device may be administered while waiting for emergency assistance. Pediatric Patients Aged 2 To Under 12 Years Of Age: The recommended dose for pediatric patients who weigh less than 45 kg is 0.5 mg GVOKE administered by subcutaneous injection into the lower abdomen, outer thigh, or outer upper arm. The recommended dose for pediatric patients who weigh 45 kg or greater is 1 mg GVOKE administered by subcutaneous injection into the lower abdomen, outer thigh, or outer upper arm. If there has been no response after 15 minutes, an additional weight appropriate dose of GVOKE from a new device may be administered while waiting for emergency assistance. | GVOKE is contraindicated in patients with: Pheochromocytoma Insulinoma because of the risk of hypoglycemia Known hypersensitivity to glucagon or to any of the excipients in GVOKE. Allergic reactions have been reported with glucagon and include anaphylactic shock with breathing difficulties and hypotension | nausea, vomiting, and swelling where the injection was given | Link | NA | NA |
| 10255 | Th1035 | Glucagon recombinant | >Th1035_Glucagon_recombinant HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | -1.197 | NA | NA | Glucagon is a 29 residue peptide hormone, synthesized in a special non- pathogenic laboratory strain of Escherichia coli bacteria that has been genetically altered by the addition of the gene for glucagons. | Used to treat severe hypoglycemia, also used in gastrointestinal imaging. | Used in the treatment of hypoglycemia and in gastric imaging, glucagon increases blood glucose concentration and is used in the treatment of hypoglycemia. Glucagon acts only on liver glycogen, converting it to glucose through the release of insulin. It also relaxes the smooth muscles of the gastrointestinal tract. | Glucagon binds the glucagon receptor(G protein-coupled receptor located in the plasma membrane) which then initiates a dual signaling pathway using both adenylate cyclase activation and increased intracellular calcium. Adenylate cyclase manufactures cAMP (cyclic AMP), which activates protein kinase A (cAMP-dependent protein kinase). This enzyme, in turn, activates phosphorylase kinase, which, in turn, phosphorylates glycogen phosphorylase, converting into the active form called phosphorylase A. Phosphorylase A is the enzyme responsible for the release of glucose-1-phosphate from glycogen polymers. This yields glucose molecules to be released into the blood. Glucagon receptors are found in the liver, kidney, brain and pancreatic islet cells. The glucagon mediated signals lead to an increase in insulin excretion | atients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium. Phentolamine may be given to control blood pressure. Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia. | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma. | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes. A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes | 0.25 L/kg | 13.5 mL/min/kg [Adults with IV 1 mg] | Amino Acids, Peptides, and Proteins, Antihypoglycemic Agent, Decreased GI Motility, Decreased GI Smooth Muscle Tone, Decreased Glycolysis, Gastrointestinal Agents, Gastrointestinal Hormones, Gastrointestinal Motility Inhibitor, Glucagon, antagonists & inhibitors, Glycogenolytic Agents, Glycogenolytic Hormones, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Increased Gluconeogenesis, Increased Glycogenolysis, Pancreatic Hormones, Peptide Hormones, Peptides, Proglucagon, Protein Precursors, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | NA | NA | NA | Walfarin- Glucagon may increase the anticoagulant effect of warfarin (Coumadin) and other anticoagulants causing an increase in the slow clotting of blood and a greater risk of developing an episode of bleeding. | NA | Glucagon | Eli Lilly, Fresenius Kabi USA, LLC,TYA Pharmaceuticals, A-S Medication Solutions, Physicians Total Care, Inc. | Eli Lilly, Fresenius Kabi USA, LLC,TYA Pharmaceuticals, A-S Medication Solutions, Physicians Total Care, Inc. | Glucagon is used to increase the blood glucose level in severe hypoglycemia (low blood glucose). Glucagon is a glucose-elevating drug | NA | Glucagon is available as an emergency kit. The kit contains freeze-dried glucagon as a powder for injection 1 ml syringe of diluent. The powder contains 1 mg (1 unit) of glucagon and 49 mg of lactose. The diluent contains 12 mg/ml of glycerine, water for | Powder | Subcutaneously or intramuSubcutaneousularly Inject | Adults and children weighing 44 pounds or more should receive 1mg (1 unit) of glucagon | Allergy | Nausea and vomiting may occur occasionally after injection of glucagon, but this may be a symptom of the hypoglycemia for which glucagon is being given. Rare allergic-type reactions may occur with glucagon including itching, respiratory distress, or low blood pressure. | Link | NA | NA |
| 10263 | Th1037 | Botulinum Toxin Type B | >Th1037_Botulinum_Toxin_Type_B MPVTINNFNYNDPIDNNNIIMMEPPFARGTGRYYKAFKITDRIWIIPERYTFGYKPEDFNKSSGIFNRDVCEYYDPDYLNTNDKKNIFLQTMIKLFNRIKSKPLGEKLLEMIINGIPYLGDRRVPLEEFNTNIASVTVNKLISNPGEVERKKGIFANLIIFGPGPVLNENETIDIGIQNHFASREGFGGIMQMKFCPEYVSVFNNVQENKGASIFNRRGYFSDPALILMHELIHVLHGLYGIKVDDLPIVPNEKKFFMQSTDAIQAEELYTFGGQDPSIITPSTDKSIYDKVLQNFRGIVDRLNKVLVCISDPNININIYKNKFKDKYKFVEDSEGKYSIDVESFDKLYKSLMFGFTETNIAENYKIKTRASYFSDSLPPVKIKNLLDNEIYTIEEGFNISDKDMEKEYRGQNKAINKQAYEEISKEHLAVYKIQMCKSVKAPGICIDVDNEDLFFIADKNSFSDDLSKNERIEYNTQSNYIENDFPINELILDTDLISKIELPSENTESLTDFNVDVPVYEKQPAIKKIFTDENTIFQYLYSQTFPLDIRDISLTSSFDDALLFSNKVYSFFSMDYIKTANKVVEAGLFAGWVKQIVNDFVIEANKSNTMDKIADISLIVPYIGLALNVGNETAKGNFENAFEIAGASILLEFIPELLIPVVGAFLLESYIDNKNKIIKTIDNALTKRNEKWSDMYGLIVAQWLSTVNTQFYTIKEGMYKALNYQAQALEEIIKYRYNIYSEKEKSNINIDFNDINSKLNEGINQAIDNINNFINGCSVSYLMKKMIPLAVEKLLDFDNTLKKNLLNYIDENKLYLIGSAEYEKSKVNKYLKTIMPFDLSIYTNDTILIEMFNKYNSEILNNIILNLRYKDNNLIDLSGYGAKVEVYDGVELNDKNQFKLTSSANSKIRVTQNQNIIFNSVFLDFSVSFWIRIPKYKNDGIQNYIHNEYTIINCMKNNSGWKISIRGNRIIWTLIDINGKTKSVFFEYNIREDISEYINRWFFVTITNNLNNAKIYINGKLESNTDIKDIREVIANGEIIFKLDGDIDRTQFIWMKYFSIFNTELSQSNIEERYKIQSYSEYLKDFWGNPLMYNKEYYMFNAGNKNSYIKLKKDSPVGEILTRSKYNQNSKYINYRDLYIGEKFIIRRKSNSQSINDDIVRKEDYIYLDFFNLNQEWRVYTYKYFKKEEEKLFLAPISDSDEFYNTIQIKEYDEQPTYSCQLLFKKDEESTDEIGLIGIHRFYESGIVFEEYKDYFCISKWYLKEVKRKPYNLKLGCNWQFIPKDEGWTE | 150804 | C690H1115N177O202S6 | NA | NA | NA | NA | Neurotoxin produced by fermentation of clostridium botulinum type B. The protein exists in noncovalent association with hemagglutinin and nonhemagglutinin proteins as a neurotoxin complex. The neurotoxin complex is recovered from the fermentation process. | To treat patients with cervical dystonia to reduce the severity of abnormal head position and neck pain associated with cervical dystonia. | Botulinum Toxin Type B inhibits acetylcholine release at the neuromuscular junction via a three stage process: 1) Heavy Chain mediated neurospecific binding of the toxin, 2) internalization of the toxin by receptor-mediated endocytosis, and 3) ATP and pH dependent translocation of the Light Chain to the neuronal cytosol where it acts as a zinc-dependent endoprotease cleaving polypeptides essential for neurotransmitter release. | Botulinum Toxin Type B binds and cleaves the synaptic Vesicle Associated Membrane Protein (VAMP, also known as synaptobrevin) which is a component of the protein complex responsible for docking and fusion of the synaptic vesicle to the presynaptic membrane, a necessary step to neurotransmitter release. | One unit of Botulinum Toxin Type B corresponds to the calculated median lethal intraperitoneal dose (LD50) in mice. | NA | Botulinum Toxin Type B is not expected to be present in the peripheral blood at measurable levels following IM injection at the recommended doses as pharmacokinetic or ADME studies were not performed | NA | NA | Acetylcholine Release Inhibitors, Agents that produce neuromuscular block (indirect), Amino Acids, Peptides, and Proteins, Amphibian Venoms, Anti-Dyskinesia Agents, Bacterial Proteins, Bacterial Toxins, Biological Factors, Botulinum Toxins, Central Nervous System Agents, Central Nervous System Depressants, Cholinergic Agents, Complex Mixtures, Endopeptidases, Enzymes, Enzymes and Coenzymes, Ganglion Blockers, Hydrolases, Membrane Transport Modulators, Metalloendopeptidases, Metalloproteases, Muscle Relaxants, Muscle Relaxants, Peripherally Acting Agents, Musculo-Skeletal System, Neurotoxins, Neurotransmitter Agents, Other Miscellaneous Therapeutic Agents, Peptide Hydrolases, Proteins, Toxins, Biological, Venoms | NA | NA | NA | The effect of administering different botulinum neurotoxin serotypes concurrently is unknown. However, in clinical studies, NeuroBloc was administered 16 weeks after the injection of Botulinum Toxin Type A. Co-administration of NeuroBloc and aminoglycos | NA | Neurobloc | Sloan Pharma S.A.R.L | Sloan Pharma S.A.R.L | NeuroBloc is indicated for the treatment of cervical dystonia (torticollis) in adults. It means Neurobloc is used to treat muscle spasms of the neck | NA | Medicines contain active ingredients and may also contain other, additional ingredients that help ensure the stability, safety and effectiveness of the medicine. Some may be used to prolong the life of the medicine. Neurobloc contains botulinum toxin type | Clear and colourless to light yellow solution | IntramuSubcutaneousular Injection | The initial dose is 10,000 U and should be divided between the two to four most affected muscles. Data from clinical studies suggest that efficacy is dose dependent, but these trials, because they were not powered for a comparison, do not show a significant difference between 5000 U and 10,000 U. | Hypersensitivity | Dry mouth, dysphagia, dyspepsia, and injection site pain. | Link | NA | NA |
| 10265 | Th1038 | Omalizumab | >Th1038_Omalizumab EVQLVESGGGLVQPGGSLRLSCAVSGYSITSGYSWNWIRQAPGKGLEWVASITYDGSTNYADSVKGRFTISRDDSKNTFYLQMNSLRAEDTAVYYCARGSHYFGHWHFAVWGQGTLVTVSSGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | C6450H9916N1714O2023S38 | 6.6 - 7.2 | -0.432 | 61(FAB fra | 624 hours | A recombinant DNA-derived humanized IgG1k monoclonal antibody that selectively binds to human immunoglobulin E. Xolair is produced by a Chinese hamster ovary cell suspension culture in a nutrient medium containing the antibiotic gentamicin. | For treatment of asthma caused by allergies | Xolair inhibits the binding of IgE to the high-affinity IgE receptor (FceRI) on the surface of mast cells and basophils. Reduction in surface-bound IgE on FceRI-bearing cells limits the degree of release of mediators of the allergic response. Xolair is used to treat severe, persisten asthma. | Xolair binds to IgE (a class of antibodies normally secreted in allergic responses), which prevents their binding to mast cells and basophils. | Anaphylaxis may occur rarely with this agent, either after the first dose or multiple doses | Most likely removed by opsonization via the reticuloendothelial system. | bioavailability of 62% | 78 ± 32 mL/kg | Liver elimination of IgG includes degradation in the liver reticuloendothelial system (RES) and endothelial cells. Intact IgG is also excreted in bile. | Agents to Treat Airway Disease, Amino Acids, Peptides, and Proteins, Anti-Allergic Agents, Anti-Asthmatic Agents, Anti-IgE, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Blood Proteins, Decreased IgE Activity, Globulins, IgE-directed Antibody Interactions, Immunoglobulins, Immunoproteins, Proteins, Respiratory Agents, Miscellaneous, Respiratory System Agents, Serum Globulins | CA2113813 | 12-Apr-2005 | 14-Aug-2012 | NA | High affinity immunoglobulin epsilon receptor subunit alpha and beta | Xolair | Genentech Inc, Novartis Europharm Limited | Genentech Inc, Novartis Europharm Limited | Xolair is used to treat moderate to severe asthma that is caused by allergies, and chronic idiopathic urticaria (a form of chronic hives) in adults and children who are at least 12 years old. Xolair is usually given after other asthma medications have bee | NA | Formulated in a single use vial that is reconstituted with sterile water for injection (SWFI), USP, and administered as a subcutaneous (SC) injection. Each 202.5 mg vial of omalizumab also contains L-histidine (1.8 mg), L-histidine hydrochloride monohydra | Sterile, white, preservative free, lyophilized powder | Subcutaneous Injection | Xolair is administered at 150 to 375 mg by subcutaneous injection every 2 or 4 weeks. Determine doses (mg) and dosing frequency by serum total IgE level (IU/mL), measured before the start of treatment, and body weight (kg) as if serum IgE is less than 30-or >700 IU/mL and <66 or >330 lb, respectively) should not be dosed. | Severe hypersensitivity | Wheezing, tightness in your chest, trouble breathing; hives or skin rash; feeling anxious or light-headed, fainting; warmth or tingling under your skin; or swelling of your face, lips, tongue, or throat. | Link | NA | NA |
| 10269 | Th1039 | Lutropin alfa | >Th1039_Lutropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 30000 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | approximately 18 hours | Lutropin alfa is a recombinant human luteinizing hormone produced in yeast with 2 subunits, alpha = 92 residues, beta = 121 residues. It is a heterodimeric glycoprotein. Each monomeric unit is a glycoprotein molecule. In females, an acute rise of LH(LH surge) triggers ovulation and the development of the corpus luteum. In males, it stimulates Leydig cell production of testosterone. Lutropin alfa was the first and only recombinant human form of luteinizing hormone (LH) developed for use in the stimulation of follicular development. | For treatment of female infertility | Used to facilitate female conception, lutropin alfa performs the same actions as luteinizing hormone, which is normally produced in the pituitary gland. Lutropin is usually given in combination with follitropin alfa. In females, a LH surge about halfway through the menstrual cycle triggers the onset of ovulation. LH also induces the ovulated follicle to become a corpus luteum, which then secretes progesterone. | Binds to the luteinizing hormone receptor which then activates adenylate cylcase through G protein mediation. Adenylate cyclase then activates many other pathways leading to steroid hormone production and other follicle maturation processes. | Lutropin alfa is not indicated for people under 16 and over 60, pregnant and lactating women, patients with uncontrolled thyroid and adrenal failure, patients with active, untreated tumours of the hypothalamus and pituitary gland, and in any patient with a condition that makes a normal pregnancy possible such as primary ovarian failure or fibroid tumors of the uterus. | <5% of dose excreted renally as unchanged drug. | bioavailability is 56% | 10 L | 2-3 L/h [healthy female following subcutaneous administration]. Total body clearance is approximately 2 to 3 L/h with less than 5 percent of the dose being excreted unchanged renally. | Genito Urinary System and Sex Hormones, Gonadotropins | US5767251 | 16-Jun-1998 | 16-Jun-2015 | Other drugs may interact with lutropin alfa, including prescription and over-the-counter medicines, vitamins, and herbal products | Lutropin-choriogonadotropic hormone receptor | Luveris | Serono, Merck Europe B.V. | Serono, Merck Europe B.V. | Luveris is used together with follitropin alfa to treat infertility in women with LH deficiency. | NA | One vial contains 75 IU of lutropin alfa (recombinant human Luteinising Hormone {r-hLH}) and following excipeint is present; Powder:Sucrose,Disodium phosphate dihydrate,Sodium dihydrogen phosphate monohydrate,Polysorbate 20,Phosphoric acid, concentrated ( | White lyophilised pellet withg clear colourless solvent to make solution | Subcutaneous (Subcutaneous) administration | It is recommended that 75 IU Luveris be concomitantly administered subcutaneously with 75 IU to 150 IU Gonal-f as two separate injections in the initial treatment cycle | Hypersensitivity | Nausea, stomach pain, diarrhea, constipation, gas; pelvic pain, menstrual cramps; breast pain; headache; pain or irritation where the injection was given; tired feeling; or cold symptoms such as stuffy nose, sneezing, sore throat. | Link | NA | NA |
| 10275 | Th1040 | Insulin Lispro | >Th1040_Insulin_Lispro GIVEQCCTSICSLYQLENYCN | 5808 | C257H387N65O76S6 | 5.39 | 0.218 | 81 | On subcutaneous administration = 1 hour | Insulin lispro is a recombinant human insulin analogue produced in a specialized laboratory strain of Escherischia coli. Plasmid DNA transfected into the bacteria encodes for an analogue of human insulin that has a lysine at residuce B28 and proline at B29; these residues are reversed in endogenous human insulin. Reversal of these amino acid residues produces a rapid-acting insulin analogue. FDA approved on 1996. | To treat type 1 or 2 diabetes mellitus. To be used in conjunction with an intermediate or long-acting insulin except when used in a continuous insulin infusion pump. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin lispro binds to the insulin receptor(IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Reversal of the proline and lysine residues at positions B28 and B29 of native insulin eliminates hydrophobic interactions and weakens some of the hydrogen bonds that contribute to the stability of the insulin dimers that comprise insulin hexamers. Hexamers of insulin lispro are produced in the presence of zinc and -cresol. These weakly associated hexamers quickly dissociate upon subcutaneous injection and are absorbed as monomers through vascular endothelial cells. These properties give insulin lispro its fast-acting properties. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process. | Rapidly absorbed following subcutaneous administration. It is also absorbed more quickly than regular human insulin. Peak serum levels occur 30-90 minutes after injection in healthy subjects. Absorption also differs depending on the site of injection. Aft | When administered intravenously as bolus injections of 0.1 and 0.2 U/kg dose in two separate groups of healthy subjects, the mean volume of distribution of insulin lispro appeared to decrease with increase in dose (1.55 and 0.72 L/kg, respectively). | Clearance is dose dependent. When a dose of 0.1 unit/kg and 0.2 unit/kg were administered intravenously, the mean clearance was 21.0 mL/min/kg and 9.6 mL/min/kg respectively. | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Insulin, Insulin Analog, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides | US5474978 | 12-Dec-1995 | 16-Jun-2014 | The beta-blocker, acebutolol, atenolol, bisoprolol, carvedilol, may decrease symptoms of hypoglycemia. | Insulin receptor,Insulin-like growth factor 1 receptor | Humalog | Eli Lilly | Eli Lilly | Humalog is used to treat type 1 diabetes in adults. It is usually given together with another long-acting insulin. Humalog is also used together with oral medications to treat type 2 diabetes in adults. | NA | Each milliliter of HUMALOG contains insulin lispro 100 units, 16 mg glycerin, 1.88 mg dibasic sodium phosphate, 3.15 mg Metacresol, zinc oxide content adjusted to provide 0.0197 mg zinc ion, trace amounts of phenol, and Water for Injection. Insulin lispro | Sterile, aqueous, clear, and colorless solution | Subcutaneous and Intravenous infusion | The total daily insulin requirement may vary and is usually between 0.5 to 1 unit/kg/day. Insulin requirements may be altered during stress, major illness, or with changes in exercise, meal patterns, or coadministered drugs. Usual maintenance range is 0.5-1 unit/kg/day in divided doses; nonobese may require 0.4-0.6 unit/kg/day; obese may require 0.8-1.2 units/kg/day. | During episodes of hypoglycemia in patients who are hypersensitive to HUMALOG or to any of its excipients. | Low blood sugar--headache, hunger, weakness, sweating, confusion, irritability, dizziness, fast heart rate, or feeling jittery. | Link | NA | NA |
| 10276 | Th1040 | Insulin Lispro | >Th1040_Insulin_Lispro GIVEQCCTSICSLYQLENYCN | 5808 | C257H387N65O76S6 | 5.39 | 0.218 | 81 | On subcutaneous administration = 1 hour | Insulin lispro is a recombinant human insulin analogue produced in a specialized laboratory strain of Escherischia coli. Plasmid DNA transfected into the bacteria encodes for an analogue of human insulin that has a lysine at residuce B28 and proline at B29; these residues are reversed in endogenous human insulin. Reversal of these amino acid residues produces a rapid-acting insulin analogue. FDA approved on 1996. | To treat type 1 or 2 diabetes mellitus. To be used in conjunction with an intermediate or long-acting insulin except when used in a continuous insulin infusion pump. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin lispro binds to the insulin receptor(IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Reversal of the proline and lysine residues at positions B28 and B29 of native insulin eliminates hydrophobic interactions and weakens some of the hydrogen bonds that contribute to the stability of the insulin dimers that comprise insulin hexamers. Hexamers of insulin lispro are produced in the presence of zinc and -cresol. These weakly associated hexamers quickly dissociate upon subcutaneous injection and are absorbed as monomers through vascular endothelial cells. These properties give insulin lispro its fast-acting properties. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process. | Rapidly absorbed following subcutaneous administration. It is also absorbed more quickly than regular human insulin. Peak serum levels occur 30-90 minutes after injection in healthy subjects. Absorption also differs depending on the site of injection. Aft | When administered intravenously as bolus injections of 0.1 and 0.2 U/kg dose in two separate groups of healthy subjects, the mean volume of distribution of insulin lispro appeared to decrease with increase in dose (1.55 and 0.72 L/kg, respectively). | Clearance is dose dependent. When a dose of 0.1 unit/kg and 0.2 unit/kg were administered intravenously, the mean clearance was 21.0 mL/min/kg and 9.6 mL/min/kg respectively. | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Insulin, Insulin Analog, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides | US5514646 | 7-May-1996 | 7-May-2013 | Concomitant therapy with drugs like Dextropropoxyphene, Pentoxifylline, Pramlintide, Fluoxetine, Fenofibrate and Disopyramide that may increase the blood-glucose-lowering effect of insulin lispro | NA | Admelog | Sanofi Aventis, REMEDYREPACK INC. | Sanofi Aventis, REMEDYREPACK INC. | symptoms of Type 1 or 2 Diabetes Mellitus. | C257H383N65O77S6 | Insulin lispro is produced by recombinant DNA technology utilizing a non-pathogenic laboratory strain of Escherichia coli. Insulin lispro differs from human insulin in that the amino acid proline at position B28 is replaced by lysine and the lysine in position B29 is replaced by proline. | sterile, aqueous, clear, and colorless solution. | Subcutaneous Injection | Dilute ADMELOG to concentrations from 0.1 unit/mL to 1 unit/mL using 0.9% sodium chloride. Administer ADMELOG intravenously ONLY under medical supervision with close monitoring of blood glucose and potassium levels to avoid hypoglycemia and hypokalemia | ADMELOG is contraindicated: during episodes of hypoglycemia. in patients who are hypersensitive to insulin lispro or to any of the excipients. Clinical Pharmacology | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, redness or swelling where an injection was given, itchy skin rash over the entire body, fast heartbeats, lightheadedness, weight gain, swelling in your hands or feet, shortness of breath, headache, hunger, sweating, irritability, dizziness, anxiety, shakiness, leg cramps, constipation, irregular heartbeats, fluttering in your chest, increased thirst or urination, numbness or tingling, muscle weakness, and limp feeling | Link | NA | NA |
| 10278 | Th1040 | Insulin Lispro | >Th1040_Insulin_Lispro GIVEQCCTSICSLYQLENYCN | 5808 | C257H387N65O76S6 | 5.39 | 0.218 | 81 | On subcutaneous administration = 1 hour | Insulin lispro is a recombinant human insulin analogue produced in a specialized laboratory strain of Escherischia coli. Plasmid DNA transfected into the bacteria encodes for an analogue of human insulin that has a lysine at residuce B28 and proline at B29; these residues are reversed in endogenous human insulin. Reversal of these amino acid residues produces a rapid-acting insulin analogue. FDA approved on 1996. | To treat type 1 or 2 diabetes mellitus. To be used in conjunction with an intermediate or long-acting insulin except when used in a continuous insulin infusion pump. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin lispro binds to the insulin receptor(IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Reversal of the proline and lysine residues at positions B28 and B29 of native insulin eliminates hydrophobic interactions and weakens some of the hydrogen bonds that contribute to the stability of the insulin dimers that comprise insulin hexamers. Hexamers of insulin lispro are produced in the presence of zinc and -cresol. These weakly associated hexamers quickly dissociate upon subcutaneous injection and are absorbed as monomers through vascular endothelial cells. These properties give insulin lispro its fast-acting properties. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process. | Rapidly absorbed following subcutaneous administration. It is also absorbed more quickly than regular human insulin. Peak serum levels occur 30-90 minutes after injection in healthy subjects. Absorption also differs depending on the site of injection. Aft | When administered intravenously as bolus injections of 0.1 and 0.2 U/kg dose in two separate groups of healthy subjects, the mean volume of distribution of insulin lispro appeared to decrease with increase in dose (1.55 and 0.72 L/kg, respectively). | Clearance is dose dependent. When a dose of 0.1 unit/kg and 0.2 unit/kg were administered intravenously, the mean clearance was 21.0 mL/min/kg and 9.6 mL/min/kg respectively. | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Insulin, Insulin Analog, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides | CA2151560 | 9-May-2000 | 12-Jun-2015 | Concomitant therapy with diuretics like Hydrochlorothiazide may reduce the blood-glucose-lowering effect of insulin lispro. | NA | Humalog KwikPen | Eli Lilly | Eli Lilly | Insulin lispro is used to treat type 1 diabetes in adults. It is usually given together with another long-acting insulin. Insulin lispro is also used together with oral medication to treat type 2 diabetes in adults. | NA | NA | Solution | Subcutaneous injection | Insulin lispro can be administered intravenously under medical supervision at concentrations from 0.1 unit/mL to 1 unit/mL in infusion systems containing 0.9% sodium chloride. Blood glucose and potassium levels should be closely monitored to avoid hypoglycemia. | During episodes of hypoglycemia in patients who are hypersensitive to HUMALOG or to any of its excipients. | Low blood sugar is the most common side effect. There are many causes of low blood sugar, including taking too much Humalog. Severe life-threatening allergic reactions (whole-body reactions) can happen.Reactions at the injection site (local allergic reaction. | Link | NA | NA |
| 10283 | Th1041 | Insulin Glargine | >Th1041_Insulin_Glargine GIVEQCCTSICSLYQLENYCG | 6063 | C267H404N72O78S6 | 6.88 | 0.098 | 81 | Not reported in humans; 30 hours in mammalian reticulocytes. | Insulin glargine is produced by recombinant DNA technology using a non-pathogenic laboratory strain of Escherichia coli (K12). It is an analogue of human insulin made by replacing the asparagine residue at position A21 of the A-chain with glycine and adding two arginines to the C-terminus (positions B31 and 32) of the B-chain. The resulting protein is soluble at pH 4 and forms microprecipitates at physiological pH 7.4. Small amounts of insulin glargine are slowly released from microprecipitates giving the drug a long duration of action (up to 24 hours) and no pronounced peak concentration. | To treat Type 1 or 2 diabetes mellitus in patients over 17 years old who require a long-acting (basal) insulin for the control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for glycemic control. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin glargine binds to the insulin receptor, a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism. Insulin glargine is completely soluble at pH 4, the pH of administered solution, and has low solubility at physiological pH 7.4. Upon subcuteous injection, the solution is neutralized resulting in the formation of microprecipitates. Small amounts of insulin glargine are released from microprecipitates giving the drug a relatively constant concentration over time profile over 24 hours with no pronounced peak. This release mechanism allows the drug to mimic basal insulin levels within the body. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Partly metabolized to two active metabolites with similar in vitro activity to insulin: A21-Gly-insulin and A21-Gly-des-B30-Thr-insulin. | Due to the modifications in the A and B chain, the isoelectric point shifts towards a neutral pH and insulin glargine is more stable in acidic conditions than regular insulin. As insulin glargine is less soluble at neutral pH, once injected, forms micro-p | NA | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Antimetabolites, Biological Products, Blood Glucose Lowering Agents, Complex Mixtures, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Hypolipidemic Agents, Insulin, Insulin Analog, Insulin, Long-Acting, Lipid Regulating Agents, Pancreatic Hormones, Peptide Hormones, Peptides | US7476652 | 13-Jan-2009 | 23-Jul-2023 | Somatropin may antagonize the hypoglycemic effect of insulin glargine. Monitor for changes in fasting and postprandial blood sugars. | Insulin receptor,Insulin-like growth factor 1 receptor | Lantus | Sanofi-Aventis | Sanofi-Aventis | Its used to improve glycemic control in adults and children with type 1 diabetes mellitus and in adults with type 2 diabetes mellitus. | 21A-Gly-30Ba-L-Arg-30Bb-L-Arg-human insulin | LANTUS consists of insulin glargine dissolved in a clear aqueous fluid. Each milliliter of LANTUS contains 100 Units (3.6378 mg) insulin glargine. The 10 mL vial presentation contains the following inactive ingredients per mL: 30 mcg zinc, 2.7 mg m-cresol | Solution | Subcutaneous Injection | LANTUS may be administered at any time during the day. LANTUS should be administered subcutaneously once a day at the same time every day. The dose of LANTUS must be individualized based on clinical response. | Hypersensitivity | Low blood sugar (headache, hunger, weakness, sweating, confusion, irritability, dizziness, fast heart rate, or feeling jittery). Sign of insulin allergy include itching skin rash over the entire body, wheezing, trouble breathing, fast heart rate, sweating. | Link | NA | NA |
| 10285 | Th1041 | Insulin Glargine | >Th1041_Insulin_Glargine GIVEQCCTSICSLYQLENYCG | 6063 | C267H404N72O78S6 | 6.88 | 0.098 | 81 | Not reported in humans; 30 hours in mammalian reticulocytes. | Insulin glargine is produced by recombinant DNA technology using a non-pathogenic laboratory strain of Escherichia coli (K12). It is an analogue of human insulin made by replacing the asparagine residue at position A21 of the A-chain with glycine and adding two arginines to the C-terminus (positions B31 and 32) of the B-chain. The resulting protein is soluble at pH 4 and forms microprecipitates at physiological pH 7.4. Small amounts of insulin glargine are slowly released from microprecipitates giving the drug a long duration of action (up to 24 hours) and no pronounced peak concentration. | To treat Type 1 or 2 diabetes mellitus in patients over 17 years old who require a long-acting (basal) insulin for the control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for glycemic control. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin glargine binds to the insulin receptor, a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism. Insulin glargine is completely soluble at pH 4, the pH of administered solution, and has low solubility at physiological pH 7.4. Upon subcuteous injection, the solution is neutralized resulting in the formation of microprecipitates. Small amounts of insulin glargine are released from microprecipitates giving the drug a relatively constant concentration over time profile over 24 hours with no pronounced peak. This release mechanism allows the drug to mimic basal insulin levels within the body. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Partly metabolized to two active metabolites with similar in vitro activity to insulin: A21-Gly-insulin and A21-Gly-des-B30-Thr-insulin. | Due to the modifications in the A and B chain, the isoelectric point shifts towards a neutral pH and insulin glargine is more stable in acidic conditions than regular insulin. As insulin glargine is less soluble at neutral pH, once injected, forms micro-p | NA | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Antimetabolites, Biological Products, Blood Glucose Lowering Agents, Complex Mixtures, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Hypolipidemic Agents, Insulin, Insulin Analog, Insulin, Long-Acting, Lipid Regulating Agents, Pancreatic Hormones, Peptide Hormones, Peptides | CA1339044 | 1-Apr-1997 | 1-Apr-2014 | NA | NA | Abasaglar/Basaglar | Eli Lilly Nederland B.V | Eli Lilly Nederland B.V | to control high blood sugar in adults and children with type 1 diabetes mellitus and adults with type 2 diabetes mellitus. | NA | BASAGLAR is produced by recombinant DNA technology utilizing a non-pathogenic laboratory strain of Escherichia coli (K12) as the production organism. Insulin glargine differs from human insulin in that the amino acid asparagine at position A21 is replaced by glycine and two arginines are added to the C-terminus of the B-chain. | clear, colorless, sterile aqueous solution | subcutaneously into the abdominal area, thigh, or deltoid, and rotate injection sites within the same region from one injection to the next | Inject between 1 and 80 units per injection. | BASAGLAR is contraindicated: During episodes of hypoglycemia. In patients with hypersensitivity to insulin glargine or one of its excipients | low blood sugar (hypoglycemia), allergic reactions, injection site reactions, body fat redistribution, itching, rash, swelling, weight gain, upper respiratory tract infection, runny or stuffy nose, back pain, cough, urinary tract infection, diarrhea, depression, or headache. | Link | NA | NA |
| 10286 | Th1041 | Insulin Glargine | >Th1041_Insulin_Glargine GIVEQCCTSICSLYQLENYCG | 6063 | C267H404N72O78S6 | 6.88 | 0.098 | 81 | Not reported in humans; 30 hours in mammalian reticulocytes. | Insulin glargine is produced by recombinant DNA technology using a non-pathogenic laboratory strain of Escherichia coli (K12). It is an analogue of human insulin made by replacing the asparagine residue at position A21 of the A-chain with glycine and adding two arginines to the C-terminus (positions B31 and 32) of the B-chain. The resulting protein is soluble at pH 4 and forms microprecipitates at physiological pH 7.4. Small amounts of insulin glargine are slowly released from microprecipitates giving the drug a long duration of action (up to 24 hours) and no pronounced peak concentration. | To treat Type 1 or 2 diabetes mellitus in patients over 17 years old who require a long-acting (basal) insulin for the control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for glycemic control. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin glargine binds to the insulin receptor, a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism. Insulin glargine is completely soluble at pH 4, the pH of administered solution, and has low solubility at physiological pH 7.4. Upon subcuteous injection, the solution is neutralized resulting in the formation of microprecipitates. Small amounts of insulin glargine are released from microprecipitates giving the drug a relatively constant concentration over time profile over 24 hours with no pronounced peak. This release mechanism allows the drug to mimic basal insulin levels within the body. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Partly metabolized to two active metabolites with similar in vitro activity to insulin: A21-Gly-insulin and A21-Gly-des-B30-Thr-insulin. | Due to the modifications in the A and B chain, the isoelectric point shifts towards a neutral pH and insulin glargine is more stable in acidic conditions than regular insulin. As insulin glargine is less soluble at neutral pH, once injected, forms micro-p | NA | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Antimetabolites, Biological Products, Blood Glucose Lowering Agents, Complex Mixtures, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Hypolipidemic Agents, Insulin, Insulin Analog, Insulin, Long-Acting, Lipid Regulating Agents, Pancreatic Hormones, Peptide Hormones, Peptides | NA | NA | NA | NA | NA | Lantus OptiSet | NA | NA | Its used to reduce high blood sugar in adults, adolescents and children of 6 years or above with diabetes mellitus. | NA | NA | Solution | Subcutaneous Injection | Patients need one injection of Lantus every day, at the same time of the day. In children, only evening injection has been studied.OptiSet delivers insulin in increments of 2 units up to a maximum single dose of 40 units. The dosage may vary from person tto person. | Hypersensitivity | Hypoglycemia, skin changes at the injection site, allergic reactions, large-scale skin reactions (rash and itching all over the body), severe swelling of skin or mucous membranes (angio-oedema), shortness of breath, a fall in blood pressure with rapid headache. | Link | NA | NA |
| 10287 | Th1041 | Insulin Glargine | >Th1041_Insulin_Glargine GIVEQCCTSICSLYQLENYCG | 6063 | C267H404N72O78S6 | 6.88 | 0.098 | 81 | Not reported in humans; 30 hours in mammalian reticulocytes. | Insulin glargine is produced by recombinant DNA technology using a non-pathogenic laboratory strain of Escherichia coli (K12). It is an analogue of human insulin made by replacing the asparagine residue at position A21 of the A-chain with glycine and adding two arginines to the C-terminus (positions B31 and 32) of the B-chain. The resulting protein is soluble at pH 4 and forms microprecipitates at physiological pH 7.4. Small amounts of insulin glargine are slowly released from microprecipitates giving the drug a long duration of action (up to 24 hours) and no pronounced peak concentration. | To treat Type 1 or 2 diabetes mellitus in patients over 17 years old who require a long-acting (basal) insulin for the control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for glycemic control. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin glargine binds to the insulin receptor, a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism. Insulin glargine is completely soluble at pH 4, the pH of administered solution, and has low solubility at physiological pH 7.4. Upon subcuteous injection, the solution is neutralized resulting in the formation of microprecipitates. Small amounts of insulin glargine are released from microprecipitates giving the drug a relatively constant concentration over time profile over 24 hours with no pronounced peak. This release mechanism allows the drug to mimic basal insulin levels within the body. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Partly metabolized to two active metabolites with similar in vitro activity to insulin: A21-Gly-insulin and A21-Gly-des-B30-Thr-insulin. | Due to the modifications in the A and B chain, the isoelectric point shifts towards a neutral pH and insulin glargine is more stable in acidic conditions than regular insulin. As insulin glargine is less soluble at neutral pH, once injected, forms micro-p | NA | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Antimetabolites, Biological Products, Blood Glucose Lowering Agents, Complex Mixtures, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Hypolipidemic Agents, Insulin, Insulin Analog, Insulin, Long-Acting, Lipid Regulating Agents, Pancreatic Hormones, Peptide Hormones, Peptides | NA | NA | NA | NA | NA | Lantus SoloStar | NA | NA | It works by helping your body to use sugar properly. This lowers the amount of glucose in the blood, which helps to treat diabetes. | NA | NA | Solution | Subcutaneous Injection | NA | Hypersensitivity | Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); changes in vision; chills; confusion; dizziness; drowsiness; fainting; fast heartbeat; fast, shallow breathing. | Link | NA | NA |
| 10300 | Th1042 | Collagenase | >Th1042_Collagenase MKRKCLSKRLMLAITMATIFTVNSTLPIYAAVDKNNATAAVQNESKRYTVSYLKTLNYYDLVDLLVKTEIENLPDLFQYSSDAKEFYGNKTRMSFIMDEIGRRAPQYTEIDHKGIPTLVEVVRAGFYLGFHNKELNEINKRSFKERVIPSILAIQKNPNFKLGTEVQDKIVSATGLLAGNETAPPEVVNNFTPILQDCIKNIDRYALDDLKSKALFNVLAAPTYDITEYLRATKEKPENTPWYGKIDGFINELKKLALYGKINDNNSWIIDNGIYHIAPLGKLHSNNKIGIETLTEVMKVYPYLSMQHLQSADQIKRHYDSKDAEGNKIPLDKFKKEGKEKYCPKTYTFDDGKVIIKAGARVEEEKVKRLYWASKEVNSQFFRVYGIDKPLEEGNPDDILTMVIYNSPEEYKLNSVLYGYDTNNGGMYIEPEGTFFTYEREAQESTYTLEELFRHEYTHYLQGRYAVPGQWGRTKLYDNDRLTWYEEGGAELFAGSTRTSGILPRKSIVSNIHNTTRNNRYKLSDTVHSKYGASFEFYNYACMFMDYMYNKDMGILNKLNDLAKNNDVDGYDNYIRDLSSNYALNDKYQDHMQERIDNYENLTVPFVADDYLVRHAYKNPNEIYSEISEVAKLKDAKSEVKKSQYFSTFTLRGSYTGGASKGKLEDQKAMNKFIDDSLKKLDTYSWSGYKTLTAYFTNYKVDSSNRVTYDVVFHGYLPNEGDSKNSLPYGKINGTYKGTEKEKIKFSSEGSFDPDGKIVSYEWDFGDGNKSNEENPEHSYDKVGTYTVKLKVTDDKGESSVSTTTAEIKDLSENKLPVIYMHVPKSGALNQKVVFYGKGTYDPDGSIAGYQWDFGDGSDFSSEQNPSHVYTKKGEYTVTLRVMDSSGQMSEKTMKIKITDPVYPIGTEKEPNNSKETASGPIVPGIPVSGTIENTSDQDYFYFDVITPGEVKIDINKLGYGGATWVVYDENNNAVSYATDDGQNLSGKFKADKPGRYYIHLYMFNGSYMPYRINIEGSVGR | 112023.2 | C5028H7666N1300O1564S21 | 5.58 | -0.714 | 49-54 | NA | This enzyme is derived from fermentation of Clostridium histolyticum | It promotes debridement of necrotic tissue and helps in the treatment of severe burns and dermal ulcers including decubitus ulcers. | Helps in the treatment of skin ulcers and severe burns, collagenase is able to digest collagen in necrotic tissue at physiological pH by hydrolyzing the peptide bonds of undenatured and denatured collagen. Collagenase thus contributes towards the formation of granulation tissue and subsequent epithelization of dermal ulcers and severely burned areas. The action of collagenase may remove substrates necessary for bacterial proliferation or may permit antibodies, leukocytes, and antibiotics better access to the infected area. | Collagenase is a protease that is specific to collagen. The triple helical region of interstitial collagens is highly resistant to most cell proteinases. However, during remodeling of the connective tissue in such processes as wound healing and metastasis, collagen becomes susceptible to cleavage by collagenases. Collagenase cleaves all 3 alpha helical chains of native Types I, II and III collagens at a single locus by hydrolyzing the peptide bond following the Gly residue of the sequence: Gly 775-(Ile or Leu) 776-(Ala or Leu) 777 located approximately three-fourths of the chain length from each N-terminus. | NA | NA | NA | NA | NA | Collagen-specific Enzyme, Collagenases, Dermatologicals, Endopeptidases, Enzymes, Enzymes and Coenzymes, Hydrolases, Metalloendopeptidases, Metalloproteases, Microbial Collagenase, antagonists & inhibitors, Misc. Skin and Mucous Membrane Agents, Musculo-Skeletal System, Peptide Hydrolases, Preparations for Treatment of Wounds and Ulcers | NA | NA | NA | silver nitrate topical | NA | Qwo | Endo Aesthetics LLC | Endo Aesthetics LLC | used for the treatment of moderate to severe cellulite in the buttocks of adult women. | NA | Each QWO 0.92-mg single-dose vial contains 0.92 mg of collagenase clostridium histolyticumaaes and mannitol (37.7 mg), sucrose (18.9 mg), tromethamine (1.1 mg), and hydrochloric acid as needed to adjust pH. Reconstitution with 4 mL of supplied Diluent for QWO yields a solution containing 0.23 mg/mL collagenase clostridium histolyticum-aaes at a pH of approximately 8.0. Each QWO 1.84-mg single-dose vial contains 1.84 mg of collagenase clostridium histolyticumaaes and mannitol (75.4 mg), sucrose (37.8 mg), tromethamine (2.2 mg), and hydrochloric acid as needed to adjust pH. Reconstitution with 8 mL of supplied Diluent for QWO yields a solution containing 0.23 mg/mL collagenase clostridium histolyticum-aaes at a pH of approximately 8.0. | sterile, preservative-free, lyophilized powder (appearing as a white cake) | injected subcutaneously | A treatment area is defined as a single buttock receiving up to 12 injections, 0.3 mL each (up to a total of 3.6 mL), of QWO. A treatment visit may consist of up to 2 treatment areas. Treatment should be repeated every 21 days for 3 treatment visits. | QWO is contraindicated in: patients with a history of hypersensitivity to collagenase or to any of the excipients. the presence of infection at the injection sites. | hives swollen face trouble breathing chest pain low blood pressure dizziness or fainting | NA | NA | NA |
| 10316 | Th1044 | Adalimumab | >Th1044_Adalimumab DIQMTQSPSSLSASVGDRVTITCRASQGIRNYLAWYQQKPGKAPKLLIYAASTLQSGVPSRFSGSGSGTDFTLTISSLQPEDVATYYCQRYNRAPYTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | NA | 240-480 hours | Adalimumab(1330 amino acids, molecular weight of approximately 148 kilodaltons) is a human monoclonal antibody against TNF-alpha. It is produced by recombinant DNA technology using a mammalian cell expression system. | For treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and Crohn's disease. | Used in the treatment of immune system mediated diseases, adalimumab binds specifically to TNF-alpha and blocks its general cytokine effects, thereby reducing TNF-induced inflammation and halting tissue destruction. | Adalimumab binds to TNF-alpha and blocks its interaction with the p55 and p75 cell surface TNF receptors. Adalimumab also lyses surface TNF expressing cells in vitro in the presence of complement. | Rare side effects include: worsening or initiation of congestive heart failure, a lupus-like syndrome, lymphoma, medically significant cytopenias, and worsening or initiation of multiple sclerosis/neurological diseases. There has been reported pancytopenia and increased liver transaminases with the use of adalimumab, which suggests that laboratory value monitoring blood counts and liver function, at least intermittently, are important | Most likely removed by opsonization via the reticuloendothelial system. | Bioavailability is 64% | 4.7-6.0 L | 12 mL/hr [RA patients with dose 0.25-10 mg/kg] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Disease-modifying Antirheumatic Agents, Globulins, Immunoglobulins, Immunomodulatory Agents, Immunoproteins, Immunosuppressive Agents, Miscellaneous GI Drugs, Proteins, Serum Globulins, Tumor Necrosis Factor Blockers, Tumor Necrosis Factor Receptor Blocking Activity | CA2243459 | 17-Sep-2002 | 10-Feb-2017 | Canakinumab and Rilonacept increase immunosuppressive effects and risk of infection. | Tumor necrosis factor,Low affinity immunoglobulin gamma Fc region receptor III-B,Complement C1r subcomponent,Complement C1q subcomponent subunit A,Complement C1q subcomponent subunit B,Complement C1q subcomponent subunit C,Low affinity immunoglobulin gamm | Humira | Abbott Laboratories | Abbott Laboratories | Humira is used to treat rheumatoid arthritis, juvenile idiopathic arthritis, psoriatic arthritis, ankylosing spondylitis, and plaque psoriasis. It is also used to treat Crohn's disease or ulcerative colitis, after other drugs have been tried without succe | NA | It is supplied for a single use. Each prefilled syringe delivers 0.8 mL (40 mg) of drug product. Each 0.8 mL of HUMIRA contains 40 mg adalimumab, 4.93 mg sodium chloride, 0.69 mg monobasic sodium phosphate dihydrate, 1.22 mg dibasic sodium phosphate dihyd | Sterile, preservative-free solution | Subcutaneous administration | The recommended dose of HUMIRA for adult patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), or ankylosing spondylitis (AS) is 40 mg administered every other week. Methotrexate (MTX), other non-biologic DMARDS, glucocorticoids, nonsteroidal anti-inflammatory drugs (NSAIDs), and/or analgesics may be continued during treatment with HUMIRA. | Hypersensitivity | Fever, chills, sore throat, vomiting, diarrhea, flu symptoms, pain or burning when you urinate; signs of tuberculosis - fever with ongoing cough, weight loss (fat or muscle); pale skin, easy bruising or bleeding (nosebleeds, bleeding gums); numbness. | Link | NA | NA |
| 10317 | Th1044 | Adalimumab | >Th1044_Adalimumab DIQMTQSPSSLSASVGDRVTITCRASQGIRNYLAWYQQKPGKAPKLLIYAASTLQSGVPSRFSGSGSGTDFTLTISSLQPEDVATYYCQRYNRAPYTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | NA | 240-480 hours | Adalimumab(1330 amino acids, molecular weight of approximately 148 kilodaltons) is a human monoclonal antibody against TNF-alpha. It is produced by recombinant DNA technology using a mammalian cell expression system. | For treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and Crohn's disease. | Used in the treatment of immune system mediated diseases, adalimumab binds specifically to TNF-alpha and blocks its general cytokine effects, thereby reducing TNF-induced inflammation and halting tissue destruction. | Adalimumab binds to TNF-alpha and blocks its interaction with the p55 and p75 cell surface TNF receptors. Adalimumab also lyses surface TNF expressing cells in vitro in the presence of complement. | Rare side effects include: worsening or initiation of congestive heart failure, a lupus-like syndrome, lymphoma, medically significant cytopenias, and worsening or initiation of multiple sclerosis/neurological diseases. There has been reported pancytopenia and increased liver transaminases with the use of adalimumab, which suggests that laboratory value monitoring blood counts and liver function, at least intermittently, are important | Most likely removed by opsonization via the reticuloendothelial system. | Bioavailability is 64% | 4.7-6.0 L | 13 mL/hr [RA patients with dose 0.25-10 mg/kg] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Disease-modifying Antirheumatic Agents, Globulins, Immunoglobulins, Immunomodulatory Agents, Immunoproteins, Immunosuppressive Agents, Miscellaneous GI Drugs, Proteins, Serum Globulins, Tumor Necrosis Factor Blockers, Tumor Necrosis Factor Receptor Blocking Activity | NA | NA | NA | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | NA | Abrilada | Pfizer Canada Ulc | Pfizer Canada Ulc | ABRILADA is indicated for reducing signs and symptoms, inducing major clinical response, inhibiting the progression of structural damage, and improving physical function in adult patients with moderately to severely active rheumatoid arthritis. ABRILADA can be used alone or in combination with methotrexate or other non-biologic disease-modifying anti-rheumatic drugs (DMARDs). | NA | Adalimumab-afzb is a recombinant human IgG1 monoclonal antibody with human derived heavy and light chain variable regions and human IgG1:k constant regions. Adalimumab-afzb is produced by recombinant DNA technology in Chinese hamster ovary cells and is purified by a process that includes specific viral inactivation and removal steps. It consists of 1330 amino acids and has a molecular weight of approximately 148 kilodaltons | sterile, preservative-free solution | Subcutaneous administration | 10 kg (22 lbs) to <15 kg (33 lbs)-10 mg every other week (10 mg prefilled syringe) 15 kg (33 lbs) to <30 kg (66 lbs)-20 mg every other week (20 mg prefilled syringe) ≥30 kg (66 lbs)-40 mg every other week (ABRILADA pen or 40 mg prefilled syringe) | NA | infections (e.g. upper respiratory, sinusitis), injection site reactions, headache, and rash | Link | NA | NA |
| 10318 | Th1044 | Adalimumab | >Th1044_Adalimumab DIQMTQSPSSLSASVGDRVTITCRASQGIRNYLAWYQQKPGKAPKLLIYAASTLQSGVPSRFSGSGSGTDFTLTISSLQPEDVATYYCQRYNRAPYTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | NA | 240-480 hours | Adalimumab(1330 amino acids, molecular weight of approximately 148 kilodaltons) is a human monoclonal antibody against TNF-alpha. It is produced by recombinant DNA technology using a mammalian cell expression system. | For treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and Crohn's disease. | Used in the treatment of immune system mediated diseases, adalimumab binds specifically to TNF-alpha and blocks its general cytokine effects, thereby reducing TNF-induced inflammation and halting tissue destruction. | Adalimumab binds to TNF-alpha and blocks its interaction with the p55 and p75 cell surface TNF receptors. Adalimumab also lyses surface TNF expressing cells in vitro in the presence of complement. | Rare side effects include: worsening or initiation of congestive heart failure, a lupus-like syndrome, lymphoma, medically significant cytopenias, and worsening or initiation of multiple sclerosis/neurological diseases. There has been reported pancytopenia and increased liver transaminases with the use of adalimumab, which suggests that laboratory value monitoring blood counts and liver function, at least intermittently, are important | Most likely removed by opsonization via the reticuloendothelial system. | Bioavailability is 64% | 4.7-6.0 L | 14 mL/hr [RA patients with dose 0.25-10 mg/kg] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Disease-modifying Antirheumatic Agents, Globulins, Immunoglobulins, Immunomodulatory Agents, Immunoproteins, Immunosuppressive Agents, Miscellaneous GI Drugs, Proteins, Serum Globulins, Tumor Necrosis Factor Blockers, Tumor Necrosis Factor Receptor Blocking Activity | NA | NA | NA | Adalimumab (and other anti-TNF immunosuppressants), when used in combination with tofacitinib, may increase the risk of added immunosuppression. It is recommended to avoid concurrent therapy. | NA | Humira Pen | Abbott Laboratories | Abbott Laboratories | It is used to treat rheumatoid arthritis, juvenile idiopathic arthritis, psoriatic arthritis, ankylosing spondylitis, and plaque psoriasis. It is also used to treat Crohn's disease or ulcerative colitis, after other drugs have been tried without successfu | NA | NA | Sterile, preservative-free solution | Subcutaneous Injection | The recommended dose of HUMIRA for adult patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), or ankylosing spondylitis (AS) is 40 mg administered every other week. Methotrexate (MTX), other non-biologic DMARDS, glucocorticoids,nonsteroidal anti-inflammatory drugs (NSAIDs), and/or analgesics may be continued during treatment with HUMIRA. | Hypersensitivity | Fever, chills, sore throat, vomiting, diarrhea, flu symptoms, pain or burning when you urinate; signs of tuberculosis - fever with ongoing cough, weight loss (fat or muscle); pale skin, easy bruising or bleeding (nosebleeds, bleeding gums); numbness. | Link | NA | NA |
| 10321 | Th1044 | Adalimumab | >Th1044_Adalimumab DIQMTQSPSSLSASVGDRVTITCRASQGIRNYLAWYQQKPGKAPKLLIYAASTLQSGVPSRFSGSGSGTDFTLTISSLQPEDVATYYCQRYNRAPYTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | NA | 240-480 hours | Adalimumab(1330 amino acids, molecular weight of approximately 148 kilodaltons) is a human monoclonal antibody against TNF-alpha. It is produced by recombinant DNA technology using a mammalian cell expression system. | For treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and Crohn's disease. | Used in the treatment of immune system mediated diseases, adalimumab binds specifically to TNF-alpha and blocks its general cytokine effects, thereby reducing TNF-induced inflammation and halting tissue destruction. | Adalimumab binds to TNF-alpha and blocks its interaction with the p55 and p75 cell surface TNF receptors. Adalimumab also lyses surface TNF expressing cells in vitro in the presence of complement. | Rare side effects include: worsening or initiation of congestive heart failure, a lupus-like syndrome, lymphoma, medically significant cytopenias, and worsening or initiation of multiple sclerosis/neurological diseases. There has been reported pancytopenia and increased liver transaminases with the use of adalimumab, which suggests that laboratory value monitoring blood counts and liver function, at least intermittently, are important | Most likely removed by opsonization via the reticuloendothelial system. | Bioavailability is 64% | 4.7-6.0 L | 17 mL/hr [RA patients with dose 0.25-10 mg/kg] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Disease-modifying Antirheumatic Agents, Globulins, Immunoglobulins, Immunomodulatory Agents, Immunoproteins, Immunosuppressive Agents, Miscellaneous GI Drugs, Proteins, Serum Globulins, Tumor Necrosis Factor Blockers, Tumor Necrosis Factor Receptor Blocking Activity | NA | NA | NA | NA | NA | Cyltezo | Boehringer Ingelheim | Boehringer Ingelheim | to treat the symptoms of Rheumatoid Arthritis, Psoriatic Arthritis, Ankylosing Spondylitis, Plaque Psoriasis, Chron Disease and Ulcerative Colitis. Cyltezo may be used alone or with other medications. | NA | Adalimumab-adbm is a recombinant human IgG1 monoclonal antibody specific for human tumor necrosis factor (TNF). Adalimumabadbm is produced by recombinant DNA technology in a mammalian cell expression system and is purified by a process that includes specific viral inactivation and removal steps. It consists of 1330 amino acids and has a molecular weight of approximately 148 kilodaltons. | sterile, preservative-free solution | subcutaneous administration. | The dosage of Cyltezo for rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis is 40 mg every other week. The dosage of Cyltezo for juvenile idiopathic arthritis in children up to 30 kg (66 lbs.) is 40 mg every other week. The initial dose of Cyltezo for adult Crohn's disease and ulcerative colitis is 160 mg on Day 1(four 40 mg injections in one day or two 40 mg injections per day for two consecutive days); second dose two weeks later (Day 15) is 80 mg; two weeks later (Day 29) begin a maintenance dose of 40 mg every other week. The dosage of Cyltezo for plaque psoriasis is an 80 mg initial dose, followed by 40 mg every other week starting one week after initial dose. | NA | infections (e.g. upper respiratory, sinusitis, urinary tract), injection site reactions, headache, rash, flu symptoms, nausea, abdominal pain, high cholesterol, blood in the urine, alkaline phosphatase increased, back pain, and high blood pressure (hypertension). | Link | NA | NA |
| 10337 | Th1048 | Pegaspargase | >Th1048_Pegaspargase MEFFKKTALAALVMGFSGAALALPNITILATGGTIAGGGDSATKSNYTVGKVGVENLVNAVPQLKDIANVKGEQVVNIGSQDMNDNVWLTLAKKINTDCDKTDGFVITHGTDTMEETAYFLDLTVKCDKPVVMVGAMRPSTSMSADGPFNLYNAVVTAADKASANRGVLVVMNDTVLDGRDVTKTNTTDVATFKSVNYGPLGYIHNGKIDYQRTPARKHTSDTPFDVSKLNELPKVGIVYNYANASDLPAKALVDAGYDGIVSAGVGNGNLYKSVFDTLATAAKTGTAVVRSSRVPTGATTQDAEVDDAKYGFVASGTLNPQKARVLLQLALTQTKDPQQIQQIFNQY | 31731.9 | C1377H2208N382O442S17 | 4.67 | 0.059 | NA | IM: ~6 days | Pegylated L-asparagine amidohydrolase from E. coli. Pegylation substantially (by a factor of 4) extends the protein half life. | For treatment of acute lymphoblastic leukemia. | In a significant number of patients with acute leukemia, the malignant cells are dependent on an exogenous source of asparagine for survival. Normal cells, however, are able to synthesize asparagine and thus are affected less by the rapid depletion produced by treatment with the enzyme asparaginase. Oncaspar exploits a metabolic defect in asparagine synthesis of some malignant cells. | Pegaspargase, more effective than asparaginase, converts asparagine to aspartic acid and ammonia. It facilitates production of oxaloacetate which is needed for general cellular metabolism. Some malignant cells lose the ability to produce asparagine and so the loss of exogenous sources of asparagine leads to cell death. | Adverse effects that occur more than 10% of the time include hepatotoxicity as it is known to increase serum transaminases (ALT, AST). Also known to induce hypersensitivity reactions including anaphylaxis, erythema and bronchospasm. | NA | Onset of Asparagine depletion by IM is within 4 days Time to peak: IM: 3 to 4 days | IV: Adults (asparaginase naive): 2.4 L/m2 Distributes into CSF (reportedly reducing CSF asparagine concentrations to a similar extent as asparaginase | NA | Alcohols, Amidohydrolases, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Asparaginase, Asparagine-specific Enzyme, Compounds used in a research, industrial, or household setting, Delayed-Action Preparations, Enzymes, Enzymes and Coenzymes, Ethylene Glycols, Glycols, Hydrolases, Immunosuppressive Agents, Macromolecular Substances, Pegylated agents, Polymers, Thyroxine-binding globulin inhibitors | NA | NA | NA | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | L-asparagine | Oncaspar | Enzon Inc, Servier Pharmaceuticals LLC, Sigma Tau Pharmaceuticals, Inc., Les Laboratoires Servier, Baxalta US Inc. | Enzon Inc, Servier Pharmaceuticals LLC, Sigma Tau Pharmaceuticals, Inc., Les Laboratoires Servier, Baxalta US Inc. | Oncaspar is indicated as a component of a multi-agent chemotherapeutic regimen for the first line treatment of patients with Acute Lymphoblastic Leukemia (ALL). | NA | Oncaspar is supplied as a clear, colorless, preservative-free, isotonic sterile solution in phosphate-buffered saline, pH 7.3. Each milliliter contains 750 ± 150 International Units of pegaspargase, dibasic sodium phosphate, USP (5.58 mg), monobasic sodiu | Solution | Intravenous or intramuSubcutaneousular administrat | The recommended dose of Oncaspar is 2,500 International Units/m_ intramuscularly or intravenously. Oncaspar should be administered no more frequently than every 14 days. When Oncaspar is administered intramuscularly, the volume at a single injection site should be limited to 2ml. | History of serious allergic reactions to Oncaspar. History of serious thrombosis with prior L-asparaginase therapy. History of pancreatitis with prior L-asparaginase therapy. History of serious hemorrhagic events with prior L-asparaginase therapy. | Hypersensitivity reactions, coagulopathy, hyperglycemia, elevated serum transaminase concentrations, hyperbilirubinemia, pancreatitis, CNS thrombosis.No apparent difference in adverse effects following IV versus IM administration. | Link | NA | NA |
| 10341 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | CA1341604 | 4-May-2010 | 4-May-2027 | NA | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | Avonex | Biogen Inc | Biogen Inc | Avonex is used to treat relapsing multiple sclerosis (MS). This medication will not cure MS, it will only decrease the frequency of relapse symptoms. | NA | AVONEX is avalible as powder vial, Single used prefillled syringe, single used prefilled autoinjector. Each vial of reconstituted AVONEX contains 30 micrograms of interferon beta-1a; 15 mg Albumin (Human), USP; 5.8 mg Sodium Chloride, USP; 5.7 mg Dibasic | Lyophilized powder vial, Sterile liquid as single used prefilled syringe and also available as single use prefilled autoinjector. | IntramuSubcutaneousular Injection | The recommended dose is 30 micrograms once a week. To reduce the incidence and severity of flu-like symptoms that may occur when initiating AVONEX therapy at a dose of 30 micrograms, AVONEX may be started at a dose of 7.5 micrograms and the dose may beincreased by 7.5 micrograms each week for the next three weeks until the recommended dose of 30 micrograms is achieved. | Hypersensitivity | Stomach pain; headache, drowsiness; or minor irritation where the injection was given. | Link | NA | NA |
| 10344 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | Betaferon | Bayer | Bayer | Betaferon is indicated for the treatment of patients with a single demyelinating event with an active inflammatory process, if it is severe enough to warrant treatment with intravenous corticosteroids, if alternative diagnoses have been excluded, and if t | NA | NA | Powder and solvent that are made upto make solution. | Subcutaneous Injection | NA | People with severe depression or thoughts of suicide. People with severe liver disease. Pregnancy. Breastfeeding. | Flu-like symptoms such as fever,chills, painful joints, malaise, sweating, headache or muscular pain. These symptoms may be reduced by taking paracetamol or steroidal anti-inflammatory medicines such as ibuprofen. | Link | NA | NA |
| 10347 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | Betaseron | Merck | Merck | Betaseron is used to treat relapsing multiple sclerosis (MS). Betaseron will not cure MS, it will only decrease the frequency of relapse symptoms. | NA | Lyophilized Betaseron is a sterile, white to off-white powder, for subcutaneous injection after reconstitution with the diluent supplied (Sodium Chloride, 0.54% Solution). Albumin (Human) USP and Mannitol, USP (15 mg each/vial) are added as stabilizers. | Sterile, white to off-white powder | Subcutaneous Injection | The recommended starting dose is 0.0625 mg (0.25 mL) subcutaneously every other day, with dose increases over a six week period to the recommended dose of 0.25 mg (1 mL) every other day | Betaseron is contraindicated in patients with a history of hypersensitivity to natural or recombinant interferon beta, Albumin (Human). | Depressed mood, anxiety, trouble sleeping, restlessness, or thoughts of suicide or hurting yourself; bruising, swelling, oozing, or skin changes where the injection was given; weight changes, pounding heartbeats, feeling too hot or cold; fever, chills, bo | Link | NA | NA |
| 10351 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | Extavia | Novartis | Novartis | Extavia is used to treat relapsing multiple sclerosis (MS). This medication will not cure MS, it will only decrease the frequency of relapse symptoms. | NA | Each vial contains 0.3 mg of interferon beta-1b. The unit measurement is derived by comparing the antiviral activity of the product to the World Health Organization (WHO) reference standard of recombinant human interferon beta. Mannitol, USP and Albumin ( | Sterile, white to off-white powder | Subcutaneous Injection | The recommended starting dose is 0.0625 mg (0.25 mL) subcutaneously every other day, with dose increases over a six week period to the recommended dose of 0.25 mg (1 mL) every other day. | Extavia is contraindicated in patients with a history of hypersensitivity to natural or recombinant interferon beta, Albumin (Human). | Depressed mood, anxiety, trouble sleeping, restlessness, or thoughts of suicide or hurting yourself; bruising, swelling, oozing, or skin changes where the injection was given; weight changes, pounding heartbeats, feeling too hot or cold; fever, chills, weating, muscle aches and tiredness. | Link | NA | NA |
| 10355 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | Rebif | Merck, EMD Serono, Inc. | Merck, EMD Serono, Inc. | Rebif is used to treat relapsing multiple sclerosis (MS). This medication will not cure MS, it will only decrease the frequency of relapse symptoms. | NA | Each 0.5 mL (0.5 cc) of REBIF contains either 22 mcg or 44 mcg of interferon beta-1a, 2 mg or 4 mg albumin (human), 27.3 mg mannitol, 0.4 mg sodium acetate, and water for injection. Each 0.2 mL (0.2 cc) of REBIF contains 8.8 mcg of interferon beta-1a, 0.8 | Sterile solution in a prefilled syringe or REBIF Rebidose autoinjector | Subcutaneous Injection | The recommended dose of REBIF is either 22 mcg or 44 mcg injected subcutaneously three times per week. REBIF should be administered, if possible, at the same time (preferably in the late afternoon or evening) on the same three days (e.g., Monday, Wednesday, and Friday) at least 48 hours apart each week. | REBIF is contraindicated in patients with a history of hypersensitivity to natural or recombinant interferon beta, human albumin | Depressed mood, anxiety, trouble sleeping, restlessness, or thoughts of suicide or hurting yourself; bruising, swelling, oozing, or skin changes where the injection was given; weight changes, pounding heartbeats, feeling too hot or cold; fever, chills. | Link | NA | NA |
| 10372 | Th1055 | Follitropin beta | >Th1055_Follitropin_beta APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 | Circulation half life of 3-4 hours, elimination half life of 35-40 hours | Follitropin beta is a human follicle stimulating hormone (FSH) preparation of recombinant DNA origin, which consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Follitropin beta is produced in genetically engineered Chinese hamster cell lines (CHO). The nomenclature “beta†differentiates it from another recombinant human FSH product that was marketed earlier as follitropin alpha. Follitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). Numerous physio-chemical tests and bioassays indicate that follitropin beta and follitropin alpha are indistinguishable. However, a more recent study showed there is may be a slight clinical difference, with the alpha form tending towards a higher pregnancy rate and the beta form tending towards a lower pregnancy rate, but with significantly higher estradiol (E2) levels. Structural analysis shows that the amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (FSH). Further, the ogliosaccharide side chains are very similar, but not completely identical to that of natural FSH. However, these small differences do not affect the bioactivity compared to natural FSH. | For treatment of female infertility | Used for the treatment of female infertility, Follitropin beta or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of Follitropin beta is the primary hormone responsible for follicular recruitment and development. | Follitropin alpha is a recombinant form of endogenous follicle stimulating hormone (FSH). FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells. | Headaches, ovarian cysts, nausea and upper respiratory tract infections occurred in more than 10% of women in clinical trials. In men, the most serious adverse events reported were testicular surgery for cryptorchidism which existed prestudy, hemoptysis, an infected pilonidal cyst, and lymphadenopathy associated with an Epstein-Barr viral infection. Other concerns include overstimulation of the ovaries, pulmonary and vascular complications and multiple births. Post-marketing reports revealed hypersensitivity reactions including anaphylactoid reactions and asthma. Follitropin is contraindicated in pregnant women. | NA | bioavailability is approximately 66-76%. | 8 L [female subjects following intravenous administration of a 300 IU dose] | 0.011 /h/kg [European women with a single intramuscular dose of 300 IU] 0.011 /h/kg [Japanese women with a single intramuscular dose of 300 IU] | Amino Acids, Peptides, and Proteins, Follicle Stimulating Hormone, Genito Urinary System and Sex Hormones, Gonadotropins, Gonadotropins and Antigonadotropins, Gonadotropins, Pituitary, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Peptides, Pituitary Hormones, Pituitary Hormones, Anterior, Proteins, Sex Hormones and Modulators of the Genital System, Thyroid Products | US7741268 | 22-Jun-2010 | 2-Apr-2024 | NA | Follicle-stimulating hormone receptor | Follistim AQ | Merck | Merck | Follistim AQ (follitropin beta injection) is indicated for the development of multiple follicles in ovulatory patients participating in an Assisted Reproductive Technology (ART) program. Follistim AQ (follitropin beta) is also indicated for the induction of ovulation and pregnancy in anovulatory infertile patients in whom the cause of infertility is functional and not due to primary ovarian failure. | NA | Each single-use vial of Follistim AQ (follitropin beta) contains the following per 0.5 mL: 75 IU or 150 IU of FSH activity; 25 mg sucrose, NF; 7.35 mg sodium citrate (dihydrate), USP; 0.25 mg L-methionine, USP; 0.1 mg polysorbate 20, NF; and water for injection, USP. Hydrochloric acid, NF and/or sodium hydroxide, NF are used to adjust the pHto 7. | Follistim AQ (follitropin beta) is presented as a Sterile aqueous solution | for Subcutaneous or INTRAMUSubcutaneousULAR admini | starting dose of 150 to 225 IU of Follistim AQ (follitropin beta injection) is recommended for at least the first four days of treatment. After this, the dose may be adjusted for the individual patient based upon their ovarian response. | Tumor of the ovary, breast, uterus, hypothalamus or pituitary gland; Pregnancy; Uncontrolled thyroid or adrenal dysfunction; High levels of FSH indicating primary ovarian failure; | The following adverse events have been reported in women treated with gonado tropins: pulmonary and vascular complications, hemoperitoneum, adnexal torsion (as a complication of ovarian enlargement), dizziness, tachycardia, dyspnea, tachypnea, febrile reactions, flu-like symptoms including fever, chills, mus culoskeletal aches, joint pains, nausea, headache and malaise, breast tenderness, and dermatological symptoms | Link | NA | NA |
| 10375 | Th1056 | Vasopressin | >Th1056_Vasopressin CYFQNCPRG | 2140.46 | C92H130N28O24S4 | NA | -4.9 | NA | 10-20 minutes | Antidiuretic hormone, also known as vasopressin, is a nine amino acid peptide secreted from the posterior pituitary. Antidiuretic hormone binds to receptors in the distal or collecting tubules of the kidney and promotes reabsorbtion of water back into the circulation. | For the treatment of enuresis, polyuria, diabetes insipidus, polydipsia and oesophageal varices with bleeding | Vasopressin is an antidiuretic hormone indicated for the prevention and treatment of postoperative abdominal distention, in abdominal roentgenography to dispel interfering gas shadows, and in diabetes insipidus. Vasopressin can cause contraction of smooth muscle of the gastrointestinal tract and of all parts of the vascular bed, especially the capillaries, small arterioles and venules. It has less effect on the smooth musculature of the large veins. Vasopressin may also be used to control bleeding in some forms of von Willebrand disease and to treat extreme cases of bed wetting in children. It may also play a role in memory formation although the mechanism is unknown. | Vasopressin acts on three different receptors, vasopressin receptor V1a (which initiates vasoconstriction, liver gluconeogenesis, platelet aggregation and release of factor VIII), vasopressin receptor V1b (which mediates corticotrophin secretion from the pituitary) and vasopressin receptor V2 which controls free water reabsorption in the renal medullar. The binding of vasopressin to the V2 receptor activates adenylate cyclase which causes the release of aquaporin 2 channels into the cells lining the renal medullar duct. This allows water to be reabsorbed down an osmotic gradient so the urine is more concentrated. | Vasopressin overdose is expected to present with consequences related to excessive vasoconstriction of peripheral, mesenteric, coronary vascular beds, hyponatremia, and possibly with ventricular tachyarrhythmias, rhabdomyolysis, and gastrointestinal symptoms. As vasopressin is rapidly metabolized and cleared, symptoms will resolve with cessation of vasopressin administration. | The majority of a dose of vasopressin is metabolized and rapidly destroyed in the liver and kidneys. | NA | NA | Vasopressin has a clearance of 9-25 mL/min/kg in patients with vasodilatory shock receiving 0.01-0.1 U/min of vasopressin. | Amino Acids, Peptides, and Proteins, Antidiuretic Agents, Arginine Vasopressin, Arginine Vasopressin, analogs & derivatives, Cardiovascular Agents, Coagulants, Decreased Diuresis, Hematologic Agents, Hemostatics, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Natriuretic Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptide Hormones, Peptides, Pituitary, Pituitary Hormones, Pituitary Hormones, Posterior, Proteins, Vasoconstriction, Vasoconstrictor Agents, Vasopressin and Analogues, Vasopressins | NA | NA | NA | NA | Vasopressin V2 receptor,Vasopressin V1a receptor,Vasopressin V1b receptor, Oxytocin receptor | Pitressin | JHP Pharmaceuticals | JHP Pharmaceuticals | Vasopressin is indicated for prevention and treatment of postoperative abdominal distention, in abdominal roentgenography to dispel interfering gas shadows, and in diabetes insipidus. | NA | Vasopressin 20 units, Sodium Chloride 9 mg, Chlorobutanol 0.5% (as a preservative), Water for Injection q.s. pH (range 2.5 - 4.5) adjusted with Acetic Acid. | Vasopressin Injection, USP is a Sterile, aqueous solution of synthetic vasopressin (8-L-arginine vasopressin) of the posterior pituitary gland | intramuSubcutaneousular or Subcutaneous use | For Abdominal Distention, Abdominal Roentgenography, Diabetes Insipidus: Ten units of vassopressin (0.5mL) will usually elicit full physiologic response in adult patients. | Anaphylaxis or hypersensitivity to the drug or its components. | anaphylaxia (cardiac arrest), circumoral pallor, arrhythmias, decreased cardiac output, angina, myocardial ischemia, peripheral vasoconstruction and gangrene, nausea, vomiting, tremor, vertigo, bronchial constriction | Link | NA | NA |
| 10376 | Th1057 | Interferon beta-1b | >Th1057_Interferon_beta-1b SYNLLGFLQRSSNFQSQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20011 | C908H1408N246O253S6 | 9.02 | -0.447 | NA | 10-20 minutes | Human interferon beta (165 residues), cysteine 17 is substituted with serine. Produced in E. coli, no carbohydrates, MW=18.5kD. | Interferon beta-1b is a drug used for the treatment of relapsing/remitting multiple sclerosis. It has been shown to slow the advance of the disease as well as to decrease the frequency of attacks. | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin, neopterin and protein kinase R. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | 0.25 to 2,88 L/kg | 9.4 - 28.9 mL/min/kg [patients with diseases other than MS receiving single intravenous doses up to 2.0 mg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Myelosuppressive Agents, Peptides, Proteins, Recombinant Human Interferon beta | CA1340861 | 28-Dec-1999 | 28-Dec-2016 | NA | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | Betaseron | Bayer | Bayer | Betaseron is used to treat relapsing multiple sclerosis (MS). Betaseron will not cure MS, it will only decrease the frequency of relapse symptoms. | NA | Each vial contains 0.3 mg of interferon beta-lb. The unit measurement is derived by comparing the antiviral activity of the product to the World Health Organization (WHO) reference standard of recombinant human interferon beta. Mannitol, USP and Albumin (Human), USP (15 mg each/vial) are added as stabilizers. | Sterile, white to off-white powder | Subcutaneous Injection | The recommended starting dose is 0.0625 mg (0.25 mL) subcutaneously every other day, with dose increases over a six week period to the recommended dose of 0.25 mg (1 mL) every other day. | Betaseron is contraindicated in patients with a history of hypersensitivity to natural or recombinant interferon beta, Albumin (Human), | serious side effects: depressed mood, anxiety, trouble sleeping, restlessness, or thoughts of suicide or hurting yourself; bruising, swelling, oozing, or skin changes where the injection was given; weight changes, pounding heartbeats, feeling too hot or cold; fever, chills, body aches, flu symptoms; or nausea, stomach pain, low fever, loss of appetite, dark urine, clay-colored stools, jaundice (yellowing of the skin or eyes). | Link | NA | NA |
| 10377 | Th1057 | Interferon beta-1b | >Th1057_Interferon_beta-1b SYNLLGFLQRSSNFQSQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20011 | C908H1408N246O253S7 | 9.02 | -0.447 | NA | 10-20 minutes | Human interferon beta (165 residues), cysteine 17 is substituted with serine. Produced in E. coli, no carbohydrates, MW=18.5kD. | Interferon beta-1b is a drug used for the treatment of relapsing/remitting multiple sclerosis. It has been shown to slow the advance of the disease as well as to decrease the frequency of attacks. | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin, neopterin and protein kinase R. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | 0.25 to 2,88 L/kg | 9.4 - 28.9 mL/min/kg [patients with diseases other than MS receiving single intravenous doses up to 2.0 mg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Myelosuppressive Agents, Peptides, Proteins, Recombinant Human Interferon beta | CA1339707 | 10-Mar-1998 | 10-Mar-2015 | NA | NA | Betaferon | Bayer | Bayer | Betaferon is indicated for the treatment of patients with a single demyelinating event with an active inflammatory process, if it is severe enough to warrant treatment with intravenous corticosteroids, if alternative diagnoses have been excluded, and if they are determined to be at high risk of developing clinically definite multiple sclerosis; patients with relapsing-remitting multiple sclerosis and two or more relapses within the last two years; patients with secondary progressive multiple sclerosis with active disease, evidenced by relapses. | NA | NA | Powder and solvent that are made upto make solution. | Subcutaneous Injection | NA | People with severe depression or thoughts of suicide; People with severe liver disease; Pregnancy; Breastfeeding. | The most frequently observed side-effects are: Flu-like symptoms- such as fever,chills, painful joints, malaise, sweating, headache or muscular pain. These symptoms may be reduced by taking paracetamol or steroidal anti-inflammatory medicines such as ibuprofen. Injection site reactions. - Symptoms can include redness, swelling, discolouration, inflammation and pain. These may be reduced by the use of an auto-injector device. | Link | NA | NA |
