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 |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 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 |
| 10030 | Th1005 | Etanercept | >Th1005_Etanercept LPAQVAFTPYAPEPGSTCRLREYYDQTAQMCCSKCSPGQHAKVFCTKTSDTVCDSCEDSTYTQLWNWVPECLSCGSRCSSDQVETQACTREQNRICTCRPGWYCALSKQEGCRLCAPLRKCRPGFGVARPGTETSDVVCKPCAPGTFSNTTSSTDICRPHQICNVVAIPGNASMDAVCTSTSPTRSMAPGAVHLPQPVSTRSQHTQPTPEPSTAPSTSFLLPMGPSPPAEGSTGDEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 51234.9 | C2224H3475N621O698S36 | 7.89 | -0.529 | 71 | 70.7-94.8 hours in pediatric JIA 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 | US7276477 | 2-Oct-2007 | 18-Nov-2024 | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | NA | Eticovo | Samsung Bioepis Co., Ltd. | Samsung Bioepis Co., Ltd. | rheumatoid arthritis (RA), polyarticular juvenile idiopathic arthritis (JIA) in patients aged 2 years or older, psoriatic arthritis (PsA), ankylosing spondylitis (AS), and plaque psoriasis (PsO) in patients 4 years or older. | NA | 8.18 mg sodium chloride 0.665 mg sodium phosphate dibasic heptahydrate 1.038 mg sodium phosphate monobasic monohydrate 10 mg sucrose Water for Injection, USP | clear to opalescent, colorless to pale yellow, sterile, and preservative-free solution | Injection in the single-dose prefilled syring | Starting Dose: 50 mg twice weekly for 3 months Maintenance Dose: 50 mg once weekly | Eticovo should not be administered to patients with sepsis. | pneumonia, cellulitis, septic arthritis, bronchitis, gastroenteritis, pyelonephritis, sepsis, abscess and osteomyelitis. | Link | NA | NA |
| 10033 | Th1006 | Bivalirudin | >Th1006_Bivalirudin FPRPGGGGNGDFEEIPEEYL | 2180.285 | C98H138N24O33 | 3.91 | -0.985 | NA | Creatinine clearance 10-29mL/min: 0.95 hours | Bivalirudin is a synthetic 20 residue peptide which acts as a thrombin inhibitor. Once bound to the active site of the inhibitor, thrombin cannot activate fibrinogen into fibrin which is a crucial step in the formation of thrombus. As it can cause blood stagnation, it is important to monitor changes in hematocrit, activated partial thromboplastin time, international normalized ratio and blood pressure. It is administered intravenously. | For treatment of heparin-induced thrombocytopenia and for the prevention of thrombosis. Bivalirudin is indicated for use in patients undergoing percutaneous coronary intervention (PCI), in patients at moderate to high risk acute coronary syndromes due to unstable angina or non-ST segment elevation in whom a PCI is planned. | Bivalirudin directly and reversibly inhibits thrombin by specifically binding to both the catalytic site and the anion-binding exosite of circulating and clot-bound thrombin. The action of bivalirudin is reversible as thrombin will slowly cleave the thrombin-bivalirudin bond which recovers the active site of thrombin. | Inhibits the action of thrombin by binding to both its catalytic site and to its anion-binding exosite. Thrombin, a serine proteinase that plays a central role in the thrombotic process, acts to cleave fibrinogen into fibrin monomers and activate Factor XIII to Factor XIIIa, allowing fibrin to develop a covalently cross-linked framework which stabilizes the thrombus; thrombin also activates Factors V and VIII, promoting further thrombin generation, and activates platelets, stimulating aggregation and granule release. | Based on a study by Gleason et al., the no observed adverse effect level (NOAEL) for bivalirudin administered to rats via Intravenous infusion over a 24-hour period, was 2000 mg/kg/24 h. | 80% proteolytic cleavage | Bivalirudin exhibits linear pharmacokinetics. The mean steady state concentration is 12.3 ± 1.7mcg/mL after administration of an intravenous bolus of 1mg/kg followd by a 2.5mg/kg/hr Intravenous infusion given over 4 hours. | 0.2L/kg | 3.4 mL/min/kg [mild renal function] | Amino Acids, Peptides, and Proteins, Anticoagulants, Antithrombins, Blood and Blood Forming Organs, Enzyme Inhibitors, Hematologic Agents, Peptides, Protease Inhibitors, Serine Protease Inhibitors, Thrombin Inhibitors | US5196404 | 23-Mar-1993 | 15-Dec-2014 | Gemcitabine, Gemcitabine may enhance the adverse/toxic effect of Bleomycin. The risk of pulmonary toxicity may be increased. Use extreme caution if using gemcitabine and bleomycin in combination. Monitor for the development of pulmonary toxicity | NA | Angiox | The Medicines Company UK Ltd | The Medicines Company UK Ltd | Used as an anticoagulant in adult patients undergoing percutaneous coronary intervention (PCI), including patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary PCI. Angiox is also indicated for the treatment of adult patients | NA | Each vial contains 250 mg bivalirudin. | Powder for concentrated solution | Injection | 0.75 mg/kg IV bolus, initially, followed by continuous infusion at rate of 1.75 mg/kg/hr for duration of procedure | Hypersensitivity, active bleeding or increased risk of bleeding because of haemostasis disorder or irreversible coagulation disorder, uncontrolled hypertension, subacute bacterial endocarditis, severe renal impairment and in dialysis dependent pateints, | NA | Link | NA | NA |
| 10039 | 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 | NA | Enantone | Takeda | Takeda | NA | NA | NA | Solution | Injection | One3.75 mg DPS mnthly or one 11.25 mg DPS every 3 month as a single SC/IM injection. | Hypersensitivity, undiagnosed abnormal vag bleeding, pregnancy, lactation | Weightloss, Parosmia (distortion of the sense of smell, as in smelling odours that are not present), Nausea (feeling of having an urge to vomit), Musculoskeletal Stiffness (stiffness of the body's muscles, joints, tendons, ligaments and nerves), Mood Swinng. | 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 |
| 10059 | Th1010 | Interferon alfa-n1 | >Th1010_Interferon_alfa-n1 CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 19241.1 | C860H1353N227O255S9 | 5.99 | -0.336 | 61 | 1.2 hours (mammalian reticulocytes, in vitro) | Purified, natural and glycosylated human interferon alpha proteins of 166 residues. | Used to treat venereal or genital warts caused by the Human Papiloma Virus. | Upregulates the expression of MHC I proteins, allowing increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes 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 namely 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 | NA | NA | NA | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, 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 Type I, Interferons, Myelosuppressive Agents, Peptides, Proteins | NA | NA | NA | Interferon increases the effect and toxicity of theophylline | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | Wellferon | GlaxoSmithKline | GlaxoSmithKline | Used for the treatment of patients with hairy cell leukemia, juvenile laryngeal papillomatosis, condylomata acuminata, chronic hepatitis B and chronic hepatitis C infections. | NA | Each vial of clear, colorless solution contains interferon alpha-n1 (lns) [purified human lymphoblastoid interferon] 3, 5 or 10 mega units. 1 mega unit (Mu)=1´10International Units (IU) of lymphoblastoid interferon. Formulated in 1 mL tris-glycine buffere | Solution | Injection | NA | Hypersensitivity | Most side/adverse effects, except the flu-like syndrome, are dose-related . They are usually mild to moderate at systemic doses less than 10 million Units per day }; hematologic and hepatic toxicities tend to be more frequent with doses above 10 million | 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 |
| 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 |
| 10088 | 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 | Nanokine | Nanogen Pharmaceutical biotechnology, Vietnam) | Nanogen Pharmaceutical biotechnology, Vietnam) | Used in treatment of anaemia associated with chronic renal failure in paediatric and adult patients on haemodialysis and adult patients on peritoneal dialysis | NA | NA | Sterile, white, lyophilized powder. The reconstituted preparation with 1 ml solvent (containing 0.9% benzyl alcohol) results in a clear, colorless solution. | Injection | NA | Uncontrolled hypertension | NA | 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 |
| 10110 | Th1015 | Interferon alfa-n3 | >Th1015_Interferon_alfa-n3 CDLPQTHSLGSRRTLMLLAQMRKISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | NA | NA | 5.99 | NA | 61 | NA | Purified, natural human interferon alpha proteins consisting of 3 forms or polymorphisms including 2a, 2b and 2c. It consists of 166 residues(MW range from 16 kD to 27 kD) out of which some are glycosylated. | For the intralesional treatment of refractory or recurring external condylomata acuminata. | Interferon alfa-n3 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 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), beta-2 microglobulin, neopterin 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. | NA | NA | NA | NA | NA | Alfa Interferons, 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 alpha, Interferon Type I, Interferon-alpha, Interferons, Myelosuppressive Agents, Peptides, Proteins | NA | NA | NA | NA | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | Alferon | AIM ImmunoTech Inc | AIM ImmunoTech Inc | Used to treat genital warts (condylomata acuminata) | NA | NA | Solution | Injection | 0.05 mL (250,000 international units) per wart, injected intralesionally twice a week for up to 8 weeks. The maximum recommended dosage per treatment session is 0.5 mL (2.5 million international units). | Allergic to any ingredient in Alferon solution, including egg protein or neomycin | Appetite loss; changes in taste or hearing; chills; diarrhea; fatigue; flu-like symptoms; headache; muscle and joint pain; nausea; pain or other reaction at the site of injection; stomach pain; vomiting. | 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 |
| 10132 | Th1018 | Secretin | >Th1018_Secretin HSDGTFTSELSRLREGARLQRLLQGLV | 3039.44 | C130H220N44O42 | 9.45 | -0.463 | NA | 0.75 hours | This drug is the synthetic form of natural secretin. It is prepared using solid phase peptide synthesis. Secretin is a peptide hormone produced in the S cells of the duodenum. Its main effect is to regulate the pH of the small intestine contents through the control of gastric acid secretion and buffering with bicarbonate. It was the first hormone to be discovered. | For diagnosis of pancreatic exocrine dysfunction and gastrinoma | Secretin is a hormone produced in the S cells of the duodenum in response to low local pH. It stimulates the secretion of bicarbonate from bicarbonate producing organs(liver, pancreas, Brunner's glands) when the pH drops below a set value. This helps neutralize the gastric acid entering the duodenum from the stomach. It also inhibits acid secretion from the stomach by reducing gastrin release from the G cells of the stomach. | Secretin binds to the secretin receptor found on the lining of S cells in the duodenum and G cells in the stomach. Binding leads to the secrection of bicarbonate or the reduction of the secretion of gastrin. Properly functioning organs (duodenum, pancreas and stomach) should be responsive to this hormone. | n acute toxicity studies with mice and rabbits, a dose of 20 μg/kg of synthetic human secretin was not lethal with no clinical symptoms of toxicity. | NA | Following intravenous bolus administration of 0.4 mcg/kg, synthetic human secretin concentration rapidly declines to baseline secretin levels within 90 to 120 minutes | 2.7 L | 580.9 ± 51.3 mL/min | Amino Acids, Peptides, and Proteins, Diagnostic Agents, Gastrointestinal Agents, Gastrointestinal Hormones, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Peptide Hormones, Peptides, Proteins, Secretin, Secretin-class Hormone, Tests for Pancreatic Function | NA | NA | NA | Trihexyphenidyl.The stimulatory effect of Secretin may be reduced by anticholinergics such as Trihexyphenidyl. Concomitant use of Secretin and drugs with substantial anticholinergic effects should be avoided. If combination therapy must be used, S | NA | Secremax | Repligen Corp | Repligen Corp | Used to treat GI spasm, irritable bowel syndrome, hyperperistalsis, peptic ulcer, functional diarrhoea, morning sickness, motion sickness and Dismenorrhoea. | NA | NA | Solution | Intravenous | NA | NA | NA | Link | NA | NA |
| 10171 | Th1022 | Antihemophilic Factor | >Th1022_Antihemophilic_Factor MQIELSTCFFLCLLRFCFSATRRYYLGAVELSWDYMQSDLGELPVDARFPPRVPKSFPFNTSVVYKKTLFVEFTVHLFNIAKPRPPWMGLLGPTIQAEVYDTVVITLKNMASHPVSLHAVGVSYWKASEGAEYDDQTSQREKEDDKVFPGGSHTYVWQVLKENGPMASDPLCLTYSYLSHVDLVKDLNSGLIGALLVCREGSLAKEKTQTLHKFILLFAVFDEGKSWHSETKNSLMQDRDAASARAWPKMHTVNGYVNRSLPGLIGCHRKSVYWHVIGMGTTPEVHSIFLEGHTFLVRNHRQASLEISPITFLTAQTLLMDLGQFLLFCHISSHQHDGMEAYVKVDSCPEEPQLRMKNNEEAEDYDDDLTDSEMDVVRFDDDNSPSFIQIRSVAKKHPKTWVHYIAAEEEDWDYAPLVLAPDDRSYKSQYLNNGPQRIGRKYKKVRFMAYTDETFKTREAIQHESGILGPLLYGEVGDTLLIIFKNQASRPYNIYPHGITDVRPLYSRRLPKGVKHLKDFPILPGEIFKYKWTVTVEDGPTKSDPRCLTRYYSSFVNMERDLASGLIGPLLICYKESVDQRGNQIMSDKRNVILFSVFDENRSWYLTENIQRFLPNPAGVQLEDPEFQASNIMHSINGYVFDSLQLSVCLHEVAYWYILSIGAQTDFLSVFFSGYTFKHKMVYEDTLTLFPFSGETVFMSMENPGLWILGCHNSDFRNRGMTALLKVSSCDKNTGDYYEDSYEDISAYLLSKNNAIEPRSFSQNSRHPSTRQKQFNATTIPENDIEKTDPWFAHRTPMPKIQNVSSSDLLMLLRQSPTPHGLSLSDLQEAKYETFSDDPSPGAIDSNNSLSEMTHFRPQLHHSGDMVFTPESGLQLRLNEKLGTTAATELKKLDFKVSSTSNNLISTIPSDNLAAGTDNTSSLGPPSMPVHYDSQLDTTLFGKKSSPLTESGGPLSLSEENNDSKLLESGLMNSQESSWGKNVSSTESGRLFKGKRAHGPALLTKDNALFKVSISLLKTNKTSNNSATNRKTHIDGPSLLIENSPSVWQNILESDTEFKKVTPLIHDRMLMDKNATALRLNHMSNKTTSSKNMEMVQQKKEGPIPPDAQNPDMSFFKMLFLPESARWIQRTHGKNSLNSGQGPSPKQLVSLGPEKSVEGQNFLSEKNKVVVGKGEFTKDVGLKEMVFPSSRNLFLTNLDNLHENNTHNQEKKIQEEIEKKETLIQENVVLPQIHTVTGTKNFMKNLFLLSTRQNVEGSYEGAYAPVLQDFRSLNDSTNRTKKHTAHFSKKGEEENLEGLGNQTKQIVEKYACTTRISPNTSQQNFVTQRSKRALKQFRLPLEETELEKRIIVDDTDTQWSKNMKHLTPSTLTQIDYNEKEKGAITQSPLSDCLTRSHSIPQANRSPLPIAKVSSFPSIRPIYLTRVLFQDNSSHLPAASYRKKDSGVQESSHFLQGAKKNNLSLAILTLEMTGDQREVGSLGTSATNSVTYKKVENTVLPKPDLPKTSGKVELLPKVHIYQKDLFPTETSNGSPGHLDLVEGSLLQGTEGAIKWNEANRPGKVPFLRVATESSAKTPSKLLDPLAWDNHYGTQIPKEEWKSQEKSPEKTAFKKKDTILSLNACESNHAIAAINEGQNKPEIEVTWAKQGRTERLCSQNPPVLKRHQREITRTTLQSDQEEIDYDDTISVEMKKEDFDIYDEDENQSPRSFQKKTRHYFIAAVERLWDYGMSSSPHVLRNRAQSGSVPQFKKVVFQEFTDGSFTQPLYRGELNEHLGLLGPYIRAEVEDNIMVTFRNQASRPYSFYSSLISYEEDQRQGAEPRKNFVKPNETKTYFWKVQHHMAPTKDEFDCKAWAYFSDVDLEKDVHSGLIGPLLVCHTNTLNPAHGRQVTVQEFALFFTIFDETKSWYFTENMERNCRAPCNIQMEDPTFKENYRFHAINGYIMDTLPGLVMAQDQRIRWYLLSMGSNENIHSIHFSGHVFTVRKKEEYKMALYNLYPGVFETVEMLPSKAGIWRVECLIGEHLHAGMSTLFLVYSNKCQTPLGMASGHIRDFQITASGQYGQWAPKLARLHYSGSINAWSTKEPFSWIKVDLLAPMIIHGIKTQGARQKFSSLYISQFIIMYSLDGKKWQTYRGNSTGTLMVFFGNVDSSGIKHNIFNPPIIARYIRLHPTHYSIRSTLRMELMGCDLNSCSMPLGMESKAISDAQITASSYFTNMFATWSPSKARLHLQGRSNAWRPQVNNPKEWLQVDFQKTMKVTGVTTQGVKSLLTSMYVKEFLISSSQDGHQWTLFFQNGKVKVFQGNQDSFTPVVNSLDPPLLTRYLRIHPQSWVHQIALRMEVLGCEAQDLY | 264725.5 | C11794H18314N3220O3553S83 | 6.97 | -0.533 | NA | 8.4-19.3 hours | Human recombinant antihemophilic factor or Factor VIII of 2332 residues(glycosylated) is produced by CHO cells. | For the treatment of hemophilia A, von Willebrand disease and Factor XIII deficiency. | Antihemophilic Factor binds factor IXa along with calcium and phospholipid, this complex converts factor X to factor Xa to facilitate clotting cascade. | Antihemophilic factor is a protein found in normal plasma which is necessary for clot formation. The administration of AHF provides an increase in plasma levels of AHF and can temporarily correct the coagulation defect of patients with hemophilia A. | The highest toxicity is the risk of viral hepatitis transmition as well as intravascular hemolyisis can occur if large or frequent doses are used in blood groups A, B or AB | The metabolism of the human antihemophilic factor is identical to the normal inactivation and elimination pathway of the natural coagulation factor VIII. After activation, the human antihemophilic factor gets metabolized by activated protein C in R336 and R562 and this action inactivates this cofactor. The proteolysis generates two major fragments which are recognized by an anti-factor VIII A2 domain antibody. This process is followed by a further degradation into smaller fragments | After intravenous administration of the human antihemophilic factor the values of Cmax, AUC and Tmax were 100 IU/ml, 1450 IU h/ml and 0.43 h respectively. In a second clinical trial, the treatment was administered for six months and the values of Cmax, AUC and Tmax were 99 units/ 100 ml, 1471 units h/ 100ml and 16 h, respectively. | The central and peripheral volume of distribution in adults weight an average of 68 kg were 2.81 L and 1.90 L respectively. | 0.15 L/h | Amino Acids, Peptides, and Proteins, Biological Factors, Blood and Blood Forming Organs, Blood Coagulation Factors, Blood Proteins, Carbohydrates, Disaccharides, Hemophilia A, Hemostatics, Human Antihemophilic Factor, Increased Coagulation Activity, Oligosaccharides, Polysaccharides, Protein Precursors, Proteins | NA | NA | NA | NA | NA | Monoclate-P | NA | NA | To control and prevent bleeding episodes in people with hemophilia A. It is also used in these patients before surgery to prevent bleeding. | NA | Each vial contains the labeled amount of antihemophilic factor (AHF) activity as expressed in terms of International Units (I.U.) of antihemophilic activity. One unit of antihemophilic activity is equivalent to that quantity of AHF present in one mL of no | Lyophilized powder for solution | Intravenous Injection | The following formula provides a guide of dosage calculations for both adult and pediatric patients:Number of AHF I.U. Required = Body weight(in kg) x desired Factor VIII increase(% normal) x 0.5 | Hypersensitivity to mouse protein | Products of this type are known to cause allergic reactions, mild chills, nausea or stinging at the infusion site. In some cases, inhibitors of FVIII may occur. | 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 |
| 10190 | Th1024 | Gramicidin D | >Th1024_Gramicidin_D VGALAVVVWLWLWLWX | 1811.253 | C96H135N19O16 | NA | NA | 229 | NA | Gramcidin D is a heterogeneous mixture of three antibiotic compounds, gramicidins A, B and C, making up 80%, 6%, and 14% respectively all of which are obtained from the soil bacterial species Bacillus brevis and called collectively gramicidin D. Gramcidins are 15 residue peptides with alternating D and L amino acids. The peptides assemble inside of the hydrophobic interior of the cellular lipid bilayer to form an alpha helix. The helix itself is not long enough to span the membrane but it dimerizes to form the elongated channel needed to span the whole membrane. Gramicidin D is used primarily as a topical antibiotic and is one of the three constituents of consumer antibiotic polysporin ophthalmic solution. | For treatment of skin lesions, surface wounds and eye infections | Gramicidin is particularly effective against gram-positive bacteria because the drug is highly hemolytic, it cannot be administered internally and so is used only on the skin as a lotion or ointment. It is used primarily in the treatment of infected surface wounds, and in eye, nose, and throat infections. It is normally given with two other antibiotics (neomycin and polymixin B) as an ophthalmic solution | Gramicidin D binds and inserts itself into bacterial membranes (preference to gram-positive cell membranes) resulting in membrane disruption and permeabilization (it acts as a channel). This leads to loss of intracellular solutes (e.g., K+ and amino acids); dissipation of the transmembrane potential; inhibition of respiration; a reduction in ATP pools; and inhibition of DNA, RNA, and protein synthesis, which leads to cell death. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Anti-Bacterial Agents, Anti-Infective Agents, Anti-Infective Agents, Local, Membrane Proteins, P-glycoprotein inhibitors, P-glycoprotein substrates, Peptides, Peptides, Cyclic, Pore Forming Cytotoxic Proteins, Proteins, Throat Preparations | NA | NA | NA | NA | NA | Sofradex | Sanofi | Sanofi | Used in the eye(s) to treat Inflammation in the eye when prevention of bacterial infection is also needed. Signs include sore, red or swollen eyes. It is used in the ear(s) to treat Inflammation of the ear canal (otitis externa) | NA | Each bottle contains 0.5% w/v of Framycetin Sulphate, Dexamethasone Sodium Metasulphobenzoate (equivalent to 0.050% w/v of Dexamethasone) and 0.005% w/v of Gramicidin. The other ingredients are citric acid, sodium citrate, lithium chloride, phenylethyl al | Sterile, clear, bright, colourless, aqueous solution | Auricular and Ocular use. | One or two drops applied to each affected eye up to six times daily or more frequently if required. Two or three drops instilled into the ear three or four times daily. | If glaucoma is present or herpetic keratitis (e.g. dendritic ulcer) is considered a possibility. Otitis Externa should not be treated when the eardrum is perforated because of the risk of ototoxicity. Hypersensitivity to framycetin sulphate, dexamethasone sodium metasulphobenzoate, gramicidin or to any of the excipients. | Stop using Sofradex if: You get any kind of skin problem, such as a rash or itching around your eyes or irritation burning, stinging, itching or swelling, your eyes have problems focussing or develop a blind spot. You may have increased pressure in the eye, you have difficulty seeing at night or notice that your eyesight is cloudy and fuzzy, or you see halos around lights. These could be signs of cataracts. This may occur after using the medicine for a long time | Link | NA | NA |