| 10378 | Th1057 | Interferon beta-1b | >Th1057_Interferon_beta-1b SYNLLGFLQRSSNFQSQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20011 | C908H1408N246O253S8 | 9.02 | -0.447 | NA | 10-20 minutes | Human interferon beta (165 residues), cysteine 17 is substituted with serine. Produced in E. coli, no carbohydrates, MW=18.5kD. | Interferon beta-1b is a drug used for the treatment of relapsing/remitting multiple sclerosis. It has been shown to slow the advance of the disease as well as to decrease the frequency of attacks. | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin, neopterin and protein kinase R. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | 0.25 to 2,88 L/kg | 9.4 - 28.9 mL/min/kg [patients with diseases other than MS receiving single intravenous doses up to 2.0 mg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Myelosuppressive Agents, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | Extavia | Novartis | Novartis | Extavia is used to treat relapsing multiple sclerosis (MS). This medication will not cure MS, it will only decrease the frequency of relapse symptoms. | NA | Each vial contains 0.3 mg of interferon beta-1b. The unit measurement is derived by comparing the antiviral activity of the product to the World Health Organization (WHO) reference standard of recombinant human interferon beta. Mannitol, USP and Albumin (Human), USP (15 mg each/vial) are added as stabilizers. | Sterile, white to off-white powder | Subcutaneous Injection | The recommended starting dose is 0.0625 mg (0.25 mL) subcutaneously every other day, with dose increases over a six week period to the recommended dose of 0.25 mg (1 mL) every other day. | Extavia is contraindicated in patients with a history of hypersensitivity to natural or recombinant interferon beta, Albumin (Human), | serious side effects: depressed mood, anxiety, trouble sleeping, restlessness, or thoughts of suicide or hurting yourself; bruising, swelling, oozing, or skin changes where the injection was given; weight changes, pounding heartbeats, feeling too hot or cold; fever, chills, body aches, flu symptoms; or nausea, stomach pain, low fever, loss of appetite, dark urine, clay-colored stools, jaundice (yellowing of the skin or eyes). | Link | NA | NA |
| 10379 | Th1058 | Interferon alfacon-1 | >Th1058_Interferon_alfacon-1 MCDLPQTHSLGNRRALILLAQMRRISPFSCLKDRHDFGFPQEEFDGNQFQKAQAISVLHEMIQQTFNLFSTKDSSAAWDESLLEKFYTELYQQLNDLEACVIQEVGVEETPLMNVDSILAVKKYFQRITLYLTEKKYSPCAWEVVRAEIMRSFSLSTNLQERLRRKE | 19343 | C860H1353N227O255S9 | 5.99 | -0.336 | 61 | 1.3 hours in golden Syrian hamsters and 3.4 hours in rhesus monkeys. | Recombinant type-I Interferon alpha 2b (human leukocyte clone hif-sn 206 protein moiety reduced), composed of 165 amino acid residues with R at position 23. It resembles leukocyte secreted interferon. Widely used as an antiviral or antineoplastic agent. | For the treatment of hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. | Interferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which upon dimerization activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | There is limited experience with overdosage. Postmarketing surveillance includes reports of patients receiving a single dose as great as 10 times the recommended dose. In general, the primary effects of an overdose are consistent with the effects seen with therapeutic doses of interferon alfa-2b. Hepatic enzyme abnormalities, renal failure, hemorrhage, and myocardial infarction have been reported with single administration overdoses and/or with longer durations of treatment than prescribed. Toxic effects after ingestion of interferon alfa-2b are not expected because interferons are poorly absorbed orally. | NA | Absorption is high (greater than 80%) when administered intramuscularly or subcutaneously. | NA | NA | Adjuvants, Immunologic, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferons, Myelosuppressive Agents, Peptides, Proteins | CA1341567 | 19-Feb-2008 | 19-Feb-2025 | Zidovudine, The interferon increases the effect and toxicity of zidovudine | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | INFERGEN | Kadmon Pharmaceuticals, LLC., Valeant Pharmaceuticals, Inc., Three Rivers Pharmaceuticals Llc | Kadmon Pharmaceuticals, LLC., Valeant Pharmaceuticals, Inc., Three Rivers Pharmaceuticals Llc | INFERGEN (interferon alfacon-1) is indicated for treatment of chronic hepatitis C in patients 18 years of age or older with compensated liver disease. | NA | single-use vials containing 9 mcg and 15 mcg interferon alfacon-1 at a fill volume of 0.3 mL and 0.5 mL, respectively. INFERGEN vials contain 0.03 mg/mL interferon alfacon-1, sodium chloride (5.9 mg/mL), and sodium phosphate (3.8 mg/mL) in Water for Injection, USP. | INFERGEN is a Sterile, clear, colorless, preservative-free liquid | Subcutaneous Injection | The recommended dose of INFERGEN monotherapy for the initial treatment of chronic HCV infection is 9 mcg administered three times a week as a single subcutaneous injection for 24 weeks. | contraindicated in patients with hepatic decompensation; autoimmune hepatitis; known hypersensitivity reactions such as urticaria, angioedema, bronchoconstriction, anaphylaxis to interferon alphas or to any component of the product. | INFERGEN alone or in combination with ribavirin causes a broad range of serious adverse reactions; | Link | NA | NA |
| 10381 | Th1059 | Hyaluronidase | >Th1059_Hyaluronidase MWTGLGPAVTLALVLVVAWATELKPTAPPIFTGRPFVVAWDVPTQDCGPR | 53870.9 | C2455H3775N617O704S21 | 5.73 | -0.117 | NA | 0.03 hours | Highly purified sheep hyaluronidase for administration by injection into the vitreous of the eye. | For increase of absorption and distribution of other injected drugs and for rehydration. | Hyaluronidase hydrolyzes hyaluronic acid and increase diffusion of injected drugs, thus facilitating their absorption. Hyaluronidase is used for enhancing absorption and distribution of other injected drugs. | Hyaluronidase is a spreading or diffusing substance. It increase the permeability of connective tissue through the hydrolysis of hyaluronic acid. Hyaluronidase hydrolyzes hyaluronic acid by splitting the glucosaminidic bond between C1 of the glucosamine moiety and C4 of glucuronic acid. This temporarily decreases the viscosity of the cellular cement and increases diffusion of injected fluids or of localized transudates or exudates, thus facilitating their absorption. | NA | NA | NA | NA | NA | Blood and Blood Forming Organs, Carbon-Oxygen Lyases, Enzymes, Enzymes and Coenzymes, Glycoside Hydrolases, Hyaluronoglucosaminidase, antagonists & inhibitors, Hydrolases, Lyases, Polysaccharide-Lyases | NA | NA | NA | NA | Hyaluronic acid, Transforming growth factor beta-1 | HYLENEX | Baxter Healthcare Corporation | Baxter Healthcare Corporation | HYLENEX recombinant is indicated as an adjuvant in subcutaneous fluid administration for achieving hydration, to increase the dispersion and absorption of other injected drug and an adjunct in subcutaneous urography for improving resorption of radioopque agents | NA | Each mL contains 150 USP units of recombinant human hyaluronidase with 8.5 mg sodium chloride, 1.4 mg dibasic sodium phosphate, 1.0 mg albumin human, 0.9 mg edentate disodium, 0.3 mg calcium chloride, and sodium hydroxide added for pH adjustment. | HYLENEX recombinant (hyaluronidase human injection) is supplied as a Sterile, clear, colorless, nonpreserved, ready for use solution. | human Injection Subcutaneous use | Most typically 150 U hyaluronidaseare used to the injection (hyaluronidase human injection) for the subcutaneous fluid administration, will facilitate absorption of 1,000 mL or more of solution. | HYLENEX is contraindicated in patients with known hypersensitivity to hyaluronidase or any of the excipients | adverse experiences have been mild local injection site reactions such as erythema and pain. Edema has been reported most frequently. | Link | NA | NA |
| 10382 | Th1060 | Insulin, porcine | >Th1060_Insulin,_porcine GIVEQCCTSICSLYQLENYCN | 5795.6 | C257H387N65O76S6 | 5.39 | 0.218 | NA | 0.03 hours | Insulin isolated from pig pancreas. Composed of alpha and beta chains, processed from pro-insulin. Forms a hexameric structure. | For the treatment of type I and II diabetes mellitus. | Insulin is used in the treatment of type I and type II diabetes. The primary activity of insulin is the regulation of glucose metabolism. In muscle and other tissues (except the brain), insulin causes rapid transport of glucose and amino acids intracellularly. It also promotes anabolism, and inhibits protein catabolism. In the liver, insulin promotes the uptake and storage of glucose in the form of glycogen, inhibits gluconeogenesis, and promotes the conversion of excess glucose into fat. | Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism. | NA | Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process. | NA | NA | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Insulin, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides, Proteins | NA | NA | NA | NA | Interferon alpha/beta receptor 2,Interferon alpha/beta receptor 1 | vetsulin | Intervet Inc (Merck Animal Health) | Intervet Inc (Merck Animal Health) | vetsulin (porcine insulin zinc suspension) is indicated for the reduction of hyperglycemia and hyperglycemia-associated clinical signs in dogs and cats with diabetes mellitus | NA | purified porcine insulin 40 IU (35% amorphous and 65% crystalline), Zinc (as chloride) 0.08 mg, Sodium acetate trihydrate 1.36 mg, Sodium chloride 7.0 mg, Methylparaben (preservative) 1.0 mg, pH is adjusted with hydrochloric acid and/or sodium hydroxide. | Vetsulin is supplied as a sterile injectable suspension in multidose vials containing 10 mL of 40 IU/mL porcine insulin zinc suspension. Vials are supplied in cartons of one, 10 mL vial. | Subcutaneous Injection | In dogs: The initial recommended vetsulin dose is 0.5 IU insulin/kg body weight. Initially, this dose should be given once daily concurrently with, or right after a meal; In Cats:The initial recommended dose in cats is 1 to 2 IU per injection. The injections should be given twice daily at approximately 12 hour intervals. | Dogs and cats known to have a systemic allergy to pork or pork products should not be treated with vetsulin. vetsulin is contraindicated during periods of hypoglycemia. | In dogs: Clinical signs of hypoglycemia were generally mild in nature (described as weakness, lethargy, stumbling, falling down, and/or depression, hematuria, vomiting, diarrhea, pancreatitis, non-specific hepatopathy/pancreatitis, development of cataracts, and urinary tract infections. In Cats: omiting, lethargy, diarrhea, decreased appetite/anorexia, pancreatitis, dermal events, respiratory disease, urinary tract disorder, renal disease, dehydration, weight loss, polydipsia, polyuria, behavioral change, and ocular discharge/conjunctivitis. | Link | NA | NA |
| 10415 | Th1069 | Pegvisomant | >Th1069_Pegvisomant FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 | 6 days | Pegvisomant is a highly selective growth hormone (GH) receptor antagonist. It is used to treat acromegaly. Unlike dopamine or somatostatin analogs (which inhibit growth hormone secretion), this drug actually blocks the hepatic (GH-mediated) production of insulin like growth factor (IGF-1), which is the main mediator of growth hormone activity. | Pegvisomant is a growth hormone receptor antagonist used for the treatment of acromegaly. | Somavert is used for the treatment of acromegaly, which arises from excessive IGF-1 levels. Somavert selectively binds to growth hormone (GH) receptors on cell surfaces, where it blocks the binding of endogenous GH, and thus interferes with GH signal transduction. Inhibition of GH action results in decreased serum concentrations of insulin-like growth factor-I (IGF-I), and IGF binding protein-3 (IGFBP-3). This reduces the symptoms of acromegaly. | Somavert selectively binds to growth hormone (GH) receptors on cell surfaces, where it blocks the binding of endogenous GH. This leads to the normalization of serum IGF-1 levels. | NA | NA | NA | 7 L | 36 ± 28 mL/h [SC doses ranging from 10 to 20 mg/day] | Acromegaly, Amino Acids, Peptides, and Proteins, Anterior Pituitary Lobe Hormones and Analogues, Cholinesterase Inhibitors, Cytochrome P-450 CYP3A Inducers, Cytochrome P-450 CYP3A4 Inducers, Cytochrome P-450 CYP3A4 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Growth Hormone Receptor Antagonist, Growth Hormone Receptor Antagonists, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Pegylated agents, Peptide Hormones, Peptides, Pituitary and Hypothalamic Hormones and Analogues, Pituitary Hormones, Pituitary Hormones, Anterior, Somatotropin Antagonists, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | US5849535 | 15-Dec-1998 | 25-Mar-2017 | Dihydrocodeine opioids may diminish the therapeutic effect of pegvisomant. It is recommended to monitor therapy | Growth hormone receptor | SOMAVERT | Pfizer | Pfizer | SOMAVERT is indicated for the treatment of acromegaly in patients who have had an inadequate response to surgery or radiation therapy, or for whom these therapies are not appropriate. The goal of treatment is to normalize serum insulin-like growth factor-I (IGF-I) levels. | NA | SOMAVERT is available in single-dose sterile vials containing 10, 15, or 20 mg of pegvisomant protein (approximately 10, 15, and 20 U activity, respectively). Each vial also contains 1.36 mg of glycine, 36.0 mg of mannitol, 1.04 mg of sodium phosphate dibasic anhydrous, and 0.36 mg of sodium phosphate monobasic monohydrate | SOMAVERT for injection is supplied as a Sterile, white lyophilized powder | Subcutaneous Injection | The recommended loading dose of SOMAVERT is 40 mg given subcutaneously, under healthcare provider supervision. Increase the dosage by 5 mg increments every 4-6 weeks if IGF-I concentrations are elevated.Decrease the dosage by 5 mg decrements every 4-6 weeks if IGF-I concentrations are below the normal range. | None. | Hypoglycemia associated with GH lowering in patients with Diabetes Mellitus, Liver test elevations, Cross-reactivity with GH assay, Lipohypertrophy, Systemic hypersensitivity, pain, nausea ,diarrhea, dizziness, Sinusitis | Link | NA | NA |
| 10419 | Th1070 | Botulinum Toxin Type A | >Th1070_Botulinum_Toxin_Type_A MPFVNKQFNYKDPVNGVDIAYIKIPNVGQMQPVKAFKIHNKIWVIPERDTFTNPEEGDLNPPPEAKQVPVSYYDSTYLSTDNEKDNYLKGVTKLFERIYSTDLGRMLLTSIVRGIPFWGGSTIDTELKVIDTNCINVIQPDGSYRSEELNLVIIGPSADIIQFECKSFGHEVLNLTRNGYGSTQYIRFSPDFTFGFEESLEVDTNPLLGAGKFATDPAVTLAHELIHAGHRLYGIAINPNRVFKVNTNAYYEMSGLEVSFEELRTFGGHDAKFIDSLQENEFRLYYYNKFKDIASTLNKAKSIVGTTASLQYMKNVFKEKYLLSEDTSGKFSVDKLKFDKLYKMLTEIYTEDNFVKFFKVLNRKTYLNFDKAVFKINIVPKVNYTIYDGFNLRNTNLAANFNGQNTEINNMNFTKLKNFTGLFEFYKLLCVRGIITSKTKSLDKGYNKALNDLCIKVNNWDLFFSPSEDNFTNDLNKGEEITSDTNIEAAEENISLDLIQQYYLTFNFDNEPENISIENLSSDIIGQLELMPNIERFPNGKKYELDKYTMFHYLRAQEFEHGKSRIALTNSVNEALLNPSRVYTFFSSDYVKKVNKATEAAMFLGWVEQLVYDFTDETSEVSTTDKIADITIIIPYIGPALNIGNMLYKDDFVGALIFSGAVILLEFIPEIAIPVLGTFALVSYIANKVLTVQTIDNALSKRNEKWDEVYKYIVTNWLAKVNTQIDLIRKKMKEALENQAEATKAIINYQYNQYTEEEKNNINFNIDDLSSKLNESINKAMININKFLNQCSVSYLMNSMIPYGVKRLEDFDASLKDALLKYIYDNRGTLIGQVDRLKDKVNNTLSTDIPFQLSKYVDNQRLLSTFTEYIKNIINTSILNLRYESNHLIDLSRYASKINIGSKVNFDPIDKNQIQLFNLESSKIEVILKNAIVYNSMYENFSTSFWIRIPKYFNSISLNNEYTIINCMENNSGWKVSLNYGEIIWTLQDTQEIKQRVVFKYSQMINISDYINRWIFVTITNNRLNNSKIYINGRLIDQKPISNLGNIHASNNIMFKLDGCRDTHRYIWIKYFNLFDKELNEKEIKDLYDNQSNSGILKDFWGDYLQYDKPYYMLNLYDPNKYVDVNNVGIRGYMYLKGPRGSVMTTNIYLNSSLYRGTKFIIKKYASGNKDNIVRNNDRVYINVVVKNKEYRLATNASQAGVEKILSALEIPDVGNLSQVVVMKSKNDQGITNKCKMNLQDNNGNDIGFIGFHQFNNIAKLVASNWYNRQIERSSRTLGCSWEFIPVDDGWGERPL | 900000 | C6760H10447N1743O2010S32 | 5.6 | -0.368 | 85.5-86.5 | 230 to 260 min in a pharmacokinetic study of rats and mice | Purified botulinum toxin from Clostridium botulinum, purified from culture via dialysis and acid precipitation. | For the treatment of cervical dystonia in adults to decrease the severity of abnormal head position and neck pain associated with cervical dystonia. Also for the treatment of severe primary axillary hyperhidrosis that is inadequately managed with topical agents and for the treatment of strabismus and blepharospasm associated with dystonia, including benign essential blepharospasm or VII nerve disorders in patients 12 years of age and above. Also used cosmetically to temporarily improve the appearance of moderate-to-severe frown lines between the eyebrows (glabellar lines) as well as for the treatment of excessive underarm sweating. | A 150 kDa neurotoxic protein produced from fermentation of Hall strain Clostridium botulinum type A grown in a medium containing casein hydrolysate, glucose and yeast extract. It is purified from the culture solution by dialysis and a series of acid precipitations to a complex consisting of the neurotoxin, and several accessory proteins. Botulinum Toxin Type A is not expected to be present in the peripheral blood at measurable levels following IM or intradermal injection at the recommended doses. The recommended quantities of neurotoxin administered at each treatment session are not expected to result in systemic, overt distant clinical effects, i.e. muscle weakness, in patients without other neuromuscular dysfunction. However, sub-clinical systemic effects have been shown by single-fiber electromyography after IM doses of botulinum toxins appropriate to produce clinically observable local muscle weakness. | Botulinum Toxin Type A blocks neuromuscular transmission by binding to acceptor sites on motor or sympathetic nerve terminals, entering the nerve terminals, and inhibiting the release of acetylcholine. This inhibition occurs as the neurotoxin cleaves SNAP-25, a protein integral to the successful docking and release of acetylcholine from vesicles situated within nerve endings. | Based on toxicological studies, it has been estimated that the human LD50 by injection is approximately 2800 Units, equivalent to 28 individual vials of BOTOX (Botulinum Toxin Type A) Purified Neurotoxin Complex (100 Units) for a 70 kg adult. When injected intramuscularly, Botulinum Toxin Type A has been shown to be teratogenic or to have embryocidal effects in some animal species. | NA | The chemical complexity of Botulinum Toxin Type A combined with its extreme potency limits the opportunity to study its pharmacokinetic profile in humans. Therefore, no human pharmacokinetic studies have been performed. Botulinum Toxin Type A is injected directly into the target organ, a skeletal muscle. Thus, bioavailability of the intravenous or oral route is not of clinical relevance. | NA | NA | Acetylcholine Release Inhibitors, Agents that produce neuromuscular block (indirect), Amino Acids, Peptides, and Proteins, Bacterial Proteins, Bacterial Toxins, Biological Factors, Botulinum Toxins, Botulinum Toxins, Type A, Central Nervous System Depressants, Cholinergic Agents, Endopeptidases, Enzymes, Enzymes and Coenzymes, Ganglion Blockers, Hydrolases, Membrane Transport Modulators, Metalloendopeptidases, Metalloproteases, Muscle Relaxants, Muscle Relaxants, Peripherally Acting Agents, Musculo-Skeletal System, Neuromuscular Agents, Neuromuscular Blocking Agents, Neurotoxins, Neurotransmitter Agents, Noxae, Other Miscellaneous Therapeutic Agents, Peptide Hydrolases, Peripheral Nervous System Agents, Proteins, Toxic Actions, Toxins, Biological | CA2280565 | 15-Nov-2005 | 20-Aug-2019 | NA | Synaptosomal-associated protein 25,Rho-related GTP-binding protein RhoB | BOTOX | Allergan | Allergan | Prescribed in cases such as Bladder Dysfunction, Chronic Migraine, Upper Limb Spasticity, Cervical Dystonia, Primary Axillary Hyperhidrosis, Blepharospasm and Strabismus | NA | Each vial of BOTOX contains either 50 Units of Clostridium botulinum type A neurotoxin complex, 0.25 mg of Albumin Human, and 0.45 mg of sodium chloride; 100 Units of Clostridium botulinum type A neurotoxin complex, 0.5 mg of Albumin Human, and 0.9 mg of sodium chloride; or 200 Units of Clostridium botulinum type A neurotoxin complex, 1 mg of Albumin Human, and 1.8 mg of sodium chloride in a sterile, vacuum-dried form without a preservative. | BOTOX (onabotulinum toxin A) For Injection is a sterile, vacuum-dried purified botulinum toxin type A, produced from fermentation of Hall strainClostridium botulinum type A | IntramuSubcutaneousular, intradetrusor and intrade | Do not exceed a total dose of 360 Units administered in a 3 month interval. | Known Hypersensitivity to Botulinum Toxin, Infection at the Injection Site, Urinary Tract Infection or Urinary Retention. | Spread of Toxin Effects, Hypersensitivity, Dysphagia and Breathing Difficulties in Treatment of Cervical Dystonia, Bronchitis and Upper Respiratory Tract Infections in Patients Treated for Spasticity, Urinary Retention in Patients Treated for Bladder Dysfunction. | Link | NA | NA |
| 10420 | Th1070 | Botulinum Toxin Type A | >Th1070_Botulinum_Toxin_Type_A MPFVNKQFNYKDPVNGVDIAYIKIPNVGQMQPVKAFKIHNKIWVIPERDTFTNPEEGDLNPPPEAKQVPVSYYDSTYLSTDNEKDNYLKGVTKLFERIYSTDLGRMLLTSIVRGIPFWGGSTIDTELKVIDTNCINVIQPDGSYRSEELNLVIIGPSADIIQFECKSFGHEVLNLTRNGYGSTQYIRFSPDFTFGFEESLEVDTNPLLGAGKFATDPAVTLAHELIHAGHRLYGIAINPNRVFKVNTNAYYEMSGLEVSFEELRTFGGHDAKFIDSLQENEFRLYYYNKFKDIASTLNKAKSIVGTTASLQYMKNVFKEKYLLSEDTSGKFSVDKLKFDKLYKMLTEIYTEDNFVKFFKVLNRKTYLNFDKAVFKINIVPKVNYTIYDGFNLRNTNLAANFNGQNTEINNMNFTKLKNFTGLFEFYKLLCVRGIITSKTKSLDKGYNKALNDLCIKVNNWDLFFSPSEDNFTNDLNKGEEITSDTNIEAAEENISLDLIQQYYLTFNFDNEPENISIENLSSDIIGQLELMPNIERFPNGKKYELDKYTMFHYLRAQEFEHGKSRIALTNSVNEALLNPSRVYTFFSSDYVKKVNKATEAAMFLGWVEQLVYDFTDETSEVSTTDKIADITIIIPYIGPALNIGNMLYKDDFVGALIFSGAVILLEFIPEIAIPVLGTFALVSYIANKVLTVQTIDNALSKRNEKWDEVYKYIVTNWLAKVNTQIDLIRKKMKEALENQAEATKAIINYQYNQYTEEEKNNINFNIDDLSSKLNESINKAMININKFLNQCSVSYLMNSMIPYGVKRLEDFDASLKDALLKYIYDNRGTLIGQVDRLKDKVNNTLSTDIPFQLSKYVDNQRLLSTFTEYIKNIINTSILNLRYESNHLIDLSRYASKINIGSKVNFDPIDKNQIQLFNLESSKIEVILKNAIVYNSMYENFSTSFWIRIPKYFNSISLNNEYTIINCMENNSGWKVSLNYGEIIWTLQDTQEIKQRVVFKYSQMINISDYINRWIFVTITNNRLNNSKIYINGRLIDQKPISNLGNIHASNNIMFKLDGCRDTHRYIWIKYFNLFDKELNEKEIKDLYDNQSNSGILKDFWGDYLQYDKPYYMLNLYDPNKYVDVNNVGIRGYMYLKGPRGSVMTTNIYLNSSLYRGTKFIIKKYASGNKDNIVRNNDRVYINVVVKNKEYRLATNASQAGVEKILSALEIPDVGNLSQVVVMKSKNDQGITNKCKMNLQDNNGNDIGFIGFHQFNNIAKLVASNWYNRQIERSSRTLGCSWEFIPVDDGWGERPL | 900000 | C6760H10447N1743O2010S32 | 5.6 | -0.368 | 85.5-86.6 | 230 to 260 min in a pharmacokinetic study of rats and mice | Purified botulinum toxin from Clostridium botulinum, purified from culture via dialysis and acid precipitation. | For the treatment of cervical dystonia in adults to decrease the severity of abnormal head position and neck pain associated with cervical dystonia. Also for the treatment of severe primary axillary hyperhidrosis that is inadequately managed with topical agents and for the treatment of strabismus and blepharospasm associated with dystonia, including benign essential blepharospasm or VII nerve disorders in patients 12 years of age and above. Also used cosmetically to temporarily improve the appearance of moderate-to-severe frown lines between the eyebrows (glabellar lines) as well as for the treatment of excessive underarm sweating. | A 150 kDa neurotoxic protein produced from fermentation of Hall strain Clostridium botulinum type A grown in a medium containing casein hydrolysate, glucose and yeast extract. It is purified from the culture solution by dialysis and a series of acid precipitations to a complex consisting of the neurotoxin, and several accessory proteins. Botulinum Toxin Type A is not expected to be present in the peripheral blood at measurable levels following IM or intradermal injection at the recommended doses. The recommended quantities of neurotoxin administered at each treatment session are not expected to result in systemic, overt distant clinical effects, i.e. muscle weakness, in patients without other neuromuscular dysfunction. However, sub-clinical systemic effects have been shown by single-fiber electromyography after IM doses of botulinum toxins appropriate to produce clinically observable local muscle weakness. | Botulinum Toxin Type A blocks neuromuscular transmission by binding to acceptor sites on motor or sympathetic nerve terminals, entering the nerve terminals, and inhibiting the release of acetylcholine. This inhibition occurs as the neurotoxin cleaves SNAP-25, a protein integral to the successful docking and release of acetylcholine from vesicles situated within nerve endings. | Based on toxicological studies, it has been estimated that the human LD50 by injection is approximately 2800 Units, equivalent to 28 individual vials of BOTOX (Botulinum Toxin Type A) Purified Neurotoxin Complex (100 Units) for a 70 kg adult. When injected intramuscularly, Botulinum Toxin Type A has been shown to be teratogenic or to have embryocidal effects in some animal species. | NA | The chemical complexity of Botulinum Toxin Type A combined with its extreme potency limits the opportunity to study its pharmacokinetic profile in humans. Therefore, no human pharmacokinetic studies have been performed. Botulinum Toxin Type A is injected directly into the target organ, a skeletal muscle. Thus, bioavailability of the intravenous or oral route is not of clinical relevance. | NA | NA | Acetylcholine Release Inhibitors, Agents that produce neuromuscular block (indirect), Amino Acids, Peptides, and Proteins, Bacterial Proteins, Bacterial Toxins, Biological Factors, Botulinum Toxins, Botulinum Toxins, Type A, Central Nervous System Depressants, Cholinergic Agents, Endopeptidases, Enzymes, Enzymes and Coenzymes, Ganglion Blockers, Hydrolases, Membrane Transport Modulators, Metalloendopeptidases, Metalloproteases, Muscle Relaxants, Muscle Relaxants, Peripherally Acting Agents, Musculo-Skeletal System, Neuromuscular Agents, Neuromuscular Blocking Agents, Neurotoxins, Neurotransmitter Agents, Noxae, Other Miscellaneous Therapeutic Agents, Peptide Hydrolases, Peripheral Nervous System Agents, Proteins, Toxic Actions, Toxins, Biological | CA2310845 | 15-May-2001 | 7-Jun-2014 | NA | Growth hormone receptor | Dysport | Ipsen Pharmaceuticals | Ipsen Pharmaceuticals | Dysport is indicated for the treatment of Cervical Dystonia and Glabellar Lines | NA | Each vial contains 500 or 300 Units of lyophilized abobotulinumtoxinA, 125 micrograms human serum albumin and 2.5 mg lactose. Dysport may contain trace amounts of cow's milk proteins | Dysport is supplied in a single-use, sterile vial for reconstitution | IntramuSubcutaneousular Injection | In Cervical Dystonia: Initial dose of DYSPORT  is 500 Units given intramuscularly. Re-treatment every 12 to 16 weeks or longer, as necessary, based on return of clinical symptoms with doses administered between 250 and 1000 Units to optimize clinical benefit. In Glabellar Lines: A total dose of 50 Units of DYSPORT , divided in five equal aliquots of 10 Units each, should be administered to affected muscles to achieve clinical effect. | DYSPORT is contraindicated in patients with known hypersensitivity to any botulinum toxin preparation or to any of the components in the formulation. | In Cervical Dystonia: Most commonly observed adverse reactions (> 5% of patients) are: muscular weakness, dysphagia, dry mouth, injection site discomfort, fatigue, headache, neck pain, musculoskeletal pain, dysphonia, injection site pain, and eye disorders. In Glabellar Lines: The most frequently reported adverse events (≥2%) are nasopharyngitis, headache, injection site pain, injection site reaction, upper respiratory tract infection, eyelid edema, eyelid ptosis, sinusitis and nausea. | Link | NA | NA |
| 10421 | Th1070 | Botulinum Toxin Type A | >Th1070_Botulinum_Toxin_Type_A MPFVNKQFNYKDPVNGVDIAYIKIPNVGQMQPVKAFKIHNKIWVIPERDTFTNPEEGDLNPPPEAKQVPVSYYDSTYLSTDNEKDNYLKGVTKLFERIYSTDLGRMLLTSIVRGIPFWGGSTIDTELKVIDTNCINVIQPDGSYRSEELNLVIIGPSADIIQFECKSFGHEVLNLTRNGYGSTQYIRFSPDFTFGFEESLEVDTNPLLGAGKFATDPAVTLAHELIHAGHRLYGIAINPNRVFKVNTNAYYEMSGLEVSFEELRTFGGHDAKFIDSLQENEFRLYYYNKFKDIASTLNKAKSIVGTTASLQYMKNVFKEKYLLSEDTSGKFSVDKLKFDKLYKMLTEIYTEDNFVKFFKVLNRKTYLNFDKAVFKINIVPKVNYTIYDGFNLRNTNLAANFNGQNTEINNMNFTKLKNFTGLFEFYKLLCVRGIITSKTKSLDKGYNKALNDLCIKVNNWDLFFSPSEDNFTNDLNKGEEITSDTNIEAAEENISLDLIQQYYLTFNFDNEPENISIENLSSDIIGQLELMPNIERFPNGKKYELDKYTMFHYLRAQEFEHGKSRIALTNSVNEALLNPSRVYTFFSSDYVKKVNKATEAAMFLGWVEQLVYDFTDETSEVSTTDKIADITIIIPYIGPALNIGNMLYKDDFVGALIFSGAVILLEFIPEIAIPVLGTFALVSYIANKVLTVQTIDNALSKRNEKWDEVYKYIVTNWLAKVNTQIDLIRKKMKEALENQAEATKAIINYQYNQYTEEEKNNINFNIDDLSSKLNESINKAMININKFLNQCSVSYLMNSMIPYGVKRLEDFDASLKDALLKYIYDNRGTLIGQVDRLKDKVNNTLSTDIPFQLSKYVDNQRLLSTFTEYIKNIINTSILNLRYESNHLIDLSRYASKINIGSKVNFDPIDKNQIQLFNLESSKIEVILKNAIVYNSMYENFSTSFWIRIPKYFNSISLNNEYTIINCMENNSGWKVSLNYGEIIWTLQDTQEIKQRVVFKYSQMINISDYINRWIFVTITNNRLNNSKIYINGRLIDQKPISNLGNIHASNNIMFKLDGCRDTHRYIWIKYFNLFDKELNEKEIKDLYDNQSNSGILKDFWGDYLQYDKPYYMLNLYDPNKYVDVNNVGIRGYMYLKGPRGSVMTTNIYLNSSLYRGTKFIIKKYASGNKDNIVRNNDRVYINVVVKNKEYRLATNASQAGVEKILSALEIPDVGNLSQVVVMKSKNDQGITNKCKMNLQDNNGNDIGFIGFHQFNNIAKLVASNWYNRQIERSSRTLGCSWEFIPVDDGWGERPL | 900000 | C6760H10447N1743O2010S32 | 5.6 | -0.368 | 85.5-86.7 | 230 to 260 min in a pharmacokinetic study of rats and mice | Purified botulinum toxin from Clostridium botulinum, purified from culture via dialysis and acid precipitation. | For the treatment of cervical dystonia in adults to decrease the severity of abnormal head position and neck pain associated with cervical dystonia. Also for the treatment of severe primary axillary hyperhidrosis that is inadequately managed with topical agents and for the treatment of strabismus and blepharospasm associated with dystonia, including benign essential blepharospasm or VII nerve disorders in patients 12 years of age and above. Also used cosmetically to temporarily improve the appearance of moderate-to-severe frown lines between the eyebrows (glabellar lines) as well as for the treatment of excessive underarm sweating. | A 150 kDa neurotoxic protein produced from fermentation of Hall strain Clostridium botulinum type A grown in a medium containing casein hydrolysate, glucose and yeast extract. It is purified from the culture solution by dialysis and a series of acid precipitations to a complex consisting of the neurotoxin, and several accessory proteins. Botulinum Toxin Type A is not expected to be present in the peripheral blood at measurable levels following IM or intradermal injection at the recommended doses. The recommended quantities of neurotoxin administered at each treatment session are not expected to result in systemic, overt distant clinical effects, i.e. muscle weakness, in patients without other neuromuscular dysfunction. However, sub-clinical systemic effects have been shown by single-fiber electromyography after IM doses of botulinum toxins appropriate to produce clinically observable local muscle weakness. | Botulinum Toxin Type A blocks neuromuscular transmission by binding to acceptor sites on motor or sympathetic nerve terminals, entering the nerve terminals, and inhibiting the release of acetylcholine. This inhibition occurs as the neurotoxin cleaves SNAP-25, a protein integral to the successful docking and release of acetylcholine from vesicles situated within nerve endings. | Based on toxicological studies, it has been estimated that the human LD50 by injection is approximately 2800 Units, equivalent to 28 individual vials of BOTOX (Botulinum Toxin Type A) Purified Neurotoxin Complex (100 Units) for a 70 kg adult. When injected intramuscularly, Botulinum Toxin Type A has been shown to be teratogenic or to have embryocidal effects in some animal species. | NA | The chemical complexity of Botulinum Toxin Type A combined with its extreme potency limits the opportunity to study its pharmacokinetic profile in humans. Therefore, no human pharmacokinetic studies have been performed. Botulinum Toxin Type A is injected directly into the target organ, a skeletal muscle. Thus, bioavailability of the intravenous or oral route is not of clinical relevance. | NA | NA | Acetylcholine Release Inhibitors, Agents that produce neuromuscular block (indirect), Amino Acids, Peptides, and Proteins, Bacterial Proteins, Bacterial Toxins, Biological Factors, Botulinum Toxins, Botulinum Toxins, Type A, Central Nervous System Depressants, Cholinergic Agents, Endopeptidases, Enzymes, Enzymes and Coenzymes, Ganglion Blockers, Hydrolases, Membrane Transport Modulators, Metalloendopeptidases, Metalloproteases, Muscle Relaxants, Muscle Relaxants, Peripherally Acting Agents, Musculo-Skeletal System, Neuromuscular Agents, Neuromuscular Blocking Agents, Neurotoxins, Neurotransmitter Agents, Noxae, Other Miscellaneous Therapeutic Agents, Peptide Hydrolases, Peripheral Nervous System Agents, Proteins, Toxic Actions, Toxins, Biological | NA | NA | NA | NA | NA | Xeomin | MERZ AESTHETICS | MERZ AESTHETICS | Xeomin is indicated in Cervical Dystonia, Blepharospasm, Glabellar Lines | NA | One vial of XEOMIN contains 50 or 100 Units of incobotulinumtoxinA, 1 mg of human albumin, and 4.7 mg sucrose. | XEOMIN is a sterile white to off-white lyophilized powder after reconstitution with preservative-free 0.9% Saline for Injection. | IntramuSubcutaneousular Injection | In Cervical Dystonia: Initial dose of Xeomin is 120 Units given intramuscularly. In Blepharospasm: The total initial dose of XEOMIN in both eyes should not exceed 70 Units (35 Units/eye).In Glabellar Lines: The total recommended XEOMIN dose is 20 Units per treatment session divided into five equal intramuscular injections of 4 Units each. | Known hypersensitivity to the active substance botulinum neurotoxin type A or to any of the excipients and Infection at the proposed injection sites | In Cervical Dystonia: The most commonly observed adverse reactions (≥5% of patients and > placebo) are dysphagia, neck pain, muscle weakness, injection site pain, and musculoskeletal pain. In Blepharospasm: The most commonly observed adverse reactions (≥5% of patients and > placebo) are eyelid ptosis, dry eye, dry mouth, diarrhea, headache, visual impairment, dyspnea, nasopharyngitis, and respiratory tract infection. In Glabellar Lines:The most commonly observed adverse reaction (>1% of patients and > placebo) is headache. | Link | NA | NA |
| 10440 | Th1077 | Urofollitropin | >Th1077_Urofollitropin APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 980.162 | C42H65N11O12S2 | 7.5 | -0.33 | 55 | Circulation half life of 3-4 hours, elimination half life of 35-40 hours | Urofollitropin is a purified form of follicle-stimulating hormone (FSH) that is manufactured by extraction from human urine and then purified. It consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Urofollitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Urofollitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). | For treatment of female infertility | Urofollitropin or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of urofollitropin is the primary hormone responsible for follicular recruitment and development. | FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells. | NA | NA | 0.74 | Time to peak in plasma: IM: 17 hours (single dose), 11 hours (multiple doses) SubQ: 21 hours (single dose), 10 hours (multiple doses) | NA | Fertility Agents | US5767067 | 16-Jun-1998 | 16-Jun-2015 | NA | Follicle-stimulating hormone receptor | BRAVELLE | Ferring Pharmaceuticals Inc. | Ferring Pharmaceuticals Inc. | BRAVELLE (urofollitropin for injection, purified) is a gonadotropin indicated for Induction of ovulation in women who have previously received pituitary suppression – intramuscular and subcutaneous administration, Development of multiple follicles as part of an Assisted Reproductive Technology (ART) cycle in ovulatory women who have previously received pituitary suppression | NA | Each vial of BRAVELLE contains 82.5 International Units (IU) of Follicle Stimulating Hormone (FSH) activity, 23 mg Lactose Monohydrate, 0.005 mg Polysorbate 20, and Sodium Phosphate buffer (Sodium Phosphate dibasic, Heptahydrate and Phosphoric acid) for pH adjustments, which, when reconstituted with diluent, will deliver 75 International Units of FSH. BRAVELLE contains up to 2% luteinizing hormone (LH) activity based on bioassay. Human Chorionic Gonadotropin(hCG) is not detected in BRAVELLE. When stored at 3° to 25, up to 40% of the α-subunits may be oxidized. | BRAVELLE is a sterile, lyophilized powder used after reconstitution with Sterile 0.9% Sodium Chloride Injection, USP | IntramuSubcutaneousular and Subcutaneous administr | Initial starting 150 International Units per day for 5 days, administered subcutaneously or intramuscularly in case of ovulation induction. In case of Assisted Reproductive Technology (ART) initial starting dose of the first cycle – 225 International Units per day for 5 days, administered subcutaneously. | RAVELLE is contraindicated in women who exhibits Prior hypersensitivity to BRAVELLE or urofollitropins, High levels of FSH indicating primary ovarian failure, Pregnancy, Presence of uncontrolled non-gonadal endocrinopathies, Sex hormone dependent tumors of the reproductive tract and accessory organ, Tumors of pituitary gland or hypothalamus, Abnormal uterine bleeding of undetermined origin, Ovarian cysts or enlargement of undetermined origin, not due to polycystic ovary syndrome. | The most common adverse reactions (≥5% incidence) in ovulation induction include: headache, hot flashes, OHSS, pain, and respiratory disorder. The most common adverse reactions (≥2% incidence) in ART include: abdominal cramps, abdominal fullness/enlargement, headache, nausea, OHSS, pain, pelvic pain, and post retrieval pain. | Link | NA | NA |
| 10441 | Th1077 | Urofollitropin | >Th1077_Urofollitropin APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 980.162 | C42H65N11O12S2 | 7.5 | -0.33 | 55 | Circulation half life of 3-4 hours, elimination half life of 35-40 hours | Urofollitropin is a purified form of follicle-stimulating hormone (FSH) that is manufactured by extraction from human urine and then purified. It consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Urofollitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Urofollitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). | For treatment of female infertility | Urofollitropin or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of urofollitropin is the primary hormone responsible for follicular recruitment and development. | FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells. | NA | NA | 0.74 | Time to peak in plasma: IM: 17 hours (single dose), 11 hours (multiple doses) SubQ: 21 hours (single dose), 10 hours (multiple doses) | NA | Fertility Agents | NA | NA | NA | NA | Follicle-stimulating hormone receptor | Metrodin | NA | NA | Metrodin (urofollitropin for injection) and hCG given in a sequential manner are indicated for the stimulation of follicular development and the induction ofovulation in patients with polycystic ovary syndrome, and infertility, who have failed to respond or conceive following adequate clomiphene citrate therapy. Metrodin (urofollitropin for injection) and hCG may also be used to stimulate the development of multiple follicles in ovulatory patients undergoing Assisted Reproductive Technologies (ART) such as in vitro fertilization. | NA | Each ampule of Metrodin (urofollitropin for injection) contains 75 or 150 IU of follicle-stimulating hormone (FSH) activity, in not more than 0.83 mg (75 IU) or 1.66 mg (150 IU) of extract, plus 10 mg lactose | Metrodin (urofollitropin for injection) is a sterile, lypholized powder form contains an acidic, water soluble glycoprotein biologically standardized for FSH gonadotropin activity | IntramuSubcutaneousular Injection. | Initial starting 75 International Units per day for 5 days administered intramuscularly in polycystic ovary syndrome. In ART the dose is 150 IU per day. | contraindicated in High levels of FSH indicating primary ovarian failure, Uncontrolled thyroid or adrenal dysfunction, An organic intracranial lesion such as a pituitary tumor, The presence of any cause of infertility other than anovulation, as stated in the Indications unless they are candidates for Assisted Reproductive Technologies, Abnormal bleeding of undetermined origin, Ovarian cysts or enlargement of undetermined origin, Prior hypersensitivity to urofollitropin. | Pulmonary and vascular complications, Ovarian Hyperstimulation Syndrome, Adnexal torsion, Mild to moderate ovarian enlargement, Abdominal pain, Ovarian cysts, nausea, vomiting, diarrhea, abdominal cramps, bloating, Pain, rash, swelling, and/or irritation at the site of injection, Ectopic pregnancy, Congenital abnormalities, dry skin, body rash, hair loss, hives, Headache. | Link | NA | NA |
| 10442 | Th1077 | Urofollitropin | >Th1077_Urofollitropin APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 980.162 | C42H65N11O12S2 | 7.5 | -0.33 | 55 | Circulation half life of 3-4 hours, elimination half life of 35-40 hours | Urofollitropin is a purified form of follicle-stimulating hormone (FSH) that is manufactured by extraction from human urine and then purified. It consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Urofollitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Urofollitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). | For treatment of female infertility | Urofollitropin or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of urofollitropin is the primary hormone responsible for follicular recruitment and development. | FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells. | NA | NA | 0.74 | Time to peak in plasma: IM: 17 hours (single dose), 11 hours (multiple doses) SubQ: 21 hours (single dose), 10 hours (multiple doses) | NA | Fertility Agents | NA | NA | NA | NA | Follicle-stimulating hormone receptor | Fertinex | NA | NA | FertinexTM (urofollitropin for injection, purified) and hCG given in a sequential manner are indicated for the stimulation of follicular recruitment and development and the induction of ovulation in patients with polycystic ovary syndrome and infertility, who have failed to respond or conceive following adequate clomiphene citrate therapy. Fertinex (urofollitropin) TM and hCG may also be used to stimulate the development of multiple follicles in ovulatory patients undergoing Assisted Reproductive Technologies (ART) such as in vitro fertilization. | NA | Each ampule of Fertinex (urofollitropin) TM contains either 75 IU or 150 IU of highly purified FSH and 10 mg lactose. If required, pH is adjusted with 0.1 M hydrochloric acid and/or 0.1 M sodium hydroxide. | Fertinex (urofollitropin) in asterile, lyophilized powder form contains an acidic, water soluble glycoprotein biologically standardized for FSH gonadotropin activity | Subcutaneous Injection. | Initial starting 75 International Units per day for 5 days administered intramuscularly in polycystic ovary syndrome. In ART the dose is 150 IU per day. | contraindicated in High levels of FSH indicating primary ovarian failure, Uncontrolled thyroid or adrenal dysfunction, An organic intracranial lesion such as a pituitary tumor, The presence of any cause of infertility other than anovulation, as stated in the Indications unless they are candidates for Assisted Reproductive Technologies, Abnormal bleeding of undetermined origin, Ovarian cysts or enlargement of undetermined origin, Prior hypersensitivity to urofollitropin. | Pulmonary and vascular complications, Ovarian Hyperstimulation Syndrome, Adnexal torsion, Mild to moderate ovarian enlargement, Abdominal pain, Ovarian cysts, nausea, vomiting, diarrhea, abdominal cramps, bloating, Pain, rash, swelling, and/or irritation at the site of injection, Ectopic pregnancy, Congenital abnormalities, dry skin, body rash, hair loss, hives, Headache. | Link | NA | NA |
| 10443 | Th1078 | Efalizumab | >Th1078_Efalizumab EVQLVESGGGLVQPGGSLRLSCAASGYSFTGHWMNWVRQAPGKGLEWVGIMIHPSDSETRYNQKFKDIRFTISVDKSKNTLYLQMNSLRAEDTAVYYCARIGIYFYGTTYFDYIWGQGTLVTVSS | 150000 | NA | NA | NA | 61 (FAB f | 5 days | Efalizumab is Humanized IgG1 kappa isotype monoclonal antibody that binds to human CD11a. It is produced in a Chinese hamster ovary mammalian cell expression system in a nutrient medium containing the antibiotic gentamicin. | Indcated in treatment of adult patients with moderate to severe chronic plaque psoriasis, who are candidates for phototherapy or systemic therapy. | In psoriatic skin, ICAM-1 cell surface expression is upregulated on endothelium and keratinocytes. Raptiva inhibits the binding of LFA-1 to the intercellular adhesion molecule-1 (ICAM-1), thereby inhibiting the adhesion of leukocytes to other cell types. | Efalizumab binds to CD11a, a subunit of leukocyte function antigen-1 (LFA-1), which is expressed on all leukocytes. As a result efalizumab decreases cell surface expression of CD11a. | NA | NA | Average efalizumab bioavailability following subcutaneous administration was estimated at 30 to 50%. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antigens, CD11,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,CD11a-directed Antibody Interactions,CD11a-directed Humanized IgG1 Antibody,Cell Migration Inhibition,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Proteins,Selective Immunosuppressants,Serum Globulins | NA | NA | NA | Ergonovine is the antiretroviral agent may increase the ergot derivative | Integrin alpha-L,Integrin alpha-X | RAPTIVA | Genentech, Inc. | Genentech, Inc. | RAPTIVA (efalizumab) is indicated for the treatment of adult patients (18 years or older) with chronic moderate to severe plaque psoriasis who are candidates for systemic therapy or phototherapy. | NA | Each single-use vial of RAPTIVA contains 150 mg of efalizumab, 123.2 mg of sucrose, 6.8 mg of L-histidine hydrochloride monohydrate, 4.3 mg of L-histidine and 3 mg of polysorbate 20 and is designed to deliver 125 mg of efalizumab in 1.25 mL. | RAPTIVA (efalizumab) is supplied as a sterile, white to off-white, lyophilized powder in single-use glass vials | Subcutaneous (Subcutaneous) Injection. | The recommended dose of RAPTIVA (efalizumab) is a single 0.7 mg/kg SCconditioning dose followed by weekly SC doses of 1 mg/kg (maximum single dose not to exceed a total of 200 mg). | RAPTIVA (efalizumab) should not be administered to patients with known hypersensitivity to RAPTIVA (efalizumab) or any of its components. | he most serious adverse reactions observed during treatment with RAPTIVA (efalizumab) are serious infections, including PML, malignancies,thrombocytopenia, hemolytic anemia, arthritis events, psoriasis worsening and variants, and neurologic events. The most common adverse reactions associated with RAPTIVA (efalizumab) were a first dose reaction complex that included headache, chills, fever, nausea, and myalgia. | Link | NA | NA |
| 10472 | Th1086 | Interferon alfa-2b | >Th1086_Interferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMNEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 19271 | C860H1353N229O255S9 | 5.99 | -0.339 | 61 | The elimination half-life following both intramuscular and subcutaneous injections was approximately 2 to 3 hours | Recombinant type-I Interferon alpha 2b (human leukocyte clone hif-sn 206 protein moiety reduced), composed of 165 amino acid residues with R at position 23. It resembles leukocyte secreted interferon. Widely used as an antiviral or antineoplastic agent. | For the treatment of hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. | Interferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which upon dimerization activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | There is limited experience with overdosage. Postmarketing surveillance includes reports of patients receiving a single dose as great as 10 times the recommended dose. In general, the primary effects of an overdose are consistent with the effects seen with therapeutic doses of interferon alfa-2b. Hepatic enzyme abnormalities, renal failure, hemorrhage, and myocardial infarction have been reported with single administration overdoses and/or with longer durations of treatment than prescribed. Toxic effects after ingestion of interferon alfa-2b are not expected because interferons are poorly absorbed orally. | NA | Absorption is high (greater than 80%) when administered intramuscularly or subcutaneously. | NA | NA | Immunosuppressive Agents | CA1341567 | 19-Feb-2008 | 19-Feb-2025 | NA | Interferon alpha/beta receptor 2,Interferon alpha/beta receptor 1 | INTRON A | Merck | Merck | Hairy Cell Leukemia, Malignant Melanoma, Follicular Lymphoma, Condylomata Acuminata, AIDS-Related Kaposi's Sarcoma, Chronic Hepatitis C, Chronic Hepatitis B, | NA | INTRON A Powder for Injection, 10 million IU per vial and Diluent for INTRON A (Sterile Water for Injection USP) 1 mL per vial, INTRON A Solution for Injection, 18 million IU multidose vial (22.8 million IU per 3.8 mL per vial); boxes containing 1 vial of INTRON A Solution for Injection | Powder or solution | IntramuSubcutaneousular, Subcutaneous, Intralesion | Not all dosage forms and strengths are appropriate for some indications. To enhance the tolerability of INTRON A, injections should be administered in the evening when possible; To reduce the incidence of certain adverse reactions, acetaminophen may be administered at the time of injection;The solution should be allowed to come to room temperature before using. | Alpha interferons, including INTRON A, cause or aggravate fatal or life-threatening neuropsychiatric, autoimmune, ischemic, and infectious disorders. Patients should be monitored closely with periodic clinical and laboratory evaluations. Patients with persistently severe or worsening signs or symptoms of these conditions should be withdrawn from therapy. In many but not all cases these disorders resolve after stopping INTRON A therapy. | most frequently reported adverse reactions were “flu-like†symptoms, particularly fever, headache, chills, myalgia, and fatigue. More severe toxicities are observed generally at higher doses and may be difficult for patients to tolerate. | Link | NA | NA |
| 10478 | Th1088 | Enfuvirtide | >Th1088_Enfuvirtide YTSLIHSLIEESQNQQEKNEQELLELDKWASLWNWF | 4491.876 | C204H301N51O64 | 4.3 | -0.875 | NA | 3.8 ± 0.6 hrs | 36 residue, synthetically prepared peptide with N-terminal acetylation and C-terminal amidation. It blocks the fusion of HIV-1 with CD4 cells. | Enfuvirtide is an antiretroviral drug used in combination therapy for the treatment of HIV-1/AIDS. | NA | Enfuvirtide binds to the first heptad-repeat (HR1) in the gp41 subunit of the viral envelope glycoprotein and prevents the conformational changes required for the fusion of viral and cellular membranes. It works by disrupting the HIV-1 molecular machinery at the final stage of fusion with the target cell, preventing uninfected cells from becoming infected. Enfuvirtide is a biomimetic peptide that was rationally designed to mimic components of the HIV-1 fusion machinery and displace them, preventing normal fusion. | NA | Expected to undergo catabolism to its constituent amino acids, with subsequent recycling of the amino acids in the body pool. | After a 90 mg single subcutaneous injection of Enfuvirtide into the abdomen in 12 HIV-1 infected subjects, the mean peak concentration is 4.59±1.5 ug/ml and the median time to peak concentration was 8 hours (ranged from 3 to12 hours). | 5.5 ± 1.1 L | 24.8 +/- 4.1 mL/h/kg [HIV-1 infected adult and pediatric subjects following a 90-mg single SC dose of enfuvirtide] 30.6 +/- 10.6 mL/h/kg [Following 90-mg twice daily dosing of FUZEON SC in combination with other antiretroviral agents in HIV-1 infected subjects] 40 +/- 17 mL/h/kg [pediatric patients in the presence of concomitant medications including antiretroviral agents receiving the 2 mg/kg twice daily dose] | Amino Acids, Peptides, and Proteins,Anti-HIV Agents,Anti-Infective Agents,Anti-Retroviral Agents,Antigens,Antigens, Viral,Antiinfectives for Systemic Use,Antiviral Agents,Antivirals for Systemic Use,Biological Factors,Cytochrome P-450 CYP2C19 Substrates,Cytochrome P-450 CYP2E1 Substrates,Cytochrome P-450 Substrates,Direct Acting Antivirals,env Gene Products, Human Immunodeficiency Virus,Fusion Protein Inhibitors,Gene Products, env,HIV Antigens,HIV Envelope Protein gp41,HIV Fusion Inhibitors,Human Immunodeficiency Virus 1 Fusion Inhibitor,Human Immunodeficiency Virus Proteins,Membrane Fusion Proteins,Membrane Proteins,Peptide Fragments,Peptides,Polyproteins,Proteins,Retroviridae Proteins,Viral Envelope Proteins,Viral Fusion Protein Inhibitors,Viral Fusion Proteins,Viral Proteins,Viral Structural Proteins | US6475491 | 5-Nov-2002 | 7-Jun-2015 | NA | Envelope glycoprotein | FUZEON | Trimeris, Roche | Trimeris, Roche | FUZEON in combination with other antiretroviral agents is indicated for the treatment of HIV-1 infection in treatment experienced patients with evidence of HIV-1 replication despite ongoing antiretroviral therapy. | NA | Each single-use vial contains 108 mg of enfuvirtide for the delivery of 90 mg. Prior to subcutaneous administration, the contents of the vial are reconstituted with 1.1 mL of Sterile Water for Injection giving a volume of approximately 1.2 mL to provide the delivery of 1 mL of the solution. Each 1 mL of the reconstituted solution contains approximately 90 mg of enfuvirtide with approximate amounts of the following excipients: 22.55 mg of mannitol, 2.39 mg of sodium carbonate (anhydrous), and sodium hydroxide and hydrochloric acid for pH adjustment as needed. The reconstituted solution has an approximate pH of 9.0 | White to off-white, sterile, lyophilized powder. Each single-use vial contains 108 mg of enfuvirtide for the delivery of 90 mg. Prior to subcutaneous administration, the contents of the vial are reconstituted with 1.1 mL of Sterile Water for Injection giving a volume of approximately 1.2 mL to provi | Subcutaneous | 90 mg (1 mL) twice daily injected subcutaneously into the upper arm, anterior thigh or abdomen. Each injection should be given at a site different from the preceding injection site, and only where there is no current injection site reaction from an earlier dose. | FUZEON is contraindicated in patients with known hypersensitivity to FUZEON or any of its components | fever, chills, chest congestion, cough with yellow or green mucus, stabbing chest pain, wheezing, feeling short of breath; signs of a new infection such as sore throat, flu symptoms, swollen glands, easy bruising or bleeding. | Link | NA | NA |
| 10509 | Th1100 | Pramlintide | >Th1100_Pramlintide KCNTATCATQRLANFLVHSSNNFGPILPPTNVGSNTY | 3949.44 | C171H267N51O53S2 | NA | NA | NA | Approximately 48 minutes | New adjunct treatment for type I and type II diabetes. It is developed by Amylin Pharmaceuticals. It is derived from amylin, a hormone released after meal, in a pattern similar to insulin. Diabetic patients are also deficient in amylin. | For the treatment of type 1 and type 2 diabetes mellitus as an adjunct to preprandial insulin therapy in patients without adequate glycemic control of insulin therapy. | Pramlintide is a synthetic analog of amylin, a glucoregulatory hormone that is synthesized by pancreatic β-cells and released into the bloodstream, in a similar pattern as insulin, after a meal. Like insulin, amylin is deficient in individuals with diabetes. It is provided as an acetate salt. Pramlintide is a 37-amino acid polypeptide that differs structurally from human amylin by the replacement of alanine, serine, and serine at positions 25, 28, and 29 respectively with proline. | Pramlintide is an amlyinomimetic, a functional analog of the naturally occurring pancreatic hormone amylin. Amylin has activity in a number of gastrointestinal and glucodynamic systems, and by mimicking its activity, pramlintide acts to improve glycemic control through modulation of the rate of gastric emptying, prevention of post-prandial rise in glucagon levels, and by increasing sensations of satiety, thereby reducing caloric intake and potentiating weight loss. There appears to be at least three distinct receptor complexes that bind with high affinity to amylin. All three complexes contain the calcitonin receptor at the core, plus one of three Receptor activity-modifying proteins, RAMP1, RAMP2, or RAMP3. | NA | Metabolized primarily by the kidneys. | The absolute bioavailability of a single subcutaneous dose of pramlintide is approximately 30 to 40%. | NA | NA | NA | US5686411 | 11-Nov-1997 | 16-Mar-2019 | NA | Calcitonin receptor,Receptor activity-modifying protein 1,Receptor activity-modifying protein 2,Receptor activity-modifying protein 3 | Symlin | Amylin Pharmaceuticals (now a wholly owned subsidiary of AstraZeneca) | Amylin Pharmaceuticals (now a wholly owned subsidiary of AstraZeneca) | SYMLIN is indicated as an adjunctive treatment in patients with type 1 or type 2 diabetes who use mealtime insulin therapy and who have failed to achieve desired glucose control despite optimal insulin therapy. | NA | The disposable multidose SymlinPen pen-injector contains 1000 mcg/mL of pramlintide (as acetate). The formulation contains 2.25 mg/mL of metacresol as a preservative, D-mannitol as a tonicity modifier, acetic acid, sodium acetate as pH modifiers, and water for injection. SYMLIN has a pH of approximately 4.0 | Clear, isotonic, sterile solution for subcutaneous administration | Subcutaneous | Reduce mealtime insulin doses by 50%, then initiate SYMLIN at 15 mcg subcutaneously, injecting immediately prior to each major meal. Increase the SYMLIN dose to the next increment (30, 45, or 60 mcg) when no clinically significant nausea has occurred for at least 3 days. If significant nausea persists at the 45 or 60 mcg dose level, the SYMLIN dose should be decreased to 30 mcg. If the 30 mcg dose is not tolerated, discontinuation of SYMLIN therapy should be considered. | NA | Nausea, Anorexia, Vomiting, Arthralgia, Fatigue, Allergic Reaction, Dizziness | Link | NA | NA |
| 10522 | Th1102 | Abatacept | >Th1102_Abatacept MHVAQPAVVLASSRGIASFVCEYASPGKATEVRVTVLRQADSQVTEVCAATYMMGNELTFLDDSICTGTSSGNQVNLTIQGLRAMDTGLYICKVELMYPPPYYLGIGNGTQIYVIDPEPCPDSDQEPKSSDKTHTSPPSPAPELLGGSSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 92300 | C3498H5458N922O1090S32 | NA | NA | NA | 16.7 (12-23) days in healthy subjects | Recombinant (CHO cell derived), soluble fusion protein that links the extracellular domain of human cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), to the modified Fc (hinge, CH2, and CH3 domains) portion of human IgG1. Abatacept is a glycosylated fusion protein with molecular weight of 92,300 Da and it is a homodimer of two polypeptide chains of 357 amino acids. The drug has activity as a selective co-stimulation modulator with inhibitory activity on T lymphocytes. | For the management of the signs and symptoms of moderate-to-severe active rheumatoid arthritis, inducing major clinical response, slowing the progression of structural damage, and improving physical function in adult patients. It is indicated both as a monotherapy and for use in combination with a continued regimen of DMARDs (not including TNF antagonists). Also used for the management of the signs and symptoms of moderately to severely active polyarticular juvenile idiopathic arthritis in children. | Abatacept is the first in a new class of drugs known as Selective Co-stimulation Modulators. Known as a recombinant fusion protein, the drug consists of the extracellular domain of human cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) linked to a modified Fc portion of human immunoglobulin G1 (IgG1. The Fc portion of the drug consists of the hinge region, the CH2 domain, and the CH3 domain of IgG1. Although there are multiple pathways and cell types involved in the pathogenesis of rheumatoid arthritis, evidence suggests that T-cell activation may play an important role in the immunopathology of the disease. Ordinarily, full T-cell activation requires binding of the T-cell receptor to an antigen-MHC complex on the antigen-presenting cell as well as a co-stimulatory signal provided by the binding of the CD28 protein on the surface of the T-cell with the CD80/86 proteins on the surface of the antigen-presenting cell. CTLA4 is a naturally occurring protein which is expressed on the surface of T-cells some hours or days after full T-cell activation and is capable of binding to CD80/86 on antigen-presenting cells with much greater affinity than CD28. Binding of CTLA4-Ig to CD80/86 provides a negative feedback mechanism which results in T-cell deactivation. Abatacept was developed by Bristol-Myers-Squibb and is licensed in the US for the treatment of Rheumatoid Arthritis in the case of inadequate response to anti-TNF-alpha therapy. | Abatacept is a selective costimulation modulator, like CTLA-4, the drug has shown to inhibit T-cell (T lymphocyte) activation by binding to CD80 and CD86, thereby blocking interaction with CD28. Blockade of this interaction has been shown to inhibit the delivery of the second co-stimulatory signal required for optimal activation of T-cells. This results in the inhibition of autoimmune T-Cell activation that has been implcated in the pathogenesis of rheumatoid arthritis. | Most common adverse events (≥10%) are headache, upper respiratory tract infection, nasopharyngitis, and nausea. Doses up to 50 mg/kg have been administered without apparent toxic effect. | NA | When a single 10 mg/kg Intravenous infusion of abatacept is administered in healthy subjects, the peak plasma concentration (Cmax) was 292 mcg/mL. When multiple doses of 10 mg/kg was given to rheumatoid arthritis (RA) patients, the Cmax was 295 mcg/mL. The bioavailability of abatacept following subcutaneous administration relative to intravenous administration is 78.6%. | 0.07 L/kg [RA Patients, IV administration] 0.09 L/kg [Healthy Subjects, IV administration] 0.11 L/kg [RA patients, subcutaneous administration] | 0.23 mL/h/kg [Healthy Subjects after 10 mg/kg Intravenous infusion 0.22 mL/h/kg [RA Patients after multiple 10 mg/kg Intravenous infusions] 0.4 mL/h/kg [juvenile idiopathic arthritis patients].The mean systemic clearance is 0.28 mL/h/kg when a subcutaneously administered to adult RA patients.The clearance of abatacept increases with increasing body weight. | Antirheumatic Agents and Immunosuppressive Agents | CA2110518 | 22-May-2007 | 16-Jun-2012 | NA | T-lymphocyte activation antigen CD80,T-lymphocyte activation antigen CD86 | ORENCIA | Bristol-Myers Squibb | Bristol-Myers Squibb | Adult Rheumatoid Arthritis (RA): ORENCIA is indicated for reducing signs and symptoms, inducing major clinical response, inhibiting the progression of structural damage, and improving physical function in adult patients with moderately to severely active rheumatoid arthritis. ORENCIA may be used as monotherapy or concomitantly with disease-modifying antirheumatic drugs (DMARDs) other than tumor necrosis factor (TNF) antagonists.; Juvenile Idiopathic Arthritis: ORENCIA is indicated for reducing signs and symptoms in pediatric patients 6 years of age and older with moderately to severely active polyarticular juvenile idiopathic arthritis. ORENCIA may be used as monotherapy or concomitantly with methotrexate | NA | Following reconstitution of the lyophilized powder with 10 mL of Sterile Water for Injection, USP, the solution of ORENCIA is clear, colorless to pale yellow, with a pH range of 7.2 to 7.8. Each single-use vial of ORENCIA provides 250 mg abatacept, maltose (500 mg), monobasic sodium phosphate (17.2 mg), and sodium chloride (14.6 mg) for administration. | Lyophilized powder for Intravenous infusion is supplied as a Sterile, white, preservative-free, lyophilized powder for intravenous administration | Intravenous infusion, Subcutaneous Injection | Adult Rheumatoid Arthritis, For adult patients with RA, ORENCIA may be administered as an Intravenous infusion or a subcutaneous injection. ORENCIA may be used as monotherapy or concomitantly with DMARDs other than TNF antagonists. For pediatric juvenile idiopathic arthritis, a dose calculated based on each patient's body weight is used. Intravenous Dosing Regimen; ORENCIA intravenous should be administered as a 30-minute Intravenous infusion utilizing the weight range-based dosing specified in Table 1. Following the initial intravenous administration, an Intravenous infusion should be given at 2 and 4 weeks after the first infusion and every 4 weeks thereafter. | NA | The most serious adverse reactions were serious infections and malignancies. The most commonly reported adverse events (occurring in ≥ 10% of patients treated with ORENCIA) were headache, upper respiratory tract infection, nasopharyngitis, and nausea. | Link | NA | NA |
| 10529 | Th1105 | Insulin aspart | >Th1105_Insulin_aspart GIVEQCCTSICSLYQLENYCN | 5825.8 | C256H381N65O79S6 | NA | NA | NA | 81 mins. SC injection | Recombinant (from S. cerevisiae),fast-acting insulin analogue. It contains a single amino acid substitution at position B28 where proline is replaced with aspartic acid. This results in a decreased hexamer formation and higher rate of absorption, compared to wild type insulin, following subcutaneous administration. | For the treatment of Type 1 or 2 diabetes mellitus. Should normally be used in conjunction with an intermediate or long-acting insulin. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin aspart is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin aspart is 10-15 minutes. Its activity peaks 60-90 minutes following subcutaneous injection and its duration of action is 4-5 hours. | Insulin aspart binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Substitution of the proline residue at B28 with aspartic acid reduces the tendency to form hexamers and results in a faster rate of absorption and onset of action and shorter duration of action. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. | NA | Rapidly absorbed following subcutaneous administration (more so than regular human insulin). Furthermore, insulin aspart has a faster absorption, a faster onset of action, and a shorter duration of action than regular human insulin after subcutaneous injection. It takes 40 - 50 minutes to reach maximum concentration. When a dose of 0.15 U/kg body weight was injected in type 1 diabetes patients, the mean maximum concentration (Cmax) was 82 mU/L. The site of injection has no impact on extent or speed of absorption. | NA | 1.2 L/h/kg [healthy Caucasian male] | Hypoglycemic Agents and Antidiabetic Agents | US5866538 | 2-Feb-1999 | 20-Jun-2017 | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NovoLog | Novo Nordisk | Novo Nordisk | NovoLog is an insulin analog indicated to improve glycemic control in adults and children with diabetes mellitus | NA | NovoLog is a sterile, aqueous, clear, and colorless solution, that contains insulin aspart 100 Units/mL, glycerin 16 mg/mL, phenol 1.50 mg/mL, metacresol 1.72 mg/mL, zinc 19.6 mcg/mL, disodium hydrogen phosphate dihydrate 1.25 mg/mL, sodium chloride 0.58 mg/mL and water for injection. NovoLog has a pH of 7.2-7.6. Hydrochloric acid 10% and/or sodium hydroxide 10% may be added to adjust pH | Sterile, aqueous, clear, and colorless solution | Subcutaneous, Intravenous | The total daily insulin requirement may vary and is usually between 0.5 to 1.0 units/kg/day. When used in a meal-related subcutaneous injection treatment regimen, 50 to 70% of total insulin requirements may be provided by NovoLog and the remainder provided by an intermediate-acting or long-acting insulin. Because of NovoLog's comparatively rapid onset and short duration of glucose lowering activity, some patients may require more basal insulin and more total insulin to prevent pre-meal hyperglycemia when using NovoLog than when using human regular insulin. | NovoLog is contraindicated during episodes of hypoglycemia in patients with hypersensitivity to NovoLog or one of its excipients | swelling in your hands or feet; or low potassium (confusion, uneven heart rate, extreme thirst, increased urination, leg discomfort, muscle weakness or limp feeling). Hypoglycemia, Lipodystrophy, Weight gain, Peripheral Edema | Link | NA | NA |
| 10530 | Th1105 | Insulin aspart | >Th1105_Insulin_aspart GIVEQCCTSICSLYQLENYCN | 5825.8 | C256H381N65O79S6 | NA | NA | NA | 81 mins. SC injection | Recombinant (from S. cerevisiae),fast-acting insulin analogue. It contains a single amino acid substitution at position B28 where proline is replaced with aspartic acid. This results in a decreased hexamer formation and higher rate of absorption, compared to wild type insulin, following subcutaneous administration. | For the treatment of Type 1 or 2 diabetes mellitus. Should normally be used in conjunction with an intermediate or long-acting insulin. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin aspart is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin aspart is 10-15 minutes. Its activity peaks 60-90 minutes following subcutaneous injection and its duration of action is 4-5 hours. | Insulin aspart binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Substitution of the proline residue at B28 with aspartic acid reduces the tendency to form hexamers and results in a faster rate of absorption and onset of action and shorter duration of action. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. | NA | Rapidly absorbed following subcutaneous administration (more so than regular human insulin). Furthermore, insulin aspart has a faster absorption, a faster onset of action, and a shorter duration of action than regular human insulin after subcutaneous injection. It takes 40 - 50 minutes to reach maximum concentration. When a dose of 0.15 U/kg body weight was injected in type 1 diabetes patients, the mean maximum concentration (Cmax) was 82 mU/L. The site of injection has no impact on extent or speed of absorption. | NA | 1.2 L/h/kg [healthy Caucasian male] | Hypoglycemic Agents and Antidiabetic Agents | US5618913 | 8-Apr-1997 | 7-Jun-2014 | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NovoLog Mix 50/50 | Novo Nordisk | Novo Nordisk | NovoLog Mix 50/50 (50% insulin aspart protamine suspension and 50% insulin aspart injection) is indicated as an adjunct to diet and exercise to improve glycemic control in patients with diabetes mellitus. | NA | NovoLog Mix 50/50 (50% insulin aspart protamine suspension and 50% insulin aspart injection) is a uniform, white, sterile suspension that contains insulin aspart (B28 asp regular human insulin analog) 100 Units/ml, 16 mg glycerol, 1.50 mg phenol, 1.72 mg metacreÂÂsol, 19.6 μg zinc, 1.25 mg disodium hydrogen phosphate dihydrate, 1.17 mg sodium chloride, and 0.23 mg protamine sulfate. NovoLog Mix 50/50 (50% insulin aspart protamine suspension and 50% insulin aspart injection) has a pH of 7.10 - 7.44. Hydrochloric acid or sodium hydroxide may be added to adjust pH | Uniform, white, sterile suspension that contains insulin aspart (B28 asp regular human insulin analog) | Subcutaneous | NovoLog Mix 50/50 (50% insulin aspart protamine suspension and 50% insulin aspart injection) should be administered within 15 minutes of meal initiation up to three times daily. It is intended only for subcutaneous injection into the abdominal wall, thigh, or upper arm. NovoLog Mix 50/50 (50% insulin aspart protamine suspension and 50% insulin aspart injection) should not be administered intravenously. | NovoLog Mix 50/50 (50% insulin aspart protamine suspension and 50% insulin aspart injection) is contraindicated during episodes of hypoglycemia and in patients hypersensitive to NovoLog Mix 50/50 (50% insulin aspart protamine suspension and 50% insulin aspart injection) or any of the excipients. | During clinical trials the overall adverse event profile of NovoLog Mix 50/50 was comparable to Novolin 70/30. Adverse events commonly associated with human insulin therapy include the following: Body as whole: allergic reactions, Skin and Appendages: Injection site reaction, lipodystrophy, pruritus, rash, Hypoglycemia | Link | NA | NA |
| 10531 | Th1105 | Insulin aspart | >Th1105_Insulin_aspart GIVEQCCTSICSLYQLENYCN | 5825.8 | C256H381N65O79S6 | NA | NA | NA | 81 mins. SC injection | Recombinant (from S. cerevisiae),fast-acting insulin analogue. It contains a single amino acid substitution at position B28 where proline is replaced with aspartic acid. This results in a decreased hexamer formation and higher rate of absorption, compared to wild type insulin, following subcutaneous administration. | For the treatment of Type 1 or 2 diabetes mellitus. Should normally be used in conjunction with an intermediate or long-acting insulin. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin aspart is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin aspart is 10-15 minutes. Its activity peaks 60-90 minutes following subcutaneous injection and its duration of action is 4-5 hours. | Insulin aspart binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Substitution of the proline residue at B28 with aspartic acid reduces the tendency to form hexamers and results in a faster rate of absorption and onset of action and shorter duration of action. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. | NA | Rapidly absorbed following subcutaneous administration (more so than regular human insulin). Furthermore, insulin aspart has a faster absorption, a faster onset of action, and a shorter duration of action than regular human insulin after subcutaneous injection. It takes 40 - 50 minutes to reach maximum concentration. When a dose of 0.15 U/kg body weight was injected in type 1 diabetes patients, the mean maximum concentration (Cmax) was 82 mU/L. The site of injection has no impact on extent or speed of absorption. | NA | 1.2 L/h/kg [healthy Caucasian male] | Hypoglycemic Agents and Antidiabetic Agents | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NovoLog Mix 70/30 | Novo Nordisk | Novo Nordisk | NovoLog Mix 70/30 (70% insulin aspart protamine suspension and 30% insulin aspart injection) is indicated as an adjunct to diet and exercise to improve glycemic control in patients with diabetes mellitus. | NA | Inactive ingredients for the 10 mL vial are mannitol 36.4 mg/mL, phenol 1.50 mg/mL, metacresol 1.72 mg/mL, zinc 19.6 μg/mL, disodium hydrogen phosphate dihydrate 1.25 mg/mL, sodium chloride 0.58 mg/mL, and protamine sulfate 0.32 mg/mL. Inactive ingredients for the NovoLog Mix 70/30 (insulin aspart protamine and insulin aspart rdna origin) FlexPen are glycerol 16.0 mg/mL, phenol 1.50 mg/mL, metacresol 1.72 mg/mL, zinc 19.6 μg/mL, disodium hydrogen phosphate dihydrate 1.25 mg/mL, sodium chloride 0.877 mg/mL, and protamine sulfate 0.32 mg/mL. NovoLog Mix 70/30 (insulin aspart protamine and insulin aspart rdna origin) has a pH of 7.20 - 7.44. Hydrochloric acid or sodium hydroxide may be added to adjust pH. | NovoLog Mix 70/30 (insulin aspart protamine and insulin aspart rdna origin) is a uniform, white, sterile suspension that contains insulin aspart 100 Units/mL. | Subcutaneous | NovoLog Mix 70/30 (insulin aspart protamine and insulin aspart (rdna origin)) is an insulin analog with an earlier onset and intermediate duration of action in comparison to the basal human insulin premix. The addition of protamine to the rapid-acting aspart insulin analog (NovoLog) results in insulin activity that is 30% short-acting and 70% long-acting. NovoLog Mix 70/30 (insulin aspart protamine and insulin aspart (rdna origin)) is typically dosed on a twice-daily basis (with each dose intended to cover 2 meals or a meal and a snack). The dosage of NovoLog Mix 70/30 (insulin aspart protamine and insulin aspart (rdna origin)) must be individualized. The written prescription for NovoLog Mix 70/30 (insulin aspart protamine and insulin aspart (rdna origin)) should include the full name, to avoid confusion with NovoLog (insulin aspart) and Novolin 70/30 (human premix). | NovoLog Mix 70/30 (insulin aspart protamine and insulin aspart (rdna origin)) is contraindicated during episodes of hypoglycemia in patients with hypersensitivity to NovoLog Mix 70/30 (insulin aspart protamine and insulin aspart (rdna origin)) or one of its excipients. | signs of insulin allergy: itching skin rash over the entire body, wheezing, trouble breathing, fast heart rate, sweating, or feeling like you might pass out. Hypoglycemia, or low blood sugar, is the most common side effect of insulin. Symptoms include headache, hunger, weakness, sweating, tremors, irritability, trouble concentrating, rapid breathing, fast heartbeat, fainting, or seizure (severe hypoglycemia can be fatal) | Link | NA | NA |
| 10538 | Th1106 | Insulin detemir | >Th1106_Insulin_detemir GIVEQCCTSICSLYQLENYCN | 5916.9 | C267H402N64O76S6 | NA | NA | NA | 5 to 7 hours | Recombinant (from yeast cells), long-acting human insulin analogue. It has a myristic acid (14-C fatty acid), bound to lysine at position B29, which increases self-association and albumin binding. Coupled with its slow systemic absorption from the injection site, prolongs its distribution into tissues enabling it to act for a longer time than native insulin. | For the treatment of type 1 or 2 diabetes mellitus. May be used in combination with oral anti-diabetic agents in type 2 diabetic patients who are not in adequate metabolic control with oral anti-diabetic agents alone. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin detemir is a long-acting insulin analogue with a flat and predictable action profile. It is used to mimic the basal levels of insulin in diabetic individuals. The onset of action of insulin detemir is 1 to 2 hours and its duration of action is up to 24 hours. Interestingly, it has a lower affinity (30%) for the insulin receptor than human insulin. | Insulin detemir binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. Insulin detemir's long duration of action appears to be a result of slow systemic absorption from the injection site and delayed distribution to target tissues. The myristic acid side chain on insulin detemir increases self-association and gives it a high binding affinity to serum albumin. These features slows its distribution into target tissues and prolongs its duration of action. | Hypoglycemia may occur with inappropriately high doses. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. Injection site reactions may also occur. Symptoms include: redness, inflammation, bruising, swelling and itching at the injection site. | As with natural insulin, all metabolites formed are inactive. | Maximum serum concentrations are reached 6 to 8 hours following subcutaneous injection. When single dose of 0.5 units/kg of insulin detemir was given to adult type 1 diabetes patients, the maximum serum concentration (Cmax) was 4,641 ± 2,299 pmol/L. Absorption is also dependent on the site of injection. When injected into the thigh, the AUC was lower than when injected into the deltoid and abdominal regions. Bioavailability is approximately 60%. | 0.1 L/kg | Apparent clearance (CL/F), type 1 diabetes adult patients = 3.41 ± 1.00 L/min·kg | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Long-Acting,Pancreatic Hormones,Peptide Hormones,Peptides | US5750497 | 12-May-1998 | 16-Jun-2019 | NA | Insulin receptor,Insulin-like growth factor 1 receptor | LEVEMIR | Novo Nordisk | Novo Nordisk | LEVEMIR is indicated to improve glycemic control in adults and children with diabetes mellitus. | NA | Each milliliter of LEVEMIR contains 100 units (14.2 mg/mL) insulin detemir, 65.4 meg inc, 2.06 mg m-cresol, 16.0 mg glycerol, 1.80 mg phenol, 0.89 mg disodium phosphate dihydrate, 1.17 mg sodium chloride, and water for injection. Hydrochloric acid and/or sodium hydroxide may be added to adjust pH. LEVEMIR has a pH of approximately 7.4 | Clear, colorless, aqueous, neutral Sterile solution | Subcutaneous | Patients who require twice-daily dosing can administer the evening dose with the evening meal, at bedtime, or 12 hours after the morning dose. The dose of LEVEMIR must be individualized based on clinical response. Blood glucose monitoring is essential in all patients receiving insulin therapy. | LEVEMIR is not recommended for the treatment of diabetic ketoacidosis. Intravenous rapid-acting or short-acting insulin is the preferred treatment for this condition. LEVEMIR is contraindicated in patients with hypersensitivity to LEVEMIR or any of its excipients. Reactions have included anaphylaxis. | Hypoglycemia, upper respiratory tract infection, Headache, Pharyngitis, Influenza-like illness, Abdominal Pain | Link | NA | NA |
| 10558 | Th1110 | Thymalfasin | >Th1110_Thymalfasin SDAAVDTSSEITTKDLKEKKEVVEEAEN | 3108.276 | C129H215N33O55 | NA | NA | NA | Approx. 2 hrs | Chemically synthesized version identicle to human acetylated polypeptide , thymosin alpha 1. It is now approved in 35 developing countries for the treatment of Hepatitis B and C and in boosting immunity against other diseases. | Indicated as an adjuvant for influenza vaccine in elderly patients and as an adjuvant for both influenza and hepatitis B vaccines in chronic hemodialysis patients who failed to achieve adequate antibody titers from previous immunization. | Thymalfasin is a 28-amino acid polypeptide produced synthetically but originally isolated from thymosin fraction 5, a bovine thymus extract containing a number of immunologically active peptides. In vitro studies have shown that Thymalfasin can influence T-cell production and maturation, stimulate production of Th1 cytokines such as interferon-gamma and interleukin-2, and activate natural killer cell-mediated cytotoxicity. | The mechanism of action of thymalfasin is not completely understood but is thought to be related to its immunomodulating activities, centered primarily around augmentation of T-cell function. In various in vitro assays, thymosin alpha 1 has been shown to promote T-cell differentiation and maturation; for example, CD4+, CD8+, and CD3+ cells have all been shown to be increased. Thymosin alpha 1 has also been shown to increase production of IFN-g, IL-2, IL-3, and expression of IL-2 receptor following activation by mitogens or antigens, increase NK cell activity, increase production of migratory inhibitory factor (MIF), and increase antibody response to T-cell dependent antigens. Thymosin alpha 1 has also been shown to antagonize dexamethasone-induced apoptosis of thymocytes in vitro. In vivo administration of thymosin alpha 1 to animals immunosuppressed by chemotherapy, tumor burden, or irradiation showed that thymosin alpha 1 protects against cytotoxic damage to bone marrow, tumor progression and opportunistic infections, thereby increasing survival time and number of survivors. Many of the in vitro and in vivo effects of thymosin alpha 1 have been interpreted as influences on either differentiation of pluripotent stem cells to thymocytes or activation of thymocytes into activated T-cells. Thymalfasin also has been shown in vitro to upregulate expression of toll like receptors (TLR) including TLR2 and TLR9 in mouse and human dendritic cells, as well as activate NF-kB and JNK/P38/AP1 pathways. Thymalfasin's activation of dendritic cells provides another possible pathway explaining thymalfasin's immunomodulatory and antiviral effects. | There are no reported instances of deliberate or accidental overdosage in humans. Animal toxicology studies have shown no adverse reactions in single doses up to 20 mg/kg and in repeated doses up to 6 mg/kg/day for 13 weeks, which were the highest doses studied. The highest single dose tested in animals represents 800-times the clinical dose. | NA | Rapidly absorbed with peak serum levels achieved at approximately 2 hours. | NA | NA | Adjuvants, Immunologic,Amino Acids, Peptides, and Proteins,Antineoplastic Agents,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Immunologic Factors,Peptide Hormones,Peptides,Proteins,Thymus Hormones | NA | NA | NA | NA | NA | Zadaxin | SciClone Pharmaceuticals (SCLN) | SciClone Pharmaceuticals (SCLN) | ZADAXIN thymosin alpha 1 (thymalfasin) is indicated as a monotherapy or combination therapy with interferon for the treatment of chronic hepatitis B. | NA | lyophilized preparation contains 1.6 mg thymosin alpha 1, 50 mg mannitol, and sodium phosphate buffer to adjust the pH to 6.8 | N. A. | Subcutaneous | The recommend-ed dose of ZADAXIN (thymalfasin) for chronic hepatitis B when used as a monotherapy or in combination with interferon (at the labeled dose and schedule for interferon) is 1.6 mg (900 µg/m2) administered subcutaneously twice a week for 6 to 12 months. Patients weighing less than 40 kg should receive a ZADAXIN (thymalfasin) dose of 40 µg/kg. | ZADAXIN (thymalfasin) is contraindicated in patients with a history of hypersensitivity to thymosin alpha 1 or any component of the injection. Because ZADAXIN (thymalfasin) therapy appears to work by enhancing the immune system, it should be considered contraindicated in patients who are being deliberately immunosuppressed, such as organ transplant patients, unless the potential benefits of the therapy clearly outweigh the potential risks. | Adverse experiences have been infrequent and mild, consisting primarily of local discomfort at the injection site, and rare instances of erythema, transient muscle atrophy, polyarthralgia combined with hand edema, and rash. | Link | NA | NA |
| 10561 | Th1112 | Natural alpha interferon OR multiferon | >Th1112_Natural_alpha_interferon_OR_multiferon CDLPETHSLDNRRTLMLLAQMSRISPSSCLMDRHDFGFPQEEFDGNQFQKAPAISVLHELIQQIFNLFTTKDSSAAWDEDLLDKFCTELYQQLNDLEACVMQEERVGETPLMNADSILAVKKYFRRITLYLTEKKYSPCAWEVVRAEIMRSLSLSTNLQERLRRKE | 19300-22100 | NA | NA | NA | NA | NA | Obtained from the leukocyte fraction of human blood following Sendai virus infection. Interferon alfa contains several naturally occurring IFN-α subtypes and is purified by affinity chromatography. Interferon alpha proteins are mainly involved in innate immune response against viral infection. They come in 13 subtypes that are called IFNA1, IFNA2, IFNA4, IFNA5, IFNA6, IFNA7, IFNA8, IFNA10, IFNA13, IFNA14, IFNA16, IFNA17, IFNA21. Multiferon consists of the 6 major subtypes are IFN-α1, IFN-α2, IFN-α8, IFN-α10, IFN-α14 and IFN-α21. Of these, IFN-α2 and IFN-α14 are glycosylated. | Investigated for use/treatment in hepatitis (viral, C), leukemia (lymphoid), leukemia (myeloid), leukemia (unspecified), and melanoma. | NA | Natural alpha interferon offers multiple subtypes of interferon which may work together as a 'cocktail-in-one', while recombinant versions only exhibit a single subtype. Viragen offers MultiferonT at a cost which is competitive with recombinant interferon regimens. Natural alpha interferon contains the multiple subtype composition that is characteristic of interferon produced by the human body. It is believed that this results in a broader spectrum of specific anti-viral and immunoregulatory activity with the subtypes acting synergistically to give a wide-ranging response. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Intron/ Roferon-A | NA | NA | Approved for use in hairy cell leukemia, malignant melanoma, AIDS-related Kaposi's sarcoma, follicular non-Hodgkin's lymphoma. Other uses: Chronic myelogenous leukemia (CML), renal cell cancer, cervical cancer, carcinoid syndrome, medullary thyroid cancer, multiple myeloma, basal and squamous cell skin cancers, low-grade non-Hodgkin's lymphoma, cutaneous T-cell lymphoma (mycosis fungoides). Blood disorders such as: polycythemia vera, essential thrombocytopenia, thrombocytopenia purpura. | NA | NA | NA | Subcutaneous, Intravenous, Intramuscular | NA | Do not take aspirin, products containing aspirin unless your doctor specifically permits this; Do not receive any kind of immunization or vaccination without your doctor's approval while taking interferon alpha; Due to differences in dosage, you should not change brands of interferons. Discuss with your doctor or health care professional if there is a problem with supply. Interferon alfa may cause patients to develop mood or behavioral problems or if you have ever been addicted to drugs or alcohol. Pregnancy category C (use in pregnancy only when benefit to the mother outweighs risk to the fetus). For both men and women: Do not conceive a child (get pregnant) while taking interferon alfa. Barrier methods of contraception, such as condoms, are recommended. Discuss with your doctor when you may safely become pregnant or conceive a child after therapy. Do not breast feed while taking this medication. | Flu-like syndrome: Fever, chills, generalized aches and pains, headache, poor appetite, Fatigue, Low blood counts, anaemia and/or bleeding. Decreases are dose dependent. Temporary blood test abnormalities: low calcium, high glucose, or high triglyceride levels. Increases in blood tests measuring liver function. These return to normal once treatment is discontinued (see liver problems). Weight loss, Hair loss. | Link | NA | NA |
| 10562 | Th1113 | Glatiramer acetate | >Th1113_Glatiramer_acetate EAYKAAEKAYAAKEAAKEAAKAKAEKKAAYAKAKAAKYEKKAKKAAAEYKKK | 5000-9000 | C254H422N70O72 | NA | NA | NA | NA | Glatiramer acetate comprises acetate salts of synthetic polypeptides, containing four naturally occurring amino acids: L-glutamic acid, L-alanine, L-tyrosine, and L-lysine with an average molar fraction of 0.141, 0.427, 0.095, and 0.338, respectively. The average molecular weight of glatiramer acetate is 5,000-9,000 daltons. It is an immunomodulator, known to reduce the frequency of relapses in relapsing-remitting multiple sclerosis | For reduction of the frequency of relapses in patients with Relapsing-Remitting Multiple Sclerosis. | Glatiramer acetate was originally designed to mimic a protein in myelin, called myelin basic protein, with the intention of inducing EAE (an animal model of MS). Quite to the contrary, it was found to suppress the disease and as a result came to be trialed in human MS. There is some evidence that Glatiramer acetate converts the body's immune response from a Th1 type to a Th2 one, promotes suppressor T cells or acts as an altered peptide ligand. Studies in animals and in vitro systems suggest that upon its administration, glatiramer acetate-specific suppressor T-cells are induced and activated in the periphery. Some fraction of the injected material, either intact or partially hydrolyzed, is presumed to enter the lymphatic circulation, enabling it to reach regional lymph nodes, and some may enter the systemic circulation intact. | Glatiramer acetate (GA) exhibits strong and promiscuous binding to MHC molecules (HLA DRB1* variants) and consequent competition with various myelin antigens for their presentation to T cells. A further aspect of its action is potent induction of specific suppressor cells of the T helper 2 (Th2) type that migrate to the brain and lead to in situ bystander suppression. Furthermore, the GA-specific cells in the brain express the anti-inflammatory cytokines IL-10 and transforming growth factor beta, in addition to brain-derived neurotrophic factor, whereas they do not express the inflammatory cytokine IFN-gamma. Recent evidence also suggests that Glatiramer acetate directly inhibits dendritic cells and monocytes - both of which are circulating antigen presenting cells. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Copaxone | Teva Pharmaceutical Industries | Teva Pharmaceutical Industries | Glatiramer acetate, the active ingredient of COPAXONE, consists of the acetate salts of synthetic polypeptides, containing four naturally occurring amino acids: L-glutamic acid, L-alanine, L-tyrosine, and L-lysine with an average molar fraction of 0.141, 0.427, 0.095, and 0.338, respectively. The average molecular weight of glatiramer acetate is 5,000 – 9,000 daltons. Glatiramer acetate is identified by specific antibodies. Chemically, glatiramer acetate is designated L-glutamic acid polymer with L-alanine, L-lysine and L-tyrosine, acetate (salt). | NA | Each 1 mL of COPAXONE solution contains 20 mg or 40 mg of glatiramer acetate and the following inactive ingredient: 40 mg of mannitol. The pH of the solutions is approximately 5.5 to 7.0. The biological activity of glatiramer acetate is determined by its ability to block the induction of experimental autoimmune encephalomyelitis (EAE) in mice. | Clear, colorless to slightly yellow, sterile, nonpyrogenic solution | Subcutaneous | COPAXONE is for subcutaneous use only. Do not administer intravenously. The dosing schedule depends on the product strength that is selected. The recommended doses are: COPAXONE 20 mg per mL: administer once per day or COPAXONE 40 mg per mL: administer three times per week and at least 48 hours apart. COPAXONE 20 mg per mL and COPAXONE 40 mg per mL are not interchangeable. | COPAXONE is contraindicated in patients with known hypersensitivity to glatiramer acetate or mannitol. | most commonly associated with discontinuation were: injection site reactions, dyspnea, urticaria, vasodilatation, and hypersensitivity. The most common adverse reactions were: injection site reactions, vasodilatation, rash, dyspnea, and chest pain. | Link | NA | NA |
| 10563 | Th1114 | Preotact | >Th1114_Preotact SVSEIQLMHNLGKHLNSMERVEWLRKKLQDVHNFVALGAPLAPRDAGSQRPRKKEDNVLVESHEKSLGEADKADVNVLTKAKSQ | 9420 | C408H674N126O126S2 | NA | NA | NA | 1.5 hrs | Recombinant, pharmaceutical form of parathyroid hormone (PTH), which is a single-chain polypeptide composed of 84 amino acids. Its sequence is identical to the full-length native 84-amino acid PTH polypeptide. It lacks disulfide bonds and glycosylation sites. Preotact is marketed in Europe by Nycomed. Preos is a registered trade mark owned by NPS Pharmaceuticals, Inc. The name Preos and the New Drug Application is pending approval by the U.S. Food and Drug Administration (FDA). | For use/treatment in osteoporosis. | Parathyroid hormone is responsible for the fine regulation of serum calcium concentration on a minute-to-minute basis. This is achieved by the acute effects of the hormone on calcium resorption in bone and calcium reabsorption in the kidney. The phosphate mobilized from bone is excreted into the urine by means of the hormone's influence on renal phosphate handling. Parathyroid hormone also stimulates calcium absorption in the intestine, this being mediated indirectly by 1,25-dihydroxyvitamin D. Thus, a hypocalcemic stimulus of parathyroid hormone secretion results in an increased influx of calcium from three sources (bone, kidney, and intestine), resulting in a normalization of the serum calcium concentration without change in the serum phosphate concentration. | The biological actions of rhPTH are mediated through binding to at least two distinct high- affinity cell-surface receptors specific for the N-terminal and C-terminal regions of the molecule, both of which are required for normal bone metabolism. The N-terminal portion of the molecule is primarily responsible for the bone building effects of parathyroid hormone. The C-terminal portion of the molecule has antiresorptive activity and is necessary for normal regulation of N-terminal fragment activity. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Parathyroid hormone/parathyroid hormone-related peptide receptor,Parathyroid hormone 2 receptor | Preotact | Nycomed | Nycomed | osteoporosis in women past menopause | NA | NA | NA | Subcutaneous | 100 micrograms given once a day. Your doctor may advise you to take supplementary calcium and vitamin D. | Do not use Preotact: if you are allergic (hypersensitive) to parathyroid hormone or any of the other ingredients of Preotact; if you have had radiation therapy to the skeleton; if you suffer from high calcium levels and other disturbances in the calcium-phosphor metabolism; if you have other bone disease (including hyperparathyroidism or Paget’s disease); if you have high levels of alkaline phosphatase; if you suffer from severe kidney problems; if you suffer from severe liver disease. | increased level of calcium in the blood, increased level of calcium in the urine, and nausea. back pain, constipation, decreased muscle strength, diarrhoea, dizziness, erythema at injection site, fast or irregular heart beats, headache, muscle cramps, pain in extremity, stomach upset, tiredness, and vomiting. | Link | NA | NA |
| 10565 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | ILARIS | Novartis Pharmaceuticals | Novartis Pharmaceuticals | Cryopyrin-Associated Periodic Syndromes (CAPS), Familial Cold Autoinflammatory Syndrome (FCAS), Muckle-Wells Syndrome (MWS), Systemic Juvenile Idiopathic Arthritis (SJIA) | NA | Reconstitution with 1 mL of preservative-free Sterile Water for Injection is required prior to subcutaneous administration of the drug. The reconstituted canakinumab is a 150 mg/mL solution essentially free of particulates, clear to slightly opalescent, and is colorless or may have a slightly brownish-yellow tint. A volume of up to 1 mL can be withdrawn for delivery of 150 mg/mL canakinumab for subcutaneous administration. Each reconstituted vial contains 180 mg canakinumab, sucrose, L-histidine, L-histidine HCL monohydrate, polysorbate 80 and Sterile Water for Injection. No preservatives are present. | 180 mg of canakinumab as a white, preservative-free, lyophilized powder | Subcutaneous | Cryopyrin-Associated Periodic Syndromes (CAPS): The recommended dose of ILARIS is 150 mg for CAPS patients with body weight greater than 40 kg. For CAPS patients with body weight greater than or equal to 15 kg and less than or equal to 40 kg, the recommended dose is 2 mg/kg. For children 15 to 40 kg with an inadequate response, the dose can be increased to 3 mg/kg. Systemic Juvenile Idiopathic Arthritis (SJIA): The recommended dose of ILARIS for SJIA patients with a body weight greater than or equal to 7.5 kg is 4mg/kg (with a maximum of 300 mg) administered every four weeks via subcutaneous injection. | Confirmed hypersensitivity to the active substance or to any of the excipients. | ILARIS has been associated with an increased risk of serious infections, Immunosuppression, Hypersensitivity , Live vaccines should not be given concurrently with ILARIS. | Link | NA | NA |
| 10566 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | Ilaris | Novartis Pharmaceuticals Corporation | Novartis Pharmaceuticals Corporation | NA | NA | NA | Injection, powder, lyophilized, for solution | Subcutaneous | 150 mg/1mL | NA | NA | NA | NA | NA |
| 10567 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | Ilaris | Novartis Pharmaceuticals Corporation | Novartis Pharmaceuticals Corporation | NA | NA | NA | Injection, solution | Subcutaneous | 150 mg/1mL | NA | NA | NA | NA | NA |
| 10568 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | Ilaris | Novartis | Novartis | NA | NA | NA | Powder, for solution | Subcutaneous | 150 mg / vial | NA | NA | NA | NA | NA |
| 10569 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | Ilaris | Novartis | Novartis | NA | NA | NA | Solution | Subcutaneous | 150 mg / mL | NA | NA | NA | NA | NA |
| 10570 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | Ilaris | Novartis Europharm Limited | Novartis Europharm Limited | NA | NA | NA | Injection, powder, for solution | Subcutaneous | 150 mg | NA | NA | NA | NA | NA |
| 10571 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | Ilaris | Novartis Europharm Limited | Novartis Europharm Limited | NA | NA | NA | Injection, powder, for solution | Subcutaneous | 150 mg | NA | NA | NA | NA | NA |
| 10572 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | Ilaris | Novartis Europharm Limited | Novartis Europharm Limited | NA | NA | NA | Injection, powder, for solution | Subcutaneous | 150 mg | NA | NA | NA | NA | NA |
| 10573 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | Ilaris | Novartis Europharm Limited | Novartis Europharm Limited | NA | NA | NA | Injection, solution | Subcutaneous | 150 mg/ml | NA | NA | NA | NA | NA |
| 10578 | Th1119 | Tocilizumab | >Th1119_Tocilizumab QVQLQESGPGLVRPSQTLSLTCTVSGYSITSDHAWSWVRQPPGRGLEWIGYISYSGITTYNPSLKSRVTMLRDTSKNQFSLRLSSVTAADTAVYYCARSLARTTAMDYWGQGSLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | 148000 | C6428H9976N1720O2018S42 | NA | NA | NA | 11 days for 4 mg/kg and up to 13 days for 8 mg/kg | Recombinant, humanized, anti-human interleukin 6 receptor (IL-6R) monoclonal antibody. The light chain is made up of 214 amino acids and the heavy chain is made up of 448 amino acids. | Indicated for the treatment of adult patients with moderately to severely active rheumatoid arthritis (RA) who have had an inadequate response to one or more Disease-Modifying Anti-Rheumatic Drugs (DMARDs). It is also indicated for the treatment of active polyarticular juvenile idiopathic arthritis (PJIA) and active systemic juvenile idiopathic arthritis (SJIA) in patients 2 years of age and older. | A decrease in C-reactive protein (CRP) was noted as early as week 2. Changes in pharmacodynamic parameters were observed (i.e., decreases in rheumatoid factor, erythrocyte sedimentation rate (ESR), serum amyloid A and increases in hemoglobin) with both doses, however the greatest improvements were observed with 8 mg per kg tocilizumab. Similar pharmacodynamic changes were also observed in active polyarticular juvenile idiopathic arthritis and active systemic juvenile idiopathic arthritis patients. | Interleukin (IL)-6 plays essential roles not only in the immune response, but also in haematopoiesis and the central nervous system. Deregulated production of IL-6 has been found in chronic inflammatory autoimmune diseases, such as rheumatoid arthritis (RA), systemic onset juvenile idiopathic arthritis (soJIA), Crohn's disease (CD) and systemic lupus erythematosus (SLE). Furthermore, IL-6 activities can explain many symptoms of these diseases. More importantly, serum levels of IL-6 are correlated with disease activity. Tocilizumab binds specifically to both soluble and membrane-bound IL-6 receptors (sIL-6R and mIL-6R), and has been shown to inhibit IL-6-mediated signaling through these receptors. | Data regarding overdoses of tocilizumab are not readily available.[L12789] Patients experiencing an overdose may develop neutropenia.[L12789] In case of overdose, monitor patients for signs of adverse reactions and provide symptomatic and supportive treatment.[L12789] | Tocilizumab, like other monoclonal antibodies, is expected to be metabolized to smaller proteins and amino acids by proteolytic enzymes.[A19126] | A 162mg subcutaneous dose given weekly has a Cmax of 51.3±23.2µg/mL and an AUC of 8254±3833µg | In rheumatoid arthritis patients, the central volume of distribution is 3.5L, the peripheral volume of distribution is 2.9L, and the volume of distribution at steady state is 6.4L.[L12789] In giant cell arteritis patients, the central volume of distribution is 4.09L, the peripheral volume of distribution if 3.37L, and the volume of distribution at steady state is 7.46L.[L12789] In pediatric patients with polyarticular juvenile arthritis, the central volume of distribution is 1.98L, the peripheral volume of distribution is 2.1L, and the volume of distribution at steady state is 4.08L.[L12789] In pediatric patients with systemic juvenile idiopathic arthritis, the central volume of distribution is 1.87L, the peripheral volume of distribution is 2.14L, and the volume of distribution at steady state is 4.01L.[L12789] | The linear clearance in rheumatoid arthritis patients is 12.5mL/h, in giant cell arteritis patients is 6.7mL/h, in polyarticular juvenile idiopathic arthritis patients is 5.8mL/h, and in systemic juvenile idiopathic arthritis is 5.7mL/h.[L12789] Clearance is dose dependent and changes from non linear at low doses to linear at higher doses.[L12789] | NA | CA2201781 | 1-Dec-2010 | 6-Jul-2015 | NA | Interleukin-6 receptor subunit alpha | ACTEMRA | Genentech | Genentech | ACTEMRA (tocilizumab) is indicated for the treatment ofRheumatoid Arthritis, Polyarticular Juvenile Idiopathic Arthritis (PJIA), Juvenile Idiopathic Arthritis (SJIA). | NA | Single-use vials are available for intravenous administration containing 80 mg per 4 mL, 200 mg per 10 mL, or 400 mg per 20 mL of ACTEMRA. Injectable solutions of ACTEMRA are formulated in an aqueous solution containing disodium phosphate dodecahydrate and sodium dihydrogen phosphate dehydrate (as a 15 mmol per L phosphate buffer), polysorbate 80 (0.5 mg per mL), and sucrose (50 mg per mL). | Sterile, preservative-free solution, colorless to pale yellow liquid, with a pH of about 6.5 | Intravenous infusion, Subcutaneous | Rheumatoid Arthritis: The recommended dosage of ACTEMRA for adult patients given as a 60-minute single intravenous drip infusion is 4 mg per kg every 4 weeks followed by an increase to 8 mg per kg every 4 weeks based on clinical response. For SC dosage: Patients less than 100 kg weight = 162 mg administered subcutaneously every other week, followed by an increase to every week based on clinical response, Patients at or above 100 kg weight = 162 mg administered subcutaneously every week. | contraindicated in patients with known hypersensitivity to ACTEMRA | Serious Infections, Gastrointestinal Perforations, Infusion Reactions, Anaphylaxis, Neutropenia, Thrombocytopenia, Elevated Liver Enzymes, Immunogenicity, Malignancies. | Link | NA | NA |
| 10584 | Th1120 | Teriparatide | >Th1120_Teriparatide SVSEIQLMHNLGKHLNSMERVEWLRKKLQDVHNF | 4117.715 | C181H291N55O51S2 | NA | NA | NA | NA | Recombinant, human parathyroid hormone (PTH). It is a potent anabolic agent used to treat osteoporosis. It is manufactured and marketed by Eli Lilly and Company. | For the treatment of osteoporosis in men and postmenopausal women who are at high risk for having a fracture. Also used to increase bone mass in men with primary or hypogonadal osteoporosis who are at high risk for fracture. | Clinical trials indicate that teriparatide increases predominantly trabecular bone in the lumbar spine and femoral neck; it has less significant effects at cortical sites. The combination of teriparatide with antiresorptive agents is not more effective than teriparatide monotherapy. The most common adverse effects associated with teriparatide include injection-site pain, nausea, headaches, leg cramps, and dizziness. After a maximum of two years of teriparatide therapy, the drug should be discontinued and antiresorptive therapy begun to maintain bone mineral density. | Teriparatide is the portion of human parathyroid hormone (PTH),amino acid sequence 1 through 34 of the complete molecule which contains amino acid sequence 1 to 84. Endogenous PTH is the primary regulator of calcium and phosphate metabolism in bone and kidney. Daily injections of teriparatide stimulate new bone formation leading to increased bone mineral density. | Effects of overexposure may include headaches, dizziness, dizziness, decreased blood pressured, decreased fetal survival, leg cramps, changes in clinical chemistry including increased in blood levels of calcium, decreased serum phosphorous, and increased urinary calcium and phosphorus. | Hepatic | Bioavailability is 95% following subcutaneous injection. | 0.12 L/kg | * 62 L/hr [Women] * 94 L/hr [Men] | Bone Density Conservation Agents | US6977077 | 20-12-2005 | 19-08-2019 | NA | Parathyroid hormone/parathyroid hormone-related peptide receptor | Forteo | Eli Lilly and Company | Eli Lilly and Company | Treatment of Postmenopausal Women with Osteoporosis at High Risk for Fracture, Increase of Bone Mass in Men with Primary or Hypogonadal Osteoporosis at High Risk for Fracture, Treatment of Men and Women with Glucocorticoid-Induced Osteoporosis at High Risk for Fracture. | NA | Each prefilled delivery device is filled with 2.7 mL to deliver 2.4 mL. Each mL contains 250 mcg teriparatide (corrected for acetate, chloride, and water content), 0.41 mg glacial acetic acid, 0.1 mg sodium acetate (anhydrous), 45.4 mg mannitol, 3 mg Metacresol, and Water for Injection. In addition, hydrochloric acid solution 10% and/or sodium hydroxide solution 10% may have been added to adjust the product to pH 4. Each cartridge, pre-assembled into a delivery device, delivers 20 mcg of teriparatide per dose each day for up to 28 days. | Sterile, colorless, clear, isotonic solution in a glass cartridge which is pre-assembled into a disposable delivery device (pen) for subcutaneous injection | Subcutaneous | Treatment of Postmenopausal Women with Osteoporosis at High Risk for Fracture. The recommended dose is 20 mcg subcutaneously once a day. Increase of Bone Mass in Men with Primary or Hypogonadal Osteoporosis at High Risk for Fracture. he recommended dose is 20 mcg subcutaneously once a day. | Hypersensitivity to teriparatide or to any of its excipients. Reactions have included angioedema and anaphylaxis | NA | Link | NA | NA |
| 10590 | Th1122 | Rilonacept | >Th1122_Rilonacept SERCDDWGLDTMRQIQVFEDEPARIKCPLFEHFLKFNYSTAHSAGLTLIWYWTRQDRDLEEPINFRLPENRISKEKDVLWFRPTLLNDTGNYTCMLRNTTYCSKVAFPLEVVQKDSCFNSPMKLPVHKLYIEYGIQRITCPNVDGYFPSSVKPTITWYMGCYKIQNFNNVIPEGMNLSFLIALISNNGNYTCVVTYPENGRTFHLTRTLTVKVVGSPKNAVPPVIHSPNDHVVYEKEPGEELLIPCTVYFSFLMDSRNEVWWTIDGKKPDDITIDVTINESISHSRTEDETRTQILSIKKVTSEDLKRSYVCHARSAKGEVAKAAKVKQKVPAPRYTVEKCKEREEKIILVSSANEIDVRPCPLNPNEHKGTITWYKDDSKTPVSTEQASRIHQHKEKLWFVPAKVEDSGHYYCVVRNSSYCLRIKISAKFVENEPNLCYNAQAIFKQKLPVAGDGGLVCPYMEFFKNENNELPKLQWYKDCKPLLLDNIHFSGVKDRLIVMNVAEKHRGNYTCHASYTYLGKQYPITRVIEFITLEENKPTRPVIVSPANETMEVDLGSQIQLICNVTGQLSDIAYWKWNGSVIDEDDPVLGEDYYSVENPANKRRSTLITVLNISEIESRFYKHPFTCFAKNTHGIDAAYIQLIYPVTNSGDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 251000 | C9030H13932N2400O2670S74 | NA | NA | NA | 8.6 days | Dimeric fusion protein consisting of portions of IL-1R and the IL-1R accessory protein, linked to the Fc portion of immunoglobulin G1. It inhibits interleukin 1 and is used in the treatment of cryopyrin-associated periodic syndromes (CAPS), in adults and children overr than 12 of ageold. | Rilonacept is currently used in the treatment of cryopyrin-associated periodic syndrome. In May 2012, an advisory panel for the FDA voted 11-0 against the use of Rilonacept for the treatment of gout. | Treatment with Rilonacept resulted in decreased levels of mean C-Reactive Protein (CRP) and Serum Amyloid A (SAA). Higher levels of CRP and SAA are associated with inflammatory disease activity found in patients with Cryopyrin-Associated Periodic Syndromes. | CAPS refer to rare genetic syndromes generally caused by mutations in the NLRP-3 [Nucleotide-binding domain, leucine rich family (NLR), pyrin domain containing 3] gene (also known as Cold-Induced Auto-inflammatory Syndtrome-1 [CIAS1]). CAPS disorders are inherited in an autosomal dominant pattern with male and female offspring equally affected. Fever, urticaria-like rash, arthralgia, myalgia, fatigue, and conjunctivitis are features common to all disorders. In most cases, inflammation in CAPS is associated with mutations in the NLRP-3 gene which encodes the protein cryopyrin, an important component of the inflammasome. Cryopyrin regulates the protease caspase-1 and controls the activation of interleukin-1 beta (IL-1β). Mutations in NLRP-3 result in an overactive inflammasome resulting in excessive release of activated IL-1β that drives inflammation. Rilonacept blocks IL-1β signaling by acting as a soluble decoy receptor that binds IL-1β and prevents its interaction with cell surface receptors. Rilonacept also binds IL-1α and IL-1 receptor antagonist (IL-1ra) with reduced affinity. By binding IL-1, rilonacept prevents the activation of IL-1 receptors, thus reducing inflammatory responses and other effects related to an excess of IL-1. | NA | NA | NA | NA | NA | Agents reducing cytokine levels,Amino Acids, Peptides, and Proteins,Anti-Inflammatory Agents,Antineoplastic and Immunomodulating Agents,Immunosuppressive Agents,Immunotherapy,Interleukin Inhibitors,Interleukin-1 Receptor Accessory Protein,Proteins,Receptors, Interleukin-1 Type I,Recombinant Proteins | US5844099 | 12-Jan-1998 | 1-Jan-2020 | NA | Interleukin-1 beta,Interleukin-1 alpha,Interleukin-1 receptor antagonist protein | Arcalyst | Regeneron Pharmaceuticals | Regeneron Pharmaceuticals | ARCALYST (rilonacept) is an interleukin-1 blocker indicated for the treatment of Cryopyrin-Associated Periodic Syndromes (CAPS), including Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS) in adults and children 12 and older. | NA | Each vial of ARCALYST (rilonacept) is to be reconstituted with 2.3 mL of Sterile Water for Injection. A volume of up to 2 mL can be withdrawn, which is designed to deliver 160 mg for subcutaneous administration only. The resulting solution is viscous, clear, colorless to pale yellow, and essentially free from particulates. Each vial contains 220 mg rilonacept (80 mg/ 1mL after reconstitution), histidine, arginine, polyethylene glycol 3350, sucrose, and glycine at a pH of 6.5±0.3. No preservatives are present | Sterile, white to off-white, lyophilized powder | Subcutaneous | Adult patients 18 years and older: Treatment should be initiated with a loading dose of 320 mg delivered as two, 2 mL, subcutaneous injections of 160 mgeach given on the same day at two different sites. Dosing should be continued with a once-weekly injection of 160 mg administered as a single, 2-mL, subcutaneous injection. ARCALYST (rilonacept) should not be given more often than once weekly. Dosage modification is not required based on advanced age or gender. Paediatric patients aged 12 to 17 years: Treatment should be initiated with a loading dose of 4.4mg/kg, up to amaximum of 320 mg, delivered as one or two subcutaneous injections with a maximum single-injection volume of 2mL.Dosing should be continued with a once-weekly injection of 2.2 mg/kg, up to a maximum of 160 mg, administered as a single subcutaneous injection, up to 2 mL. If the initial dose is given as two injections, they should be given on the same day at two different sites. ARCALYST (rilonacept) should not be given more often than once weekly. | Certain type of bulging blood vessel (aneurysm), have a heart attack or blood clot in the lung and you also have had recent brain or spinal injury. | Six serious adverse reactions These serious adverse reactions were Mycobacterium intracellular infection; gastrointestinal bleeding and colitis; sinusitis and bronchitis; and Streptococcus pneumoniae meningitis. | Link | NA | NA |
| 10604 | Th1124 | Liraglutide | >Th1124_Liraglutide HAEGTFTSDVSSYLEGQAAKEEFIAWLVRGRG | 3751.2 | C172H265N43O51 | 4.9 | NA | NA | approx. 13 hrs | Contains liraglutide, an analog of human GLP-1, and acts as a GLP-1 receptor agonist. The recombinant peptide precursor of liraglutide, produced by its expression in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting R for K at position 34. Liraglutide was designed by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor. | For use in/treatment of diabetes mellitus type 2. | Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. GLP-1, in its natural form, is short-lived in the body (the half-life after subcutaneous injection is approximately one hour), so it is not very useful as a therapeutic agent. However, liraglutide has a half-life after subcutaneous injection of 11–15 hours, making it suitable for once-daily dosing. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at one position of the GLP-1 molecule, enabling it to bind to albumin within the subcutaneous tissue and bloodstream. The active GLP-1 is then released from albumin at a slow, consistent rate. Binding with albumin also results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1. | Liraglutide is an acylated GLP-1 (Glucagon-Like Peptide-1) receptor agonist. Liraglutide upregulates intracellular cAMP resulting in the release of insulin given elevated blood glucose concentrations. Glucagon secretion is also decreased in a glucose-dependent fashion by liraglutide. | There is no clinical significance of race or ethnicity on the safety or efficacy of liraglutide[Label]. Geriatric patients do not experience clinically significant differences in pharmacokinetics though patients at an especially advanced age may be more susceptible to adverse effects[Label]. Female patients have reduced clearance of liraglutide but no dose adjustment is necessary[Label]. The risk and benefit of liraglutide in pregnancy must be weighed before prescribing[Label]. In animal studies, liraglutide is associated with an increased risk of embryonic death and fetal abnormalities though an HbA1c > 7 is also associated with a 20-25% risk of birth defects[Label]. In animal studies, liraglutide is present in the milk of lactating rats at half the plasma concentration of the mother but these results may not translate to humans[Label]. Because it is not known if liraglutide is present in breast milk and the effects on infants are also unknown, the risk and benefit of liraglutide in breastfeeding must be considered before prescribing[Label]. Liraglutide was shown to be safe and effective in patients up to 160kg in weight but has not been studied in patients at a higher weight[Label]. A patient's weight significantly affects the pharmacokinetics of liraglutide[Label]. Liraglutide has not been investigated for use in pediatric patients[Label]. No dosage adjustments are necessary in patients with renal impairment but studies have not been performed in patients with end stage renal disease[Label]. There are no recommendations on dosage adjustment in patients with hepatic impairment, though caution should still be exercised when prescribing to this population[Label]. | Liraglutide is less sensitive to metabolism than the endogenous GLP-1 and so is more slowly metabolized by dipeptidyl peptidase-4 and neutral endopeptidase to various smaller polypeptides which have not all been structurally determined[A6932]. A portion of Liraglutide may be completely metabolized to carbon dioxide and water[A6932]. | Bioavailability of liraglutide after subcutaneous injection is approximately 55%[Label] and maximum concentrations are reached after 11.7 hours[A6932]. | 13L[Label]. | 1.2L/h[Label]. | NA | US6268343 | 31-07-2001 | 22-02-2023 | NA | Glucagon-like peptide 1 receptor | Saxenda | Novo Nordisk | Novo Nordisk | obese | NA | Each 1 mL of Saxenda solution contains 6 mg of liraglutide and the following inactive ingredients: disodium phosphate dihydrate, 1.42 mg; propylene glycol, 14 mg; phenol, 5.5 mg; and water for injection. Each pre-filled pen contains a 3 mL solution of Saxenda equivalent to 18 mg liraglutide (free-base, anhydrous). | Saxenda is a clear, colorless solution | Subcutaneous | 3 mg daily | medullary thyroid carcinoma, Multiple Endocrine Neoplasia syndrome type 2 , hypersensitivity, Pregnancy | Risk of Thyroid C-Cell Tumors, Acute Pancreatitis, Acute Gallbladder, Risk for Hypoglycemia with Concomitant Use of Anti-Diabetic Therapy , Heart Rate Increase, Renal Impairment, Hypersensitivity Reactions, Suicidal Behavior and Ideation. | Link | NA | NA |
| 10605 | Th1124 | Liraglutide | >Th1124_Liraglutide HAEGTFTSDVSSYLEGQAAKEEFIAWLVRGRG | 3751.2 | C172H265N43O51 | 4.9 | NA | NA | approx. 13 hrs | Contains liraglutide, an analog of human GLP-1, and acts as a GLP-1 receptor agonist. The recombinant peptide precursor of liraglutide, produced by its expression in Saccharomyces cerevisiae, has been engineered to be 97% homologous to native human GLP-1 by substituting R for K at position 34. Liraglutide was designed by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor. | For use in/treatment of diabetes mellitus type 2. | Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. GLP-1, in its natural form, is short-lived in the body (the half-life after subcutaneous injection is approximately one hour), so it is not very useful as a therapeutic agent. However, liraglutide has a half-life after subcutaneous injection of 11–15 hours, making it suitable for once-daily dosing. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at one position of the GLP-1 molecule, enabling it to bind to albumin within the subcutaneous tissue and bloodstream. The active GLP-1 is then released from albumin at a slow, consistent rate. Binding with albumin also results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1. | Liraglutide is an acylated GLP-1 (Glucagon-Like Peptide-1) receptor agonist. Liraglutide upregulates intracellular cAMP resulting in the release of insulin given elevated blood glucose concentrations. Glucagon secretion is also decreased in a glucose-dependent fashion by liraglutide. | There is no clinical significance of race or ethnicity on the safety or efficacy of liraglutide[Label]. Geriatric patients do not experience clinically significant differences in pharmacokinetics though patients at an especially advanced age may be more susceptible to adverse effects[Label]. Female patients have reduced clearance of liraglutide but no dose adjustment is necessary[Label]. The risk and benefit of liraglutide in pregnancy must be weighed before prescribing[Label]. In animal studies, liraglutide is associated with an increased risk of embryonic death and fetal abnormalities though an HbA1c > 7 is also associated with a 20-25% risk of birth defects[Label]. In animal studies, liraglutide is present in the milk of lactating rats at half the plasma concentration of the mother but these results may not translate to humans[Label]. Because it is not known if liraglutide is present in breast milk and the effects on infants are also unknown, the risk and benefit of liraglutide in breastfeeding must be considered before prescribing[Label]. Liraglutide was shown to be safe and effective in patients up to 160kg in weight but has not been studied in patients at a higher weight[Label]. A patient's weight significantly affects the pharmacokinetics of liraglutide[Label]. Liraglutide has not been investigated for use in pediatric patients[Label]. No dosage adjustments are necessary in patients with renal impairment but studies have not been performed in patients with end stage renal disease[Label]. There are no recommendations on dosage adjustment in patients with hepatic impairment, though caution should still be exercised when prescribing to this population[Label]. | Liraglutide is less sensitive to metabolism than the endogenous GLP-1 and so is more slowly metabolized by dipeptidyl peptidase-4 and neutral endopeptidase to various smaller polypeptides which have not all been structurally determined[A6932]. A portion of Liraglutide may be completely metabolized to carbon dioxide and water[A6932]. | Bioavailability of liraglutide after subcutaneous injection is approximately 55%[Label] and maximum concentrations are reached after 11.7 hours[A6932]. | 13L[Label]. | 1.2L/h[Label]. | NA | CA2264243 | 10-May-2004 | 22-08-2017 | NA | Glucagon-like peptide 1 receptor | Victoza | Novo Nordisk | Novo Nordisk | type 2 diabetes mellitus | NA | Each 1 mL of Victoza solution contains 6 mg of liraglutide. Each pre-filled pen contains a 3 mL solution of Victoza equivalent to 18 mg liraglutide (free-base, anhydrous) and the following inactive ingredients: disodium phosphate dihydrate, 1.42 mg; propylene glycol, 14 mg; phenol, 5.5 mg; and water for injection. | Victoza is a clear, colorless solution. | Subcutaneous | 0.6 mg per day for one week. The 0.6 mg dose is a starting dose intended to reduce gastrointestinal symptoms during initial titration, and is not effective for glycemic control. After one week at 0.6 mg per day, the dose should be increased to 1.2 mg. If the 1.2 mg dose does not result in acceptable glycemic control, the dose can be increased to 1.8 mg. | medullary thyroid carcinoma, Multiple Endocrine Neoplasia syndrome type 2, prior serious hypersensitivity reaction to Victoza. | Nausea, Diarrhea, Vomiting, Constipation, Headache | Link | NA | NA |
| 10611 | Th1125 | Golimumab | NA | 146943.2 | C6530H10068N1752O2026S44 | NA | NA | NA | About 2 weeks | Human IgG1Ò› monoclonal antibody derived from immunizing genetically engineered mice with human TNFα. It binds and inhibits soluble and transmembrane human TNFα. Increased TNFα is associated with chronic inflammation. Thus golimumab is indicated for use in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. In the U.S. and Canada, golimumab is marketed under the brand name Simponi. The FDA label includes a black box warning of serious infections and malignancy. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | Used in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. | Golimumab inhibits the activity of the cytokine, tumor necrosis factor alpha (TNFα). In areas such as the joints and blood, increased TNFαis associated with chronic inflammation seen in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. Thus golimumab decreases the inflammation in these conditions. Concerning ulcerative colitis, the physiological effects of golimumab has yet to be determined. | As a human monoclonal antibody, golimumab binds and inhibits soluble and transmembrane human TNFα. Inhibition of TNFα prevents it binding to its receptors, which prevents both leukocyte infiltration through prevention of cell adhesion proteins such as E-selectin, ICAM-1 and VCAM-1, and pro-inflammatory cytokine secretion such as IL-6, IL-8, G-CSF and GM-CSF in vitro. Consequently, in patients with chronic inflammatory conditions, decreases in ICAM-1 and IL-6 as well as C-reactive protein (CRP), matrix metalloproteinase 3 (MMP-3), and vascular endothelial growth factor (VEGF) were observed. | The FDA label includes a black box warning of serious infections and malignancy. Specifically there have been hospitalizations or death from infections such as bacterial sepsis, tuberculosis (TB), and invasive fungal (histoplasmosis) and other opportunistic infections. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. | The metabolism of golimumab has yet to be determined. | After subcutaneous administration, golimumab can achieve maximum serum concentrations in 2 to 6 days and has an approximate bioavailability of 53%. In healthy volunteers, the maximum average concentration reached was 3.2 ± 1.4 µg/mL. | After IV administration, golimumab has a volume of distribution of about 58 to 126 mL/kg. This means that golimumab stays mostly in the circulatory system. | After one IV dose of golimumab, the systemic clearance was about 4.9 to 6.7 mL/day/kg. | Antipsoriatic Agents and Monoclonal antibodies and TNF inhibitor | NA | NA | NA | NA | Tumor necrosis factor | Simponi Injection | NA | NA | Rheumatoid Arthritis, Psoriatic Arthritis, Ankylosing Spondylitis, Ulcerative Colitis | NA | pH of approximately 5.5. SIMPONI is provided in two strengths: 50 mg of the golimumab antibody in 0.5 mL of solution and 100 mg of the golimumab antibody in 1 mL of solution. In the 50 mg strength, 0.5 mL of SIMPONI contains 50 mg of the golimumab antibody, 0.44 mg of L-histidine and L-histidine monohydrochloride monohydrate, 20.5 mg of sorbitol, 0.08 mg of polysorbate 80, and Water for Injection. In the 100 mg strength, 1 mL of SIMPONI contains 100 mg of the golimumab antibody, 0.87 mg of L-histidine and L-histidine monohydrochloride monohydrate, 41.0 mg of sorbitol, 0.15 mg of polysorbate 80, and Water for Injection. | The solution is clear to slightly opalescent, colorless to light yellow | Subcutaneous | 50 mg once a month | NA | sepsis, alanine aminotransferase, aspartate aminotransferase, tuberculosis, anemia | Link | NA | NA |
| 10629 | Th1127 | Buserelin | >Th1127_Buserelin XHWSYXLRP | 1239.447 | C60H86N16O13 | NA | NA | NA | 50-80 minutes by IV dose, 80 mins. By SC dose, 1-2 hrs by Intranasal dose | Buserelin is a luteinizing hormone-releasing hormone (LHRH) agonist. It is a synthetic hormone which stimulates the pituitary gland's gonadotrophin-releasing hormone receptor (GnRHR) and is used in prostate cancer treatment. | Buserelin may be used in the treatment of hormone-responsive cancers such as prostate cancer or breast cancer, estrogen-dependent conditions (such as endometriosis or uterine fibroids), and in assisted reproduction. | NA | Buserelin stimulates the pituitary gland's gonadotrophin-releasing hormone receptor (GnRHR). Buserelin desensitizes the GnRH receptor, reducing the amount of LH and testosterone. However, there is a concomitant surge in LH and testosterone levels with the decrease in androgens, so antiandrogens must administered. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Lutropin-choriogonadotropic hormone receptor,Gonadotropin-releasing hormone receptor | Suprecur (injection) | Sanofi-Aventis | Sanofi-Aventis | infertility | NA | Each 1ml of solution contains 1 milligram of the active substance, buserelin as buserelin acetate. The other ingredients are, sodium chloride, sodium dihydrogen phosphate, sodium hydroxide, benzyl alcohol and water for injections | 1mg/ml Injection | Subcutaneous | Treatment starts on day 1 or day 21 of menstrual cycle. Daily dose is: 200 to 500 micrograms given as a single daily injection or 500 micrograms twice a day; Daily injections until blood tests show that levels of sex hormones are lowered. This usually takes one to three weeks; After this other hormones along with Suprecur Injection;Doctor determines the treatment time | Do not have this medicine and tell your doctor if: Allergy (hypersensitive) to buserelin or other similar medicines such as goserelin, or any of the other ingredients of Suprecur Injection. Abnormal menstrual bleeding Pregnancy or breast-feeding A tumour that is not affected by changes in hormone levels. This medicine is for use in women only. However there is another form of this medicine that can be used in men. Men should not use either form of this medicine if they have had their testicles removed. | NA | Link | NA | NA |
| 10631 | Th1129 | Tesamorelin | >Th1129_Tesamorelin YADAIFTNSYRKVLGQLSARKLLQDIMSRQQGESNQERGARARL | 5005.76 | C216H360N72O63S | NA | NA | NA | 26 and 38 minutes in healthy subjects and HIV-infected patients, respectively. | Stabilized synthetic peptide analogue of Growth Hormone Releasing Hormone (GHRH). It is used to treat excess abdominal fat in HIV-infected patients with lipodystrophy. It is a metabolic condition characterized by insulin resistance, fat redistribution and hyperlipidemia associated with antiretroviral therapy for HIV infection. | Tesamorelin acetate is a synthetic analogue of human hypothalamic Growth Hormone Releasing Factor (hGRF) indicated to induce and maintain a reduction of excess abdominal fat in HIV-infected patients with lipodystrophy. | Tesamorelin stimulates growth hormone secretion, and subsequently increases IGF-1 and IGFBP-3 levels. | By acting on the pituitary cells in the brain, tesamorelin stimulates production and release of the endogenous hormone (hGRF). Tesamorelin therapy predisposes the patient to glucose intolerance and can also increase the risk of type 2 diabetes, so the drug is contraindicated in pregnancy. | NA | NA | NA | NA | NA | NA | US5861379 | 19-01-1999 | 26-05-2020 | NA | Growth hormone-releasing hormone receptor | Egrifta | Theratechnologies | Theratechnologies | excess abdominal fat in HIV-infected patients with lipodystrophy | NA | After reconstitution with the supplied diluent (Sterile Water for Injection, USP), a solution of EGRIFTA is clear and colorless. Each single-use vial of EGRIFTA contains 2 mg of tesamorelin as the free base (2.2 mg tesamorelin acetate, anhydrous) and the following inactive ingredient: 100 mg mannitol, USP. | EGRIFTA is a sterile, white to off-white, preservative-free lyophilized powder for subcutaneous injection | Subcutaneous | The recommended dose of EGRIFTA is 2 mg injected subcutaneously once a day. | Disruption of the Hypothalamic-pituitary Axis, Active Malignancy, Hypersensitivity and Pregnancy | rash, urticaria, arthralgia, extremity pain, peripheral edema, hyperglycemia, carpal tunnel syndrome, erythema, pruritis, pain, urticaria, irritation, swelling, hemorrhage | Link | NA | NA |
| 10652 | Th1137 | Teduglutide | >Th1137_Teduglutide HGDGSFSDEMNTILDNLAARDFINWLIQTKITD | 3752 | C164H252N44O55S | NA | NA | NA | Terminal half-life - 2 hrs. | Recombinant (E.coli derived) glucagon-like peptide-2 (GLP-2) analogue, made up of 33 amino acids. It differs from GLP-2 by one amino acid (A to G), which makes it more resistant to dipeptidyl peptidase-4 proteolysis, giving it a longer half-life as compared to endogenous GLP-2. FDA approved on December 21, 2012. | Treatment of short bowel syndrome (SBS), malabsorption associated with the removal of the intestine, in adults patients who are dependent on parenteral support. | An enhancement of gastrointestinal fluid absorption (750-1000 mL/day) was observed following daily administrations of teduglutide. An increase in villus height and crypt depth of the intestinal mucosa was also noted. A decrease in fecal weight has also been observed. Teduglutide does not prolong the QTc interval. | Teduglutide is an analog of naturally occurring human glucagon-like peptide-2 (GLP-2), a peptide secreted by L-cells of the distal intestine in response to meals. GLP-2 increases intestinal and portal blood flow and inhibit gastric acid secretion. Teduglutide binds to the glucagon-like peptide-2 receptors located in enteroendocrine cells, subepithelial myofibroblasts and enteric neurons of the submucosal and myenteric plexus. This causes the release of insulin-like growth factor (IGF)-1, nitric oxide and keratinocyte growth factor (KGF). These growth factors may contribute to the increase in crypt cell growth and surface area of the gastric mucosa. Ultimately, absorption through the intestine is enhanced. | The most common adverse reactions (= 10%) across all studies with GATTEX are abdominal pain, injection site reactions, nausea, headaches, abdominal distension, upper respiratory tract infection. In addition, vomiting and fluid overload were reported in the SBS studies (1 and 3) at rates = 10%. | Although a formal investigation has not been conducted, it is expected because teduglutide is a peptide-based drug, it will be degraded into smaller peptides and amino acids via catabolic pathways. The cytochrome P450 enzyme system is not involved in the metabolism of this drug. | The pharmacokinetic profile of teduglutide (when administered subcutaneously) is described by a one-compartment model with first order absorption in the abdomen, arm, and thigh. With escalating doses, teduglutide demonstrates linear pharmacokinetics. Absolute bioavailability, SubQ = 88%; Tmax, SubQ = 3-5 hours; Cmax, 0.05 mg/kg SubQ, SBS patients = 36 ng/mL; AUC, 0.05 mg/kg SubQ, SBS patients = 0.15 µg•hr/mL; Teduglutide does not accumulate following multiple subcutaneous administrations. | Vd, healthy subjects = 103 mL/kg | Plasma clearance, healthy subjects = 123 mL/hr/kg; This value indicates that teduglutide is primarily cleared by the kidney. | NA | US5789379 | 8-Apr-1998 | 14-10-2020 | NA | Glucagon-like peptide 2 receptor | Gattex | NPS Pharmaceuticals, Inc | NPS Pharmaceuticals, Inc | Short Bowel Syndrome (SBS) | NA | Each single-use vial of GATTEX contains 5 mg of teduglutide as a white lyophilized powder for solution for subcutaneous injection. In addition to the active pharmaceutical ingredient (teduglutide), each vial of GATTEX contains 3.88 mg L-histidine, 15 mg mannitol, 0.644 mg monobasic sodium phosphate monohydrate, 3.434 mg dibasic sodium phosphate heptahydrate as excipients. No preservatives are present. | Teduglutide drug substance is a clear, colorless to light-straw–colored liquid. | Subcutaneous | 0.05 mg/kg body weight administered by subcutaneous injection once daily | NA | abdominal pain , injection site reactions, nausea, headaches , abdominal distension, upper respiratory tract infection. | Link | NA | NA |
| 10656 | Th1139 | Certolizumab pegol | >Th1139_Certolizumab_pegol EVQLVESGGGLVQPGGSLRLSCAASGYVFTDYGMNWVRQAPGKGLEWMGWINTYIGEPIYADSVKGRFTFSLDTSKSTAYLQMNSLRAEDTAVYYCARGYRSYAMDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCAA | 91000 | C2115H3252N556O673S16 | 6.6 - 7.2 | NA | 61ºC | Elimination half life- 14 days | Recombinant Fab' antibody fragment against TNF-alpha, which is conjugated to a ~40kDa Polyethylene glycol (PEG2MAL40K) moiety. PEG helps delay drug elimination. The light chain is made up of 214 amino acid residues while the heavy chain is composed of 229 amino acid residues. The molecular mass of the Fab' antibody fragment itself is 47.8 kDa (i.e. Excluding the PEG moiety). FDA approved on April 22, 2008. | Reducing signs and symptoms of Crohn's disease and treatment of moderately to severely active rheumatoid arthritis (RA). | TNFα is a key pro-inflammatory cytokine with a central role in inflammatory processes. Biological activity associated to TNFα include the upregulation of cellular adhesion molecules and chemokines, upregulation of major histocompatibility complex (MHC) class I and class II molecules, and direct leukocyte activation. TNFα stimulates the production of downstream inflammatory mediators, including interleukin-1, prostaglandins, platelet activating factor, and nitric oxide. After treatment with certolizumab pegol, patients with Crohn's disease demonstrated a decrease in the levels of C-reactive protein (CRP). | NA | The oral ld50 observed in mice is determined to be of 300 mg/kg.[MSDS] To this date, there have not been reports of overdosage, however, in case of accidental overexposure close monitoring is recommended.[FDA label] Certolizumab pegol does not present mutagenic potential nor presents effects in fertility and reproductive performance. On the other hand, carcinogenicity studies have not been performed.[FDA label] | The presence of PEG group in certolizumab pegol delays the metabolism and elimination of this drug. However, once under metabolism, the PEG group gets cleaved from the parent compound and the antibody section is thought to be internalized cells and rescued from metabolism by recycling. Later, it is degraded in the reticuloendothelial system to small peptides and amino acids which can be used for de-novo protein synthesis.[A31470] On the other hand, the PEG section is processed normally by the action of the alcohol dehydrogenase to the formation of carboxylic acid.[A176672] | After subcutaneous administration, the peak plasma concentration is reached between 54 and 171 hours with a bioavailability of 80%.[A176606] Certolizumab presents a linear pharmacokinetic profile with a peak plasma concentration of 43-49 mcg/ml.[F4232] | Certolizumab pegol volume of distribution is reported to be in the range of 4-8 L.[A176666] It is known to have a very good distribution in the joints when compared to other TNF-alpha inhibitors.[A176645] | The clearance rate of certolizumab pegol ranged between 9-14 ml/h when administered intravenously. However, when administered subcutaneously, the clearance rate is estimated to range between 14-21 ml/h depending on the patient condition.[F4232] | TNF inhibitor | CA2380298 | 28-09-2010 | 6-May-2021 | NA | Tumor necrosis factor | Cimzia | UCB | UCB | Crohn's Disease, Rheumatoid Arthritis, Psoriatic Arthritis | NA | Each single-use prefilled syringe of CIMZIA delivers 200 mg in 1 mL of solution with a pH of approximately 4.7 for subcutaneous use. Each 1 mL syringe of CIMZIA contains certolizumab pegol (200 mg), sodium acetate (1.36 mg), sodium chloride (7.31 mg), and Water for Injection, USP. | CIMZIA is supplied as either a sterile, white, lyophilized powder for solution or as a sterile, solution in a single-use prefilled 1 mL glass syringe for subcutaneous injection | Subcutaneous | 400 mg dose is needed (given as two subcutaneous injections of 200 mg), injections should occur at separate sites in the thigh or abdomen. | NA | Serious Infections, Malignancies, Heart Failure | Link | NA | NA |
| 10662 | Th1140 | Insulin,isophane | >Th1140_Insulin,isophane GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | 9 | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Recombinant (E.coli derived), Intermediate-acting insulin to improve glycemic control. It consists of a crystalline suspension of human insulin with protamine and zinc, which results in an intermediate-acting insulin with a slower onset of action and longer duration of activity compared to regular human insulin. | Used to improve glycemic control in patients with type 1 or type 2 diabetes mellitus. | When 0.3 Units/kg of NPH insulin was subcutaneously administered, the onset of action was approximately 0.8 hours. The duration of action was 13.2 hours. The peak activity of NPH insulin occurs 4-6 hours post-dose. Compared to insulin glargine, NPH insulin has a quicker onset of action and shorter duration of action. | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism | NA | NA | NA | NA | NA | Hypoglycemic Agents and Antidiabetic Agents | NA | NA | NA | NA | Insulin receptor | Novolin N | Novo Nordisk | Novo Nordisk | Type 1 Diabetes Mellitus, Type 2 Diabetes Mellitus, | NA | Novolin N in an InnoLet disposable prefilled insulin syringe. Novolin N is commonly known as NPH, Human Insulin Isophane Suspension (recombinant DNA origin). The concentration of this product is 100 units of insulin per milliliter. It is a cloudy or milky suspension of human insulin with protamine and zinc. The insulin substance (the cloudy material) settles at the bottom of the insulin reservoir, therefore, the Novolin N InnoLet (nph, human insulin isophane suspension 3 ml disposable prefilled syringe) must be rotated up and down so that the contents are uniformly mixed before a dose is given | Novolin N InnoLet (nph, human insulin isophane suspension 3 ml disposable prefilled syringe) | Subcutaneous | 0.5 U/kg/day SC (Type 1 Diabetes Mellitus), 0.5-1 units/kg/day in divided doses (Type 2 Diabetes Mellitus) | Tell your doctor or pharmacist if you have any medical conditions, pregnant, planning to become pregnant, or are breast-feeding; taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement; allergies to medicines, foods, or other substances; drink alcoholic beverages or smoke; heart problems (eg, heart failure); kidney or liver problems; nerve problems; adrenal, pituitary, or thyroid problems; or diabetic ketoacidosis; use 3 or more insulin injections per day; if you are fasting, have high blood sodium levels, or are on a low-salt (sodium) diet. Some MEDICINES MAY INTERACT with insulin isophane vials. Tell your health care provider if you are taking any other medicines, especially any of the following: Beta-blockers, Angiotensin-converting enzyme, (ACE) inhibitors, Thiazolidinediones Corticosteroids . | insulin allergy, Hypoglycemia, or low blood sugar, is the most common side effect of insulin. Symptoms of low blood sugar may include headache, hunger, sweating, pale skin, irritability, dizziness, feeling shaky, or trouble concentrating. Watch for signs of low blood sugar. Carry a piece of non-dietetic hard candy or glucose tablets with you in case you have low blood sugar. Tell your doctor if you have itching, swelling, redness, or thickening of the skin where you inject insulin isophane. | Link | NA | NA |
| 10666 | Th1144 | Follitropin alpha | >Th1144_Follitropin_alpha APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | NA | NA | 24-53 hours in females, 32-41 hours in males | Recombinant (CHO cell derived) human follicle stimulating hormone (FSH). It consists of two non-covalently linked, non-identical glycoproteins designated as the alpha (92 amino acids)- and beta (111 amino acids)- subunits. The alpha subunit is glycosylated at N51 and N78 while the beta subunit is glycosylated at N7 and N24. Follitropin alpha was the world's first recombinant human FSH preparation. The term “alpha†differentiates it from another recombinant human FSH product that was marketed later as follitropin beta. Follitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). Numerous physio-chemical tests and bioassays indicate that follitropin beta and follitropin alpha are indistinguishable. However, a more recent study showed there is may be a slight clinical difference, with the alpha form tending towards a higher pregnancy rate than beta but with significantly higher estradiol (E2) levels. The amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (FSH). Further, the ogliosaccharide side-chains are very similar, but not completely identical to that of natural FSH. However, these small differences do not affect the bioactivity compared to natural FSH. | In women having been diagnosed with primary ovarian failure, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. In men with hypogonadotrophic hypogonadism, it is used to induce spermatogenesis. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF) | The main pharmacodynamic parameters are serum inhibin, estradiol and total follicular volume with daily injections of follitropin. The quickest response was noticed with serum inhibin, which declined rapidly after discontinuation. Follicular growth showed late response and continued even after discontinuation of the drug and after decline of the serum concentrations. Thus follicular growth was better correlated with serum inhibin and estradiol rather than peal levels of the drug. It should be noted that there is great inter-individual variability | Follitropin is important for spermatogenesis, gonadal steroid production and follicule growth and maturation | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Gonal-F | Serono Laboratories | Serono Laboratories | induction of ovulation and pregnancy anovulatory infertile patients in whom the cause of infertility is functional and not due to primary ovarian failure, for the development of multiple follicles in the ovulatory patient participating in an Assisted Reproductive Technology (ART) program. | NA | Each Gonal-f (follitropin alfa) RFF single-dose vial is filled with 82 IU (6 µg)follitropin alfa to deliver 75 IU (5.5 µg) follitropin alfa and contains 30 mg sucrose, 1.11 mg dibasic sodium phosphate dihydrate, 0.45 mg monobasic sodium phosphate monohydrate, 0.1 mg methionine, and 0.05 mg polysorbate 20. Phosphoric acid and/or sodium hydroxide may be used prior to lyophilization for pH adjustment. Vials are reconstituted with Sterile Water for Injection, USP. | Gonal-f (follitropin alfa) RFF is a sterile, lyophilized powder intended for subcutaneous injection after reconstitution. | Subcutaneous Injection | 300 IU per day | Prior hypersensitivity to recombinant FSH preparations or one of their excipients, High levels of FSH indicating primary ovarian failure., Uncontrolled thyroid or adrenal dysfunction, An organic intracranial lesion such as a pituitary tumor, Abnormal uterine bleeding of undetermined origin, Ovarian cyst or enlargement of undetermined origin, Sex hormone dependent tumors of the reproductive tract and accessory organs, Pregnancy. | headache, ovarian cyst, nausea, and upper respiratory tract infection | Link | NA | NA |
| 10667 | Th1144 | Follitropin alpha | >Th1144_Follitropin_alpha APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | NA | NA | NA | Recombinant (CHO cell derived) human follicle stimulating hormone (FSH). It consists of two non-covalently linked, non-identical glycoproteins designated as the alpha (92 amino acids)- and beta (111 amino acids)- subunits. The alpha subunit is glycosylated at N51 and N78 while the beta subunit is glycosylated at N7 and N24. Follitropin alpha was the world's first recombinant human FSH preparation. The term “alpha†differentiates it from another recombinant human FSH product that was marketed later as follitropin beta. Follitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). Numerous physio-chemical tests and bioassays indicate that follitropin beta and follitropin alpha are indistinguishable. However, a more recent study showed there is may be a slight clinical difference, with the alpha form tending towards a higher pregnancy rate than beta but with significantly higher estradiol (E2) levels. The amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (FSH). Further, the ogliosaccharide side-chains are very similar, but not completely identical to that of natural FSH. However, these small differences do not affect the bioactivity compared to natural FSH. | In women having been diagnosed with primary ovarian failure, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. In men with hypogonadotrophic hypogonadism, it is used to induce spermatogenesis. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF) | The main pharmacodynamic parameters are serum inhibin, estradiol and total follicular volume with daily injections of follitropin. The quickest response was noticed with serum inhibin, which declined rapidly after discontinuation. Follicular growth showed late response and continued even after discontinuation of the drug and after decline of the serum concentrations. Thus follicular growth was better correlated with serum inhibin and estradiol rather than peal levels of the drug. It should be noted that there is great inter-individual variability | Follitropin is important for spermatogenesis, gonadal steroid production and follicule growth and maturation | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Gonal-f RFF | EMD SERONO | EMD SERONO | ovulation and pregnancy in the oligo-anovulatory infertile patient in whom the cause of infertility is functional and not due to primary ovarian failure, development of multiple follicles in the ovulatory patient participating in an Assisted Reproductive Technology (ART) program. | NA | Each Gonal-f RFF single-dose vial is filled with 82 IU (6 µg)follitropin alfa to deliver 75 IU (5.5 µg) follitropin alfa and contains 30 mg sucrose, 1.11 mg dibasic sodium phosphate dihydrate, 0.45 mg monobasic sodium phosphate monohydrate, 0.1 mg methionine, and 0.05 mg polysorbate 20. Phosphoric acid and/or sodium hydroxide may be used prior to lyophilization for pH adjustment. Vials are reconstituted with Sterile Water for Injection, USP. | Gonal-f RFF (follitropin alfa injection) is a sterile, lyophilized powder intended for subcutaneous injection after reconstitution. | Subcutaneous Injection | 300 IU per day | Prior hypersensitivity to recombinant FSH preparations or one of their excipients, High levels of FSH indicating primary ovarian failure., Uncontrolled thyroid or adrenal dysfunction, An organic intracranial lesion such as a pituitary tumor, Sex hormone dependent tumors of the reproductive tract and accessory organs, Abnormal uterine bleeding of undetermined origin, Ovarian cyst or enlargement of undetermined origin, Pregnancy. | Headache, Dizziness, Migraine, Abdominal Pain, Nausea, Flatulence, Diarrhea, Toothache, Dyspepsia, Constipation, Stomatitis Ulcerative, Ovarian Cyst, Reproductive, Female, Ovarian Hyperstimulation, Breast Pain Female, Vaginal Haemorrhage, Gynecological-related pain, Uterine haemorrhage, Sinusitis, Pharyngitis, Rhinitis, Coughing, Injection Site Pain, Injection Site Inflammation, Back Pain, Pain, Fever, Hot Flushes, Malaise, Acne, Micturition Frequency, Cystitis, Infection viral. | Link | NA | NA |
| 10668 | Th1145 | Romiplostim | >Th1145_Romiplostim IEGPTLRQWLAARA | 59000 | C2634H4086N722O790S18 | NA | NA | NA | Immunen thrombocytopenia patients, subQ = 3.5 days (median) (range 1-34 days) | Romiplostim is a thrombopoiesis stimulating dimer Fc-peptide fusion protein (peptibody) to increase platelet production through activation of the thrombopoietin receptor. The peptibody molecule has two identical single-chain subunits, each one is made up of 269 amino acid residues. Each subunit consists of an IgG1 Fc carrier domain that is covalently attached to a polypeptide sequence that contains two binding domains to interact with thrombopoietin receptor c-Mpl. Each domain consists of 14 amino acids. Interestingly, romiplostim's amino acid sequence is not similar to that of endogenous thrombopoietin. Romiplostim is produced by recombinant DNA technology in Escherichia coli. FDA approved on August 22, 2008. | Treatment of chronic immune thrombocytopenic purpura. | Responses to platelet increase varies between patients thus indicating a need for individualization of dose. However, a dose dependent-increase in platelet counts have been observed in clinical trials. Does not affect platelet destruction. | Romiplostim is a thrombopoietin receptor agonist that activates intracellular transcriptional pathways via c-Mpl to increase production of platelets. It also works similarly to thrombopoietin (TPO), an endogenous glycoprotein hormone that regulates the production of platelets in the bone marrow. | The most common adverse reactions (= 5% higher patient incidence in Nplate versus placebo) are arthralgia, dizziness, insomnia, myalgia, pain in extremity, abdominal pain, shoulder pain, dyspepsia, and paresthesia. Headache was the most commonly reported adverse reaction that did not occur at = 5% higher patient incidence in Nplate versus placebo. LD50 = 980 mg/kg. | NA | Cmax, healthy volunteers, subQ = 24-36 hours; Cmax, immune thrombocytopenia patients, subQ = 7-50 hours (median = 14 hours). Not affected by age, weight, or gender. Accumulation does not occur after six weekly doses of 3 mcg/kg romiplostim. | In healthy volunteers, non-linear decrease in Vd with increase IV dose of romiplostim which indicates saturation of c-Mpl receptors. Vd, 0.3 µg/kg = 122 mL/kg Vd, 10 µg/kg = 48.2 mL/kg | NA | Amino Acids, Peptides, and Proteins,Biological Factors,Blood and Blood Forming Organs,Carbohydrates,Colony-Stimulating Factors,Cytokines,Glycoconjugates,Glycoproteins,Hematinics,Hematopoietic Cell Growth Factors,Hemostatics,Increased Megakaryocyte Maturation,Increased Platelet Production,Intercellular Signaling Peptides and Proteins,Membrane Proteins,Peptides,Proteins,Receptors, Thrombopoietin, agonists,Recombinant Proteins,Thrombopoietin Receptor Agonist,Thrombopoietin Receptor Agonists | NA | NA | NA | NA | Thrombopoietin receptor | Nplate | Amgen | Amgen | Nplate is indicated for the treatment of thrombocytopenia in patients with chronic immune thrombocytopenia (ITP) who have had an insufficient response to corticosteroids, immunoglobulins or splenectomy. | NA | Two vial presentations are available, which contain a sufficient amount of active ingredient to provide either 250 mcg or 500 mcg of deliverable romiplostim, respectively. Each single-use 250 mcg vial of Nplate contains the following: 375 mcg romiplostim, 30 mg mannitol, 15 mg sucrose, 1.2 mg L-histidine, 0.03 mg polysorbate 20, and sufficient HCl to adjust the pH to a target of 5.0. Each single-use 500 mcg vial of Nplate contains the following: 625 mcg romiplostim, 50 mg mannitol, 25 mg sucrose, 1.9 mg L-histidine, 0.05 mg polysorbate 20, and sufficient HCl to adjust the pH to a target of 5.0 | Sterile, preservative-free, lyophilized, solid white powder | Subcutaneous Injection | Use the lowest dose of Nplate to achieve and maintain a platelet count ≥ 50 x 109/L as necessary to reduce the risk for bleeding. Administer Nplate as a weekly subcutaneous injection with dose adjustments based upon the platelet count response. The prescribed Nplate dose may consist of a very small volume (eg, 0.15 mL). Administer Nplate only with a syringe that contains 0.01 mL graduations. The initial dose for Nplate is 1 mcg/kg based on actual body weight. Dose AdjustmentsUse the actual body weight at initiation of therapy, then adjust the weekly dose of Nplate by increments of 1 mcg/kg until the patient achieves a platelet count ≥ 50 x 109/L as necessary to reduce the risk for bleeding; do not exceed a maximum weekly dose of 10 mcg/kg. In clinical studies, most patients who responded to Nplate achieved and maintained platelet counts ≥ 50 x 109/L with a median dose of 2 mcg/kg. During Nplate therapy, assess CBCs, including platelet counts, weekly until a stable platelet count ( ≥ 50 x 109/L for at least 4 weeks without dose adjustment) has been achieved. Obtain CBCs, including platelet counts, monthly thereafter. | NA | The following serious adverse reactions: Progression of Myelodysplastic Syndromes, Thrombotic/Thromboembolic Complications, Loss of Response to Nplate, Overdoses due to medication errors have been reported in patients receiving Nplate. In the event of overdose, platelet counts may increase excessively and result in thrombotic/thromboembolic complications. In this case, discontinue Nplate and monitor platelet counts. Reinitiate treatment with Nplate in accordance with dosing and administration recommendations. | Link | NA | NA |
| 10682 | Th1150 | Secukinumab | >Th1150_Secukinumab EVQLVESGGGLVQPGGSLRLSCAASGFTFSNYWMNWVRQAPGKGLEWVAAINQDGSEKYYVGSVKGRFTISRDNAKNSLYLQMNSLRVEDTAVYYCVRDYYDILTDYYIHYWYFDLWGRGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 147940 | C6584H10134N1754O2042S44 | NA | NA | NA | 22-31 days | A human monoclonal antibody, secukinumab (cosentyx) was designed for the treatment of uveitis, rheumatoid arthritis, ankylosing spondylitis, and psoriasis. Secukinumab is an interleukin-17A inhibitor marketed by Novartis. On January 19, 2015, secukinumab was approved by the European Commission as a first line systemic treatment in moderate to severe adult plaque psoriasis. On January 21, 2015, the United States Food and Drug Administration announced that it had approved secukinumab to treat adults with moderate-to-severe plaque psoriasis. | It is a human interleukin-17A antagonist indicated for the treatment of moderate to severe plaque psoriasis in adult patients who are candidates for systemic therapy or phototherapy. | Elevated levels of IL-17A are found in psoriatic plaques. Treatment with cosentyx may reduce epidermal neutrophils and IL-17A levels in psoriatic plaques. Serum levels of total IL-17A (free and secukinumab-bound IL-17A) measured at Week 4 and Week 12 were increased following secukinumab treatment. These pharmacodynamic activities are based on small exploratory studies. The relationship between these pharmacodynamic activities and the mechanism(s) by which secukinumab exerts its clinical effects is unknown. | Secukinumab is a human IgG1 monoclonal antibody that selectively binds to the interleukin-17A (IL-17A) cytokine and inhibits its interaction with the IL-17 receptor. IL-17A is a naturally occurring cytokine that is involved in normal inflammatory and immune responses. Secukinumab inhibits the release of proinflammatory cytokines and chemokines. | NA | Mainly intracellular breakdown. | Bioavailability after subcutaneous administration was 55-77%. | Volume of distribution (Vd) in interstitial fluid of skin (+/- psoriasis) was 27-40% of that in serum after single subcutaneous dose of 300 mg. Vd increased at higher body weights. | Serum clearance was increased with higher body weights. | Inhibitor | US20130202610 | 10-Aug-2010 | 10-Aug-2020 | NA | Interleukin-17A | Cosentyx | Novartis Pharmaceuticals Corporation | Novartis Pharmaceuticals Corporation | Cosentyx is indicated for the treatment of moderate to severe plaque psoriasis in adult patients who are candidates for systemic therapy or phototherapy. | NA | Each cosentyx sensoready pen or prefilled syringe contains 150 mg of secukinumab formulated in: Lhistidine/ histidine hydrochloride monohydrate (3.103 mg), L-methionine (0.746 mg), polysorbate 80 (0.2 mg), trehalose dihydrate (75.67 mg), and Sterile Water for Injection, USP, at pH of 5.8. | Cosentyx injection is a sterile, preservative-free, clear to slightly opalescent, colorless to slightly yellow solution. | Subcutaneous injection | The recommended dose is 300 mg by subcutaneous injection at Weeks 0, 1, 2, 3, and 4 followed by 300 mg every 4 weeks. Each 300 mg dose is given as 2 subcutaneous injections of 150 mg. For some patients, a dose of 150 mg may be acceptable. | Patients with a previous serious hypersensitivity reaction to secukinumab or to any of the excipients | Crohn’s disease “flare-ups†(worsening Crohn’s disease), serious allergic reactions, chest tightness, swelling of your face, eyelids, lips, mouth, tongue, or throat, trouble breathing or throat tightness, skin rash and upper respiratory infections | Link | NA | NA |
| 10683 | Th1151 | Somatotropin Recombinant | >Th1151_Somatotropin_Recombinant FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 at pH 3 | 21.1 (±5.1) minutes | Somatropin (rDNA origin - nonrefrigerated) is a growth hormone. It works by increasing the flow of water, electrolytes, and nutrients into the bowels. | For treatment of dwarfism, acromegaly and prevention of HIV-induced weight loss | Used in the treatment of dwarfism and growth failure, growth hormone (hGH) stimulates skeletal growth in pediatric patients with growth failure due to a lack of adequate secretion of endogenous GH. Skeletal growth is accomplished at the epiphyseal plates at the ends of a growing bone. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and one of its mediators, IGF-I (insulin-like growth factor). | hGH binds to the human growth hormone receptor (GHR). Upon binding, hGH causes dimerization of GHR, activation of the GHR-associated JAK2 tyrosine kinase, and tyrosyl phosphorylation of both JAK2 and GHR. These events recruit and/or activate a variety of signaling molecules, including MAP kinases, insulin receptor substrates, phosphatidylinositol 3' phosphate kinase, diacylglycerol, protein kinase C, intracellular calcium, and Stat transcription factors. These signaling molecules contribute to the GH-induced changes in enzymatic activity, transport function, and gene expression that ultimately culminate in changes in growth and metabolism. | NA | NA | NA | NA | NA | Hormone Replacement Agents | CA1326439 | 25-01-1994 | 25-01-2011 | NA | Growth hormone receptor | NutropinAQ | Genentech Inc. | Genentech Inc. | Various brands of this medication are used for the treatment of one of the following medical conditions: growth failure, growth hormone deficiency, intestinal disorder (short bowel syndrome) or HIV-related weight loss or wasting. Somatropin is also used to increase height in children with a certain genetic disorder (Noonan syndrome). | Growth hormon (human), r-DNA derived | Nutropin is a sterile, white lyophilized powder intended for subcutaneous administration after reconstitution with Bacteriostatic Water for Injection, USP (benzyl alcohol preserved). The reconstituted product is nearly isotonic at a concentration of 5 mg/mL GH and has a pH of approximately 7.4. | Sterile, white lyophilized powder intended for subcutaneous administration after reconstitution with Bacteriostatic Water | Subcutaneous administration | Not to exceed 0.006 mg/kg/day SC initially for 6 weeks; may increase up to 0.025 mg/kg/day if patient <35 years of age and up to 0.0125 mg/kg/day if patient >35 years | Acute Critical Illness, Prader-Willi Syndrome (PWS) in Children, Active MalignancyIn, Diabetic Retinopathy and Hypersensitivity | Sudden death in pediatric patients with Prader-Willi syndrome (PWS) with risk factors includingsevere obesity, history of upper airway obstruction or sleep apnea and unidentified respiratoryinfection, Intracranial tumors, in particular meningiomas, in teenagers/young adults treated with radiationto the head as children for a first neoplasm and somatropin, Glucose intolerance including impaired glucose tolerance/impaired fasting glucose as well asovert diabetes mellitus, Intracranial hypertension, Unmasking of latent central hypothyroidism, Significant diabetic retinopathy , Slipped capital femoral epiphysis in pediatric patients, Progression of preexisting scoliosis in pediatric patients and Fluid retention manifested by edema, arthralgia, myalgia, nerve compression syndromes including carpal tunnel syndrome/paraesthesias. | Link | NA | NA |