| 10198 | Th1025 | Intravenous Immunoglobulin | >Th1025_Intravenous_Immunoglobulin PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 71 | 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 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 taggingor 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 | Amino Acids, Peptides, and Proteins, Antibodies, Antigen Neutralization, Blood Proteins, Globulins, Human Immunoglobulin G, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Passively Acquired Immunity, Proteins, Serum, Serum Globulins | NA | NA | NA | NA | NA | Gamastan | Grifols Therapeutics Llc | Grifols Therapeutics Llc | used to treat the symptoms of Hepatitis A, Measles, Rubella, and Varicella. | NA | In the manufacturing process of GAMASTAN, there are several steps with the capacity for viral inactivation or removal. The main steps of the manufacturing process that contribute to the virus clearance capacity are as follows: Caprylate precipitation/depth filtration Caprylate incubation Depth filtration Column chromatography Nanofiltration Low pH final container incubation | clear or slightly opalescent, and colorless or pale yellow or light brown sterile solution | Intravenous | 0.1 mL/kg 0.2 mL/kg 0.2 mL/kg | GAMASTAN is contraindicated in: Anaphylactic or severe systemic hypersensitivity reactions to immune globulin (human). | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, itching, red, swollen, blistered, or peeling skin with or without fever, wheezing, tightness in the chest or throat, trouble breathing, swallowing, or talking, and unusual hoarseness | Link | NA | NA |
| 10199 | Th1025 | Intravenous Immunoglobulin | >Th1025_Intravenous_Immunoglobulin PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S42 | 8.13 | -0.331 | 71 | 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 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 taggingor 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 | Amino Acids, Peptides, and Proteins, Antibodies, Antigen Neutralization, Blood Proteins, Globulins, Human Immunoglobulin G, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Passively Acquired Immunity, Proteins, Serum, Serum Globulins | NA | NA | NA | NA | NA | Gamunex | Talecris Biotherapeutics | Talecris Biotherapeutics | Gamunex-C is used to treat primary immunodeficiency (PI). This includes, but is not limited to, congenital agammaglobulinemia, common variable immunodeficiency, X-linked agammaglobulinemia, Wiskott-Aldrich syndrome, and severe combined immunodeficiencies. | NA | GAMUNEX (immune globulin intravenous human 10%) consists of 9%–11% protein in 0.16–0.24 M glycine. Not less than 98% of the protein has the electrophoretic mobility of gamma globulin. GAMUNEX (immune globulin intravenous human 10%) contains trace levels o | Sterile solution | Intravenous infusion | Treatment of Primary Humoral Immunodeficiency = The dose of GAMUNEX (immune globulin intravenous (human) 10%) for replacement therapy in primary immune deficiency diseases is 300 to 600 mg/kg body weight (3-6 mL/kg) administered every 3 to 4 weeks. The dosage may be adjusted over time to achieve the desired trough levels and clinical responses. | GAMUNEX (immune globulin intravenous (human) 10%) is contraindicated in individuals with acute severe hypersensitivity reactions to Immune Globulin (Human). GAMUNEX (immune globulin intravenous (human) 10%) contains trace amounts of IgA. It is contraindic in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. | Mild headache; dizziness; tired feeling; back pain, muscle cramps; minor chest pain; or flushing (warmth, redness, or tingly feeling). | 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 |
| 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 |
| 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 |
| 10260 | 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 | NA | Vesicle-associated membrane protein 2,Vesicle-associated membrane protein 1,Synaptotagmin-2 | Myobloc | Solstice Neurosciences | Solstice Neurosciences | It is used for reducing the severity of abnormal head position and neck pain associated with a certain neck problem (cervical dystonia) | NA | It is supplied in 3.5-mL glass vials. Each single-use vial of formulated MYOBLOC contains 5,000 Units of botulinum toxin type B per milliliter in 0.05% human serum albumin, 0.01 M sodium succinate, and 0.1 M sodium chloride at approximately pH 5.6. | Clear and colorless to light-yellow Sterile injectable solution | Injection | The recommended initial dose of MYOBLOC (botulinum toxin type b) for patients with a prior history of tolerating botulinum toxin injections is 2,500 to 5,000 Units divided among affected muscles. Patients without a prior history of tolerating botulinum toxin injections should receive lower initial dose. | MYOBLOC is contraindicated in patients with a known hypersensitivity to any botulinum toxin preparation or to any of the components in the formulation and in patients with infection at the proposed injection site | Anxiety; back pain; dizziness; drowsiness; dry eyes; dry mouth; flu-like symptoms; headache; increased cough; indigestion; nausea; neck pain; pain, redness, swelling, or tenderness at the injection site; runny nose; sensitivity to light; sweating; upset stomach. | 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 |
| 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 |
| 10308 | Th1043 | Rasburicase | >Th1043_Rasburicase SAVKAARYGKDNVRVYKVHKDEKTGVQTVYEMTVCVLLEGEIETSYTKADNSVIVATDSIKNTIYITAKQNPVTPPELFGSILGTHFIEKYNHIHAAHVNIVCHRWTRMDIDGKPHPHSFIRDSEEKRNVQVDVVEGKGIDIKSSLSGLTVLKSTNSQFWGFLRDEYTTLKETWDRILSTDVDATWQWKNFSGLQEVRSHVPKFDATWATAREVTLKTFAEDNSASVQATMYKMAEQILARQQLIETVEYSLPNKHYFEIDLSWHKGLQNTGKNAEVFAPQSDPNGLIKCTVGRSSLKSKL | 34109.5 | C1521H2381N417O461S7 | 7.16 | -0.465 | NA | 18 hours | Rasburicase is a recombinant urate-oxidase enzyme produced by a genetically modified Saccharomyces cerevisiae< strain. The cDNA coding for rasburicase was cloned from a strain of Aspergillus flavus. | For treatment of hyperuricemia, reduces elevated plasma uric acid levels (from chemotherapy). | Drugs used to treat lympohoid leukemia, non-Hodgkin's lymphoma and acute myelogenous leukemia often lead to the accumulation of toxic plasma levels of purine metabolites (i.e. uric acid). The injection of rasburicase reduces levels of uric acid and mitigates the toxic effects of chemotherapy induced tumor lysis. | Rasburicase catalyzes enzymatic oxidation of uric acid into an inactive and soluble metabolite (allantoin). | NA | NA | NA | NA | NA | Antigout Preparations, Detoxifying Agents for Antineoplastic Treatment, Enzymes, Enzymes and Coenzymes, Methemoglobinemia Associated Agents, Musculo-Skeletal System, Oxidoreductases, Recombinant Proteins, Uric Acid-specific Enzyme | NA | NA | NA | Cyanide Antidote Kit (amyl nitrite / sodium nitrite / sodium thiosulfate) | NA | Fasturtec | Sanofi Aventis | Sanofi Aventis | Fasturtec is used to treat and prevent high levels of uric acid in the blood in order to prevent kidney failure. It is used in adults and children with blood cancers who are at risk of a sudden rise in uric acid levels when they start to receive chemother | NA | NA | Powder and solvent that are made upto make solution. | Intravenous administartion | The recommended dose is 0.2 mg per kilogram body weight in both children and adults, given as a daily infusion for up to seven days. The duration of treatment is adjusted depending on the patient’s blood levels of uric acid and the doctor’s judgment. | Hypersensitivity | Rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue; blue or gray skin color; chest pain; chills; coughing up blood; dark urine; fever; irregular heartbeat; numbness or tingling of the skin; persistent sore throat; severe dizziness; shortness of breath, trouble breathing, or wheezing; swelling of the hands or feet; weakness; yellowing of the eyes and skin. | Link | 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 |
| 10327 | Th1046 | Abciximab | >Th1046_Abciximab EVQLQQSGTVLARPGASVKMSCEASGYTFTNYWMHWVKQRPGQGLEWIGAIYPGNSDTSYIQKFKGKAKLTAVTSTTSVYMELSSLTNEDSAVYYCTLYDGYYVFAYWGQGTLVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTH | 145651.1 | C6462H9964N1690O2049S48 | 6.16 | -0.424 | 71 | initial half-life of less than 10 minutes and a second phase half-life of about 30 minutes | Abciximab is a Fab fragment of the chimeric human-murine monoclonal antibody 7E3. Abciximab binds to the glycoprotein (GP) IIb/IIIa receptor of human platelets and inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules. It also binds to vitronectin (αvβ3) receptor found on platelets and vessel wall endothelial and smooth muscle cells. | Abciximab is indicated as an adjunct to percutaneous coronary intervention for the prevention of cardiac ischemic complications in patients undergoing percutaneous coronary intervention and in patients with unstable angina not responding to conventional medical therapy when percutaneous coronary intervention is planned within 24 hours. Abciximab is intended for use with aspirin and heparin and has been studied only in that setting. | Abciximab inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules to GPIIb/IIIa receptor sites on activated platelets. A single intravenous bolus dose from 0.15 mg/kg to 0.30 mg/kg produced rapid dose-dependent inhibition of platelet function. After two hours post-injection with a dose of 0.25 - 0.30 mg/kg, 80% of the GPIIb/IIIa receptors were blocked and platelet aggregation was prevented. GPIIb/IIIa is the major surface receptor involved in the final pathway of platelet aggregation. Bleeding time increases to over 30 minutes at the aforementioned doses. To compare, baseline values were five minutes. | Abciximab binds to the intact platelet GPIIb/IIIa receptor, which is a member of the integrin family of adhesion receptors and the major platelet surface receptor involved in platelet aggregation. This binding is thought to involve steric hindrance and/orconformational alterations which block access of large molecules to the receptor rather than direct interaction with the RGD (arginine-glycine-aspartic acid) binding site of GPIIb/IIIa. By binding to the vitronectin receptor (also known as the αvβ3 integrin), abciximab blocks effects mediated by this integrin which include cell adhesion. Furthermore, abciximab blocks Mac-1 receptor on monocytes and neutrophils thus inhibiting monocyte adhesion. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to platelets, or by human antimurine antibody production. Excreted renally. | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Anticoagulants, Antiplatelet agents, Blood and Blood Forming Organs, Blood Proteins, Globulins, Hematologic Agents, Immunoglobulin Fab Fragments, Immunoglobulin Fragments, Immunoglobulins, Immunoproteins, Miscellaneous Therapeutic Agents, Peptide Fragments, Peptides, Platelet Aggregation Inhibitors Excl. Heparin, Proteins, Serum Globulins | CA1341357 | 7-May-2002 | 7-May-2019 | Additive anticoagulant/antiplatelet effects may increase bleed risk. Concomitant therapy should be avoided with Ginkgo biloba. | Integrin beta-3,Integrin alpha-IIb,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 immuno | ReoPro | Eli Lilly and Company, Janssen Pharmaceuticals, Janssen Biotech, Inc. | Eli Lilly and Company, Janssen Pharmaceuticals, Janssen Biotech, Inc. | ReoPro is used to lessen the chance of heart attack in people who need percutaneous coronary intervention (PCI), a procedure to open blocked arteries of the heart. | NA | Each single use vial contains 2 mg/mL of Abciximab in a buffered solution (pH 7.2) of 0.01 M sodium phosphate, 0.15 M sodium chloride and 0.001% polysorbate 80 in Water for Injection. No preservatives are added. | Clear, colorless, Sterile, non-pyrogenic solution | Intravenous administartion | The recommended dosage of Abciximab in adults is a 0.25 mg/kg intravenous bolus administered 10-60 minutes before the start of PCI, followed by a continuous Intravenous infusion of 0.125 _g/kg/min (to a maximum of 10 _g/min) for 12 hours. | Active internal bleeding, Recent (within six weeks) gastrointestinal (GI) or genitourinary (GU) bleeding of clinical significance, History of cerebrovascular accident (CVA) within two years, or CVA with a significant residual neurological deficit, Bleeding diathesis; Administration of oral anticoagulants within seven days unless prothrombin time is I 1.2 times control; Thrombocytopenia (< 100,000 cells/pL); Recent (within six weeks) major surgery or trauma; Intracranial neoplasm, arteriovenous malformation, or aneurysm; Severe uncontrolled hypertension; Presumed or documented history of vasculitis; Use of intravenous dextran before percutaneous coronary intervention, or intent to use it during an intervention. | Bleeding; blurred vision; confusion; dizziness, faintness, or lightheadedness when getting up from a lying or sitting position suddenly; sweating; unusual tiredness or weakness | 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 |
| 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 |
| 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 |
| 10358 | Th1050 | Pegademase bovine | >Th1050_Pegademase_bovine MAQTPAFNKPKVELHVHLDGAIKPETILYYGRKRGIALPADTPEELQNIIGMDKPLSLPEFLAKFDYYMPAIAGCREAVKRIAYEFVEMKAKDGVVYVEVRYSPHLLANSKVEPIPWNQAEGDLTPDEVVSLVNQGLQEGERDFGVKVRSILCCMRHQPSWSSEVVELCKKYREQTVVAIDLAGDETIEGSSLFPGHVKAYAEAVKSGVHRTVHAGEVGSANVVKEAVDTLKTERLGHGYHTLEDATLYNRLRQENMHFEVCPWSSYLTGAWKPDTEHPVVRFKNDQVNYSLNTDDPLIFKSTLDTDYQMTKNEMGFTEEEFKRLNINAAKSSFLPEDEKKELLDLLYKAYGMPSPASAEQCL | 40788.2 | C1821H2834N484O552S14 | 5.33 | -0.428 | NA | 72-144 hours | Bovine adenosine deaminase derived from bovine intestine that has been extensively pegylated for extended serum half life. | For treatment of adenosine deaminase deficiency | Used to replace deficient or inactive adenosine deaminase which leads to severe combined immunodeficiency disease (SCID). The enzyme is responsible for converting adenosine to inosine. In the absence of adenosine deaminase, the purine substrates adenosine 2-deoxyadenosine and their metabolites are actually toxic to lymphocytes thereby leading to diminished immune function. | Pegademase converts adenosine (toxic) to inosine (less toxic) by deamination. It also converts 2'-deoxyadenosine to 2'-deoxyinosine via deamination. | NA | NA | NA | NA | NA | Adjuvants, Immunologic, Aminohydrolases, Antineoplastic and Immunomodulating Agents, Bovine Intestinal Adenosine Deaminase, Enzymes, Enzymes and Coenzymes, Hydrolases, Nucleoside Deaminases, Pegylated agents, Severe Combined Immunodeficiency | NA | NA | NA | Krystexxa (pegloticase) | Adenosine,Growth factor receptor-bound protein 2 | Adagen | Enzon Inc. | Enzon Inc. | It is used for Treating severe combined immunodeficiency disease (SCID) in certain patients with adenosine deaminase (ADA) deficiency. | (monomethoxypolyethylene glycol succinimidyl) 11-17_ adenosine deaminase | Each ml of ADAGEN injection contains, 250 units of Pegademase bovine, 20 mg of Monobasic sodium phoshphate, USP, 5.58 mg of Dibasic sodium phoshphate, USP, 8.50 mg of Sodiium chloride, USP and q.s. to 0 ml of water for injection. | Isotonic, pyrogen free, Sterile solution, pH 7.2-7.4 | Intramusular Injection | The dosage of ADAGEN (pegademase bovine) Injection should be individualized. The recommended dosing schedule is 10 U/kg for the first dose, 15 U/kg for the second dose, and 20 U/kg for the third dose. The usual maintenance dose is 20 U/kg per week. Further increases of 5 U/kg/week may be necessary, but a maximum single dose of 30 U/kg should not be exceeded. | Allergic | Rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue; dark urine; severe or persistent tiredness or weakness; unusual bruising or bleeding | Link | NA | NA |
| 10361 | Th1051 | Human Serum Albumin | >Th1051_Human_Serum_Albumin MKWVTFISLLFLFSSAYSRGVFRRDAHKSEVAHRFKDLGEENFKALVLIAFAQYLQQCPFEDHVKLVNEVTEFAKTCVADESAENCDKSLHTLFGDKLCTVATLRETYGEMADCCAKQEPERNECFLQHKDDNPNLPRLVRPEVDVMCTAFHDNEETFLKKYLYEIARRHPYFYAPELLFFAKRYKAAFTECCQAADKAACLLPKLDELRDEGKASSAKQRLKCASLQKFGERAFKAWAVARLSQRFPKAEFAEVSKLVTDLTKVHTECCHGDLLECADDRADLAKYICENQDSISSKLKECCEKPLLEKSHCIAEVENDEMPADLPSLAADFVESKDVCKNYAEAKDVFLGMFLYEYARRHPDYSVVLLLRLAKTYETTLEKCCAAADPHECYAKVFDEFKPLVEEPQNLIKQNCELFEQLGEYKFQNALLVRYTKKVPQVSTPTLVEVSRNLGKVGSKCCKHPEAKRMPCAEDYLSVVLNQLCVLHEKTPVSDRVTKCCTESLVNRRPCFSALEVDETYVPKEFNAETFTFHADICTLSEKERQIKKQTALVELVKHKPKATKEQLKAVMDDFAAFVEKCCKADDKETCFAEEGKKLVAASQAALGL | 66472.2 | C2936H4624N786O889S41 | 5.67 | -0.395 | 62 | NA | Human serum albumin isolated from expired blood plasma. | Human Serum Albumin is indicated for treatment of severe blood loss, hypervolemia, hypoproteinemia. | Human Serum Albumin regulates the colloidal osmotic pressure of blood. It is used to increase the circulating plasma volume, thereby reducing hemoconcentrtion and blood viscosity. Also used as a transport protein that binds naturally occurring, therapeutic and toxic materials in circulation. | Human Serum albumin acts as a high molecular weight, very soluble osmolyte. | NA | NA | NA | NA | NA | Albumins, Amino Acids, Peptides, and Proteins, Blood and Blood Forming Organs, Blood and Related Products, Blood Derivatives, Blood Proteins, Blood Substitutes and Perfusion Solutions, Blood Substitutes and Plasma Protein Fractions, Cardiac Function, Diluents, Human Serum Albumin, Increased Intravascular Volume, Increased Oncotic Pressure, Osmotic Activity, Proteins, Serum Albumin | US6723303 | 20-Apr-2004 | 20-Nov-2025 | NA | Nitric oxide | Albuminar | CSL Behring | CSL Behring | precscribed in treatment of Shock, Burns, Hypoproteinemia with or without edema | NA | Albumin (Human) 25% (albumin human) is a solution containing in each 100 mL, 25 grams of serum albumin, osmotically equivalent to 500 mL of normal human plasma. The pH of the solution is adjusted with sodium bicarbonate, sodium hydroxide, or acetic acid. Approximate concentrations of significant electrolytes per liter are: sodium - 130-160 mEq; and potassium - n.m.t. 1 mEq. | Albumin (Human) 25%, is a Sterile aqueous solution of albumin obtained from large pools of adult human venous plasma by low temperature controlled fractionation according to the Cohn process. | Albumin (Human) 25%, Albuminar-25 (albumin human) | Albumin (Human) 25%, Albuminar-25 (albumin (human)) may be given intravenously without dilution or it may be diluted with normal saline or 5% dextrose before administration. 200 mL per liter gives a solution which is approximately isotonic and iso-osmotic with citrated plasma. | Albumin (Human) 25% may be contraindicated in patients with severe anemia or cardiac failure and in patients with a history of allergic reactions to human albumin. | Allergic or pyrogenic reactions are characterized primarily by fever and chills; rash, nausea, vomiting, tachycardia and hypotension have also been reported. if administered rapidly, may result in vascular overload with resultant pulmonary edema. | Link | NA | NA |
| 10362 | Th1051 | Human Serum Albumin | >Th1051_Human_Serum_Albumin MKWVTFISLLFLFSSAYSRGVFRRDAHKSEVAHRFKDLGEENFKALVLIAFAQYLQQCPFEDHVKLVNEVTEFAKTCVADESAENCDKSLHTLFGDKLCTVATLRETYGEMADCCAKQEPERNECFLQHKDDNPNLPRLVRPEVDVMCTAFHDNEETFLKKYLYEIARRHPYFYAPELLFFAKRYKAAFTECCQAADKAACLLPKLDELRDEGKASSAKQRLKCASLQKFGERAFKAWAVARLSQRFPKAEFAEVSKLVTDLTKVHTECCHGDLLECADDRADLAKYICENQDSISSKLKECCEKPLLEKSHCIAEVENDEMPADLPSLAADFVESKDVCKNYAEAKDVFLGMFLYEYARRHPDYSVVLLLRLAKTYETTLEKCCAAADPHECYAKVFDEFKPLVEEPQNLIKQNCELFEQLGEYKFQNALLVRYTKKVPQVSTPTLVEVSRNLGKVGSKCCKHPEAKRMPCAEDYLSVVLNQLCVLHEKTPVSDRVTKCCTESLVNRRPCFSALEVDETYVPKEFNAETFTFHADICTLSEKERQIKKQTALVELVKHKPKATKEQLKAVMDDFAAFVEKCCKADDKETCFAEEGKKLVAASQAALGL | 66472.2 | C2936H4624N786O889S41 | 5.67 | -0.395 | 62 | NA | Human serum albumin isolated from expired blood plasma. | Human Serum Albumin is indicated for treatment of severe blood loss, hypervolemia, hypoproteinemia. | Human Serum Albumin regulates the colloidal osmotic pressure of blood. It is used to increase the circulating plasma volume, thereby reducing hemoconcentrtion and blood viscosity. Also used as a transport protein that binds naturally occurring, therapeutic and toxic materials in circulation. | Human Serum albumin acts as a high molecular weight, very soluble osmolyte. | NA | NA | NA | NA | NA | Albumins, Amino Acids, Peptides, and Proteins, Blood and Blood Forming Organs, Blood and Related Products, Blood Derivatives, Blood Proteins, Blood Substitutes and Perfusion Solutions, Blood Substitutes and Plasma Protein Fractions, Cardiac Function, Diluents, Human Serum Albumin, Increased Intravascular Volume, Increased Oncotic Pressure, Osmotic Activity, Proteins, Serum Albumin | US5558094 | 24-Sep-1996 | 19-Jan-2016 | NA | NA | Albutein | GRIFOLS | GRIFOLS | For treatment of hypovolemic shock,As an adjunct in hemodialysis for patients undergoing long-term dialysis or for those patients who are fluid-overloaded and cannot tolerate substantial volumes of salt solution for therapy of shock or hypotension | NA | Albutein 20% is clinically desirable, compatible diluents include sterile 0.9% Sodium Chloride solution or sterile 5% Dextrose in Water. | Albutein 20% is a Sterile, aqueous solution for single dose intravenous administration containing 20% human albumin (weight/volume). | Albutein 20% is to be administered by the Intraven | Albutein 20% is administered intravenously. The total dosage will vary with the individual. In adults, an initial infusion of 100 mL is suggested. | Albutein 20% is contraindicated in patients with severe anemia or cardiac failure in the presence of normal or increased intravascular volume. | The most common adverse reactions include fever and chills, rash, nausea, vomiting, tachycardia and hypotension. Should an adverse reaction occur, slow or stop the infusion for a short period of time which may result in the disappearance of the symptoms. If administration has been stopped and the patient requires additional Albutein 20%, material from a different lot should be used. | Link | NA | NA |