| 10684 | Th1151 | Somatotropin Recombinant | >Th1151_Somatotropin_Recombinant FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 at pH 3 | 21.1 (±5.1) minutes | Somatropin (rDNA origin - nonrefrigerated) is a growth hormone. It works by increasing the flow of water, electrolytes, and nutrients into the bowels. | For treatment of dwarfism, acromegaly and prevention of HIV-induced weight loss | Used in the treatment of dwarfism and growth failure, growth hormone (hGH) stimulates skeletal growth in pediatric patients with growth failure due to a lack of adequate secretion of endogenous GH. Skeletal growth is accomplished at the epiphyseal plates at the ends of a growing bone. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and one of its mediators, IGF-I (insulin-like growth factor). | hGH binds to the human growth hormone receptor (GHR). Upon binding, hGH causes dimerization of GHR, activation of the GHR-associated JAK2 tyrosine kinase, and tyrosyl phosphorylation of both JAK2 and GHR. These events recruit and/or activate a variety of signaling molecules, including MAP kinases, insulin receptor substrates, phosphatidylinositol 3' phosphate kinase, diacylglycerol, protein kinase C, intracellular calcium, and Stat transcription factors. These signaling molecules contribute to the GH-induced changes in enzymatic activity, transport function, and gene expression that ultimately culminate in changes in growth and metabolism. | NA | NA | NA | NA | NA | Hormone Replacement Agents | CA2252535 | 23-06-2009 | 24-04-2017 | NA | Growth hormone receptor | BioTropin | Bio-Technology General (Israel) Ltd. | Bio-Technology General (Israel) Ltd. | Various brands of this medication are used for the treatment of one of the following medical conditions: growth failure, growth hormone deficiency, intestinal disorder (short bowel syndrome) or HIV-related weight loss or wasting. Somatropin is also used to increase height in children with a certain genetic disorder (Noonan syndrome). | Growth hormon (human), r-DNA derived | Bio-Tropin is provided as a sterile, white, lyophilized powder, available 4 mg presentations. It is intended for subcutaneous administration after reconstitution with bacteriostatic sodium chloride injection, USP, (benzyl alcohol preserved).The diluent for the 4 mg presentation contains solution of 0.9% sodium chloride in water for injection and 0.9% benzyl alcohol as a preservative (bacteriostatic normal saline, USP). A 5 ml vial of the diluent is provided with each dispensed vial of Bio-Tropin. | Sterile, white, lyophilized powder | Subcutaneous administration | Growth hormone insufficiency:25-35 µg/kg/day or 0.7-1.0 mg/m2/day, Turner syndrome:50 µg/kg/day or 1.4 mg/m2/day, Chronic Renal Disease:50 µg/kg/day or 1.4 mg/m2/day, In children born small for gestational age (SGA):35 microgram/kg/day or 1 mg/m2/day. A dose of 0.035 mg/kg/day is usually recommended until final height is reached. Treatment should be discontinued after the first year of treatment, if the height velocity SDS is below +1. Treatment should be discontinued if height velocity is < 2cm/year and, if confirmation is required, bone age is>14 years (girls) or >16 years (boys), corresponding to closure of the epiphyseal growth plates. | Bio-Tropin should not be used in subjects with closed epiphyses.Patients with evidence of progression of an underlying intracranial lesion should not receive Bio-Tropin. Prior to the initiation of the therapy with Bio-Tropin, intracranial tumors must be inactive and antitumor therapy, including a reasonable period of observation, should be completed. Bio-Tropin should be discontinued if there is evidence of recurrent tumor growth. Bio-Tropin reconstituted with bacteriostatic sodium chloride injection, USP (benzyl alcohol preserved) should not be administered to patients with a known sensitivity to benzyl alcohol. Bio-Tropin is not indicated for the treatment of short stature in genetically confirmed Prader-Willi syndrome. | Irritability, Mental Disorder, Insomnia, Depression, Asocial Behaviour, Aggression, Nephrotic Syndrome, Blood Cholesterol Increased | Link | NA | NA |
| 10685 | Th1151 | Somatotropin Recombinant | >Th1151_Somatotropin_Recombinant FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 at pH 3 | 21.1 (±5.1) minutes | Somatropin (rDNA origin - nonrefrigerated) is a growth hormone. It works by increasing the flow of water, electrolytes, and nutrients into the bowels. | For treatment of dwarfism, acromegaly and prevention of HIV-induced weight loss | Used in the treatment of dwarfism and growth failure, growth hormone (hGH) stimulates skeletal growth in pediatric patients with growth failure due to a lack of adequate secretion of endogenous GH. Skeletal growth is accomplished at the epiphyseal plates at the ends of a growing bone. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and one of its mediators, IGF-I (insulin-like growth factor). | hGH binds to the human growth hormone receptor (GHR). Upon binding, hGH causes dimerization of GHR, activation of the GHR-associated JAK2 tyrosine kinase, and tyrosyl phosphorylation of both JAK2 and GHR. These events recruit and/or activate a variety of signaling molecules, including MAP kinases, insulin receptor substrates, phosphatidylinositol 3' phosphate kinase, diacylglycerol, protein kinase C, intracellular calcium, and Stat transcription factors. These signaling molecules contribute to the GH-induced changes in enzymatic activity, transport function, and gene expression that ultimately culminate in changes in growth and metabolism. | NA | NA | NA | NA | NA | Hormone Replacement Agents | US5288703 | 22-02-1994 | 10-Jul-2011 | Concomitant glucocorticoid therapy may inhibit the growth promoting effect of Protropin (somatrem) . If glucocorticoid replacement is required, the dose should be carefully adjusted. | Growth hormone receptor | Protropin | Genentech Inc. | Genentech Inc. | Protropin is indicated only for the long- term treatment of children who have growth failure due to a lack of adequateendogenous growth hormone secretion. Other etiologies of short stature should be excluded. | Growth hormon (human), r-DNA derived | Each 5 mg Protropin vial contains 5 mg (approximately 15 IU) somatrem, lyophilized with 40 mg mannitol, and 1.7 mg sodium phosphates (0.1 mg sodium phosphate monobasic and 1.6 mg sodium phosphate dibasic). | Protropin (somatrem) is a sterile, white, lyophilized powder intended forintramuscular or subcutaneous administration after reconstitution withBacteriostatic Water for Injection, USP (benzyl alcohol preserved). | Intramuscular or subcutaneous administration | A weekly dosage of 0.30 mg/kg (approximately 0.90 IU/kg) of body weight administered by daily intramuscular or subcutaneous injection is recommended. | Protropin (somatrem for injection) should not be used in subjects with closed epiphyses, protropin should not be used in patients with active neoplasia. Growth hormone therapy should be discontinued if evidence of neoplasia develops and when reconstituted with Bacteriostatic Water for Injection, USP (benzyl alcohol preserved) should not be used in patients with a known sensitivity to benzyl alcohol. | As with all protein pharmaceuticals, a small percentage of patients may develop antibodies to the protein. Growth hormone antibody binding capacities below 2 mg/L have not been associated with growth attenuation. In some cases when binding capacity exceeds 2 mg/L, growth attenuation has been observed. Common side effects include headache, fatigue, or muscle pain. | Link | NA | NA |
| 10694 | Th1157 | Sermorelin | >Th1157_Sermorelin YADAIFTNSYRKVLGQLSARKLLQDIMSRQ | 3357.882 | C149H246N44O42S | 9.99 | -0.33 | NA | 11-12 minutes | Sermorelin acetate is the acetate salt of an amidated synthetic 29-amino acid peptide (GRF 1-29 NH 2 ) that corresponds to the amino-terminal segment of the naturally occurring human growth hormone-releasing hormone (GHRH or GRF) consisting of 44 amino acid residues. | For the treatment of dwarfism, prevention of HIV-induced weight loss | Sermorelin is used in the treatment of children with growth hormone deficiency or growth failure. Geref increases plasma growth hormone (GH) concentration by stimulating the pituitary gland to release GH. Geref is similar to the full-length native hormone (44 residues) in its ability to stimulate GH secretion in humans. | Sermorelin binds to the growth hormone releasing hormone receptor and mimics native GRF in its ability to stimulate growth hormone secretion. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins,Anterior Pituitary Lobe Hormones and Analogues,Diagnostic Agents,Growth Hormone-Releasing Hormone,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypothalamic Hormones,Nerve Tissue Proteins,Neuropeptides,Peptide Hormones,Peptides,Pituitary and Hypothalamic Hormones and Analogues,Pituitary Hormone-Releasing Hormones,Somatropin and Somatropin Agonists,Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins,Tests for Pituitary Function | NA | NA | NA | NA | Growth hormone-releasing hormone receptor | Sermorelin acetate | Emd serono inc | Emd serono inc | Sermorelin is approved for diagnostic evaluation of pituitary function and also for increasing growth in children. Off label usage may include acute or age-related growth hormone insufficiency | NA | Two vial presentations are available, Each vial contains 0.5 mg sermorelin (as the acetate) and 5 mg mannitol. The pH is adjusted with dibasic sodium phosphate and monobasic sodium phosphate buffer. Each vial contains 3.0 mg sermorelin (as the acetate) and 5 mg mannitol. The pH is adjusted with dibasic sodium phosphate and monobasic sodium phosphate buffer. | Sermorelin is a sterile, non-pyrogenic, lyophilized powder | Subcutaneous Injection | A dosage of 0.2 - 0.3 mcg once daily at bedtime by subcutaneous injection is recommended. It is also recommended that subcutaneous injection sites be periodically rotated. | Sermorelin should not be used by patients with a known sensitivity to sermorelin or any of the excipients | The most common treatment-related adverse event (occurring in about 1 patient in 6) is local injection reaction characterized by pain, swelling or redness. Other treatment-related adverse events had individual occurrence rates of less than 1% and include: headache, flushing, dysphagia, dizziness, hyperactivity, somnolence and urticaria. | Link | NA | NA |
| 10702 | Th1161 | Albiglutide | >Th1161_Albiglutide HGEGTFTSDVSSYLEGQAAKEFIAWLVKGRHGEGTFTSDVSSYLEGQAAKEFIAWLVKGRDAHKSEVAHRFKDLGEENFKALVLIAFAQYLQQCPFEDHVKLVNEVTEFAKTCVADESAENCDKSLHTLFGDKLCTVATLRETYGEMADCCAKQEPERNECFLQHKDDNPNLPRLVRPEVDVMCTAFHDNEETFLKKYLYEIARRHPYFYAPELLFFAKRYKAAFTECCQAADKAACLLPKLDELRDEGKASSAKQRLKCASLQKFGERAFKAWAVARLSQRFPKAEFAEVSKLVTDLTKVHTECCHGDLLECADDRADLAKYICENQDSISSKLKECCEKPLLEKSHCIAEVENDEMPADLPSLAADFVESKDVCKNYAEAKDVFLGMFLYEYARRHPDYSVVLLLRLAKTYETTLEKCCAAADPHECYAKVFDEFKPLVEEPQNLIKQNCELFEQLGEYKFQNALLVRYTKKVPQVSTPTLVEVSRNLGKVGSKCCKHPEAKRMPCAEDYLSVVLNQLCVLHEKTPVSDRVTKCCTESLVNRRPCFSALEVDETYVPKEFNAETFTFHADICTLSEKERQIKKQTALVELVKHKPKATKEQLKAVMDDFAAFVEKCCKADDKETCFAEEGKKLVAASQAALGL | 72970 | C3232H5032N864O979S41 | NA | NA | NA | 4-7 days. | Albiglutide is a glucagon-like peptide-1 agonist (GLP-1) biologic drug indicated in the treatment of type 2 diabetes. It is marketed under the brands Eperzan and Tanzeum by GSK (GlaxoSmithKline). It is a dipeptidyl peptidase-4-resistant glucagon-like peptide-1 dimer fused to human albumin. Albiglutide was approved on April 15, 2014 by the FDA. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | It lowers fasting glucose and reduces postprandial glucose excursions in patients with type 2 diabetes mellitus. The majority of the observed reduction in fasting plasma glucose occurs after a single dose, consistent with the pharmacokinetic profile of albiglutide. | Albiglutide is an agonist of the GLP-1 (glucagon-like peptide 1) receptor and augments glucose-dependent insulin secretion. Albiglutide also slows gastric emptying. | -RISK OF THYROID C-CELL TUMORS -Albiglutide is contraindicated in patients with a personal or family history of MTC or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN2). Routine serum calcitonin or thyroid ultrasound monitoring is of uncertain value in patients treated with Albiglutide. | Biotransformation studies have not been performed. Because albiglutide is an albumin fusion protein, it likely follows a metabolic pathway similar to native human serum albumin, which is catabolized primarily in the vascular endothelium. | Maximum concentrations of albiglutide were reached at 3 to 5 days post-dosing following a single 30mg dose. The mean peak concentration (Cmax) and mean area under the time-concentration curve (AUC) of albiglutide were 1.74 mcg/mL and 465 mcg.h/mL, respectively | 11 L. | 67 mL/h. | Drugs used in diabetes; alimentary tract and metabolism; blood glucose lowering drugs, excl. insulins. | NA | NA | NA | Acetylsalicylic acid may increase the hypoglycemic activities of Albiglutide; Albiglutide may increase the hypoglycemic activities of Chlorpropamide; Dihydrotestosterone may increase the hypoglycemic activities of Albiglutide; Albiglutide may increase the hypoglycemic activities of Insulin Regular; Albiglutide may increase the hypoglycemic activities of Insulin Lispro; The therapeutic efficacy of Albiglutide can be decreased when used in combination with Leuprolide; Lipoic Acid may increase the hypoglycemic activities of Albiglutide; Oxandrolone may increase the hypoglycemic activities of Albiglutide; Paroxetine may increase the hypoglycemic activities of Albiglutide; Pegvisomant may increase the hypoglycemic activities of Albiglutide. | Glucagon-like peptide 1 receptor | Eperzan | Glaxosmithkline Inc | Glaxosmithkline Inc | NA | NA | 50 mg | powder for solution | Subcutaneous | NA | NA | NA | NA | NA | NA |
| 10703 | Th1161 | Albiglutide | >Th1161_Albiglutide HGEGTFTSDVSSYLEGQAAKEFIAWLVKGRHGEGTFTSDVSSYLEGQAAKEFIAWLVKGRDAHKSEVAHRFKDLGEENFKALVLIAFAQYLQQCPFEDHVKLVNEVTEFAKTCVADESAENCDKSLHTLFGDKLCTVATLRETYGEMADCCAKQEPERNECFLQHKDDNPNLPRLVRPEVDVMCTAFHDNEETFLKKYLYEIARRHPYFYAPELLFFAKRYKAAFTECCQAADKAACLLPKLDELRDEGKASSAKQRLKCASLQKFGERAFKAWAVARLSQRFPKAEFAEVSKLVTDLTKVHTECCHGDLLECADDRADLAKYICENQDSISSKLKECCEKPLLEKSHCIAEVENDEMPADLPSLAADFVESKDVCKNYAEAKDVFLGMFLYEYARRHPDYSVVLLLRLAKTYETTLEKCCAAADPHECYAKVFDEFKPLVEEPQNLIKQNCELFEQLGEYKFQNALLVRYTKKVPQVSTPTLVEVSRNLGKVGSKCCKHPEAKRMPCAEDYLSVVLNQLCVLHEKTPVSDRVTKCCTESLVNRRPCFSALEVDETYVPKEFNAETFTFHADICTLSEKERQIKKQTALVELVKHKPKATKEQLKAVMDDFAAFVEKCCKADDKETCFAEEGKKLVAASQAALGL | 72971 | C3232H5032N864O979S42 | NA | NA | NA | 4-7 days. | Albiglutide is a glucagon-like peptide-1 agonist (GLP-1) biologic drug indicated in the treatment of type 2 diabetes. It is marketed under the brands Eperzan and Tanzeum by GSK (GlaxoSmithKline). It is a dipeptidyl peptidase-4-resistant glucagon-like peptide-1 dimer fused to human albumin. Albiglutide was approved on April 15, 2014 by the FDA. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | It lowers fasting glucose and reduces postprandial glucose excursions in patients with type 2 diabetes mellitus. The majority of the observed reduction in fasting plasma glucose occurs after a single dose, consistent with the pharmacokinetic profile of albiglutide. | Albiglutide is an agonist of the GLP-1 (glucagon-like peptide 1) receptor and augments glucose-dependent insulin secretion. Albiglutide also slows gastric emptying. | -RISK OF THYROID C-CELL TUMORS -Albiglutide is contraindicated in patients with a personal or family history of MTC or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN2). Routine serum calcitonin or thyroid ultrasound monitoring is of uncertain value in patients treated with Albiglutide. | Biotransformation studies have not been performed. Because albiglutide is an albumin fusion protein, it likely follows a metabolic pathway similar to native human serum albumin, which is catabolized primarily in the vascular endothelium. | Maximum concentrations of albiglutide were reached at 3 to 5 days post-dosing following a single 30mg dose. The mean peak concentration (Cmax) and mean area under the time-concentration curve (AUC) of albiglutide were 1.74 mcg/mL and 465 mcg.h/mL, respectively | 11 L. | 67 mL/h. | Drugs used in diabetes; alimentary tract and metabolism; blood glucose lowering drugs, excl. insulins. | NA | NA | NA | Acetylsalicylic acid may increase the hypoglycemic activities of Albiglutide; Albiglutide may increase the hypoglycemic activities of Chlorpropamide; Dihydrotestosterone may increase the hypoglycemic activities of Albiglutide; Albiglutide may increase the hypoglycemic activities of Insulin Regular; Albiglutide may increase the hypoglycemic activities of Insulin Lispro; The therapeutic efficacy of Albiglutide can be decreased when used in combination with Leuprolide; Lipoic Acid may increase the hypoglycemic activities of Albiglutide; Oxandrolone may increase the hypoglycemic activities of Albiglutide; Paroxetine may increase the hypoglycemic activities of Albiglutide; Pegvisomant may increase the hypoglycemic activities of Albiglutide. | Glucagon-like peptide 1 receptor | Eperzan | Glaxosmithkline Inc | Glaxosmithkline Inc | NA | NA | 30 mg | powder for solution | Subcutaneous | NA | NA | NA | NA | NA | NA |
| 10704 | Th1161 | Albiglutide | >Th1161_Albiglutide HGEGTFTSDVSSYLEGQAAKEFIAWLVKGRHGEGTFTSDVSSYLEGQAAKEFIAWLVKGRDAHKSEVAHRFKDLGEENFKALVLIAFAQYLQQCPFEDHVKLVNEVTEFAKTCVADESAENCDKSLHTLFGDKLCTVATLRETYGEMADCCAKQEPERNECFLQHKDDNPNLPRLVRPEVDVMCTAFHDNEETFLKKYLYEIARRHPYFYAPELLFFAKRYKAAFTECCQAADKAACLLPKLDELRDEGKASSAKQRLKCASLQKFGERAFKAWAVARLSQRFPKAEFAEVSKLVTDLTKVHTECCHGDLLECADDRADLAKYICENQDSISSKLKECCEKPLLEKSHCIAEVENDEMPADLPSLAADFVESKDVCKNYAEAKDVFLGMFLYEYARRHPDYSVVLLLRLAKTYETTLEKCCAAADPHECYAKVFDEFKPLVEEPQNLIKQNCELFEQLGEYKFQNALLVRYTKKVPQVSTPTLVEVSRNLGKVGSKCCKHPEAKRMPCAEDYLSVVLNQLCVLHEKTPVSDRVTKCCTESLVNRRPCFSALEVDETYVPKEFNAETFTFHADICTLSEKERQIKKQTALVELVKHKPKATKEQLKAVMDDFAAFVEKCCKADDKETCFAEEGKKLVAASQAALGL | 72972 | C3232H5032N864O979S43 | NA | NA | NA | 4-7 days. | Albiglutide is a glucagon-like peptide-1 agonist (GLP-1) biologic drug indicated in the treatment of type 2 diabetes. It is marketed under the brands Eperzan and Tanzeum by GSK (GlaxoSmithKline). It is a dipeptidyl peptidase-4-resistant glucagon-like peptide-1 dimer fused to human albumin. Albiglutide was approved on April 15, 2014 by the FDA. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | It lowers fasting glucose and reduces postprandial glucose excursions in patients with type 2 diabetes mellitus. The majority of the observed reduction in fasting plasma glucose occurs after a single dose, consistent with the pharmacokinetic profile of albiglutide. | Albiglutide is an agonist of the GLP-1 (glucagon-like peptide 1) receptor and augments glucose-dependent insulin secretion. Albiglutide also slows gastric emptying. | -RISK OF THYROID C-CELL TUMORS -Albiglutide is contraindicated in patients with a personal or family history of MTC or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN2). Routine serum calcitonin or thyroid ultrasound monitoring is of uncertain value in patients treated with Albiglutide. | Biotransformation studies have not been performed. Because albiglutide is an albumin fusion protein, it likely follows a metabolic pathway similar to native human serum albumin, which is catabolized primarily in the vascular endothelium. | Maximum concentrations of albiglutide were reached at 3 to 5 days post-dosing following a single 30mg dose. The mean peak concentration (Cmax) and mean area under the time-concentration curve (AUC) of albiglutide were 1.74 mcg/mL and 465 mcg.h/mL, respectively | 11 L. | 67 mL/h. | Drugs used in diabetes; alimentary tract and metabolism; blood glucose lowering drugs, excl. insulins. | NA | NA | NA | Acetylsalicylic acid may increase the hypoglycemic activities of Albiglutide; Albiglutide may increase the hypoglycemic activities of Chlorpropamide; Dihydrotestosterone may increase the hypoglycemic activities of Albiglutide; Albiglutide may increase the hypoglycemic activities of Insulin Regular; Albiglutide may increase the hypoglycemic activities of Insulin Lispro; The therapeutic efficacy of Albiglutide can be decreased when used in combination with Leuprolide; Lipoic Acid may increase the hypoglycemic activities of Albiglutide; Oxandrolone may increase the hypoglycemic activities of Albiglutide; Paroxetine may increase the hypoglycemic activities of Albiglutide; Pegvisomant may increase the hypoglycemic activities of Albiglutide. | Glucagon-like peptide 1 receptor | Tanzeum | Glaxo Smith Kline Llc | Glaxo Smith Kline Llc | A GLP-1 receptor agonist indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus | NA | 30 mg/.5mL | injection, powder, lyophilized, for solution | Subcutaneous | The recommended dosage of TANZEUM is 30 mg once weekly given as a subcutaneous injection in the abdomen, thigh, or upper arm region. The dosage may be increased to 50 mg once weekly if the glycemic response is inadequate. | Contraindicated in patients with a personal or family history of medullary thyroid carcinoma (MTC) or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2); in patients with a prior serious hypersensitivity reaction to albiglutide or to any of the product components | Risk of Thyroid C-cell Tumors; Acute Pancreatitis; Hypoglycemia with Concomitant Use of Insulin Secretagogues or Insulin ; Hypersensitivity Reactions; Renal Impairment. | Link | NA | NA |
| 10705 | Th1161 | Albiglutide | >Th1161_Albiglutide HGEGTFTSDVSSYLEGQAAKEFIAWLVKGRHGEGTFTSDVSSYLEGQAAKEFIAWLVKGRDAHKSEVAHRFKDLGEENFKALVLIAFAQYLQQCPFEDHVKLVNEVTEFAKTCVADESAENCDKSLHTLFGDKLCTVATLRETYGEMADCCAKQEPERNECFLQHKDDNPNLPRLVRPEVDVMCTAFHDNEETFLKKYLYEIARRHPYFYAPELLFFAKRYKAAFTECCQAADKAACLLPKLDELRDEGKASSAKQRLKCASLQKFGERAFKAWAVARLSQRFPKAEFAEVSKLVTDLTKVHTECCHGDLLECADDRADLAKYICENQDSISSKLKECCEKPLLEKSHCIAEVENDEMPADLPSLAADFVESKDVCKNYAEAKDVFLGMFLYEYARRHPDYSVVLLLRLAKTYETTLEKCCAAADPHECYAKVFDEFKPLVEEPQNLIKQNCELFEQLGEYKFQNALLVRYTKKVPQVSTPTLVEVSRNLGKVGSKCCKHPEAKRMPCAEDYLSVVLNQLCVLHEKTPVSDRVTKCCTESLVNRRPCFSALEVDETYVPKEFNAETFTFHADICTLSEKERQIKKQTALVELVKHKPKATKEQLKAVMDDFAAFVEKCCKADDKETCFAEEGKKLVAASQAALGL | 72973 | C3232H5032N864O979S44 | NA | NA | NA | 4-7 days. | Albiglutide is a glucagon-like peptide-1 agonist (GLP-1) biologic drug indicated in the treatment of type 2 diabetes. It is marketed under the brands Eperzan and Tanzeum by GSK (GlaxoSmithKline). It is a dipeptidyl peptidase-4-resistant glucagon-like peptide-1 dimer fused to human albumin. Albiglutide was approved on April 15, 2014 by the FDA. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | It lowers fasting glucose and reduces postprandial glucose excursions in patients with type 2 diabetes mellitus. The majority of the observed reduction in fasting plasma glucose occurs after a single dose, consistent with the pharmacokinetic profile of albiglutide. | Albiglutide is an agonist of the GLP-1 (glucagon-like peptide 1) receptor and augments glucose-dependent insulin secretion. Albiglutide also slows gastric emptying. | -RISK OF THYROID C-CELL TUMORS -Albiglutide is contraindicated in patients with a personal or family history of MTC or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN2). Routine serum calcitonin or thyroid ultrasound monitoring is of uncertain value in patients treated with Albiglutide. | Biotransformation studies have not been performed. Because albiglutide is an albumin fusion protein, it likely follows a metabolic pathway similar to native human serum albumin, which is catabolized primarily in the vascular endothelium. | Maximum concentrations of albiglutide were reached at 3 to 5 days post-dosing following a single 30mg dose. The mean peak concentration (Cmax) and mean area under the time-concentration curve (AUC) of albiglutide were 1.74 mcg/mL and 465 mcg.h/mL, respectively | 11 L. | 67 mL/h. | Drugs used in diabetes; alimentary tract and metabolism; blood glucose lowering drugs, excl. insulins. | NA | NA | NA | Acetylsalicylic acid may increase the hypoglycemic activities of Albiglutide; Albiglutide may increase the hypoglycemic activities of Chlorpropamide; Dihydrotestosterone may increase the hypoglycemic activities of Albiglutide; Albiglutide may increase the hypoglycemic activities of Insulin Regular; Albiglutide may increase the hypoglycemic activities of Insulin Lispro; The therapeutic efficacy of Albiglutide can be decreased when used in combination with Leuprolide; Lipoic Acid may increase the hypoglycemic activities of Albiglutide; Oxandrolone may increase the hypoglycemic activities of Albiglutide; Paroxetine may increase the hypoglycemic activities of Albiglutide; Pegvisomant may increase the hypoglycemic activities of Albiglutide. | Glucagon-like peptide 1 receptor | Tanzeum | Glaxo Smith Kline Llc | Glaxo Smith Kline Llc | A GLP-1 receptor agonist indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus | NA | 50 mg/.5mL | injection, powder, lyophilized, for solution | Subcutaneous | The recommended dosage of TANZEUM is 30 mg once weekly given as a subcutaneous injection in the abdomen, thigh, or upper arm region. The dosage may be increased to 50 mg once weekly if the glycemic response is inadequate. | Contraindicated in patients with a personal or family history of medullary thyroid carcinoma (MTC) or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2); in patients with a prior serious hypersensitivity reaction to albiglutide or to any of the product components | Risk of Thyroid C-cell Tumors; Acute Pancreatitis; Hypoglycemia with Concomitant Use of Insulin Secretagogues or Insulin ; Hypersensitivity Reactions; Renal Impairment. | Link | NA | NA |
| 10706 | Th1162 | Alirocumab | NA | 146000 | C6472H9996N1736O2032S42 | NA | NA | NA | In monotherapy, the median half-life of alirocumab at steady state was 17–20 days in patients receiving alirocumab at SC doses of 75 or 150 mg every 2 weeks. | Alirocumab is a biopharmaceutical drug approved by the FDA in July 2015 as a second line treatment for high cholesterol for adults whose LDL-cholesterol (LDL-C) is not controlled by diet and statin treatment. It is a human monoclonal antibody administered by subcutaneous injection that belongs to a novel class of anti-cholesterol drugs, known as PCSK9 inhibitors, and it was the first such agent to receive FDA approval. The FDA approval was contingent on the completion of further clinical trials to better determine efficacy and safety. PCSK9 inhibition facilitates more LDL-C clearance from the blood. | Alirocumab is indicated as an adjunct to diet and maximally tolerated statin therapy in adults who require additional LDL-cholesterol (LDL-C) lowering due to heterozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease. | Alirocumab reduces levels of PCSK9 in a concentration-dependent manner. | Alirocumab is a fully human IgG1 monoclonal antibody that binds and inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9), an enzyme found to have gain of function mutations in autosomal dominant hypercholesterolemia. PCSK9 is secreted by the liver and typically binds to the LDL receptors in serum and marks them for lysosomal degradation. In result, the LDL receptors are not able to recycle to the plasma membrane, reducing their binding to LDL-C and therefore reducing the clearance of LDL-C from plasma. Therefore by inhibiting PCSK9's actions, alirocumab allows for more LDL-C reuptake by the liver and facilitates a higher rate of clearance. Lower LDL cholesterol concentrations are associated with a reduced risk of coronary heart disease. | NA | Antibodies are generally metabolized by the reticuloendothelial system and degraded into small peptides and individual amino acids - therefore specific metabolism studies were not conducted. Alirocumab did not show evidence of affecting CYP 450 enzymes or transporter proteins in co-administration with statins. | Following subcutaneous (SC) administration, alirocumab is absorbed into the bloodstream and maximum concentrations are reached at a median time of 3-7 days. The absolute availability after SC administration was 85%. | Alirocumab is mainly distributed through the circulatory system, with minimal extravascular distribution. | NA | NA | NA | NA | NA | The risk or severity of adverse effects can be increased when Alirocumab is combined with Belimumab. | Proprotein convertase subtilisin/kexin type 9 | Praluent | Sanofi Aventis U.S. Llc | Sanofi Aventis U.S. Llc | It is indicated as an adjunct to diet and maximally tolerated statin therapy for the treatment of adults with heterozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease, who require additional lowering of LDL-C. | NA | 75 mg/mL | injection, solution | Subcutaneous | The recommended starting dose of PRALUENT is 75 mg administered subcutaneously once every 2 weeks, since the majority of patients achieve sufficient LDL-C reduction with this dosage. If the LDL-C response is inadequate, the dosage may be increased to the maximum dosage of 150 mg administered every 2 weeks. | It is contraindicated in patients with a history of a serious hypersensitivity reaction to PRALUENT. Reactions have included hypersensitivity vasculitis and hypersensitivity reactions requiring hospitalization. | Allergic Reactions | Link | NA | NA |
| 10707 | Th1162 | Alirocumab | NA | 146001 | C6472H9996N1736O2032S43 | NA | NA | NA | In monotherapy, the median half-life of alirocumab at steady state was 17–20 days in patients receiving alirocumab at SC doses of 75 or 150 mg every 2 weeks. | Alirocumab is a biopharmaceutical drug approved by the FDA in July 2015 as a second line treatment for high cholesterol for adults whose LDL-cholesterol (LDL-C) is not controlled by diet and statin treatment. It is a human monoclonal antibody administered by subcutaneous injection that belongs to a novel class of anti-cholesterol drugs, known as PCSK9 inhibitors, and it was the first such agent to receive FDA approval. The FDA approval was contingent on the completion of further clinical trials to better determine efficacy and safety. PCSK9 inhibition facilitates more LDL-C clearance from the blood. | Alirocumab is indicated as an adjunct to diet and maximally tolerated statin therapy in adults who require additional LDL-cholesterol (LDL-C) lowering due to heterozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease. | Alirocumab reduces levels of PCSK9 in a concentration-dependent manner. | Alirocumab is a fully human IgG1 monoclonal antibody that binds and inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9), an enzyme found to have gain of function mutations in autosomal dominant hypercholesterolemia. PCSK9 is secreted by the liver and typically binds to the LDL receptors in serum and marks them for lysosomal degradation. In result, the LDL receptors are not able to recycle to the plasma membrane, reducing their binding to LDL-C and therefore reducing the clearance of LDL-C from plasma. Therefore by inhibiting PCSK9's actions, alirocumab allows for more LDL-C reuptake by the liver and facilitates a higher rate of clearance. Lower LDL cholesterol concentrations are associated with a reduced risk of coronary heart disease. | NA | Antibodies are generally metabolized by the reticuloendothelial system and degraded into small peptides and individual amino acids - therefore specific metabolism studies were not conducted. Alirocumab did not show evidence of affecting CYP 450 enzymes or transporter proteins in co-administration with statins. | Following subcutaneous (SC) administration, alirocumab is absorbed into the bloodstream and maximum concentrations are reached at a median time of 3-7 days. The absolute availability after SC administration was 85%. | Alirocumab is mainly distributed through the circulatory system, with minimal extravascular distribution. | NA | NA | NA | NA | NA | The risk or severity of adverse effects can be increased when Alirocumab is combined with Belimumab. | Proprotein convertase subtilisin/kexin type 9 | Praluent | Sanofi Aventis Canada Inc | Sanofi Aventis Canada Inc | It is indicated as an adjunct to diet and maximally tolerated statin therapy for the treatment of adults with heterozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease, who require additional lowering of LDL-C. | NA | 150 mg | solution | Subcutaneous | The recommended starting dose of PRALUENT is 75 mg administered subcutaneously once every 2 weeks, since the majority of patients achieve sufficient LDL-C reduction with this dosage. If the LDL-C response is inadequate, the dosage may be increased to the maximum dosage of 150 mg administered every 2 weeks. | It is contraindicated in patients with a history of a serious hypersensitivity reaction to PRALUENT. Reactions have included hypersensitivity vasculitis and hypersensitivity reactions requiring hospitalization. | Allergic Reactions | Link | NA | NA |
| 10708 | Th1162 | Alirocumab | NA | 146002 | C6472H9996N1736O2032S44 | NA | NA | NA | In monotherapy, the median half-life of alirocumab at steady state was 17–20 days in patients receiving alirocumab at SC doses of 75 or 150 mg every 2 weeks. | Alirocumab is a biopharmaceutical drug approved by the FDA in July 2015 as a second line treatment for high cholesterol for adults whose LDL-cholesterol (LDL-C) is not controlled by diet and statin treatment. It is a human monoclonal antibody administered by subcutaneous injection that belongs to a novel class of anti-cholesterol drugs, known as PCSK9 inhibitors, and it was the first such agent to receive FDA approval. The FDA approval was contingent on the completion of further clinical trials to better determine efficacy and safety. PCSK9 inhibition facilitates more LDL-C clearance from the blood. | Alirocumab is indicated as an adjunct to diet and maximally tolerated statin therapy in adults who require additional LDL-cholesterol (LDL-C) lowering due to heterozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease. | Alirocumab reduces levels of PCSK9 in a concentration-dependent manner. | Alirocumab is a fully human IgG1 monoclonal antibody that binds and inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9), an enzyme found to have gain of function mutations in autosomal dominant hypercholesterolemia. PCSK9 is secreted by the liver and typically binds to the LDL receptors in serum and marks them for lysosomal degradation. In result, the LDL receptors are not able to recycle to the plasma membrane, reducing their binding to LDL-C and therefore reducing the clearance of LDL-C from plasma. Therefore by inhibiting PCSK9's actions, alirocumab allows for more LDL-C reuptake by the liver and facilitates a higher rate of clearance. Lower LDL cholesterol concentrations are associated with a reduced risk of coronary heart disease. | NA | Antibodies are generally metabolized by the reticuloendothelial system and degraded into small peptides and individual amino acids - therefore specific metabolism studies were not conducted. Alirocumab did not show evidence of affecting CYP 450 enzymes or transporter proteins in co-administration with statins. | Following subcutaneous (SC) administration, alirocumab is absorbed into the bloodstream and maximum concentrations are reached at a median time of 3-7 days. The absolute availability after SC administration was 85%. | Alirocumab is mainly distributed through the circulatory system, with minimal extravascular distribution. | NA | NA | NA | NA | NA | The risk or severity of adverse effects can be increased when Alirocumab is combined with Belimumab. | Proprotein convertase subtilisin/kexin type 9 | Praluent | Sanofi Aventis Canada Inc | Sanofi Aventis Canada Inc | It is indicated as an adjunct to diet and maximally tolerated statin therapy for the treatment of adults with heterozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease, who require additional lowering of LDL-C. | NA | 75 mg | solution | Subcutaneous | The recommended starting dose of PRALUENT is 75 mg administered subcutaneously once every 2 weeks, since the majority of patients achieve sufficient LDL-C reduction with this dosage. If the LDL-C response is inadequate, the dosage may be increased to the maximum dosage of 150 mg administered every 2 weeks. | It is contraindicated in patients with a history of a serious hypersensitivity reaction to PRALUENT. Reactions have included hypersensitivity vasculitis and hypersensitivity reactions requiring hospitalization. | Allergic Reactions | Link | NA | NA |
| 10709 | Th1162 | Alirocumab | NA | 146005 | C6472H9996N1736O2032S47 | NA | NA | NA | In monotherapy, the median half-life of alirocumab at steady state was 17–20 days in patients receiving alirocumab at SC doses of 75 or 150 mg every 2 weeks. | Alirocumab is a biopharmaceutical drug approved by the FDA in July 2015 as a second line treatment for high cholesterol for adults whose LDL-cholesterol (LDL-C) is not controlled by diet and statin treatment. It is a human monoclonal antibody administered by subcutaneous injection that belongs to a novel class of anti-cholesterol drugs, known as PCSK9 inhibitors, and it was the first such agent to receive FDA approval. The FDA approval was contingent on the completion of further clinical trials to better determine efficacy and safety. PCSK9 inhibition facilitates more LDL-C clearance from the blood. | Alirocumab is indicated as an adjunct to diet and maximally tolerated statin therapy in adults who require additional LDL-cholesterol (LDL-C) lowering due to heterozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease. | Alirocumab reduces levels of PCSK9 in a concentration-dependent manner. | Alirocumab is a fully human IgG1 monoclonal antibody that binds and inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9), an enzyme found to have gain of function mutations in autosomal dominant hypercholesterolemia. PCSK9 is secreted by the liver and typically binds to the LDL receptors in serum and marks them for lysosomal degradation. In result, the LDL receptors are not able to recycle to the plasma membrane, reducing their binding to LDL-C and therefore reducing the clearance of LDL-C from plasma. Therefore by inhibiting PCSK9's actions, alirocumab allows for more LDL-C reuptake by the liver and facilitates a higher rate of clearance. Lower LDL cholesterol concentrations are associated with a reduced risk of coronary heart disease. | NA | Antibodies are generally metabolized by the reticuloendothelial system and degraded into small peptides and individual amino acids - therefore specific metabolism studies were not conducted. Alirocumab did not show evidence of affecting CYP 450 enzymes or transporter proteins in co-administration with statins. | Following subcutaneous (SC) administration, alirocumab is absorbed into the bloodstream and maximum concentrations are reached at a median time of 3-7 days. The absolute availability after SC administration was 85%. | Alirocumab is mainly distributed through the circulatory system, with minimal extravascular distribution. | NA | NA | NA | NA | NA | The risk or severity of adverse effects can be increased when Alirocumab is combined with Belimumab. | Proprotein convertase subtilisin/kexin type 9 | Praluent | Sanofi Aventis U.S. Llc | Sanofi Aventis U.S. Llc | It is indicated as an adjunct to diet and maximally tolerated statin therapy for the treatment of adults with heterozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease, who require additional lowering of LDL-C. | NA | 150 mg/mL | injection, solution | Subcutaneous | The recommended starting dose of PRALUENT is 75 mg administered subcutaneously once every 2 weeks, since the majority of patients achieve sufficient LDL-C reduction with this dosage. If the LDL-C response is inadequate, the dosage may be increased to the maximum dosage of 150 mg administered every 2 weeks. | It is contraindicated in patients with a history of a serious hypersensitivity reaction to PRALUENT. Reactions have included hypersensitivity vasculitis and hypersensitivity reactions requiring hospitalization. | Allergic Reactions | Link | NA | NA |
| 10710 | Th1163 | Ancestim | >Th1163_Ancestim MEGICRNRVTNNVKDVTKLVANLPKDYMITLKYVPGMDVLPSHCWISEMVVQLSDSLTDLLDKFSNISEGLSNYSIIDKLVNIVDDLVECVKENSSKDLKKSFKSPEPRLFTPEEFFRIFNRSIDAFKDFVVASETSDCVVSSTLSPEKDSRVSVTKPFMLPPVA | 18540 | C1662H2650N422O512S18 | 5.86 | NA | 230ºC | 2-5 hours | Ancestim is a recombinant methionyl human stem cell factor, branded by Amgen as StemGen. It was developed by Amgen and sold to Biovitrium, now Swedish Orphan Biovitrum, in December, 2008. It is a 166 amino acid protein produced by E. coli bacteria into which a gene has been inserted for soluble human stem cell factor. It has a monomeric molecular weight of approximately 18,500 daltons and normally exists as a noncovalently associated dimer. The protein has an amino acid sequence that is identical to the natural sequence predicted from human DNA sequence analysis, except for the addition of an N-terminal methionine retained after expression in E. coli. Because Ancestim is produced in E. coli, it is nonglycosylated. Ancestim is supplied as a sterile, white, preservative-free, lyophilised powder for reconstitution and administration as a subcutaneous (SC) injection and is indicated for use in combination with filgrastim for mobilizing peripheral hematopoietic stem cells for later transplanation in certain cancer patients | Indicated for use in combination with filgrastim for mobilizing peripheral hematopoietic stem cells for later transplanation in certain cancer patients | NA | Recombinant human stem cell factor | Ancestim was not genotoxic for gene mutation or chromosomal damage and it did not have any effect in fertility.[L1089] | Administration of ancestim in preclinical trials have proven that from the excreted dose all of it is formed by degraded ancestim into lower molecular weigth products.[L1089] | The pharmacokinetics of ancestim has a dose-linear profile. After subcutaneous administration, ancestim has an absorption half-life of 35-41 hours following a mean lag of 2 hours. When a dose of 5-25 mcg/kg is administered, the peak concentration of 3.6-13.7 ng/ml is reached after 15-24 hours. In preclinical studies, the bioavailability of ancestim was reported to be greater than 60%. After multiple dosing, the steady state was reached after 4-5 days from the beginning of the treatment.[L1089] | Preclinical reports demonstrate that after intravenous administration of ancestim, the distribution profile is primarily in plasma and kidneys with a subsequent and rapid loss from all tissues.[L1089] | The apparent clearance reported for ancestim is approximately 35-40 ml/h/kg.[L1089] | NA | NA | NA | NA | NA | Mast/stem cell growth factor receptor Kit | Stemgen | Biovitrum Ab (publ) | Biovitrum Ab (publ) | indicated for use in combination with NEUPOGEN® (filgrastim) in the setting of autologous peripheral blood progenitor cell (PBPC) transplantation for patients at risk of poor PBPC mobilisation to increase the number of PBPC collected in the apheresis harvest, thereby increasing the proportion of patients reaching a PBPC target for transplantation. | NA | Reconstitute with 1.2 mL sterlie water for injection to yield a concentration of 1.5 mg/mL with a withdrawable volume of 1 mL. Compatibility with saline or other diluents is unknown. During reconstitution, the vial contents may be gently swirled to avoid foaming during dissolution. Avoid excess or vigorous agitation | NA | Subcutaneous | 20 mcg/kg/day SC | It is contraindicated in patients with known hypersensitivity to E coli-derived proteins, ancestim or any component of the product; increased risk of systemic allergic reactions (greater incidence and severity) when STEMGEN® was administered by the IV route | Injection site reactions (92%); Paresthesia (29%); Respiratory symptoms (28%); Distant skin reactions (21%);Nausea (16%); Headache (13%); Dizziness (12%); Tachycardia (8%) | Link | NA | NA |
| 10722 | Th1166 | Asfotase Alfa | >Th1166_Asfotase_Alfa LVPEKEKDPKYWRDQAQETLKYALELQKLNTNVAKNVIMFLGDGMGVSTVTAARILKGQLHHNPGEETRLEMDKFPFVALSKTYNTNAQVPDSAGTATAYLCGVKANEGTVGVSAATERSRCNTTQGNEVTSILRWAKDAGKSVGIVTTTRVNHATPSAAYAHSADRDWYSDNEMPPEALSQGCKDIAYQLMHNIRDIDVIMGGGRKYMYPKNKTDVEYESDEKARGTRLDGLDLVDTWKSFKPRYKHSHFIWNRTELLTLDPHNVDYLLGLFEPGDMQYELNRNNVTDPSLSEMVVVAIQILRKNPKGFFLLVEGGRIDHGHHEGKAKQALHEAVEMDRAIGQAGSLTSSEDTLTVVTADHSHVFTFGGYTPRGNSIFGLAPMLSDTDKKPFTAILYGNGPGYKVVGGERENVSMVDYAHNNYQAQSAVPLRHETHGGEDVAVFSKGPMAHLLHGVHEQNYVPHVMAYAACIGANLGHCAPASSLKDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGKDIDDDDDDDDDD | 180001 | C7108H11008N1968O2206S57 | NA | NA | NA | Approximately 5 days. | Asfotase Alfa is a first-in-class bone-targeted enzyme replacement therapy designed to address the underlying cause of hypophosphatasia (HPP)â€â€deficient alkaline phosphatase (ALP). Hypophosphatasia is almost always fatal when severe skeletal disease is obvious at birth. By replacing deficient ALP, treatment with Asfotase Alfa aims to improve the elevated enzyme substrate levels and improve the body’s ability to mineralize bone, thereby preventing serious skeletal and systemic patient morbidity and premature death. Asfotase alfa was first approved by Pharmaceuticals and Medicals Devices Agency of Japan (PMDA) on July 3, 2015, then approved by the European Medicine Agency (EMA) on August 28, 2015, and was approved by the U.S. Food and Drug Administration (FDA) on October 23, 2015. | Indicated for the treatment of patients with perinatal/infantile and juvenile onset hypophosphatasia (HPP). | Perinatal/infantile- and juvenile-onset HPP patients treated with Asfotase alfa had reductions in plasma TNSALP (tissue non-specific alkaline phosphatase) substrates, PPi and pyridoxal 5'-phosphate (PLP) within 6 to 12 weeks of treatment. Reductions in plasma PPi and PLP levels did not correlate with clinical outcomes. Bone biopsy data from perinatal/infantile-onset and juvenile-onset HPP patients treated with Asfotase alfa demonstrated decreases in osteoid volume and thickness indicating improved bone mineralization. | HPP is caused by a deficiency in TNSALP (tissue non-specific alkaline phosphatase) enzyme activity, which leads to elevations in several TNSALP substrates, including inorganic pyrophosphate (PPi). Elevated extracellular levels of PPi block hydroxyapatite crystal growth which inhibits bone mineralization and causes an accumulation of unmineralized bone matrix which manifests as rickets and bone deformation in infants and children and as osteomalacia (softening of bones) once growth plates close, along with muscle weakness. Replacement of the TNSALP enzyme upon Asfotase alfa treatment reduces the enzyme substrate levels. | There are no available human data on Asfotase Alfa use in pregnant women to inform a drug associated risk. In animal reproduction studies, Asfotase Alfa administered intravenously to pregnant rats and rabbits during the period of organogenesis showed no evidence of fetotoxicity, embryolethality or teratogenicity at doses causing plasma exposures up to 21 and 24 times, respectively, the exposure at the recommended human dose. | NA | NA | NA | NA | Enzymes Alimentary Tract and Metabolism | NA | NA | NA | NA | Pyrophosphate | Strensiq | Alexion Pharma Ghbh | Alexion Pharma Ghbh | STRENSIQâ„¢ is indicated for the treatment of patients with perinatal/infantile-and juvenile-onset hypophosphatasia (HPP). | NA | 100 mg | Solution | Subcutaneous | The recommended dosage regimen of STRENSIQ for the treatment of perinatal/infantileonset HPP is 6 mg/kg per week administered subcutaneously as either: 2 mg/kg three times per week, or 1 mg/kg six times per week. Injection site reactions may limit the tolerability of the six times per week regimen | NA | Hypersensitivity Reactions; Lipodystrophy; Ectopic Calcifications. | Link | NA | NA |
| 10723 | Th1166 | Asfotase Alfa | >Th1166_Asfotase_Alfa LVPEKEKDPKYWRDQAQETLKYALELQKLNTNVAKNVIMFLGDGMGVSTVTAARILKGQLHHNPGEETRLEMDKFPFVALSKTYNTNAQVPDSAGTATAYLCGVKANEGTVGVSAATERSRCNTTQGNEVTSILRWAKDAGKSVGIVTTTRVNHATPSAAYAHSADRDWYSDNEMPPEALSQGCKDIAYQLMHNIRDIDVIMGGGRKYMYPKNKTDVEYESDEKARGTRLDGLDLVDTWKSFKPRYKHSHFIWNRTELLTLDPHNVDYLLGLFEPGDMQYELNRNNVTDPSLSEMVVVAIQILRKNPKGFFLLVEGGRIDHGHHEGKAKQALHEAVEMDRAIGQAGSLTSSEDTLTVVTADHSHVFTFGGYTPRGNSIFGLAPMLSDTDKKPFTAILYGNGPGYKVVGGERENVSMVDYAHNNYQAQSAVPLRHETHGGEDVAVFSKGPMAHLLHGVHEQNYVPHVMAYAACIGANLGHCAPASSLKDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGKDIDDDDDDDDDD | 180002 | C7108H11008N1968O2206S58 | NA | NA | NA | Approximately 5 days. | Asfotase Alfa is a first-in-class bone-targeted enzyme replacement therapy designed to address the underlying cause of hypophosphatasia (HPP)â€â€deficient alkaline phosphatase (ALP). Hypophosphatasia is almost always fatal when severe skeletal disease is obvious at birth. By replacing deficient ALP, treatment with Asfotase Alfa aims to improve the elevated enzyme substrate levels and improve the body’s ability to mineralize bone, thereby preventing serious skeletal and systemic patient morbidity and premature death. Asfotase alfa was first approved by Pharmaceuticals and Medicals Devices Agency of Japan (PMDA) on July 3, 2015, then approved by the European Medicine Agency (EMA) on August 28, 2015, and was approved by the U.S. Food and Drug Administration (FDA) on October 23, 2015. | Indicated for the treatment of patients with perinatal/infantile and juvenile onset hypophosphatasia (HPP). | Perinatal/infantile- and juvenile-onset HPP patients treated with Asfotase alfa had reductions in plasma TNSALP (tissue non-specific alkaline phosphatase) substrates, PPi and pyridoxal 5'-phosphate (PLP) within 6 to 12 weeks of treatment. Reductions in plasma PPi and PLP levels did not correlate with clinical outcomes. Bone biopsy data from perinatal/infantile-onset and juvenile-onset HPP patients treated with Asfotase alfa demonstrated decreases in osteoid volume and thickness indicating improved bone mineralization. | HPP is caused by a deficiency in TNSALP (tissue non-specific alkaline phosphatase) enzyme activity, which leads to elevations in several TNSALP substrates, including inorganic pyrophosphate (PPi). Elevated extracellular levels of PPi block hydroxyapatite crystal growth which inhibits bone mineralization and causes an accumulation of unmineralized bone matrix which manifests as rickets and bone deformation in infants and children and as osteomalacia (softening of bones) once growth plates close, along with muscle weakness. Replacement of the TNSALP enzyme upon Asfotase alfa treatment reduces the enzyme substrate levels. | There are no available human data on Asfotase Alfa use in pregnant women to inform a drug associated risk. In animal reproduction studies, Asfotase Alfa administered intravenously to pregnant rats and rabbits during the period of organogenesis showed no evidence of fetotoxicity, embryolethality or teratogenicity at doses causing plasma exposures up to 21 and 24 times, respectively, the exposure at the recommended human dose. | NA | NA | NA | NA | Enzymes Alimentary Tract and Metabolism | NA | NA | NA | NA | Pyrophosphate | Strensiq | Alexion Pharmaceuticals Inc. | Alexion Pharmaceuticals Inc. | STRENSIQâ„¢ is indicated for the treatment of patients with perinatal/infantile-and juvenile-onset hypophosphatasia (HPP). | NA | 18 mg/.45mL | Solution | Subcutaneous | The recommended dosage regimen of STRENSIQ for the treatment of perinatal/infantileonset HPP is 6 mg/kg per week administered subcutaneously as either: 2 mg/kg three times per week, or 1 mg/kg six times per week. Injection site reactions may limit the tolerability of the six times per week regimen | NA | Hypersensitivity Reactions; Lipodystrophy; Ectopic Calcifications. | Link | NA | NA |
| 10724 | Th1166 | Asfotase Alfa | >Th1166_Asfotase_Alfa LVPEKEKDPKYWRDQAQETLKYALELQKLNTNVAKNVIMFLGDGMGVSTVTAARILKGQLHHNPGEETRLEMDKFPFVALSKTYNTNAQVPDSAGTATAYLCGVKANEGTVGVSAATERSRCNTTQGNEVTSILRWAKDAGKSVGIVTTTRVNHATPSAAYAHSADRDWYSDNEMPPEALSQGCKDIAYQLMHNIRDIDVIMGGGRKYMYPKNKTDVEYESDEKARGTRLDGLDLVDTWKSFKPRYKHSHFIWNRTELLTLDPHNVDYLLGLFEPGDMQYELNRNNVTDPSLSEMVVVAIQILRKNPKGFFLLVEGGRIDHGHHEGKAKQALHEAVEMDRAIGQAGSLTSSEDTLTVVTADHSHVFTFGGYTPRGNSIFGLAPMLSDTDKKPFTAILYGNGPGYKVVGGERENVSMVDYAHNNYQAQSAVPLRHETHGGEDVAVFSKGPMAHLLHGVHEQNYVPHVMAYAACIGANLGHCAPASSLKDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGKDIDDDDDDDDDD | 180003 | C7108H11008N1968O2206S59 | NA | NA | NA | Approximately 5 days. | Asfotase Alfa is a first-in-class bone-targeted enzyme replacement therapy designed to address the underlying cause of hypophosphatasia (HPP)â€â€deficient alkaline phosphatase (ALP). Hypophosphatasia is almost always fatal when severe skeletal disease is obvious at birth. By replacing deficient ALP, treatment with Asfotase Alfa aims to improve the elevated enzyme substrate levels and improve the body’s ability to mineralize bone, thereby preventing serious skeletal and systemic patient morbidity and premature death. Asfotase alfa was first approved by Pharmaceuticals and Medicals Devices Agency of Japan (PMDA) on July 3, 2015, then approved by the European Medicine Agency (EMA) on August 28, 2015, and was approved by the U.S. Food and Drug Administration (FDA) on October 23, 2015. | Indicated for the treatment of patients with perinatal/infantile and juvenile onset hypophosphatasia (HPP). | Perinatal/infantile- and juvenile-onset HPP patients treated with Asfotase alfa had reductions in plasma TNSALP (tissue non-specific alkaline phosphatase) substrates, PPi and pyridoxal 5'-phosphate (PLP) within 6 to 12 weeks of treatment. Reductions in plasma PPi and PLP levels did not correlate with clinical outcomes. Bone biopsy data from perinatal/infantile-onset and juvenile-onset HPP patients treated with Asfotase alfa demonstrated decreases in osteoid volume and thickness indicating improved bone mineralization. | HPP is caused by a deficiency in TNSALP (tissue non-specific alkaline phosphatase) enzyme activity, which leads to elevations in several TNSALP substrates, including inorganic pyrophosphate (PPi). Elevated extracellular levels of PPi block hydroxyapatite crystal growth which inhibits bone mineralization and causes an accumulation of unmineralized bone matrix which manifests as rickets and bone deformation in infants and children and as osteomalacia (softening of bones) once growth plates close, along with muscle weakness. Replacement of the TNSALP enzyme upon Asfotase alfa treatment reduces the enzyme substrate levels. | There are no available human data on Asfotase Alfa use in pregnant women to inform a drug associated risk. In animal reproduction studies, Asfotase Alfa administered intravenously to pregnant rats and rabbits during the period of organogenesis showed no evidence of fetotoxicity, embryolethality or teratogenicity at doses causing plasma exposures up to 21 and 24 times, respectively, the exposure at the recommended human dose. | NA | NA | NA | NA | Enzymes Alimentary Tract and Metabolism | NA | NA | NA | NA | Pyrophosphate | Strensiq | Alexion Pharma Ghbh | Alexion Pharma Ghbh | STRENSIQâ„¢ is indicated for the treatment of patients with perinatal/infantile-and juvenile-onset hypophosphatasia (HPP). | NA | 40 mg | Solution | Subcutaneous | The recommended dosage regimen of STRENSIQ for the treatment of perinatal/infantileonset HPP is 6 mg/kg per week administered subcutaneously as either: 2 mg/kg three times per week, or 1 mg/kg six times per week. Injection site reactions may limit the tolerability of the six times per week regimen | NA | Hypersensitivity Reactions; Lipodystrophy; Ectopic Calcifications. | Link | NA | NA |
| 10725 | Th1166 | Asfotase Alfa | >Th1166_Asfotase_Alfa LVPEKEKDPKYWRDQAQETLKYALELQKLNTNVAKNVIMFLGDGMGVSTVTAARILKGQLHHNPGEETRLEMDKFPFVALSKTYNTNAQVPDSAGTATAYLCGVKANEGTVGVSAATERSRCNTTQGNEVTSILRWAKDAGKSVGIVTTTRVNHATPSAAYAHSADRDWYSDNEMPPEALSQGCKDIAYQLMHNIRDIDVIMGGGRKYMYPKNKTDVEYESDEKARGTRLDGLDLVDTWKSFKPRYKHSHFIWNRTELLTLDPHNVDYLLGLFEPGDMQYELNRNNVTDPSLSEMVVVAIQILRKNPKGFFLLVEGGRIDHGHHEGKAKQALHEAVEMDRAIGQAGSLTSSEDTLTVVTADHSHVFTFGGYTPRGNSIFGLAPMLSDTDKKPFTAILYGNGPGYKVVGGERENVSMVDYAHNNYQAQSAVPLRHETHGGEDVAVFSKGPMAHLLHGVHEQNYVPHVMAYAACIGANLGHCAPASSLKDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGKDIDDDDDDDDDD | 180004 | C7108H11008N1968O2206S60 | NA | NA | NA | Approximately 5 days. | Asfotase Alfa is a first-in-class bone-targeted enzyme replacement therapy designed to address the underlying cause of hypophosphatasia (HPP)â€â€deficient alkaline phosphatase (ALP). Hypophosphatasia is almost always fatal when severe skeletal disease is obvious at birth. By replacing deficient ALP, treatment with Asfotase Alfa aims to improve the elevated enzyme substrate levels and improve the body’s ability to mineralize bone, thereby preventing serious skeletal and systemic patient morbidity and premature death. Asfotase alfa was first approved by Pharmaceuticals and Medicals Devices Agency of Japan (PMDA) on July 3, 2015, then approved by the European Medicine Agency (EMA) on August 28, 2015, and was approved by the U.S. Food and Drug Administration (FDA) on October 23, 2015. | Indicated for the treatment of patients with perinatal/infantile and juvenile onset hypophosphatasia (HPP). | Perinatal/infantile- and juvenile-onset HPP patients treated with Asfotase alfa had reductions in plasma TNSALP (tissue non-specific alkaline phosphatase) substrates, PPi and pyridoxal 5'-phosphate (PLP) within 6 to 12 weeks of treatment. Reductions in plasma PPi and PLP levels did not correlate with clinical outcomes. Bone biopsy data from perinatal/infantile-onset and juvenile-onset HPP patients treated with Asfotase alfa demonstrated decreases in osteoid volume and thickness indicating improved bone mineralization. | HPP is caused by a deficiency in TNSALP (tissue non-specific alkaline phosphatase) enzyme activity, which leads to elevations in several TNSALP substrates, including inorganic pyrophosphate (PPi). Elevated extracellular levels of PPi block hydroxyapatite crystal growth which inhibits bone mineralization and causes an accumulation of unmineralized bone matrix which manifests as rickets and bone deformation in infants and children and as osteomalacia (softening of bones) once growth plates close, along with muscle weakness. Replacement of the TNSALP enzyme upon Asfotase alfa treatment reduces the enzyme substrate levels. | There are no available human data on Asfotase Alfa use in pregnant women to inform a drug associated risk. In animal reproduction studies, Asfotase Alfa administered intravenously to pregnant rats and rabbits during the period of organogenesis showed no evidence of fetotoxicity, embryolethality or teratogenicity at doses causing plasma exposures up to 21 and 24 times, respectively, the exposure at the recommended human dose. | NA | NA | NA | NA | Enzymes Alimentary Tract and Metabolism | NA | NA | NA | NA | Pyrophosphate | Strensiq | Alexion Pharma Ghbh | Alexion Pharma Ghbh | STRENSIQâ„¢ is indicated for the treatment of patients with perinatal/infantile-and juvenile-onset hypophosphatasia (HPP). | NA | 40 mg | Solution | Subcutaneous | The recommended dosage regimen of STRENSIQ for the treatment of perinatal/infantileonset HPP is 6 mg/kg per week administered subcutaneously as either: 2 mg/kg three times per week, or 1 mg/kg six times per week. Injection site reactions may limit the tolerability of the six times per week regimen | NA | Hypersensitivity Reactions; Lipodystrophy; Ectopic Calcifications. | Link | NA | NA |
| 10726 | Th1166 | Asfotase Alfa | >Th1166_Asfotase_Alfa LVPEKEKDPKYWRDQAQETLKYALELQKLNTNVAKNVIMFLGDGMGVSTVTAARILKGQLHHNPGEETRLEMDKFPFVALSKTYNTNAQVPDSAGTATAYLCGVKANEGTVGVSAATERSRCNTTQGNEVTSILRWAKDAGKSVGIVTTTRVNHATPSAAYAHSADRDWYSDNEMPPEALSQGCKDIAYQLMHNIRDIDVIMGGGRKYMYPKNKTDVEYESDEKARGTRLDGLDLVDTWKSFKPRYKHSHFIWNRTELLTLDPHNVDYLLGLFEPGDMQYELNRNNVTDPSLSEMVVVAIQILRKNPKGFFLLVEGGRIDHGHHEGKAKQALHEAVEMDRAIGQAGSLTSSEDTLTVVTADHSHVFTFGGYTPRGNSIFGLAPMLSDTDKKPFTAILYGNGPGYKVVGGERENVSMVDYAHNNYQAQSAVPLRHETHGGEDVAVFSKGPMAHLLHGVHEQNYVPHVMAYAACIGANLGHCAPASSLKDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGKDIDDDDDDDDDD | 180005 | C7108H11008N1968O2206S61 | NA | NA | NA | Approximately 5 days. | Asfotase Alfa is a first-in-class bone-targeted enzyme replacement therapy designed to address the underlying cause of hypophosphatasia (HPP)â€â€deficient alkaline phosphatase (ALP). Hypophosphatasia is almost always fatal when severe skeletal disease is obvious at birth. By replacing deficient ALP, treatment with Asfotase Alfa aims to improve the elevated enzyme substrate levels and improve the body’s ability to mineralize bone, thereby preventing serious skeletal and systemic patient morbidity and premature death. Asfotase alfa was first approved by Pharmaceuticals and Medicals Devices Agency of Japan (PMDA) on July 3, 2015, then approved by the European Medicine Agency (EMA) on August 28, 2015, and was approved by the U.S. Food and Drug Administration (FDA) on October 23, 2015. | Indicated for the treatment of patients with perinatal/infantile and juvenile onset hypophosphatasia (HPP). | Perinatal/infantile- and juvenile-onset HPP patients treated with Asfotase alfa had reductions in plasma TNSALP (tissue non-specific alkaline phosphatase) substrates, PPi and pyridoxal 5'-phosphate (PLP) within 6 to 12 weeks of treatment. Reductions in plasma PPi and PLP levels did not correlate with clinical outcomes. Bone biopsy data from perinatal/infantile-onset and juvenile-onset HPP patients treated with Asfotase alfa demonstrated decreases in osteoid volume and thickness indicating improved bone mineralization. | HPP is caused by a deficiency in TNSALP (tissue non-specific alkaline phosphatase) enzyme activity, which leads to elevations in several TNSALP substrates, including inorganic pyrophosphate (PPi). Elevated extracellular levels of PPi block hydroxyapatite crystal growth which inhibits bone mineralization and causes an accumulation of unmineralized bone matrix which manifests as rickets and bone deformation in infants and children and as osteomalacia (softening of bones) once growth plates close, along with muscle weakness. Replacement of the TNSALP enzyme upon Asfotase alfa treatment reduces the enzyme substrate levels. | There are no available human data on Asfotase Alfa use in pregnant women to inform a drug associated risk. In animal reproduction studies, Asfotase Alfa administered intravenously to pregnant rats and rabbits during the period of organogenesis showed no evidence of fetotoxicity, embryolethality or teratogenicity at doses causing plasma exposures up to 21 and 24 times, respectively, the exposure at the recommended human dose. | NA | NA | NA | NA | Enzymes Alimentary Tract and Metabolism | NA | NA | NA | NA | Pyrophosphate | Strensiq | Alexion Pharma Ghbh | Alexion Pharma Ghbh | STRENSIQâ„¢ is indicated for the treatment of patients with perinatal/infantile-and juvenile-onset hypophosphatasia (HPP). | NA | 40 mg | Solution | Subcutaneous | The recommended dosage regimen of STRENSIQ for the treatment of perinatal/infantileonset HPP is 6 mg/kg per week administered subcutaneously as either: 2 mg/kg three times per week, or 1 mg/kg six times per week. Injection site reactions may limit the tolerability of the six times per week regimen | NA | Hypersensitivity Reactions; Lipodystrophy; Ectopic Calcifications. | Link | NA | NA |
| 10727 | Th1166 | Asfotase Alfa | >Th1166_Asfotase_Alfa LVPEKEKDPKYWRDQAQETLKYALELQKLNTNVAKNVIMFLGDGMGVSTVTAARILKGQLHHNPGEETRLEMDKFPFVALSKTYNTNAQVPDSAGTATAYLCGVKANEGTVGVSAATERSRCNTTQGNEVTSILRWAKDAGKSVGIVTTTRVNHATPSAAYAHSADRDWYSDNEMPPEALSQGCKDIAYQLMHNIRDIDVIMGGGRKYMYPKNKTDVEYESDEKARGTRLDGLDLVDTWKSFKPRYKHSHFIWNRTELLTLDPHNVDYLLGLFEPGDMQYELNRNNVTDPSLSEMVVVAIQILRKNPKGFFLLVEGGRIDHGHHEGKAKQALHEAVEMDRAIGQAGSLTSSEDTLTVVTADHSHVFTFGGYTPRGNSIFGLAPMLSDTDKKPFTAILYGNGPGYKVVGGERENVSMVDYAHNNYQAQSAVPLRHETHGGEDVAVFSKGPMAHLLHGVHEQNYVPHVMAYAACIGANLGHCAPASSLKDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGKDIDDDDDDDDDD | 180006 | C7108H11008N1968O2206S62 | NA | NA | NA | Approximately 5 days. | Asfotase Alfa is a first-in-class bone-targeted enzyme replacement therapy designed to address the underlying cause of hypophosphatasia (HPP)â€â€deficient alkaline phosphatase (ALP). Hypophosphatasia is almost always fatal when severe skeletal disease is obvious at birth. By replacing deficient ALP, treatment with Asfotase Alfa aims to improve the elevated enzyme substrate levels and improve the body’s ability to mineralize bone, thereby preventing serious skeletal and systemic patient morbidity and premature death. Asfotase alfa was first approved by Pharmaceuticals and Medicals Devices Agency of Japan (PMDA) on July 3, 2015, then approved by the European Medicine Agency (EMA) on August 28, 2015, and was approved by the U.S. Food and Drug Administration (FDA) on October 23, 2015. | Indicated for the treatment of patients with perinatal/infantile and juvenile onset hypophosphatasia (HPP). | Perinatal/infantile- and juvenile-onset HPP patients treated with Asfotase alfa had reductions in plasma TNSALP (tissue non-specific alkaline phosphatase) substrates, PPi and pyridoxal 5'-phosphate (PLP) within 6 to 12 weeks of treatment. Reductions in plasma PPi and PLP levels did not correlate with clinical outcomes. Bone biopsy data from perinatal/infantile-onset and juvenile-onset HPP patients treated with Asfotase alfa demonstrated decreases in osteoid volume and thickness indicating improved bone mineralization. | HPP is caused by a deficiency in TNSALP (tissue non-specific alkaline phosphatase) enzyme activity, which leads to elevations in several TNSALP substrates, including inorganic pyrophosphate (PPi). Elevated extracellular levels of PPi block hydroxyapatite crystal growth which inhibits bone mineralization and causes an accumulation of unmineralized bone matrix which manifests as rickets and bone deformation in infants and children and as osteomalacia (softening of bones) once growth plates close, along with muscle weakness. Replacement of the TNSALP enzyme upon Asfotase alfa treatment reduces the enzyme substrate levels. | There are no available human data on Asfotase Alfa use in pregnant women to inform a drug associated risk. In animal reproduction studies, Asfotase Alfa administered intravenously to pregnant rats and rabbits during the period of organogenesis showed no evidence of fetotoxicity, embryolethality or teratogenicity at doses causing plasma exposures up to 21 and 24 times, respectively, the exposure at the recommended human dose. | NA | NA | NA | NA | Enzymes Alimentary Tract and Metabolism | NA | NA | NA | NA | Pyrophosphate | Strensiq | Alexion Pharma Ghbh | Alexion Pharma Ghbh | STRENSIQâ„¢ is indicated for the treatment of patients with perinatal/infantile-and juvenile-onset hypophosphatasia (HPP). | NA | 40 mg | Solution | Subcutaneous | The recommended dosage regimen of STRENSIQ for the treatment of perinatal/infantileonset HPP is 6 mg/kg per week administered subcutaneously as either: 2 mg/kg three times per week, or 1 mg/kg six times per week. Injection site reactions may limit the tolerability of the six times per week regimen | NA | Hypersensitivity Reactions; Lipodystrophy; Ectopic Calcifications. | Link | NA | NA |
| 10728 | Th1166 | Asfotase Alfa | >Th1166_Asfotase_Alfa LVPEKEKDPKYWRDQAQETLKYALELQKLNTNVAKNVIMFLGDGMGVSTVTAARILKGQLHHNPGEETRLEMDKFPFVALSKTYNTNAQVPDSAGTATAYLCGVKANEGTVGVSAATERSRCNTTQGNEVTSILRWAKDAGKSVGIVTTTRVNHATPSAAYAHSADRDWYSDNEMPPEALSQGCKDIAYQLMHNIRDIDVIMGGGRKYMYPKNKTDVEYESDEKARGTRLDGLDLVDTWKSFKPRYKHSHFIWNRTELLTLDPHNVDYLLGLFEPGDMQYELNRNNVTDPSLSEMVVVAIQILRKNPKGFFLLVEGGRIDHGHHEGKAKQALHEAVEMDRAIGQAGSLTSSEDTLTVVTADHSHVFTFGGYTPRGNSIFGLAPMLSDTDKKPFTAILYGNGPGYKVVGGERENVSMVDYAHNNYQAQSAVPLRHETHGGEDVAVFSKGPMAHLLHGVHEQNYVPHVMAYAACIGANLGHCAPASSLKDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGKDIDDDDDDDDDD | 180007 | C7108H11008N1968O2206S63 | NA | NA | NA | Approximately 5 days. | Asfotase Alfa is a first-in-class bone-targeted enzyme replacement therapy designed to address the underlying cause of hypophosphatasia (HPP)â€â€deficient alkaline phosphatase (ALP). Hypophosphatasia is almost always fatal when severe skeletal disease is obvious at birth. By replacing deficient ALP, treatment with Asfotase Alfa aims to improve the elevated enzyme substrate levels and improve the body’s ability to mineralize bone, thereby preventing serious skeletal and systemic patient morbidity and premature death. Asfotase alfa was first approved by Pharmaceuticals and Medicals Devices Agency of Japan (PMDA) on July 3, 2015, then approved by the European Medicine Agency (EMA) on August 28, 2015, and was approved by the U.S. Food and Drug Administration (FDA) on October 23, 2015. | Indicated for the treatment of patients with perinatal/infantile and juvenile onset hypophosphatasia (HPP). | Perinatal/infantile- and juvenile-onset HPP patients treated with Asfotase alfa had reductions in plasma TNSALP (tissue non-specific alkaline phosphatase) substrates, PPi and pyridoxal 5'-phosphate (PLP) within 6 to 12 weeks of treatment. Reductions in plasma PPi and PLP levels did not correlate with clinical outcomes. Bone biopsy data from perinatal/infantile-onset and juvenile-onset HPP patients treated with Asfotase alfa demonstrated decreases in osteoid volume and thickness indicating improved bone mineralization. | HPP is caused by a deficiency in TNSALP (tissue non-specific alkaline phosphatase) enzyme activity, which leads to elevations in several TNSALP substrates, including inorganic pyrophosphate (PPi). Elevated extracellular levels of PPi block hydroxyapatite crystal growth which inhibits bone mineralization and causes an accumulation of unmineralized bone matrix which manifests as rickets and bone deformation in infants and children and as osteomalacia (softening of bones) once growth plates close, along with muscle weakness. Replacement of the TNSALP enzyme upon Asfotase alfa treatment reduces the enzyme substrate levels. | There are no available human data on Asfotase Alfa use in pregnant women to inform a drug associated risk. In animal reproduction studies, Asfotase Alfa administered intravenously to pregnant rats and rabbits during the period of organogenesis showed no evidence of fetotoxicity, embryolethality or teratogenicity at doses causing plasma exposures up to 21 and 24 times, respectively, the exposure at the recommended human dose. | NA | NA | NA | NA | Enzymes Alimentary Tract and Metabolism | NA | NA | NA | NA | Pyrophosphate | Strensiq | Alexion Pharmaceuticals Inc. | Alexion Pharmaceuticals Inc. | STRENSIQâ„¢ is indicated for the treatment of patients with perinatal/infantile-and juvenile-onset hypophosphatasia (HPP). | NA | 80 mg/.8mL | Solution | Subcutaneous | The recommended dosage regimen of STRENSIQ for the treatment of perinatal/infantileonset HPP is 6 mg/kg per week administered subcutaneously as either: 2 mg/kg three times per week, or 1 mg/kg six times per week. Injection site reactions may limit the tolerability of the six times per week regimen | NA | Hypersensitivity Reactions; Lipodystrophy; Ectopic Calcifications. | Link | NA | NA |
| 10729 | Th1166 | Asfotase Alfa | >Th1166_Asfotase_Alfa LVPEKEKDPKYWRDQAQETLKYALELQKLNTNVAKNVIMFLGDGMGVSTVTAARILKGQLHHNPGEETRLEMDKFPFVALSKTYNTNAQVPDSAGTATAYLCGVKANEGTVGVSAATERSRCNTTQGNEVTSILRWAKDAGKSVGIVTTTRVNHATPSAAYAHSADRDWYSDNEMPPEALSQGCKDIAYQLMHNIRDIDVIMGGGRKYMYPKNKTDVEYESDEKARGTRLDGLDLVDTWKSFKPRYKHSHFIWNRTELLTLDPHNVDYLLGLFEPGDMQYELNRNNVTDPSLSEMVVVAIQILRKNPKGFFLLVEGGRIDHGHHEGKAKQALHEAVEMDRAIGQAGSLTSSEDTLTVVTADHSHVFTFGGYTPRGNSIFGLAPMLSDTDKKPFTAILYGNGPGYKVVGGERENVSMVDYAHNNYQAQSAVPLRHETHGGEDVAVFSKGPMAHLLHGVHEQNYVPHVMAYAACIGANLGHCAPASSLKDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGKDIDDDDDDDDDD | 180008 | C7108H11008N1968O2206S64 | NA | NA | NA | Approximately 5 days. | Asfotase Alfa is a first-in-class bone-targeted enzyme replacement therapy designed to address the underlying cause of hypophosphatasia (HPP)â€â€deficient alkaline phosphatase (ALP). Hypophosphatasia is almost always fatal when severe skeletal disease is obvious at birth. By replacing deficient ALP, treatment with Asfotase Alfa aims to improve the elevated enzyme substrate levels and improve the body’s ability to mineralize bone, thereby preventing serious skeletal and systemic patient morbidity and premature death. Asfotase alfa was first approved by Pharmaceuticals and Medicals Devices Agency of Japan (PMDA) on July 3, 2015, then approved by the European Medicine Agency (EMA) on August 28, 2015, and was approved by the U.S. Food and Drug Administration (FDA) on October 23, 2015. | Indicated for the treatment of patients with perinatal/infantile and juvenile onset hypophosphatasia (HPP). | Perinatal/infantile- and juvenile-onset HPP patients treated with Asfotase alfa had reductions in plasma TNSALP (tissue non-specific alkaline phosphatase) substrates, PPi and pyridoxal 5'-phosphate (PLP) within 6 to 12 weeks of treatment. Reductions in plasma PPi and PLP levels did not correlate with clinical outcomes. Bone biopsy data from perinatal/infantile-onset and juvenile-onset HPP patients treated with Asfotase alfa demonstrated decreases in osteoid volume and thickness indicating improved bone mineralization. | HPP is caused by a deficiency in TNSALP (tissue non-specific alkaline phosphatase) enzyme activity, which leads to elevations in several TNSALP substrates, including inorganic pyrophosphate (PPi). Elevated extracellular levels of PPi block hydroxyapatite crystal growth which inhibits bone mineralization and causes an accumulation of unmineralized bone matrix which manifests as rickets and bone deformation in infants and children and as osteomalacia (softening of bones) once growth plates close, along with muscle weakness. Replacement of the TNSALP enzyme upon Asfotase alfa treatment reduces the enzyme substrate levels. | There are no available human data on Asfotase Alfa use in pregnant women to inform a drug associated risk. In animal reproduction studies, Asfotase Alfa administered intravenously to pregnant rats and rabbits during the period of organogenesis showed no evidence of fetotoxicity, embryolethality or teratogenicity at doses causing plasma exposures up to 21 and 24 times, respectively, the exposure at the recommended human dose. | NA | NA | NA | NA | Enzymes Alimentary Tract and Metabolism | NA | NA | NA | NA | Pyrophosphate | Strensiq | Alexion Pharmaceuticals Inc. | Alexion Pharmaceuticals Inc. | STRENSIQâ„¢ is indicated for the treatment of patients with perinatal/infantile-and juvenile-onset hypophosphatasia (HPP). | NA | 40 mg/mL | Solution | Subcutaneous | The recommended dosage regimen of STRENSIQ for the treatment of perinatal/infantileonset HPP is 6 mg/kg per week administered subcutaneously as either: 2 mg/kg three times per week, or 1 mg/kg six times per week. Injection site reactions may limit the tolerability of the six times per week regimen | NA | Hypersensitivity Reactions; Lipodystrophy; Ectopic Calcifications. | Link | NA | NA |
| 10730 | Th1166 | Asfotase Alfa | >Th1166_Asfotase_Alfa LVPEKEKDPKYWRDQAQETLKYALELQKLNTNVAKNVIMFLGDGMGVSTVTAARILKGQLHHNPGEETRLEMDKFPFVALSKTYNTNAQVPDSAGTATAYLCGVKANEGTVGVSAATERSRCNTTQGNEVTSILRWAKDAGKSVGIVTTTRVNHATPSAAYAHSADRDWYSDNEMPPEALSQGCKDIAYQLMHNIRDIDVIMGGGRKYMYPKNKTDVEYESDEKARGTRLDGLDLVDTWKSFKPRYKHSHFIWNRTELLTLDPHNVDYLLGLFEPGDMQYELNRNNVTDPSLSEMVVVAIQILRKNPKGFFLLVEGGRIDHGHHEGKAKQALHEAVEMDRAIGQAGSLTSSEDTLTVVTADHSHVFTFGGYTPRGNSIFGLAPMLSDTDKKPFTAILYGNGPGYKVVGGERENVSMVDYAHNNYQAQSAVPLRHETHGGEDVAVFSKGPMAHLLHGVHEQNYVPHVMAYAACIGANLGHCAPASSLKDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGKDIDDDDDDDDDD | 180009 | C7108H11008N1968O2206S65 | NA | NA | NA | Approximately 5 days. | Asfotase Alfa is a first-in-class bone-targeted enzyme replacement therapy designed to address the underlying cause of hypophosphatasia (HPP)â€â€deficient alkaline phosphatase (ALP). Hypophosphatasia is almost always fatal when severe skeletal disease is obvious at birth. By replacing deficient ALP, treatment with Asfotase Alfa aims to improve the elevated enzyme substrate levels and improve the body’s ability to mineralize bone, thereby preventing serious skeletal and systemic patient morbidity and premature death. Asfotase alfa was first approved by Pharmaceuticals and Medicals Devices Agency of Japan (PMDA) on July 3, 2015, then approved by the European Medicine Agency (EMA) on August 28, 2015, and was approved by the U.S. Food and Drug Administration (FDA) on October 23, 2015. | Indicated for the treatment of patients with perinatal/infantile and juvenile onset hypophosphatasia (HPP). | Perinatal/infantile- and juvenile-onset HPP patients treated with Asfotase alfa had reductions in plasma TNSALP (tissue non-specific alkaline phosphatase) substrates, PPi and pyridoxal 5'-phosphate (PLP) within 6 to 12 weeks of treatment. Reductions in plasma PPi and PLP levels did not correlate with clinical outcomes. Bone biopsy data from perinatal/infantile-onset and juvenile-onset HPP patients treated with Asfotase alfa demonstrated decreases in osteoid volume and thickness indicating improved bone mineralization. | HPP is caused by a deficiency in TNSALP (tissue non-specific alkaline phosphatase) enzyme activity, which leads to elevations in several TNSALP substrates, including inorganic pyrophosphate (PPi). Elevated extracellular levels of PPi block hydroxyapatite crystal growth which inhibits bone mineralization and causes an accumulation of unmineralized bone matrix which manifests as rickets and bone deformation in infants and children and as osteomalacia (softening of bones) once growth plates close, along with muscle weakness. Replacement of the TNSALP enzyme upon Asfotase alfa treatment reduces the enzyme substrate levels. | There are no available human data on Asfotase Alfa use in pregnant women to inform a drug associated risk. In animal reproduction studies, Asfotase Alfa administered intravenously to pregnant rats and rabbits during the period of organogenesis showed no evidence of fetotoxicity, embryolethality or teratogenicity at doses causing plasma exposures up to 21 and 24 times, respectively, the exposure at the recommended human dose. | NA | NA | NA | NA | Enzymes Alimentary Tract and Metabolism | NA | NA | NA | NA | Pyrophosphate | Strensiq | Alexion Pharmaceuticals Inc. | Alexion Pharmaceuticals Inc. | STRENSIQâ„¢ is indicated for the treatment of patients with perinatal/infantile-and juvenile-onset hypophosphatasia (HPP). | NA | 28 mg/.7mL | Solution | Subcutaneous | The recommended dosage regimen of STRENSIQ for the treatment of perinatal/infantileonset HPP is 6 mg/kg per week administered subcutaneously as either: 2 mg/kg three times per week, or 1 mg/kg six times per week. Injection site reactions may limit the tolerability of the six times per week regimen | NA | Hypersensitivity Reactions; Lipodystrophy; Ectopic Calcifications. | Link | NA | NA |
| 10754 | Th1175 | Desirudin | NA | 6963.52 | C287H440N80O110 S7 | NA | NA | NA | Mean terminal elimination half-life of 2 to 3 hours | Desirudin is a direct, highly selective thrombin inhibitor. Reversibly binds to the active thrombin site of free and clot-associated thrombin. Inhibits fibrin formation, activation of coagulation factors V, VII, and XIII, and thrombin-induced platelet aggregation resulting in a dose-dependent prolongation of the activated partial thromboplastin time (aPTT). | Preventing blood clots in patients having hip replacement surgery. It may also be used for other conditions as determined by your doctor. Desirudin is a thrombin inhibitor. It works by blocking the activity of thrombin, which helps to prevent the formation of blood clots. | The pharmacodynamic effect of desirudin on proteolytic activity of thrombin was assessed as an increase in aPTT. A mean peak aPTT prolongation of about 1.38 times baseline value (range 0.58 to 3.41) was observed following subcutaneous b.i.d. injections of 15 mg desirudin. Thrombin time (TT) frequently exceeds 200 seconds even at low plasma concentrations of desirudin, which renders this test unsuitable for routine monitoring of Iprivask therapy. At therapeutic serum concentrations, desirudin has no effect on other enzymes of the hemostatic system such as factors IXa, Xa, kallikrein, plasmin, tissue plasminogen activator, or activated protein C. In addition, it does not display any effect on other serine proteases, such as the digestive enzymes trypsin, chymotrypsin, or on complement activation by the classical or alternative pathways. | Desirudin is a direct inhibitor of free circulating and clot-bound thrombin. The anticoagulant properties of desirudin are demonstrated by its ability to prolong the clotting time of human plasma. One molecule of desirudin binds to one molecule of thrombin and thereby blocks the thrombogenic activity of thrombin. As a result, all thrombin-dependent coagulation assays are affected. Activated partial thromboplastin time (aPTT) is a measure of the anticoagulant activity of desirudin and increases in a dose-dependent fashion. | No data available. | Human and animal data suggest that desirudin is primarily eliminated and metabolized by the kidney. The total urinary excretion of unchanged desirudin amounts to 40 to 50% of the administered dose. Metabolites lacking one or two C-terminal amino acids constitute a minor proportion of the material recovered from urine (< 7%). There is no evidence for the presence of other metabolites. This indicates that desirudin is metabolized by stepwise degradation from the C-terminus probably catalyzed by carboxypeptidase(s) such as carboxypeptidase A. | Absorption is complete after subcutaneous administration. Time to peak in plasma is 1 to 3 hours. | 0.25 L/kg. | 1.5 to 2.7 mL/min/kg. | NA | NA | NA | NA | Abciximab may increase the anticoagulant activities of Desirudin; Acenocoumarol may increase the anticoagulant activities of Desirudin; Acetylsalicylic acid may increase the anticoagulant activities of Desirudin; Alteplase may increase the anticoagulant activities of Desirudin; Anistreplase may increase the anticoagulant activities of Desirudin; Apixaban may increase the anticoagulant activities of Desirudin; Chlorotrianisene may decrease the anticoagulant activities of Desirudin; Citric Acid may increase the anticoagulant activities of Desirudin; The risk or severity of adverse effects can be increased when Desirudin is combined with Collagenase; Dabigatran etexilate may increase the anticoagulant activities of Desirudin. | NA | Iprivask | Valeant Pharmaceuticals North America LLC | Valeant Pharmaceuticals North America LLC | Iprivask is indicated for the prophylaxis of deep vein thrombosis, which may lead to pulmonary embolism, in patients undergoing elective hip replacement surgery. | NA | NA | NA | Subcutaneous | Initial Dosage: In patients undergoing hip replacement surgery, the recommended dose of Iprivask is 15 mg every 12 hours administered by subcutaneous injection with the initial dose given up to 5 to 15 minutes prior to surgery, but after induction of regional block anesthesia, if used | Iprivask is contraindicated in patients with known hypersensitivity to natural or recombinant hirudins due to risk of anaphylaxis, and in patients with active bleeding and/or irreversible coagulation disorders due to risk of hemorrhage. | Spinal/Epidural Hematoma; Hemorrhagic Events; Increased Risk of Bleeding with Renal Impairment; Antibodies/Re-exposure. | Link | NA | NA |
| 10757 | Th1176 | Dulaglutide | >Th1176_Dulaglutide HGEGTFTSDVSSYLEEQAAKEFIAWLVKGGGGGGGSGGGGSGGGGSAESKYGPPCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 59669.81 | C2646H4044N704O836S19 | NA | NA | NA | Approximately 5 days. | Dulaglutide is a novel glucagon-like peptide-1 agonist (GLP-1) biologic drug consisting of a dipeptidyl peptidase-IV-protected GLP-1 analogue covalently linked to a human IgG4-Fc heavy chain by a small peptide linker. Dulaglutide is indicated in the treatment of type 2 diabetes and can be used once a week. It was approved by the FDA in September 2014. Dulaglutide is manufactured and marketed by Eli Lily under the brand Trulicityâ„¢. It is not known if dulaglutide can increase the risk of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2, and is thus not recommended for use in populations with a personal or family history of these conditions. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | Dulaglutide activates human glucagon-like peptide-1 receptors, thus increasing intracellular cyclic AMP in beta cells. This, in turn, increases glucose-dependent insulin release. Dulaglutide also reduces glucagon secretion and slows gastric emptying. | Dulaglutide is a human GLP-1 receptor agonist with 90% amino acid sequence homology to endogenous human GLP-1 (7-37). Dulaglutide activates the GLP-1 receptor, a membrane-bound cell-surface receptor coupled to adenylyl cyclase in pancreatic beta cells. Dulaglutide increases intracellular cyclic AMP (cAMP) in beta cells leading to glucose-dependent insulin release. Dulaglutide also decreases glucagon secretion and slows gastric emptying. | LD50 information for dulaglutide is not readily available in the literature.[L34685] Cases of overdose with dulaglutide have resulted in gastrointestinal disturbance. Appropriate supportive treatment is recommended to manage signs and symptoms.[L34670] Additionally, hypoglycemia has been observed after an overdose with dulaglutide; frequent plasma glucose monitoring should be performed.[L30380] | Dulaglutide is presumed to be degraded into its component amino acids by general protein catabolism pathways.[L30380] | Dulaglutide is slowly absorbed after subcutaneous injection.[L34670] In a pharmacokinetic study of 20 healthy adults, Cmax occurred within 24-48 hours after dosing.[A234419] The average absolute bioavailability of dulaglutide after subcutaneous injections of single 0.75 mg and 1.5 mg doses was 65% and 47%, respectively.[L30380] | The apparent volume of distribution of dulaglutide was 3.09 L in a pharmacokinetic study; the apparent population mean peripheral volume of distribution was approximately 6 L.[L30380] | The apparent population mean clearance of dulaglutide was 0.142 L/h in a pharmacokinetic study.[L30380] | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Blood Proteins,Drugs Used in Diabetes,Gastrointestinal Hormones,Globulins,GLP-1 Agonists,Glucagon-like peptide-1 (GLP-1) analogues,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Immunoglobulin Fragments,Immunoglobulins,Immunoproteins,Incretin Mimetics,Pancreatic Hormones,Peptide Fragments,Peptide Hormones,Peptides,Proglucagon,Protein Precursors,Proteins,Recombinant Proteins,Serum Globulins | NA | NA | NA | Acetylsalicylic acid may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Chlorpropamide; Dihydrotestosterone may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Insulin Regular; Dulaglutide may increase the hypoglycemic activities of Insulin Lispro; The therapeutic efficacy of Dulaglutide can be decreased when used in combination with Leuprolide; Lipoic Acid may increase the hypoglycemic activities of Dulaglutide; Oxandrolone may increase the hypoglycemic activities of Dulaglutide; Paroxetine may increase the hypoglycemic activities of Dulaglutide; Pegvisomant may increase the hypoglycemic activities of Dulaglutide. | Glucagon-like peptide 1 receptor | Trulicity | Eli Lilly and Company | Eli Lilly and Company | TRULICITYâ„¢ is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | NA | TRULICITY solution contains 0.75 mg or 1.5 mg of dulaglutide. Each single-dose pen or prefilled syringe contains 0.5 mL of solution and the following excipients: citric acid anhydrous (0.07 mg), mannitol (23.2 mg), polysorbate 80 (0.10 mg), trisodium citrate dihydrate (1.37 mg), in water for injection. | Solution, Injection | Subcutaneous | The recommended initiating dose of TRULICITY is 0.75 mg once weekly. The dose may be increased to 1.5 mg once weekly for additional glycemic control. The maximum recommended dose is 1.5 mg once weekly. Administer TRULICITY once weekly, any time of day, with or without food. TRULICITY should be injected subcutaneously in the abdomen, thigh, or upper arm. If a dose is missed, instruct patients to administer as soon as possible if there are at least 3 days (72 hours) until the next scheduled dose. If less than 3 days remain before the next scheduled dose, skip the missed dose and administer the next dose on the regularly scheduled day. In each case, patients can then resume their regular once weekly dosing schedule. The day of weekly administration can be changed if necessary as long as the last dose was administered 3 or more days before. | TRULICITY is contraindicated in patients with a personal or family history of medullary thyroid carcinoma (MTC) or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2); TRULICITY is also contraindicated in patients with a prior serious hypersensitivity reaction to dulaglutide or to any of the product components | Risk of Thyroid C-cell Tumors; Pancreatitis; Hypoglycemia with Concomitant Use of Insulin Secretagogues or Insulin; Hypersensitivity reactions; Renal impairment; Severe Gastrointestinal Disease. | Link | NA | NA |
| 10758 | Th1176 | Dulaglutide | >Th1176_Dulaglutide HGEGTFTSDVSSYLEEQAAKEFIAWLVKGGGGGGGSGGGGSGGGGSAESKYGPPCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 59669.81 | C2646H4044N704O836S20 | NA | NA | NA | Approximately 5 days. | Dulaglutide is a novel glucagon-like peptide-1 agonist (GLP-1) biologic drug consisting of a dipeptidyl peptidase-IV-protected GLP-1 analogue covalently linked to a human IgG4-Fc heavy chain by a small peptide linker. Dulaglutide is indicated in the treatment of type 2 diabetes and can be used once a week. It was approved by the FDA in September 2014. Dulaglutide is manufactured and marketed by Eli Lily under the brand Trulicityâ„¢. It is not known if dulaglutide can increase the risk of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2, and is thus not recommended for use in populations with a personal or family history of these conditions. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | Dulaglutide activates human glucagon-like peptide-1 receptors, thus increasing intracellular cyclic AMP in beta cells. This, in turn, increases glucose-dependent insulin release. Dulaglutide also reduces glucagon secretion and slows gastric emptying. | Dulaglutide is a human GLP-1 receptor agonist with 90% amino acid sequence homology to endogenous human GLP-1 (7-37). Dulaglutide activates the GLP-1 receptor, a membrane-bound cell-surface receptor coupled to adenylyl cyclase in pancreatic beta cells. Dulaglutide increases intracellular cyclic AMP (cAMP) in beta cells leading to glucose-dependent insulin release. Dulaglutide also decreases glucagon secretion and slows gastric emptying. | LD50 information for dulaglutide is not readily available in the literature.[L34685] Cases of overdose with dulaglutide have resulted in gastrointestinal disturbance. Appropriate supportive treatment is recommended to manage signs and symptoms.[L34670] Additionally, hypoglycemia has been observed after an overdose with dulaglutide; frequent plasma glucose monitoring should be performed.[L30380] | Dulaglutide is presumed to be degraded into its component amino acids by general protein catabolism pathways.[L30380] | Dulaglutide is slowly absorbed after subcutaneous injection.[L34670] In a pharmacokinetic study of 20 healthy adults, Cmax occurred within 24-48 hours after dosing.[A234419] The average absolute bioavailability of dulaglutide after subcutaneous injections of single 0.75 mg and 1.5 mg doses was 65% and 47%, respectively.[L30380] | The apparent volume of distribution of dulaglutide was 3.09 L in a pharmacokinetic study; the apparent population mean peripheral volume of distribution was approximately 6 L.[L30380] | The apparent population mean clearance of dulaglutide was 0.142 L/h in a pharmacokinetic study.[L30380] | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Blood Proteins,Drugs Used in Diabetes,Gastrointestinal Hormones,Globulins,GLP-1 Agonists,Glucagon-like peptide-1 (GLP-1) analogues,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Immunoglobulin Fragments,Immunoglobulins,Immunoproteins,Incretin Mimetics,Pancreatic Hormones,Peptide Fragments,Peptide Hormones,Peptides,Proglucagon,Protein Precursors,Proteins,Recombinant Proteins,Serum Globulins | NA | NA | NA | Acetylsalicylic acid may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Chlorpropamide; Dihydrotestosterone may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Insulin Regular; Dulaglutide may increase the hypoglycemic activities of Insulin Lispro; The therapeutic efficacy of Dulaglutide can be decreased when used in combination with Leuprolide; Lipoic Acid may increase the hypoglycemic activities of Dulaglutide; Oxandrolone may increase the hypoglycemic activities of Dulaglutide; Paroxetine may increase the hypoglycemic activities of Dulaglutide; Pegvisomant may increase the hypoglycemic activities of Dulaglutide. | Glucagon-like peptide 1 receptor | Trulicity | Eli Lilly Canada Inc | Eli Lilly Canada Inc | TRULICITYâ„¢ is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | NA | TRULICITY solution contains 0.75 mg or 1.5 mg of dulaglutide. Each single-dose pen or prefilled syringe contains 0.5 mL of solution and the following excipients: citric acid anhydrous (0.07 mg), mannitol (23.2 mg), polysorbate 80 (0.10 mg), trisodium citrate dihydrate (1.37 mg), in water for injection. | Solution | Subcutaneous | The recommended initiating dose of TRULICITY is 0.75 mg once weekly. The dose may be increased to 1.5 mg once weekly for additional glycemic control. The maximum recommended dose is 1.5 mg once weekly. Administer TRULICITY once weekly, any time of day, with or without food. TRULICITY should be injected subcutaneously in the abdomen, thigh, or upper arm. If a dose is missed, instruct patients to administer as soon as possible if there are at least 3 days (72 hours) until the next scheduled dose. If less than 3 days remain before the next scheduled dose, skip the missed dose and administer the next dose on the regularly scheduled day. In each case, patients can then resume their regular once weekly dosing schedule. The day of weekly administration can be changed if necessary as long as the last dose was administered 3 or more days before. | TRULICITY is contraindicated in patients with a personal or family history of medullary thyroid carcinoma (MTC) or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2); TRULICITY is also contraindicated in patients with a prior serious hypersensitivity reaction to dulaglutide or to any of the product components | Risk of Thyroid C-cell Tumors; Pancreatitis; Hypoglycemia with Concomitant Use of Insulin Secretagogues or Insulin; Hypersensitivity reactions; Renal impairment; Severe Gastrointestinal Disease. | Link | NA | NA |
| 10759 | Th1176 | Dulaglutide | >Th1176_Dulaglutide HGEGTFTSDVSSYLEEQAAKEFIAWLVKGGGGGGGSGGGGSGGGGSAESKYGPPCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 59669.81 | C2646H4044N704O836S21 | NA | NA | NA | Approximately 5 days. | Dulaglutide is a novel glucagon-like peptide-1 agonist (GLP-1) biologic drug consisting of a dipeptidyl peptidase-IV-protected GLP-1 analogue covalently linked to a human IgG4-Fc heavy chain by a small peptide linker. Dulaglutide is indicated in the treatment of type 2 diabetes and can be used once a week. It was approved by the FDA in September 2014. Dulaglutide is manufactured and marketed by Eli Lily under the brand Trulicityâ„¢. It is not known if dulaglutide can increase the risk of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2, and is thus not recommended for use in populations with a personal or family history of these conditions. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | Dulaglutide activates human glucagon-like peptide-1 receptors, thus increasing intracellular cyclic AMP in beta cells. This, in turn, increases glucose-dependent insulin release. Dulaglutide also reduces glucagon secretion and slows gastric emptying. | Dulaglutide is a human GLP-1 receptor agonist with 90% amino acid sequence homology to endogenous human GLP-1 (7-37). Dulaglutide activates the GLP-1 receptor, a membrane-bound cell-surface receptor coupled to adenylyl cyclase in pancreatic beta cells. Dulaglutide increases intracellular cyclic AMP (cAMP) in beta cells leading to glucose-dependent insulin release. Dulaglutide also decreases glucagon secretion and slows gastric emptying. | LD50 information for dulaglutide is not readily available in the literature.[L34685] Cases of overdose with dulaglutide have resulted in gastrointestinal disturbance. Appropriate supportive treatment is recommended to manage signs and symptoms.[L34670] Additionally, hypoglycemia has been observed after an overdose with dulaglutide; frequent plasma glucose monitoring should be performed.[L30380] | Dulaglutide is presumed to be degraded into its component amino acids by general protein catabolism pathways.[L30380] | Dulaglutide is slowly absorbed after subcutaneous injection.[L34670] In a pharmacokinetic study of 20 healthy adults, Cmax occurred within 24-48 hours after dosing.[A234419] The average absolute bioavailability of dulaglutide after subcutaneous injections of single 0.75 mg and 1.5 mg doses was 65% and 47%, respectively.[L30380] | The apparent volume of distribution of dulaglutide was 3.09 L in a pharmacokinetic study; the apparent population mean peripheral volume of distribution was approximately 6 L.[L30380] | The apparent population mean clearance of dulaglutide was 0.142 L/h in a pharmacokinetic study.[L30380] | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Blood Proteins,Drugs Used in Diabetes,Gastrointestinal Hormones,Globulins,GLP-1 Agonists,Glucagon-like peptide-1 (GLP-1) analogues,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Immunoglobulin Fragments,Immunoglobulins,Immunoproteins,Incretin Mimetics,Pancreatic Hormones,Peptide Fragments,Peptide Hormones,Peptides,Proglucagon,Protein Precursors,Proteins,Recombinant Proteins,Serum Globulins | NA | NA | NA | Acetylsalicylic acid may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Chlorpropamide; Dihydrotestosterone may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Insulin Regular; Dulaglutide may increase the hypoglycemic activities of Insulin Lispro; The therapeutic efficacy of Dulaglutide can be decreased when used in combination with Leuprolide; Lipoic Acid may increase the hypoglycemic activities of Dulaglutide; Oxandrolone may increase the hypoglycemic activities of Dulaglutide; Paroxetine may increase the hypoglycemic activities of Dulaglutide; Pegvisomant may increase the hypoglycemic activities of Dulaglutide. | Glucagon-like peptide 1 receptor | Trulicity | Eli Lilly Canada Inc | Eli Lilly Canada Inc | TRULICITYâ„¢ is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | NA | TRULICITY solution contains 0.75 mg or 1.5 mg of dulaglutide. Each single-dose pen or prefilled syringe contains 0.5 mL of solution and the following excipients: citric acid anhydrous (0.07 mg), mannitol (23.2 mg), polysorbate 80 (0.10 mg), trisodium citrate dihydrate (1.37 mg), in water for injection. | Solution | Subcutaneous | The recommended initiating dose of TRULICITY is 0.75 mg once weekly. The dose may be increased to 1.5 mg once weekly for additional glycemic control. The maximum recommended dose is 1.5 mg once weekly. Administer TRULICITY once weekly, any time of day, with or without food. TRULICITY should be injected subcutaneously in the abdomen, thigh, or upper arm. If a dose is missed, instruct patients to administer as soon as possible if there are at least 3 days (72 hours) until the next scheduled dose. If less than 3 days remain before the next scheduled dose, skip the missed dose and administer the next dose on the regularly scheduled day. In each case, patients can then resume their regular once weekly dosing schedule. The day of weekly administration can be changed if necessary as long as the last dose was administered 3 or more days before. | TRULICITY is contraindicated in patients with a personal or family history of medullary thyroid carcinoma (MTC) or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2); TRULICITY is also contraindicated in patients with a prior serious hypersensitivity reaction to dulaglutide or to any of the product components | Risk of Thyroid C-cell Tumors; Pancreatitis; Hypoglycemia with Concomitant Use of Insulin Secretagogues or Insulin; Hypersensitivity reactions; Renal impairment; Severe Gastrointestinal Disease. | Link | NA | NA |
| 10760 | Th1176 | Dulaglutide | >Th1176_Dulaglutide HGEGTFTSDVSSYLEEQAAKEFIAWLVKGGGGGGGSGGGGSGGGGSAESKYGPPCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 59669.81 | C2646H4044N704O836S22 | NA | NA | NA | Approximately 5 days. | Dulaglutide is a novel glucagon-like peptide-1 agonist (GLP-1) biologic drug consisting of a dipeptidyl peptidase-IV-protected GLP-1 analogue covalently linked to a human IgG4-Fc heavy chain by a small peptide linker. Dulaglutide is indicated in the treatment of type 2 diabetes and can be used once a week. It was approved by the FDA in September 2014. Dulaglutide is manufactured and marketed by Eli Lily under the brand Trulicityâ„¢. It is not known if dulaglutide can increase the risk of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2, and is thus not recommended for use in populations with a personal or family history of these conditions. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | Dulaglutide activates human glucagon-like peptide-1 receptors, thus increasing intracellular cyclic AMP in beta cells. This, in turn, increases glucose-dependent insulin release. Dulaglutide also reduces glucagon secretion and slows gastric emptying. | Dulaglutide is a human GLP-1 receptor agonist with 90% amino acid sequence homology to endogenous human GLP-1 (7-37). Dulaglutide activates the GLP-1 receptor, a membrane-bound cell-surface receptor coupled to adenylyl cyclase in pancreatic beta cells. Dulaglutide increases intracellular cyclic AMP (cAMP) in beta cells leading to glucose-dependent insulin release. Dulaglutide also decreases glucagon secretion and slows gastric emptying. | LD50 information for dulaglutide is not readily available in the literature.[L34685] Cases of overdose with dulaglutide have resulted in gastrointestinal disturbance. Appropriate supportive treatment is recommended to manage signs and symptoms.[L34670] Additionally, hypoglycemia has been observed after an overdose with dulaglutide; frequent plasma glucose monitoring should be performed.[L30380] | Dulaglutide is presumed to be degraded into its component amino acids by general protein catabolism pathways.[L30380] | Dulaglutide is slowly absorbed after subcutaneous injection.[L34670] In a pharmacokinetic study of 20 healthy adults, Cmax occurred within 24-48 hours after dosing.[A234419] The average absolute bioavailability of dulaglutide after subcutaneous injections of single 0.75 mg and 1.5 mg doses was 65% and 47%, respectively.[L30380] | The apparent volume of distribution of dulaglutide was 3.09 L in a pharmacokinetic study; the apparent population mean peripheral volume of distribution was approximately 6 L.[L30380] | The apparent population mean clearance of dulaglutide was 0.142 L/h in a pharmacokinetic study.[L30380] | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Blood Proteins,Drugs Used in Diabetes,Gastrointestinal Hormones,Globulins,GLP-1 Agonists,Glucagon-like peptide-1 (GLP-1) analogues,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Immunoglobulin Fragments,Immunoglobulins,Immunoproteins,Incretin Mimetics,Pancreatic Hormones,Peptide Fragments,Peptide Hormones,Peptides,Proglucagon,Protein Precursors,Proteins,Recombinant Proteins,Serum Globulins | NA | NA | NA | Acetylsalicylic acid may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Chlorpropamide; Dihydrotestosterone may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Insulin Regular; Dulaglutide may increase the hypoglycemic activities of Insulin Lispro; The therapeutic efficacy of Dulaglutide can be decreased when used in combination with Leuprolide; Lipoic Acid may increase the hypoglycemic activities of Dulaglutide; Oxandrolone may increase the hypoglycemic activities of Dulaglutide; Paroxetine may increase the hypoglycemic activities of Dulaglutide; Pegvisomant may increase the hypoglycemic activities of Dulaglutide. | Glucagon-like peptide 1 receptor | Trulicity | Eli Lilly Canada Inc | Eli Lilly Canada Inc | TRULICITYâ„¢ is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | NA | TRULICITY solution contains 0.75 mg or 1.5 mg of dulaglutide. Each single-dose pen or prefilled syringe contains 0.5 mL of solution and the following excipients: citric acid anhydrous (0.07 mg), mannitol (23.2 mg), polysorbate 80 (0.10 mg), trisodium citrate dihydrate (1.37 mg), in water for injection. | Solution | Subcutaneous | The recommended initiating dose of TRULICITY is 0.75 mg once weekly. The dose may be increased to 1.5 mg once weekly for additional glycemic control. The maximum recommended dose is 1.5 mg once weekly. Administer TRULICITY once weekly, any time of day, with or without food. TRULICITY should be injected subcutaneously in the abdomen, thigh, or upper arm. If a dose is missed, instruct patients to administer as soon as possible if there are at least 3 days (72 hours) until the next scheduled dose. If less than 3 days remain before the next scheduled dose, skip the missed dose and administer the next dose on the regularly scheduled day. In each case, patients can then resume their regular once weekly dosing schedule. The day of weekly administration can be changed if necessary as long as the last dose was administered 3 or more days before. | TRULICITY is contraindicated in patients with a personal or family history of medullary thyroid carcinoma (MTC) or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2); TRULICITY is also contraindicated in patients with a prior serious hypersensitivity reaction to dulaglutide or to any of the product components | Risk of Thyroid C-cell Tumors; Pancreatitis; Hypoglycemia with Concomitant Use of Insulin Secretagogues or Insulin; Hypersensitivity reactions; Renal impairment; Severe Gastrointestinal Disease. | Link | NA | NA |
| 10761 | Th1176 | Dulaglutide | >Th1176_Dulaglutide HGEGTFTSDVSSYLEEQAAKEFIAWLVKGGGGGGGSGGGGSGGGGSAESKYGPPCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 59669.81 | C2646H4044N704O836S23 | NA | NA | NA | Approximately 5 days. | Dulaglutide is a novel glucagon-like peptide-1 agonist (GLP-1) biologic drug consisting of a dipeptidyl peptidase-IV-protected GLP-1 analogue covalently linked to a human IgG4-Fc heavy chain by a small peptide linker. Dulaglutide is indicated in the treatment of type 2 diabetes and can be used once a week. It was approved by the FDA in September 2014. Dulaglutide is manufactured and marketed by Eli Lily under the brand Trulicityâ„¢. It is not known if dulaglutide can increase the risk of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2, and is thus not recommended for use in populations with a personal or family history of these conditions. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | Dulaglutide activates human glucagon-like peptide-1 receptors, thus increasing intracellular cyclic AMP in beta cells. This, in turn, increases glucose-dependent insulin release. Dulaglutide also reduces glucagon secretion and slows gastric emptying. | Dulaglutide is a human GLP-1 receptor agonist with 90% amino acid sequence homology to endogenous human GLP-1 (7-37). Dulaglutide activates the GLP-1 receptor, a membrane-bound cell-surface receptor coupled to adenylyl cyclase in pancreatic beta cells. Dulaglutide increases intracellular cyclic AMP (cAMP) in beta cells leading to glucose-dependent insulin release. Dulaglutide also decreases glucagon secretion and slows gastric emptying. | LD50 information for dulaglutide is not readily available in the literature.[L34685] Cases of overdose with dulaglutide have resulted in gastrointestinal disturbance. Appropriate supportive treatment is recommended to manage signs and symptoms.[L34670] Additionally, hypoglycemia has been observed after an overdose with dulaglutide; frequent plasma glucose monitoring should be performed.[L30380] | Dulaglutide is presumed to be degraded into its component amino acids by general protein catabolism pathways.[L30380] | Dulaglutide is slowly absorbed after subcutaneous injection.[L34670] In a pharmacokinetic study of 20 healthy adults, Cmax occurred within 24-48 hours after dosing.[A234419] The average absolute bioavailability of dulaglutide after subcutaneous injections of single 0.75 mg and 1.5 mg doses was 65% and 47%, respectively.[L30380] | The apparent volume of distribution of dulaglutide was 3.09 L in a pharmacokinetic study; the apparent population mean peripheral volume of distribution was approximately 6 L.[L30380] | The apparent population mean clearance of dulaglutide was 0.142 L/h in a pharmacokinetic study.[L30380] | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Blood Proteins,Drugs Used in Diabetes,Gastrointestinal Hormones,Globulins,GLP-1 Agonists,Glucagon-like peptide-1 (GLP-1) analogues,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Immunoglobulin Fragments,Immunoglobulins,Immunoproteins,Incretin Mimetics,Pancreatic Hormones,Peptide Fragments,Peptide Hormones,Peptides,Proglucagon,Protein Precursors,Proteins,Recombinant Proteins,Serum Globulins | NA | NA | NA | Acetylsalicylic acid may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Chlorpropamide; Dihydrotestosterone may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Insulin Regular; Dulaglutide may increase the hypoglycemic activities of Insulin Lispro; The therapeutic efficacy of Dulaglutide can be decreased when used in combination with Leuprolide; Lipoic Acid may increase the hypoglycemic activities of Dulaglutide; Oxandrolone may increase the hypoglycemic activities of Dulaglutide; Paroxetine may increase the hypoglycemic activities of Dulaglutide; Pegvisomant may increase the hypoglycemic activities of Dulaglutide. | Glucagon-like peptide 1 receptor | Trulicity | Eli Lilly Canada Inc | Eli Lilly Canada Inc | TRULICITYâ„¢ is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | NA | TRULICITY solution contains 0.75 mg or 1.5 mg of dulaglutide. Each single-dose pen or prefilled syringe contains 0.5 mL of solution and the following excipients: citric acid anhydrous (0.07 mg), mannitol (23.2 mg), polysorbate 80 (0.10 mg), trisodium citrate dihydrate (1.37 mg), in water for injection. | Solution | Subcutaneous | The recommended initiating dose of TRULICITY is 0.75 mg once weekly. The dose may be increased to 1.5 mg once weekly for additional glycemic control. The maximum recommended dose is 1.5 mg once weekly. Administer TRULICITY once weekly, any time of day, with or without food. TRULICITY should be injected subcutaneously in the abdomen, thigh, or upper arm. If a dose is missed, instruct patients to administer as soon as possible if there are at least 3 days (72 hours) until the next scheduled dose. If less than 3 days remain before the next scheduled dose, skip the missed dose and administer the next dose on the regularly scheduled day. In each case, patients can then resume their regular once weekly dosing schedule. The day of weekly administration can be changed if necessary as long as the last dose was administered 3 or more days before. | TRULICITY is contraindicated in patients with a personal or family history of medullary thyroid carcinoma (MTC) or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2); TRULICITY is also contraindicated in patients with a prior serious hypersensitivity reaction to dulaglutide or to any of the product components | Risk of Thyroid C-cell Tumors; Pancreatitis; Hypoglycemia with Concomitant Use of Insulin Secretagogues or Insulin; Hypersensitivity reactions; Renal impairment; Severe Gastrointestinal Disease. | Link | NA | NA |
| 10762 | Th1176 | Dulaglutide | >Th1176_Dulaglutide HGEGTFTSDVSSYLEEQAAKEFIAWLVKGGGGGGGSGGGGSGGGGSAESKYGPPCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 59670.81 | C2646H4044N704O836S24 | NA | NA | NA | Approximately 5 days. | Dulaglutide is a novel glucagon-like peptide-1 agonist (GLP-1) biologic drug consisting of a dipeptidyl peptidase-IV-protected GLP-1 analogue covalently linked to a human IgG4-Fc heavy chain by a small peptide linker. Dulaglutide is indicated in the treatment of type 2 diabetes and can be used once a week. It was approved by the FDA in September 2014. Dulaglutide is manufactured and marketed by Eli Lily under the brand Trulicityâ„¢. It is not known if dulaglutide can increase the risk of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2, and is thus not recommended for use in populations with a personal or family history of these conditions. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | Dulaglutide activates human glucagon-like peptide-1 receptors, thus increasing intracellular cyclic AMP in beta cells. This, in turn, increases glucose-dependent insulin release. Dulaglutide also reduces glucagon secretion and slows gastric emptying. | Dulaglutide is a human GLP-1 receptor agonist with 90% amino acid sequence homology to endogenous human GLP-1 (7-37). Dulaglutide activates the GLP-1 receptor, a membrane-bound cell-surface receptor coupled to adenylyl cyclase in pancreatic beta cells. Dulaglutide increases intracellular cyclic AMP (cAMP) in beta cells leading to glucose-dependent insulin release. Dulaglutide also decreases glucagon secretion and slows gastric emptying. | LD50 information for dulaglutide is not readily available in the literature.[L34685] Cases of overdose with dulaglutide have resulted in gastrointestinal disturbance. Appropriate supportive treatment is recommended to manage signs and symptoms.[L34670] Additionally, hypoglycemia has been observed after an overdose with dulaglutide; frequent plasma glucose monitoring should be performed.[L30380] | Dulaglutide is presumed to be degraded into its component amino acids by general protein catabolism pathways.[L30380] | Dulaglutide is slowly absorbed after subcutaneous injection.[L34670] In a pharmacokinetic study of 20 healthy adults, Cmax occurred within 24-48 hours after dosing.[A234419] The average absolute bioavailability of dulaglutide after subcutaneous injections of single 0.75 mg and 1.5 mg doses was 65% and 47%, respectively.[L30380] | The apparent volume of distribution of dulaglutide was 3.09 L in a pharmacokinetic study; the apparent population mean peripheral volume of distribution was approximately 6 L.[L30380] | The apparent population mean clearance of dulaglutide was 0.142 L/h in a pharmacokinetic study.[L30380] | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Blood Proteins,Drugs Used in Diabetes,Gastrointestinal Hormones,Globulins,GLP-1 Agonists,Glucagon-like peptide-1 (GLP-1) analogues,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Immunoglobulin Fragments,Immunoglobulins,Immunoproteins,Incretin Mimetics,Pancreatic Hormones,Peptide Fragments,Peptide Hormones,Peptides,Proglucagon,Protein Precursors,Proteins,Recombinant Proteins,Serum Globulins | NA | NA | NA | Acetylsalicylic acid may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Chlorpropamide; Dihydrotestosterone may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Insulin Regular; Dulaglutide may increase the hypoglycemic activities of Insulin Lispro; The therapeutic efficacy of Dulaglutide can be decreased when used in combination with Leuprolide; Lipoic Acid may increase the hypoglycemic activities of Dulaglutide; Oxandrolone may increase the hypoglycemic activities of Dulaglutide; Paroxetine may increase the hypoglycemic activities of Dulaglutide; Pegvisomant may increase the hypoglycemic activities of Dulaglutide. | Glucagon-like peptide 1 receptor | Trulicity | Eli Lilly and Company | Eli Lilly and Company | TRULICITYâ„¢ is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | NA | TRULICITY solution contains 0.75 mg or 1.5 mg of dulaglutide. Each single-dose pen or prefilled syringe contains 0.5 mL of solution and the following excipients: citric acid anhydrous (0.07 mg), mannitol (23.2 mg), polysorbate 80 (0.10 mg), trisodium citrate dihydrate (1.37 mg), in water for injection. | Solution, Injection | Subcutaneous | The recommended initiating dose of TRULICITY is 0.75 mg once weekly. The dose may be increased to 1.5 mg once weekly for additional glycemic control. The maximum recommended dose is 1.5 mg once weekly. Administer TRULICITY once weekly, any time of day, with or without food. TRULICITY should be injected subcutaneously in the abdomen, thigh, or upper arm. If a dose is missed, instruct patients to administer as soon as possible if there are at least 3 days (72 hours) until the next scheduled dose. If less than 3 days remain before the next scheduled dose, skip the missed dose and administer the next dose on the regularly scheduled day. In each case, patients can then resume their regular once weekly dosing schedule. The day of weekly administration can be changed if necessary as long as the last dose was administered 3 or more days before. | TRULICITY is contraindicated in patients with a personal or family history of medullary thyroid carcinoma (MTC) or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2); TRULICITY is also contraindicated in patients with a prior serious hypersensitivity reaction to dulaglutide or to any of the product components | Risk of Thyroid C-cell Tumors; Pancreatitis; Hypoglycemia with Concomitant Use of Insulin Secretagogues or Insulin; Hypersensitivity reactions; Renal impairment; Severe Gastrointestinal Disease. | Link | NA | NA |
| 10769 | Th1179 | Evolocumab | NA | 141800 | C6242H9648N1668O1996S56 | NA | NA | NA | NA | Evolocumab is a monoclonal antibody designed for the treatment of hyperlipidemia by Amgen. It is a subcutaneous injection approved by the FDA for individuals on maximum statin therapy who still require additional LDL-cholesterol lowering. It is approved for both homozygous and heterozygous familial cholesterolemia as an adjunct to other first-line therapies. Evolocumab is a human IgG2 monoclonal antibody that inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9). PCSK9 is a protein that targets LDL receptors for degradation, therefore reducing the liver’s ability to remove LDL-cholesterol (LDL-C), or “bad†cholesterol, from the blood. Evolocumab is designed to bind to PCSK9 and inhibit PCSK9 from binding to LDL receptors on the liver surface, resulting in more LDL receptors on the surface of the liver to remove LDL-C from the blood. Evolocumab is the second PCSK9 inhibitor on the market, first being alirocumab. | For the treatment of heterozygous/homozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease in patients on maximum tolerated statin therapy requiring additional LDL-cholesterol lowering. | Following single subcutaneous administration of 140 mg or 420 mg of evolocumab, maximum suppression of circulating unbound PCSK9 occurred by 4 hours. Unbound PCSK9 concentrations returned toward baseline when evolocumab concentrations decreased below the limit of quantitation. | Evolocumab is a human IgG monoclonal antibody which targets PCSK9 (proprotein convertase subtilisin/kexin type 9). PCSK9 is a serine protease produced by the liver which binds LDL receptors and creates a complex to be targeted for lysosomal degradation. LDL receptors typically bind LDL-cholesterol (bad cholesterol) for cellular reuptake, therefore the formation of these complexes with PCSK9 inhibits LDL receptor recycling to the cell surface, resulting in decreased cellular reuptake of LDL-C and increased levels of free LDL-C in the plasma. Individuals with familial hypercholesterolemia often may have gain of function mutations in the PCSK9 molecules in their body, resulting in increased LDL-C plasma levels and a consequent cardiovascular risk. Evolocumab is able to bind both the normal PCSK9 and the gain of function mutant, D374Y. The exact mechanism of the binding has not been published, however the precursor molecule, mAb1, is indicative of the interaction. The mAb1 molecule binds on the catalytic site of PCSK9 next to the binding site for the LDL receptor and creates hydrogen bonds and hydrophobic interactions, resulting in the steric inhibition of binding between PCSK9 and the LDL receptor. Because the formation of complexes between LDL receptor and PCSK9 are prevented, the internalized LDL receptors are less likely to be degrated by lysosomes and may recycle to the surface of the cell to serve their function of removing LDL from the blood. | NA | NA | Total bioavailability from subcutaneous injection was 82% in cynomolgus monkeys. | NA | Evolocumab showed non-linear, dose-dependent clearance in healthy volunteers; clearance decreased with increasing dose. | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Anticholesteremic Agents,Antimetabolites,Blood Proteins,Globulins,Hypolipidemic Agents,Hypolipidemic Agents Indicated for Hyperlipidemia,Immunoglobulins,Immunoproteins,Lipid Modifying Agents,Lipid Modifying Agents, Plain,Lipid Regulating Agents,Non-statin Hypolipidemic Agents Indicated for Hyperlipidemia,Noxae,PCSK9 Inhibitor,Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Inhibitors,Proteins,Serum Globulins,Toxic Actions | NA | NA | NA | The risk or severity of adverse effects can be increased when Evolocumab is combined with Belimumab. | Proprotein convertase subtilisin/kexin type 9 | NA | NA | NA | NA | NA | 140 mg/mL; 140 mg | Injection, solution; Injection | Subcutaneous | NA | NA | NA | NA | NA | NA |
| 10770 | Th1179 | Evolocumab | NA | 141800 | C6242H9648N1668O1996S57 | NA | NA | NA | NA | Evolocumab is a monoclonal antibody designed for the treatment of hyperlipidemia by Amgen. It is a subcutaneous injection approved by the FDA for individuals on maximum statin therapy who still require additional LDL-cholesterol lowering. It is approved for both homozygous and heterozygous familial cholesterolemia as an adjunct to other first-line therapies. Evolocumab is a human IgG2 monoclonal antibody that inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9). PCSK9 is a protein that targets LDL receptors for degradation, therefore reducing the liver’s ability to remove LDL-cholesterol (LDL-C), or “bad†cholesterol, from the blood. Evolocumab is designed to bind to PCSK9 and inhibit PCSK9 from binding to LDL receptors on the liver surface, resulting in more LDL receptors on the surface of the liver to remove LDL-C from the blood. Evolocumab is the second PCSK9 inhibitor on the market, first being alirocumab. | For the treatment of heterozygous/homozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease in patients on maximum tolerated statin therapy requiring additional LDL-cholesterol lowering. | Following single subcutaneous administration of 140 mg or 420 mg of evolocumab, maximum suppression of circulating unbound PCSK9 occurred by 4 hours. Unbound PCSK9 concentrations returned toward baseline when evolocumab concentrations decreased below the limit of quantitation. | Evolocumab is a human IgG monoclonal antibody which targets PCSK9 (proprotein convertase subtilisin/kexin type 9). PCSK9 is a serine protease produced by the liver which binds LDL receptors and creates a complex to be targeted for lysosomal degradation. LDL receptors typically bind LDL-cholesterol (bad cholesterol) for cellular reuptake, therefore the formation of these complexes with PCSK9 inhibits LDL receptor recycling to the cell surface, resulting in decreased cellular reuptake of LDL-C and increased levels of free LDL-C in the plasma. Individuals with familial hypercholesterolemia often may have gain of function mutations in the PCSK9 molecules in their body, resulting in increased LDL-C plasma levels and a consequent cardiovascular risk. Evolocumab is able to bind both the normal PCSK9 and the gain of function mutant, D374Y. The exact mechanism of the binding has not been published, however the precursor molecule, mAb1, is indicative of the interaction. The mAb1 molecule binds on the catalytic site of PCSK9 next to the binding site for the LDL receptor and creates hydrogen bonds and hydrophobic interactions, resulting in the steric inhibition of binding between PCSK9 and the LDL receptor. Because the formation of complexes between LDL receptor and PCSK9 are prevented, the internalized LDL receptors are less likely to be degrated by lysosomes and may recycle to the surface of the cell to serve their function of removing LDL from the blood. | NA | NA | Total bioavailability from subcutaneous injection was 82% in cynomolgus monkeys. | NA | Evolocumab showed non-linear, dose-dependent clearance in healthy volunteers; clearance decreased with increasing dose. | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Anticholesteremic Agents,Antimetabolites,Blood Proteins,Globulins,Hypolipidemic Agents,Hypolipidemic Agents Indicated for Hyperlipidemia,Immunoglobulins,Immunoproteins,Lipid Modifying Agents,Lipid Modifying Agents, Plain,Lipid Regulating Agents,Non-statin Hypolipidemic Agents Indicated for Hyperlipidemia,Noxae,PCSK9 Inhibitor,Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Inhibitors,Proteins,Serum Globulins,Toxic Actions | NA | NA | NA | The risk or severity of adverse effects can be increased when Evolocumab is combined with Belimumab. | Proprotein convertase subtilisin/kexin type 9 | Repatha | Amgen Inc | Amgen Inc | REPATHA™ is indicated as an adjunct to diet and maximally tolerated statin therapy for the treatment of adults with heterozygous familial hypercholesterolemia (HeFH) or clinical atherosclerotic cardiovascular disease (CVD), who require additional lowering of low density lipoprotein cholesterol (LDL-C); Also indicated as an adjunct to diet and other LDL-lowering therapies (e.g., statins, ezetimibe, LDL apheresis) for the treatment of patients with homozygous familial hypercholesterolemia (HoFH) who require additional lowering of LDL-C. | NA | 140 mg/mL | injection, solution | Subcutaneous | The recommended subcutaneous dosage of REPATHA in patients with HeFH or patients with primary hyperlipidemia with established clinical atherosclerotic CVD is either 140 mg every 2 weeks OR 420 mg once monthly. When switching dosage regimens, administer the first dose of the new regimen on the next scheduled date of the prior regimen. The recommended subcutaneous dosage of REPATHA in patients with HoFH is 420 mg once monthly. In patients with HoFH, measure LDL-C levels 4 to 8 weeks after starting REPATHA, since response to therapy will depend on the degree of LDL-receptor function. | REPATHA is contraindicated in patients with a history of a serious hypersensitivity reaction to REPATHA | Allergic reactions | Link | NA | NA |
| 10771 | Th1179 | Evolocumab | NA | 141800 | C6242H9648N1668O1996S58 | NA | NA | NA | NA | Evolocumab is a monoclonal antibody designed for the treatment of hyperlipidemia by Amgen. It is a subcutaneous injection approved by the FDA for individuals on maximum statin therapy who still require additional LDL-cholesterol lowering. It is approved for both homozygous and heterozygous familial cholesterolemia as an adjunct to other first-line therapies. Evolocumab is a human IgG2 monoclonal antibody that inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9). PCSK9 is a protein that targets LDL receptors for degradation, therefore reducing the liver’s ability to remove LDL-cholesterol (LDL-C), or “bad†cholesterol, from the blood. Evolocumab is designed to bind to PCSK9 and inhibit PCSK9 from binding to LDL receptors on the liver surface, resulting in more LDL receptors on the surface of the liver to remove LDL-C from the blood. Evolocumab is the second PCSK9 inhibitor on the market, first being alirocumab. | For the treatment of heterozygous/homozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease in patients on maximum tolerated statin therapy requiring additional LDL-cholesterol lowering. | Following single subcutaneous administration of 140 mg or 420 mg of evolocumab, maximum suppression of circulating unbound PCSK9 occurred by 4 hours. Unbound PCSK9 concentrations returned toward baseline when evolocumab concentrations decreased below the limit of quantitation. | Evolocumab is a human IgG monoclonal antibody which targets PCSK9 (proprotein convertase subtilisin/kexin type 9). PCSK9 is a serine protease produced by the liver which binds LDL receptors and creates a complex to be targeted for lysosomal degradation. LDL receptors typically bind LDL-cholesterol (bad cholesterol) for cellular reuptake, therefore the formation of these complexes with PCSK9 inhibits LDL receptor recycling to the cell surface, resulting in decreased cellular reuptake of LDL-C and increased levels of free LDL-C in the plasma. Individuals with familial hypercholesterolemia often may have gain of function mutations in the PCSK9 molecules in their body, resulting in increased LDL-C plasma levels and a consequent cardiovascular risk. Evolocumab is able to bind both the normal PCSK9 and the gain of function mutant, D374Y. The exact mechanism of the binding has not been published, however the precursor molecule, mAb1, is indicative of the interaction. The mAb1 molecule binds on the catalytic site of PCSK9 next to the binding site for the LDL receptor and creates hydrogen bonds and hydrophobic interactions, resulting in the steric inhibition of binding between PCSK9 and the LDL receptor. Because the formation of complexes between LDL receptor and PCSK9 are prevented, the internalized LDL receptors are less likely to be degrated by lysosomes and may recycle to the surface of the cell to serve their function of removing LDL from the blood. | NA | NA | Total bioavailability from subcutaneous injection was 82% in cynomolgus monkeys. | NA | Evolocumab showed non-linear, dose-dependent clearance in healthy volunteers; clearance decreased with increasing dose. | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Anticholesteremic Agents,Antimetabolites,Blood Proteins,Globulins,Hypolipidemic Agents,Hypolipidemic Agents Indicated for Hyperlipidemia,Immunoglobulins,Immunoproteins,Lipid Modifying Agents,Lipid Modifying Agents, Plain,Lipid Regulating Agents,Non-statin Hypolipidemic Agents Indicated for Hyperlipidemia,Noxae,PCSK9 Inhibitor,Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Inhibitors,Proteins,Serum Globulins,Toxic Actions | NA | NA | NA | The risk or severity of adverse effects can be increased when Evolocumab is combined with Belimumab. | Proprotein convertase subtilisin/kexin type 9 | Repatha | Amgen Canada Inc | Amgen Canada Inc | REPATHA™ is indicated as an adjunct to diet and maximally tolerated statin therapy for the treatment of adults with heterozygous familial hypercholesterolemia (HeFH) or clinical atherosclerotic cardiovascular disease (CVD), who require additional lowering of low density lipoprotein cholesterol (LDL-C); Also indicated as an adjunct to diet and other LDL-lowering therapies (e.g., statins, ezetimibe, LDL apheresis) for the treatment of patients with homozygous familial hypercholesterolemia (HoFH) who require additional lowering of LDL-C. | NA | 140 mg | solution | Subcutaneous | The recommended subcutaneous dosage of REPATHA in patients with HeFH or patients with primary hyperlipidemia with established clinical atherosclerotic CVD is either 140 mg every 2 weeks OR 420 mg once monthly. When switching dosage regimens, administer the first dose of the new regimen on the next scheduled date of the prior regimen. The recommended subcutaneous dosage of REPATHA in patients with HoFH is 420 mg once monthly. In patients with HoFH, measure LDL-C levels 4 to 8 weeks after starting REPATHA, since response to therapy will depend on the degree of LDL-receptor function. | REPATHA is contraindicated in patients with a history of a serious hypersensitivity reaction to REPATHA | Allergic reactions | Link | NA | NA |
| 10772 | Th1179 | Evolocumab | NA | 141800 | C6242H9648N1668O1996S59 | NA | NA | NA | NA | Evolocumab is a monoclonal antibody designed for the treatment of hyperlipidemia by Amgen. It is a subcutaneous injection approved by the FDA for individuals on maximum statin therapy who still require additional LDL-cholesterol lowering. It is approved for both homozygous and heterozygous familial cholesterolemia as an adjunct to other first-line therapies. Evolocumab is a human IgG2 monoclonal antibody that inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9). PCSK9 is a protein that targets LDL receptors for degradation, therefore reducing the liver’s ability to remove LDL-cholesterol (LDL-C), or “bad†cholesterol, from the blood. Evolocumab is designed to bind to PCSK9 and inhibit PCSK9 from binding to LDL receptors on the liver surface, resulting in more LDL receptors on the surface of the liver to remove LDL-C from the blood. Evolocumab is the second PCSK9 inhibitor on the market, first being alirocumab. | For the treatment of heterozygous/homozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease in patients on maximum tolerated statin therapy requiring additional LDL-cholesterol lowering. | Following single subcutaneous administration of 140 mg or 420 mg of evolocumab, maximum suppression of circulating unbound PCSK9 occurred by 4 hours. Unbound PCSK9 concentrations returned toward baseline when evolocumab concentrations decreased below the limit of quantitation. | Evolocumab is a human IgG monoclonal antibody which targets PCSK9 (proprotein convertase subtilisin/kexin type 9). PCSK9 is a serine protease produced by the liver which binds LDL receptors and creates a complex to be targeted for lysosomal degradation. LDL receptors typically bind LDL-cholesterol (bad cholesterol) for cellular reuptake, therefore the formation of these complexes with PCSK9 inhibits LDL receptor recycling to the cell surface, resulting in decreased cellular reuptake of LDL-C and increased levels of free LDL-C in the plasma. Individuals with familial hypercholesterolemia often may have gain of function mutations in the PCSK9 molecules in their body, resulting in increased LDL-C plasma levels and a consequent cardiovascular risk. Evolocumab is able to bind both the normal PCSK9 and the gain of function mutant, D374Y. The exact mechanism of the binding has not been published, however the precursor molecule, mAb1, is indicative of the interaction. The mAb1 molecule binds on the catalytic site of PCSK9 next to the binding site for the LDL receptor and creates hydrogen bonds and hydrophobic interactions, resulting in the steric inhibition of binding between PCSK9 and the LDL receptor. Because the formation of complexes between LDL receptor and PCSK9 are prevented, the internalized LDL receptors are less likely to be degrated by lysosomes and may recycle to the surface of the cell to serve their function of removing LDL from the blood. | NA | NA | Total bioavailability from subcutaneous injection was 82% in cynomolgus monkeys. | NA | Evolocumab showed non-linear, dose-dependent clearance in healthy volunteers; clearance decreased with increasing dose. | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Anticholesteremic Agents,Antimetabolites,Blood Proteins,Globulins,Hypolipidemic Agents,Hypolipidemic Agents Indicated for Hyperlipidemia,Immunoglobulins,Immunoproteins,Lipid Modifying Agents,Lipid Modifying Agents, Plain,Lipid Regulating Agents,Non-statin Hypolipidemic Agents Indicated for Hyperlipidemia,Noxae,PCSK9 Inhibitor,Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Inhibitors,Proteins,Serum Globulins,Toxic Actions | NA | NA | NA | The risk or severity of adverse effects can be increased when Evolocumab is combined with Belimumab. | Proprotein convertase subtilisin/kexin type 9 | Repatha | Amgen Inc | Amgen Inc | REPATHA™ is indicated as an adjunct to diet and maximally tolerated statin therapy for the treatment of adults with heterozygous familial hypercholesterolemia (HeFH) or clinical atherosclerotic cardiovascular disease (CVD), who require additional lowering of low density lipoprotein cholesterol (LDL-C); Also indicated as an adjunct to diet and other LDL-lowering therapies (e.g., statins, ezetimibe, LDL apheresis) for the treatment of patients with homozygous familial hypercholesterolemia (HoFH) who require additional lowering of LDL-C. | NA | 140 mg/mL | injection, solution | Subcutaneous | The recommended subcutaneous dosage of REPATHA in patients with HeFH or patients with primary hyperlipidemia with established clinical atherosclerotic CVD is either 140 mg every 2 weeks OR 420 mg once monthly. When switching dosage regimens, administer the first dose of the new regimen on the next scheduled date of the prior regimen. The recommended subcutaneous dosage of REPATHA in patients with HoFH is 420 mg once monthly. In patients with HoFH, measure LDL-C levels 4 to 8 weeks after starting REPATHA, since response to therapy will depend on the degree of LDL-receptor function. | REPATHA is contraindicated in patients with a history of a serious hypersensitivity reaction to REPATHA | Allergic reactions | Link | NA | NA |
| 10781 | Th1181 | Filgrastim-sndz | >Th1181_Filgrastim-sndz MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S9 | 5.65 | NA | NA | Approximately 3.5 hours | NA | Patients with Cancer Receiving Myelosuppressive Chemotherapy: to decrease the incidence of infection, as manifested by febrile neutropenia, in patients with nonmyeloid malignancies receiving myelosuppressive anti-cancer drugs associated with a significant incidence of severe neutropenia with fever. Patients with Acute Myeloid Leukemia Receiving Induction or Consolidation Chemotherapy: to reduce the time to neutrophil recovery and the duration of fever, following induction or consolidation chemotherapy treatment of patients with acute myeloid leukemia (AML). Patients with Cancer Undergoing Bone Marrow Transplantation: to reduce the duration of neutropenia and neutropenia-related clinical sequelae, e.g., febrile neutropenia, in patients with nonmyeloid malignancies undergoing myeloablative chemotherapy followed by bone marrow transplantation. Patients Undergoing Autologous Peripheral Blood Progenitor Cell Collection and Therapy: for the mobilization of autologous hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis. Patients with Severe Chronic Neutropenia: for chronic administration to reduce the incidence and duration of sequelae of neutropenia (e.g, fever, infections, oropharyngeal ulcers) in symptomatic patients with congenital neutropenia, cyclic neutropenia, or idiopathic neutropenia. | In patients with patients with various nonmyeloid malignancies‚ administration of filgrastim resulted in a dose-dependent increase in circulating neutrophil counts over the dose range of 1 to 70 mcg/kg/day. This increase in neutrophil counts was observed whether filgrastim was administered intravenous (1 to70 mcg/kg twice daily)‚ subcutaneous (1 to 3 mcg/kg once daily)‚ or by continuous subcutaneous infusion (3 to 11 mcg/kg/day). With discontinuation of filgrastim therapy‚ neutrophil counts returned to baseline in most cases within 4 days. Isolated neutrophils displayed normal phagocytic (measured by zymosan-stimulated chemoluminescence) and chemotactic (measured by migration under agarose using N-formyl-methionyl-leucyl- phenylalanine [fMLP] as the chemotaxin) activity in vitro. | Colony-stimulating factors are glycoproteins which act on hematopoietic cells by binding to specific cell surface receptors and stimulating proliferation‚ differentiation commitment‚ and some end-cell functional activation. Endogenous G-CSF is a lineage-specific colony-stimulating factor that is produced by monocytes‚ fibroblasts, and endothelial cells. G-CSF regulates the production of neutrophils within the bone marrow and affects neutrophil progenitor proliferation‚ differentiation, and selected end-cell functions (including enhanced phagocytic ability‚ priming of the cellular metabolism associated with respiratory burst‚ antibody-dependent killing, and the increased expression of some cell surface antigens). G-CSF is not species-specific and has been shown to have minimal direct in vivo or in vitro effects on the production or activity of hematopoietic cell types other than the neutrophil lineage. | NA | NA | NA | NA | NA | NA | NA | NA | NA | The risk or severity of adverse effects can be increased when Filgrastim-sndz is combined with Bleomycin; The risk or severity of adverse effects can be increased when Filgrastim-sndz is combined with Cyclophosphamide; The risk or severity of adverse effects can be increased when Filgrastim-sndz is combined with Topotecan. | NA | Zarxio | Sandoz Inc | Sandoz Inc | NA | NA | 300 ug/.5mL Injection | solution | intravenous; subcutaneous | The recommended starting dosage of ZARXIO is 5 mcg/kg/day‚ administered as a single daily injection by subcutaneous injection‚ by short intravenous infusion (15 to 30 minutes)‚ or by continuous intravenous infusion. Obtain a complete blood count (CBC) and platelet count before instituting ZARXIO therapy and monitor twice weekly during therapy. Consider dose escalation in increments of 5 mcg/kg for each chemotherapy cycle‚ according to the duration and severity of the absolute neutrophil count (ANC) nadir. Recommend stopping ZARXIO if the ANC increases beyond 10‚000/mm³ | ZARXIO is contraindicated in patients with a history of serious allergic reactions to human granulocyte colony-stimulating factors such as filgrastim or pegfilgrastim products | Splenic Rupture; Acute Respiratory Distress Syndrome; Serious Allergic Reactions ; Sickle Cell Disorders; Glomerulonephritis; Alveolar Hemorrhage and Hemoptysis; Capillary Leak Syndrome; Thrombocytopenia; Leukocytosis; Cutaneous Vasculitis. | Link | NA | NA |
| 10782 | Th1181 | Filgrastim-sndz | >Th1181_Filgrastim-sndz MTPLGPASSLPQSFLLKCLEQVRKIQGDGAALQEKLCATYKLCHPEELVLLGHSLGIPWAPLSSCPSQALQLAGCLSQLHSGLFLYQGLLQALEGISPELGPTLDTLQLDVADFATTIWQQMEELGMAPALQPTQGAMPAFASAFQRRAGGVLVASHLQSFLEVSYRVLRHLAQP | 18800 | C845H1339N223O243S9 | 5.65 | NA | NA | Approximately 3.5 hours | NA | Patients with Cancer Receiving Myelosuppressive Chemotherapy: to decrease the incidence of infection, as manifested by febrile neutropenia, in patients with nonmyeloid malignancies receiving myelosuppressive anti-cancer drugs associated with a significant incidence of severe neutropenia with fever. Patients with Acute Myeloid Leukemia Receiving Induction or Consolidation Chemotherapy: to reduce the time to neutrophil recovery and the duration of fever, following induction or consolidation chemotherapy treatment of patients with acute myeloid leukemia (AML). Patients with Cancer Undergoing Bone Marrow Transplantation: to reduce the duration of neutropenia and neutropenia-related clinical sequelae, e.g., febrile neutropenia, in patients with nonmyeloid malignancies undergoing myeloablative chemotherapy followed by bone marrow transplantation. Patients Undergoing Autologous Peripheral Blood Progenitor Cell Collection and Therapy: for the mobilization of autologous hematopoietic progenitor cells into the peripheral blood for collection by leukapheresis. Patients with Severe Chronic Neutropenia: for chronic administration to reduce the incidence and duration of sequelae of neutropenia (e.g, fever, infections, oropharyngeal ulcers) in symptomatic patients with congenital neutropenia, cyclic neutropenia, or idiopathic neutropenia. | In patients with patients with various nonmyeloid malignancies‚ administration of filgrastim resulted in a dose-dependent increase in circulating neutrophil counts over the dose range of 1 to 70 mcg/kg/day. This increase in neutrophil counts was observed whether filgrastim was administered intravenous (1 to70 mcg/kg twice daily)‚ subcutaneous (1 to 3 mcg/kg once daily)‚ or by continuous subcutaneous infusion (3 to 11 mcg/kg/day). With discontinuation of filgrastim therapy‚ neutrophil counts returned to baseline in most cases within 4 days. Isolated neutrophils displayed normal phagocytic (measured by zymosan-stimulated chemoluminescence) and chemotactic (measured by migration under agarose using N-formyl-methionyl-leucyl- phenylalanine [fMLP] as the chemotaxin) activity in vitro. | Colony-stimulating factors are glycoproteins which act on hematopoietic cells by binding to specific cell surface receptors and stimulating proliferation‚ differentiation commitment‚ and some end-cell functional activation. Endogenous G-CSF is a lineage-specific colony-stimulating factor that is produced by monocytes‚ fibroblasts, and endothelial cells. G-CSF regulates the production of neutrophils within the bone marrow and affects neutrophil progenitor proliferation‚ differentiation, and selected end-cell functions (including enhanced phagocytic ability‚ priming of the cellular metabolism associated with respiratory burst‚ antibody-dependent killing, and the increased expression of some cell surface antigens). G-CSF is not species-specific and has been shown to have minimal direct in vivo or in vitro effects on the production or activity of hematopoietic cell types other than the neutrophil lineage. | NA | NA | NA | NA | NA | NA | NA | NA | NA | The risk or severity of adverse effects can be increased when Filgrastim-sndz is combined with Bleomycin; The risk or severity of adverse effects can be increased when Filgrastim-sndz is combined with Cyclophosphamide; The risk or severity of adverse effects can be increased when Filgrastim-sndz is combined with Topotecan. | NA | Zarxio | Sandoz Inc | Sandoz Inc | NA | NA | 480 ug/.8mL Injection | solution | intravenous; subcutaneous | The recommended starting dosage of ZARXIO is 5 mcg/kg/day‚ administered as a single daily injection by subcutaneous injection‚ by short intravenous infusion (15 to 30 minutes)‚ or by continuous intravenous infusion. Obtain a complete blood count (CBC) and platelet count before instituting ZARXIO therapy and monitor twice weekly during therapy. Consider dose escalation in increments of 5 mcg/kg for each chemotherapy cycle‚ according to the duration and severity of the absolute neutrophil count (ANC) nadir. Recommend stopping ZARXIO if the ANC increases beyond 10‚000/mm³ | ZARXIO is contraindicated in patients with a history of serious allergic reactions to human granulocyte colony-stimulating factors such as filgrastim or pegfilgrastim products | Splenic Rupture; Acute Respiratory Distress Syndrome; Serious Allergic Reactions ; Sickle Cell Disorders; Glomerulonephritis; Alveolar Hemorrhage and Hemoptysis; Capillary Leak Syndrome; Thrombocytopenia; Leukocytosis; Cutaneous Vasculitis. | Link | NA | NA |
| 10812 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. | Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging†or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab′)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. | NA | NA | NA | NA | NA | Immunologic Factors; Immunosuppressive Agents; Anti-Infective Agents | NA | NA | NA | Estradiol may increase the thrombogenic activities of Intravenous Immunoglobulin; Estropipate may increase the thrombogenic activities of Intravenous Immunoglobulin. | High affinity immunoglobulin gamma Fc receptor I; High affinity immunoglobulin gamma Fc receptor IB; Low affinity immunoglobulin gamma Fc region receptor II-a; Low affinity immunoglobulin gamma Fc region receptor II-b; Low affinity immunoglobulin gamma Fc region receptor II-c; Low affinity immunoglobulin gamma Fc region receptor III-A; Low affinity immunoglobulin gamma Fc region receptor III-B; Complement C3; Complement C4-A; Complement C4-B; Complement C5. | NA | NA | NA | NA | NA | .165 g/mL; 10 g/100mL; 12 g/1; 3 g/1; v; 1 g/10mL; 10 g/100mL; 5 g/50mL; .05 g/mL; 100 mg/mL | Injection; Injection, powder, lyophilized, for solution; Injection, solution. | intramuscular; intravenous; subcutaneous | NA | NA | NA | NA | NA | NA |
| 10826 | Th1192 | Ustekinumab | >Th1192_Ustekinumab EVQLVQSGAEVKKPGESLKISCKGSGYSFTTYWLGWVRQMPGKGLDWIGIMSPVDSDIRYSPSFQGQVTMSVDKSITTAYLQWNSLKASDTAMYYCARRRPGQGYFDFWGQGTLVTVSSSSTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTH | 148600 | NA | NA | NA | NA | Following administration of a single subcutaneous dose of 45 mg or 90 mg in patients with psoriasis, the median half-life was 19.8 days and 21.2, respectively. | CNTO 1275 is the experimental name for the human immunosuppressive drug ustekinumab developed by the biotechnology company Centocor. It is a laboratory manufactured, monoclonal antibody directed against interleukins IL-12 and IL-23. | For treatment in psoriasis and psoriatic disorders. | NA | Similar to the immunosuppressive function of Etanercept (Enbrel), CNTO 1275 is designed to interfere with the triggering of the body's inflamatory response through the suppression of certain cytokines. Specifically, CNTO 1275 blocks interleukin IL-12 and IL-23 (via the p40 subunit of IL-12 and IL-23) which help activate certain T-cells. | Signs of dose-limiting toxicity were not observed with intravenous administration of single doses up to 6 mg/kg in clinical trials. Information on overdose of ustekinumab is limited: in the event of overdose, patients should be monitored for any signs and symptoms of drug-related adverse events and appropriate symptomatic treatment should be initiated.[L9383,L9386] | The metabolic pathway of ustekinumab has not been fully characterized; it is expected to undergo nonspecific protein degradation via catabolic pathways in the same manner as endogenous IgG.[L9383,L9386] | The median Tmax following a single subcutaneous dose administration of 45mg and 90mg in adults with psoriasis was 13.5 days and 7 days, respectively. The median Cmax in the same group of patients was 2.4 µg/mL and 5.3 µg/mL at doses of 45mg and 90mg, respectively. The median AUC was 84.9 µg·day/mL and 226.9 µg·day/mL, respectively.[L9491] Following an intravenous induction dose administration, the mean ± SD Cmax was 125.2 ± 33.6 mcg/mL in patients with Crohn’s disease and 129.1 ± 27.6 mcg/mL in patients with ulcerative colitis.[L9386] The systemic exposure of ustekinumab (Cmax and AUC) increases in a linear or dose-proportional manner following a single subcutaneous administration at doses ranging from approximately 24 mg to 240 mg in patients with psoriasis. The estimated absolute bioavailability (F) of ustekinumab following a single subcutaneous dose administration in patients with psoriasis is 57.2%.[L9491] | The total volume of distribution at steady-state was 4.62 L in patients with Crohn’s disease and 4.4 L in patients with ulcerative colitis.[L9386] The median apparent volume of distribution during the terminal phase (Vz/F) ranged from 76 to 161 mL/kg in patients with psoriasis receiving a single subcutaneous dose.[L9491] | The median apparent clearance (CL/F) following a single subcutaneous administration to patients with psoriasis ranged from 2.7 to 5.3 mL/day/kg.[L9491] In patients with Crohn’s disease, the clearance was 0.19 L/day in patients with Crohn’s disease or ulcerative colitis.[L9383,L9386] | Deramtologic agent, Immunosuppressive agent, antineoplastic agent | NA | NA | NA | Belimumab, Denosumab, Infliximab, Leflunomide, Natalizumab, Pimecrolimus, Roflumilast, Sipuleucel-T, Tacrolimus, Tofacitinib, Trastuzumab | Interleukin-12 subunit beta,Interleukin-23 | Stelara | Janssen Biotech, Inc. | Janssen Biotech, Inc. | Psoriasis (Ps) and Psoriatic Arthritis (PsA) | NA | Each 45 mg ustekinumab prefilled syringe also contains: L-histidine and L-histidine monohydrochloride monohydrate (0.5 mg), Polysorbate 80 (0.02 mg), and sucrose (38 mg) to fill to a final volume of 0.5 mL. | solution fro injection | Subcutaneous | In case of psoriasis, for patients weighing ≤ 100 kg (220 lbs), the recommended dose is 45 mg initially and 4 weeks later, followed by 45 mg every 12 weeks. In case of Psoriatic Arthritis ecommended dose is 45 mg initially and 4 weeks later, followed by 45 mg every 12 weeks. | NA | Adverse reactions that occurred at rates less than 1% in the controlled period of Ps STUDIES 1 and 2 through week 12 included: cellulitis, herpes zoster, diverticulitis and certain injection site reaction | Link | NA | NA |
| 10840 | Th1203 | Peginterferon beta-1a | >Th1203_Peginterferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 22500 | NA | 9.02 | NA | NA | Approximately 78 hours | Peginterferon beta-1a is an interferon beta-1a to which a single, linear 20,000 dalton (Da) methoxy poly(ethyleneglycol)-O-2-methylpropionaldehyde molecule is covalently attached to the alpha amino group of the N-terminal amino acid residue. The interferon beta-1a portion is produced as a glycosylated protein using genetically-engineered Chinese hamster ovary cells into which the human interferon beta gene has been introduced. The amino acid sequence of the recombinant interferon beta-1a is identical to that of the human interferon beta counterpart. | For the treatment of patients with relapsing forms of multiple sclerosis. | There is no biochemical or physiologic effect known to relate directly to the clinical effect of PLEGRIDY. | The mechanism by which PLEGRIDY exerts its effects in patients with multiple sclerosis is unknown. | LD50 information for peginterferon beta-1a is not readily available in the literature. In clinical trials, no cases of overdoses occurred with the administration of interferon beta-1a at a dose of 75 µg administered subcutaneously 3 times a week.[L31428] In a case report, a 38-year-old patient attempted suicide with about 6 or 7 pre-filled syringes containing 44 mug (12 MIU) of subcutaneous interferon beta-1a; symptoms were limited to malaise and skin erythema, which resolved within 24 hours with no intervention. Laboratory test results were unremarkable.[A191871] In the case of an overdose with interferon-beta 1a, prescribing information suggests to contact the local poison control centre.[L31438] | Peginterferon beta-1a is not extensively metabolized in the liver.[L31428] | Peginterferon beta-1a is almost completely absorbed after subcutaneous administration. After 125 microgram subcutaneous doses of peginterferon beta-1a to patient with MS, a Cmax of 280 pg/mL was reached between 1 and 1.5 days[A227983], and the AUC over a 14 day dosing interval was 34.8 ng.hr/mL.[L31428] The AUC ranges from 23.5-29.5 ng ml-1h, according to one pharmacokinetic study of patients with MS. Impairment of renal function may alter the Cmax and AUC of interferon beta-1a.[A227983] | The volume of distribution of peginterferon beta-1a is about 481 L.[L31428] One pharmacokinetic study of patients administered interferon beta-1a revealed a volume of distribution in the range of 248-726 L, depending on the week of treatment.[A227983] | The average steady state clearance of peginterferon beta-1a is about 4.1 L/h.[L31428] One pharmacokinetic study revealed a clearance within the range of 3.68-7.89 L/h, depending on the week of treatment.[A227983] | NA | NA | NA | NA | Theophylline, Zidovudine | Interferon alpha/beta receptor 1 | Plegridy | Biogen Canada Inc | Biogen Canada Inc | PLEGRIDY (peginterferon beta-1a) is indicated for the treatment of patients with relapsing forms of multiple sclerosis. | Methoxy poly(ethyleneglycol)-O-2-methylpropionaldehyde | Prefilled glass syringe containing 0.5 mL of a sterile solution in water for injection of 63, 94, or 125 micrograms of peginterferon beta-1a | Sterile Solution | Subcutaneous | The recommended dosage of PLEGRIDY is 125 micrograms injected subcutaneously every 14 days. | PLEGRIDY is contraindicated in patients with a history of hypersensitivity to natural or recombinant interferon beta or peginterferon, or any other component of the formulation | Hepatic Injury; Depression and Suicide; Seizures; Anaphylaxis and Other Allergic Reactions; Injection Site Reactions; Congestive Heart Failure; Decreased Peripheral Blood Counts; Thrombotic Microangiopathy; Autoimmune Disorders. | Link | NA | NA |
| 10845 | Th1208 | Metreleptin | >Th1208_Metreleptin MVPIQKVQDDTKTLIKTIVTRINDISHTQSVSSKQKVTGLDFIPGLHPILTLSKMDQTLAVYQQILTSMPSRNVIQISNDLENLRDLLHVLAFSKSCHLPWASGLETLDSLGGVLEASGYSTEVVALSRLQGSLQDMLWQLDLSPGC | 16155.44 | C714H1167N191O221S6 | NA | NA | NA | 3.8 to 4.7 hours | Metreleptin, a recombinant analog of the human hormone leptin, is an orphan drug used to treat complications of leptin deficiency in people with congenital or acquired lipodystrophy. Affecting less than 500 people worldwide, lipodystrophy is characterized by a lack of adipose tissue, fat deposition in the muscles and liver, and metabolic complications such as hypertriglyceridemia, insulin resistance, diabetes mellitus, and fatty liver disease. These metabolic abnormalities are often aggravated by excessive food intake, which is further aggravated by leptin deficiency, a protein secreted by adipose tissue. Administration of Metreleptin results in improvement of metabolic symptoms including improvements in insulin resistance, reduced HbA1c and fasting glucose, reduced triglycerides, and reductions in food intake. Metreleptin is produced in E. coli and differs from native human leptin by the addition of a methionine residue at its amino terminus. It is administered as a once daily subcutaneous injection. On Feb. 24, 2014, Metreleptin was approved by the FDA for the treatment of complications of leptin deficiency, in addition to diet, in patients with congenital generalized or acquired generalized lipodystrophy. Metreleptin is marketed under the brand Myalept® by Aegerion Pharmaceuticals, Inc. | It is indicated as an adjunct to diet as replacement therapy to treat the complications of leptin deficiency in patients with congenital or acquired generalized lipodystrophy. | In patients with leptin deficiency, clinical trials demonstrated that exogenous leptin administration results in weight loss, reduction in mean HbA1c and fasting glucose levels, reduced blood insulin, and reduced triglyceride levels leading to improved insulin sensitivity and reductions in food intake. | Metreleptin functions by binding to and activating the human leptin receptor (ObR), which belongs to the Class I cytokine family of receptors that signals through the JAK/STAT transduction pathway. | The most common adverse events reported for metreleptin use have been headache, hypoglycemia, weight loss, and abdominal pain. A boxed warning states that anti-metreleptin antibodies, serious infections, and worsening metabolic control have been reported in patients taking the drug, and that some patients with acquired generalized lipodystrophy taking metreleptin have developed T-cell lymphoma. Anti-metreleptin antibodies with neutralizing activity have been identified in patients treated with metreleptin which can lead to inhibition of endogenous leptin action and loss of drug efficacy. As part of a Risk Evaluation and Mitigation Strategy (REMS), the FDA has required healthcare providers to be trained in the use of metreleptin before prescribing it and to attest that patients for whom they prescribe metreleptin have a labeled indication for the drug. Metreleptin is classified as category C (no adequate studies in women) for use during pregnancy. Two-year carcinogenicity studies in rodents have not been conducted with metreleptin. No proliferative or preneoplastic lesions were observed in mice or dogs following treatment up to six months. However, leptin is reported in the literature to promote cell proliferation in vitro and tumor progression in some mouse models of cancer. Metreleptin was not mutagenic in the Ames bacterial mutagenicity assay or clastogenic in an in vitro chromosomal aberration assay in Chinese hamster ovary cells and human peripheral blood lymphocytes. Metreleptin was not mutagenic or clastogenic in an in vivo mouse micronucleus assay. In a fertility study in mice, metreleptin had no adverse effects on mating, fertility, or early embryonic development at doses ranging between 7 and 15 times the maximum recommended clinical dose based on body surface area of a 20- and 60-kg patient, respectively. | No formal metabolism studies have been conducted with metreleptin. Nonclinical data indicate renal clearance is the major route of metreleptin elimination, with no apparent contribution of systemic metabolism or degradation. | Peak serum leptin concentration (Cmax) occurred approximately 4.0 to 4.3 hours after subcutaneous administration of single doses ranging from 0.1 to 0.3 mg/kg in healthy subjects. | Following intravenous administration of metreleptin, leptin volume of distribution was approximately 4 to 5 times plasma volume; volumes (mean ± SD) were 370 ± 184 mL/kg, 398 ± 92 mL/kg, and 463 ± 116 mL/kg for 0.3, 1.0, and 3.0 mg/kg/day doses, respectively. | The clearance of metreleptin is expected to be delayed in the presence of leptin antibodies. | Adipokines,Alimentary Tract and Metabolism,Amino Acids and Derivatives,Amino Acids, Peptides, and Proteins,Analogs/Derivatives,Biological Factors,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Intercellular Signaling Peptides and Proteins,Leptin Analog,Obesity, drug therapy,Peptide Hormones,Peptides,Proteins | US20070099836 | 29-11-2006 | 29-11-2026 | Chlorotrianisene, Chlorpropamide, Cyclosporine, Dienogest, Etonogestrel, Gliclazide, Glimepiride, Glipizide, Glyburide, Insulin Aspart, Insulin Degludec, Insulin Detemir, Insulin Glargine, Insulin Glulisine, Insulin Human, Insulin Lispro, Levonorgestrel, Medroxyprogesterone acetate, Norethisterone, Theophylline, Tolazamide, Tolbutamide, Warfarin | Leptin receptor | Myalept | Amylin Pharmaceuticals, LLC | Amylin Pharmaceuticals, LLC | MYALEPT (metreleptin) for injection is indicated as an adjunct to diet as replacement therapy to treat the complications of leptin deficiency in patients with congenital or acquired generalized lipodystrophy. | NA | NA | Lyophilized powder for solution | subcutaneous | The starting daily dose (injection volume) should be 0.06 mg/kg for a baseline weight of less than 40kg. For a weight greater than 40 kg, the starting dose should be 2.5 mg (0.5 mL) for males and 5 mg (1 mL) for females. | MYALEPT is contraindicated in patients with general obesity not associated with congenital leptin deficiency. MYALEPT has not been shown to be effective in treating general obesity, and the development of anti-metreleptin antibodies with neutralizing activity has been reported in obese patients treated with MYALEPT; Also, is contraindicated in patients with prior severe hypersensitivity reactions to metreleptin or to any of the product components. Known hypersensitivity reactions have included urticaria and generalized rash. | As observed from an open-lable single-arm study the most frequesnt reactions were headache, hypoglycaemia, decreased weight, abdominal pain, athralgia, dizziness, ear infection, fatigue, nausea, ovarian cyst, upper respiratory tract infection, anaemia, diarrhea, back pain, paresthesia, proteinuria, pyrexia. | Link | NA | NA |