| 10363 | Th1052 | Eptifibatide | >Th1052_Eptifibatide CXGDWPC | 831.962 | C35H49N11O9S2 | NA | -2.3 | NA | Approximately 2.5 hours | Synthetic cyclic hexapeptide that binds to platelet receptor glycoprotein and inhibits platelet aggregation. | For treatment of myocardial infarction and acute coronary syndrome. | Eptifibatide is an anti-coagulant that selectively blocks the platelet glycoprotein IIb/IIIa receptor. Eptifibatide is a cyclic heptapeptide derived from a protein found in the venom of the southeastern pygmy rattlesnake (Sistrurus miliarus barbouri). It belongs to the class of the so called arginin-glycin-aspartat-mimetics and reversibly binds to platelets. | Eptifibatide inhibits platelet aggregation by reversibly binding to the platelet receptor glycoprotein (GP) IIb/IIIa of human platelets, thus preventing the binding of fibrinogen, von Willebrand factor, and other adhesive ligands. Inhibition of platelet aggregation occurs in a dose- and concentration-dependent manner. | Eptifibatide was not lethal to rats, rabbits, or monkeys when administered by continuous Intravenous infusion for 90 minutes at a total dose of 45 mg/kg (about 2 to 5 times the recommended maximum daily human dose on a body surface area basis). | No major metabolites have been detected in human plasma. Deamidated eptifibatide and other, more polar metabolites have been detected in urine. | The mean absolute bioavailability following a single subcutaneous injection to healthy female volunteers is about 40%. | NA | 55 mL/kg/h [patients with coronary artery disease] | Amino Acids, Peptides, and Proteins, Antiplatelet agents, Blood and Blood Forming Organs, Decreased Platelet Aggregation, Hematologic Agents, Peptides, Peptides, Cyclic, Platelet Aggregation Inhibitors Excl. Heparin | US6706681 | 16-Mar-2004 | 16-Mar-2021 | NA | Lutropin-choriogonadotropic hormone receptor,Follicle-stimulating hormone receptor, Integrin beta-3, Voltage-dependent N-type calcium channel (Protein Group) | INTEGRILIN | Schering-Plough/Essex | Schering-Plough/Essex | Acute Coronary Syndrome (ACS), Percutaneous Coronary Intervention (PCI) | N6-(aminoiminomethyl)-N2-(3-mercapto-1-oxopropyl)-Llysylglycyl-L-α-aspartyl-L-tryptophyl-L-prolyl-L-cysteinamide, cyclic (1→6)-disulfide. | Each 10-mL vial contains 2 mg/mL of INTEGRILIN and each 100-mL vial contains either 0.75 mg/mL of INTEGRILIN or 2 mg/mL of INTEGRILIN. Each vial of either size also contains 5.25 mg/mL citric acid and sodium hydroxide to adjust the pH to 5.35. | INTEGRILIN Injection is a clear, colorless, Sterile, non-pyrogenic solution of Eptifibatide | Injection Solution for Intravenous Use | Dosage in Acute Coronary Syndrome (ACS): 180 mcg/kg intravenous (IV) bolus as soon as possible after diagnosis, followed by continuous infusion of 2 mcg/kg/min Dosage in 180 mcg/kg IV bolus immediately before PCI followed by continuous infusion of 2 mcg/kg/min and a second bolus of 180 mcg/kg (given 10 minutes after the first bolus). | 1. Severe hypertension (systolic blood pressure > 200 mm Hg or diastolic blood pressure > 110 mm Hg) not adequately controlled onantihypertensive therapy. 2. History of stroke within 30 days or any history of hemorrhagic stroke. 3. Current or planned administration of another parenteral GP IIb/IIIa inhibitor. 4.Hypersensitivity to INTEGRILIN or any component of the product (hypersensitivity reactions that occurred included anaphylaxis and urticaria). | Bleeding, Intracranial Hemorrhage and Stroke, Immunogenicity/Thrombocytopenia. | Link | NA | NA |
| 10365 | Th1053 | Serum albumin iodonated | >Th1053_Serum_albumin_iodonated MKWVTFISLLFLFSSAYSRGVFRRDAHKSEVAHRFKDLGEENFKALVLIAFAQYLQQCPFEDHVKLVNEVTEFAKTCVADESAENCDKSLHTLFGDKLCTVATLRETYGEMADCCAKQEPERNECFLQHKDDNPNLPRLVRPEVDVMCTAFHDNEETFLKKYLYEIARRHPYFYAPELLFFAKRYKAAFTECCQAADKAACLLPKLDELRDEGKASSAKQRLKCASLQKFGERAFKAWAVARLSQRFPKAEFAEVSKLVTDLTKVHTECCHGDLLECADDRADLAKYICENQDSISSKLKECCEKPLLEKSHCIAEVENDEMPADLPSLAADFVESKDVCKNYAEAKDVFLGMFLYEYARRHPDYSVVLLLRLAKTYETTLEKCCAAADPHECYAKVFDEFKPLVEEPQNLIKQNCELFEQLGEYKFQNALLVRYTKKVPQVSTPTLVEVSRNLGKVGSKCCKHPEAKRMPCAEDYLSVVLNQLCVLHEKTPVSDRVTKCCTESLVNRRPCFSALEVDETYVPKEFNAETFTFHADICTLSEKERQIKKQTALVELVKHKPKATKEQLKAVMDDFAAFVEKCCKADDKETCFAEEGKKLVAASQAALGL | 66472.2 | C2936H4624N786O889S41 | 5.67 | -0.395 | 62 | NA | A diagnostic radiopharmaceutical containing iodinated I 131 albumin for intravenous imaging. Following Intravenous infusion, radioiodinated albumin human is uniformly distributed throughout the intravascular pool within 10 minutes; extravascular distribution takes place more slowly (2 days). Indicated for use in determinations of total blood and plasma volumes, cardiac output, cardiac and pulmonary blood volumes and circulation times | For determination of total blood and plasma volumes | Regulates the colloidal osmotic pressure of blood. It is used to increase the circulating plasma volume, thereby reducing hemoconcentrtion and blood viscosity. Also used as a transport protein that binds naturally occurring, therapeutic and toxic materials in circulation. | Serum albumin acts as a high molecular weight, very soluble osmolyte. | In general, human albumin solutions are well-tolerated and no specific, clinically relevant alterations in organ function or coagulopathy have been substantiated. The most common adverse reactions are rigors, hypotension, tachycardia with increased heart rate, fever, chills, nausea, vomiting, dyspnea and/or bronchospasm, skin rash/pruritus. Stop the infusion immediately if anaphylaxis, with or without shock is observed. Hypervolemia may occur if the dosage and rate of infusion are not adjusted to the volume status of the patient. When clinical signs of cardiovascular overload occur (headache, dyspnea, jugular venous distention, increased blood pressure), the infusion must be slowed or stopped immediately. | NA | NA | Albumin is distributed throughout the extracellular space and more than 60% of the body albumin pool is located in the extravascular fluid space . In healthy adults, less than 10% of infused albumin leaves the intravascular compartment during the first 2 hours following infusion of albumin. There is considerable individual variation in the effect of albumin on plasma volume, however. In some patients, the plasma volume can remain elevated for several hours. In critically ill patients, however, albumin can leak out of the vascular space in substantial amounts at an unpredictable rate that is difficult to predict. | NA | Albumins, Amino Acids, Peptides, and Proteins, Blood and Blood Forming Organs, Blood and Related Products, Blood Derivatives, Blood Proteins, Blood Substitutes and Perfusion Solutions, Blood Substitutes and Plasma Protein Fractions, Cardiac Function, Diluents, Human Serum Albumin, Increased Intravascular Volume, Increased Oncotic Pressure, Osmotic Activity, Proteins, Serum Albumin | NA | NA | NA | NA | Apolipoprotein E,Serum amyloid A-1 protein,Protein AMBP, Nitric oxide | Megatope | IsoTex Diagnostics | IsoTex Diagnostics | Megatope (Iodinated I 131 Albumin Injection) is indicated for use in determinations of total blood and plasma volumes, cardiac output, cardiac and pulmonary blood volumes and circulation times, and in protein turnover studies, heart and great vessel,dilineation, localization of the placenta, and localization of celebral neospasms | NA | Each mL of sterile, nonpyrogenic, aqueous, colorless to very pale yellow solution provides approximate 10 mg, protein (albumin human), 16 mg dibasic sodium phosphate, 1.6 mg monobasic, sodium phosphate, not more than 0.4 guanidine hydrochloride, sodium chloride, for isotonicity, and 9 mg benzyl alcohol as a preservative. | Megatope (Iodinated I 131 Albumin Injection) may be colorless to very pale yellow solution | Injection for Intravenous administration | The total dosage administered in any one week should not exceed 200 microcuries | None Known. | Although the immunological properties of albumin human are believed to be virtually unaltered by the iodination process, there is a theoretical possibility that allergic reactions may occur in patients receiving additional doses a number of weeks after an initial dose. | Link | NA | NA |
| 10366 | Th1053 | Serum albumin iodonated | >Th1053_Serum_albumin_iodonated MKWVTFISLLFLFSSAYSRGVFRRDAHKSEVAHRFKDLGEENFKALVLIAFAQYLQQCPFEDHVKLVNEVTEFAKTCVADESAENCDKSLHTLFGDKLCTVATLRETYGEMADCCAKQEPERNECFLQHKDDNPNLPRLVRPEVDVMCTAFHDNEETFLKKYLYEIARRHPYFYAPELLFFAKRYKAAFTECCQAADKAACLLPKLDELRDEGKASSAKQRLKCASLQKFGERAFKAWAVARLSQRFPKAEFAEVSKLVTDLTKVHTECCHGDLLECADDRADLAKYICENQDSISSKLKECCEKPLLEKSHCIAEVENDEMPADLPSLAADFVESKDVCKNYAEAKDVFLGMFLYEYARRHPDYSVVLLLRLAKTYETTLEKCCAAADPHECYAKVFDEFKPLVEEPQNLIKQNCELFEQLGEYKFQNALLVRYTKKVPQVSTPTLVEVSRNLGKVGSKCCKHPEAKRMPCAEDYLSVVLNQLCVLHEKTPVSDRVTKCCTESLVNRRPCFSALEVDETYVPKEFNAETFTFHADICTLSEKERQIKKQTALVELVKHKPKATKEQLKAVMDDFAAFVEKCCKADDKETCFAEEGKKLVAASQAALGL | 66472.2 | C2936H4624N786O889S41 | 5.67 | -0.395 | 62 | NA | A diagnostic radiopharmaceutical containing iodinated I 131 albumin for intravenous imaging. Following Intravenous infusion, radioiodinated albumin human is uniformly distributed throughout the intravascular pool within 10 minutes; extravascular distribution takes place more slowly (2 days). Indicated for use in determinations of total blood and plasma volumes, cardiac output, cardiac and pulmonary blood volumes and circulation times | For determination of total blood and plasma volumes | Regulates the colloidal osmotic pressure of blood. It is used to increase the circulating plasma volume, thereby reducing hemoconcentrtion and blood viscosity. Also used as a transport protein that binds naturally occurring, therapeutic and toxic materials in circulation. | Serum albumin acts as a high molecular weight, very soluble osmolyte | In general, human albumin solutions are well-tolerated and no specific, clinically relevant alterations in organ function or coagulopathy have been substantiated. The most common adverse reactions are rigors, hypotension, tachycardia with increased heart rate, fever, chills, nausea, vomiting, dyspnea and/or bronchospasm, skin rash/pruritus. Stop the infusion immediately if anaphylaxis, with or without shock is observed. Hypervolemia may occur if the dosage and rate of infusion are not adjusted to the volume status of the patient. When clinical signs of cardiovascular overload occur (headache, dyspnea, jugular venous distention, increased blood pressure), the infusion must be slowed or stopped immediately. | NA | NA | Albumin is distributed throughout the extracellular space and more than 60% of the body albumin pool is located in the extravascular fluid space . In healthy adults, less than 10% of infused albumin leaves the intravascular compartment during the first 2 hours following infusion of albumin. There is considerable individual variation in the effect of albumin on plasma volume, however. In some patients, the plasma volume can remain elevated for several hours. In critically ill patients, however, albumin can leak out of the vascular space in substantial amounts at an unpredictable rate that is difficult to predict. | NA | Albumins, Amino Acids, Peptides, and Proteins, Blood and Blood Forming Organs, Blood and Related Products, Blood Derivatives, Blood Proteins, Blood Substitutes and Perfusion Solutions, Blood Substitutes and Plasma Protein Fractions, Cardiac Function, Diluents, Human Serum Albumin, Increased Intravascular Volume, Increased Oncotic Pressure, Osmotic Activity, Proteins, Serum Albumin | NA | NA | NA | Rilonacept results in increased immunosuppressive effects; increases the risk of infection | NA | Jeanotope | IsoTex Diagnostics | IsoTex Diagnostics | Jeanotope I-125 is indicated for use in the determination of total blood and plasma volume. | NA | Each milliliter provides approximately 10 mg protein (normal human serum albumin), 1.6 mg sodium phosphate, 16 mg sodium biphosphate, not more than 0.4 mg guanidine hydrochloride, sodium chloride for isotonicity, and 9 mg benzyl alcohol as a preservative. The stabilizer aceryltryptophanate and sodium caprylate have a concentration of less, than 0.0089M. | Jeanatope 1-125 (Iodinated 1-125 Albumin Injection) is a Sterile, nonpyrogenic, aqueos solution | Intravenous infusion | When a procedure such as a blood volume determination is to be repeated, the total dosage administered in any one week should not exceed 7.4 megabecquerels, (200 microcuries). | At present there are no known contraindications to the use of this preparation | Although the immunological properties of albumin human are believed to be virtually unaltered by the iodination process, there is a theoretical possibility that allergic reactions may occur in patients receiving additional doses a number of weeks after an initial dose. | Link | NA | NA |
| 10367 | Th1053 | Serum albumin iodonated | >Th1053_Serum_albumin_iodonated MKWVTFISLLFLFSSAYSRGVFRRDAHKSEVAHRFKDLGEENFKALVLIAFAQYLQQCPFEDHVKLVNEVTEFAKTCVADESAENCDKSLHTLFGDKLCTVATLRETYGEMADCCAKQEPERNECFLQHKDDNPNLPRLVRPEVDVMCTAFHDNEETFLKKYLYEIARRHPYFYAPELLFFAKRYKAAFTECCQAADKAACLLPKLDELRDEGKASSAKQRLKCASLQKFGERAFKAWAVARLSQRFPKAEFAEVSKLVTDLTKVHTECCHGDLLECADDRADLAKYICENQDSISSKLKECCEKPLLEKSHCIAEVENDEMPADLPSLAADFVESKDVCKNYAEAKDVFLGMFLYEYARRHPDYSVVLLLRLAKTYETTLEKCCAAADPHECYAKVFDEFKPLVEEPQNLIKQNCELFEQLGEYKFQNALLVRYTKKVPQVSTPTLVEVSRNLGKVGSKCCKHPEAKRMPCAEDYLSVVLNQLCVLHEKTPVSDRVTKCCTESLVNRRPCFSALEVDETYVPKEFNAETFTFHADICTLSEKERQIKKQTALVELVKHKPKATKEQLKAVMDDFAAFVEKCCKADDKETCFAEEGKKLVAASQAALGL | 66472.2 | C2936H4624N786O889S41 | 5.67 | -0.395 | 62 | NA | A diagnostic radiopharmaceutical containing iodinated I 131 albumin for intravenous imaging. Following Intravenous infusion, radioiodinated albumin human is uniformly distributed throughout the intravascular pool within 10 minutes; extravascular distribution takes place more slowly (2 days). Indicated for use in determinations of total blood and plasma volumes, cardiac output, cardiac and pulmonary blood volumes and circulation times | For determination of total blood and plasma volumes | Regulates the colloidal osmotic pressure of blood. It is used to increase the circulating plasma volume, thereby reducing hemoconcentrtion and blood viscosity. Also used as a transport protein that binds naturally occurring, therapeutic and toxic materials in circulation. | Serum albumin acts as a high molecular weight, very soluble osmolyte | In general, human albumin solutions are well-tolerated and no specific, clinically relevant alterations in organ function or coagulopathy have been substantiated. The most common adverse reactions are rigors, hypotension, tachycardia with increased heart rate, fever, chills, nausea, vomiting, dyspnea and/or bronchospasm, skin rash/pruritus. Stop the infusion immediately if anaphylaxis, with or without shock is observed. Hypervolemia may occur if the dosage and rate of infusion are not adjusted to the volume status of the patient. When clinical signs of cardiovascular overload occur (headache, dyspnea, jugular venous distention, increased blood pressure), the infusion must be slowed or stopped immediately. | NA | NA | Albumin is distributed throughout the extracellular space and more than 60% of the body albumin pool is located in the extravascular fluid space . In healthy adults, less than 10% of infused albumin leaves the intravascular compartment during the first 2 hours following infusion of albumin. There is considerable individual variation in the effect of albumin on plasma volume, however. In some patients, the plasma volume can remain elevated for several hours. In critically ill patients, however, albumin can leak out of the vascular space in substantial amounts at an unpredictable rate that is difficult to predict. | NA | Albumins, Amino Acids, Peptides, and Proteins, Blood and Blood Forming Organs, Blood and Related Products, Blood Derivatives, Blood Proteins, Blood Substitutes and Perfusion Solutions, Blood Substitutes and Plasma Protein Fractions, Cardiac Function, Diluents, Human Serum Albumin, Increased Intravascular Volume, Increased Oncotic Pressure, Osmotic Activity, Proteins, Serum Albumin | NA | NA | NA | NA | NA | Volumex | IsoTex Diagnostics | IsoTex Diagnostics | Volumex (Iodinated I 131 Allbumin injection) is indicated for use in determination of total blood and plasma volumes and in protein turnover studies | NA | Each ml of nonpyrogenic, aqueous, colorless to very pale yellow solution provides approximately 10 mg protein (albumin human), 16 mg dibasic sodium phosphate, 1.6 mg monobasic sodium phosphate, not more, than 0.4 mg guanidine hydrochloride, sodium chloride for isotonicity, and 9 mg benzyl alcohol as a preservative. | Volumex (Iodinated I 131 Albumin Injection) may be colorless to very pale yellow solution. | Intravenous infusion | When a procedure such as a blood volume determination is to be repeated, the total dosage administered in any one week should not exceed 200 microcuries | None Known. | Although the immunological properties of albumin human are believed to be virtually unaltered by the iodination process, there is a theoretical possibility that allergic reactions may occur in patients receiving additional doses a number of weeks after an initial dose. | 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 |
| 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 |
| 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 |
| 10392 | Th1062 | Rituximab | >Th1062_Rituximab QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143859.7 | C6416H9874N1688O1987S44 | 8.68 | -0.414 | 61 (FAB f | 23 days: Granulomatosis with Polyangitis and Microscopic Polyangitis | Rituxan is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. The antibody is an IgG1 kappa immunoglobulin containing murine light- and heavy-chain variable region sequences and human constant region sequences. Rituximab is composed of two heavy chains of 451 amino acids and two light chains of 213 amino acids. | For treatment of CD20-positive non-Hodgkins lymphoma, chronic lymphocytic leukemia, and rheumatoid arthritis. | Rituximab binds to the CD20 antigen, which is predominantly expressed on mature B cells and 90% of B-cell non-Hodgkin's lympohomas. The antibody leads to selective killing of B-cells. | The Fab regions of rituximab binds to the CD20 antigen on B lymphocytes, while the Fc domain recruits antibodies and complements to mediate cell lysis. | NA | Most likely removed by opsonization via the reticuloendothelial system. | Following the administration of 2 doses of rituximab in patients with rheumatoid arthritis (RA), the mean (± S.D.; % CV) concentrations after the first infusion (Cmax first) and second infusion (Cmax second) were : 157 ( ± 46; 29%) and 183 ( ± 55; 30%) mcg/mL, and 318 ( ± 86; 27%) and 381 ( ± 98; 26%) mcg/mL for the 2 × 500 mg and 2 × 1000 mg doses, respectively | 3.1 L | 0.34 L/day [RA patients] | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Murine-Derived, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antirheumatic Agents, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Cancer immunotherapy, CD20-directed Antibody Interactions, CD20-directed Cytolytic Antibody, Globulins, Immunoglobulins, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Telmisartan may increase the hypotensive effect of Rituximab. Telmisartan should be withheld prior to and throughout Rituximab administration | NA | Riabni | AMGEN INC | AMGEN INC | RIABNI is a prescription medicine used to treat adults with: Non-Hodgkin’s Lymphoma (NHL): alone or with other chemotherapy medicines. Chronic Lymphocytic Leukemia (CLL): with the chemotherapy medicines fludarabine and cyclophosphamide. Granulomatosis with Polyangiitis (GPA) (Wegener’s Granulomatosis) and Microscopic Polyangiitis (MPA): with glucocorticoids, to treat GPA and MPA. | NA | RIABNI is supplied at a concentration of 10 mg/mL in either 100 mg/10 mL or 500 mg/50 mL single-dose vials. Each mL of solution contains 10 mg rituximabarrx, polysorbate 80 (0.7 mg), sodium chloride (9 mg), sodium citrate dihydrate (7.35 mg), and Water for Injection, USP. Hydrochloric acid is used to adjust the buffer solution pH. The pH is 6.5. | sterile, preservative-free, clear to slightly opalescent, colorless to slightly yellow solution | intravenous infusion. | Initiate at a rate of 20% of the total dose given in the first 30 minutes and the remaining 80% of the total dose given over the next 60 minutes. If the 90-minute infusion is tolerated in Cycle 2, the same rate can be used when administering the remainder of the treatment regimen (through Cycle 6 or 8). | NA | fever cold symptoms, such as runny nose or sore throat that do not go away flu symptoms, such as cough, tiredness, and body aches earache or headache pain during urination cold sores in the mouth or throat cuts, scrapes or incisions that are red, warm, swollen or painful | Link | NA | NA |
| 10397 | Th1062 | Rituximab | >Th1062_Rituximab QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143859.7 | C6416H9874N1688O1987S44 | 8.68 | -0.414 | 61 (FAB f | NA | Rituxan is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. The antibody is an IgG1 kappa immunoglobulin containing murine light- and heavy-chain variable region sequences and human constant region sequences. Rituximab is composed of two heavy chains of 451 amino acids and two light chains of 213 amino acids. | For treatment of CD20-positive non-Hodgkins lymphoma, chronic lymphocytic leukemia, and rheumatoid arthritis. | Rituximab binds to the CD20 antigen, which is predominantly expressed on mature B cells and 90% of B-cell non-Hodgkin's lympohomas. The antibody leads to selective killing of B-cells. | The Fab regions of rituximab binds to the CD20 antigen on B lymphocytes, while the Fc domain recruits antibodies and complements to mediate cell lysis. | NA | Most likely removed by opsonization via the reticuloendothelial system. | Following the administration of 2 doses of rituximab in patients with rheumatoid arthritis (RA), the mean (± S.D.; % CV) concentrations after the first infusion (Cmax first) and second infusion (Cmax second) were : 157 ( ± 46; 29%) and 183 ( ± 55; 30%) mcg/mL, and 318 ( ± 86; 27%) and 381 ( ± 98; 26%) mcg/mL for the 2 × 500 mg and 2 × 1000 mg doses, respectively | 3.1 L | 0.34 L/day [RA patients] | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Murine-Derived, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antirheumatic Agents, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Cancer immunotherapy, CD20-directed Antibody Interactions, CD20-directed Cytolytic Antibody, Globulins, Immunoglobulins, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Myelosuppressive Agents, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | NA | Ruxience | Pfizer | Pfizer | Non-Hodgkin’s Lymphoma (NHL): alone or with other chemotherapy medicines. Chronic Lymphocytic Leukemia (CLL): with the chemotherapy medicines fludarabine and cyclophosphamide. Granulomatosis with Polyangiitis (GPA) (Wegener's Granulomatosis) and Microscopic Polyangiitis (MPA): with glucocorticoids, to treat GPA and MPA. | NA | RUXIENCE is supplied at a concentration of 10 mg/mL in either 100 mg/10 mL or 500 mg/50 mL single-dose vials. Each mL of solution contains 10 mg rituximab-pvvr, 0.056 mg of edetate disodium dihydrate, 1.2 mg of L-histidine, 2.57 mg of L-histidine hydrochloride monohydrate, 0.2 mg of polysorbate 80, 85 mg of sucrose, and Water for Injection, USP. The pH is 5.8. | sterile, preservative-free, clear to slightly opalescent, colorless to pale brownish-yellow solution | intravenous infusion | First Infusion: Initiate infusion at a rate of 50 mg/hour. In the absence of infusion toxicity, increase infusion rate by 50 mg/hour increments every 30 minutes, to a maximum of 400 mg/hour. Subsequent Infusions: Standard Infusion: Initiate infusion at a rate of 100 mg/hour. In the absence of infusion toxicity, increase rate by 100 mg/hour increments at 30-minute intervals, to a maximum of 400 mg/hour. For Previously Untreated Follicular NHL and DLBCL Patients: If patients did not experience a Grade 3 or 4 infusion-related adverse event during Cycle 1, a 90-minute infusion can be administered in Cycle 2 with a glucocorticoid-containing chemotherapy regimen. Initiate at a rate of 20% of the total dose given in the first 30 minutes and the remaining 80% of the total dose given over the next 60 minutes. If the 90-minute infusion is tolerated in Cycle 2, the same rate can be used when administering the remainder of the treatment regimen (through Cycle 6 or 8). Patients who have clinically significant cardiovascular disease or who have a circulating lymphocyte count ≥5,000/mm³ before Cycle 2 should not be administered the 90-minute infusion | NA | fever cold symptoms, such as runny nose or sore throat that do not go away flu symptoms, such as cough, tiredness, and body aches earache or headache pain during urination cold sores in the mouth or throat cuts, scrapes or incisions that are red, warm, swollen or painful | Link | NA | NA |