| 10847 | Th1210 | Mepolizumab | NA | 149000 | NA | NA | NA | NA | 16 to 22 days. | Mepolizumab is a humanized IL-5 antagonist monoclonal antibody produced by recombinant DNA technology in Chinese hamster ovary cells. It has a molecular weight of approximately 149 kDa. It was approved by the FDA in November, 2015 for the treatment of asthma under the brand name Nucala (marketed by GlaxoSmithKline). Mepolizumab has been investigated in the treatment of severe nasal polyposis, among numerous other conditions. | Mepolizumab is indicated for add-on maintenance treatment of severe eosinophilic asthma, as identified by blood eosinophils greater than or equal to 150 cells/μl at initiation of treatment or blood eosinophils greater than or equal to 300 cells/μl in the past 12 months, in patients aged 12 years and older. Mepolizumab has been shown to reduce exacerbations of asthma in patients with an exacerbation history | The pharmacodynamic response (blood eosinophil reduction) following repeat doses of mepolizumab administered subcutaneously or intravenously was evaluated in subjects with asthma and blood eosinophil levels greater than 200 cells/mcL. Subjects received 1 of 4 mepolizumab treatments (administered every 28 days for a total of 3 doses): 12.5 mg SC, 125 mg SC, 250 mg SC, or 75 mg IV. Sixty-six (66) of the 70 randomized subjects completed the trial. Compared with baseline levels, blood eosinophils decreased in a dose-dependent manner. A reduction in blood eosinophil levels was observed in all treatment groups by Day 3. On Day 84 (4 weeks post-last dose), the observed geometric mean reduction from baseline in blood eosinophils was 64%, 78%, 84%, and 90% in the 12.5-mg SC, 75-mg IV, 125-mg SC, and 250-mg SC treatment groups, respectively. The model-predicted SC doses providing 50% and 90% of maximal reduction of blood eosinophils at Day 84 were estimated to be 11 and 99 mg, respectively. These results, along with the clinical efficacy data from the dose-ranging exacerbation trial (Trial 1) supported the evaluation of mepolizumab 75 mg IV and 100 mg SC in the confirmatory trials [see Clinical Studies (14)]. Following SC administration of mepolizumab 100 mg every 4 weeks for 32 weeks (Trial 2), blood eosinophils were reduced to a geometric mean count of 40 cells/mcL, which corresponds to a geometric mean reduction of 84% compared with placebo. This magnitude of reduction was observed within 4 weeks of treatment and was maintained throughout the treatment period | Mepolizumab is an interleukin-5 antagonist (IgG1 kappa). IL-5 is the major cytokine responsible for the growth and differentiation, recruitment, activation, and survival of eosinophils. Mepolizumab binds to IL-5 with a dissociation constant of 100 pM, inhibiting the bioactivity of IL-5 by blocking its binding to the alpha chain of the IL-5 receptor complex expressed on the eosinophil cell surface. Inflammation is an important component in the pathogenesis of asthma. Multiple cell types (e.g., mast cells, eosinophils, neutrophils, macrophages, lymphocytes) and mediators (e.g., histamine, eicosanoids, leukotrienes, cytokines) are involved in inflammation. Mepolizumab, by inhibiting IL-5 signaling, reduces the production and survival of eosinophils; however, the mechanism of mepolizumab action in asthma has not been definitively established. | Toxicity information regarding mepolizumab is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as newly established or worsening chronic infections, including those caused by helminths, and generalized immune depression. Symptomatic and supportive measures are recommended.[L16518] | As a monoclonal antibody, mepolizumab is subject to proteolytic degradation at sites distributed throughout the body.[L16518] | Mepolizumab is administered subcutaneously and has a bioavailability of approximately 80% based on a 100 mg dose given to both adult and adolescent subjects with asthma. With the recommended four-week dosing schedule, there is an approximately two-fold accumulation of mepolizumab at steady-state.[L16518] | Mepolizumab has a population central volume of distribution of 3.6 L (for a 70 kg individual) in adult asthma patients.[L16518] | Mepolizumab has an estimated apparent population systemic clearance of 0.28 L/day (for a 70-kg individual) in adult and adolescent subjects.[L16518] | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Blood Proteins,Drugs for Obstructive Airway Diseases,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Interleukin-5 Antagonist,Proteins,Serum Globulins | US2008134721 | NA | NA | NA | Interleukin-5 | Nucala | Glaxosmithkline Inc | Glaxosmithkline Inc | NUCALA® is indicated for the add-on maintenance treatment of patients with severe asthma aged 12 years and older, and with an eosinophilic phenotype. | NA | 100 mg/mL | lyophilized powder | subcutaneous | The recommended dose of NUCALA is 100 mg administered once every 4 weeks by subcutaneous injection into the upper arm, thigh, or abdomen. | NUCALA should not be administered to patients with a history of hypersensitivity to mepolizumab or excipients in the formulation. | Hypersensitivity reactions; Opportunistic infections: herpes zoster | Link | NA | NA |
| 10848 | Th1211 | Ixekizumab | >Th1211_Ixekizumab QVQLVQSGAEVKKPGSSVKVSCKASGYSFTDYHIHWVRQAPGQGLEWMGVINPMYGTTDYNQRFKGRVTITADESTSTAYMELSSLRSEDTAVYYCARYDYFTGTGVYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 1,46,158 | C6492H10012N1728O2028S46 | NA | NA | NA | 13 days | Ixekizumab is a humanized immunoglobulin G subclass 4 (IgG4) monoclonal antibody (mAb) with neutralizing activity against IL-17A. Ixekizumab is produced by recombinant DNA technology in a recombinant mammalian cell line and purified using standard technology for bioprocessing. Ixekizumab is comprised of two identical light chain polypeptides of 219 amino acids each and two identical heavy chain polypeptides of 445 amino acids each, and has a molecular weight of 146,158 Daltons for the protein backbone of the molecule. | For the treatment of adults with moderate-to-severe plaque psoriasis who are candidates for systemic therapy or phototherapy | No formal pharmacodynamic studies have been conducted with TALTZ. | Ixekizumab is a humanized IgG4 monoclonal antibody that selectively binds with the interleukin 17A (IL-17A) cytokine and inhibits its interaction with the IL-17 receptor. IL-17A is a naturally occurring cytokine that is involved in normal inflammatory and immune responses. Ixekizumab inhibits the release of proinflammatory cytokines and chemokines. | The most common adverse reactions associated with Ixekizumab treatment are injection site reactions, upper respiratory tract infections, nausea, and tinea infections. | The metabolic pathway of ixekizumab has not been characterized. As a humanized IgG4 monoclonal antibody ixekizumab is expected to be degraded into small peptides and amino acids via catabolic pathways in the same manner as endogenous IgG. | Following a single subcutaneous dose of 160 mg in subjects with plaque psoriasis, ixekizumab reached peak mean (±SD) serum concentrations (Cmax) of 16.2 ±6.6 mcg/mL by approximately 4 days post dose. | The mean (geometric CV%) volume of distribution at steady-state was 7.11 L (29%) in subjects with plaque psoriasis. | 0.39 L/day | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic and Immunomodulating Agents,Blood Proteins,Dermatologicals,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Interleukin Inhibitors,Interleukin-17,Interleukin-17A Antagonist,Misc. Skin and Mucous Membrane Agents,Proteins,Serum Globulins | NA | NA | NA | NA | Interleukin-17A | Taltz | Eli lilly | Eli lilly | Taltz is indicated for the treatment of moderate to severe plaque psoriasis in adults who are candidates for systemic therapy or phototherapy. | NA | 80 mg of ixekizumab in a 1 mL single-dose prefilled autoinjector or a single-dose prefilled syringe | Sterile, preservative free, clear and colorless to slightly yellow solution | Subcutaneous | TALTZ is administered by subcutaneous injection. The recommended dose is 160 mg (two 80 mg injections) at Week 0, followed by 80 mg at Weeks 2, 4, 6, 8, 10, and 12, then 80 mg every 4 weeks. | TALTZ is contraindicated in patients with a previous serious hypersensitivity reaction, such as anaphylaxis, to ixekizumab or to any of the excipients | Infections; Hypersensitivity Reactions; Inflammatory Bowel Disease | Link | NA | NA |
| 10849 | Th1212 | Insulin Pork | >Th1212_Insulin_Pork GIVEQCCTSICSLYQLENYCN | 5795.6 | C257H387N65O76S6 | 5.39 | 0.218 | NA | NA | Insulin isolated from pig pancreas. Composed of alpha and beta chains, processed from pro-insulin. Forms a hexameric structure. | For the treatment of type I and II diabetes mellitus. | Insulin is used in the treatment of type I and type II diabetes. The primary activity of insulin is the regulation of glucose metabolism. In muscle and other tissues (except the brain), insulin causes rapid transport of glucose and amino acids intracellularly. It also promotes anabolism, and inhibits protein catabolism. In the liver, insulin promotes the uptake and storage of glucose in the form of glycogen, inhibits gluconeogenesis, and promotes the conversion of excess glucose into fat. | Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism. | NA | Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process. | NA | NA | NA | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Insulin,Insulin, Short-Acting,Insulins and Analogues for Injection, Fast-Acting,Pancreatic Hormones,Peptide Hormones,Peptides,Protein Precursors,Proteins | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | Iletin II | Lilly | Lilly | NA | NA | 100 units/mL (U-100) | sterile suspension | Subcutaneous | NA | NA | NA | Link | NA | NA |
| 10850 | Th1213 | Insulin Degludec | >Th1213_Insulin_Degludec GIVEQCCTSICSLYQLENYCN | 6103.97 | C274H411N65O81S6 | NA | NA | NA | approximately 25 hours | Insulin degludec differs from human insulin in that the amino acid threonine in position B30 has been omitted and a side-chain consisting of glutamic acid and a C16 fatty acid has been attached. | Indicated to improve glycemic control in adults with diabetes mellitus. | The glucose-lowering effect of TRESIBA after 8 days of once-daily dosing was measured in a euglycemic glucose clamp study enrolling 21 patients with type 1 diabetes. Figure 2 shows the pharmacodynamic effect of TRESIBA over time following 8 once-daily subcutaneous injections of 0.4 U/kg of TRESIBA in patients with type 1 diabetes. | The primary activity of insulin, including TRESIBA, is regulation of glucose metabolism. Insulin and its analogs lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production. Insulin also inhibits lipolysis and proteolysis, and enhances protein synthesis. TRESIBA forms multi-hexamers when injected into the subcutaneous tissue resulting in a subcutanous insulin degludec depot. The protracted time action profile of TRESIBA is predominantly due to delayed absorption of insulin degludec from the subcutaneous tissue to the systemic circulation and to a lesser extent due to binding of insulin-degludec to circulating albumin. | Observe for signs and symptoms of hypoglycemia, hypokalemia, and fluid retention and heart failure with concomitant use of Thiazolidinediones. Pregnancy Category C | All insulin degludec metabolites are inactive. | In patients with type 1 diabetes, after 8 days of once daily subcutaneous dosing with 0.4 U/kg, maximum degludec concentrations of 4472 pmol/L were attained at a median of 9 hours (tmax). After the first dose of, median onset of appearance was around one hour. The glucose lowering effect lasted at least 42 hours after the last of 8 once-daily injections. Insulin degludec concentration reach steady state levels after 3-4 days. | NA | The mean apparent clearance of insulin degludec is 0.03 L/kg (2.1 L/h in 70 kg individual) after single subcutaneous dose of 0.4 units/kg. | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | Tresiba | Novo Nordisk | Novo Nordisk | TRESIBA is indicated to improve glycemic control in adults with diabetes mellitus. | LysB29(Ns-hexadecandioyl-y-Glu) des(B30) human insulin | 100 units/mL (U-100) or 200 units/mL (U-200). | sterile, aqueous, clear, and colorless solution | Subcutaneous | Inject TRESIBA subcutaneously once-daily at any time of day. The recommended starting dose of TRESIBA in insulin naive patients with type 1 diabetes is approximately one-third to one-half of the total daily insulin dose. As a general rule, 0.2 to 0.4 units of insulin per kilogram of body weight can be used to calculate the initial total daily insulin dose in insulin naive patients with type 1 diabetes. The recommended starting dose of TRESIBA in insulin naive patients with type 2 diabetes mellitus is 10 units once daily. | During episodes of hypoglycemia; In patients with hypersensitivity to TRESIBA or one of its excipients. | Hypoglycemia; Hypersensitivity and allergic reactions; Hypokalemia. | Link | NA | NA |
| 10858 | Th1220 | Brodalumab | NA | 1,44,000 | C6372H9840N1712O1988S52 | NA | NA | NA | NA | Brodalumab has been used in trials studying the treatment of Asthma, Psoriasis, Crohn's Disease, Psoriatic Arthritis, and Rheumatoid Arthritis. Brodalumab was FDA approved in February, 2017 as Siliq for the treatment of moderate-to-severe plaque psoriasis. | Brodalumab has been approved for the treatment of psoriasis vulgaris, psoriatic arthritis, pustular psoriasis and psoriatic erythroderma. | Increase in the level of IL-17 due to blocking of its receptors. | Brodalumab binds with high affinity to interleukin (IL)-17 receptor A, thereby inhibiting several pro-inflammatory cytokines from the IL-17 family. | NA | NA | NA | 4.62 L. | 0.223 L/day. | Antineoplastic and Immunomodulating Agents | NA | NA | NA | The risk or severity of adverse effects can be increased with combination of drugs like BCG, Denosumab, Fingolimod, G17DT, GI-5005, INGN 201, INGN 225, Leflunomide, Natalizumab, Pimecrolimus. | Interleukin 17 receptor A | Siliq | NA | NA | SILIQ™ is indicated for the treatment of moderate to severe plaque psoriasis in adult patients who are candidates for systemic therapy or phototherapy and have failed to respond or have lost response to other systemic therapies. | NA | Each SILIQ single-dose prefilled syringe delivers 1.5 mL of solution containing 210 mg of brodalumab formulated in glutamate (6.5 mg), polysorbate 20 (0.15 mg), proline (36 mg), and Water for Injection, USP at pH 4.8. | sterile, preservative-free, clear to slightly opalescent, colorless to slightly yellow solution | Subcutaneous | The recommended SILIQ dose is 210 mg administered by subcutaneous injection at Weeks 0, 1, and 2 followed by 210 mg every 2 weeks. | SILIQ is contraindicated in patients with Crohn’s disease because SILIQ may cause worsening of disease | Suicidal Ideation and Behavior, Infection and Crohn’s Disease | Link | NA | NA |
| 10860 | Th1222 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant, human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It is expressed in a murine Sp2/0-Ag14 cell line and comprised of two 447- (or 448-) residue heavy chains and two 214-residue light chains, with a molecular mass of 145157 Daltons when deglycosylated. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at asparagine 298 (Asn 298). Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). Canakinumab is marketed under the brand name Ilaris and indicated for patients 4 years of age and older to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS) as well as for patients 2 years of age and older to treat systemic juvenile idiopathic arthritis (SJIA). Clinical trials have established the administration of canakinumab every 2 weeks to be safe and effective, offering a considerable advantage over the existing treatment with the human IL-1 receptor antagonist, anakinra, which must be injected daily and which is often poorly tolerated by patients. | Used in patients 4 years of age and older to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS) as well as for patients 2 years of age and older to treat systemic juvenile idiopathic arthritis (SJIA). | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | * 6.01 L [typical CAPS patient weighing 70 kg] | * 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | The risk or severity of adverse effects can be increased when Canakinumab is combined with Adalimumab, Afelimomab, Anakinra, BCG, Certolizumab pegol, Denosumab, Etanercept, Fingolimod, G17DT, GI-5005 etc | Interleukin-1 beta | Ilaris | Novartis | Novartis | Ilaris is used to treat certain types of periodic fever syndromes, sometimes called auto-inflammatory syndromes. | NA | Each vial of sterile, white, preservative-free, lyophilized powder contains canakinumab 150 mg. Nonmedicinal ingredients: sucrose, L-histidine, L-histidine HCL monohydrate, polysorbate 80. | Lyphilized powder | Subcutaneous | The recommended dose of Ilaris is 150 mg for CAPS patients with body weight greater than 40 kg. For CAPS patients with body weight greater than or equal to 15 kg and less than or equal to 40 kg, the recommended dose is 2 mg/kg. For children 15 to 40 kg with an inadequate response, the dose can be increased to 3 mg | Confirmed hypersensitivity to the active substance or to any of the excipients. | The most common adverse reactionsgreater than 10% reported by patients treated with ILARISare nasopharyngitis, diarrhea, influenza, rhinitis, nausea, headache, bronchitis, gastroenteritis, pharyngitis, weight increased, musculoskeletal pain, and vertigo. | Link | NA | NA |
| 10861 | Th1223 | Chorionic Gonadotropin (Human) | >Th1223_Chorionic_Gonadotropin_(Human) APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | NA | NA | NA | NA | NA | NA | Human chorionic gonadotropin (HCG), a polypeptide hormone produced by the human placenta. Endogenously produced HCG interacts with the LHCG receptor of the ovary and promotes the maintenance of the corpus luteum during the beginning of pregnancy. This allows the corpus luteum to continuously secrete the hormone progesterone during the first trimester, which is required for maintenance of the uterus and prevents menstruation. In males, HCG also stimulates the production of gonadal steroid hormones by stimulating the interstitial cells (Leydig cells) of the testis to produce androgens. HCG is composed of an alpha and a beta sub-unit. The alpha sub-unit is essentially identical to the alpha sub units of the human pituitary gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), as well as to the alpha sub-unit of human thyroid-stimulating hormone (TSH), while the beta sub units of these hormones differ in amino acid sequence. As a drug product, chorionic gonadotropin is a highly purified pyrogen-free preparation obtained from the urine of pregnant females. | For the treatment of prepubertal cryptorchidism (not due to anatomical obstruction), for the treatment of selected cases of hypogonadotropic hypogonadism (hypogonadism secondary to a pituitary deficiency) in males and for the induction of ovulation and pregnancy in the anovulatory, infertile woman in whom the cause of anovulation is secondary and not due to primary ovarian failure, and who has been appropriately pretreated with human menotropins. | he action of HCG is virtually identical to that of pituitary LH, although HCG appears to have a small degree of FSH activity as well. It stimulates production of gonadal steroid hormones by stimulating the interstitial cells (Leydig cells) of the testis to produce androgens and the corpus luteum of the ovary to produce progesterone. | NA | NA | NA | NA | NA | NA | Hormones | US6706681 | 16-03-2004 | 16-03-2021 | NA | Lutropin-choriogonadotropic hormone receptor | Ovidrel | Emd Serono | Emd Serono | It is indicated for the induction of final follicular maturation and early luteinization in infertile women who have undergone pituitary desensitization and who have been appropriately pretreated with follicle stimulating hormones as part of an Assisted Reproductive Technology (ART) program such as in vitro fertilization and embryo transfer. It is also indicated for the induction of ovulation (OI) and pregnancy in anovulatory infertile patients in whom the cause of infertility is functional and not due to primary ovarian failure. | NA | Each Ovidrel® PreFilled Syringe is filled with 0.515 mL containing 257.5 μg of choriogonadotropin alfa, 28.1 mg mannitol, 505 μg 85% O-phosphoric acid, 103 μg L-methionine, 51.5 μg Poloxamer 188, Sodium Hydroxide (for pH adjustment), and Water for Injection to deliver 250 μg of choriogonadotropin alfa in 0.5 mL. The pH of the solution is 6.5 to 7.5. | Injection, solution | Subcutaneous | Ovidrel® PreFilled Syringe 250 μg should be administered one day following the last dose of the follicle stimulating agent. Ovidrel® PreFilled Syringe should not be administered until adequate follicular development is indicated by serum estradiol and vaginal ultrasonography. | Ovidrel® PreFilled Syringe (choriogonadotropin alfa injection) is contraindicated in women who exhibit:Prior hypersensitivity to hCG preparations or one of their excipients.Primary ovarian failure.Uncontrolled thyroid or adrenal dysfunction.An uncontrolled organic intracranial lesion such as a pituitary tumor.Abnormal uterine bleeding of undetermined origin (see “Selection of Patientsâ€Â).Ovarian cyst or enlargement of undetermined origin (see “Selection of Patientsâ€Â).Sex hormone dependent tumors of the reproductive tract and accessory organs.Pregnancy. | Redness or pain at the injection site, mild abdominal pain, mood changes, or mild nausea/vomiting may occur. | Link | NA | NA |
| 10862 | Th1223 | Chorionic Gonadotropin (Human) | >Th1223_Chorionic_Gonadotropin_(Human) APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | NA | NA | NA | NA | NA | NA | Human chorionic gonadotropin (HCG), a polypeptide hormone produced by the human placenta. Endogenously produced HCG interacts with the LHCG receptor of the ovary and promotes the maintenance of the corpus luteum during the beginning of pregnancy. This allows the corpus luteum to continuously secrete the hormone progesterone during the first trimester, which is required for maintenance of the uterus and prevents menstruation. In males, HCG also stimulates the production of gonadal steroid hormones by stimulating the interstitial cells (Leydig cells) of the testis to produce androgens. HCG is composed of an alpha and a beta sub-unit. The alpha sub-unit is essentially identical to the alpha sub units of the human pituitary gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), as well as to the alpha sub-unit of human thyroid-stimulating hormone (TSH), while the beta sub units of these hormones differ in amino acid sequence. As a drug product, chorionic gonadotropin is a highly purified pyrogen-free preparation obtained from the urine of pregnant females. | For the treatment of prepubertal cryptorchidism (not due to anatomical obstruction), for the treatment of selected cases of hypogonadotropic hypogonadism (hypogonadism secondary to a pituitary deficiency) in males and for the induction of ovulation and pregnancy in the anovulatory, infertile woman in whom the cause of anovulation is secondary and not due to primary ovarian failure, and who has been appropriately pretreated with human menotropins. | he action of HCG is virtually identical to that of pituitary LH, although HCG appears to have a small degree of FSH activity as well. It stimulates production of gonadal steroid hormones by stimulating the interstitial cells (Leydig cells) of the testis to produce androgens and the corpus luteum of the ovary to produce progesterone. | NA | NA | NA | NA | NA | NA | Hormones | US6706681 | 16-03-2004 | 16-03-2021 | NA | Lutropin-choriogonadotropic hormone receptor | Pregnyl | Physicians Total Care, Inc. | Physicians Total Care, Inc. | It is used for treating fertility problems in certain women who have not gone through menopause. Treating certain testicular development problems and stimulating the development of secondary sexual characteristics in certain patients. It is also used to treat boys 4 to 9 years old who have testicles that have not moved into the scrotum. | NA | Available in vials containing 10,000 USP units of sterile dried powder with 5 mg monobasic sodium phosphate and 4.4 mg dibasic sodium phosphate. If required, pH is adjusted with sodium hydroxide and/or phosphoric acid. Each package also contains a 10-mL vial of solvent containing: water for injection with 0.56% sodium chloride and 0.9% BENZYL ALCOHOL, WHICH IS NOT FOR USE IN NEWBORNS. If required, pH is adjusted with sodium hydroxide and/or hydrochloric acid. | Injection, Solution | Intramuscular, Subcutaneous | 4000 USP units 3 times weekly for 3 weeks. | Precocious puberty, prostatic carcinoma or other androgen-dependent neoplasm, prior allergic reaction to HCG. | Headache, irritability, restlessness, depression, fatigue, edema, precocious puberty, gynecomastia, pain at the site of injection. | Link | NA | NA |
| 10863 | Th1224 | Chorionic Gonadotropin (Recombinant) | >Th1224_Chorionic_Gonadotropin_(Recombinant) APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 25719.7 | C1105H1770N318O336S26 | 8.61 | -0.258 | 55 °C | The mean terminal half-life is about 29 ± 6 hours (initial half-life is 4.5 ± 0.5 hours). | Recombinant human chorionic gonadotropin with 2 subunits, alpha = 92 residues, beta = 145 residues, each with N-and O-linked carbohydrate moieties linked to ASN-52 and ASN-78 (on alpha subunit) and ASN-13, ASN-30, SER-121, SER-127, SER-132 and SER-138 (on beta subunit). The primary structure of the alpha-chain of r-hCG is identical to that of the alpha-chain of hCG, FSH and LH. | For the treatment of female infertility | Choriogonadotropin alfa is used to treat female infertility, Choriogonadotropin alfa stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Ovidrel is an analogue of Luteinizing Hormone (LH) and binds to the LH/hCG receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Choriogonadotropin alfa binds to the Follicle stimulating hormone receptor which results in ovulation in the absence of sufficient endogenous Luteinizing hormone. | NA | NA | NA | NA | NA | Hormones | US5767251 | 16-06-1998 | 16-06-2015 | NA | Lutropin-choriogonadotropic hormone receptor, Follicle-stimulating hormone receptor | Ovitrelle | Merck Serono Europe Limited | Merck Serono Europe Limited | Ovitrelle is indicated in the treatment of:women undergoing superovulation prior to assisted reproductive techniques such as in vitro fertilisation (IVF): Ovitrelle is administered to trigger final follicular maturation and luteinisation after stimulation of follicular growth;anovulatory or oligo-ovulatory women: Ovitrelle is administered to trigger ovulation and luteinisation in anovulatory or oligo-ovulatory patients after stimulation of follicular growth. | NA | Each pre-filled syringe contains 250 micrograms choriogonadotropin alfa* (equivalent to approximately 6,500 IU) in 0.5 mL solution | powder and solvent to be made up into a solution | Subcutaneous | One pre-filled syringe of Ovitrelle (250 micrograms) is administered 24 to 48 hours after the last administration of a follicle stimulating hormone (FSH) or human menopausal gonadotropin (hMG) preparation, i.e. when optimal stimulation of follicular growth is achieved. | hypersensitive (allergic) to choriogonadotropin alfa or any of the other ingredients. | The most common side effects with Ovitrelle (seen in between 1 and 10 patients in 100) are reactions at the injection site, headache, tiredness, vomiting, nausea (feeling sick), abdominal pain (stomach ache) and ovarian hyperstimulation syndrome (such as feeling sick, weight gain and diarrhoea). Ovarian hyperstimulation syndrome occurs when the ovaries over respond to treatment, especially when medicines to trigger ovulation have been used. | Link | NA | NA |
| 10872 | Th1232 | Lenograstim | NA | 18668 | C840-H1330-N222-O242-S8 | NA | NA | NA | The pharmacokinetic profile of lenograstim is similar in healthy volunteers and cancer patients with elimination half-life (t½β) values of 2.3 - 3.3 hrs (volunteers); 2.8-7.5 hrs (cancer patients) following sc administration, and 0.8 - 2.1 hrs (volunteers); 1.1 - 4.0 hrs (cancer patients) following iv administration. | Lenograstim is a recombinant granulocyte colony-stimulating factor which functions as an immunostimulator. | The drug is used to reduce the risk of life-threatening infection in patients with neutropenia, particularly after cytotoxic chemotherapy. GRANOCYTE ( Lenograstim) is indicated as a treatment to reduce the duration of neutropenia and the severity of infections in patients with non-myeloid malignancy who have undergone autologous or allogeneic bone marrow transplantation, or treatment with established cytotoxic chemotherapy and in addition to reduce the incidence of infection associated with established cytotoxic chemotherapy. GRANOCYTE is also indicated to mobilise peripheral blood progenitor cells (PBPCs) with GRANOCYTE alone, or after myelosuppressive chemotherapy, in order to accelerate haematopoietic recovery by infusion of such cells, after myelosuppressive or myeloablative therapy. GRANOCYTE is also indicated to accelerate the engraftment of these cells after their reinfusion. GRANOCYTE is also indicated for the treatment of severe chronic neutropenia including congenital agranulocytosis (Kostmann's syndrome). | Lenograstim has been confirmed as a valuable adjunct to minimise the haematological toxicity of myelosuppressive chemotherapy in patients with malignant disease. The drug also enhances neutrophil recovery in patients undergoing stem cell rescue, and assists PBSC mobilisation. | Lenograstim is the glycosylated recombinant form of human granulocyte colony stimulating factor. Lenograstim accelerates neutrophil recovery significantly after chemotherapy, with beneficial effects on clinical end-points such as incidence of laboratory-confirmed infection and length of hospital stay. Chemotherapy dose intensity has also been increased in patients receiving lenograstim, notably those with breast or small cell lung cancer, although improvements in tumour response and survival have not been demonstrated. Lenograstim also assists neutrophil recovery in patients undergoing bone marrow transplantation, and stimulates the production of peripheral blood stem cells (PBSCs) for autologous transfusion after aggressive chemotherapy. | Species observed : Human (Man) Test type: TDLo ( Lowest Published Toxic Dose) Route of exposure: Subcutaneous Dose/Duration: 21428mg/kg/15 Toxic Effect: Skin and appendages: Dermatitis, allergic ( after systemic exposure ) Species observed : Rodent - Rat Test type: LD50 Route of exposure: Oral Dose/Duration: >5mg/kg Toxic Effect: Details of toxic effects not reported other than lethal dose value Species observed : Rodent - Rat Test type: LD50 Route of exposure: Subcutaneous Dose/Duration: >5mg/kg Toxic Effect: Details of toxic effects not reported other than lethal dose value Species observed : Rodent - Rat Test type: LD50 Route of exposure: Intravenous Dose/Duration: >5mg/kg Toxic Effect: Details of toxic effects not reported other than lethal dose value Species observed : Mammal - Dog Test type: LD50 Route of exposure: Intravenous Dose/Duration: >5mg/kg Toxic Effect: Details of toxic effects not reported other than lethal dose value Species observed : Mammal - Dog Test type: LD50 Route of exposure: Subcutaneous Dose/Duration: >5mg/kg Toxic Effect: Details of toxic effects not reported other than lethal dose value | Lenograstim is metabolised to peptides. | During repeated dosing (iv and sc routes), peak serum concentrations (at the end of iv infusion or after sc injection) are proportional to the injected dose. Repeated dosing with lenograstim by the two injection routes results in no evidence of drug accumulation. | Apparent distribution volume (Vd area) is approximately 52 ± 5 mL/kg body weight. | Plasma clearance of lenograstim increased 3-fold (from 50 up to 150 mL/min) during repeated sc dosing. | Antineoplastic and Immunomodulating Agents | NA | NA | NA | NA | Granulocyte colony-stimulating factor receptor | Granocyte | NA | NA | Reducing the duration of neutropenia and risk of infection in people treated with chemotherapy for cancer. | L-treonine-colony-stimulating factor | NA | Solid | Subcutaneous or Intravenous | NA | People with malignancies affecting myeloid cell | Decrease in the number of platelets in the blood (thrombocytopenia), Headache, Feeling weak, Bone pain, Back pain, Elevated levels of liver enzymes | Link | NA | NA |
| 10877 | Th1237 | Somatropin recombinant | >Th1237_Somatropin_recombinant FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 °C at pH 3.5 | 21.1 (±5.1) minutes | Recombinant human growth hormone (somatotropin) 191 residues, MW 22.1 kD, synthesized in E. coli | For treatment of dwarfism, acromegaly and prevention of HIV-induced weight loss | Used in the treatment of dwarfism and growth failure, growth hormone (hGH) stimulates skeletal growth in pediatric patients with growth failure due to a lack of adequate secretion of endogenous GH. Skeletal growth is accomplished at the epiphyseal plates at the ends of a growing bone. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and one of its mediators, IGF-I (insulin-like growth factor). | hGH binds to the human growth hormone receptor (GHR). Upon binding, hGH causes dimerization of GHR, activation of the GHR-associated JAK2 tyrosine kinase, and tyrosyl phosphorylation of both JAK2 and GHR. These events recruit and/or activate a variety of signaling molecules, including MAP kinases, insulin receptor substrates, phosphatidylinositol 3' phosphate kinase, diacylglycerol, protein kinase C, intracellular calcium, and Stat transcription factors. These signaling molecules contribute to the GH-induced changes in enzymatic activity, transport function, and gene expression that ultimately culminate in changes in growth and metabolism. | NA | NA | NA | NA | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | CA1326439,CA2252535 | Mostly fro | Mostly 202 | The therapeutic efficacy of Somatropin recombinant can be decreased when used in combination with Bazedoxifene, Chlorotrianisene, Conjugated Equine Estrogens, Cortisone acetate, Dienestrol, Diethylstilbestrol, Estradiol, Estriol, Estrone, Ethinyl Estradiol. | Growth hormone receptor, Prolactin receptor | BioTropin | Biotech General | Biotech General | It is indicate dfor short stature due to pitutary growth hormone deficency, turner Syndorme, Children suffering from renal insuuficiency. | NA | NA | Powder and Solvent for Solution | Subcutaneous | The reequired dose is 10mg/ml | children with closed epiphyses. | may lead to loss or increase of adipose tissue as well as punctual haemorrhage and bruising at the injection site. | Link | NA | NA |
| 10878 | Th1237 | Somatropin recombinant | >Th1237_Somatropin_recombinant FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 °C at pH 3.5 | 21.1 (±5.1) minutes | Recombinant human growth hormone (somatotropin) 191 residues, MW 22.1 kD, synthesized in E. coli | For treatment of dwarfism, acromegaly and prevention of HIV-induced weight loss | Used in the treatment of dwarfism and growth failure, growth hormone (hGH) stimulates skeletal growth in pediatric patients with growth failure due to a lack of adequate secretion of endogenous GH. Skeletal growth is accomplished at the epiphyseal plates at the ends of a growing bone. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and one of its mediators, IGF-I (insulin-like growth factor). | hGH binds to the human growth hormone receptor (GHR). Upon binding, hGH causes dimerization of GHR, activation of the GHR-associated JAK2 tyrosine kinase, and tyrosyl phosphorylation of both JAK2 and GHR. These events recruit and/or activate a variety of signaling molecules, including MAP kinases, insulin receptor substrates, phosphatidylinositol 3' phosphate kinase, diacylglycerol, protein kinase C, intracellular calcium, and Stat transcription factors. These signaling molecules contribute to the GH-induced changes in enzymatic activity, transport function, and gene expression that ultimately culminate in changes in growth and metabolism. | NA | NA | NA | NA | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | CA1326439,CA2252535 | Mostly fro | Mostly 202 | The therapeutic efficacy of Somatropin recombinant can be decreased when used in combination with Bazedoxifene, Chlorotrianisene, Conjugated Equine Estrogens, Cortisone acetate, Dienestrol, Diethylstilbestrol, Estradiol, Estriol, Estrone, Ethinyl Estradiol. | Growth hormone receptor, Prolactin receptor | NutropinAQ | Genentech Inc. | Genentech Inc. | Treating certain children or adults when the body does not produce enough growth hormone. It is also used to treat certain children who are not growing normally due to Turner syndrome or other conditions (eg, chronic kidney problems, idiopathic short stature). | NA | Each pen cartridge or NuSpin contain either 5 mg, 10 mg or 20 mg of somatropin formulated in 17.4 mg sodium chloride, 5 mg phenol, 4 mg polysorbate 20, and 10 mM sodium citrate | Sterile liquid | Subcutaneous | A weekly dosage of up to 0.3 mg/kg of body weight divided into daily subcutaneous injections is recommended for Idiopathic Short Stature (ISS) | Acute Critical Illness, Prader-Willi Syndrome (PWS) In Children, Active Malignancy, Diabetic Retinopathy, Hypersensitivity, Closed Epiphysis | Abnormal or decreased touch sensation, bleeding, blistering, burning, coldness, discoloration of the skin, feeling of pressure, hives, infection, inflammation, itching, lumps, numbness, pain, rash, redness, scarring, soreness, stinging, swelling, tenderness, tingling, ulceration, or warmth at the injection site | Link | NA | NA |
| 10945 | Th1240 | Erythropoietin | >Th1240_Erythropoietin APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 °C | **Healthy volunteers:** The half life is approximately 4 hours in healthy volunteers receiving an intravenous injection [F85]. A half-life of approximately 6 hours has been reported in children [F85]., **Adult and paediatric patients with CRF:** The elimination half life following intravenous administration ranges from 4 to 13 hours, which is about 20% longer in CRF patients than that in healthy subjects. The half life is reported to be similar between adult patients receiving or not receiving dialysis [FDA Label]. , **Cancer patients receiving cyclic chemotherapy:** Following subcutaneous administration, the average half life is 40 hours with range of 16 to 67 hours [FDA Label]. | Erythropoietin (EPO) is a growth factor produced in the kidneys that stimulates the production of red blood cells. It works by promoting the division and differentiation of committed erythroid progenitors in the bone marrow [FDA Label]. Epoetin alfa (Epoge) was developed by Amgen Inc. in 1983 as the first rhEPO commercialized in the United States, followed by other alfa and beta formulations. Epoetin alfa is a 165-amino acid erythropoiesis-stimulating glycoprotein produced in cell culture using recombinant DNA technology and is used for the treatment of patients with anemia associated with various clinical conditions, such as chronic renal failure, antiviral drug therapy, chemotherapy, or a high risk for perioperative blood loss from surgical procedures [FDA Label]. It has a molecular weight of approximately 30,400 daltons and is produced by mammalian cells into which the human erythropoietin gene has been introduced. The product contains the identical amino acid sequence of isolated natural erythropoietin and has the same biological activity as the endogenous erythropoietin. Epoetin alfa biosimilar, such as Retacrit (epoetin alfa-epbx or epoetin zeta), has been formulated to allow more access to treatment options for patients in the market [L2784]. The biosimilar is approved by the FDA and EMA as a safe, effective and affordable biological product and displays equivalent clinical efficacy, potency, and purity to the reference product [A7504]. Epoetin alfa formulations can be administered intravenously or subcutaneously. | Indicated in adult and paediatric patients for the treatment of anemia due to Chronic Kidney Disease (CKD) in patients on dialysis and not on dialysis, treatment of anemia due to zidovudine in patients with HIV-infection, treatment of anemia due to the effects of concomitant myelosuppressive chemotherapy, and upon initiation, there is a minimum of two additional months of planned chemotherapy, reduction of allogeneic RBC transfusions in patients undergoing elective, noncardiac, nonvascular surgery. | Erythropoietin and epoetin alfa are involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is reported to increase the reticulocyte count within 10 days of initiation, followed by increases in the RBC count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [F85]. Depending on the dose administered, the rate of hemoglobin increase may vary. In patients receiving hemodialysis, a greater biologic response is not observed at doses exceeding 300 Units/kg 3 times weekly [F85]. Epoetin alfa serves to restore erythropoietin deficiency in pathological and other clinical conditions where normal production of erythropoietin is impaired or compromised. In anemic patients with chronic renal failure (CRF), administration with epoetin alfa stimulated erythropoiesis by increasing the reticulocyte count within 10 days, followed by increases in the red cell count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [FDA Label]. Epoetin alfa was shown to be effective in increasing hematocrit in zidovudine-treated HIV-infected patients and anemic cancer patients undergoing chemotherapy [FDA Label]. | Erythropoietin or exogenous epoetin alfa binds to the erythropoietin receptor (EPO-R) and activates intracellular signal transduction pathways [A33079]. The affinity (Kd) of EPO for its receptor on human cells is ~100 to 200 pM [A33080]. Upon binding to EPO-R on the surface of erythroid progenitor cells, a conformational change is induced which brings EPO-R-associated Janus family tyrosine protein kinase 2 (JAK2) molecules into close proximity. JAK2 molecules are subsequently activated via phosphorylation, then phosphorylate tyrosine residues in the cytoplasmic domain of the EPO-R that serve as docking sites for Src homology 2-domain-containing intracellular signaling proteins [A33079]. The signalling proteins include STAT5 that once phosphorylated by JAK2, dissociates from the EPO-R, dimerizes, and translocates to the nucleus where they serve as transcription factors to activate target genes involved in cell division or differentiation, including the apoptosis inhibitor Bcl-x [A33079]. The inhibition of apoptosis by the EPO-activated JAK2/STAT5/Bcl-x pathway is critical in erythroid differentiation. Via JAK2-mediated tyrosine phosphorylation, erythropoietin and epoetin alfa also activates other intracellular proteins involved in erythroid cell proliferation and survival, such as Shc , phosphatidylinositol 3-kinase (PI3K), and phospholipase C- | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. Polycythemia should be managed acutely with phlebotomy, as clinically indicated. Following resolution of the overdose, reintroduction of epoetin alfa therapy should be accompanied by close monitoring for evidence of rapid increases in hemoglobin concentration (>1 gm/dL per 14 days). In patients with an excessive hematopoietic response, reduce the dose in accordance with the recommendations described in the drug label [FDA Label]. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system [A33080]. | The time to reach peak concentration is slower via the subcutaneous route than the intravenous route which ranges from 20 to 25 hours, and the peak is always well below the peak achieved using the intravenous route (5–10% of those seen with IV administration) [A33080, L85]. The bioavailability of subcutaneous injectable erythropoietin is much lower than that of the intravenously administered product and is approximately 20-40% [A33080, L85]. **Adult and paediatric patients with CRF:** Following subcutaneous administration, the peak plasma levels are achieved within 5 to 24 hours [FDA Label]. **Cancer patients receiving cyclic chemotherapy:** The average time to reach peak plasma concentration was approximately 13.3 ± 12.4 hours after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing. The Cmax is expected be 3- to 7- fold higher and the Tmax is expected to be 2- to 3-fold longer in patients receiving a 40,000 Units SC weekly dosing regimen [FDA Label]. | In healthy volunteers, the volume of distribution of intravenous epoetin alfa was generally similar to the plasma volume (range of 40–63.80 mL/kg), indicating limited extravascular distribution [A33080, A33076]. | **Healthy volunteers: ** In male volunteers receiving intravenous epoetin alfa, the total body clearance was approximately 8.12 ± 1.00 mL/h/kg [A33076]. **Cancer patients receiving cyclic chemotherapy:** The average clearance was approximately 20.2 ± 15.9 mL/h/kg after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing [FDA Label]. The patients receiving a 40,000 Units SC weekly dosing regimen display a lower clearance (9.2 ± 4.7 mL/h/kg) [FDA Label]. | NA | NA | NA | NA | NA | Erythropoietin receptor | Eprex Sterile Solution | Janssen Pharmaceuticals | Janssen Pharmaceuticals | Intravenous; Subcutaneous | 20000 unit / 0.5 mL | NA | headache joint or muscle aches, pain, or soreness nausea vomiting weight loss sores in the mouth difficulty falling asleep or staying asleep depression muscle spasms runny nose, sneezing, and congestion fever, cough, or chills redness, swelling, pain, or itching at the injection spot | Epoetin alfa injection products come as a solution (liquid) to inject subcutaneously (just under the skin) or intravenously (into a vein). It is usually injected one to three times weekly. When epoetin alfa injection products are used to decrease the risk that blood transfusions will be required due to surgery, it is sometimes injected once daily for 10 days before surgery, on the day of surgery and for 4 days after surgery. Alternatively, epoetin alfa injection products are sometimes injected once weekly, beginning 3 weeks before surgery and on the day of surgery. | Epoetin alfa injection products are used to treat anemia (a lower than normal number of red blood cells) in people with chronic kidney failure (condition in which the kidneys slowly and permanently stop working over a period of time). Epoetin alfa injection products are also used to treat anemia caused by chemotherapy in people with certain types of cancer or caused by zidovudine (AZT, Retrovir, in Trizivir, in Combivir), a medication used to treat human immunodeficiency virus (HIV). | potassium;[2-butyl-5-chloro-3-[[4-[2-(1,2,3-triaza-4-azanidacyclopenta-2,5-dien-5-yl)phenyl]phenyl]methyl]imidazol-4-yl]methanol | NA | Link | Link | NA |
| 10946 | Th1240 | Erythropoietin | >Th1240_Erythropoietin APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 °C | **Healthy volunteers:** The half life is approximately 4 hours in healthy volunteers receiving an intravenous injection [F85]. A half-life of approximately 6 hours has been reported in children [F85]., **Adult and paediatric patients with CRF:** The elimination half life following intravenous administration ranges from 4 to 13 hours, which is about 20% longer in CRF patients than that in healthy subjects. The half life is reported to be similar between adult patients receiving or not receiving dialysis [FDA Label]. , **Cancer patients receiving cyclic chemotherapy:** Following subcutaneous administration, the average half life is 40 hours with range of 16 to 67 hours [FDA Label]. | Erythropoietin (EPO) is a growth factor produced in the kidneys that stimulates the production of red blood cells. It works by promoting the division and differentiation of committed erythroid progenitors in the bone marrow [FDA Label]. Epoetin alfa (Epoge) was developed by Amgen Inc. in 1983 as the first rhEPO commercialized in the United States, followed by other alfa and beta formulations. Epoetin alfa is a 165-amino acid erythropoiesis-stimulating glycoprotein produced in cell culture using recombinant DNA technology and is used for the treatment of patients with anemia associated with various clinical conditions, such as chronic renal failure, antiviral drug therapy, chemotherapy, or a high risk for perioperative blood loss from surgical procedures [FDA Label]. It has a molecular weight of approximately 30,400 daltons and is produced by mammalian cells into which the human erythropoietin gene has been introduced. The product contains the identical amino acid sequence of isolated natural erythropoietin and has the same biological activity as the endogenous erythropoietin. Epoetin alfa biosimilar, such as Retacrit (epoetin alfa-epbx or epoetin zeta), has been formulated to allow more access to treatment options for patients in the market [L2784]. The biosimilar is approved by the FDA and EMA as a safe, effective and affordable biological product and displays equivalent clinical efficacy, potency, and purity to the reference product [A7504]. Epoetin alfa formulations can be administered intravenously or subcutaneously. | Indicated in adult and paediatric patients for the treatment of anemia due to Chronic Kidney Disease (CKD) in patients on dialysis and not on dialysis, treatment of anemia due to zidovudine in patients with HIV-infection, treatment of anemia due to the effects of concomitant myelosuppressive chemotherapy, and upon initiation, there is a minimum of two additional months of planned chemotherapy, reduction of allogeneic RBC transfusions in patients undergoing elective, noncardiac, nonvascular surgery. | Erythropoietin and epoetin alfa are involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is reported to increase the reticulocyte count within 10 days of initiation, followed by increases in the RBC count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [F85]. Depending on the dose administered, the rate of hemoglobin increase may vary. In patients receiving hemodialysis, a greater biologic response is not observed at doses exceeding 300 Units/kg 3 times weekly [F85]. Epoetin alfa serves to restore erythropoietin deficiency in pathological and other clinical conditions where normal production of erythropoietin is impaired or compromised. In anemic patients with chronic renal failure (CRF), administration with epoetin alfa stimulated erythropoiesis by increasing the reticulocyte count within 10 days, followed by increases in the red cell count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [FDA Label]. Epoetin alfa was shown to be effective in increasing hematocrit in zidovudine-treated HIV-infected patients and anemic cancer patients undergoing chemotherapy [FDA Label]. | Erythropoietin or exogenous epoetin alfa binds to the erythropoietin receptor (EPO-R) and activates intracellular signal transduction pathways [A33079]. The affinity (Kd) of EPO for its receptor on human cells is ~100 to 200 pM [A33080]. Upon binding to EPO-R on the surface of erythroid progenitor cells, a conformational change is induced which brings EPO-R-associated Janus family tyrosine protein kinase 2 (JAK2) molecules into close proximity. JAK2 molecules are subsequently activated via phosphorylation, then phosphorylate tyrosine residues in the cytoplasmic domain of the EPO-R that serve as docking sites for Src homology 2-domain-containing intracellular signaling proteins [A33079]. The signalling proteins include STAT5 that once phosphorylated by JAK2, dissociates from the EPO-R, dimerizes, and translocates to the nucleus where they serve as transcription factors to activate target genes involved in cell division or differentiation, including the apoptosis inhibitor Bcl-x [A33079]. The inhibition of apoptosis by the EPO-activated JAK2/STAT5/Bcl-x pathway is critical in erythroid differentiation. Via JAK2-mediated tyrosine phosphorylation, erythropoietin and epoetin alfa also activates other intracellular proteins involved in erythroid cell proliferation and survival, such as Shc , phosphatidylinositol 3-kinase (PI3K), and phospholipase C- | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. Polycythemia should be managed acutely with phlebotomy, as clinically indicated. Following resolution of the overdose, reintroduction of epoetin alfa therapy should be accompanied by close monitoring for evidence of rapid increases in hemoglobin concentration (>1 gm/dL per 14 days). In patients with an excessive hematopoietic response, reduce the dose in accordance with the recommendations described in the drug label [FDA Label]. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system [A33080]. | The time to reach peak concentration is slower via the subcutaneous route than the intravenous route which ranges from 20 to 25 hours, and the peak is always well below the peak achieved using the intravenous route (5–10% of those seen with IV administration) [A33080, L85]. The bioavailability of subcutaneous injectable erythropoietin is much lower than that of the intravenously administered product and is approximately 20-40% [A33080, L85]. **Adult and paediatric patients with CRF:** Following subcutaneous administration, the peak plasma levels are achieved within 5 to 24 hours [FDA Label]. **Cancer patients receiving cyclic chemotherapy:** The average time to reach peak plasma concentration was approximately 13.3 ± 12.4 hours after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing. The Cmax is expected be 3- to 7- fold higher and the Tmax is expected to be 2- to 3-fold longer in patients receiving a 40,000 Units SC weekly dosing regimen [FDA Label]. | In healthy volunteers, the volume of distribution of intravenous epoetin alfa was generally similar to the plasma volume (range of 40–63.80 mL/kg), indicating limited extravascular distribution [A33080, A33076]. | **Healthy volunteers: ** In male volunteers receiving intravenous epoetin alfa, the total body clearance was approximately 8.12 ± 1.00 mL/h/kg [A33076]. **Cancer patients receiving cyclic chemotherapy:** The average clearance was approximately 20.2 ± 15.9 mL/h/kg after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing [FDA Label]. The patients receiving a 40,000 Units SC weekly dosing regimen display a lower clearance (9.2 ± 4.7 mL/h/kg) [FDA Label]. | NA | NA | NA | NA | NA | Erythropoietin receptor | Eprex Sterile Solution | Janssen Pharmaceuticals | Janssen Pharmaceuticals | Intravenous; Subcutaneous | 30000 unit / 0.75 mL | NA | headache joint or muscle aches, pain, or soreness nausea vomiting weight loss sores in the mouth difficulty falling asleep or staying asleep depression muscle spasms runny nose, sneezing, and congestion fever, cough, or chills redness, swelling, pain, or itching at the injection spot | Epoetin alfa injection products come as a solution (liquid) to inject subcutaneously (just under the skin) or intravenously (into a vein). It is usually injected one to three times weekly. When epoetin alfa injection products are used to decrease the risk that blood transfusions will be required due to surgery, it is sometimes injected once daily for 10 days before surgery, on the day of surgery and for 4 days after surgery. Alternatively, epoetin alfa injection products are sometimes injected once weekly, beginning 3 weeks before surgery and on the day of surgery. | Epoetin alfa injection products are used to treat anemia (a lower than normal number of red blood cells) in people with chronic kidney failure (condition in which the kidneys slowly and permanently stop working over a period of time). Epoetin alfa injection products are also used to treat anemia caused by chemotherapy in people with certain types of cancer or caused by zidovudine (AZT, Retrovir, in Trizivir, in Combivir), a medication used to treat human immunodeficiency virus (HIV). | potassium;[2-butyl-5-chloro-3-[[4-[2-(1,2,3-triaza-4-azanidacyclopenta-2,5-dien-5-yl)phenyl]phenyl]methyl]imidazol-4-yl]methanol | NA | Link | Link | NA |
| 10947 | Th1240 | Erythropoietin | >Th1240_Erythropoietin APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 °C | **Healthy volunteers:** The half life is approximately 4 hours in healthy volunteers receiving an intravenous injection [F85]. A half-life of approximately 6 hours has been reported in children [F85]., **Adult and paediatric patients with CRF:** The elimination half life following intravenous administration ranges from 4 to 13 hours, which is about 20% longer in CRF patients than that in healthy subjects. The half life is reported to be similar between adult patients receiving or not receiving dialysis [FDA Label]. , **Cancer patients receiving cyclic chemotherapy:** Following subcutaneous administration, the average half life is 40 hours with range of 16 to 67 hours [FDA Label]. | Erythropoietin (EPO) is a growth factor produced in the kidneys that stimulates the production of red blood cells. It works by promoting the division and differentiation of committed erythroid progenitors in the bone marrow [FDA Label]. Epoetin alfa (Epoge) was developed by Amgen Inc. in 1983 as the first rhEPO commercialized in the United States, followed by other alfa and beta formulations. Epoetin alfa is a 165-amino acid erythropoiesis-stimulating glycoprotein produced in cell culture using recombinant DNA technology and is used for the treatment of patients with anemia associated with various clinical conditions, such as chronic renal failure, antiviral drug therapy, chemotherapy, or a high risk for perioperative blood loss from surgical procedures [FDA Label]. It has a molecular weight of approximately 30,400 daltons and is produced by mammalian cells into which the human erythropoietin gene has been introduced. The product contains the identical amino acid sequence of isolated natural erythropoietin and has the same biological activity as the endogenous erythropoietin. Epoetin alfa biosimilar, such as Retacrit (epoetin alfa-epbx or epoetin zeta), has been formulated to allow more access to treatment options for patients in the market [L2784]. The biosimilar is approved by the FDA and EMA as a safe, effective and affordable biological product and displays equivalent clinical efficacy, potency, and purity to the reference product [A7504]. Epoetin alfa formulations can be administered intravenously or subcutaneously. | Indicated in adult and paediatric patients for the treatment of anemia due to Chronic Kidney Disease (CKD) in patients on dialysis and not on dialysis, treatment of anemia due to zidovudine in patients with HIV-infection, treatment of anemia due to the effects of concomitant myelosuppressive chemotherapy, and upon initiation, there is a minimum of two additional months of planned chemotherapy, reduction of allogeneic RBC transfusions in patients undergoing elective, noncardiac, nonvascular surgery. | Erythropoietin and epoetin alfa are involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is reported to increase the reticulocyte count within 10 days of initiation, followed by increases in the RBC count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [F85]. Depending on the dose administered, the rate of hemoglobin increase may vary. In patients receiving hemodialysis, a greater biologic response is not observed at doses exceeding 300 Units/kg 3 times weekly [F85]. Epoetin alfa serves to restore erythropoietin deficiency in pathological and other clinical conditions where normal production of erythropoietin is impaired or compromised. In anemic patients with chronic renal failure (CRF), administration with epoetin alfa stimulated erythropoiesis by increasing the reticulocyte count within 10 days, followed by increases in the red cell count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [FDA Label]. Epoetin alfa was shown to be effective in increasing hematocrit in zidovudine-treated HIV-infected patients and anemic cancer patients undergoing chemotherapy [FDA Label]. | Erythropoietin or exogenous epoetin alfa binds to the erythropoietin receptor (EPO-R) and activates intracellular signal transduction pathways [A33079]. The affinity (Kd) of EPO for its receptor on human cells is ~100 to 200 pM [A33080]. Upon binding to EPO-R on the surface of erythroid progenitor cells, a conformational change is induced which brings EPO-R-associated Janus family tyrosine protein kinase 2 (JAK2) molecules into close proximity. JAK2 molecules are subsequently activated via phosphorylation, then phosphorylate tyrosine residues in the cytoplasmic domain of the EPO-R that serve as docking sites for Src homology 2-domain-containing intracellular signaling proteins [A33079]. The signalling proteins include STAT5 that once phosphorylated by JAK2, dissociates from the EPO-R, dimerizes, and translocates to the nucleus where they serve as transcription factors to activate target genes involved in cell division or differentiation, including the apoptosis inhibitor Bcl-x [A33079]. The inhibition of apoptosis by the EPO-activated JAK2/STAT5/Bcl-x pathway is critical in erythroid differentiation. Via JAK2-mediated tyrosine phosphorylation, erythropoietin and epoetin alfa also activates other intracellular proteins involved in erythroid cell proliferation and survival, such as Shc , phosphatidylinositol 3-kinase (PI3K), and phospholipase C- | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. Polycythemia should be managed acutely with phlebotomy, as clinically indicated. Following resolution of the overdose, reintroduction of epoetin alfa therapy should be accompanied by close monitoring for evidence of rapid increases in hemoglobin concentration (>1 gm/dL per 14 days). In patients with an excessive hematopoietic response, reduce the dose in accordance with the recommendations described in the drug label [FDA Label]. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system [A33080]. | The time to reach peak concentration is slower via the subcutaneous route than the intravenous route which ranges from 20 to 25 hours, and the peak is always well below the peak achieved using the intravenous route (5–10% of those seen with IV administration) [A33080, L85]. The bioavailability of subcutaneous injectable erythropoietin is much lower than that of the intravenously administered product and is approximately 20-40% [A33080, L85]. **Adult and paediatric patients with CRF:** Following subcutaneous administration, the peak plasma levels are achieved within 5 to 24 hours [FDA Label]. **Cancer patients receiving cyclic chemotherapy:** The average time to reach peak plasma concentration was approximately 13.3 ± 12.4 hours after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing. The Cmax is expected be 3- to 7- fold higher and the Tmax is expected to be 2- to 3-fold longer in patients receiving a 40,000 Units SC weekly dosing regimen [FDA Label]. | In healthy volunteers, the volume of distribution of intravenous epoetin alfa was generally similar to the plasma volume (range of 40–63.80 mL/kg), indicating limited extravascular distribution [A33080, A33076]. | **Healthy volunteers: ** In male volunteers receiving intravenous epoetin alfa, the total body clearance was approximately 8.12 ± 1.00 mL/h/kg [A33076]. **Cancer patients receiving cyclic chemotherapy:** The average clearance was approximately 20.2 ± 15.9 mL/h/kg after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing [FDA Label]. The patients receiving a 40,000 Units SC weekly dosing regimen display a lower clearance (9.2 ± 4.7 mL/h/kg) [FDA Label]. | NA | NA | NA | NA | NA | Erythropoietin receptor | Eprex Sterile Solution 10000iu/1.0ml | Janssen Pharmaceuticals | Janssen Pharmaceuticals | Intravenous; Subcutaneous | 10000 unit / mL | NA | headache joint or muscle aches, pain, or soreness nausea vomiting weight loss sores in the mouth difficulty falling asleep or staying asleep depression muscle spasms runny nose, sneezing, and congestion fever, cough, or chills redness, swelling, pain, or itching at the injection spot | Epoetin alfa injection products come as a solution (liquid) to inject subcutaneously (just under the skin) or intravenously (into a vein). It is usually injected one to three times weekly. When epoetin alfa injection products are used to decrease the risk that blood transfusions will be required due to surgery, it is sometimes injected once daily for 10 days before surgery, on the day of surgery and for 4 days after surgery. Alternatively, epoetin alfa injection products are sometimes injected once weekly, beginning 3 weeks before surgery and on the day of surgery. | Epoetin alfa injection products are used to treat anemia (a lower than normal number of red blood cells) in people with chronic kidney failure (condition in which the kidneys slowly and permanently stop working over a period of time). Epoetin alfa injection products are also used to treat anemia caused by chemotherapy in people with certain types of cancer or caused by zidovudine (AZT, Retrovir, in Trizivir, in Combivir), a medication used to treat human immunodeficiency virus (HIV). | potassium;[2-butyl-5-chloro-3-[[4-[2-(1,2,3-triaza-4-azanidacyclopenta-2,5-dien-5-yl)phenyl]phenyl]methyl]imidazol-4-yl]methanol | NA | Link | Link | NA |
| 10948 | Th1240 | Erythropoietin | >Th1240_Erythropoietin APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 °C | **Healthy volunteers:** The half life is approximately 4 hours in healthy volunteers receiving an intravenous injection [F85]. A half-life of approximately 6 hours has been reported in children [F85]., **Adult and paediatric patients with CRF:** The elimination half life following intravenous administration ranges from 4 to 13 hours, which is about 20% longer in CRF patients than that in healthy subjects. The half life is reported to be similar between adult patients receiving or not receiving dialysis [FDA Label]. , **Cancer patients receiving cyclic chemotherapy:** Following subcutaneous administration, the average half life is 40 hours with range of 16 to 67 hours [FDA Label]. | Erythropoietin (EPO) is a growth factor produced in the kidneys that stimulates the production of red blood cells. It works by promoting the division and differentiation of committed erythroid progenitors in the bone marrow [FDA Label]. Epoetin alfa (Epoge) was developed by Amgen Inc. in 1983 as the first rhEPO commercialized in the United States, followed by other alfa and beta formulations. Epoetin alfa is a 165-amino acid erythropoiesis-stimulating glycoprotein produced in cell culture using recombinant DNA technology and is used for the treatment of patients with anemia associated with various clinical conditions, such as chronic renal failure, antiviral drug therapy, chemotherapy, or a high risk for perioperative blood loss from surgical procedures [FDA Label]. It has a molecular weight of approximately 30,400 daltons and is produced by mammalian cells into which the human erythropoietin gene has been introduced. The product contains the identical amino acid sequence of isolated natural erythropoietin and has the same biological activity as the endogenous erythropoietin. Epoetin alfa biosimilar, such as Retacrit (epoetin alfa-epbx or epoetin zeta), has been formulated to allow more access to treatment options for patients in the market [L2784]. The biosimilar is approved by the FDA and EMA as a safe, effective and affordable biological product and displays equivalent clinical efficacy, potency, and purity to the reference product [A7504]. Epoetin alfa formulations can be administered intravenously or subcutaneously. | Indicated in adult and paediatric patients for the treatment of anemia due to Chronic Kidney Disease (CKD) in patients on dialysis and not on dialysis, treatment of anemia due to zidovudine in patients with HIV-infection, treatment of anemia due to the effects of concomitant myelosuppressive chemotherapy, and upon initiation, there is a minimum of two additional months of planned chemotherapy, reduction of allogeneic RBC transfusions in patients undergoing elective, noncardiac, nonvascular surgery. | Erythropoietin and epoetin alfa are involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is reported to increase the reticulocyte count within 10 days of initiation, followed by increases in the RBC count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [F85]. Depending on the dose administered, the rate of hemoglobin increase may vary. In patients receiving hemodialysis, a greater biologic response is not observed at doses exceeding 300 Units/kg 3 times weekly [F85]. Epoetin alfa serves to restore erythropoietin deficiency in pathological and other clinical conditions where normal production of erythropoietin is impaired or compromised. In anemic patients with chronic renal failure (CRF), administration with epoetin alfa stimulated erythropoiesis by increasing the reticulocyte count within 10 days, followed by increases in the red cell count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [FDA Label]. Epoetin alfa was shown to be effective in increasing hematocrit in zidovudine-treated HIV-infected patients and anemic cancer patients undergoing chemotherapy [FDA Label]. | Erythropoietin or exogenous epoetin alfa binds to the erythropoietin receptor (EPO-R) and activates intracellular signal transduction pathways [A33079]. The affinity (Kd) of EPO for its receptor on human cells is ~100 to 200 pM [A33080]. Upon binding to EPO-R on the surface of erythroid progenitor cells, a conformational change is induced which brings EPO-R-associated Janus family tyrosine protein kinase 2 (JAK2) molecules into close proximity. JAK2 molecules are subsequently activated via phosphorylation, then phosphorylate tyrosine residues in the cytoplasmic domain of the EPO-R that serve as docking sites for Src homology 2-domain-containing intracellular signaling proteins [A33079]. The signalling proteins include STAT5 that once phosphorylated by JAK2, dissociates from the EPO-R, dimerizes, and translocates to the nucleus where they serve as transcription factors to activate target genes involved in cell division or differentiation, including the apoptosis inhibitor Bcl-x [A33079]. The inhibition of apoptosis by the EPO-activated JAK2/STAT5/Bcl-x pathway is critical in erythroid differentiation. Via JAK2-mediated tyrosine phosphorylation, erythropoietin and epoetin alfa also activates other intracellular proteins involved in erythroid cell proliferation and survival, such as Shc , phosphatidylinositol 3-kinase (PI3K), and phospholipase C- | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. Polycythemia should be managed acutely with phlebotomy, as clinically indicated. Following resolution of the overdose, reintroduction of epoetin alfa therapy should be accompanied by close monitoring for evidence of rapid increases in hemoglobin concentration (>1 gm/dL per 14 days). In patients with an excessive hematopoietic response, reduce the dose in accordance with the recommendations described in the drug label [FDA Label]. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system [A33080]. | The time to reach peak concentration is slower via the subcutaneous route than the intravenous route which ranges from 20 to 25 hours, and the peak is always well below the peak achieved using the intravenous route (5–10% of those seen with IV administration) [A33080, L85]. The bioavailability of subcutaneous injectable erythropoietin is much lower than that of the intravenously administered product and is approximately 20-40% [A33080, L85]. **Adult and paediatric patients with CRF:** Following subcutaneous administration, the peak plasma levels are achieved within 5 to 24 hours [FDA Label]. **Cancer patients receiving cyclic chemotherapy:** The average time to reach peak plasma concentration was approximately 13.3 ± 12.4 hours after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing. The Cmax is expected be 3- to 7- fold higher and the Tmax is expected to be 2- to 3-fold longer in patients receiving a 40,000 Units SC weekly dosing regimen [FDA Label]. | In healthy volunteers, the volume of distribution of intravenous epoetin alfa was generally similar to the plasma volume (range of 40–63.80 mL/kg), indicating limited extravascular distribution [A33080, A33076]. | **Healthy volunteers: ** In male volunteers receiving intravenous epoetin alfa, the total body clearance was approximately 8.12 ± 1.00 mL/h/kg [A33076]. **Cancer patients receiving cyclic chemotherapy:** The average clearance was approximately 20.2 ± 15.9 mL/h/kg after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing [FDA Label]. The patients receiving a 40,000 Units SC weekly dosing regimen display a lower clearance (9.2 ± 4.7 mL/h/kg) [FDA Label]. | NA | NA | NA | NA | NA | Erythropoietin receptor | Eprex Sterile Solution 10000iu/ml | Janssen Pharmaceuticals | Janssen Pharmaceuticals | Intravenous; Subcutaneous | 10000 unit / mL | NA | headache joint or muscle aches, pain, or soreness nausea vomiting weight loss sores in the mouth difficulty falling asleep or staying asleep depression muscle spasms runny nose, sneezing, and congestion fever, cough, or chills redness, swelling, pain, or itching at the injection spot | Epoetin alfa injection products come as a solution (liquid) to inject subcutaneously (just under the skin) or intravenously (into a vein). It is usually injected one to three times weekly. When epoetin alfa injection products are used to decrease the risk that blood transfusions will be required due to surgery, it is sometimes injected once daily for 10 days before surgery, on the day of surgery and for 4 days after surgery. Alternatively, epoetin alfa injection products are sometimes injected once weekly, beginning 3 weeks before surgery and on the day of surgery. | Epoetin alfa injection products are used to treat anemia (a lower than normal number of red blood cells) in people with chronic kidney failure (condition in which the kidneys slowly and permanently stop working over a period of time). Epoetin alfa injection products are also used to treat anemia caused by chemotherapy in people with certain types of cancer or caused by zidovudine (AZT, Retrovir, in Trizivir, in Combivir), a medication used to treat human immunodeficiency virus (HIV). | potassium;[2-butyl-5-chloro-3-[[4-[2-(1,2,3-triaza-4-azanidacyclopenta-2,5-dien-5-yl)phenyl]phenyl]methyl]imidazol-4-yl]methanol | NA | Link | Link | NA |
| 10949 | Th1240 | Erythropoietin | >Th1240_Erythropoietin APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 °C | **Healthy volunteers:** The half life is approximately 4 hours in healthy volunteers receiving an intravenous injection [F85]. A half-life of approximately 6 hours has been reported in children [F85]., **Adult and paediatric patients with CRF:** The elimination half life following intravenous administration ranges from 4 to 13 hours, which is about 20% longer in CRF patients than that in healthy subjects. The half life is reported to be similar between adult patients receiving or not receiving dialysis [FDA Label]. , **Cancer patients receiving cyclic chemotherapy:** Following subcutaneous administration, the average half life is 40 hours with range of 16 to 67 hours [FDA Label]. | Erythropoietin (EPO) is a growth factor produced in the kidneys that stimulates the production of red blood cells. It works by promoting the division and differentiation of committed erythroid progenitors in the bone marrow [FDA Label]. Epoetin alfa (Epoge) was developed by Amgen Inc. in 1983 as the first rhEPO commercialized in the United States, followed by other alfa and beta formulations. Epoetin alfa is a 165-amino acid erythropoiesis-stimulating glycoprotein produced in cell culture using recombinant DNA technology and is used for the treatment of patients with anemia associated with various clinical conditions, such as chronic renal failure, antiviral drug therapy, chemotherapy, or a high risk for perioperative blood loss from surgical procedures [FDA Label]. It has a molecular weight of approximately 30,400 daltons and is produced by mammalian cells into which the human erythropoietin gene has been introduced. The product contains the identical amino acid sequence of isolated natural erythropoietin and has the same biological activity as the endogenous erythropoietin. Epoetin alfa biosimilar, such as Retacrit (epoetin alfa-epbx or epoetin zeta), has been formulated to allow more access to treatment options for patients in the market [L2784]. The biosimilar is approved by the FDA and EMA as a safe, effective and affordable biological product and displays equivalent clinical efficacy, potency, and purity to the reference product [A7504]. Epoetin alfa formulations can be administered intravenously or subcutaneously. | Indicated in adult and paediatric patients for the treatment of anemia due to Chronic Kidney Disease (CKD) in patients on dialysis and not on dialysis, treatment of anemia due to zidovudine in patients with HIV-infection, treatment of anemia due to the effects of concomitant myelosuppressive chemotherapy, and upon initiation, there is a minimum of two additional months of planned chemotherapy, reduction of allogeneic RBC transfusions in patients undergoing elective, noncardiac, nonvascular surgery. | Erythropoietin and epoetin alfa are involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is reported to increase the reticulocyte count within 10 days of initiation, followed by increases in the RBC count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [F85]. Depending on the dose administered, the rate of hemoglobin increase may vary. In patients receiving hemodialysis, a greater biologic response is not observed at doses exceeding 300 Units/kg 3 times weekly [F85]. Epoetin alfa serves to restore erythropoietin deficiency in pathological and other clinical conditions where normal production of erythropoietin is impaired or compromised. In anemic patients with chronic renal failure (CRF), administration with epoetin alfa stimulated erythropoiesis by increasing the reticulocyte count within 10 days, followed by increases in the red cell count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [FDA Label]. Epoetin alfa was shown to be effective in increasing hematocrit in zidovudine-treated HIV-infected patients and anemic cancer patients undergoing chemotherapy [FDA Label]. | Erythropoietin or exogenous epoetin alfa binds to the erythropoietin receptor (EPO-R) and activates intracellular signal transduction pathways [A33079]. The affinity (Kd) of EPO for its receptor on human cells is ~100 to 200 pM [A33080]. Upon binding to EPO-R on the surface of erythroid progenitor cells, a conformational change is induced which brings EPO-R-associated Janus family tyrosine protein kinase 2 (JAK2) molecules into close proximity. JAK2 molecules are subsequently activated via phosphorylation, then phosphorylate tyrosine residues in the cytoplasmic domain of the EPO-R that serve as docking sites for Src homology 2-domain-containing intracellular signaling proteins [A33079]. The signalling proteins include STAT5 that once phosphorylated by JAK2, dissociates from the EPO-R, dimerizes, and translocates to the nucleus where they serve as transcription factors to activate target genes involved in cell division or differentiation, including the apoptosis inhibitor Bcl-x [A33079]. The inhibition of apoptosis by the EPO-activated JAK2/STAT5/Bcl-x pathway is critical in erythroid differentiation. Via JAK2-mediated tyrosine phosphorylation, erythropoietin and epoetin alfa also activates other intracellular proteins involved in erythroid cell proliferation and survival, such as Shc , phosphatidylinositol 3-kinase (PI3K), and phospholipase C- | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. Polycythemia should be managed acutely with phlebotomy, as clinically indicated. Following resolution of the overdose, reintroduction of epoetin alfa therapy should be accompanied by close monitoring for evidence of rapid increases in hemoglobin concentration (>1 gm/dL per 14 days). In patients with an excessive hematopoietic response, reduce the dose in accordance with the recommendations described in the drug label [FDA Label]. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system [A33080]. | The time to reach peak concentration is slower via the subcutaneous route than the intravenous route which ranges from 20 to 25 hours, and the peak is always well below the peak achieved using the intravenous route (5–10% of those seen with IV administration) [A33080, L85]. The bioavailability of subcutaneous injectable erythropoietin is much lower than that of the intravenously administered product and is approximately 20-40% [A33080, L85]. **Adult and paediatric patients with CRF:** Following subcutaneous administration, the peak plasma levels are achieved within 5 to 24 hours [FDA Label]. **Cancer patients receiving cyclic chemotherapy:** The average time to reach peak plasma concentration was approximately 13.3 ± 12.4 hours after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing. The Cmax is expected be 3- to 7- fold higher and the Tmax is expected to be 2- to 3-fold longer in patients receiving a 40,000 Units SC weekly dosing regimen [FDA Label]. | In healthy volunteers, the volume of distribution of intravenous epoetin alfa was generally similar to the plasma volume (range of 40–63.80 mL/kg), indicating limited extravascular distribution [A33080, A33076]. | **Healthy volunteers: ** In male volunteers receiving intravenous epoetin alfa, the total body clearance was approximately 8.12 ± 1.00 mL/h/kg [A33076]. **Cancer patients receiving cyclic chemotherapy:** The average clearance was approximately 20.2 ± 15.9 mL/h/kg after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing [FDA Label]. The patients receiving a 40,000 Units SC weekly dosing regimen display a lower clearance (9.2 ± 4.7 mL/h/kg) [FDA Label]. | NA | NA | NA | NA | NA | Erythropoietin receptor | Eprex Sterile Solution 1000iu/0.5ml | Janssen Pharmaceuticals | Janssen Pharmaceuticals | Intravenous; Subcutaneous | 1000 unit / 0.5 mL | NA | headache joint or muscle aches, pain, or soreness nausea vomiting weight loss sores in the mouth difficulty falling asleep or staying asleep depression muscle spasms runny nose, sneezing, and congestion fever, cough, or chills redness, swelling, pain, or itching at the injection spot | Epoetin alfa injection products come as a solution (liquid) to inject subcutaneously (just under the skin) or intravenously (into a vein). It is usually injected one to three times weekly. When epoetin alfa injection products are used to decrease the risk that blood transfusions will be required due to surgery, it is sometimes injected once daily for 10 days before surgery, on the day of surgery and for 4 days after surgery. Alternatively, epoetin alfa injection products are sometimes injected once weekly, beginning 3 weeks before surgery and on the day of surgery. | Epoetin alfa injection products are used to treat anemia (a lower than normal number of red blood cells) in people with chronic kidney failure (condition in which the kidneys slowly and permanently stop working over a period of time). Epoetin alfa injection products are also used to treat anemia caused by chemotherapy in people with certain types of cancer or caused by zidovudine (AZT, Retrovir, in Trizivir, in Combivir), a medication used to treat human immunodeficiency virus (HIV). | potassium;[2-butyl-5-chloro-3-[[4-[2-(1,2,3-triaza-4-azanidacyclopenta-2,5-dien-5-yl)phenyl]phenyl]methyl]imidazol-4-yl]methanol | NA | Link | Link | NA |
| 10950 | Th1240 | Erythropoietin | >Th1240_Erythropoietin APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 °C | **Healthy volunteers:** The half life is approximately 4 hours in healthy volunteers receiving an intravenous injection [F85]. A half-life of approximately 6 hours has been reported in children [F85]., **Adult and paediatric patients with CRF:** The elimination half life following intravenous administration ranges from 4 to 13 hours, which is about 20% longer in CRF patients than that in healthy subjects. The half life is reported to be similar between adult patients receiving or not receiving dialysis [FDA Label]. , **Cancer patients receiving cyclic chemotherapy:** Following subcutaneous administration, the average half life is 40 hours with range of 16 to 67 hours [FDA Label]. | Erythropoietin (EPO) is a growth factor produced in the kidneys that stimulates the production of red blood cells. It works by promoting the division and differentiation of committed erythroid progenitors in the bone marrow [FDA Label]. Epoetin alfa (Epoge) was developed by Amgen Inc. in 1983 as the first rhEPO commercialized in the United States, followed by other alfa and beta formulations. Epoetin alfa is a 165-amino acid erythropoiesis-stimulating glycoprotein produced in cell culture using recombinant DNA technology and is used for the treatment of patients with anemia associated with various clinical conditions, such as chronic renal failure, antiviral drug therapy, chemotherapy, or a high risk for perioperative blood loss from surgical procedures [FDA Label]. It has a molecular weight of approximately 30,400 daltons and is produced by mammalian cells into which the human erythropoietin gene has been introduced. The product contains the identical amino acid sequence of isolated natural erythropoietin and has the same biological activity as the endogenous erythropoietin. Epoetin alfa biosimilar, such as Retacrit (epoetin alfa-epbx or epoetin zeta), has been formulated to allow more access to treatment options for patients in the market [L2784]. The biosimilar is approved by the FDA and EMA as a safe, effective and affordable biological product and displays equivalent clinical efficacy, potency, and purity to the reference product [A7504]. Epoetin alfa formulations can be administered intravenously or subcutaneously. | Indicated in adult and paediatric patients for the treatment of anemia due to Chronic Kidney Disease (CKD) in patients on dialysis and not on dialysis, treatment of anemia due to zidovudine in patients with HIV-infection, treatment of anemia due to the effects of concomitant myelosuppressive chemotherapy, and upon initiation, there is a minimum of two additional months of planned chemotherapy, reduction of allogeneic RBC transfusions in patients undergoing elective, noncardiac, nonvascular surgery. | Erythropoietin and epoetin alfa are involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is reported to increase the reticulocyte count within 10 days of initiation, followed by increases in the RBC count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [F85]. Depending on the dose administered, the rate of hemoglobin increase may vary. In patients receiving hemodialysis, a greater biologic response is not observed at doses exceeding 300 Units/kg 3 times weekly [F85]. Epoetin alfa serves to restore erythropoietin deficiency in pathological and other clinical conditions where normal production of erythropoietin is impaired or compromised. In anemic patients with chronic renal failure (CRF), administration with epoetin alfa stimulated erythropoiesis by increasing the reticulocyte count within 10 days, followed by increases in the red cell count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [FDA Label]. Epoetin alfa was shown to be effective in increasing hematocrit in zidovudine-treated HIV-infected patients and anemic cancer patients undergoing chemotherapy [FDA Label]. | Erythropoietin or exogenous epoetin alfa binds to the erythropoietin receptor (EPO-R) and activates intracellular signal transduction pathways [A33079]. The affinity (Kd) of EPO for its receptor on human cells is ~100 to 200 pM [A33080]. Upon binding to EPO-R on the surface of erythroid progenitor cells, a conformational change is induced which brings EPO-R-associated Janus family tyrosine protein kinase 2 (JAK2) molecules into close proximity. JAK2 molecules are subsequently activated via phosphorylation, then phosphorylate tyrosine residues in the cytoplasmic domain of the EPO-R that serve as docking sites for Src homology 2-domain-containing intracellular signaling proteins [A33079]. The signalling proteins include STAT5 that once phosphorylated by JAK2, dissociates from the EPO-R, dimerizes, and translocates to the nucleus where they serve as transcription factors to activate target genes involved in cell division or differentiation, including the apoptosis inhibitor Bcl-x [A33079]. The inhibition of apoptosis by the EPO-activated JAK2/STAT5/Bcl-x pathway is critical in erythroid differentiation. Via JAK2-mediated tyrosine phosphorylation, erythropoietin and epoetin alfa also activates other intracellular proteins involved in erythroid cell proliferation and survival, such as Shc , phosphatidylinositol 3-kinase (PI3K), and phospholipase C- | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. Polycythemia should be managed acutely with phlebotomy, as clinically indicated. Following resolution of the overdose, reintroduction of epoetin alfa therapy should be accompanied by close monitoring for evidence of rapid increases in hemoglobin concentration (>1 gm/dL per 14 days). In patients with an excessive hematopoietic response, reduce the dose in accordance with the recommendations described in the drug label [FDA Label]. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system [A33080]. | The time to reach peak concentration is slower via the subcutaneous route than the intravenous route which ranges from 20 to 25 hours, and the peak is always well below the peak achieved using the intravenous route (5–10% of those seen with IV administration) [A33080, L85]. The bioavailability of subcutaneous injectable erythropoietin is much lower than that of the intravenously administered product and is approximately 20-40% [A33080, L85]. **Adult and paediatric patients with CRF:** Following subcutaneous administration, the peak plasma levels are achieved within 5 to 24 hours [FDA Label]. **Cancer patients receiving cyclic chemotherapy:** The average time to reach peak plasma concentration was approximately 13.3 ± 12.4 hours after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing. The Cmax is expected be 3- to 7- fold higher and the Tmax is expected to be 2- to 3-fold longer in patients receiving a 40,000 Units SC weekly dosing regimen [FDA Label]. | In healthy volunteers, the volume of distribution of intravenous epoetin alfa was generally similar to the plasma volume (range of 40–63.80 mL/kg), indicating limited extravascular distribution [A33080, A33076]. | **Healthy volunteers: ** In male volunteers receiving intravenous epoetin alfa, the total body clearance was approximately 8.12 ± 1.00 mL/h/kg [A33076]. **Cancer patients receiving cyclic chemotherapy:** The average clearance was approximately 20.2 ± 15.9 mL/h/kg after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing [FDA Label]. The patients receiving a 40,000 Units SC weekly dosing regimen display a lower clearance (9.2 ± 4.7 mL/h/kg) [FDA Label]. | NA | NA | NA | NA | NA | Erythropoietin receptor | Eprex Sterile Solution 20000iu/ml | Janssen Pharmaceuticals | Janssen Pharmaceuticals | Intravenous; Subcutaneous | 20000 unit / mL | NA | headache joint or muscle aches, pain, or soreness nausea vomiting weight loss sores in the mouth difficulty falling asleep or staying asleep depression muscle spasms runny nose, sneezing, and congestion fever, cough, or chills redness, swelling, pain, or itching at the injection spot | Epoetin alfa injection products come as a solution (liquid) to inject subcutaneously (just under the skin) or intravenously (into a vein). It is usually injected one to three times weekly. When epoetin alfa injection products are used to decrease the risk that blood transfusions will be required due to surgery, it is sometimes injected once daily for 10 days before surgery, on the day of surgery and for 4 days after surgery. Alternatively, epoetin alfa injection products are sometimes injected once weekly, beginning 3 weeks before surgery and on the day of surgery. | Epoetin alfa injection products are used to treat anemia (a lower than normal number of red blood cells) in people with chronic kidney failure (condition in which the kidneys slowly and permanently stop working over a period of time). Epoetin alfa injection products are also used to treat anemia caused by chemotherapy in people with certain types of cancer or caused by zidovudine (AZT, Retrovir, in Trizivir, in Combivir), a medication used to treat human immunodeficiency virus (HIV). | potassium;[2-butyl-5-chloro-3-[[4-[2-(1,2,3-triaza-4-azanidacyclopenta-2,5-dien-5-yl)phenyl]phenyl]methyl]imidazol-4-yl]methanol | NA | Link | Link | NA |
| 10951 | Th1240 | Erythropoietin | >Th1240_Erythropoietin APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 °C | **Healthy volunteers:** The half life is approximately 4 hours in healthy volunteers receiving an intravenous injection [F85]. A half-life of approximately 6 hours has been reported in children [F85]., **Adult and paediatric patients with CRF:** The elimination half life following intravenous administration ranges from 4 to 13 hours, which is about 20% longer in CRF patients than that in healthy subjects. The half life is reported to be similar between adult patients receiving or not receiving dialysis [FDA Label]. , **Cancer patients receiving cyclic chemotherapy:** Following subcutaneous administration, the average half life is 40 hours with range of 16 to 67 hours [FDA Label]. | Erythropoietin (EPO) is a growth factor produced in the kidneys that stimulates the production of red blood cells. It works by promoting the division and differentiation of committed erythroid progenitors in the bone marrow [FDA Label]. Epoetin alfa (Epoge) was developed by Amgen Inc. in 1983 as the first rhEPO commercialized in the United States, followed by other alfa and beta formulations. Epoetin alfa is a 165-amino acid erythropoiesis-stimulating glycoprotein produced in cell culture using recombinant DNA technology and is used for the treatment of patients with anemia associated with various clinical conditions, such as chronic renal failure, antiviral drug therapy, chemotherapy, or a high risk for perioperative blood loss from surgical procedures [FDA Label]. It has a molecular weight of approximately 30,400 daltons and is produced by mammalian cells into which the human erythropoietin gene has been introduced. The product contains the identical amino acid sequence of isolated natural erythropoietin and has the same biological activity as the endogenous erythropoietin. Epoetin alfa biosimilar, such as Retacrit (epoetin alfa-epbx or epoetin zeta), has been formulated to allow more access to treatment options for patients in the market [L2784]. The biosimilar is approved by the FDA and EMA as a safe, effective and affordable biological product and displays equivalent clinical efficacy, potency, and purity to the reference product [A7504]. Epoetin alfa formulations can be administered intravenously or subcutaneously. | Indicated in adult and paediatric patients for the treatment of anemia due to Chronic Kidney Disease (CKD) in patients on dialysis and not on dialysis, treatment of anemia due to zidovudine in patients with HIV-infection, treatment of anemia due to the effects of concomitant myelosuppressive chemotherapy, and upon initiation, there is a minimum of two additional months of planned chemotherapy, reduction of allogeneic RBC transfusions in patients undergoing elective, noncardiac, nonvascular surgery. | Erythropoietin and epoetin alfa are involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is reported to increase the reticulocyte count within 10 days of initiation, followed by increases in the RBC count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [F85]. Depending on the dose administered, the rate of hemoglobin increase may vary. In patients receiving hemodialysis, a greater biologic response is not observed at doses exceeding 300 Units/kg 3 times weekly [F85]. Epoetin alfa serves to restore erythropoietin deficiency in pathological and other clinical conditions where normal production of erythropoietin is impaired or compromised. In anemic patients with chronic renal failure (CRF), administration with epoetin alfa stimulated erythropoiesis by increasing the reticulocyte count within 10 days, followed by increases in the red cell count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [FDA Label]. Epoetin alfa was shown to be effective in increasing hematocrit in zidovudine-treated HIV-infected patients and anemic cancer patients undergoing chemotherapy [FDA Label]. | Erythropoietin or exogenous epoetin alfa binds to the erythropoietin receptor (EPO-R) and activates intracellular signal transduction pathways [A33079]. The affinity (Kd) of EPO for its receptor on human cells is ~100 to 200 pM [A33080]. Upon binding to EPO-R on the surface of erythroid progenitor cells, a conformational change is induced which brings EPO-R-associated Janus family tyrosine protein kinase 2 (JAK2) molecules into close proximity. JAK2 molecules are subsequently activated via phosphorylation, then phosphorylate tyrosine residues in the cytoplasmic domain of the EPO-R that serve as docking sites for Src homology 2-domain-containing intracellular signaling proteins [A33079]. The signalling proteins include STAT5 that once phosphorylated by JAK2, dissociates from the EPO-R, dimerizes, and translocates to the nucleus where they serve as transcription factors to activate target genes involved in cell division or differentiation, including the apoptosis inhibitor Bcl-x [A33079]. The inhibition of apoptosis by the EPO-activated JAK2/STAT5/Bcl-x pathway is critical in erythroid differentiation. Via JAK2-mediated tyrosine phosphorylation, erythropoietin and epoetin alfa also activates other intracellular proteins involved in erythroid cell proliferation and survival, such as Shc , phosphatidylinositol 3-kinase (PI3K), and phospholipase C- | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. Polycythemia should be managed acutely with phlebotomy, as clinically indicated. Following resolution of the overdose, reintroduction of epoetin alfa therapy should be accompanied by close monitoring for evidence of rapid increases in hemoglobin concentration (>1 gm/dL per 14 days). In patients with an excessive hematopoietic response, reduce the dose in accordance with the recommendations described in the drug label [FDA Label]. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system [A33080]. | The time to reach peak concentration is slower via the subcutaneous route than the intravenous route which ranges from 20 to 25 hours, and the peak is always well below the peak achieved using the intravenous route (5–10% of those seen with IV administration) [A33080, L85]. The bioavailability of subcutaneous injectable erythropoietin is much lower than that of the intravenously administered product and is approximately 20-40% [A33080, L85]. **Adult and paediatric patients with CRF:** Following subcutaneous administration, the peak plasma levels are achieved within 5 to 24 hours [FDA Label]. **Cancer patients receiving cyclic chemotherapy:** The average time to reach peak plasma concentration was approximately 13.3 ± 12.4 hours after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing. The Cmax is expected be 3- to 7- fold higher and the Tmax is expected to be 2- to 3-fold longer in patients receiving a 40,000 Units SC weekly dosing regimen [FDA Label]. | In healthy volunteers, the volume of distribution of intravenous epoetin alfa was generally similar to the plasma volume (range of 40–63.80 mL/kg), indicating limited extravascular distribution [A33080, A33076]. | **Healthy volunteers: ** In male volunteers receiving intravenous epoetin alfa, the total body clearance was approximately 8.12 ± 1.00 mL/h/kg [A33076]. **Cancer patients receiving cyclic chemotherapy:** The average clearance was approximately 20.2 ± 15.9 mL/h/kg after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing [FDA Label]. The patients receiving a 40,000 Units SC weekly dosing regimen display a lower clearance (9.2 ± 4.7 mL/h/kg) [FDA Label]. | NA | NA | NA | NA | NA | Erythropoietin receptor | Eprex Sterile Solution 2000iu/0.5ml | Janssen Pharmaceuticals | Janssen Pharmaceuticals | Intravenous; Subcutaneous | 2000 unit / 0.5 mL | NA | headache joint or muscle aches, pain, or soreness nausea vomiting weight loss sores in the mouth difficulty falling asleep or staying asleep depression muscle spasms runny nose, sneezing, and congestion fever, cough, or chills redness, swelling, pain, or itching at the injection spot | Epoetin alfa injection products come as a solution (liquid) to inject subcutaneously (just under the skin) or intravenously (into a vein). It is usually injected one to three times weekly. When epoetin alfa injection products are used to decrease the risk that blood transfusions will be required due to surgery, it is sometimes injected once daily for 10 days before surgery, on the day of surgery and for 4 days after surgery. Alternatively, epoetin alfa injection products are sometimes injected once weekly, beginning 3 weeks before surgery and on the day of surgery. | Epoetin alfa injection products are used to treat anemia (a lower than normal number of red blood cells) in people with chronic kidney failure (condition in which the kidneys slowly and permanently stop working over a period of time). Epoetin alfa injection products are also used to treat anemia caused by chemotherapy in people with certain types of cancer or caused by zidovudine (AZT, Retrovir, in Trizivir, in Combivir), a medication used to treat human immunodeficiency virus (HIV). | potassium;[2-butyl-5-chloro-3-[[4-[2-(1,2,3-triaza-4-azanidacyclopenta-2,5-dien-5-yl)phenyl]phenyl]methyl]imidazol-4-yl]methanol | NA | Link | Link | NA |
| 10952 | Th1240 | Erythropoietin | >Th1240_Erythropoietin APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 °C | **Healthy volunteers:** The half life is approximately 4 hours in healthy volunteers receiving an intravenous injection [F85]. A half-life of approximately 6 hours has been reported in children [F85]., **Adult and paediatric patients with CRF:** The elimination half life following intravenous administration ranges from 4 to 13 hours, which is about 20% longer in CRF patients than that in healthy subjects. The half life is reported to be similar between adult patients receiving or not receiving dialysis [FDA Label]. , **Cancer patients receiving cyclic chemotherapy:** Following subcutaneous administration, the average half life is 40 hours with range of 16 to 67 hours [FDA Label]. | Erythropoietin (EPO) is a growth factor produced in the kidneys that stimulates the production of red blood cells. It works by promoting the division and differentiation of committed erythroid progenitors in the bone marrow [FDA Label]. Epoetin alfa (Epoge) was developed by Amgen Inc. in 1983 as the first rhEPO commercialized in the United States, followed by other alfa and beta formulations. Epoetin alfa is a 165-amino acid erythropoiesis-stimulating glycoprotein produced in cell culture using recombinant DNA technology and is used for the treatment of patients with anemia associated with various clinical conditions, such as chronic renal failure, antiviral drug therapy, chemotherapy, or a high risk for perioperative blood loss from surgical procedures [FDA Label]. It has a molecular weight of approximately 30,400 daltons and is produced by mammalian cells into which the human erythropoietin gene has been introduced. The product contains the identical amino acid sequence of isolated natural erythropoietin and has the same biological activity as the endogenous erythropoietin. Epoetin alfa biosimilar, such as Retacrit (epoetin alfa-epbx or epoetin zeta), has been formulated to allow more access to treatment options for patients in the market [L2784]. The biosimilar is approved by the FDA and EMA as a safe, effective and affordable biological product and displays equivalent clinical efficacy, potency, and purity to the reference product [A7504]. Epoetin alfa formulations can be administered intravenously or subcutaneously. | Indicated in adult and paediatric patients for the treatment of anemia due to Chronic Kidney Disease (CKD) in patients on dialysis and not on dialysis, treatment of anemia due to zidovudine in patients with HIV-infection, treatment of anemia due to the effects of concomitant myelosuppressive chemotherapy, and upon initiation, there is a minimum of two additional months of planned chemotherapy, reduction of allogeneic RBC transfusions in patients undergoing elective, noncardiac, nonvascular surgery. | Erythropoietin and epoetin alfa are involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is reported to increase the reticulocyte count within 10 days of initiation, followed by increases in the RBC count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [F85]. Depending on the dose administered, the rate of hemoglobin increase may vary. In patients receiving hemodialysis, a greater biologic response is not observed at doses exceeding 300 Units/kg 3 times weekly [F85]. Epoetin alfa serves to restore erythropoietin deficiency in pathological and other clinical conditions where normal production of erythropoietin is impaired or compromised. In anemic patients with chronic renal failure (CRF), administration with epoetin alfa stimulated erythropoiesis by increasing the reticulocyte count within 10 days, followed by increases in the red cell count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [FDA Label]. Epoetin alfa was shown to be effective in increasing hematocrit in zidovudine-treated HIV-infected patients and anemic cancer patients undergoing chemotherapy [FDA Label]. | Erythropoietin or exogenous epoetin alfa binds to the erythropoietin receptor (EPO-R) and activates intracellular signal transduction pathways [A33079]. The affinity (Kd) of EPO for its receptor on human cells is ~100 to 200 pM [A33080]. Upon binding to EPO-R on the surface of erythroid progenitor cells, a conformational change is induced which brings EPO-R-associated Janus family tyrosine protein kinase 2 (JAK2) molecules into close proximity. JAK2 molecules are subsequently activated via phosphorylation, then phosphorylate tyrosine residues in the cytoplasmic domain of the EPO-R that serve as docking sites for Src homology 2-domain-containing intracellular signaling proteins [A33079]. The signalling proteins include STAT5 that once phosphorylated by JAK2, dissociates from the EPO-R, dimerizes, and translocates to the nucleus where they serve as transcription factors to activate target genes involved in cell division or differentiation, including the apoptosis inhibitor Bcl-x [A33079]. The inhibition of apoptosis by the EPO-activated JAK2/STAT5/Bcl-x pathway is critical in erythroid differentiation. Via JAK2-mediated tyrosine phosphorylation, erythropoietin and epoetin alfa also activates other intracellular proteins involved in erythroid cell proliferation and survival, such as Shc , phosphatidylinositol 3-kinase (PI3K), and phospholipase C- | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. Polycythemia should be managed acutely with phlebotomy, as clinically indicated. Following resolution of the overdose, reintroduction of epoetin alfa therapy should be accompanied by close monitoring for evidence of rapid increases in hemoglobin concentration (>1 gm/dL per 14 days). In patients with an excessive hematopoietic response, reduce the dose in accordance with the recommendations described in the drug label [FDA Label]. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system [A33080]. | The time to reach peak concentration is slower via the subcutaneous route than the intravenous route which ranges from 20 to 25 hours, and the peak is always well below the peak achieved using the intravenous route (5–10% of those seen with IV administration) [A33080, L85]. The bioavailability of subcutaneous injectable erythropoietin is much lower than that of the intravenously administered product and is approximately 20-40% [A33080, L85]. **Adult and paediatric patients with CRF:** Following subcutaneous administration, the peak plasma levels are achieved within 5 to 24 hours [FDA Label]. **Cancer patients receiving cyclic chemotherapy:** The average time to reach peak plasma concentration was approximately 13.3 ± 12.4 hours after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing. The Cmax is expected be 3- to 7- fold higher and the Tmax is expected to be 2- to 3-fold longer in patients receiving a 40,000 Units SC weekly dosing regimen [FDA Label]. | In healthy volunteers, the volume of distribution of intravenous epoetin alfa was generally similar to the plasma volume (range of 40–63.80 mL/kg), indicating limited extravascular distribution [A33080, A33076]. | **Healthy volunteers: ** In male volunteers receiving intravenous epoetin alfa, the total body clearance was approximately 8.12 ± 1.00 mL/h/kg [A33076]. **Cancer patients receiving cyclic chemotherapy:** The average clearance was approximately 20.2 ± 15.9 mL/h/kg after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing [FDA Label]. The patients receiving a 40,000 Units SC weekly dosing regimen display a lower clearance (9.2 ± 4.7 mL/h/kg) [FDA Label]. | NA | NA | NA | NA | NA | Erythropoietin receptor | Eprex Sterile Solution 2000iu/ml | Janssen Pharmaceuticals | Janssen Pharmaceuticals | Intravenous; Subcutaneous | 2000 unit / mL | NA | headache joint or muscle aches, pain, or soreness nausea vomiting weight loss sores in the mouth difficulty falling asleep or staying asleep depression muscle spasms runny nose, sneezing, and congestion fever, cough, or chills redness, swelling, pain, or itching at the injection spot | Epoetin alfa injection products come as a solution (liquid) to inject subcutaneously (just under the skin) or intravenously (into a vein). It is usually injected one to three times weekly. When epoetin alfa injection products are used to decrease the risk that blood transfusions will be required due to surgery, it is sometimes injected once daily for 10 days before surgery, on the day of surgery and for 4 days after surgery. Alternatively, epoetin alfa injection products are sometimes injected once weekly, beginning 3 weeks before surgery and on the day of surgery. | Epoetin alfa injection products are used to treat anemia (a lower than normal number of red blood cells) in people with chronic kidney failure (condition in which the kidneys slowly and permanently stop working over a period of time). Epoetin alfa injection products are also used to treat anemia caused by chemotherapy in people with certain types of cancer or caused by zidovudine (AZT, Retrovir, in Trizivir, in Combivir), a medication used to treat human immunodeficiency virus (HIV). | potassium;[2-butyl-5-chloro-3-[[4-[2-(1,2,3-triaza-4-azanidacyclopenta-2,5-dien-5-yl)phenyl]phenyl]methyl]imidazol-4-yl]methanol | NA | Link | Link | NA |
| 10953 | Th1240 | Erythropoietin | >Th1240_Erythropoietin APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 °C | **Healthy volunteers:** The half life is approximately 4 hours in healthy volunteers receiving an intravenous injection [F85]. A half-life of approximately 6 hours has been reported in children [F85]., **Adult and paediatric patients with CRF:** The elimination half life following intravenous administration ranges from 4 to 13 hours, which is about 20% longer in CRF patients than that in healthy subjects. The half life is reported to be similar between adult patients receiving or not receiving dialysis [FDA Label]. , **Cancer patients receiving cyclic chemotherapy:** Following subcutaneous administration, the average half life is 40 hours with range of 16 to 67 hours [FDA Label]. | Erythropoietin (EPO) is a growth factor produced in the kidneys that stimulates the production of red blood cells. It works by promoting the division and differentiation of committed erythroid progenitors in the bone marrow [FDA Label]. Epoetin alfa (Epoge) was developed by Amgen Inc. in 1983 as the first rhEPO commercialized in the United States, followed by other alfa and beta formulations. Epoetin alfa is a 165-amino acid erythropoiesis-stimulating glycoprotein produced in cell culture using recombinant DNA technology and is used for the treatment of patients with anemia associated with various clinical conditions, such as chronic renal failure, antiviral drug therapy, chemotherapy, or a high risk for perioperative blood loss from surgical procedures [FDA Label]. It has a molecular weight of approximately 30,400 daltons and is produced by mammalian cells into which the human erythropoietin gene has been introduced. The product contains the identical amino acid sequence of isolated natural erythropoietin and has the same biological activity as the endogenous erythropoietin. Epoetin alfa biosimilar, such as Retacrit (epoetin alfa-epbx or epoetin zeta), has been formulated to allow more access to treatment options for patients in the market [L2784]. The biosimilar is approved by the FDA and EMA as a safe, effective and affordable biological product and displays equivalent clinical efficacy, potency, and purity to the reference product [A7504]. Epoetin alfa formulations can be administered intravenously or subcutaneously. | Indicated in adult and paediatric patients for the treatment of anemia due to Chronic Kidney Disease (CKD) in patients on dialysis and not on dialysis, treatment of anemia due to zidovudine in patients with HIV-infection, treatment of anemia due to the effects of concomitant myelosuppressive chemotherapy, and upon initiation, there is a minimum of two additional months of planned chemotherapy, reduction of allogeneic RBC transfusions in patients undergoing elective, noncardiac, nonvascular surgery. | Erythropoietin and epoetin alfa are involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is reported to increase the reticulocyte count within 10 days of initiation, followed by increases in the RBC count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [F85]. Depending on the dose administered, the rate of hemoglobin increase may vary. In patients receiving hemodialysis, a greater biologic response is not observed at doses exceeding 300 Units/kg 3 times weekly [F85]. Epoetin alfa serves to restore erythropoietin deficiency in pathological and other clinical conditions where normal production of erythropoietin is impaired or compromised. In anemic patients with chronic renal failure (CRF), administration with epoetin alfa stimulated erythropoiesis by increasing the reticulocyte count within 10 days, followed by increases in the red cell count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [FDA Label]. Epoetin alfa was shown to be effective in increasing hematocrit in zidovudine-treated HIV-infected patients and anemic cancer patients undergoing chemotherapy [FDA Label]. | Erythropoietin or exogenous epoetin alfa binds to the erythropoietin receptor (EPO-R) and activates intracellular signal transduction pathways [A33079]. The affinity (Kd) of EPO for its receptor on human cells is ~100 to 200 pM [A33080]. Upon binding to EPO-R on the surface of erythroid progenitor cells, a conformational change is induced which brings EPO-R-associated Janus family tyrosine protein kinase 2 (JAK2) molecules into close proximity. JAK2 molecules are subsequently activated via phosphorylation, then phosphorylate tyrosine residues in the cytoplasmic domain of the EPO-R that serve as docking sites for Src homology 2-domain-containing intracellular signaling proteins [A33079]. The signalling proteins include STAT5 that once phosphorylated by JAK2, dissociates from the EPO-R, dimerizes, and translocates to the nucleus where they serve as transcription factors to activate target genes involved in cell division or differentiation, including the apoptosis inhibitor Bcl-x [A33079]. The inhibition of apoptosis by the EPO-activated JAK2/STAT5/Bcl-x pathway is critical in erythroid differentiation. Via JAK2-mediated tyrosine phosphorylation, erythropoietin and epoetin alfa also activates other intracellular proteins involved in erythroid cell proliferation and survival, such as Shc , phosphatidylinositol 3-kinase (PI3K), and phospholipase C- | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. Polycythemia should be managed acutely with phlebotomy, as clinically indicated. Following resolution of the overdose, reintroduction of epoetin alfa therapy should be accompanied by close monitoring for evidence of rapid increases in hemoglobin concentration (>1 gm/dL per 14 days). In patients with an excessive hematopoietic response, reduce the dose in accordance with the recommendations described in the drug label [FDA Label]. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system [A33080]. | The time to reach peak concentration is slower via the subcutaneous route than the intravenous route which ranges from 20 to 25 hours, and the peak is always well below the peak achieved using the intravenous route (5–10% of those seen with IV administration) [A33080, L85]. The bioavailability of subcutaneous injectable erythropoietin is much lower than that of the intravenously administered product and is approximately 20-40% [A33080, L85]. **Adult and paediatric patients with CRF:** Following subcutaneous administration, the peak plasma levels are achieved within 5 to 24 hours [FDA Label]. **Cancer patients receiving cyclic chemotherapy:** The average time to reach peak plasma concentration was approximately 13.3 ± 12.4 hours after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing. The Cmax is expected be 3- to 7- fold higher and the Tmax is expected to be 2- to 3-fold longer in patients receiving a 40,000 Units SC weekly dosing regimen [FDA Label]. | In healthy volunteers, the volume of distribution of intravenous epoetin alfa was generally similar to the plasma volume (range of 40–63.80 mL/kg), indicating limited extravascular distribution [A33080, A33076]. | **Healthy volunteers: ** In male volunteers receiving intravenous epoetin alfa, the total body clearance was approximately 8.12 ± 1.00 mL/h/kg [A33076]. **Cancer patients receiving cyclic chemotherapy:** The average clearance was approximately 20.2 ± 15.9 mL/h/kg after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing [FDA Label]. The patients receiving a 40,000 Units SC weekly dosing regimen display a lower clearance (9.2 ± 4.7 mL/h/kg) [FDA Label]. | NA | NA | NA | NA | NA | Erythropoietin receptor | Eprex Sterile Solution 3000iu/0.3ml | Janssen Pharmaceuticals | Janssen Pharmaceuticals | Intravenous; Subcutaneous | 3000 unit / 0.3 mL | NA | headache joint or muscle aches, pain, or soreness nausea vomiting weight loss sores in the mouth difficulty falling asleep or staying asleep depression muscle spasms runny nose, sneezing, and congestion fever, cough, or chills redness, swelling, pain, or itching at the injection spot | Epoetin alfa injection products come as a solution (liquid) to inject subcutaneously (just under the skin) or intravenously (into a vein). It is usually injected one to three times weekly. When epoetin alfa injection products are used to decrease the risk that blood transfusions will be required due to surgery, it is sometimes injected once daily for 10 days before surgery, on the day of surgery and for 4 days after surgery. Alternatively, epoetin alfa injection products are sometimes injected once weekly, beginning 3 weeks before surgery and on the day of surgery. | Epoetin alfa injection products are used to treat anemia (a lower than normal number of red blood cells) in people with chronic kidney failure (condition in which the kidneys slowly and permanently stop working over a period of time). Epoetin alfa injection products are also used to treat anemia caused by chemotherapy in people with certain types of cancer or caused by zidovudine (AZT, Retrovir, in Trizivir, in Combivir), a medication used to treat human immunodeficiency virus (HIV). | potassium;[2-butyl-5-chloro-3-[[4-[2-(1,2,3-triaza-4-azanidacyclopenta-2,5-dien-5-yl)phenyl]phenyl]methyl]imidazol-4-yl]methanol | NA | Link | Link | NA |
| 10954 | Th1240 | Erythropoietin | >Th1240_Erythropoietin APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 °C | **Healthy volunteers:** The half life is approximately 4 hours in healthy volunteers receiving an intravenous injection [F85]. A half-life of approximately 6 hours has been reported in children [F85]., **Adult and paediatric patients with CRF:** The elimination half life following intravenous administration ranges from 4 to 13 hours, which is about 20% longer in CRF patients than that in healthy subjects. The half life is reported to be similar between adult patients receiving or not receiving dialysis [FDA Label]. , **Cancer patients receiving cyclic chemotherapy:** Following subcutaneous administration, the average half life is 40 hours with range of 16 to 67 hours [FDA Label]. | Erythropoietin (EPO) is a growth factor produced in the kidneys that stimulates the production of red blood cells. It works by promoting the division and differentiation of committed erythroid progenitors in the bone marrow [FDA Label]. Epoetin alfa (Epoge) was developed by Amgen Inc. in 1983 as the first rhEPO commercialized in the United States, followed by other alfa and beta formulations. Epoetin alfa is a 165-amino acid erythropoiesis-stimulating glycoprotein produced in cell culture using recombinant DNA technology and is used for the treatment of patients with anemia associated with various clinical conditions, such as chronic renal failure, antiviral drug therapy, chemotherapy, or a high risk for perioperative blood loss from surgical procedures [FDA Label]. It has a molecular weight of approximately 30,400 daltons and is produced by mammalian cells into which the human erythropoietin gene has been introduced. The product contains the identical amino acid sequence of isolated natural erythropoietin and has the same biological activity as the endogenous erythropoietin. Epoetin alfa biosimilar, such as Retacrit (epoetin alfa-epbx or epoetin zeta), has been formulated to allow more access to treatment options for patients in the market [L2784]. The biosimilar is approved by the FDA and EMA as a safe, effective and affordable biological product and displays equivalent clinical efficacy, potency, and purity to the reference product [A7504]. Epoetin alfa formulations can be administered intravenously or subcutaneously. | Indicated in adult and paediatric patients for the treatment of anemia due to Chronic Kidney Disease (CKD) in patients on dialysis and not on dialysis, treatment of anemia due to zidovudine in patients with HIV-infection, treatment of anemia due to the effects of concomitant myelosuppressive chemotherapy, and upon initiation, there is a minimum of two additional months of planned chemotherapy, reduction of allogeneic RBC transfusions in patients undergoing elective, noncardiac, nonvascular surgery. | Erythropoietin and epoetin alfa are involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is reported to increase the reticulocyte count within 10 days of initiation, followed by increases in the RBC count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [F85]. Depending on the dose administered, the rate of hemoglobin increase may vary. In patients receiving hemodialysis, a greater biologic response is not observed at doses exceeding 300 Units/kg 3 times weekly [F85]. Epoetin alfa serves to restore erythropoietin deficiency in pathological and other clinical conditions where normal production of erythropoietin is impaired or compromised. In anemic patients with chronic renal failure (CRF), administration with epoetin alfa stimulated erythropoiesis by increasing the reticulocyte count within 10 days, followed by increases in the red cell count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [FDA Label]. Epoetin alfa was shown to be effective in increasing hematocrit in zidovudine-treated HIV-infected patients and anemic cancer patients undergoing chemotherapy [FDA Label]. | Erythropoietin or exogenous epoetin alfa binds to the erythropoietin receptor (EPO-R) and activates intracellular signal transduction pathways [A33079]. The affinity (Kd) of EPO for its receptor on human cells is ~100 to 200 pM [A33080]. Upon binding to EPO-R on the surface of erythroid progenitor cells, a conformational change is induced which brings EPO-R-associated Janus family tyrosine protein kinase 2 (JAK2) molecules into close proximity. JAK2 molecules are subsequently activated via phosphorylation, then phosphorylate tyrosine residues in the cytoplasmic domain of the EPO-R that serve as docking sites for Src homology 2-domain-containing intracellular signaling proteins [A33079]. The signalling proteins include STAT5 that once phosphorylated by JAK2, dissociates from the EPO-R, dimerizes, and translocates to the nucleus where they serve as transcription factors to activate target genes involved in cell division or differentiation, including the apoptosis inhibitor Bcl-x [A33079]. The inhibition of apoptosis by the EPO-activated JAK2/STAT5/Bcl-x pathway is critical in erythroid differentiation. Via JAK2-mediated tyrosine phosphorylation, erythropoietin and epoetin alfa also activates other intracellular proteins involved in erythroid cell proliferation and survival, such as Shc , phosphatidylinositol 3-kinase (PI3K), and phospholipase C- | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. Polycythemia should be managed acutely with phlebotomy, as clinically indicated. Following resolution of the overdose, reintroduction of epoetin alfa therapy should be accompanied by close monitoring for evidence of rapid increases in hemoglobin concentration (>1 gm/dL per 14 days). In patients with an excessive hematopoietic response, reduce the dose in accordance with the recommendations described in the drug label [FDA Label]. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system [A33080]. | The time to reach peak concentration is slower via the subcutaneous route than the intravenous route which ranges from 20 to 25 hours, and the peak is always well below the peak achieved using the intravenous route (5–10% of those seen with IV administration) [A33080, L85]. The bioavailability of subcutaneous injectable erythropoietin is much lower than that of the intravenously administered product and is approximately 20-40% [A33080, L85]. **Adult and paediatric patients with CRF:** Following subcutaneous administration, the peak plasma levels are achieved within 5 to 24 hours [FDA Label]. **Cancer patients receiving cyclic chemotherapy:** The average time to reach peak plasma concentration was approximately 13.3 ± 12.4 hours after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing. The Cmax is expected be 3- to 7- fold higher and the Tmax is expected to be 2- to 3-fold longer in patients receiving a 40,000 Units SC weekly dosing regimen [FDA Label]. | In healthy volunteers, the volume of distribution of intravenous epoetin alfa was generally similar to the plasma volume (range of 40–63.80 mL/kg), indicating limited extravascular distribution [A33080, A33076]. | **Healthy volunteers: ** In male volunteers receiving intravenous epoetin alfa, the total body clearance was approximately 8.12 ± 1.00 mL/h/kg [A33076]. **Cancer patients receiving cyclic chemotherapy:** The average clearance was approximately 20.2 ± 15.9 mL/h/kg after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing [FDA Label]. The patients receiving a 40,000 Units SC weekly dosing regimen display a lower clearance (9.2 ± 4.7 mL/h/kg) [FDA Label]. | NA | NA | NA | NA | NA | Erythropoietin receptor | Eprex Sterile Solution 40000iu/ml | Janssen Pharmaceuticals | Janssen Pharmaceuticals | Intravenous; Subcutaneous | 40000 unit / mL | NA | headache joint or muscle aches, pain, or soreness nausea vomiting weight loss sores in the mouth difficulty falling asleep or staying asleep depression muscle spasms runny nose, sneezing, and congestion fever, cough, or chills redness, swelling, pain, or itching at the injection spot | Epoetin alfa injection products come as a solution (liquid) to inject subcutaneously (just under the skin) or intravenously (into a vein). It is usually injected one to three times weekly. When epoetin alfa injection products are used to decrease the risk that blood transfusions will be required due to surgery, it is sometimes injected once daily for 10 days before surgery, on the day of surgery and for 4 days after surgery. Alternatively, epoetin alfa injection products are sometimes injected once weekly, beginning 3 weeks before surgery and on the day of surgery. | Epoetin alfa injection products are used to treat anemia (a lower than normal number of red blood cells) in people with chronic kidney failure (condition in which the kidneys slowly and permanently stop working over a period of time). Epoetin alfa injection products are also used to treat anemia caused by chemotherapy in people with certain types of cancer or caused by zidovudine (AZT, Retrovir, in Trizivir, in Combivir), a medication used to treat human immunodeficiency virus (HIV). | potassium;[2-butyl-5-chloro-3-[[4-[2-(1,2,3-triaza-4-azanidacyclopenta-2,5-dien-5-yl)phenyl]phenyl]methyl]imidazol-4-yl]methanol | NA | Link | Link | NA |
| 10955 | Th1240 | Erythropoietin | >Th1240_Erythropoietin APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 °C | **Healthy volunteers:** The half life is approximately 4 hours in healthy volunteers receiving an intravenous injection [F85]. A half-life of approximately 6 hours has been reported in children [F85]., **Adult and paediatric patients with CRF:** The elimination half life following intravenous administration ranges from 4 to 13 hours, which is about 20% longer in CRF patients than that in healthy subjects. The half life is reported to be similar between adult patients receiving or not receiving dialysis [FDA Label]. , **Cancer patients receiving cyclic chemotherapy:** Following subcutaneous administration, the average half life is 40 hours with range of 16 to 67 hours [FDA Label]. | Erythropoietin (EPO) is a growth factor produced in the kidneys that stimulates the production of red blood cells. It works by promoting the division and differentiation of committed erythroid progenitors in the bone marrow [FDA Label]. Epoetin alfa (Epoge) was developed by Amgen Inc. in 1983 as the first rhEPO commercialized in the United States, followed by other alfa and beta formulations. Epoetin alfa is a 165-amino acid erythropoiesis-stimulating glycoprotein produced in cell culture using recombinant DNA technology and is used for the treatment of patients with anemia associated with various clinical conditions, such as chronic renal failure, antiviral drug therapy, chemotherapy, or a high risk for perioperative blood loss from surgical procedures [FDA Label]. It has a molecular weight of approximately 30,400 daltons and is produced by mammalian cells into which the human erythropoietin gene has been introduced. The product contains the identical amino acid sequence of isolated natural erythropoietin and has the same biological activity as the endogenous erythropoietin. Epoetin alfa biosimilar, such as Retacrit (epoetin alfa-epbx or epoetin zeta), has been formulated to allow more access to treatment options for patients in the market [L2784]. The biosimilar is approved by the FDA and EMA as a safe, effective and affordable biological product and displays equivalent clinical efficacy, potency, and purity to the reference product [A7504]. Epoetin alfa formulations can be administered intravenously or subcutaneously. | Indicated in adult and paediatric patients for the treatment of anemia due to Chronic Kidney Disease (CKD) in patients on dialysis and not on dialysis, treatment of anemia due to zidovudine in patients with HIV-infection, treatment of anemia due to the effects of concomitant myelosuppressive chemotherapy, and upon initiation, there is a minimum of two additional months of planned chemotherapy, reduction of allogeneic RBC transfusions in patients undergoing elective, noncardiac, nonvascular surgery. | Erythropoietin and epoetin alfa are involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is reported to increase the reticulocyte count within 10 days of initiation, followed by increases in the RBC count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [F85]. Depending on the dose administered, the rate of hemoglobin increase may vary. In patients receiving hemodialysis, a greater biologic response is not observed at doses exceeding 300 Units/kg 3 times weekly [F85]. Epoetin alfa serves to restore erythropoietin deficiency in pathological and other clinical conditions where normal production of erythropoietin is impaired or compromised. In anemic patients with chronic renal failure (CRF), administration with epoetin alfa stimulated erythropoiesis by increasing the reticulocyte count within 10 days, followed by increases in the red cell count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [FDA Label]. Epoetin alfa was shown to be effective in increasing hematocrit in zidovudine-treated HIV-infected patients and anemic cancer patients undergoing chemotherapy [FDA Label]. | Erythropoietin or exogenous epoetin alfa binds to the erythropoietin receptor (EPO-R) and activates intracellular signal transduction pathways [A33079]. The affinity (Kd) of EPO for its receptor on human cells is ~100 to 200 pM [A33080]. Upon binding to EPO-R on the surface of erythroid progenitor cells, a conformational change is induced which brings EPO-R-associated Janus family tyrosine protein kinase 2 (JAK2) molecules into close proximity. JAK2 molecules are subsequently activated via phosphorylation, then phosphorylate tyrosine residues in the cytoplasmic domain of the EPO-R that serve as docking sites for Src homology 2-domain-containing intracellular signaling proteins [A33079]. The signalling proteins include STAT5 that once phosphorylated by JAK2, dissociates from the EPO-R, dimerizes, and translocates to the nucleus where they serve as transcription factors to activate target genes involved in cell division or differentiation, including the apoptosis inhibitor Bcl-x [A33079]. The inhibition of apoptosis by the EPO-activated JAK2/STAT5/Bcl-x pathway is critical in erythroid differentiation. Via JAK2-mediated tyrosine phosphorylation, erythropoietin and epoetin alfa also activates other intracellular proteins involved in erythroid cell proliferation and survival, such as Shc , phosphatidylinositol 3-kinase (PI3K), and phospholipase C- | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. Polycythemia should be managed acutely with phlebotomy, as clinically indicated. Following resolution of the overdose, reintroduction of epoetin alfa therapy should be accompanied by close monitoring for evidence of rapid increases in hemoglobin concentration (>1 gm/dL per 14 days). In patients with an excessive hematopoietic response, reduce the dose in accordance with the recommendations described in the drug label [FDA Label]. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system [A33080]. | The time to reach peak concentration is slower via the subcutaneous route than the intravenous route which ranges from 20 to 25 hours, and the peak is always well below the peak achieved using the intravenous route (5–10% of those seen with IV administration) [A33080, L85]. The bioavailability of subcutaneous injectable erythropoietin is much lower than that of the intravenously administered product and is approximately 20-40% [A33080, L85]. **Adult and paediatric patients with CRF:** Following subcutaneous administration, the peak plasma levels are achieved within 5 to 24 hours [FDA Label]. **Cancer patients receiving cyclic chemotherapy:** The average time to reach peak plasma concentration was approximately 13.3 ± 12.4 hours after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing. The Cmax is expected be 3- to 7- fold higher and the Tmax is expected to be 2- to 3-fold longer in patients receiving a 40,000 Units SC weekly dosing regimen [FDA Label]. | In healthy volunteers, the volume of distribution of intravenous epoetin alfa was generally similar to the plasma volume (range of 40–63.80 mL/kg), indicating limited extravascular distribution [A33080, A33076]. | **Healthy volunteers: ** In male volunteers receiving intravenous epoetin alfa, the total body clearance was approximately 8.12 ± 1.00 mL/h/kg [A33076]. **Cancer patients receiving cyclic chemotherapy:** The average clearance was approximately 20.2 ± 15.9 mL/h/kg after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing [FDA Label]. The patients receiving a 40,000 Units SC weekly dosing regimen display a lower clearance (9.2 ± 4.7 mL/h/kg) [FDA Label]. | NA | NA | NA | NA | NA | Erythropoietin receptor | Eprex Sterile Solution 4000iu/0.4ml | Janssen Pharmaceuticals | Janssen Pharmaceuticals | Intravenous; Subcutaneous | 4000 unit / 0.4 mL | NA | headache joint or muscle aches, pain, or soreness nausea vomiting weight loss sores in the mouth difficulty falling asleep or staying asleep depression muscle spasms runny nose, sneezing, and congestion fever, cough, or chills redness, swelling, pain, or itching at the injection spot | Epoetin alfa injection products come as a solution (liquid) to inject subcutaneously (just under the skin) or intravenously (into a vein). It is usually injected one to three times weekly. When epoetin alfa injection products are used to decrease the risk that blood transfusions will be required due to surgery, it is sometimes injected once daily for 10 days before surgery, on the day of surgery and for 4 days after surgery. Alternatively, epoetin alfa injection products are sometimes injected once weekly, beginning 3 weeks before surgery and on the day of surgery. | Epoetin alfa injection products are used to treat anemia (a lower than normal number of red blood cells) in people with chronic kidney failure (condition in which the kidneys slowly and permanently stop working over a period of time). Epoetin alfa injection products are also used to treat anemia caused by chemotherapy in people with certain types of cancer or caused by zidovudine (AZT, Retrovir, in Trizivir, in Combivir), a medication used to treat human immunodeficiency virus (HIV). | potassium;[2-butyl-5-chloro-3-[[4-[2-(1,2,3-triaza-4-azanidacyclopenta-2,5-dien-5-yl)phenyl]phenyl]methyl]imidazol-4-yl]methanol | NA | Link | Link | NA |
| 10956 | Th1240 | Erythropoietin | >Th1240_Erythropoietin APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 °C | **Healthy volunteers:** The half life is approximately 4 hours in healthy volunteers receiving an intravenous injection [F85]. A half-life of approximately 6 hours has been reported in children [F85]., **Adult and paediatric patients with CRF:** The elimination half life following intravenous administration ranges from 4 to 13 hours, which is about 20% longer in CRF patients than that in healthy subjects. The half life is reported to be similar between adult patients receiving or not receiving dialysis [FDA Label]. , **Cancer patients receiving cyclic chemotherapy:** Following subcutaneous administration, the average half life is 40 hours with range of 16 to 67 hours [FDA Label]. | Erythropoietin (EPO) is a growth factor produced in the kidneys that stimulates the production of red blood cells. It works by promoting the division and differentiation of committed erythroid progenitors in the bone marrow [FDA Label]. Epoetin alfa (Epoge) was developed by Amgen Inc. in 1983 as the first rhEPO commercialized in the United States, followed by other alfa and beta formulations. Epoetin alfa is a 165-amino acid erythropoiesis-stimulating glycoprotein produced in cell culture using recombinant DNA technology and is used for the treatment of patients with anemia associated with various clinical conditions, such as chronic renal failure, antiviral drug therapy, chemotherapy, or a high risk for perioperative blood loss from surgical procedures [FDA Label]. It has a molecular weight of approximately 30,400 daltons and is produced by mammalian cells into which the human erythropoietin gene has been introduced. The product contains the identical amino acid sequence of isolated natural erythropoietin and has the same biological activity as the endogenous erythropoietin. Epoetin alfa biosimilar, such as Retacrit (epoetin alfa-epbx or epoetin zeta), has been formulated to allow more access to treatment options for patients in the market [L2784]. The biosimilar is approved by the FDA and EMA as a safe, effective and affordable biological product and displays equivalent clinical efficacy, potency, and purity to the reference product [A7504]. Epoetin alfa formulations can be administered intravenously or subcutaneously. | Indicated in adult and paediatric patients for the treatment of anemia due to Chronic Kidney Disease (CKD) in patients on dialysis and not on dialysis, treatment of anemia due to zidovudine in patients with HIV-infection, treatment of anemia due to the effects of concomitant myelosuppressive chemotherapy, and upon initiation, there is a minimum of two additional months of planned chemotherapy, reduction of allogeneic RBC transfusions in patients undergoing elective, noncardiac, nonvascular surgery. | Erythropoietin and epoetin alfa are involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is reported to increase the reticulocyte count within 10 days of initiation, followed by increases in the RBC count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [F85]. Depending on the dose administered, the rate of hemoglobin increase may vary. In patients receiving hemodialysis, a greater biologic response is not observed at doses exceeding 300 Units/kg 3 times weekly [F85]. Epoetin alfa serves to restore erythropoietin deficiency in pathological and other clinical conditions where normal production of erythropoietin is impaired or compromised. In anemic patients with chronic renal failure (CRF), administration with epoetin alfa stimulated erythropoiesis by increasing the reticulocyte count within 10 days, followed by increases in the red cell count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [FDA Label]. Epoetin alfa was shown to be effective in increasing hematocrit in zidovudine-treated HIV-infected patients and anemic cancer patients undergoing chemotherapy [FDA Label]. | Erythropoietin or exogenous epoetin alfa binds to the erythropoietin receptor (EPO-R) and activates intracellular signal transduction pathways [A33079]. The affinity (Kd) of EPO for its receptor on human cells is ~100 to 200 pM [A33080]. Upon binding to EPO-R on the surface of erythroid progenitor cells, a conformational change is induced which brings EPO-R-associated Janus family tyrosine protein kinase 2 (JAK2) molecules into close proximity. JAK2 molecules are subsequently activated via phosphorylation, then phosphorylate tyrosine residues in the cytoplasmic domain of the EPO-R that serve as docking sites for Src homology 2-domain-containing intracellular signaling proteins [A33079]. The signalling proteins include STAT5 that once phosphorylated by JAK2, dissociates from the EPO-R, dimerizes, and translocates to the nucleus where they serve as transcription factors to activate target genes involved in cell division or differentiation, including the apoptosis inhibitor Bcl-x [A33079]. The inhibition of apoptosis by the EPO-activated JAK2/STAT5/Bcl-x pathway is critical in erythroid differentiation. Via JAK2-mediated tyrosine phosphorylation, erythropoietin and epoetin alfa also activates other intracellular proteins involved in erythroid cell proliferation and survival, such as Shc , phosphatidylinositol 3-kinase (PI3K), and phospholipase C- | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. Polycythemia should be managed acutely with phlebotomy, as clinically indicated. Following resolution of the overdose, reintroduction of epoetin alfa therapy should be accompanied by close monitoring for evidence of rapid increases in hemoglobin concentration (>1 gm/dL per 14 days). In patients with an excessive hematopoietic response, reduce the dose in accordance with the recommendations described in the drug label [FDA Label]. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system [A33080]. | The time to reach peak concentration is slower via the subcutaneous route than the intravenous route which ranges from 20 to 25 hours, and the peak is always well below the peak achieved using the intravenous route (5–10% of those seen with IV administration) [A33080, L85]. The bioavailability of subcutaneous injectable erythropoietin is much lower than that of the intravenously administered product and is approximately 20-40% [A33080, L85]. **Adult and paediatric patients with CRF:** Following subcutaneous administration, the peak plasma levels are achieved within 5 to 24 hours [FDA Label]. **Cancer patients receiving cyclic chemotherapy:** The average time to reach peak plasma concentration was approximately 13.3 ± 12.4 hours after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing. The Cmax is expected be 3- to 7- fold higher and the Tmax is expected to be 2- to 3-fold longer in patients receiving a 40,000 Units SC weekly dosing regimen [FDA Label]. | In healthy volunteers, the volume of distribution of intravenous epoetin alfa was generally similar to the plasma volume (range of 40–63.80 mL/kg), indicating limited extravascular distribution [A33080, A33076]. | **Healthy volunteers: ** In male volunteers receiving intravenous epoetin alfa, the total body clearance was approximately 8.12 ± 1.00 mL/h/kg [A33076]. **Cancer patients receiving cyclic chemotherapy:** The average clearance was approximately 20.2 ± 15.9 mL/h/kg after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing [FDA Label]. The patients receiving a 40,000 Units SC weekly dosing regimen display a lower clearance (9.2 ± 4.7 mL/h/kg) [FDA Label]. | NA | NA | NA | NA | NA | Erythropoietin receptor | Eprex Sterile Solution 4000iu/ml | Janssen Pharmaceuticals | Janssen Pharmaceuticals | Intravenous; Subcutaneous | 4000 unit / mL | NA | headache joint or muscle aches, pain, or soreness nausea vomiting weight loss sores in the mouth difficulty falling asleep or staying asleep depression muscle spasms runny nose, sneezing, and congestion fever, cough, or chills redness, swelling, pain, or itching at the injection spot | Epoetin alfa injection products come as a solution (liquid) to inject subcutaneously (just under the skin) or intravenously (into a vein). It is usually injected one to three times weekly. When epoetin alfa injection products are used to decrease the risk that blood transfusions will be required due to surgery, it is sometimes injected once daily for 10 days before surgery, on the day of surgery and for 4 days after surgery. Alternatively, epoetin alfa injection products are sometimes injected once weekly, beginning 3 weeks before surgery and on the day of surgery. | Epoetin alfa injection products are used to treat anemia (a lower than normal number of red blood cells) in people with chronic kidney failure (condition in which the kidneys slowly and permanently stop working over a period of time). Epoetin alfa injection products are also used to treat anemia caused by chemotherapy in people with certain types of cancer or caused by zidovudine (AZT, Retrovir, in Trizivir, in Combivir), a medication used to treat human immunodeficiency virus (HIV). | potassium;[2-butyl-5-chloro-3-[[4-[2-(1,2,3-triaza-4-azanidacyclopenta-2,5-dien-5-yl)phenyl]phenyl]methyl]imidazol-4-yl]methanol | NA | Link | Link | NA |
| 10957 | Th1240 | Erythropoietin | >Th1240_Erythropoietin APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 °C | **Healthy volunteers:** The half life is approximately 4 hours in healthy volunteers receiving an intravenous injection [F85]. A half-life of approximately 6 hours has been reported in children [F85]., **Adult and paediatric patients with CRF:** The elimination half life following intravenous administration ranges from 4 to 13 hours, which is about 20% longer in CRF patients than that in healthy subjects. The half life is reported to be similar between adult patients receiving or not receiving dialysis [FDA Label]. , **Cancer patients receiving cyclic chemotherapy:** Following subcutaneous administration, the average half life is 40 hours with range of 16 to 67 hours [FDA Label]. | Erythropoietin (EPO) is a growth factor produced in the kidneys that stimulates the production of red blood cells. It works by promoting the division and differentiation of committed erythroid progenitors in the bone marrow [FDA Label]. Epoetin alfa (Epoge) was developed by Amgen Inc. in 1983 as the first rhEPO commercialized in the United States, followed by other alfa and beta formulations. Epoetin alfa is a 165-amino acid erythropoiesis-stimulating glycoprotein produced in cell culture using recombinant DNA technology and is used for the treatment of patients with anemia associated with various clinical conditions, such as chronic renal failure, antiviral drug therapy, chemotherapy, or a high risk for perioperative blood loss from surgical procedures [FDA Label]. It has a molecular weight of approximately 30,400 daltons and is produced by mammalian cells into which the human erythropoietin gene has been introduced. The product contains the identical amino acid sequence of isolated natural erythropoietin and has the same biological activity as the endogenous erythropoietin. Epoetin alfa biosimilar, such as Retacrit (epoetin alfa-epbx or epoetin zeta), has been formulated to allow more access to treatment options for patients in the market [L2784]. The biosimilar is approved by the FDA and EMA as a safe, effective and affordable biological product and displays equivalent clinical efficacy, potency, and purity to the reference product [A7504]. Epoetin alfa formulations can be administered intravenously or subcutaneously. | Indicated in adult and paediatric patients for the treatment of anemia due to Chronic Kidney Disease (CKD) in patients on dialysis and not on dialysis, treatment of anemia due to zidovudine in patients with HIV-infection, treatment of anemia due to the effects of concomitant myelosuppressive chemotherapy, and upon initiation, there is a minimum of two additional months of planned chemotherapy, reduction of allogeneic RBC transfusions in patients undergoing elective, noncardiac, nonvascular surgery. | Erythropoietin and epoetin alfa are involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is reported to increase the reticulocyte count within 10 days of initiation, followed by increases in the RBC count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [F85]. Depending on the dose administered, the rate of hemoglobin increase may vary. In patients receiving hemodialysis, a greater biologic response is not observed at doses exceeding 300 Units/kg 3 times weekly [F85]. Epoetin alfa serves to restore erythropoietin deficiency in pathological and other clinical conditions where normal production of erythropoietin is impaired or compromised. In anemic patients with chronic renal failure (CRF), administration with epoetin alfa stimulated erythropoiesis by increasing the reticulocyte count within 10 days, followed by increases in the red cell count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [FDA Label]. Epoetin alfa was shown to be effective in increasing hematocrit in zidovudine-treated HIV-infected patients and anemic cancer patients undergoing chemotherapy [FDA Label]. | Erythropoietin or exogenous epoetin alfa binds to the erythropoietin receptor (EPO-R) and activates intracellular signal transduction pathways [A33079]. The affinity (Kd) of EPO for its receptor on human cells is ~100 to 200 pM [A33080]. Upon binding to EPO-R on the surface of erythroid progenitor cells, a conformational change is induced which brings EPO-R-associated Janus family tyrosine protein kinase 2 (JAK2) molecules into close proximity. JAK2 molecules are subsequently activated via phosphorylation, then phosphorylate tyrosine residues in the cytoplasmic domain of the EPO-R that serve as docking sites for Src homology 2-domain-containing intracellular signaling proteins [A33079]. The signalling proteins include STAT5 that once phosphorylated by JAK2, dissociates from the EPO-R, dimerizes, and translocates to the nucleus where they serve as transcription factors to activate target genes involved in cell division or differentiation, including the apoptosis inhibitor Bcl-x [A33079]. The inhibition of apoptosis by the EPO-activated JAK2/STAT5/Bcl-x pathway is critical in erythroid differentiation. Via JAK2-mediated tyrosine phosphorylation, erythropoietin and epoetin alfa also activates other intracellular proteins involved in erythroid cell proliferation and survival, such as Shc , phosphatidylinositol 3-kinase (PI3K), and phospholipase C- | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. Polycythemia should be managed acutely with phlebotomy, as clinically indicated. Following resolution of the overdose, reintroduction of epoetin alfa therapy should be accompanied by close monitoring for evidence of rapid increases in hemoglobin concentration (>1 gm/dL per 14 days). In patients with an excessive hematopoietic response, reduce the dose in accordance with the recommendations described in the drug label [FDA Label]. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system [A33080]. | The time to reach peak concentration is slower via the subcutaneous route than the intravenous route which ranges from 20 to 25 hours, and the peak is always well below the peak achieved using the intravenous route (5–10% of those seen with IV administration) [A33080, L85]. The bioavailability of subcutaneous injectable erythropoietin is much lower than that of the intravenously administered product and is approximately 20-40% [A33080, L85]. **Adult and paediatric patients with CRF:** Following subcutaneous administration, the peak plasma levels are achieved within 5 to 24 hours [FDA Label]. **Cancer patients receiving cyclic chemotherapy:** The average time to reach peak plasma concentration was approximately 13.3 ± 12.4 hours after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing. The Cmax is expected be 3- to 7- fold higher and the Tmax is expected to be 2- to 3-fold longer in patients receiving a 40,000 Units SC weekly dosing regimen [FDA Label]. | In healthy volunteers, the volume of distribution of intravenous epoetin alfa was generally similar to the plasma volume (range of 40–63.80 mL/kg), indicating limited extravascular distribution [A33080, A33076]. | **Healthy volunteers: ** In male volunteers receiving intravenous epoetin alfa, the total body clearance was approximately 8.12 ± 1.00 mL/h/kg [A33076]. **Cancer patients receiving cyclic chemotherapy:** The average clearance was approximately 20.2 ± 15.9 mL/h/kg after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing [FDA Label]. The patients receiving a 40,000 Units SC weekly dosing regimen display a lower clearance (9.2 ± 4.7 mL/h/kg) [FDA Label]. | NA | NA | NA | NA | NA | Erythropoietin receptor | Eprex Sterile Solution 5000iu/0.5ml | Janssen Pharmaceuticals | Janssen Pharmaceuticals | Intravenous; Subcutaneous | 5000 unit / 0.5 mL | NA | headache joint or muscle aches, pain, or soreness nausea vomiting weight loss sores in the mouth difficulty falling asleep or staying asleep depression muscle spasms runny nose, sneezing, and congestion fever, cough, or chills redness, swelling, pain, or itching at the injection spot | Epoetin alfa injection products come as a solution (liquid) to inject subcutaneously (just under the skin) or intravenously (into a vein). It is usually injected one to three times weekly. When epoetin alfa injection products are used to decrease the risk that blood transfusions will be required due to surgery, it is sometimes injected once daily for 10 days before surgery, on the day of surgery and for 4 days after surgery. Alternatively, epoetin alfa injection products are sometimes injected once weekly, beginning 3 weeks before surgery and on the day of surgery. | Epoetin alfa injection products are used to treat anemia (a lower than normal number of red blood cells) in people with chronic kidney failure (condition in which the kidneys slowly and permanently stop working over a period of time). Epoetin alfa injection products are also used to treat anemia caused by chemotherapy in people with certain types of cancer or caused by zidovudine (AZT, Retrovir, in Trizivir, in Combivir), a medication used to treat human immunodeficiency virus (HIV). | potassium;[2-butyl-5-chloro-3-[[4-[2-(1,2,3-triaza-4-azanidacyclopenta-2,5-dien-5-yl)phenyl]phenyl]methyl]imidazol-4-yl]methanol | NA | Link | Link | NA |
| 10958 | Th1240 | Erythropoietin | >Th1240_Erythropoietin APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 °C | **Healthy volunteers:** The half life is approximately 4 hours in healthy volunteers receiving an intravenous injection [F85]. A half-life of approximately 6 hours has been reported in children [F85]., **Adult and paediatric patients with CRF:** The elimination half life following intravenous administration ranges from 4 to 13 hours, which is about 20% longer in CRF patients than that in healthy subjects. The half life is reported to be similar between adult patients receiving or not receiving dialysis [FDA Label]. , **Cancer patients receiving cyclic chemotherapy:** Following subcutaneous administration, the average half life is 40 hours with range of 16 to 67 hours [FDA Label]. | Erythropoietin (EPO) is a growth factor produced in the kidneys that stimulates the production of red blood cells. It works by promoting the division and differentiation of committed erythroid progenitors in the bone marrow [FDA Label]. Epoetin alfa (Epoge) was developed by Amgen Inc. in 1983 as the first rhEPO commercialized in the United States, followed by other alfa and beta formulations. Epoetin alfa is a 165-amino acid erythropoiesis-stimulating glycoprotein produced in cell culture using recombinant DNA technology and is used for the treatment of patients with anemia associated with various clinical conditions, such as chronic renal failure, antiviral drug therapy, chemotherapy, or a high risk for perioperative blood loss from surgical procedures [FDA Label]. It has a molecular weight of approximately 30,400 daltons and is produced by mammalian cells into which the human erythropoietin gene has been introduced. The product contains the identical amino acid sequence of isolated natural erythropoietin and has the same biological activity as the endogenous erythropoietin. Epoetin alfa biosimilar, such as Retacrit (epoetin alfa-epbx or epoetin zeta), has been formulated to allow more access to treatment options for patients in the market [L2784]. The biosimilar is approved by the FDA and EMA as a safe, effective and affordable biological product and displays equivalent clinical efficacy, potency, and purity to the reference product [A7504]. Epoetin alfa formulations can be administered intravenously or subcutaneously. | Indicated in adult and paediatric patients for the treatment of anemia due to Chronic Kidney Disease (CKD) in patients on dialysis and not on dialysis, treatment of anemia due to zidovudine in patients with HIV-infection, treatment of anemia due to the effects of concomitant myelosuppressive chemotherapy, and upon initiation, there is a minimum of two additional months of planned chemotherapy, reduction of allogeneic RBC transfusions in patients undergoing elective, noncardiac, nonvascular surgery. | Erythropoietin and epoetin alfa are involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is reported to increase the reticulocyte count within 10 days of initiation, followed by increases in the RBC count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [F85]. Depending on the dose administered, the rate of hemoglobin increase may vary. In patients receiving hemodialysis, a greater biologic response is not observed at doses exceeding 300 Units/kg 3 times weekly [F85]. Epoetin alfa serves to restore erythropoietin deficiency in pathological and other clinical conditions where normal production of erythropoietin is impaired or compromised. In anemic patients with chronic renal failure (CRF), administration with epoetin alfa stimulated erythropoiesis by increasing the reticulocyte count within 10 days, followed by increases in the red cell count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [FDA Label]. Epoetin alfa was shown to be effective in increasing hematocrit in zidovudine-treated HIV-infected patients and anemic cancer patients undergoing chemotherapy [FDA Label]. | Erythropoietin or exogenous epoetin alfa binds to the erythropoietin receptor (EPO-R) and activates intracellular signal transduction pathways [A33079]. The affinity (Kd) of EPO for its receptor on human cells is ~100 to 200 pM [A33080]. Upon binding to EPO-R on the surface of erythroid progenitor cells, a conformational change is induced which brings EPO-R-associated Janus family tyrosine protein kinase 2 (JAK2) molecules into close proximity. JAK2 molecules are subsequently activated via phosphorylation, then phosphorylate tyrosine residues in the cytoplasmic domain of the EPO-R that serve as docking sites for Src homology 2-domain-containing intracellular signaling proteins [A33079]. The signalling proteins include STAT5 that once phosphorylated by JAK2, dissociates from the EPO-R, dimerizes, and translocates to the nucleus where they serve as transcription factors to activate target genes involved in cell division or differentiation, including the apoptosis inhibitor Bcl-x [A33079]. The inhibition of apoptosis by the EPO-activated JAK2/STAT5/Bcl-x pathway is critical in erythroid differentiation. Via JAK2-mediated tyrosine phosphorylation, erythropoietin and epoetin alfa also activates other intracellular proteins involved in erythroid cell proliferation and survival, such as Shc , phosphatidylinositol 3-kinase (PI3K), and phospholipase C- | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. Polycythemia should be managed acutely with phlebotomy, as clinically indicated. Following resolution of the overdose, reintroduction of epoetin alfa therapy should be accompanied by close monitoring for evidence of rapid increases in hemoglobin concentration (>1 gm/dL per 14 days). In patients with an excessive hematopoietic response, reduce the dose in accordance with the recommendations described in the drug label [FDA Label]. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system [A33080]. | The time to reach peak concentration is slower via the subcutaneous route than the intravenous route which ranges from 20 to 25 hours, and the peak is always well below the peak achieved using the intravenous route (5–10% of those seen with IV administration) [A33080, L85]. The bioavailability of subcutaneous injectable erythropoietin is much lower than that of the intravenously administered product and is approximately 20-40% [A33080, L85]. **Adult and paediatric patients with CRF:** Following subcutaneous administration, the peak plasma levels are achieved within 5 to 24 hours [FDA Label]. **Cancer patients receiving cyclic chemotherapy:** The average time to reach peak plasma concentration was approximately 13.3 ± 12.4 hours after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing. The Cmax is expected be 3- to 7- fold higher and the Tmax is expected to be 2- to 3-fold longer in patients receiving a 40,000 Units SC weekly dosing regimen [FDA Label]. | In healthy volunteers, the volume of distribution of intravenous epoetin alfa was generally similar to the plasma volume (range of 40–63.80 mL/kg), indicating limited extravascular distribution [A33080, A33076]. | **Healthy volunteers: ** In male volunteers receiving intravenous epoetin alfa, the total body clearance was approximately 8.12 ± 1.00 mL/h/kg [A33076]. **Cancer patients receiving cyclic chemotherapy:** The average clearance was approximately 20.2 ± 15.9 mL/h/kg after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing [FDA Label]. The patients receiving a 40,000 Units SC weekly dosing regimen display a lower clearance (9.2 ± 4.7 mL/h/kg) [FDA Label]. | NA | NA | NA | NA | NA | Erythropoietin receptor | Eprex Sterile Solution 6000 Iu/0.6 Ml | Janssen Pharmaceuticals | Janssen Pharmaceuticals | Intravenous; Subcutaneous | 6000 unit / 0.6 mL | NA | headache joint or muscle aches, pain, or soreness nausea vomiting weight loss sores in the mouth difficulty falling asleep or staying asleep depression muscle spasms runny nose, sneezing, and congestion fever, cough, or chills redness, swelling, pain, or itching at the injection spot | Epoetin alfa injection products come as a solution (liquid) to inject subcutaneously (just under the skin) or intravenously (into a vein). It is usually injected one to three times weekly. When epoetin alfa injection products are used to decrease the risk that blood transfusions will be required due to surgery, it is sometimes injected once daily for 10 days before surgery, on the day of surgery and for 4 days after surgery. Alternatively, epoetin alfa injection products are sometimes injected once weekly, beginning 3 weeks before surgery and on the day of surgery. | Epoetin alfa injection products are used to treat anemia (a lower than normal number of red blood cells) in people with chronic kidney failure (condition in which the kidneys slowly and permanently stop working over a period of time). Epoetin alfa injection products are also used to treat anemia caused by chemotherapy in people with certain types of cancer or caused by zidovudine (AZT, Retrovir, in Trizivir, in Combivir), a medication used to treat human immunodeficiency virus (HIV). | potassium;[2-butyl-5-chloro-3-[[4-[2-(1,2,3-triaza-4-azanidacyclopenta-2,5-dien-5-yl)phenyl]phenyl]methyl]imidazol-4-yl]methanol | NA | Link | Link | NA |