| 10400 | Th1064 | Muromonab | >Th1064_Muromonab QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146189.7 | C6460H9946N1720O2043S56 | 8.31 | -0.513 | 71 | 0.8 hours (mammalian reticulocytes, in vitro) | Murine monoclonal antibody specific to CD3 T-cell lymphocyte antigens. More specifically it is a purified murine (mouse) monoclonal antibody, directed against the CD3 (T3) receptor on the surface of human T-cells (T-lymphocytes) cultured using the murine ascites method. Muromonab is 93% monomeric immune globulin G type 2a (IgG2a). | For treatment of organ transplant recipients, prevention of organ rejection | Used in organ transplant prophylaxis, Muromonab or OKT-3 binds specifically to the CD-3 complex, which is involved in antigen recognition and cell stimulation, on the surface of T lymphocytes. Immediately after administration CD-3-positive T lymphocytes are abruptly removed from circulation. It has been effective in reversing corticosteroid-resistant acute rejection in renal, liver, and cardiac transplant recipients. | Muromonab binds to the T-cell surface glycoprotein CD3 epsilon chain. It appears to kill CD-3 positive cells by inducing Fc mediated apoptosis, antibody mediated cytotoxicity and complement-dependent cytotoxicity. | NA | Most likely removed by opsonization via the reticuloendothelial system. | NA | NA | NA | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Murine-Derived, Antineoplastic and Immunomodulating Agents, Blood Proteins, CD3 Blocker Immunosuppressant, CD3 Receptor Antagonists, CD3-directed Antibody Interactions, Decreased Immunologic Activity, Globulins, Immunoglobulin G, Immunoglobulin Isotypes, Immunoglobulins, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Proteins, Selective Immunosuppressants, Serum Globulins | NA | NA | NA | Cyclosporine with Muromonab increases the levels of cyclosporine | T-cell surface glycoprotein CD3 delta chain, T-cell surface glycoprotein CD3 epsilon chain, T-cell surface glycoprotein CD3 gamma chain,T-cell surface glycoprotein CD3 zeta chain, Low affinity immunoglobulin gamma Fc region receptor III-B | ORTHOCLONE OKT3 STERILE SOLUTION | Centocor Ortho Biotech, L.P., Janssen Pharmaceuticals | Centocor Ortho Biotech, L.P., Janssen Pharmaceuticals | ORTHOCLONE OKT3 is indicated for the treatment of acute allograft rejection in renal transplant patients. ORTHOCLONE OKT3 is indicated for the treatment of steroid-resistant acute allograft rejection in cardiac and hepatic transplant patients. | NA | Each 5 mL ampule of ORTHOCLONE OKT3 Sterile Solution contains 5 mg (1 mg/mL) of muromonab-CD3 in a clear colorless solution which may contain a few fine translucent protein particles. Each ampule contains a buffered solution (pH 7.0 ± 0.5) of monobasic sodium phosphate (2.25 mg), dibasic sodium phosphate (9.0 mg), sodium chloride (43 mg), and polysorbate 80 (1.0 mg) in water for injection. | ORTHOCLONE OKT3 (muromonab-CD3)sterile solution is a murine monoclonal antibody to the CD3 antigen of human T cells which functions as an immunosuppressant. | For Intravenous Use Only | The recommended dose of ORTHOCLONE OKT3 for the treatment of acute renal, steroid-resistant cardiac, or steroid-resistant hepatic allograft rejection is 5 mg per day in a single (bolus) Intravenous infusion in less than one minute for 10 to 14 days. | not given to patient which are hypersensitive to this or any other product of murine origin, have anti-mouse antibody titers ≥1:1000; are in (uncompensated) heart failure or in fluid overload, as evidenced by chest X-ray or a greater than 3 percent weight gain within the week prior to planned ORTHOCLONE OKT3 administration; have uncontrolled hypertension; have a history of seizures, or are predisposed to seizures. | RTHOCLONE OKT3 therapy includes adverse effects: Dyspnea(21%), nausea(19%), vomiting (19%), chest pain (14%), diarrhea (14%), tremor (13%), wheezing (13%), headache (11%), tachycardia (10%), rigor (8%), and hypertension (8%), Angina, Cardiac Arrest, Fluctuation in Blood Pressure, Heart Failure, Myocardial Infarction, Shock, Thrombosis, Coma, Encephalopathy, Epilepsy, Hypotonia, Gastrointestinal Hemorrhage, Coagulation Disorder, Lymphadenopathy, Lymphopenia, Anuria, Oliguria, Apnea, Pneumonitis, Conjunctivitis, Hearing Decreases. | Link | NA | NA |
| 10406 | Th1066 | Ibritumomab | >Th1066_Ibritumomab QAYLQQSGAELVRPGASVKMSCKASGYTFTSYNMHWVKQTPRQGLEWIGAIYPGNGDTSYNQKFKGKATLTVDKSSSTAYMQLSSLTSEDSAVYFCARVVYYSNSYWYFDVWGTGTTVTVSAPSVYPLAPVCGDTTGSSVTLGCLVKGYFPEPVTLTWNSGSLSSGVHTFPAVLQSDLYTLSSSVTVTSSTWPSQSITCNVAHPASSTKVDKKIEPRGPTIKPCPPCKCPAPNLLGGPSVFIFPPKIKDVLMISLSPIVTCVVVDVSEDDPDVQISWFVNNVEVHTAQTQTHREDYNSTLRVVSALPIQHQDWMSGKEFKCKVNNKDLPAPIERTISKPKGSVRAPQVYVLPPPEEEMTKKQVTLTCMVTDFMPEDIYVEWTNNGKTELNYKNTEPVLDSDGSYFMYSKLRVEKKNWVERNSYSCSVVHEGLHNHHTTKSFSR | 143375.5 | C6382H9830N1672O1979S54 | 7.91 | -0.359 | 71 | 0.8 hours (mammalian reticulocytes, in vitro) | Indium conjugated murine IgG1 kappa monoclonal antibody directed against the CD20 antigen, which is found on the surface of normal and malignant B lymphocytes. Ibritumomab is produced in Chinese hamster ovary cells and is composed of two murine gamma 1 heavy chains of 445 amino acids each and two kappa light chains of 213 amino acids each. | For treatment of non-Hodgkin's lymphoma | Ibritumomab is a murine monoclonal antibody against CD20 that has been radiolabeled with yttrium-90. | The Fab segment of the antibody targets the CD20 epitope on B-cells, allowing the radioactive yttrium to destroy the cell via production of beta particles. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to B cells, or by human antimurine antibody production | NA | NA | Approximately 7.2% of injected dose of yttrium Y 90 ibritumomab tiuxetan is excreted in urine within 7 days. | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antigens, CD20, Blood Proteins, Cancer immunotherapy, CD20-directed Antibody Interactions, CD20-directed Radiotherapeutic Antibody, Globulins, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Lymphoma, B-Cell, Myelosuppressive Agents, Proteins, Radiopharmaceutical Activity, Serum Globulins, Therapeutic Radiopharmaceuticals, Various Therapeutic Radiopharmaceuticals, Yttrium Radioisotopes | CA2149329 | 15-Jul-2008 | 12-Nov-2013 | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | B-lymphocyte antigen CD20 | Zevalin | Spectrum Pharmaceuticals, Ceft Biopharma S.R.O., Acrotech Biopharma Llc | Spectrum Pharmaceuticals, Ceft Biopharma S.R.O., Acrotech Biopharma Llc | Zevalin is indicated for the treatment of relapsed or refractory, low-grade or follicular B-cell non-Hodgkin's lymphoma (NHL). Zevalin is indicated for the treatment of previously untreated follicular NHL in patients who achieve a partial or complete response to first-line chemotherapy. | NA |  Each single-use vial includes 3.2 mg of ibritumomab tiuxetan in 2 mL of 0.9% Sodium Chloride. | Ibritumomab tiuxetan is a clear, colorless, sterile, pyrogen-free, preservative-free solution that may contain translucent particles. | Intravenous infusion | Day 1: Administer rituximab 250 mg/m2 intravenous ; Day 7,8, or 9: Administer rituximab 250 mg/m2 Intravenous infusion If platelets ≥ 150,000/mm3: Within 4 hours after rituximab infusion, administer 0.4 mCi/kg (14.8 MBq per kg) Y-90 Zevalin intravenous. If platelets ≥ 100,000 but ≤ 149,000/mm3 in relapsed or refractory patients: Within 4 hours after rituximab infusion, administer 0.3 mCi/kg (11.1 MBq per kg) Y-90 Zevalin intravenous. | None. | Serious Infusion Reactions, prolonged and Severe Cytopenias, Severe Cutaneous and Mucocutaneous Reactions, Leukemia and Myelodysplastic Syndrome, Cytopenias, fatigue, nasopharyngitis, nausea, abdominal pain, asthenia, cough, diarrhea, and pyrexia. | Link | NA | NA |
| 10412 | Th1068 | Tositumomab | >Th1068_Tositumomab QAYLQQSGAELVRPGASVKMSCKASGYTFTSYNMHWVKQTPRQGLEWIGAIYPGNGDTSYNQKFKGKATLTVDKSSSTAYMQLSSLTSEDSAVYFCARVVYYSNSYWYFDVWGTGTTVTVSGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143859.7 | C6416H9874N1688O1987S44 | 8.68 | -0.4144 | 71 | 0.8 hours (mammalian reticulocytes, in vitro) | Murine IgG2a lambda monoclonal antibody against CD20 antigen (2 heavy chains of 451 residues, 2 lambda chains of 220 residues). It is produced in an antibiotic-free culture of mammalian cells. It can be covalently linked to Iodine 131 (a radioactive isotope of iodine). | For treatment of non-Hodgkin's lymphoma (CD20 positive, follicular) | Tositumomab binds to the CD20 antigen, which is predominantly expressed on mature B cells and on >90% of B-cell non-Hodgkin's lympohomas. The antibody leads to selective killing of B-cells. | Binds to the CD20 antigen which is found on mature B lymphocytes. The antibody binding appears to induce apoptosis, complement-dependent cytotoxicity and cell death through ionizing radiation. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to B lymphocytes, or by human antimurine antibody production | NA | NA | 68.2 mg/hr [patients with NHL] | Amino Acids, Peptides, and Proteins, Antibodies, Antigens, CD20, Antineoplastic Agents, Blood Proteins, CD20-directed Antibody Interactions, CD20-directed Radiotherapeutic Antibody, Drugs that are Mainly Renally Excreted, Globulins, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Iodine (131I) Compounds, Myelosuppressive Agents, Proteins, Radioimmunotherapy, Radiopharmaceutical Activity, Serum Globulins, Therapeutic Radiopharmaceutical | NA | NA | NA | Natalizumab with immunosuppressant, Tositumomab, may increase the adverse effects. Increased risk of Progressive Multifocal Leukoencephalopathy (PML) and other infections. Concurrent therapy should be avoided | B-lymphocyte antigen CD20,Low affinity immunoglobulin gamma Fc region receptor II-b | Bexxar | Galaxo Smith Kline | Galaxo Smith Kline | The BEXXAR therapeutic regimen (Tositumomab and Iodine I 131 Tositumomab) is indicated for the treatment of patients with CD20 antigen-expressing relapsed or refractory, low grade, follicular, or transformed non-Hodgkin's lymphoma, including patients with Rituximab-refractory non-Hodgkin’s lymphoma. Determination of the effectiveness of the BEXXAR therapeutic regimen is based on overall response rates in patients whose disease is refractory to chemotherapy alone or to chemotherapy and Rituximab. The effects of the BEXXAR therapeutic regimen on survival are not known. | NA | The formulation contains 100 mg/mL maltose, 8.5 mg/mL sodium chloride, 1 mg/mL phosphate, 1 mg/mL potassium hydroxide, and Water for Injection, USP. The pH is approximately 7.2. | Tositumomab is supplied as a Sterile, pyrogen-free, clear to opalescent, colorless to slightly yellow, preservative-free solution | Intravenous (Intravenous) administration | The BEXXAR therapeutic regimen consists of 2 separate components (tositumomab and iodine I 131 tositumomab) administered in 2 separate steps (dosimetric dose and therapeutic dose) separated by 7 to 14 days.Tositumomab 450 mg by Intravenous infusion.I-131 tositumomab (5 mCi I-131 and 35 mg protein) by Intravenous infusion | The BEXXAR therapeutic regimen is contraindicated in patients with known hypersensitivity to murine proteins or any other component of the BEXXAR therapeutic regimen. | Serious Allergic Reactions, Including Anaphylaxis, Prolonged and Severe Cytopenias, Secondary malignancies, Hypothyroidism, neutropenia, thrombocytopenia, anemia, infections (including pneumonia, bacteremia, septicemia, bronchitis, and skin infections), infusion reactions, asthenia, fever, and nausea. | Link | NA | NA |
| 10431 | Th1073 | Alemtuzumab | >Th1073_Alemtuzumab QVQLQESGPGLVRPSQTLSLTCTVSGFTFTDFYMNWVRQPPGRGLEWIGFIRDKAKGYTTEYNPSVKGRVTMLVDTSKNQFSLRLSSVTAADTAVYYCAREGHTAAPFDYWGQGSLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145453.8 | C6468H10066N1732O2005S40 | 8.76 | -0.431 | 61 (FAB f | 288 hrs | Humanized monoclonal antibody specific to lymphocyte antigens. It is a recombinant DNA-derived humanized monoclonal antibody (Campath-1H) that is directed against the 21-28 kD cell surface glycoprotein,CD52. The Campath-1H antibody is an IgG1 kappa with human variable framework and constant regions, and complementarity-determining regions from a murine (rat) monoclonal antibody (Campath-1G). Campath is produced in mammalian cell (Chinese hamster ovary) suspension culture in a medium containing neomycin. | Alemtuzumab (Campath) is a monoclonal antibody therapy used for treatment of B-cell chronic lymphocytic leukemia. | Campath is used to treat leukemia by exploiting antibody mediated lysis of CD52 presenting cells. The CD52 antigen is a cell surface protein found on essentially all B and T lymphocytes, a majority of monocytes, macrophages and most granulocytes. The CD52 antigen is not present on erythrocytes or hematopoetic stem cells. In leukemia there is an excess of B and T cells, so Campath permits selective reduction of lymphocyte populations. | Campath binds to the CD52 antigen present on most B and T lymphocytes. This binding leads to antibody-dependent lysis of leukemic cells. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to B or T lymphocytes | NA | 0.18 L/kg | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,CD52-directed Antibody Interactions,CD52-directed Cytolytic Antibody,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Myelosuppressive Agents,Narrow Therapeutic Index Drugs,Proteins,Selective Immunosuppressants,Serum Globulins | CA1339198 | 5-Aug-1997 | 5-Aug-2014 | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | CAMPATH-1 antigen,Low affinity immunoglobulin gamma Fc region receptor III-B,Low affinity immunoglobulin gamma Fc region receptor III-A,High affinity immunoglobulin gamma Fc receptor I,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 | CAMPATH | Genzyme Corporation | Genzyme Corporation | Campath is a CD52-directed cytolytic antibody indicated as a single agent for the treatment of B-cell chronic lymphocytic leukemia (B-CLL) | NA | Each single use vial of Campath contains 30 mg alemtuzumab, 8.0 mg sodium chloride, 1.44 mg dibasic sodium phosphate, 0.2 mg potassium chloride, 0.2 mg monobasic potassium phosphate, 0.1 mg polysorbate 80, and 0.0187 mg disodium edetate dihydrate. No preservatives are added. | Campath is a sterile, clear, colorless, isotonic solution (pH 6.8-7.4) for injection. | Intravenous infusion | Administer as an IV infusion over 2 hours, Escalate to recommended dose of 30 mg/day three times per week for 12 weeks, Premedicate with oral antihistamine and acetaminophen prior to dosing | None | Most common adverse reactions (>=10%): cytopenias, infusion reactions, cytomegalovirus (CMV) and other infections, nausea, emesis, diarrhea, and insomnia. | Link | NA | NA |
| 10432 | Th1073 | Alemtuzumab | >Th1073_Alemtuzumab QVQLQESGPGLVRPSQTLSLTCTVSGFTFTDFYMNWVRQPPGRGLEWIGFIRDKAKGYTTEYNPSVKGRVTMLVDTSKNQFSLRLSSVTAADTAVYYCAREGHTAAPFDYWGQGSLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145453.8 | C6468H10066N1732O2005S40 | 8.76 | -0.431 | 62 (FAB f | 289 hrs | Humanized monoclonal antibody specific to lymphocyte antigens. It is a recombinant DNA-derived humanized monoclonal antibody (Campath-1H) that is directed against the 21-28 kD cell surface glycoprotein,CD52. The Campath-1H antibody is an IgG1 kappa with human variable framework and constant regions, and complementarity-determining regions from a murine (rat) monoclonal antibody (Campath-1G). Campath is produced in mammalian cell (Chinese hamster ovary) suspension culture in a medium containing neomycin. | Alemtuzumab (Campath) is a monoclonal antibody therapy used for treatment of B-cell chronic lymphocytic leukemia. | Campath is used to treat leukemia by exploiting antibody mediated lysis of CD52 presenting cells. The CD52 antigen is a cell surface protein found on essentially all B and T lymphocytes, a majority of monocytes, macrophages and most granulocytes. The CD52 antigen is not present on erythrocytes or hematopoetic stem cells. In leukemia there is an excess of B and T cells, so Campath permits selective reduction of lymphocyte populations. | Campath binds to the CD52 antigen present on most B and T lymphocytes. This binding leads to antibody-dependent lysis of leukemic cells. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to B or T lymphocytes | NA | 0.18 L/kg | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,CD52-directed Antibody Interactions,CD52-directed Cytolytic Antibody,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Myelosuppressive Agents,Narrow Therapeutic Index Drugs,Proteins,Selective Immunosuppressants,Serum Globulins | NA | NA | NA | NA | CAMPATH-1 antigen,Low affinity immunoglobulin gamma Fc region receptor III-B,Low affinity immunoglobulin gamma Fc region receptor III-A,High affinity immunoglobulin gamma Fc receptor I,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 | LEMTRADA | Sanofi Genzyme, a Division of Sanofi Aventis Canada Inc | Sanofi Genzyme, a Division of Sanofi Aventis Canada Inc | LEMTRADA is a CD52-directed cytolytic monoclonal antibody indicated for the treatment of patients with relapsing forms of multiple sclerosis (MS). Because of its safety profile, the use of LEMTRADA should generally be reserved for patients who have had an inadequate response to two or more drugs indicated for the treatment of MS. | NA | Each 1 mL of solution contains alemtuzumab 10 mg, dibasic sodium phosphate (1.15 mg), disodium edetate dihydrate (0.0187 mg), polysorbate 80 (0.1 mg), potassium chloride (0.2 mg), potassium dihydrogen phosphate (0.2 mg), sodium chloride (8 mg), and water for injection. | LEMTRADA is a sterile, clear and colorless to slightly yellow, solution (pH 7.2±0.2) for infusion. | Intravenous infusion | Administer LEMTRADA by Intravenous infusion over 4 hours for 2 treatment courses. First course: 12 mg/day on 5 consecutive days. Second course: 12 mg/day on 3 consecutive days 12 months after first treatment course. | LEMTRADA is contraindicated in patients who are infected with Human Immunodeficiency Virus (HIV) because LEMTRADA causes prolonged reductions of CD4+ lymphocyte counts. | Most common adverse reactions (incidence >= 10% and > interferon beta-1a): rash, headache, pyrexia, nasopharyngitis, nausea, urinary tract infection, fatigue, insomnia, upper respiratory tract infection, herpes viral infection, urticaria, pruritus, thyroid gland disorders, fungal infection, arthralgia, pain in extremity, back pain, diarrhea, sinusitis, oropharyngeal pain, paresthesia, dizziness, abdominal pain, flushing, and vomiting. | Link | NA | NA |
| 10434 | Th1074 | Alglucerase | >Th1074_Alglucerase ARPCIPKSFGYSSVVCVCNATYCDSFDPPTFPALGTFSRYESTRSGRRMELSMGPIQANHTGTGLLLTLQPEQKFQKVKGFGGAMTDAAALNILALSPPAQNLLLKSYFSEEGIGYNIIRVPMASCDFSIRTYTYADTPDDFQLHNFSLPEEDTKLKIPLIHRALQLAQRPVSLLASPWTSPTWLKTNGAVNGKGSLKGQPGDIYHQTWARYFVKFLDAYAEHKLQFWAVTAENEPSAGLLSGYPFQCLGFTPEHQRDFIARDLGPTLANSTHHNVRLLMLDDQRLLLPHWAKVVLTDPEAAKYVHGIAVHWYLDFLAPAKATLGETHRLFPNTMLFASEACVGSKFWEQSVRLGSWDRGMQYSHSIITNLLYHVVGWTDWNLALNPEGGPNWVRNFVDSPIIVDITKDTFYKQPMFYHLGHFSKFIPEGSQRVGLVASQKNDLDAVALMHPDGSAVVVVLNRSSKDVPLTIKDPAVGFLETISPGYSIHTYLWRRQ | 55597.4 | C2532H3854N672O711S16 | 7.41 | -0.168 | NA | 3.6-10.4 min | Human Beta-glucocerebrosidase or Beta-D-glucosyl-N-acylsphingosine glucohydrolase E.C. 3.2.1.45. 497 residue protein with N-linked carbohydrates. Alglucerase is prepared by modification of the oligosaccharide chains of human Beta-glucocerebrosidase. The modification alters the sugar residues at the non-reducing ends of the oligosaccharide chains of the glycoprotein so that they are predominantly terminated with mannose residues | For the treatment of Gaucher's disease (deficiency in glucocerebrosidase) | Gaucher disease is characterized by a functional deficiency in Beta-glucocerebrosidase enzymatic activity and the resultant accumulation of lipid glucocerebroside in tissue macrophages which become engorged and are termed Gaucher cells. Gaucher cells are typically found in liver, spleen and bone marrow. This can lead to an enlarged spleen and liver (hepatosplenomegaly). Secondary hematologic sequelae include severe anemia and thrombocytopenia. Injections of alglucerase into Gaucher disease patients leads to elevated serum levels of the enzyme and reduction in the accumulation of glucocerebroside | Alglucerase catalyzes the hydrolysis of the glycolipid, glucocerebroside, to glucose and ceramide as part of the normal degradation pathway for membrane lipids. | NA | NA | NA | 49.4 to 282.1 mL/kg | NA | Alimentary Tract and Metabolism,Enzyme Replacement Therapy,Enzymes,Enzymes and Coenzymes,Gaucher Disease,Glucosidases,Glycoside Hydrolases,Hydrolases,Hydrolytic Lysosomal Glucocerebroside-specific Enzyme,Recombinant Proteins | NA | NA | NA | NA | Glucocerebroside | Ceredase | Genzyme Corporation | Genzyme Corporation | Ceredase (alglucerase injection) is indicated for use as long-term enzyme replacement therapy for children, adolescents and adult patients with a confirmed diagnosis of Type I Gaucher disease who exhibit signs and symptoms that are severe enough to result in moderate-to-severe anemia, thrombocytopenia with bleeding tendency, bone disease, significant hepatomegaly or splenomegaly. | NA | Ceredase citrate is supplied as buffered solution (53 mM citrate, 143 mM sodium) containing 1% albumin human USP. The enzyme is supplied in one concentration, 400 units per bottle (80 units/mL) with a fill volume of 5 mL per bottle. An enzyme unit (U) is defined as the amount of enzyme required to hydrolyze in one minute one micromole of the synthetic substrate, p-nitrophenyl-β-D-glucopyranoside. | Ceredase (alglucerase injection) is supplied as a clear sterile non-pyrogenic solution of alglucerase in a citrate buffered solution | Intravenous infusion | Ceredase (alglucerase injection) is administered by Intravenous infusion over 1-2 hours. Dosage should be individualized for each patient. Initial dosage may be as little as 2.5 units/kg of body weight 3 times a week up to as much as 60 units/kg administered as frequently as once a week or as infrequently as every 4 weeks. 60 units/kg every 2 weeks is the dose for which the most data are available. Disease severity may dictate that drug be initiated with relatively high doses or relatively frequent administration. After patient response is well-established, a reduction in dosage may be attempted for maintenance therapy. Progressive reductions can be made at intervals of 3-6 months while carefully monitoring response parameters. | There are no known contraindications to the use of Ceredase (alglucerase injection). | Events were related to the route of administration including discomfort,pruritus, burning and swelling or sterile abscess at the site of venipuncture. The remaining experiences consisted of slight fever, chills, abdominaldiscomfort, nausea or vomiting. Additional adverse symptoms which have been reported include: fatigue, vasomotor irritability or hot flash, weakness, headache, light headedness, dysosmia, oral ulcerations, backache and transient peripheral edema, and diarrhea. Menstrual abnormalities and false positive pregnancy tests | Link | NA | NA |
| 10436 | Th1075 | Capromab | NA | NA | NA | NA | NA | 61 °C (FAB fragment), 71 °C (whole mAb) | NA | Capromab is a Murine IgG1 monoclonal antibody that recognizes prostate specific membrane antigen from prostate cancer cells and normal prostate tissue. It is linked to pendetide, a derivative of DTPA. Pendetide acts as a chelating agent for the radionuclide indium-111. Capromab is used to image the extent of prostate cancer. | For diagnosis of prostate cancer and detection of intra-pelvic metastases. | Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. | Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors. | NA | Most likely removed by opsonization via the reticuloendothelial system or by human antimurine antibody production | NA | 4 ± 2.1 L | 42 +/- 22 mL/hr | Indicators, Reagents and Diagnostic Agents | NA | NA | NA | NA | NA | ProstaScint | Jazz Pharmaceuticals, Inc. | Jazz Pharmaceuticals, Inc. | Indium In 111 ProstaScint (capromab pendetide) is indicated as a diagnostic imaging agent in newly-diagnosed patients with biopsy-proven prostate cancer, thought to be clinically-localized after standard diagnostic evaluation (e.g. chest x-ray, bone scan, CT scan, or MRI), who are at high-risk for pelvic lymph node metastases. ProstaScint is not indicated as a screening tool for carcinoma of the prostate nor for readministration for the purpose of assessment of response to treatment. | NA | Each ProstaScint kit consists of two vials which contain all of the non-radioactive ingredients necessary to produce a single unit dose of Indium In 111 ProstaScint, an immunoscintigraphic agent for administration by Intravenous infusion only. The ProstaScint vial contains 0.5 mg of capromab pendetide in 1 mL of sodium phosphate buffered saline solution adjusted to pH 6; a sterile, pyrogen-free, clear, colorless solution that may contain some translucent particles. The vial of sodium acetate buffer contains 82 mg of sodium acetate in 2 mL of Water for Injection adjusted to pH 5-7 with glacial acetic acid; it is a sterile, pyrogen-free, clear, and colorless solution. Neither solution contains a preservative. Each kit also includes one sterile 0.22 μm Millex GV filter, prescribing information, and two identification labels. | Indium In 111 ProstaScint is a sterile, pyrogen-free, clear, colorless solution that may contain some translucent particles. | Intravenous infusion | he recommended dose of ProstaScint (capromab pendetide) is 0.5 mg radiolabeled with 5 mCi of Indium In 111 chloride. Each dose is administered intravenously over 5 minutes and should not be mixed with any other medication during its administration. Indium In 111 ProstaScint may be readministered following infiltration or a technically inadequate scan; however, it is not indicated for readministration for the purpose of assessment of response to treatment . | Indium In 111 ProstaScint (capromab pendetide) should not be used in patients who are hypersensitive to this or any other product of murine origin or to Indium In 111 chloride. | ProstaScint (capromab pendetide) was generally well tolerated in the clinical trials. After administration of 529 single doses of Indium In 111 ProstaScint, adverse reactions were observed in 4% of patients. The most commonly reported adverse reactions were increases in bilirubin, hypotension, and hypertension, which occurred in 1% of patients. Elevated liver enzymes and injection site reactions occurred in slightly less than 1% of patients. Other adverse reactions, listed in order of decreasing frequency, were: pruritus, fever, rash, headache, myalgia, asthenia, burning sensation in thigh, shortness of breath, and alteration of taste. Most adverse reactions were mild and readily reversible. Data from repeat administration in 61 patients revealed a similar incidence of adverse reactions (5%). No deaths were attributable to Indium In 111 ProstaScint administration. | Link | NA | NA |
| 10438 | Th1076 | Laronidase | >Th1076_Laronidase APHLVQVDAARALWPLRRFWRSTGFCPPLPHSQADQYVLSWDQQLNLAYVGAVPHRGIKQVRTHWLLELVTTRGSTGRGLSYNFTHLDGYLDLLRENQLLPGFELMGSASGHFTDFEDKQQVFEWKDLVSSLARRYIGRYGLAHVSKWNFETWNEPDHHDFDNVSMTMQGFLNYYDACSEGLRAASPALRLGGPGDSFHTPPRSPLSWGLLRHCHDGTNFFTGEAGVRLDYISLHRKGARSSISILEQEKVVAQQIRQLFPKFADTPIYNDEADPLVGWSLPQPWRADVTYAAMVVKVIAQHQNLLLANTTSAFPYALLSNDNAFLSYHPHPFAQRTLTARFQVNNTRPPHVQLLRKPVLTAMGLLALLDEEQLWAEVSQAGTVLDSNHTVGVLASAHRPQGPADAWRAAVLIYASDDTRAHPNRSVAVTLRLRGVPPGPGLVYVTRYLDNGLCSPDGEWRRLGRPVFPTAEQFRRMRAAEDPVAAAPRPLPAGGRLTLRPALRLPSLLLVHVCARPEKPPGQVTRLRALPLTQGQLVLVWSDEHVGSKCLWTYEIQFSQDGKAYTPVSRKPSTFNLFVFSPDTGAVSGSYRVRALDYWARPGPFSDPVPYLEVPVPRGPPSPGNP | 69899.4 | C3160H4848N898O881S12 | 9.09 | -0.3 | NA | 1.5-3.6 hrs | Human recombinant alpha-L-iduronidase, produced by recombinant DNAtechnology in a Chinese hamster ovary cell line. Laronidase is a glycoprotein with a predicted amino acid sequence of the recombinant form, as well as the nucleotide sequence that encodes it, are identical to a polymorphic form of human a-L-iduronidase. It contains 6 N-linked oligosaccharide modification sites. | For the treatment of mucopolysaccharidosis | Laronidase is used to treat mucopolysaccharide storage disorders (Hurlers syndrome) caused by deficiencies of alpha-L-iduronidase. Reduced or absent a-L-iduronidase activity results in the accumulation of the GAG substrates, dermatan sulfate and heparan sulfate, throughout the body and leads to widespread cellular, tissue, and organ dysfunction. | Laronidase catalyses the hydrolysis of terminal alpha-L-iduronic acid residues of dermatan sulfate and heparin sulfate. | NA | NA | NA | NA | NA | Alimentary Tract and Metabolism,Enzymes,Enzymes and Coenzymes,Hydrolytic Lysosomal Glycosaminoglycan-specific Enzyme | NA | NA | NA | NA | Iduronic acid | ALDURAZYME | Genzyme Corporation | Genzyme Corporation | ALDURAZYME is a hydrolytic lysosomal glycosaminoglycan (GAG)-specific enzyme indicated for patients with Hurler and Hurler-Scheie forms of Mucopolysaccharidosis I (MPS I) and for patients with the Scheie form who have moderate to severe symptoms. The risks and benefits of treating mildly affected patients with the Scheie form have not been established. ALDURAZYME has been shown to improve pulmonary function and walking capacity. ALDURAZYME has not been evaluated for effects on the central nervous system manifestations of the disorder | NA | The solution in each vial contains a nominal laronidase concentration of 0.58 mg/mL and a pH of approximately 5.5. The extractable volume of 5.0 mL from each vial provides 2.9 mg laronidase, 43.9 mg sodium chloride, 63.5 mg sodium phosphate monobasic monohydrate, 10.7 mg sodium phosphate dibasic heptahydrate, and 0.05 mg polysorbate 80. ALDURAZYME does not contain preservatives; vials are for single use only. | ALDURAZYME, for IV infusion, is supplied as a sterile, nonpyrogenic, colorless to pale yellow, clear to slightly opalescent solution that must be diluted prior to administration in 0.9% Sodium Chloride Injection | Intravenous (Intravenous) infusion | 0.58 mg/kg of body weight administered once weekly | None | The most commonly reported infusion reactions occurring in at least 10% of patients 6 months of age and older were pyrexia, chills, blood pressure increased, tachycardia, and oxygen saturation decreased (6). The most frequently occurring adverse reactions occurring in at least 10% of patients 6 years and older are rash, upper respiratory tract infection, injection site reaction, hyperreflexia, paresthesia, flushing, and poor venous access. | 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 |
| 10476 | Th1087 | Oxytocin | >Th1087_Oxytocin CYIQNCPLG | 1007.187 | C43H66N12O12S2 | 5.51 | -2.7 | 192-194 ℃ | 1-6 min | 9-residue cyclic peptide, synthetically prepared to avert possible contamination with vasopressin and small polypeptides | To assist in labor, elective labor induction, uterine contraction induction | Used to induce labor or to enhance uterine contractions during labor. Uterine motility depends on the formation of the contractile protein actomyosin under the influence of the Ca2+-dependent phosphorylating enzyme myosin light-chain kinase. Oxytocin promotes contractions by increasing the intracellular Ca2+, which in turn activates myosins light chain kinase.. Oxytocin has specific receptors in the muscle llining of the uterus and the receptor concentration increases greatly during pregnancy, reaching a maximum in early labor at term. | Binds the oxytocin receptor which leads to an increase in intracellular calcium levels. The oxytocin-oxytocin receptor system plays an important role as an inducer of uterine contractions during parturition and of milk ejection. | Administration of supratherapeutic doses of exogenous oxytocin can lead to myocardial ischemia, tachycardia, and arrhythmias. High doses can also lead to uterine spasms, hypertonicity, or rupture. Oxytocin has antidiuretic properties, thus, high daily doses (as a single dose or administered slowly over 24 hours) may lead to extreme water intoxication resulting in maternal seizures, coma, and even death. The risk of antidiuresis and water intoxication in the mother appears to be greater when fluids are given orally | Oxytocin is rapidly removed from the plasma by the liver and kidney. The enzyme oxytocinase is largely responsible for the metabolism and regulation of oxytocin levels in pregnancy and only a small percentage of the neurohormone is excreted in the urine unchanged.Oxytocinase activity increases throughout pregnancy and peaks in the plasma, placenta and uterus near term. The placenta is a key source of oxytocinase during gestation and produces increasing amounts of the enzyme in response to increasing levels of oxytocin produced by the mother. Oxytocinase activity is also expressed in mammary glands, heart, kidney, and the small intestine.Lower levels of activity can be found in the brain, spleen, liver, skeletal muscle, testes, and colon. The level of oxytocin degradation is negligible in non-pregnant women, men, and cord blood | Oxytocin is administered parenterally and is fully bioavailable. It takes approximately 40 minutes for oxytocin to reach steady-state concentrations in the plasma after parenteral administration. | NA | In a study that observed 10 women who were given oxytocin to induce labor, the mean metabolic clearance rate was 7.87 mL/min. | Oxytocics, Anti-tocolytic Agents and Labor Induction Agents | NA | NA | NA | NA | Oxytocin receptor | Pitocin | JHP Pharmaceuticals | JHP Pharmaceuticals | Induction or Stimulation of Labor, Control of Postpartum Uterine Bleeding, Treatment of Incomplete, Inevitable, or Elective Abortion | NA | NA | Pitocin (oxytocin injection, USP) is a sterile, clear, colorless aqueous solution of synthetic oxytocin, for Intravenous infusion or intramuscular injection. Pitocin is a nonapeptide found in pituitary extracts from mammals. It is standardized to contain 10 units of oxytocic hormone/mL and contains | Intravenous infusion | initial dose should be 0.5–1 mU/min (equal to 3–6 mL of the dilute oxytocin solution per hour). At 30–60 minute intervals the dose should be gradually increased in increments of 1–2 mU/min until the desired contraction pattern has been established. | Do NOT use Pitocin if: you are allergic to any ingredient in Pitocin; your birth canal is too small compared with the fetus's head; you have other complications that require medical intervention for birth; you have bacteria in the blood; you cannot have a child through vaginal delivery because of certain conditions (eg, genital herpes, cervical cancer) | Symptoms of overdose: Restlessness, shakiness, sleepiness, slow to respond, slurred speech, unconsciousness. | Link | NA | NA |
| 10481 | Th1089 | Palivizumab | >Th1089_Palivizumab QVTLRESGPALVKPTQTLTLTCTFSGFSLSTSGMSVGWIRQPPGKALEWLADIWWDDKKDYNPSLKSRLTISKDTSKNQVVLKVTNMDPADTATYYCARSMITNWYFDVWGAGTTVTVSS | NA | NA | NA | NA | 61 (FAB fr | 18-20 days (in adults) | Humanized, recombinant, monoclonal antibody (IgG1k) directed agaisnt the epitope in the A antigenic site of the F protein of respiratory syncytial virus (RSV). Synagis is a composite of human (95%) and murine (5%) antibody sequences. The human heavy chain sequence is derived from the constant domains of human IgG1 and the variable framework regions of the VH genes Cor (1) and Cess (2). The human light chain sequence is derived from the constant domain of Ck and the variable framework regions of the VL gene K104 withJk-4. Palivizumab is expressed from a stable murine myeloma cell line (NS0). Palivizumab is composed of to heavy chains (50.6 kDa each) and two light chains (27.6 kDa each), contains 1-2% carbohydrate by weight and has a molecular weight of 147.7 kDa ± 1 kDa (MALDI-TOF). | For prophylaxis of respiratory diseases casued by respiratory syncytial virus. | Synagis exhibits neutralizing and fusion-inhibitory activity against Respiratory syncytial virus (RSV). These activities inhibit RSV replication or spread. Synagis is given to prevent the development of lower respiratory tract disease in pediatric patients. | Palivizumab binds to the fusion glycoprotein of RSV. This prevents its binding and uptake by host cellular receptors. | NA | Most likely removed by opsonization via the reticuloendothelial system. | NA | NA | NA | Amino Acids, Peptides, and Proteins,Anti-Infective Agents,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antiinfectives for Systemic Use,Antiviral Agents,Blood Proteins,Fusion Protein Inhibitors,Globulins,Immune Sera and Immunoglobulins,Immunoglobulins,Immunoproteins,Proteins,Respiratory Syncytial Virus Anti-F Protein Monoclonal Antibody,Serum Globulins,Specific Immunoglobulins | CA2197684 | 31-Oct-2000 | 9-Aug-2015 | NA | Fusion glycoprotein F0,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 gamma Fc region receptor III-A,High affinity immunoglobulin gamma Fc receptor I,Low affinity immunoglobulin gamma Fc region receptor II-b | Synagis | MedImmune | MedImmune | Palivizumab inhibits the actions of respiratory syncytial virus (RSV) and helps to prevent the disease | NA | 100 mg single-dose vial of Synagis liquid solution contains 100 mg of palivizumab and also contains chloride (0.5 mg), glycine (0.1 mg), and histidine (3.9 mg), in a volume of 1 mL. | Sterile, preservative-free liquid solution | Intramuscular | recommended dose of Synagis is 15 mg per kg of body weight given monthly by intramuscular injection. The first dose of Synagis should be administered prior to commencement of the RSV season and the remaining doses should be administered monthly throughout the RSV season. Children who develop an RSV infection should continue to receive monthly doses throughout the RSV season. In the northern hemisphere, the RSV season typically commences in November and lasts through April, but it may begin earlier or persist later in certain communities. | indicated for the prevention of serious lower respiratory tract disease caused by respiratory syncytial virus (RSV) in children at high risk of RSV disease.The following points should be considered when prescribing Synagis: Safety and efficacy were established in children with bronchopulmonary dysplasia (BPD), infants with a history of premature birth (less than or equal to 35 weeks gestational age), and children with hemodynamically significant congenital heart disease (CHD). | high fever, ear pain or drainage, tugging at the ear; warmth or swelling of the ear; crying or fussiness, especially while lying down; change in sleeping patterns; poor feeding or loss of appetite; easy bruising or bleeding; or trouble breathing. | Link | NA | NA |
| 10484 | Th1091 | Bevacizumab | >Th1091_Bevacizumab EVQLVESGGGLVQPGGSLRLSCAASGYTFTNYGMNWVRQAPGKGLEWVGWINTYTGEPTYAADFKRRFTFSLDTSKSTAYLQMNSLRAEDTAVYYCAKYPHYYGSSHWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | C6538H10034N1716O2033S44 | NA | NA | 61 (FAB fr | 20 days (range of 11-50 days) | Recombinant (derived from CHO-gentamycin), humanized, monoclonal IgG1 antibody. It Inhibits the biologic activity of human vascular endothelial growth factor (VEGF) by binding to it. Comprises human framework regions and murine complementarity-determining regions. | As part of combination therapy for metastatic colorectal cancer and HER2-negative metastatic breast cancer. | Bevacizumab prevents or reduces the formation of blood vessels (angiogenesis) thereby preventing or reducing metatstatic disease progressing. Bevacizumab binds VEGF and prevents vascular endothelial growth and endothelial cell proliferation. | Bevacizumab binds VEGF and prevents the interaction of VEGF to its receptors (Flt-1 and KDR) on the surface of endothelial cells. This prevents blood vessel proliferation and tumour metastasis. | Bevacizumab toxicities are distinct from the effects of cytotoxic agents used in chemotherapy, and are normally linked to impaired VEGF function.18,19 Common toxicities associated with bevacizumab include hypertension, gastrointestinal perforation, arterial thromboembolism, reversible posterior leukoencephalopathy syndrome (RPLS), venous thromboembolism, proteinuria, bleeding/hemorrhage, and wound-healing complications | There are several pathways through which monoclonal antibodies (mAbs) may be cleared. Non-specific clearance of mAbs refers to target independent pinocytosis, and proteolysis of the protein into small amino acids and peptides in the reticuloendothelial system (RES) and the liver. Target-mediated clearance is a result of specific interactions between the mAb and its target antigen. Once bound, the antibody-antigen complex may be cleared via lysosomal degradation. Additionally, the production of anti-drug antibodies (ADA), which are a result of an immunogenic response to mAb-based treatment, can form complexes with mAb’s and may impact the rate of mAb clearance | Monoclonal antibodies (mAbs) are large in size, do not readily cross cell membranes, and are unable to withstand proteolysis in the gastrointestinal tract.Given these characteristics, mAbs are poorly absorbed via the oral route and are instead administered intravenously, intramuscularly or subcutaneously.In a single dose (1mg/kg) pharmacokinetic study assessing the bioequivalence of bevacizumab and TAB008 (a biosimilar product), the pharmacokinetic parameters of Avastin (bevacizumab) were as follows: Geometric mean Cmax = 17.38 ug/mL Geometric mean AUCinf = 5,358 ugxh/mL Geometric mean Tmax = 2.50 hrs | The volume of distribution of bevacizumab is approximately 3.29 L and 2.39 L for the average male and female, respectively. | The clearance (CL) of bevacizumab is approximately 0.207 L/day. The CL of bevacizumab can increase or decrease by 30% in patients who weigh >114 kg or <49 kg respectively. Males tend to clear bevacizumab at a faster rate than females (26% faster on average). Other factors including alkaline phosphatase (ALP), serum aspartate aminotransferase (AST), serum albumin, and tumor burden may cause the CL to fluctuate | Amino Acids, Peptides, and Proteins,Angiogenesis Inhibitors,Angiogenesis Modulating Agents,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,Cardiotoxic antineoplastic agents,Experimental Unapproved Treatments for COVID-19,Globulins,Growth Inhibitors,Immunoglobulins,Immunoproteins,Immunotherapy,Narrow Therapeutic Index Drugs,Proteins,Serum Globulins,Vascular Endothelial Growth Factor Inhibitor,Vascular Endothelial Growth Factor Inhibitors,Vascular Endothelial Growth Factor-directed Antibody Interactions | CA2286330 | 10-Jun-2008 | 3-Apr-2018 | NA | Vascular endothelial growth factor A,Complement C1q subcomponent subunit A,Complement C1q subcomponent subunit B,Complement C1q subcomponent subunit C,Low affinity immunoglobulin gamma Fc region receptor III-A,High affinity immunoglobulin gamma Fc receptor I,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 | Avastin | Genentech | Genentech | Metastatic Colorectal Cancer (mCRC): Avastin is indicated for the first- or second-line treatment of patients with metastatic carcinoma of the colon or rectum. Non-Squamous Non-Small Cell Lung Cancer (NSCLC), glioblastoma with progressive disease in adult patients. Metastatic Renal Cell Carcinoma (mRCC): Avastin is indicated for the treatment of metastatic renal cell carcinoma in combination with interferon alfa. Persistent, Recurrent, Or Metastatic Carcinoma Of The Cervix: Avastin in combination with paclitaxel and cisplatin or paclitaxel and topotecan is indicated for the treatment of persistent, recurrent, or metastatic carcinoma of the cervix. | NA | 100 mg product is formulated in 240 mg a,a-trehalose dihydrate, 23.2 mg sodium phosphate (monobasic, monohydrate), 4.8 mg sodium phosphate (dibasic, anhydrous), 1.6 mg polysorbate 20, and Water for Injection, USP. The 400 mg product is formulated in 960 mg a,a-trehalose dihydrate, 92.8 mg sodium phosphate (monobasic, monohydrate), 19.2 mg sodium phosphate (dibasic, anhydrous), 6.4 mg polysorbate 20, and Water for Injection, USP. | Slightly opalescent, colorless to pale brown, sterile, pH 6.2 solution | Intravenous infusion | First infusion: Administer infusion over 90 minutes. Subsequent infusions: Administer second infusion over 60 minutes if first infusion is tolerated; Recommended Doses And Schedules: Metastatic Colorectal Cancer (mCRC).The recommended doses are 5 mg/kg or 10 mg/kg every 2 weeks when used in combination with intravenous 5-FU-based chemotherapy. Administer 5 mg/kg when used in combination with bolus-IFL. Administer 10 mg/kg when used in combination with FOLFOX4. Administer 5 mg/kg every 2 weeks or 7.5 mg/kg every 3 weeks when used in combination with a fluoropyrimidine-irinotecan or fluoropyrimidine-oxaliplatin based chemotherapy regimen in patients who have progressed on a first-line Avastin-containing regimen. Non-Squamous Non-Small Cell Lung Cancer (NSCLC): The recommended dose is 15 mg/kg every 3 weeks in combination with carboplatin and paclitaxel. Glioblastoma: The recommended dose is 10 mg/kg every 2 weeks. Metastatic Renal Cell Carcinoma (mRCC): The recommended dose is 10 mg/kg every 2 weeks in combination with interferon alfa. Cervical Cancer: The recommended dose of Avastin is 15 mg/kg every 3 weeks as an Intravenous infusion administered in combination with one of the following chemotherapy regimens: paclitaxel and cisplatin, or paclitaxel and topotecan. | Do not administer as an intravenous push or bolus. Administer only as an intravenous (IV) infusion.. Do not initiate Avastin until at least 28 days following major surgery. Administer Avastin after the surgical incision has fully healed. | headache, confusion, vision problems, feeling very weak or tired, fainting, and seizure (blackout or convulsions) | Link | NA | NA |