| 10959 | Th1240 | Erythropoietin | >Th1240_Erythropoietin APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 | C815H1317N233O241S5 | 8.75 | NA | 53 °C | **Healthy volunteers:** The half life is approximately 4 hours in healthy volunteers receiving an intravenous injection [F85]. A half-life of approximately 6 hours has been reported in children [F85]., **Adult and paediatric patients with CRF:** The elimination half life following intravenous administration ranges from 4 to 13 hours, which is about 20% longer in CRF patients than that in healthy subjects. The half life is reported to be similar between adult patients receiving or not receiving dialysis [FDA Label]. , **Cancer patients receiving cyclic chemotherapy:** Following subcutaneous administration, the average half life is 40 hours with range of 16 to 67 hours [FDA Label]. | Erythropoietin (EPO) is a growth factor produced in the kidneys that stimulates the production of red blood cells. It works by promoting the division and differentiation of committed erythroid progenitors in the bone marrow [FDA Label]. Epoetin alfa (Epoge) was developed by Amgen Inc. in 1983 as the first rhEPO commercialized in the United States, followed by other alfa and beta formulations. Epoetin alfa is a 165-amino acid erythropoiesis-stimulating glycoprotein produced in cell culture using recombinant DNA technology and is used for the treatment of patients with anemia associated with various clinical conditions, such as chronic renal failure, antiviral drug therapy, chemotherapy, or a high risk for perioperative blood loss from surgical procedures [FDA Label]. It has a molecular weight of approximately 30,400 daltons and is produced by mammalian cells into which the human erythropoietin gene has been introduced. The product contains the identical amino acid sequence of isolated natural erythropoietin and has the same biological activity as the endogenous erythropoietin. Epoetin alfa biosimilar, such as Retacrit (epoetin alfa-epbx or epoetin zeta), has been formulated to allow more access to treatment options for patients in the market [L2784]. The biosimilar is approved by the FDA and EMA as a safe, effective and affordable biological product and displays equivalent clinical efficacy, potency, and purity to the reference product [A7504]. Epoetin alfa formulations can be administered intravenously or subcutaneously. | Indicated in adult and paediatric patients for the treatment of anemia due to Chronic Kidney Disease (CKD) in patients on dialysis and not on dialysis, treatment of anemia due to zidovudine in patients with HIV-infection, treatment of anemia due to the effects of concomitant myelosuppressive chemotherapy, and upon initiation, there is a minimum of two additional months of planned chemotherapy, reduction of allogeneic RBC transfusions in patients undergoing elective, noncardiac, nonvascular surgery. | Erythropoietin and epoetin alfa are involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is reported to increase the reticulocyte count within 10 days of initiation, followed by increases in the RBC count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [F85]. Depending on the dose administered, the rate of hemoglobin increase may vary. In patients receiving hemodialysis, a greater biologic response is not observed at doses exceeding 300 Units/kg 3 times weekly [F85]. Epoetin alfa serves to restore erythropoietin deficiency in pathological and other clinical conditions where normal production of erythropoietin is impaired or compromised. In anemic patients with chronic renal failure (CRF), administration with epoetin alfa stimulated erythropoiesis by increasing the reticulocyte count within 10 days, followed by increases in the red cell count, hemoglobin, and hematocrit, usually within 2 to 6 weeks [FDA Label]. Epoetin alfa was shown to be effective in increasing hematocrit in zidovudine-treated HIV-infected patients and anemic cancer patients undergoing chemotherapy [FDA Label]. | Erythropoietin or exogenous epoetin alfa binds to the erythropoietin receptor (EPO-R) and activates intracellular signal transduction pathways [A33079]. The affinity (Kd) of EPO for its receptor on human cells is ~100 to 200 pM [A33080]. Upon binding to EPO-R on the surface of erythroid progenitor cells, a conformational change is induced which brings EPO-R-associated Janus family tyrosine protein kinase 2 (JAK2) molecules into close proximity. JAK2 molecules are subsequently activated via phosphorylation, then phosphorylate tyrosine residues in the cytoplasmic domain of the EPO-R that serve as docking sites for Src homology 2-domain-containing intracellular signaling proteins [A33079]. The signalling proteins include STAT5 that once phosphorylated by JAK2, dissociates from the EPO-R, dimerizes, and translocates to the nucleus where they serve as transcription factors to activate target genes involved in cell division or differentiation, including the apoptosis inhibitor Bcl-x [A33079]. The inhibition of apoptosis by the EPO-activated JAK2/STAT5/Bcl-x pathway is critical in erythroid differentiation. Via JAK2-mediated tyrosine phosphorylation, erythropoietin and epoetin alfa also activates other intracellular proteins involved in erythroid cell proliferation and survival, such as Shc , phosphatidylinositol 3-kinase (PI3K), and phospholipase C- | Overdose from epoetin alfa include signs and symptoms associated with an excessive and/or rapid increase in hemoglobin concentration, including cardiovascular events. Patients with suspected or known overdose should be monitored closely for cardiovascular events and hematologic abnormalities. Polycythemia should be managed acutely with phlebotomy, as clinically indicated. Following resolution of the overdose, reintroduction of epoetin alfa therapy should be accompanied by close monitoring for evidence of rapid increases in hemoglobin concentration (>1 gm/dL per 14 days). In patients with an excessive hematopoietic response, reduce the dose in accordance with the recommendations described in the drug label [FDA Label]. | Binding of erythropoietin and epoetin alfa to EPO-R leads to cellular internalization, which involves the degradation of the ligand. Erythropoietin and epoetin alfa may also be degraded by the reticuloendothelial scavenging pathway or lymphatic system [A33080]. | The time to reach peak concentration is slower via the subcutaneous route than the intravenous route which ranges from 20 to 25 hours, and the peak is always well below the peak achieved using the intravenous route (5–10% of those seen with IV administration) [A33080, L85]. The bioavailability of subcutaneous injectable erythropoietin is much lower than that of the intravenously administered product and is approximately 20-40% [A33080, L85]. **Adult and paediatric patients with CRF:** Following subcutaneous administration, the peak plasma levels are achieved within 5 to 24 hours [FDA Label]. **Cancer patients receiving cyclic chemotherapy:** The average time to reach peak plasma concentration was approximately 13.3 ± 12.4 hours after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing. The Cmax is expected be 3- to 7- fold higher and the Tmax is expected to be 2- to 3-fold longer in patients receiving a 40,000 Units SC weekly dosing regimen [FDA Label]. | In healthy volunteers, the volume of distribution of intravenous epoetin alfa was generally similar to the plasma volume (range of 40–63.80 mL/kg), indicating limited extravascular distribution [A33080, A33076]. | **Healthy volunteers: ** In male volunteers receiving intravenous epoetin alfa, the total body clearance was approximately 8.12 ± 1.00 mL/h/kg [A33076]. **Cancer patients receiving cyclic chemotherapy:** The average clearance was approximately 20.2 ± 15.9 mL/h/kg after 150 Units/kg three times per week (TIW) subcutaneous (SC) dosing [FDA Label]. The patients receiving a 40,000 Units SC weekly dosing regimen display a lower clearance (9.2 ± 4.7 mL/h/kg) [FDA Label]. | NA | NA | NA | NA | NA | Erythropoietin receptor | Eprex Sterile Solution 8000 Iu/0.8 Ml | Janssen Pharmaceuticals | Janssen Pharmaceuticals | Intravenous; Subcutaneous | 8000 unit / 0.8 mL | NA | headache joint or muscle aches, pain, or soreness nausea vomiting weight loss sores in the mouth difficulty falling asleep or staying asleep depression muscle spasms runny nose, sneezing, and congestion fever, cough, or chills redness, swelling, pain, or itching at the injection spot | Epoetin alfa injection products come as a solution (liquid) to inject subcutaneously (just under the skin) or intravenously (into a vein). It is usually injected one to three times weekly. When epoetin alfa injection products are used to decrease the risk that blood transfusions will be required due to surgery, it is sometimes injected once daily for 10 days before surgery, on the day of surgery and for 4 days after surgery. Alternatively, epoetin alfa injection products are sometimes injected once weekly, beginning 3 weeks before surgery and on the day of surgery. | Epoetin alfa injection products are used to treat anemia (a lower than normal number of red blood cells) in people with chronic kidney failure (condition in which the kidneys slowly and permanently stop working over a period of time). Epoetin alfa injection products are also used to treat anemia caused by chemotherapy in people with certain types of cancer or caused by zidovudine (AZT, Retrovir, in Trizivir, in Combivir), a medication used to treat human immunodeficiency virus (HIV). | potassium;[2-butyl-5-chloro-3-[[4-[2-(1,2,3-triaza-4-azanidacyclopenta-2,5-dien-5-yl)phenyl]phenyl]methyl]imidazol-4-yl]methanol | NA | Link | Link | NA |
| 11196 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. | Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging” or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab')2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,High affinity immunoglobulin gamma Fc receptor IB,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c,Low affinity immunoglobulin gamma Fc region receptor III-A,Low affinity immunoglobulin gamma Fc region receptor III-B,Complement C3,Complement C4-A,Complement C4-B,Complement C5 | Hizentra | Csl Behring Ag | Csl Behring Ag | Subcutaneous | 0.2 g/1mL | Hizentra is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin or to components of Hizentra, such as polysorbate 80. Hizentra is contraindicated in patients with hyperprolinemia (type I or II) because it contains the stabilizer L-proline [see DESCRIPTION]. Hizentra is contraindicated in IgA-deficient patients with antibodies against IgA and a history of hypersensitivity [see DESCRIPTION]. | local injection site reactions (swelling redness heat pain and itching) headache, diarrhea, fatigue, back pain, nausea, pain in extremities, cough, rash, itching, vomiting , abdominal pain (upper), migraine , pain, joint pain, bruising, rash, and hives | Hizentra is a sterilized solution made from human plasma. It contains the antibodies to help your body protect itself against infection from various diseases. Hizentra subcutaneous injection(for injection under the skin) is used to treat primary immunodeficiency diseases. This includes, but is not limited... | Hizentra is a prescription medicine used to treat the symptoms of Primary Immune Deficiency and Chronic Inflammatory Demyelinating Polyneuropathy. Hizentra may be used alone or with other medications. | NA | Hizentra, Immune Globulin Subcutaneous (Human), 20% Liquid, is a ready-to-use, sterile 20% (0.2 g/mL) protein liquid preparation of polyvalent human immunoglobulin G (IgG) for subcutaneous administration. Hizentra is manufactured from large pools of human plasma by a combination of cold alcohol fractionation, octanoic acid fractionation, and anion exchange chromatography. The IgG proteins are not subjected to heating or to chemical or enzymatic modification. The Fc and Fab functions of the IgG molecule are retained. Fab functions tested include antigen binding capacities, and Fc functions tested include complement activation and Fc-receptor-mediated leukocyte activation (determined with complexed IgG). | Link | Link | NA |
| 11197 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. | Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging” or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab')2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,High affinity immunoglobulin gamma Fc receptor IB,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c,Low affinity immunoglobulin gamma Fc region receptor III-A,Low affinity immunoglobulin gamma Fc region receptor III-B,Complement C3,Complement C4-A,Complement C4-B,Complement C5 | Hizentra | Csl Behring | Csl Behring | Subcutaneous | 200 mg / mL | Hizentra is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin or to components of Hizentra, such as polysorbate 80. Hizentra is contraindicated in patients with hyperprolinemia (type I or II) because it contains the stabilizer L-proline [see DESCRIPTION]. Hizentra is contraindicated in IgA-deficient patients with antibodies against IgA and a history of hypersensitivity [see DESCRIPTION]. | local injection site reactions (swelling redness heat pain and itching) headache, diarrhea, fatigue, back pain, nausea, pain in extremities, cough, rash, itching, vomiting , abdominal pain (upper), migraine , pain, joint pain, bruising, rash, and hives | Hizentra is a sterilized solution made from human plasma. It contains the antibodies to help your body protect itself against infection from various diseases. Hizentra subcutaneous injection(for injection under the skin) is used to treat primary immunodeficiency diseases. This includes, but is not limited... | Hizentra is a prescription medicine used to treat the symptoms of Primary Immune Deficiency and Chronic Inflammatory Demyelinating Polyneuropathy. Hizentra may be used alone or with other medications. | NA | Hizentra, Immune Globulin Subcutaneous (Human), 20% Liquid, is a ready-to-use, sterile 20% (0.2 g/mL) protein liquid preparation of polyvalent human immunoglobulin G (IgG) for subcutaneous administration. Hizentra is manufactured from large pools of human plasma by a combination of cold alcohol fractionation, octanoic acid fractionation, and anion exchange chromatography. The IgG proteins are not subjected to heating or to chemical or enzymatic modification. The Fc and Fab functions of the IgG molecule are retained. Fab functions tested include antigen binding capacities, and Fc functions tested include complement activation and Fc-receptor-mediated leukocyte activation (determined with complexed IgG). | Link | Link | NA |
| 11198 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. | Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging” or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab')2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,High affinity immunoglobulin gamma Fc receptor IB,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c,Low affinity immunoglobulin gamma Fc region receptor III-A,Low affinity immunoglobulin gamma Fc region receptor III-B,Complement C3,Complement C4-A,Complement C4-B,Complement C5 | Hizentra | Csl Behring | Csl Behring | Subcutaneous | 200 mg/ml | Hizentra is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin or to components of Hizentra, such as polysorbate 80. Hizentra is contraindicated in patients with hyperprolinemia (type I or II) because it contains the stabilizer L-proline [see DESCRIPTION]. Hizentra is contraindicated in IgA-deficient patients with antibodies against IgA and a history of hypersensitivity [see DESCRIPTION]. | local injection site reactions (swelling redness heat pain and itching) headache, diarrhea, fatigue, back pain, nausea, pain in extremities, cough, rash, itching, vomiting , abdominal pain (upper), migraine , pain, joint pain, bruising, rash, and hives | Hizentra is a sterilized solution made from human plasma. It contains the antibodies to help your body protect itself against infection from various diseases. Hizentra subcutaneous injection(for injection under the skin) is used to treat primary immunodeficiency diseases. This includes, but is not limited... | Hizentra is a prescription medicine used to treat the symptoms of Primary Immune Deficiency and Chronic Inflammatory Demyelinating Polyneuropathy. Hizentra may be used alone or with other medications. | NA | Hizentra, Immune Globulin Subcutaneous (Human), 20% Liquid, is a ready-to-use, sterile 20% (0.2 g/mL) protein liquid preparation of polyvalent human immunoglobulin G (IgG) for subcutaneous administration. Hizentra is manufactured from large pools of human plasma by a combination of cold alcohol fractionation, octanoic acid fractionation, and anion exchange chromatography. The IgG proteins are not subjected to heating or to chemical or enzymatic modification. The Fc and Fab functions of the IgG molecule are retained. Fab functions tested include antigen binding capacities, and Fc functions tested include complement activation and Fc-receptor-mediated leukocyte activation (determined with complexed IgG). | Link | Link | NA |
| 11226 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. | Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging” or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab')2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,High affinity immunoglobulin gamma Fc receptor IB,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c,Low affinity immunoglobulin gamma Fc region receptor III-A,Low affinity immunoglobulin gamma Fc region receptor III-B,Complement C3,Complement C4-A,Complement C4-B,Complement C5 | Vivaglobin | Csl Behring | Csl Behring | Subcutaneous | 160 mg/1mL | As with all immune globulin products, Vivaglobin® (immune globulin subcutaneous (human)) Immune Globulin Subcutaneous (Human) is contraindicated in individuals with a history of anaphylactic or severe systemic response to immune globulin preparations and in persons with selective immunoglobulin A (IgA) deficiency (serum IgA < 0.05 g/L) who have known antibody against IgA. | injection site reactions (mild swelling, redness, itching, bruising, pain, or warmth) that will usually lessen as your body adjusts to the medication headache upset stomach fever nausea vomiting stomach pain diarrhea bloating sore throat cough back pain itching or skin rash joint or muscle pain tiredness, or pain anywhere in the body | Vivaglobin is a sterilized solution made from human plasma. It contains the antibodies to help your body protect itself against infection from various diseases. Vivaglobin subcutaneous (for injection under the skin) is used to treat primary immunodeficiency (PI). This includes, but is not limited to,... | Vivaglobin® Immune Globulin Subcutaneous (Human), is indicated for the treatment of patients with primary immune deficiency (PID). | NA | NA | Link | Link | NA |
| 11227 | Th1243 | Human immunoglobulin G | >Th1243_Human_immunoglobulin_G PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 61 °C (FAB fragment), 71 °C (whole mAb) | >20 hours (mammalian reticulocytes, in vitro). | Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. | IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. | Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. | IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging” or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab')2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | High affinity immunoglobulin gamma Fc receptor I,High affinity immunoglobulin gamma Fc receptor IB,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c,Low affinity immunoglobulin gamma Fc region receptor III-A,Low affinity immunoglobulin gamma Fc region receptor III-B,Complement C3,Complement C4-A,Complement C4-B,Complement C5 | Vivaglobin | Csl Behring | Csl Behring | Subcutaneous | 160 mg / mL | As with all immune globulin products, Vivaglobin® (immune globulin subcutaneous (human)) Immune Globulin Subcutaneous (Human) is contraindicated in individuals with a history of anaphylactic or severe systemic response to immune globulin preparations and in persons with selective immunoglobulin A (IgA) deficiency (serum IgA < 0.05 g/L) who have known antibody against IgA. | injection site reactions (mild swelling, redness, itching, bruising, pain, or warmth) that will usually lessen as your body adjusts to the medication headache upset stomach fever nausea vomiting stomach pain diarrhea bloating sore throat cough back pain itching or skin rash joint or muscle pain tiredness, or pain anywhere in the body | Vivaglobin is a sterilized solution made from human plasma. It contains the antibodies to help your body protect itself against infection from various diseases. Vivaglobin subcutaneous (for injection under the skin) is used to treat primary immunodeficiency (PI). This includes, but is not limited to,... | Vivaglobin® Immune Globulin Subcutaneous (Human), is indicated for the treatment of patients with primary immune deficiency (PID). | NA | NA | Link | Link | NA |
| 11259 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 8485180 | 16-07-2013 | 25-03-2030 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin 10/90 Cartridge | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Subcutaneous | NA | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11260 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 9283193 | 15-03-2016 | 14-09-2026 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin 10/90 Inj | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Subcutaneous | NA | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11261 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 8636001 | 28-01-2014 | 12-07-2032 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin 20/80 Cartridge | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Subcutaneous | NA | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11262 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 8424518 | 23-04-2013 | 17-10-2031 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin 20/80 Inj | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Subcutaneous | NA | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11263 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 8551528 | 08-10-2013 | 11-06-2030 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin 30/70 (insulin Human Biosynth Inj) | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Subcutaneous | NA | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11264 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 7464706 | 16-12-2008 | 02-03-2023 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin 30/70 Cartridge | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Subcutaneous | NA | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11265 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 8729019 | 20-05-2014 | 26-12-2028 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin 40/60 Cartridge | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Subcutaneous | NA | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11266 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 7305986 | 11-12-2007 | 16-01-2023 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin 40/60 Inj | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Subcutaneous | NA | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11267 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 8499757 | 06-08-2013 | 19-02-2032 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin 50/50 | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Subcutaneous | 100 [iU]/1mL | No information provided. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11268 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 8156936 | 17-04-2012 | 16-01-2023 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin 50/50 Cartridge | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Subcutaneous | NA | No information provided. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11269 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 8734845 | 27-05-2014 | 11-06-2030 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin 50/50 Inj | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Subcutaneous | NA | No information provided. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11270 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 8227409 | 24-07-2012 | 08-03-2031 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin 70/30 | A-S Medication Solutions | A-S Medication Solutions | Subcutaneous | 100 [iU]/1mL | HUMULIN 70/30 is contraindicated: During episodes of hypoglycemia, and In patients who have had hypersensitivity reactions to HUMULIN 70/30 or any of its excipients. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11271 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 9393372 | 19-07-2016 | 04-07-2029 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin 70/30 | Eli Lilly and Company | Eli Lilly and Company | Subcutaneous | 100 | HUMULIN 70/30 is contraindicated: During episodes of hypoglycemia, and In patients who have had hypersensitivity reactions to HUMULIN 70/30 or any of its excipients. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11272 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 9339615 | 17-05-2016 | 20-10-2029 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin 70/30 | Eli Lilly and Company | Eli Lilly and Company | Subcutaneous | 100 [iU]/1mL | HUMULIN 70/30 is contraindicated: During episodes of hypoglycemia, and In patients who have had hypersensitivity reactions to HUMULIN 70/30 or any of its excipients. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11273 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 9511198 | 06-12-2016 | 16-02-2030 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin 70/30 70/30 | REMEDYREPACK INC. | REMEDYREPACK INC. | Subcutaneous | 100 [iU]/1mL | HUMULIN 70/30 is contraindicated: During episodes of hypoglycemia, and In patients who have had hypersensitivity reactions to HUMULIN 70/30 or any of its excipients. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11274 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 9597374 | 21-03-2017 | 08-10-2031 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin 70/30 KwikPen | Eli Lilly and Company | Eli Lilly and Company | Subcutaneous | 100 [iU]/1mL | HUMULIN 70/30 is contraindicated: During episodes of hypoglycemia, and In patients who have had hypersensitivity reactions to HUMULIN 70/30 or any of its excipients. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11275 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 9358352 | 07-06-2016 | 15-02-2031 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin L | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Subcutaneous | 100 [iU]/1mL | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11281 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 10201672 | 12-02-2019 | 02-08-2030 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin N (cartridge) | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Subcutaneous | 100 unit / mL | HUMULIN N is contraindicated: During episodes of hypoglycemia, and In patients who have had hypersensitivity reactions to HUMULIN N or any of its excipients. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11282 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | 10342938 | 09-07-2019 | 12-06-2029 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin N (kwikpen) | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Subcutaneous | 100 unit / mL | HUMULIN N is contraindicated: During episodes of hypoglycemia, and In patients who have had hypersensitivity reactions to HUMULIN N or any of its excipients. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11287 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin R (kwikpen) | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Intramuscular; Subcutaneous | 100 unit/mL | Humulin R (insulin (human recombinant)) U-100 is contraindicated during episodes of hypoglycemia and in patients hypersensitive to Humulin R (insulin (human recombinant)) U-100 or any of its excipients. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11288 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin R Cartridge | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Intramuscular; Intravenous; Subcutaneous | 100 unit / mL | Humulin R (insulin (human recombinant)) U-100 is contraindicated during episodes of hypoglycemia and in patients hypersensitive to Humulin R (insulin (human recombinant)) U-100 or any of its excipients. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11289 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin R U-500 | Eli Lilly and Company | Eli Lilly and Company | Subcutaneous | 500 [iU]/1mL | Humulin R (insulin (human recombinant)) U-100 is contraindicated during episodes of hypoglycemia and in patients hypersensitive to Humulin R (insulin (human recombinant)) U-100 or any of its excipients. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11291 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Humulin U | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | Subcutaneous | 100 [iU]/1mL | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. Follow these directions carefully. Do not use more or less insulin or use it more often than prescribed by your doctor. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11333 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolin 70/30 | Physicians Total Care, Inc. | Physicians Total Care, Inc. | Subcutaneous | 100 [USP'U]/1mL | No Information Provided. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11334 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolin 70/30 | Novo Nordisk | Novo Nordisk | Subcutaneous | 100 [USP'U]/1mL | No Information Provided. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11335 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolin 70/30 | A S Medication Solutions | A S Medication Solutions | Subcutaneous | 100 [USP'U]/1mL | No Information Provided. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11336 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolin 70/30 | TYA Pharmaceuticals | TYA Pharmaceuticals | Subcutaneous | 100 [USP'U]/1mL | No Information Provided. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11337 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolin 70/30 | A-S Medication Solutions | A-S Medication Solutions | Subcutaneous | 100 [USP'U]/1mL | No Information Provided. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11338 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolin 70/30 | Remedy Repack | Remedy Repack | Subcutaneous | 100 [USP'U]/1mL | No Information Provided. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11339 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolin 70/30 | Novo Nordisk | Novo Nordisk | Subcutaneous | 100 [iU]/1mL | No Information Provided. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11340 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolin Ge 10/90 Penfill Inj Sus | Novo Nordisk | Novo Nordisk | Subcutaneous | NA | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11341 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolin Ge 20/80 Penfill Inj Sus | Novo Nordisk | Novo Nordisk | Subcutaneous | NA | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11342 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolin Ge 30/70 | Novo Nordisk | Novo Nordisk | Subcutaneous | NA | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11343 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolin Ge 30/70 Penfill | Novo Nordisk | Novo Nordisk | Subcutaneous | NA | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11344 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolin Ge 40/60 Penfill | Novo Nordisk | Novo Nordisk | Subcutaneous | NA | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11345 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolin Ge 50/50 Penfill | Novo Nordisk | Novo Nordisk | Subcutaneous | NA | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11346 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolin Ge Nph | Novo Nordisk | Novo Nordisk | Subcutaneous | 100 unit / mL | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11347 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolin Ge Nph Penfill | Novo Nordisk | Novo Nordisk | Subcutaneous | 100 unit / mL | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11348 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolin Ge Toronto | Novo Nordisk | Novo Nordisk | Intramuscular; Intravenous; Subcutaneous | 100 unit / mL | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11349 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolin Ge Toronto Penfill | Novo Nordisk | Novo Nordisk | Intramuscular; Intravenous; Subcutaneous | 100 unit / mL | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11361 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolin70/30 70/30 | Remedy Repack | Remedy Repack | Subcutaneous | 100 [USP'U]/1mL | No Information Provided. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11362 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | NovolinN N | Remedy Repack | Remedy Repack | Subcutaneous | 100 [iU]/1mL | No Information Provided. | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11363 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolinset Ge 30/70 Inj Sus | Novo Nordisk | Novo Nordisk | Subcutaneous | NA | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11364 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolinset Ge Nph Inj Sus 100u/ml | Novo Nordisk | Novo Nordisk | Subcutaneous | 100 unit / mL | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11365 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | NA | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Novolinset Ge Toronto Inj Liq 100u/ml | Novo Nordisk | Novo Nordisk | Intramuscular; Intravenous; Subcutaneous | 100 unit / mL | NA | rash and/or itching over the whole body shortness of breath wheezing dizziness blurred vision fast heartbeat sweating difficulty breathing or swallowing weakness muscle cramps abnormal heartbeat large weight gain in a short period of time swelling of the arms, hands, feet, ankles, or lower legs | Human insulin comes as a solution (liquid) and a suspension (liquid with particles that will settle on standing). to be injected subcutaneously (under the skin). Human insulin is usually injected subcutaneously several times a day, and more than one type of insulin may be needed. Your doctor will tell you which type(s) of insulin to use, how much insulin to use, and how often to inject insulin. | Human insulin is used to control blood sugar in people who have type 1 diabetes (condition in which the body does not make insulin and therefore cannot control the amount of sugar in the blood) or in people who have type 2 diabetes (condition in which the blood sugar is too high because the body does not produce or use insulin normally) that cannot be controlled with oral medications alone. Human insulin is in a class of medications called hormones. Human insulin is used to take the place of insulin that is normally produced by the body. It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way. | NA | NA | Link | Link | NA |
| 11425 | Th1247 | Glucagon | >Th1247_Glucagon HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | NA | NA | The half life of glucagon is 26 minutes for an intramuscular dose.[L7634] The half life of glucagon nasal powder is approximately 35 minutes.[L7643] The half life of glucagon by a subcutaneous auto-injector or pre-filled syringe is 32 minutes.[L8519] | Glucagon is a 29 amino acid hormone used as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon was granted FDA approval on 14 November 1960.[L7631] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and severe hypoglycemia.[A19402,L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon has a short duration of action.[L7634,L7637,L7640,L7643] Glucagon may cause hyperglycemia in diabetic patients.[L7634,L7637,L7640,L7643] | Glucagon binds to the glucagon receptor activating Gsa and Gq.[A19402] This activation activates adenylate cyclase, which increases intracellular cyclic AMP and activates protein kinase A.[A19402] Activating Gq activates phospholipase C, increases production of inositol 1,4,5-triphosphate, and releases intracellular calcium.[A19402] Protein kinase A phosphorylates glycogen phosphorylase kinase, which phosphorylates glycogen phosphorylase, which phosphorylates glycogen, causing its breakdown.[A19402] Glucagon also relaxes smooth muscle of the stomach, duodenum, small bowel, and colon.[L7634,L7643] | Patients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium.[L7634,L7637,L7640,L7643] Phentolamine may be given to control blood pressure.[L7634,L7637,L7640,L7643] Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia.[L7637] The LD50 for intravenous glucagon in mice is 300mg/kg and in rats is 38.6mg/kg.[L7637] | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma.[L7634,L7643] | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.[L7637] An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes.[L7637] A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes.[L7643] | The volume of distribution of glucagon is 0.25L/kg.[L7637] The apparent volume of distribution is 885L.[L7643] | A 1mg intravenous dose of glucagon has a clearance of 13.5mL/min/kg.[L7637] | Proteins | NA | NA | NA | NA | Glucagon receptor,Glucagon-like peptide 2 receptor,Glucagon-like peptide 1 receptor | Gvoke HypoPen 0.5 mg Auto-Injector | Xeris Pharmaceuticals, Inc. | Xeris Pharmaceuticals, Inc. | Subcutaneous | 0.5 mg/0.1mL | GVOKE is contraindicated in patients with: Pheochromocytoma Insulinoma [ see WARNINGS AND PRECAUTIONS] because of the risk of hypoglycemia Known hypersensitivity to glucagon or to any of the excipients in GVOKE. Allergic reactions have been reported with glucagon and include anaphylactic shock with breathing difficulties and hypotension. | nausea vomiting hives injection site swelling or redness headache fast heartbeat | Glucagon comes as a solution (liquid) in a prefilled syringe and an auto-injector device to inject subcutaneously (just under the skin). It also comes as a powder to be mixed with a provided liquid to be injected subcutaneously, intramuscularly (into the muscle), or intravenously (into a vein). It is usually injected as needed at the first sign of severe hypoglycemia. | Glucagon is used along with emergency medical treatment to treat very low blood sugar. Glucagon is also used in diagnostic testing of the stomach and other digestive organs. Glucagon is in a class of medications called glycogenolytic agents. It works by causing the liver to release stored sugar to the blood. It also works by relaxing smooth muscles of the stomach and other digestive organs for diagnostic testing. | (3S)-3-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-5-oxopentanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-oxopentanoyl]amino]-4-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-4-amino-1-[[(1S,2R)-1-carboxy-2-hydroxypropyl]amino]-1,4-dioxobutan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-oxobutanoic acid | NA | Link | Link | NA |
| 11426 | Th1247 | Glucagon | >Th1247_Glucagon HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | NA | NA | The half life of glucagon is 26 minutes for an intramuscular dose.[L7634] The half life of glucagon nasal powder is approximately 35 minutes.[L7643] The half life of glucagon by a subcutaneous auto-injector or pre-filled syringe is 32 minutes.[L8519] | Glucagon is a 29 amino acid hormone used as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon was granted FDA approval on 14 November 1960.[L7631] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and severe hypoglycemia.[A19402,L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon has a short duration of action.[L7634,L7637,L7640,L7643] Glucagon may cause hyperglycemia in diabetic patients.[L7634,L7637,L7640,L7643] | Glucagon binds to the glucagon receptor activating Gsa and Gq.[A19402] This activation activates adenylate cyclase, which increases intracellular cyclic AMP and activates protein kinase A.[A19402] Activating Gq activates phospholipase C, increases production of inositol 1,4,5-triphosphate, and releases intracellular calcium.[A19402] Protein kinase A phosphorylates glycogen phosphorylase kinase, which phosphorylates glycogen phosphorylase, which phosphorylates glycogen, causing its breakdown.[A19402] Glucagon also relaxes smooth muscle of the stomach, duodenum, small bowel, and colon.[L7634,L7643] | Patients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium.[L7634,L7637,L7640,L7643] Phentolamine may be given to control blood pressure.[L7634,L7637,L7640,L7643] Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia.[L7637] The LD50 for intravenous glucagon in mice is 300mg/kg and in rats is 38.6mg/kg.[L7637] | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma.[L7634,L7643] | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.[L7637] An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes.[L7637] A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes.[L7643] | The volume of distribution of glucagon is 0.25L/kg.[L7637] The apparent volume of distribution is 885L.[L7643] | A 1mg intravenous dose of glucagon has a clearance of 13.5mL/min/kg.[L7637] | Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | NA | NA | NA | NA | Glucagon receptor,Glucagon-like peptide 2 receptor,Glucagon-like peptide 1 receptor | Gvoke HypoPen 1 mg Auto-Injector | Xeris Pharmaceuticals, Inc. | Xeris Pharmaceuticals, Inc. | Subcutaneous | 1 mg/0.2mL | GVOKE is contraindicated in patients with: Pheochromocytoma Insulinoma [ see WARNINGS AND PRECAUTIONS] because of the risk of hypoglycemia Known hypersensitivity to glucagon or to any of the excipients in GVOKE. Allergic reactions have been reported with glucagon and include anaphylactic shock with breathing difficulties and hypotension. | nausea vomiting hives injection site swelling or redness headache fast heartbeat | Glucagon comes as a solution (liquid) in a prefilled syringe and an auto-injector device to inject subcutaneously (just under the skin). It also comes as a powder to be mixed with a provided liquid to be injected subcutaneously, intramuscularly (into the muscle), or intravenously (into a vein). It is usually injected as needed at the first sign of severe hypoglycemia. | Glucagon is used along with emergency medical treatment to treat very low blood sugar. Glucagon is also used in diagnostic testing of the stomach and other digestive organs. Glucagon is in a class of medications called glycogenolytic agents. It works by causing the liver to release stored sugar to the blood. It also works by relaxing smooth muscles of the stomach and other digestive organs for diagnostic testing. | (3S)-3-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-5-oxopentanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-oxopentanoyl]amino]-4-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-4-amino-1-[[(1S,2R)-1-carboxy-2-hydroxypropyl]amino]-1,4-dioxobutan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-oxobutanoic acid | NA | Link | Link | NA |
| 11427 | Th1247 | Glucagon | >Th1247_Glucagon HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | NA | NA | The half life of glucagon is 26 minutes for an intramuscular dose.[L7634] The half life of glucagon nasal powder is approximately 35 minutes.[L7643] The half life of glucagon by a subcutaneous auto-injector or pre-filled syringe is 32 minutes.[L8519] | Glucagon is a 29 amino acid hormone used as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon was granted FDA approval on 14 November 1960.[L7631] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and severe hypoglycemia.[A19402,L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon has a short duration of action.[L7634,L7637,L7640,L7643] Glucagon may cause hyperglycemia in diabetic patients.[L7634,L7637,L7640,L7643] | Glucagon binds to the glucagon receptor activating Gsa and Gq.[A19402] This activation activates adenylate cyclase, which increases intracellular cyclic AMP and activates protein kinase A.[A19402] Activating Gq activates phospholipase C, increases production of inositol 1,4,5-triphosphate, and releases intracellular calcium.[A19402] Protein kinase A phosphorylates glycogen phosphorylase kinase, which phosphorylates glycogen phosphorylase, which phosphorylates glycogen, causing its breakdown.[A19402] Glucagon also relaxes smooth muscle of the stomach, duodenum, small bowel, and colon.[L7634,L7643] | Patients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium.[L7634,L7637,L7640,L7643] Phentolamine may be given to control blood pressure.[L7634,L7637,L7640,L7643] Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia.[L7637] The LD50 for intravenous glucagon in mice is 300mg/kg and in rats is 38.6mg/kg.[L7637] | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma.[L7634,L7643] | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.[L7637] An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes.[L7637] A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes.[L7643] | The volume of distribution of glucagon is 0.25L/kg.[L7637] The apparent volume of distribution is 885L.[L7643] | A 1mg intravenous dose of glucagon has a clearance of 13.5mL/min/kg.[L7637] | NA | NA | NA | NA | NA | Glucagon receptor,Glucagon-like peptide 2 receptor,Glucagon-like peptide 1 receptor | Gvoke Kit | Xeris Pharmaceuticals, Inc. | Xeris Pharmaceuticals, Inc. | Subcutaneous | 1 mg/0.2mL | GVOKE is contraindicated in patients with: Pheochromocytoma Insulinoma [ see WARNINGS AND PRECAUTIONS] because of the risk of hypoglycemia Known hypersensitivity to glucagon or to any of the excipients in GVOKE. Allergic reactions have been reported with glucagon and include anaphylactic shock with breathing difficulties and hypotension. | nausea vomiting hives injection site swelling or redness headache fast heartbeat | Glucagon comes as a solution (liquid) in a prefilled syringe and an auto-injector device to inject subcutaneously (just under the skin). It also comes as a powder to be mixed with a provided liquid to be injected subcutaneously, intramuscularly (into the muscle), or intravenously (into a vein). It is usually injected as needed at the first sign of severe hypoglycemia. | Glucagon is used along with emergency medical treatment to treat very low blood sugar. Glucagon is also used in diagnostic testing of the stomach and other digestive organs. Glucagon is in a class of medications called glycogenolytic agents. It works by causing the liver to release stored sugar to the blood. It also works by relaxing smooth muscles of the stomach and other digestive organs for diagnostic testing. | (3S)-3-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-5-oxopentanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-oxopentanoyl]amino]-4-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-4-amino-1-[[(1S,2R)-1-carboxy-2-hydroxypropyl]amino]-1,4-dioxobutan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-oxobutanoic acid | NA | Link | Link | NA |
| 11428 | Th1247 | Glucagon | >Th1247_Glucagon HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | NA | NA | The half life of glucagon is 26 minutes for an intramuscular dose.[L7634] The half life of glucagon nasal powder is approximately 35 minutes.[L7643] The half life of glucagon by a subcutaneous auto-injector or pre-filled syringe is 32 minutes.[L8519] | Glucagon is a 29 amino acid hormone used as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon was granted FDA approval on 14 November 1960.[L7631] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and severe hypoglycemia.[A19402,L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon has a short duration of action.[L7634,L7637,L7640,L7643] Glucagon may cause hyperglycemia in diabetic patients.[L7634,L7637,L7640,L7643] | Glucagon binds to the glucagon receptor activating Gsa and Gq.[A19402] This activation activates adenylate cyclase, which increases intracellular cyclic AMP and activates protein kinase A.[A19402] Activating Gq activates phospholipase C, increases production of inositol 1,4,5-triphosphate, and releases intracellular calcium.[A19402] Protein kinase A phosphorylates glycogen phosphorylase kinase, which phosphorylates glycogen phosphorylase, which phosphorylates glycogen, causing its breakdown.[A19402] Glucagon also relaxes smooth muscle of the stomach, duodenum, small bowel, and colon.[L7634,L7643] | Patients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium.[L7634,L7637,L7640,L7643] Phentolamine may be given to control blood pressure.[L7634,L7637,L7640,L7643] Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia.[L7637] The LD50 for intravenous glucagon in mice is 300mg/kg and in rats is 38.6mg/kg.[L7637] | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma.[L7634,L7643] | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.[L7637] An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes.[L7637] A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes.[L7643] | The volume of distribution of glucagon is 0.25L/kg.[L7637] The apparent volume of distribution is 885L.[L7643] | A 1mg intravenous dose of glucagon has a clearance of 13.5mL/min/kg.[L7637] | NA | NA | NA | NA | NA | Glucagon receptor,Glucagon-like peptide 2 receptor,Glucagon-like peptide 1 receptor | Gvoke Kit Vial | Xeris Pharmaceuticals, Inc. | Xeris Pharmaceuticals, Inc. | Subcutaneous | 1 mg/0.2mL | GVOKE is contraindicated in patients with: Pheochromocytoma Insulinoma [ see WARNINGS AND PRECAUTIONS] because of the risk of hypoglycemia Known hypersensitivity to glucagon or to any of the excipients in GVOKE. Allergic reactions have been reported with glucagon and include anaphylactic shock with breathing difficulties and hypotension. | nausea vomiting hives injection site swelling or redness headache fast heartbeat | Glucagon comes as a solution (liquid) in a prefilled syringe and an auto-injector device to inject subcutaneously (just under the skin). It also comes as a powder to be mixed with a provided liquid to be injected subcutaneously, intramuscularly (into the muscle), or intravenously (into a vein). It is usually injected as needed at the first sign of severe hypoglycemia. | Glucagon is used along with emergency medical treatment to treat very low blood sugar. Glucagon is also used in diagnostic testing of the stomach and other digestive organs. Glucagon is in a class of medications called glycogenolytic agents. It works by causing the liver to release stored sugar to the blood. It also works by relaxing smooth muscles of the stomach and other digestive organs for diagnostic testing. | (3S)-3-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-5-oxopentanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-oxopentanoyl]amino]-4-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-4-amino-1-[[(1S,2R)-1-carboxy-2-hydroxypropyl]amino]-1,4-dioxobutan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-oxobutanoic acid | NA | Link | Link | NA |
| 11429 | Th1247 | Glucagon | >Th1247_Glucagon HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | NA | NA | The half life of glucagon is 26 minutes for an intramuscular dose.[L7634] The half life of glucagon nasal powder is approximately 35 minutes.[L7643] The half life of glucagon by a subcutaneous auto-injector or pre-filled syringe is 32 minutes.[L8519] | Glucagon is a 29 amino acid hormone used as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon was granted FDA approval on 14 November 1960.[L7631] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and severe hypoglycemia.[A19402,L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon has a short duration of action.[L7634,L7637,L7640,L7643] Glucagon may cause hyperglycemia in diabetic patients.[L7634,L7637,L7640,L7643] | Glucagon binds to the glucagon receptor activating Gsa and Gq.[A19402] This activation activates adenylate cyclase, which increases intracellular cyclic AMP and activates protein kinase A.[A19402] Activating Gq activates phospholipase C, increases production of inositol 1,4,5-triphosphate, and releases intracellular calcium.[A19402] Protein kinase A phosphorylates glycogen phosphorylase kinase, which phosphorylates glycogen phosphorylase, which phosphorylates glycogen, causing its breakdown.[A19402] Glucagon also relaxes smooth muscle of the stomach, duodenum, small bowel, and colon.[L7634,L7643] | Patients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium.[L7634,L7637,L7640,L7643] Phentolamine may be given to control blood pressure.[L7634,L7637,L7640,L7643] Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia.[L7637] The LD50 for intravenous glucagon in mice is 300mg/kg and in rats is 38.6mg/kg.[L7637] | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma.[L7634,L7643] | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.[L7637] An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes.[L7637] A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes.[L7643] | The volume of distribution of glucagon is 0.25L/kg.[L7637] The apparent volume of distribution is 885L.[L7643] | A 1mg intravenous dose of glucagon has a clearance of 13.5mL/min/kg.[L7637] | NA | NA | NA | NA | NA | Glucagon receptor,Glucagon-like peptide 2 receptor,Glucagon-like peptide 1 receptor | Gvoke PFS 0.5 mg Pre-filled Syringe | Xeris Pharmaceuticals, Inc. | Xeris Pharmaceuticals, Inc. | Subcutaneous | 0.5 mg/0.1mL | GVOKE is contraindicated in patients with: Pheochromocytoma Insulinoma [ see WARNINGS AND PRECAUTIONS] because of the risk of hypoglycemia Known hypersensitivity to glucagon or to any of the excipients in GVOKE. Allergic reactions have been reported with glucagon and include anaphylactic shock with breathing difficulties and hypotension. | nausea vomiting hives injection site swelling or redness headache fast heartbeat | Glucagon comes as a solution (liquid) in a prefilled syringe and an auto-injector device to inject subcutaneously (just under the skin). It also comes as a powder to be mixed with a provided liquid to be injected subcutaneously, intramuscularly (into the muscle), or intravenously (into a vein). It is usually injected as needed at the first sign of severe hypoglycemia. | Glucagon is used along with emergency medical treatment to treat very low blood sugar. Glucagon is also used in diagnostic testing of the stomach and other digestive organs. Glucagon is in a class of medications called glycogenolytic agents. It works by causing the liver to release stored sugar to the blood. It also works by relaxing smooth muscles of the stomach and other digestive organs for diagnostic testing. | (3S)-3-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-5-oxopentanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-oxopentanoyl]amino]-4-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-4-amino-1-[[(1S,2R)-1-carboxy-2-hydroxypropyl]amino]-1,4-dioxobutan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-oxobutanoic acid | NA | Link | Link | NA |
| 11430 | Th1247 | Glucagon | >Th1247_Glucagon HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | NA | NA | The half life of glucagon is 26 minutes for an intramuscular dose.[L7634] The half life of glucagon nasal powder is approximately 35 minutes.[L7643] The half life of glucagon by a subcutaneous auto-injector or pre-filled syringe is 32 minutes.[L8519] | Glucagon is a 29 amino acid hormone used as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon was granted FDA approval on 14 November 1960.[L7631] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and severe hypoglycemia.[A19402,L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon has a short duration of action.[L7634,L7637,L7640,L7643] Glucagon may cause hyperglycemia in diabetic patients.[L7634,L7637,L7640,L7643] | Glucagon binds to the glucagon receptor activating Gsa and Gq.[A19402] This activation activates adenylate cyclase, which increases intracellular cyclic AMP and activates protein kinase A.[A19402] Activating Gq activates phospholipase C, increases production of inositol 1,4,5-triphosphate, and releases intracellular calcium.[A19402] Protein kinase A phosphorylates glycogen phosphorylase kinase, which phosphorylates glycogen phosphorylase, which phosphorylates glycogen, causing its breakdown.[A19402] Glucagon also relaxes smooth muscle of the stomach, duodenum, small bowel, and colon.[L7634,L7643] | Patients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium.[L7634,L7637,L7640,L7643] Phentolamine may be given to control blood pressure.[L7634,L7637,L7640,L7643] Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia.[L7637] The LD50 for intravenous glucagon in mice is 300mg/kg and in rats is 38.6mg/kg.[L7637] | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma.[L7634,L7643] | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.[L7637] An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes.[L7637] A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes.[L7643] | The volume of distribution of glucagon is 0.25L/kg.[L7637] The apparent volume of distribution is 885L.[L7643] | A 1mg intravenous dose of glucagon has a clearance of 13.5mL/min/kg.[L7637] | NA | NA | NA | NA | NA | Glucagon receptor,Glucagon-like peptide 2 receptor,Glucagon-like peptide 1 receptor | Gvoke PFS 1 mg Pre-filled Syringe | Xeris Pharmaceuticals, Inc. | Xeris Pharmaceuticals, Inc. | Subcutaneous | 1 mg/0.2mL | GVOKE is contraindicated in patients with: Pheochromocytoma Insulinoma [ see WARNINGS AND PRECAUTIONS] because of the risk of hypoglycemia Known hypersensitivity to glucagon or to any of the excipients in GVOKE. Allergic reactions have been reported with glucagon and include anaphylactic shock with breathing difficulties and hypotension. | nausea vomiting hives injection site swelling or redness headache fast heartbeat | Glucagon comes as a solution (liquid) in a prefilled syringe and an auto-injector device to inject subcutaneously (just under the skin). It also comes as a powder to be mixed with a provided liquid to be injected subcutaneously, intramuscularly (into the muscle), or intravenously (into a vein). It is usually injected as needed at the first sign of severe hypoglycemia. | Glucagon is used along with emergency medical treatment to treat very low blood sugar. Glucagon is also used in diagnostic testing of the stomach and other digestive organs. Glucagon is in a class of medications called glycogenolytic agents. It works by causing the liver to release stored sugar to the blood. It also works by relaxing smooth muscles of the stomach and other digestive organs for diagnostic testing. | (3S)-3-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-5-oxopentanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-oxopentanoyl]amino]-4-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-4-amino-1-[[(1S,2R)-1-carboxy-2-hydroxypropyl]amino]-1,4-dioxobutan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-oxobutanoic acid | NA | Link | Link | NA |
| 15732 | Th1622 | Somapacitan | >Th1622_Somapacitan FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSCVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | NA | C1038H1609N273O319S9 | NA | NA | NA | The elimination half life of somapacitan is 2-3 days.[L15661] | Somapacitan, also known as NNC0195-0092,[A219136] is a growth hormone analog indicated to treat adults with growth hormone deficiency.[A219126,L15661] This human growth hormone analog differs by the creation of an albumin binding site, and prolonging the effect so that it requires weekly dosing rather than daily.[A219146] Somapacitan was granted FDA approval on 28 August 2020.[L15666] | Somapacitan is indicated as a replacement for growth hormone in adult patients with growth hormone deficiency.[L15661] | Somapacitan stimulates the growth hormone receptor.[L15661] Somapacitan has a long duration of action as it is given once weekly.[L15661] It has a moderately wide therapeutic window as an acute overdose may cause hypoglycemia followed by hyperglycemia.[L15661] Patients should be counselled regarding the risk of increased mortality in patients with critical illness, risk of neoplasms, glucose intolerance in diabetes mellitus, intracranial hypertension, hypersensitivity, fluid retention, hypoadrenalism, hypothyroidism, pancreatitis, lipohypertrophy, and lipoatrophy.[L15661] | Somapacitan binds to the growth hormone receptor and induces intracellular signalling to up-regulate insulin-like growth factor I (IGF-1).[A219096,L15661] IGF-1 causes growth in bones and muscle tissue.[A219096] Growth hormones more directly cause the fusion of myoblasts and myotubes to cause muscle fibre growth, activate neural stem cells, and induce chondrocyte proliferation.[A219096] | Patients experiencing an acute overdose of somapacitan may present with fluid retention.[L15661] Chronic overdose may resemble gigantism or acromegaly.[L15661] Treat patients with symptomatic and supportive measures to minimize the permanent effects.[A219141] | Studies in humans and rats show that somapacitan is metabolized through cleavage of the albumin-binding moiety and linker sidechain before further non-specific mechanisms.[A219096,L15661] | A 0.02mg/kg single dose of somapacitan reaches a Cmax of 14.4 ng/mL, with a Tmax of 11.1 hours, and an AUC of 475 ng | The approximate volume of distribution of somapacitan is 14.6 L.[L15661] | The apparent maximum rate of saturable elimination is estimated to be 0.268 ± 0.03 mg/h.[A219126] | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Growth hormone receptor | Sogroya | Novo Nordisk | Novo Nordisk | Subcutaneous | 10 mg/1.5ml | SOGROYA is contraindicated in patients with:Acute critical illness after open-heart surgery, abdominal surgery or multiple accidental trauma, or those with acute respiratory failure because of the risk of increased mortality with use of pharmacologic doses of SOGROYA [see WARNINGS AND PRECAUTIONS].Active malignancy [see WARNINGS AND PRECAUTIONS].Hypersensitivity to SOGROYA or any of its excipients. Systemic hypersensitivity reactions have been reported postmarketing with other growth hormone products [see WARNINGS AND PRECAUTIONS].Active proliferative or severe non-proliferative diabetic retinopathy. | back pain, joint pain, indigestion/heartburn, sleep disorder, dizziness, tonsillitis, swelling of extremities, vomiting, adrenal insufficiency, high blood pressure (hypertension), increased blood creatine phosphokinase, weight gain, and anemia | Sogroya is a prescription medicine that contains human growth hormone, the same growth hormone made by the human body. Sogroya is given by injection under the skin (subcutaneous) and is used to treat adults who do not make enough growth hormone. It is not known if Sogroya is safe and effective in children.... | SOGROYA is indicated for the replacement of endogenous growth hormone (GH) in adults with growth hormone deficiency (GHD). | (2S)-5-[2-[2-[2-[[(2S)-1-amino-6-[[2-[(2R)-2-amino-2-carboxyethyl]sulfanylacetyl]amino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]ethoxy]ethylamino]-2-[[(4S)-4-carboxy-4-[[2-[2-[2-[4-[16-(2H-tetrazol-5-yl)hexadecanoylsulfamoyl]butanoylamino]ethoxy]ethoxy]acetyl]amino]butanoyl]amino]-5-oxopentanoic acid | NA | Link | Link | NA |
| 15733 | Th1622 | Somapacitan | >Th1622_Somapacitan FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSCVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | NA | C1038H1609N273O319S9 | NA | NA | NA | The elimination half life of somapacitan is 2-3 days.[L15661] | Somapacitan, also known as NNC0195-0092,[A219136] is a growth hormone analog indicated to treat adults with growth hormone deficiency.[A219126,L15661] This human growth hormone analog differs by the creation of an albumin binding site, and prolonging the effect so that it requires weekly dosing rather than daily.[A219146] Somapacitan was granted FDA approval on 28 August 2020.[L15666] | Somapacitan is indicated as a replacement for growth hormone in adult patients with growth hormone deficiency.[L15661] | Somapacitan stimulates the growth hormone receptor.[L15661] Somapacitan has a long duration of action as it is given once weekly.[L15661] It has a moderately wide therapeutic window as an acute overdose may cause hypoglycemia followed by hyperglycemia.[L15661] Patients should be counselled regarding the risk of increased mortality in patients with critical illness, risk of neoplasms, glucose intolerance in diabetes mellitus, intracranial hypertension, hypersensitivity, fluid retention, hypoadrenalism, hypothyroidism, pancreatitis, lipohypertrophy, and lipoatrophy.[L15661] | Somapacitan binds to the growth hormone receptor and induces intracellular signalling to up-regulate insulin-like growth factor I (IGF-1).[A219096,L15661] IGF-1 causes growth in bones and muscle tissue.[A219096] Growth hormones more directly cause the fusion of myoblasts and myotubes to cause muscle fibre growth, activate neural stem cells, and induce chondrocyte proliferation.[A219096] | Patients experiencing an acute overdose of somapacitan may present with fluid retention.[L15661] Chronic overdose may resemble gigantism or acromegaly.[L15661] Treat patients with symptomatic and supportive measures to minimize the permanent effects.[A219141] | Studies in humans and rats show that somapacitan is metabolized through cleavage of the albumin-binding moiety and linker sidechain before further non-specific mechanisms.[A219096,L15661] | A 0.02mg/kg single dose of somapacitan reaches a Cmax of 14.4 ng/mL, with a Tmax of 11.1 hours, and an AUC of 475 ng | The approximate volume of distribution of somapacitan is 14.6 L.[L15661] | The apparent maximum rate of saturable elimination is estimated to be 0.268 ± 0.03 mg/h.[A219126] | Cytochrome P-450 CYP1A2 Inducers | NA | NA | NA | NA | Growth hormone receptor | Sogroya | Novo Nordisk | Novo Nordisk | Subcutaneous | 6.7 mg/1mL | SOGROYA is contraindicated in patients with:Acute critical illness after open-heart surgery, abdominal surgery or multiple accidental trauma, or those with acute respiratory failure because of the risk of increased mortality with use of pharmacologic doses of SOGROYA [see WARNINGS AND PRECAUTIONS].Active malignancy [see WARNINGS AND PRECAUTIONS].Hypersensitivity to SOGROYA or any of its excipients. Systemic hypersensitivity reactions have been reported postmarketing with other growth hormone products [see WARNINGS AND PRECAUTIONS].Active proliferative or severe non-proliferative diabetic retinopathy. | back pain, joint pain, indigestion/heartburn, sleep disorder, dizziness, tonsillitis, swelling of extremities, vomiting, adrenal insufficiency, high blood pressure (hypertension), increased blood creatine phosphokinase, weight gain, and anemia | Sogroya is a prescription medicine that contains human growth hormone, the same growth hormone made by the human body. Sogroya is given by injection under the skin (subcutaneous) and is used to treat adults who do not make enough growth hormone. It is not known if Sogroya is safe and effective in children.... | SOGROYA is indicated for the replacement of endogenous growth hormone (GH) in adults with growth hormone deficiency (GHD). | (2S)-5-[2-[2-[2-[[(2S)-1-amino-6-[[2-[(2R)-2-amino-2-carboxyethyl]sulfanylacetyl]amino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]ethoxy]ethylamino]-2-[[(4S)-4-carboxy-4-[[2-[2-[2-[4-[16-(2H-tetrazol-5-yl)hexadecanoylsulfamoyl]butanoylamino]ethoxy]ethoxy]acetyl]amino]butanoyl]amino]-5-oxopentanoic acid | NA | Link | Link | NA |
| 15734 | Th1622 | Somapacitan | >Th1622_Somapacitan FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSCVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | NA | C1038H1609N273O319S9 | NA | NA | NA | The elimination half life of somapacitan is 2-3 days.[L15661] | Somapacitan, also known as NNC0195-0092,[A219136] is a growth hormone analog indicated to treat adults with growth hormone deficiency.[A219126,L15661] This human growth hormone analog differs by the creation of an albumin binding site, and prolonging the effect so that it requires weekly dosing rather than daily.[A219146] Somapacitan was granted FDA approval on 28 August 2020.[L15666] | Somapacitan is indicated as a replacement for growth hormone in adult patients with growth hormone deficiency.[L15661] | Somapacitan stimulates the growth hormone receptor.[L15661] Somapacitan has a long duration of action as it is given once weekly.[L15661] It has a moderately wide therapeutic window as an acute overdose may cause hypoglycemia followed by hyperglycemia.[L15661] Patients should be counselled regarding the risk of increased mortality in patients with critical illness, risk of neoplasms, glucose intolerance in diabetes mellitus, intracranial hypertension, hypersensitivity, fluid retention, hypoadrenalism, hypothyroidism, pancreatitis, lipohypertrophy, and lipoatrophy.[L15661] | Somapacitan binds to the growth hormone receptor and induces intracellular signalling to up-regulate insulin-like growth factor I (IGF-1).[A219096,L15661] IGF-1 causes growth in bones and muscle tissue.[A219096] Growth hormones more directly cause the fusion of myoblasts and myotubes to cause muscle fibre growth, activate neural stem cells, and induce chondrocyte proliferation.[A219096] | Patients experiencing an acute overdose of somapacitan may present with fluid retention.[L15661] Chronic overdose may resemble gigantism or acromegaly.[L15661] Treat patients with symptomatic and supportive measures to minimize the permanent effects.[A219141] | Studies in humans and rats show that somapacitan is metabolized through cleavage of the albumin-binding moiety and linker sidechain before further non-specific mechanisms.[A219096,L15661] | A 0.02mg/kg single dose of somapacitan reaches a Cmax of 14.4 ng/mL, with a Tmax of 11.1 hours, and an AUC of 475 ng | The approximate volume of distribution of somapacitan is 14.6 L.[L15661] | The apparent maximum rate of saturable elimination is estimated to be 0.268 ± 0.03 mg/h.[A219126] | Cytochrome P-450 CYP1A2 Inducers (strength unknown) | NA | NA | NA | NA | Growth hormone receptor | Sogroya | Novo Nordisk | Novo Nordisk | Subcutaneous | 3.3 mg/1mL | SOGROYA is contraindicated in patients with:Acute critical illness after open-heart surgery, abdominal surgery or multiple accidental trauma, or those with acute respiratory failure because of the risk of increased mortality with use of pharmacologic doses of SOGROYA [see WARNINGS AND PRECAUTIONS].Active malignancy [see WARNINGS AND PRECAUTIONS].Hypersensitivity to SOGROYA or any of its excipients. Systemic hypersensitivity reactions have been reported postmarketing with other growth hormone products [see WARNINGS AND PRECAUTIONS].Active proliferative or severe non-proliferative diabetic retinopathy. | back pain, joint pain, indigestion/heartburn, sleep disorder, dizziness, tonsillitis, swelling of extremities, vomiting, adrenal insufficiency, high blood pressure (hypertension), increased blood creatine phosphokinase, weight gain, and anemia | Sogroya is a prescription medicine that contains human growth hormone, the same growth hormone made by the human body. Sogroya is given by injection under the skin (subcutaneous) and is used to treat adults who do not make enough growth hormone. It is not known if Sogroya is safe and effective in children.... | SOGROYA is indicated for the replacement of endogenous growth hormone (GH) in adults with growth hormone deficiency (GHD). | (2S)-5-[2-[2-[2-[[(2S)-1-amino-6-[[2-[(2R)-2-amino-2-carboxyethyl]sulfanylacetyl]amino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]ethoxy]ethylamino]-2-[[(4S)-4-carboxy-4-[[2-[2-[2-[4-[16-(2H-tetrazol-5-yl)hexadecanoylsulfamoyl]butanoylamino]ethoxy]ethoxy]acetyl]amino]butanoyl]amino]-5-oxopentanoic acid | NA | Link | Link | NA |
| 16384 | Th1894 | Tirzepatide | >Th1894_Tirzepatide YXEGTFTSDYSIXLDKIAQKAFVQWLIAGGPSSGAPPPS | 4810.52 Da | C225H348N48O68 | NA | NA | NA | ,The half-life is approximately five days. | Tirzepatide is a novel dual glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptor agonist. Dual GIP/GLP-1 agonists gained increasing attention as new therapeutic agents for glycemic and weight control as they demonstrated better glucose control and weight loss compared to selective GLP-1 receptor agonists in preclinical and clinical trials. | Tirzepatide is a dual GIP and GLP-1 receptor agonist used for the treatment of type II diabetes in adults as an adjunct to diet and exercise. | Tirzepatide is a synthetic peptide with glucose-lowering effects. It works to stimulate first- and second-phase insulin secretion, and reduces glucagon levels, both in a glucose-dependent manner. Tirzepatide was also shown to delay gastric emptying, lower fasting and postprandial glucose concentration, decrease food intake,4 and reduce body weight in patients with type 2 diabetes. Tirzepatide can increase insulin sensitivity. | Glucagon-like peptide-1 (GLP-1) receptors (GLP-1R) are expressed throughout the body, including pancreatic beta-cells and the gastrointestinal tract. They have been implicated in the pathophysiology of type II diabetes mellitus as GLP-1R signalling is involved in glucose control by enhancing glucose-stimulated insulin secretion, delaying gastric transit, decreasing plasma glucagon levels, and reducing body weight by activating anorexigenic pathways in the brain. Both glucose-dependent insulinotropic polypeptide (GIP) and GLP-1 are peptide hormones involved in glucose homeostasis: they promote glucose-stimulated insulin secretion from the pancreatic beta-cells. However, GIP is the main incretin hormone that exerts insulinotropic effects in response to food intake. | There is limited information regarding the LD50 and overdose of tirzepatide. In case of an overdosage, appropriate supportive treatment should be initiated with a sufficient amount of time for observation and treatment, as tirzepatide has a long half-life. | Tirzepatide is metabolized by proteolytic cleavage of the peptide backbone, beta-oxidation of the C20 fatty diacid moiety, and amide hydrolysis. | Over the dose range of 1-5 mg, the Cmax of tirzepatide ranged from 108 to 397 ng/mL.The mean absolute bioavailability of tirzepatide following subcutaneous administration is 80%. Following subcutaneous administration, the Tmax ranged from eight to 72 hours. The steady-state plasma concentrations were achieved following four weeks of once-weekly subcutaneous administration. | Following subcutaneous administration, the mean steady-state volume of distribution was 9.5 L. The mean apparent steady-state volume of distribution of tirzepatide following subcutaneous administration in patients with type 2 diabetes mellitus was approximately 10.3 L. | The apparent population mean clearance of tirzepatide is 0.061 L/h.4 The mean steady-state apparent clearance of tirzepatide was 0.056 L/h. | Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Gastrointestinal Hormones,GLP-1 Agonists,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Incretins,Nerve Tissue Proteins,Neuropeptides,Peptide Hormones,Peptides,Proteins | NA | NA | NA | NA | Glucagon-like peptide 1 receptor, Gastric inhibitory polypeptide | Mounjaro | Eli Lilly and Company | Eli Lilly and Company | Subcutaneous | 12.5 mg/0.5mL | MOUNJARO is contraindicated in patients with: A personal or family history of medullary thyroid carcinoma (MTC) or in patients with Multiple Endocrine Neoplasia syndrome type 2 | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, dizziness, fast heart rate, shaking, sweating, nervousness, anxiety, irritability, confusion, dizziness, hunger, pain in the upper right side of your abdomen, pain spreading to your back or below the shoulder blade, nausea, vomiting, fever, yellowing of the skin and eyes (jaundice), clay-colored stools, and bloating of the abdomen | MOUNJARO (tirzepatide) injection, for subcutaneous use, contains tirzepatide, a once weekly GIP receptor and GLP-1 receptor agonist. It is a 39-amino-acid modified peptide based on the GIP sequence. Tirzepatide contains 2 non-coded amino acids (aminoisobutyric acid, Aib) in positions 2 and 13, a C-terminal amide, and Lys residue at position 20 that is attached to 1,20-eicosanedioic acid via a linker. | Mounjaro (tirzepatide) Injection is a prescription medicine used to treat the symptoms of Type 2 Diabetes Mellitus. | NA | MOUNJARO is a clear, colorless to slightly yellow, sterile, preservative-free solution for subcutaneous use. Each singledose pen contains a 0.5 mL solution of 2.5 mg, 5 mg, 7.5 mg, 10 mg, 12.5 mg, or 15 mg of tirzepatide and the following excipients: sodium chloride (4.1 mg), sodium phosphate dibasic heptahydrate (0.7 mg), and water for injection. Hydrochloric acid solution and/or sodium hydroxide solution may have been added to adjust the pH. MOUNJARO has a pH of 6.5 – 7.5. | Link | Link | NA |