| 10497 | Th1093 | Eculizumab | NA | 148000 | NA | NA | NA | NA | 272 ± 82 hrs (mean ± SD) | Soliris is a formulation of eculizumab which is a recombinant humanized monoclonal IgG2/4;K antibody. Recombinant; produced in murine myeloma cell culture. Eculizumab contains human constant regions from human IgG2 sequences and human IgG4 sequences and murine complementarity-determining regions grafted onto the human framework light- and heavy-chain variable regions and has a molecular weight of approximately 148 kDa. | For the treatment of patients with paroxysmal nocturnal hemoglobinuria (PNH) to reduce hemolysis. | Eculizumab is a monoclonal antibody directed against the complement protein C5. This antibody blocks the cleavage of C5 and halts the process of complement-mediated cell destruction. Eculizumab is a product of Alexion Pharmaceuticals and has been shown to be effective in treating paroxysmal nocturnal hemoglobinuria. Eculizumab was approved by the FDA in March, 2007. | A genetic mutation in PNH patients leads to the generation of populations of abnormal RBCs (known as PNH cells) that are deficient in terminal complement inhibitors (CD-59), rendering PNH RBCs sensitive to persistent terminal complement-mediated destruction. The destruction and loss of these PNH cells (intravascular hemolysis) results in low RBC counts (anemia) and also fatigue, difficulty in functioning, pain, dark urine, shortness of breath, and blood clots. Eculizumab, the active ingredient in Soliris, is a monoclonal antibody that binds to the complement protein C5 specifically and with high affinity, thereby inhibiting its cleavage to C5a and C5b and subsequent generation of the terminal complement complex C5b-9. Soliris inhibits terminal complement mediated intravascular hemolysis in PNH patients and therefore the destruction of PNH erythrocytes that lack complement protection with CD-59. | Overdoses of eculizumab are unlikely as it is administered under specialist supervision.8 In case of overdose, contact local poison control | Eculizumab is a monoclonal antibody and is expected to be metabolized to small peptides and amino acids. | Eculizumab is administered by intravenous infusion so the bioavailability is 100%.7 This drug reaches a Cmax of 194±76µg/mL and Ctrough of 97±60µg/mL.7 The AUC was calculated to be 24,467.6µg*h/mL | The volume of distribution of eculizumab is 5-8L | Pharmacokinetic properties in healthy patients have not been determined.4 In patients with rhematoid arthritis, there is an average clearance of 0.26mL/kg/h. | NA | CA2189015 | 13-Apr-2010 | 1-May-2015 | NA | Complement C5 | Soliris | Alexion, Inc | Alexion, Inc | indicated for the treatment of patients with paroxysmal nocturnal hemoglobinuria (PNH) to reduce hemolysis | NA | The product is formulated at pH 7 and each vial contains 300 mg of eculizumab, 13.8 mg sodium phosphate monobasic, 53.4 mg sodium phosphate dibasic, 263.1 mg sodium chloride, 6.6 mg polysorbate 80 (vegetable origin) and Water for Injection, USP. | Sterile, clear, colorless, preservative-free 10 mg/mL solution for Intravenous infusion and is supplied in 30-mL single-use vials | NA | 600 mg weekly for the first 4 weeks, followed by 900 mg for the fifth dose 1 week later, then 900 mg every 2 weeks thereafter. | NA | Life-threatening and fatal meningococcal infections have occurred in patients treated with Soliris. Meningococcal infection may become rapidly life-threatening or fatal if not recognized and treated early. | Link | NA | NA |
| 10499 | Th1095 | Ranibizumab | >Th1095_Ranibizumab EVQLVESGGGLVQPGGSLRLSCAASGYDFTHYGMNWVRQAPGKGLEWVGWINTYTGEPTYAADFKRRFTFSLDTSKSTAYLQMNSLRAEDTAVYYCAKYPYYYGTSHWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHL | 48349.61 | C2158H3282N562O681S12 | NA | NA | NA | Approximately 9 days. | Recombinant (E.coli derived), humanized IgG1 kappa isotype monoclonal antibody (intraocular use). It binds to and inhibits the biologic activity of human vascular endothelial growth factor A (VEGF-A). Ranibizumab is marketed under the name Lucentis. | For the treatment of patients with macular edema after retinal vein occlusion, age-related macular degeneration (wet), and diabetic macular edema. | Ranibizumab is a recombinant humanized IgG1 kappa isotype monoclonal antibody fragment designed for intraocular use. Ranibizumab is a VEGF-A antagonist that binds to and inhibits the biologic activity of active forms of human VEGF-A, including the cleaved form (VEGF110). VEGF-A has been shown to cause neovascularization (angiogenesis) and an increase in vascular permeability, which is thought to contribute to the progression of the neovascular form of age-related macular degeneration (AMD). | Ranibizumab binds to the receptor binding site of active forms of VEGF-A, including the biologically active, cleaved form of this molecule, (VEGF110). The binding of ranibizumab to VEGF-A prevents the interaction of VEGF-A with its receptors (VEGFR1 and VEGFR2) on the surface of endothelial cells, reducing endothelial cell proliferation, vascular leakage, and new blood vessel formation. | There is no information available regarding the LD50 values of ranibizumab. There is also limited clinical experience of ranibizumab overdose: concentrated doses as high as 2 mg ranibizumab in 0.05 mL have been administered to patients, with no additional unexpected adverse reactions that were observed | The metabolism of ranibizumab has not been studied. Since it is a monoclonal antibody fragment, ranibizumab is expected to undergo catabolism. | Ranibizumab rapidly penetrates through the retina to reach the choroid after intravitreal injection. Following monthly intravitreal administration of 0.5 mg ranibizumab in patients with neovascular (wet) age-related macular degeneration, the mean Cmax (±SD) was 1.7 (± 1.1) ng/mL. Following an implant insertion, the mean (±SD) Cmax of ranibizumab was 0.48 (±0.17) ng/mL and median Tmax was 26 days, with a range of one to 89 days. | The apparent volume of the central compartment (Vd/F) is 2.77 L. Ranibizumab is not shown to accumulate in serum. Due to its small size from lacking the Fc region of an antibody, ranibizumab achieves enhanced diffusion into the retina and choroid | In patients with retinal vein occlusion or diabetic macular edema, the apparent clearance (CL/F) of ranibizumab was 24.8 L/day. | Amino Acids, Peptides, and Proteins,Angiogenesis Inhibitors,Angiogenesis Modulating Agents,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineovascularisation Agents,Blood Proteins,EENT Drugs, Miscellaneous,Globulins,Growth Inhibitors,Growth Substances,Immunoglobulins,Immunoproteins,Ocular Vascular Disorder Agents,Ophthalmics,Ophthalmologicals,Proteins,Sensory Organs,Serum Globulins,Vascular Endothelial Growth Factor Inhibitor,Vascular Endothelial Growth Factor Inhibitors | CA2286330 | 10-Jun-2008 | 3-Apr-2018 | NA | Vascular endothelial growth factor A | Lucentis | Genentech | Genentech | Neovascular (Wet) Age-Related Macular Degeneration (AMD), Macular Edema Following Retinal Vein Occlusion (RVO), Diabetic Macular Edema (DME), Diabetic Retinopathy (Non Proliferative Diabetic Retinopathy (NPDR), Proliferative Diabetic Retinopathy (PDR)) In patients With Diabetic Macular Edema (DME) | NA | supplied as a preservative-free, sterile solution in a single-use glass vial designed to deliver 0.05 mL of 10 mg/mL LUCENTIS (0.5 mg dose vial) or 6 mg/mL LUCENTIS (0.3 mg dose vial) aqueous solution with 10 mM histidine HCl, 10% α,α-trehalose dihydrate, 0.01% polysorbate 20, pH 5.5. | Sterile, colorless to pale yellow solution in a single-use glass vial | Intravitreal Injection ONLY | Neovascular (Wet) Age-Related Macular Degeneration (AMD): LUCENTIS 0.5 mg (0.05 mL of 10 mg/mL LUCENTIS solution) is recommended to be administered by intravitreal injection once a month (approximately 28 days). LUCENTIS 0.5 mg (0.05 mL of 10 mg/mL LUCENTIS solution) is recommended to be administered by intravitreal injection once a month (approximately 28 days). Diabetic Macular Edema (DME): LUCENTIS 0.3 mg (0.05 mL of 6 mg/mL LUCENTIS solution) is recommended to be administered by intravitreal injection once a month (approximately 28 days).; Diabetic Retinopathy In Patients With Diabetic Macular Edema: LUCENTIS 0.3 mg (0.05 mL of 6 mg/mL LUCENTIS solution) is recommended to be administered by intravitreal injection once a month (approximately 28 days). | Ocular Or Periocular Infections LUCENTIS is contraindicated in patients with ocular or periocular infections. Hypersensitivity to ranibizumab or any of the excipients in LUCENTIS. Hypersensitivity reactions may manifest as severe intraocular inflammation. | Endophthalmitis and Retinal Detachments Increases in Intraocular Pressure, Thromboembolic Events, Fatal Events in patients with DME and DR at baseline. | Link | NA | NA |
| 10502 | Th1096 | Idursulfase | >Th1096_Idursulfase SETQANSTTDALNVLLIIVDDLRPSLGCYGDKLVRSPNIDQLASHSLLFQNAFAQQAVCAPSRVSFLTGRRPDTTRLYDFNSYWRVHAGNFSTIPQYFKENGYVTMSVGKVFHPGISSNHTDDSPYSWSFPPYHPSSEKYENTKTCRGPDGELHANLLCPVDVLDVPEGTLPDKQSTEQAIQLLEKMKTSASPFFLAVGYHKPHIPFRYPKEFQKLYPLENITLAPDPEVPDGLPPVAYNPWMDIRQREDVQALNISVPYGPIPVDFQRKIRQSYFASVSYLDTQVGRLLSALDDLQLANSTIIAFTSDHGWALGEHGEWAKYSNFDVATHVPLIFYVPGRTASLPEAGEKLFPYLDPFDSASQLMEPGRQSMDLVELVSLFPTLAGLAGLQVPPRCPVPSFHVELCREGKNLLKHFRFRDLEEDPYLPG | 76000 | C2654H4000N688O774S14 | NA | NA | NA | 44 ± 19 minutes | Recombinant (from human cell line) form of human lysosomal enzyme, iduronate-2-sulfatase. Idursulfase is a 525-amino acid glycoprotein, which contains 8 N-linked glycosylation sites, occupied by complex oligosaccharide structures. Its enzyme activity depends on the post-translational modification of a specific cysteine to formylglycine. | For the treatment of Hunter syndrome in adults and children ages 5 and older. | Idursulfase is a purified form of the lysosomal enzyme human iduronate-2-sulfatase of recombinant DNA origin. It is designed to replace the natural enzyme, increasing catabolism of certain accumulated glycosaminoglycans (GAG), which abnormally accumulate in multiple tissue types in patients with mucopolysaccharidosis II (MPS-II, or Hunter syndrome). | Hunter's Syndrome is an X-linked recessive disease caused by insufficient levels of the lysosomal enzyme iduronate-2-sulfatase. This enzyme cleaves the terminal 2-O-sulfate moieties from the glycosaminoglycans (GAG) dermatan sulfate and heparan sulfate. Due to the missing or defective iduronate-2-sulfatase enzyme in patients with Hunter's Syndrome, GAG progressively accumulate in the lysosomes of a variety of cells, leading to cellular engorgement, organomegaly, tissue destruction and organ system dysfunction. Treatment of Hunter's Syndrome patients with idursulfase provides exogenous enzyme for uptake into cellular lysosomes. Targeting of idursulfase to the lysosome occurs by endocytosis from the cell surface. Mannose-6-phosphate (M6P) residues on the oligosaccharide chains allow specific binding of the enzymes to the M6P receptors on the cell surface, leading to cellular internalization of the enzyme, targeting to intracellular lysosomes and subsequent catabolism of accumulated GAG. | There is no experience with overdosage of Idursulfase in humans. Single intravenous doses of idursulfase up to 20 mg/kg were not lethal in male rats and cynomolgus monkeys (approximately 6.5 and 13 times, respectively, of the recommended human dose based on body surface area) and there were no clinical signs of toxicity. | NA | NA | NA | 3 mL/min/kg [Patients (7.7 - 27 years) with Hunter syndrome with treatment week 1(0.5 mg/kg ELAPRASE administered weekly as a 3-hour infusion)] . 3.4 mL/min/kg [patients (7.7 - 27 years) with Hunter syndrome with treatment week 27 (0.5 mg/kg ELAPRASE administered weekly as a 3-hour infusion)] | Alimentary Tract and Metabolism,Enzymes,Enzymes and Coenzymes,Esterases,Hydrolases,Hydrolytic Lysosomal Glycosaminoglycan-specific Enzyme,Sulfatases | NA | NA | NA | NA | Dermatan sulfate,Heparan sulfate,Perilipin-3 | Elaprase | SHIRE | SHIRE | indicated for patients with Hunter syndrome (Mucopolysaccharidosis II, MPS II). ELAPRASE has been shown to improve walking capacity in patients 5 years and older. The safety and efficacy of ELAPRASE have not been established in pediatric patients less than 16 months of age | NA | Each vial contains an extractable volume of 3 mL with an idursulfase concentration of 2 mg/mL at a pH of approximately 6. Each vial contains 6 mg idursulfase, sodium chloride (24 mg), sodium phosphate monobasic monohydrate (6.75 mg), sodium phosphate dibasic heptahydrate (2.97 mg), and polysorbate 20 (0.66 mg). ELAPRASE does not contain preservatives. Each vial is for single use only. | Sterile, nonpyrogenic clear to slightly opalescent, colorless solution that must be diluted prior to administration in 0.9% Sodium Chloride Injection, USP | Intravenous infusion | dosage regimen of ELAPRASE is 0.5 mg per kg of body weight administered once weekly as an Intravenous infusion. | Life-threatening anaphylactic reactions have occurred in some patients during and up to 24 hours after ELAPRASE infusions. Anaphylaxis, presenting as respiratory distress, hypoxia, hypotension, urticaria and/or angioedema of throat or tongue have been reported to occur during and after ELAPRASE infusions, regardless of duration of the course of treatment. Closely observe patients during and after ELAPRASE administration and be prepared to manage anaphylaxis. Inform patients of the signs and symptoms of anaphylaxis and have them seek immediate medical care should symptoms occur. Patients with compromised respiratory function or acute respiratory disease may be at risk of serious acute exacerbation of their respiratory compromise due to hypersensitivity reactions, and require additional monitoring | Bone or muscle pain, chest pain, chills, cough, fast, pounding, or irregular heartbeat or pulse, feeling of warmth, fever, headache, hives or welts, itching, rash, redness of the face, neck, arms, and occasionally, upper chest redness of the skin, sneezing, sore throat, tightness in the chest, unusual tiredness or weakness. | 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 |
| 10521 | Th1101 | Galsulfase | >Th1101_Galsulfase SGAGASRPPHLVFLLADDLGWNDVGFHGSRIRTPHLDALAAGGVLLDNYYTQPLCTPSRSQLLTGRYQIRTGLQHQIIWPCQPSCVPLDEKLLPQLLKEAGYTTHMVGKWHLGMYRKECLPTRRGFDTYFGYLLGSEDYYSHERCTLIDALNVTRCALDFRDGEEVATGYKNMYSTNIFTKRAIALITNHPPEKPLFLYLALQSVHEPLQVPEEYLKPYDFIQDKNRHHYAGMVSLMDEAVGNVTAALKSSGLWNNTVFIFSTDNGGQTLAGGNNWPLRGRKWSLWEGGVRGVGFVASPLLKQKGVKNRELIHISDWLPTLVKLARGHTNGTKPLDGFDVWKTISEGSPSPRIELLHNIDPNFVDSSPCPRNSMAPAKDDSSLPEYSAFNTSVHAAIRHGNWKLLTGYPGCGYWFPPPSQYNVSEIPSSDPPTKTLWLFDIDRDPEERHDLSREYPHIVTKLLSRLQFYHKHSVPVYFPAQDPRCDPKATGVWGPWM | 56012.6 | C2534H3851N691O719S16 | NA | NA | NA | 9 (6 to 21) minutes during the first week of treatment, 26 (8 to 40) minutes by the 24th week.. | A recombinant variant form of the polymorphic human enzyme, N-acetylgalactosamine 4-sulfatase. It is a glycoprotein with a molecular weight of approximately 56 kD and comprises 495 amino acids. It contains 6 N-linked glycosylation sites, four of which carry a bis-mannose-6-phosphate manose7 oligosaccharide for specific cellular recognition. It requires Ca-formylglycine for its catalytic activity. This residue is a post-translational modification of Cys53 and conserved in all members of the sulfatase enzyme family. | For the treatment of adults and children with Mucopolysaccharidosis VI. | Mucopolysaccharide storage disorders are caused by the deficiency of specific lysosomal enzymes required for the catabolism of GAG. Mucopolysaccharidosis VI (MPS VI, Maroteaux-Lamy syndrome) is characterized by the absence or marked reduction in N-acetylgalactosamine 4-sulfatase. The sulfatase activity deficiency results in the accumulation of the GAG substrate dermatan sulfate, throughout the body. This accumulation leads to widespread cellular, tissue, and organ dysfunction. Galsulfase is intended to provide an exogenous enzyme that will be taken up into lysosomes and increase the catabolism of GAG. Galsulfase uptake by cells into lysosomes is most likely mediated by the binding of mannose-6-phosphate-terminated oligosaccharide chains of galsulfase to specific mannose-6-phosphate receptors. | Galsulfase supplies recombinant-engineered galsulfase, a normal variant form of the polymorphic human enzyme, N-acetylgalactosamine 4-sulfatase. It is a lysosomal hydrolase that catalyzes the cleavage of the sulfate ester from terminal N-acetylgalactosamine 4-sulfate residues of GAG chondroitin 4-sulfate and dermatan sulfate. Increased catabolism of GAG in turn reduces systemic dermatan sulfate accumulation, thereby reducing the primary symptoms of MPS VI. | There is no experience with overdose of galsulfase. | NA | NA | Week 1: 56-323 mL/kg and 59-2799 mL/kg by week 24 | NA | Enzyme Replacement Agents | NA | NA | NA | NA | Dermatan sulfate,Perilipin-3 | Naglazyme | BioMarin | BioMarin | NAGLAZYME (galsulfase) is indicated for patients with Mucopolysaccharidosis VI (MPS VI, Maroteaux-Lamy syndrome). NAGLAZYME has been shown to improve walking and stair-climbing capacity. | NA | NAGLAZYME is supplied in clear Type I glass 5 mL vials. Each vial provides 5 mg galsulfase, 43.8 mg sodium chloride, 6.20 mg sodium phosphate monobasic monohydrate, 1.34 mg sodium phosphate dibasic heptahydrate, and 0.25 mg polysorbate 80 in a 5 mL extractable solution with pH of approximately 5.8. NAGLAZYME does not contain preservatives. Each vial is for single use only. | Sterile, nonpyrogenic, colorless to pale yellow, clear to slightly opalescent solution that must be diluted with 0.9% Sodium Chloride Injection, USP, prior to administration | Intravenous infusion | The recommended dosage regimen of NAGLAZYME is 1 mg per kg of body weight administered once weekly as an Intravenous infusion. Pretreatment with antihistamines with or without antipyretics is recommended 30 to 60 minutes prior to the start of the infusion. | NA | Serious adverse reactions experienced in this trial include apnea, pyrexia, and respiratory distress. Severe adverse reactions include chest pain, dyspnea, laryngeal edema, and conjunctivitis. The most common adverse reactions requiring interventions were infusion reactions. | 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 |
| 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 |
| 10547 | Th1107 | Insulin glulisine | >Th1107_Insulin_glulisine GIVEQCCTSICSLYQLENYCN | 5823 | C258H384N64O78S6 | NA | NA | NA | Elimination half life= 42 minutes (SC injection) | Insulin glulisine is a recombinant (E. Coli derived), rapid-acting analog of human insulin. It contains two mutations, one at position B3, where R is replaced by K and the other at position B29, where K is replaced by E. This results in decrease hexamer formation and increased stability of the monomer, thus increasing the rate of absorption and quicker action as compared to native insulin. | For the treatment of Type 1 and 2 diabetes mellitus. Should be used in regimens including a long-acting or basal insulin analogue unless it is used in a continuous infusion pump. May be used with oral antidiabetic agents. | 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 glulisine is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin glulisine is approximately 15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 2-4 hours. | Insulin glulisine 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 arginine at position B3 for lysine and replacement of the B29 lysine with glutamic acid decreases the propensity to form hexamers, stabilizes the hormone in monomeric form and results in a rapid rate of absorption and short 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 | Compared to regular human insulin, insulin glulisine is faster absorbed. When 0.15 units/kg was subcutaneously administered to type 1 diabetes patients, the pharmacokinetic parameters are as follows: Tmax = 60 minutes (range of 40 - 120 minutes); Cmax = 83 microUnits/mL (range of 40 - 131 microUnits/mL). Absolute bioavailability following subcutaneous administration is approximately 70%, regardless of site of injection. | 13 L | 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 Analog,Insulin, Short-Acting,Insulins and Analogues for Injection, Fast-Acting,Pancreatic Hormones,Peptide Hormones,Peptides,Proteins | US6960561 | 11-Jan-2005 | 25-01-2023 | NA | Insulin receptor,Insulin-like growth factor 1 receptor | APIDRA | sanofi-aventis | sanofi-aventis | APIDRA is indicated to improve glycemic control in adults and children with diabetes mellitus. | NA | Each milliliter of APIDRA contains 100 units (3.49 mg) insulin glulisine, 3.15 mg metacresol, 6 mg tromethamine, 5 mg sodium chloride, 0.01 mg polysorbate 20, and water for injection. APIDRA has a pH of approximately 7.3. The pH is adjusted by addition of aqueous solutions of hydrochloric acid and/or sodium hydroxide | Sterile, aqueous, clear, and colorless solution | NA | APIDRA is a recombinant insulin analog that is equipotent to human insulin (i.e. one unit of APIDRA has the same glucose-lowering effect as one unit of regular human insulin) when given intravenously. When given subcutaneously, APIDRA has a more rapid onset of action and a shorter duration of action than regular human insulin. The dosage of APIDRA must be individualized. Blood glucose monitoring is essential in all patients receiving insulin therapy. 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. | APIDRA is contraindicated: during episodes of hypoglycemia, in patients who are hypersensitive to APIDRA or to any of its excipients When used in patients with known hypersensitivity to APIDRA or its excipients, patients may develop localized or generalized hypersensitivity reactions. | Hypoglycemia, Hypokalemia | Link | NA | NA |
| 10556 | Th1108 | Pegaptanib | NA | 541.6 | C22H44N3O10P | NA | NA | NA | 10 ± 4 days | It is a polynucleotide aptamer, which specifically binds to VEGF 165, a protein that plays a critical role in angiogenesis and increased permeability of blood vessels; two of the primary pathological processes responsible for vision loss associated with neovascular AMD. [Wikipedia] | For the treatment of neovascular (wet) age-related macular degeneration. | Pegaptanib is a selective vascular endothelial growth factor (VEGF) antagonist. VEGF is a secreted protein that selectively binds and activates its receptors located primarily on the surface of vascular endothelial cells. VEGF induces angiogenesis, and increases vascular permeability and inflammation, all of which are thought to contribute to the progression of the neovascular (wet) form of age-related macular degeneration (AMD), a leading cause of blindness. VEGF has been implicated in blood retinal barrier breakdown and pathological ocular neovascularization. | Pegaptanib binds to the major pathological VEGF isoform, extracellular VEGF165, thereby inhibiting VEGF165 binding to its VEGF receptors. The inhibition of VEGF164, the rodent counterpart of human VEGF165, was effective at suppressing pathological neovascularization. | It is not known if pegaptanib is safe in pregnant women or if it is excreted in breast milk. Likewise, no studies have been done in the pediatric population. Most adverse events elated to the drug are ocular however non-ocular adverse events related to the drug or the injection procedure also occurred, among which headaches and rhinorrhoea appeared in more than 1% of patients. Pegaptanib is contraindicated when the patient has an ocular or periocular infection. | Based on preclinical data, pegaptanib is metabolized by endo- and exonucleases. | In animals, pegaptanib is slowly absorbed into the systemic circulation from the eye after intravitreous administration. | It is distributed into vitreous fluid, retina, aqueous fluid, and kidneys. As well, it has been shown to cross the placenta in mice but whether or not it crosses the placenta in humans is unknown. | NA | Intended for the prevention of respiratory distress syndrome (RDS) in premature infants at high risk for RDS. | NA | NA | NA | NA | Vascular endothelial growth factor A | Macugen | Gilead Sciences | Gilead Sciences | Macugen is indicated for the treatment of neovascular (wet) age-related macular degeneration. | NA | Macugen is supplied in a single-dose, pre-filled syringe and is formulated as a 3.47 mg/mL solution, measured as the free acid form of the oligonucleotide. The active ingredient is 0.3 mg of the free acid form of the oligonucleotide without polyethylene glycol, in a nominal volume of 90 μL. This dose is equivalent to 1.6 mg of pegaptanib sodium (pegylated oligonucleotide) or 0.32 mg when expressed as the sodium salt form of the oligonucleotide moiety. The product is a sterile, clear, preservative-free solution containing sodium chloride, monobasic sodium phosphate monohydrate, dibasic sodium phosphate heptahydrate, hydrochloric acid, and/or sodium hydroxide to adjust the pH and water for injection. | Sterile, aqueous solution containing pegaptanib sodium for intravitreous injection | Intravitreal Injection ONLY | Macugen 0.3 mg should be administered once every six weeks into the eye to be treated. | Ocular or Periocular Infections: Macugen is contraindicated in patients with ocular or periocular infections.Hypersensitivity to pegaptanib sodium or any other excipient in this product. | The most frequently reported adverse events in patients treated with Macugen 0.3 mg for up to two years were anterior chamber inflammation, blurred vision, cataract, conjunctival hemorrhage, corneal edema, eye discharge, eye irritation, eye pain, hypertension, increased intraocular pressure (IOP), ocular discomfort, punctate keratitis, reduced visual acuity, visual disturbance, vitreous floaters, and vitreous opacities; Ocular: blepharitis, conjunctivitis, photopsia, vitreous disorder.; Non-Ocular: bronchitis, diarrhea, dizziness, headache, nausea, urinary tract infection. | 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 |
| 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 |
| 10576 | Th1117 | Ipilimumab | >Th1117_Ipilimumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSSYTMHWVRQAPGKGLEWVTFISYDGNNKYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAIYYCARTGWLGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | C6572H10126N1734O2080S40 | 6.1-8.5 | NA | 80-90 ºC | 14.7 days | Recombinant, human monoclonal IgG1 kappa immunoglobin. It is an antineoplastic agent developed by Bristol-Myers Squibb and Medarex for the treatment of unresectable or metastatic melanoma in adults. Ipilimumab received FDA approval on March 25, 2011. | Ipilimumab is indicated for the treatment of unresectable or metastatic melanoma in adults. | The pharmacodynamics of Ipilimumab are not completely understood. In melanoma patients receiving Ipilimumab, the mean peripheral blood absolute lymphocyte counts (ALC) increased throughout the induction dosing period. This increase occurred in a dose-dependent fashion in Phase 2 studies. Ipilimumab given with or without gp100 at 3 mg/kg increased ALC throughout the induction dosing period, but no meaningful change in ALC occurred in the control group who received an investigational peptide vaccine alone. Furthermore, ipilimumab binds to CTLA-4 with high affinity (Kd = 5.24 ± 3.62 nM). As a result, ligands CD80 and CD86 are blocked from binding to CTLA-4 with a minimum EC50 value of 0.2 μg/mL. | Ipilimumab is a fully human IgG1K antibody that binds to CTLA-4 (cytotoxic T lymphocyte-associated antigen 4), a molecule on T-cells that is indicated for unresectable or metastatic melanoma. The absence or presence of CTLA-4 can augment or suppress the immune system's T-cell response in fighting disease. Ipilimumab is designed to block the activity of CTLA-4, thereby sustaining an active immune response in its attack on cancer cells. The proposed mechanism of action is indirect, and may be through T-cell - mediated anti-tumor immune responses. | Data regarding ipilumumab overdose is not readily available.[L12126] However, the most common adverse reactions to ipilumumab are fatigue, diarrhea, pruritus, rash, and colitis.[L12126] | The metabolism of ipilimumab does not involve the cytochrome P450 enzyme system.[L12126,L12642] Because ipilimumab is a protein, it is expected to be degraded into small peptides and amino acids by proteolytic enzymes.[A35122] | Cmax was 65.8µg/mL for 2-6 year olds, 70.1µg/mL for 6-<12 year olds, and 73.3µg/mL in patients 12 years and older.[L12126] Data regarding the AUC and Tmax of ipilumumab are not readily available.[A35118,L12126] | The volume of distribution at steady-state of ipilimumab is 7.21L.[A35118] | Ipilimumab has a clearance of 15.3 mL/hr.[A35118] Systemic clearance increases proportionally with body weight.[L12642] | Antineoplastic Agents and Monoclonal antibodies | CA2381770 | 8-Jul-2007 | 8-Aug-2020 | NA | Cytotoxic T-lymphocyte protein 4 | YERVOY | Bristol-Myers Squibb | Bristol-Myers Squibb | YERVOY is a human cytotoxic T-lymphocyte antigen 4 (CTLA-4)-blocking antibody indicated for the treatment of unresectable or metastatic melanoma | NA | It is supplied in single-use vials of 50 mg/10 mL and 200 mg/40 mL. Each milliliter contains 5 mg of ipilimumab and the following inactive ingredients: diethylene triamine pentaacetic acid (DTPA) (0.04 mg), mannitol (10 mg), polysorbate 80 (vegetable origin) (0.1 mg), sodium chloride (5.85 mg), tris hydrochloride (3.15 mg), and Water for Injection, USP at a pH of 7. | Sterile, preservative-free, clear to slightly opalescent, colorless to pale-yellow solution | Intravenous | The recommended dose of YERVOY is 3 mg/kg administered intravenously over 90 minutes every 3 weeks for a total of 4 doses. | Immune-mediated adverse reactions: Permanently discontinue for severe reactions. Less than 7.5 mg prednisone or equivalent per day is administered or systemic high-dose corticosteroids are adminstered for severe, persistent, or recurring immune-mediated reactions. | Most common adverse reactions are fatigue, diarrhea, pruritus, rash, and colitis. | Link | 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 |
| 10598 | Th1123 | Denosumab | >Th1123_Denosumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYAMSWVRQAPGKGLEWVSGITGSGGSTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKDPGTTVIMSWFDPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144700 | C6404H9912N1724O2004S50 | NA | NA | NA | 25.4 days | Novel, fully human IgG2 monoclonal antibody, specific to receptor activator of nuclear factor kappa-B ligand (RANKL). It suppresses bone resorption markers in patients suffering from metastatic tumors and is being investigated in multiple clinical trials for the prevention and treatment of bone metastases. Each light chain consists of 215 amino acids and the heavy chain consists of 448 amino acids. FDA approved on June 1, 2010. | Prolia is indicated for the treatment of postmenopausal women with osteoporosis at high risk for fracture. It reduces the incidence of vertebral, nonvertebral, and hip fractures. Prolia is also indicated as a treatment to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer. It can also be used in men with osteoporosis at high risk for fracture or in men receiving androgen deprivation therapy for nonmetastatic prostate cancer to increase bone mass. Xgeva is indicated for the prevention of skeletal-related events in patients with bone metastases from solid tumors. | In clinical studies, treatment with 60 mg of Prolia resulted in reduction in the bone resorption marker serum type 1 C-telopeptide (CTX) by approximately 85% by 3 days. Consistent with the physiological coupling of bone formation and resorption in skeletal remodeling, subsequent reductions in bone formation markers (i.e. osteocalcin and procollagen type 1 N-terminal peptide [PlNP]) were observed starting 1 month after the first dose of Prolia. | Denosumab is designed to target RANKL (RANK ligand), a protein that acts as the primary signal to promote bone removal/resorption. In many bone loss conditions, RANKL overwhelms the body's natural defense against bone destruction. Denosumab prevents RANKL from activating its receptor, RANK, on the surface of osteoclasts and their precursors. Prevention of the RANKL/RANK interaction inhibits osteoclast formation, function, and survival, thereby decreasing bone resorption and increasing bone mass and strength in both cortical and trabecular bone. | In patients with postmenopausal osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, pain in extremity, hypercholesterolemia, musculoskeletal pain, and cystitis. Pancreatitis has been reported in clinical trials. In male patients with osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, arthralgia, and nasopharyngitis. In patients experiencing bone loss due to hormone ablation for cancer, the most common adverse reactions (= 10% and more common than placebo) were: arthralgia and back pain. Pain in extremity and musculoskeletal pain have also been reported in clinical trials | NA | When 60 mg of denosumab was subcutaneously administered to healthy subjects after fasting for 12 hours, the pharmacokinetic parameters are as follows: Cmax = 6.75 mcg/mL; Tmax= 10 days (range of 3 to 21 days); AUC (0-16 weeks) = 316 mcg•day/mL. Denosumab does not accumulate following multiple doses once every 6 months. The pharmacokinetics of denosumab were not affected by the formation of antibodies. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Blood Proteins,Bone Density Conservation Agents,Cancer immunotherapy,Drugs Affecting Bone Structure and Mineralization,Drugs for Treatment of Bone Diseases,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Musculo-Skeletal System,Proteins,RANK Ligand Blocking Activity,RANK Ligand Inhibitor,Serum Globulins | CA2257247 | 9-Nov-2012 | 15-04-2018 | NA | Tumor necrosis factor ligand superfamily member 11 | Xgeva | Amgen. | Amgen. | Bone Metastasis From Solid Tumors, Giant Cell Tumor Of Bone, Hypercalcemia Of Malignancy | NA | Each single-use vial of Xgeva contains 120 mg denosumab, acetate (18 mM), sorbitol (4.6%), Water for Injection (USP), and sodium hydroxide to a pH of 5.2 | Sterile, preservative-free, clear, colorless to pale yellow solution | NA | Bone Metastasis From Solid Tumors: The recommended dose of Xgeva is 120 mg administered as a subcutaneous injection every 4 weeks. Administer calcium and vitamin D as necessary to treat or prevent hypocalcemia.; Giant Cell Tumor Of Bone: The recommended dose of Xgeva is 120 mg administered every 4 weeks with additional 120 mg doses on Days 8 and 15 of the first month of therapy. Administer calcium and vitamin D as necessary to treat or prevent hypocalcemia.; Hypercalcemia Of Malignancy: The recommended dose of Xgeva is 120 mg administered every 4 weeks with additional 120 mg doses on Days 8 and 15 of the first month of therapy. | Xgeva is not indicated for the prevention of skeletal-related events in patients with multiple myeloma. | Hypocalcemia, Osteonecrosis of the Jaw. | Link | NA | NA |
| 10599 | Th1123 | Denosumab | >Th1123_Denosumab EVQLLESGGGLVQPGGSLRLSCAASGFTFSSYAMSWVRQAPGKGLEWVSGITGSGGSTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYYCAKDPGTTVIMSWFDPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144700 | C6404H9912N1724O2004S50 | NA | NA | NA | 25.4 days | Novel, fully human IgG2 monoclonal antibody, specific to receptor activator of nuclear factor kappa-B ligand (RANKL). It suppresses bone resorption markers in patients suffering from metastatic tumors and is being investigated in multiple clinical trials for the prevention and treatment of bone metastases. Each light chain consists of 215 amino acids and the heavy chain consists of 448 amino acids. FDA approved on June 1, 2010. | Prolia is indicated for the treatment of postmenopausal women with osteoporosis at high risk for fracture. It reduces the incidence of vertebral, nonvertebral, and hip fractures. Prolia is also indicated as a treatment to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer. It can also be used in men with osteoporosis at high risk for fracture or in men receiving androgen deprivation therapy for nonmetastatic prostate cancer to increase bone mass. Xgeva is indicated for the prevention of skeletal-related events in patients with bone metastases from solid tumors. | In clinical studies, treatment with 60 mg of Prolia resulted in reduction in the bone resorption marker serum type 1 C-telopeptide (CTX) by approximately 85% by 3 days. Consistent with the physiological coupling of bone formation and resorption in skeletal remodeling, subsequent reductions in bone formation markers (i.e. osteocalcin and procollagen type 1 N-terminal peptide [PlNP]) were observed starting 1 month after the first dose of Prolia. | Denosumab is designed to target RANKL (RANK ligand), a protein that acts as the primary signal to promote bone removal/resorption. In many bone loss conditions, RANKL overwhelms the body's natural defense against bone destruction. Denosumab prevents RANKL from activating its receptor, RANK, on the surface of osteoclasts and their precursors. Prevention of the RANKL/RANK interaction inhibits osteoclast formation, function, and survival, thereby decreasing bone resorption and increasing bone mass and strength in both cortical and trabecular bone. | In patients with postmenopausal osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, pain in extremity, hypercholesterolemia, musculoskeletal pain, and cystitis. Pancreatitis has been reported in clinical trials. In male patients with osteoporosis, the most common adverse reactions (> 5% and more common than placebo) were: back pain, arthralgia, and nasopharyngitis. In patients experiencing bone loss due to hormone ablation for cancer, the most common adverse reactions (= 10% and more common than placebo) were: arthralgia and back pain. Pain in extremity and musculoskeletal pain have also been reported in clinical trials | NA | When 60 mg of denosumab was subcutaneously administered to healthy subjects after fasting for 12 hours, the pharmacokinetic parameters are as follows: Cmax = 6.75 mcg/mL; Tmax= 10 days (range of 3 to 21 days); AUC (0-16 weeks) = 316 mcg•day/mL. Denosumab does not accumulate following multiple doses once every 6 months. The pharmacokinetics of denosumab were not affected by the formation of antibodies. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Blood Proteins,Bone Density Conservation Agents,Cancer immunotherapy,Drugs Affecting Bone Structure and Mineralization,Drugs for Treatment of Bone Diseases,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Musculo-Skeletal System,Proteins,RANK Ligand Blocking Activity,RANK Ligand Inhibitor,Serum Globulins | CA2274987 | 24-01-2012 | 22-12-2017 | NA | Tumor necrosis factor ligand superfamily member 11 | Prolia | Amgen. | Amgen. | Treatment Of Postmenopausal Women With Osteoporosis At High Risk For Fracture,Treatment To Increase Bone Mass In Men With Osteoporosis, Treatment Of Bone Loss In Men Receiving Androgen Deprivation Therapy For Prostate Cancer, Treatment Of Bone Loss In Women Receiving Adjuvant Aromatase Inhibitor Therapy For Breast Cancer | NA | Each 1 mL single-use prefilled syringe of Prolia contains 60 mg denosumab (60 mg/mL solution), 4.7% sorbitol, 17 mM acetate, 0.01% polysorbate 20, Water for Injection (USP), and sodium hydroxide to a pH of 5.2. Each 1 mL single-use vial of Prolia contains 60 mg denosumab (60 mg/mL solution), 4.7% sorbitol, 17 mM acetate, Water for Injection (USP), and sodium hydroxide to a pH of 5.2 | Sterile, preservative-free, clear, colorless to pale yellow solution | NA | NA | Hypocalcemia. Pregnancy. Hypersensitivity | Hypocalcemia, Serious Infections, Dermatologic Adverse Reactions, Osteonecrosis of the Jaw, Atypical Subtrochanteric and Diaphyseal Femoral Fractures | 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 |
| 10612 | 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 Aria | NA | NA | rheumatoid arthritis. | NA | SIMPONI ARIA does not contain preservatives, natural rubber or latex. The solution is colorless to light yellow with a pH of approximately 5.5. Each 4 mL vial of SIMPONI ARIA contains 50 mg golimumab, 9.5 mM histidine, 4.5% (w/v) sorbitol, and 0.015% (w/v) polysorbate 80. | The SIMPONI ARIA drug product is a sterile concentrated solution of the golimumab antibody supplied in a 4 mL glass vial for Intravenous infusion. | Intravenous infusion | 2 mg per kg | NA | sepsis, pneumonia, cellulitis, abscess, opportunistic infections, tuberculosis (TB), and invasive fungal infections, Malignancies, Liver Enzyme Elevations, Autoimmune Disorders And Autoantibodies | Link | NA | NA |
| 10628 | 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 (Nasal Spray Solution) | Sanofi-Aventis | Sanofi-Aventis | Treatment of endometriosis – an illness where some of the tissues that line the womb are found elsewhere in the body. As part of a treatment for infertility – it works by stopping the natural production of hormones that control ovulation. Synthetic hormones are then used to artificially stimulate ovulation. Your doctor should give you more information about how your treatment works | NA | Each spray dose contains 150 micrograms of the active substance, buserelin as buserelin acetate. The other ingredients are citric acid, sodium citrate, sodium chloride and benzalkonium chloride in aqueous solution | 150 micrograms Nasal Spray Solution | Nasal spray | Treatment of endometriosis: The usual dose is one spray in each nostril three times each day. This is to make a total daily dose of 900 micrograms; Use the spray in the morning, at mid-day and in the evening; Treatment will be for a maximum of 6 months;Treatment should be started on the first or second day of your menstrual period.This is to lower the chances you may be pregnant. Your doctor may perform a pregnancy test if there is any doubt; You may get a menstrual period after the first few weeks of using this medicine. You may also carry on getting breakthrough bleeding or spotting As part of treatment for infertility. | Do not use this medicine and tell your doctor if: You are allergic (hypersensitive) to buserelin or goserelin, benzalkonium chloride or other ingredients of Suprecur Nasal Spray. Signs of an allergic reaction include: a rash, swallowing or breathing problems, swelling of your lips, face, throat or tongue; You have abnormal menstrual bleeding where the cause is not endometriosis; You have a tumour that is not affected by hormones; You are pregnant or breast-feeding.This medicine is for use in women only. If you are not sure, talk to your doctor or pharmacist before using Suprecur Nasal Spray. | Allergic reaction, diarrhoea, pain, swelling or a feeling of tension in stomach, weight gain, difficulty in breathing, decreased urination. These could be signs of a serious side effect called ’Ovarian Hyperstimulation Syndrome’. This is more likely if you are taking other hormones as well as Suprecur Nasal Spray (buserelin) as part of a treatment for infertility. | Link | NA | NA |
| 10643 | Th1133 | Aflibercept | >Th1133_Aflibercept SDTGRPFVEMYSEIPEIIHMTEGRELVIPCRVTSPNITVTLKKFPLDTLIPDGKRIIWDSRKGFIISNATYKEIGLLTCEATVNGHLYKTNYLTHRQTNTIIDVVLSPSHGIELSVGEKLVLNCTARTELNVGIDFNWEYPSSKHQHKKLVNRDLKTQSGSEMKKFLSTLTIDGVTRSDQGLYTCAASSGLMTKKNSTFVRVHEKDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | 115000 | C4318H6788N1164O1304S32 | NA | NA | NA | Intravitreal half life - 7.13 days | Aflibercept is a vascular endothelial growth factor (VEGF) inhibitor. It is a recombinant dimeric fusion glycoprotein that comprises (VEGF) binding portions from the extracellular domains of human VEGF receptors 1 and 2, this is fused to the Fc portion of human IgG1. It contains approximately 15% glycosylation to give a total molecular weight of 115 kDa (protein part = 96.9 kDa). It has 5 putative N-glycosylation sites on each polypeptide chain and the attached carbohydrates exhibit some degree of chain heterogeneity, including heterogeneity in terminal sialic acid residues, except at the site associated with the Fc domain, which is unsialylated. | The opthalmic agent is used for the treatment of neovascular (wet) age-related mascular degeneration (AMD) and macular edema following central retinal vein occulsion (CRVO). The systemic injection, known as ziv-aflibercept, in combination with 5-fluorouracil, leucovorin, irinotecan-(FOLFIRI), is for the treatment of metastatic colorectal cancer that is resistant to or progressed following treatment with oxaliplatin. | Compared to other anti-VEGF drugs like bevacizumab and ranibizumab, aflibercept has a higher binding affinity to VEGF-A (Kd = 0.5 pM). | Ablibercept is a recombinant fusion protein that acts as a decoy receptor for the ligands, vascular endothelial growth factor-A (VEGF-A) and placental growth factor (PIGF). It prevents these ligands to binding to endothelial receptors, VEGFR-1 and VEGFR-2, to suppress neovascularization and decrease vascular permeability. This ultimately will slow vision loss or the progression of metastatic colorectal cancer. | For all intravitreal VEGF inhibitors, there is increased risk of stroke and myocardial infarction. An increase in intraocular pressure may also occur. When used intravenously, most common adverse reactions were leukopenia, diarrhea, neutropenia, proteinuria, AST increased, stomatitis, fatigue, thrombocytopenia, ALT increased, hypertension, weight decreased, decreased appetite, epistaxis, abdominal pain, dysphonia, serum creatinine increased, and headache. | Because aflibercept is a protein, it is expected to be broken down via proteolysis into smaller peptides and amino acids. The cytochrome P450 enzyme system is not involved in the metabolism of aflibercept. | In patients with wet AMD and CRVO, the mean peak plasma concentration (Cmax) was 0.02 mcg/mL and 0.05 mcg/mL respectively. These concentrations were reached in 1 to 3 days. Aflibercept did not accumulate when administered as repeated doses intravitreally every 4 weeks. | After intravenous injection of aflibercept, the volume of distribution is 6 L. | When cancer patients were given 2-9 mg/kg every 2 or 3 week; 1 hour IV infusion of aflibercept the typical estimated clearances were as follows: CL of free aflibercept (CLf) = 0.88 L/day; CL of bound aflibercept (CLf) = 0.19 L/day; Patients clear free aflibercept faster if they had low albumin or high alkaline phosphatase levels. | Antineoplastic Agents and Ophthalmics | US7306799 | 12-Nov-2007 | 23-05-2020 | NA | Vascular endothelial growth factor A,Placenta growth factor,Vascular endothelial growth factor B | Eylea | Regeneron Pharmaceuticals | Regeneron Pharmaceuticals | Neovascular (Wet) Age-Related Macular Degeneration (AMD), Macular Edema Following Central Retinal Vein Occlusion (CRVO) | NA | EYLEA is supplied as a preservative-free, sterile, aqueous solution in a single-use, glass vial designed to deliver 0.05 mL (50 microliters) of EYLEA (40 mg/mL in 10 mM sodium phosphate, 40 mM sodium chloride, 0.03% polysorbate 20, and 5% sucrose, pH 6.2). | EYLEA is a sterile, clear, and colorless to pale yellow solution. | Intravitreal Injection | The recommended dose for EYLEA is 2 mg (0.05 mL or 50 microliters) administered by intravitreal injection every 4 weeks (monthly) for the first 12 weeks (3 months), followed by 2 mg (0.05 mL) via intravitreal injection once every 8 weeks (2 months). | ocular or periocular infections, active intraocular inflammation, Hypersensitivity | Endophthalmitis and retinal detachments, Increased intraocular pressure, Thromboembolic events | Link | NA | NA |
| 10644 | Th1133 | Aflibercept | >Th1133_Aflibercept SDTGRPFVEMYSEIPEIIHMTEGRELVIPCRVTSPNITVTLKKFPLDTLIPDGKRIIWDSRKGFIISNATYKEIGLLTCEATVNGHLYKTNYLTHRQTNTIIDVVLSPSHGIELSVGEKLVLNCTARTELNVGIDFNWEYPSSKHQHKKLVNRDLKTQSGSEMKKFLSTLTIDGVTRSDQGLYTCAASSGLMTKKNSTFVRVHEKDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | 115000 | C4318H6788N1164O1304S32 | NA | NA | NA | Intravitreal half life - 7.13 days | Aflibercept is a vascular endothelial growth factor (VEGF) inhibitor. It is a recombinant dimeric fusion glycoprotein that comprises (VEGF) binding portions from the extracellular domains of human VEGF receptors 1 and 2, this is fused to the Fc portion of human IgG1. It contains approximately 15% glycosylation to give a total molecular weight of 115 kDa (protein part = 96.9 kDa). It has 5 putative N-glycosylation sites on each polypeptide chain and the attached carbohydrates exhibit some degree of chain heterogeneity, including heterogeneity in terminal sialic acid residues, except at the site associated with the Fc domain, which is unsialylated | The opthalmic agent is used for the treatment of neovascular (wet) age-related mascular degeneration (AMD) and macular edema following central retinal vein occulsion (CRVO). The systemic injection, known as ziv-aflibercept, in combination with 5-fluorouracil, leucovorin, irinotecan-(FOLFIRI), is for the treatment of metastatic colorectal cancer that is resistant to or progressed following treatment with oxaliplatin. | Compared to other anti-VEGF drugs like bevacizumab and ranibizumab, aflibercept has a higher binding affinity to VEGF-A (Kd = 0.5 pM). | Ablibercept is a recombinant fusion protein that acts as a decoy receptor for the ligands, vascular endothelial growth factor-A (VEGF-A) and placental growth factor (PIGF). It prevents these ligands to binding to endothelial receptors, VEGFR-1 and VEGFR-2, to suppress neovascularization and decrease vascular permeability. This ultimately will slow vision loss or the progression of metastatic colorectal cancer. | For all intravitreal VEGF inhibitors, there is increased risk of stroke and myocardial infarction. An increase in intraocular pressure may also occur. When used intravenously, most common adverse reactions were leukopenia, diarrhea, neutropenia, proteinuria, AST increased, stomatitis, fatigue, thrombocytopenia, ALT increased, hypertension, weight decreased, decreased appetite, epistaxis, abdominal pain, dysphonia, serum creatinine increased, and headache. | Because aflibercept is a protein, it is expected to be broken down via proteolysis into smaller peptides and amino acids. The cytochrome P450 enzyme system is not involved in the metabolism of aflibercept. | In patients with wet AMD and CRVO, the mean peak plasma concentration (Cmax) was 0.02 mcg/mL and 0.05 mcg/mL respectively. These concentrations were reached in 1 to 3 days. Aflibercept did not accumulate when administered as repeated doses intravitreally every 4 weeks. | After intravenous injection of aflibercept, the volume of distribution is 6 L. | When cancer patients were given 2-9 mg/kg every 2 or 3 week; 1 hour IV infusion of aflibercept the typical estimated clearances were as follows: CL of free aflibercept (CLf) = 0.88 L/day; CL of bound aflibercept (CLf) = 0.19 L/day; Patients clear free aflibercept faster if they had low albumin or high alkaline phosphatase levels. | Antineoplastic Agents and Ophthalmics | US7531173 | 5-Dec-2009 | 2-Feb-2026 | NA | Vascular endothelial growth factor A,Placenta growth factor,Vascular endothelial growth factor B | Zaltrap | Sanofi and Regeneron Pharmaceuticals, Inc. | Sanofi and Regeneron Pharmaceuticals, Inc. | metastatic colorectal cancer (mCRC) that is resistant to or has progressed following an oxaliplatin-containing regimen | NA | ZALTRAP is supplied in single-use vials of 100 mg per 4 ml and 200 mg per 8 ml formulated as 25 mg/mL ziv-aflibercept in polysorbate 20 (0.1%), sodium chloride (100 mM), sodium citrate (5 mM), sodium phosphate (5 mM), and sucrose (20%), in Water for Injection USP, at a pH of 6.2. | ZALTRAP is a sterile, clear, colorless to pale yellow, non-pyrogenic, preservative-free, solution for administration by Intravenous infusion. | Intravenous infusion | 4 mg per kg as an intravenous (IV) infusion over 1 hour every two weeks. | NA | Hemorrhage, Gastrointestinal, Compromised Wound Healing, Fistula Formation, Hypertension, Arterial Thromboembolic Events, Proteinuria, Neutropenia and Neutropenic Complications, Diarrhea and Dehydration, Reversible Posterior Leukoencephalopathy Syndrome | Link | NA | NA |
| 10650 | Th1135 | Ocriplasmin | >Th1135_Ocriplasmin APSFDCGKPQVEPKKCPGR | 27250 | C1214H1890N338O348S14 | NA | NA | NA | NA | Ocriplasmin is a recombinant (derived from Pichia pastoris) truncated form of human plasmin with a molecular weight of 27.2 kDa. It is a 249 amino acid protein that is made up of two peptide chains. Agent for pharmacologic vitreolysis; thrombolytic agent. FDA approved on October 17, 2012. | Ocriplasmin is a proteolytic enzyme indicated for the treatment for symptomatic vitreomacular adhesion. | NA | Ocriplasmin has proteolytic activity against protein components of the vitreous body and the vitreoretinal interface (VRI) (e.g. laminin, fibronectin and collagen), thereby dissolving the protein matrix responsible for the vitreomacular adhesion (VMA). | The most commonly reported reactions (= 5%) in patients treated with ocriplasmin were vitreous floaters, conjunctival hemorrhage, eye pain, photopsia, blurred vision, macular hole, reduced visual acuity, visual impairment, and retinal edema. | Ocriplasmin is quickly inactivated by protease inhibitor a2-antiplasmin or a2-macroglobulin. | Because of the small dose administered (0.125 mg), ocriplasmin is not expected to be in the systemic circulation following injection. Within 30 minutes after injection, levels of ocriplasmin in the vitreous are 12 mcg/mL. 24 hours after injection, levels in the virtreous are 0.5 mcg/mL | NA | NA | Ophthalmics | NA | NA | NA | NA | Fibronectin,Alpha-2-macroglobulin,Alpha-2-antiplasmin | Jetrea | ThromboGenics NV | ThromboGenics NV | symptomatic vitreomacular adhesion. | NA | Each vial contains 0.5 mg ocriplasmin (active) and 0.21 mg citric acid, 0.75 mg mannitol, sodium hydroxide (for pH adjustment) and water for injection. The pH of the solution is 3.1. | JETREA is a Sterile, clear and colorless solution with no preservatives | Intravitreal Injection | 0.125 mg (0.1 mL of the diluted solution) | NA | Decreased Vision, Intravitreal Injection Procedure Associated Effects, Potential for Lens Subluxation, Retinal Breaks | 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 |
| 10663 | Th1141 | Epoetin zeta | >Th1141_Epoetin_zeta APPRLICDSRVLERYLLEAKEAENITTGCAEHCSLNENITVPDTKVNFYAWKRMEVGQQAVEVWQGLALLSEAVLRGQALLVNSSQPWEPLQLHVDKAVSGLRSLTTLLRALGAQKEAISPPDAASAAPLRTITADTFRKLFRVYSNFLRGKLKLYTGEACRTGDR | 18396.1 (unglycosylated), 30600 (glycosylated) | C815H1317N233O241S5 | 8.75 | NA | NA | For subcutaneous dose: 7.37 hours | Recombinant (CHO cell derived) erythropoietin with a sequence identicle to the Epoietin alfa. The molecular weight of the glycosylated protein is 30.6 kDa, of which nearly 40% is contributed by carbohydrates. The oligosaccharide chains are subject to posttranslational modifications and display heterogeneity. | For use in the treatment of symptomatic anaemia associated with chronic renal failure (CRF) in adult and paediatric patients. Also for use in the treatment of anaemia and reduction of transfusion requirements in adult patients receiving chemotherapy for solid tumours, malignant lymphoma or multiple myeloma, and at risk of transfusion as assessed by the patient's general status (e.g. cardiovascular status, pre-existing anaemia at the start of chemotherapy). Also for used to increase the yield of autologous blood from patients in a predonation program. When administered subcutaneously, Epoetin Zeta is equivalent to Epoetin Alfa in terms of clinical effectiveness. | Used in the treatment of anemia. Involved in the regulation of erythrocyte differentiation and the 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. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Erythropoietin receptor | Retacrit | Norbitec | Norbitec | Treatment of anaemia associated with chronic renal failure in adult and paediatric patients on haemodialysis and adult patients on peritoneal dialysis. Treatment of severe anaemia of renal origin accompanied by clinical symptoms in adult patients with renal insufficiency not yet undergoing dialysis. Treatment of anaemia and reduction of transfusion requirements in adult patients receiving chemotherapy for solid tumours, malignant lymphoma or multiple myeloma, and at risk of transfusion as assessed by the patient's general status (e.g. cardiovascular status, pre-existing anaemia at the start of chemotherapy). Retacrit can be used to increase the yield of autologous blood from patients in a predonation programme. Its use in this indication must be balanced against the reported risk of thromboembolic events. Treatment should only be given to patients with moderate anaemia (haemoglobin (Hb) 10-13 g/dl [6.2-8.1 mmol/l], no iron deficiency), if blood saving procedures are not available or insufficient when the scheduled major elective surgery requires a large volume of blood (4 or more units of blood for females or 5 or more units for males). | NA | The drug product is presented as a solution for injection in pre-filled syringes in the following strengths: 3,333 IU/ml (presentation of 0.3, 0.6 and 0.9 ml), 10,000 IU/ml (presentations of 0.4, 0.5, 0.6, 0.8 and 1 ml) and 40,000 IU/ml (presentations of 0.5, 0.75 and 1 ml), with all strengths exhibiting the same qualitative composition. | Retacrit [epoetin zeta (INN)] solution for injection in pre-filled syringes contains recombinant human erythropoietin (rhu-EPO, epoetin) as drug substance and water for injection, sodium monohydrogen phosphate, sodium dihydrogen phosphate, sodium chloride, calcium chloride, polysorbate 20, glycine, | NA | 50 IU/kg (International Units per kilogram), 3 times a week. If the solution is given into a vein, it should be injected over 1-5 minutes. | Hypersensitivity to the active substance or to any of the excipients. Patients who develop Pure Red Cell Aplasia (PRCA) following treatment with any erythropoietin must not receive Retacrit or any other erythropoietin, Uncontrolled hypertension, In the indication increasing the yield of autologous blood: myocardial infarction or stroke in the month preceding treatment, unstable angina pectoris, increased risk of deep venous thrombosis such as history of venous thromboembolic disease. Patients who for any reason cannot receive adequate antithrombotic prophylaxis. | Flu-like symptoms, headache, joint pain, feeling of weakness, tiredness and dizziness. Respiratory tract congestion, such as stuffy nose and sore throat, has been reported in patients with kidney disease not yet on dialysis. Increased blood pressure. Chest pain, breathlessness, painful swelling in the leg which may be symptoms of blood clots (pulmonary embolism, deep vein thrombosis). Stroke (insufficient blood supply to the brain, which may lead to inability to move one or more limbs on one side of the body, inability to understand or formulate speech, or an inability to see one side of the visual field). Skin rash and swelling around the eyes (oedema), which may result from an allergic reaction. Blood clot in an artificial kidney. | Link | NA | NA |
| 10674 | Th1147 | Natalizumab | NA | NA | NA | NA | NA | 61 (FAB fr | 11 ± 4 days | Humanized IgG4k monoclonal antibody produced in murine myeloma cells. Natalizumab contains human framework regions and the complementarity-determining regions of a murine antibody that binds to a4-integrin. Natalizumab was voluntarily withdrawn from U.S. market because of risk of Progressive multifocal leukoencephalopathy (PML). It was returned to market July, 2006. | For treatment of multiple sclerosis. | In multiple sclerosis, lesions are believed to occur when activated inflammatory cells, including T-lymphocytes, cross the blood-brain barrier (BBB). Leukocyte migration across the BBB involves interaction between adhesion molecules on inflammatory cells, and their counter-receptors present on endothelial cells of the vessel wall. The clinical effect of natalizumab in multiple sclerosis may be a secondary result of its blockade of the molecular interaction of a 4b 1-integrin expressed by inflammatory cells with VCAM-1 on vascular endothelial cells, and with CS-1 and/or osteopontin expressed by parenchymal cells in the brain. α4-integrin is required for white blood cells to move into organs, therefore, natalizumab prevents these immune cells from crossing blood vessel walls to reach affected organs thereby decreasing inflamation. | Binds to the α4-subunit of α4b 1 and α4b 7 integrins expressed on the surface of all leukocytes except neutrophils, and inhibits the α4-mediated adhesion of leukocytes to their counter-receptor(s). | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to leukocytes. | NA | 5.7 ± 1.9 L [Multiple Sclerosis (MS) Patients, 5.2 ± 2.8 L [Crohn's Disease (CD) Patients] | * 16 +/- 5 mL/hour [patients with MS who did not have PML receiving the repeat IV administration of a 300 mg dose] * 22 +/- 22 mL/hour [Patients with Crohn's Disease receiving the repeat IV administration of a 300 mg dose] | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic and Immunomodulating Agents,Blood Proteins,Globulins,Immunoglobulins,Immunologic Factors,Immunomodulatory Agents,Immunoproteins,Immunosuppressive Agents,Integrin Receptor Antagonist,Proteins,Selective Immunosuppressants,Serum Globulins | NA | NA | NA | NA | Integrin alpha-4,Low affinity immunoglobulin gamma Fc region receptor III-B,Intercellular adhesion molecule 1,High affinity immunoglobulin gamma Fc receptor I | NA | Biogen Idec Canada Inc | Biogen Idec Canada Inc | NA | NA | NA | Solution | NA | NA | NA | NA | 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 |
| 10695 | Th1158 | Aprotinin | >Th1158_Aprotinin RPDFCLEPPYTGPCKARIIRYFYNAKAGLCQTFVYGGCRAKRNNFKSAEDCMRTCGGA | 6511.439 | C284H432N84O79S7 | NA | NA | >100 | Plasma half life: 150 minutes, Elimination half life: 10hrs | Aprotinin, also known as bovine pancreatic trypsin inhibitor, BPTI (Trasylol, Bayer) is a protein, that is used as medication administered by injection to reduce bleeding during complex surgery, such as heart and liver surgery. Its main effect is the slowing down of fibrinolysis, the process that leads to the breakdown of blood clots. The aim in its use is to decrease the need for blood transfusions during surgery, as well as end-organ damage due to hypotension (low blood pressure) as a result of marked blood loss. | For prophylactic use to reduce perioperative blood loss and the need for blood transfusion in patients undergoing cardiopulmonary bypass in the course of coronary artery bypass graft surgery who are at an increased risk for blood loss and blood transfusion. | Aprotinin is a broad spectrum protease inhibitor which modulates the systemic inflammatory response (SIR) associated with cardiopulmonary bypass (CPB) surgery. SIR results in the interrelated activation of the hemostatic, fibrinolytic, cellular and humoral inflammatory systems. Aprotinin, through its inhibition of multiple mediators [e.g., kallikrein, plasmin] results in the attenuation of inflammatory responses, fibrinolysis, and thrombin generation. Aprotinin inhibits pro-inflammatory cytokine release and maintains glycoprotein homeostasis. In platelets, aprotinin reduces glycoprotein loss (e.g., GpIb, GpIIb/IIIa), while in granulocytes it prevents the expression of pro-inflammatory adhesive glycoproteins. | Aprotinin inhibits several serine proteases, specifically trypsin, chymotrypsin and plasmin at a concentration of about 125,000 IU/ml, and kallikrein at 300,000 IU/ml. Its action on kallikrein leads to the inhibition of the formation of factor XIIa. As a result, both the intrinsic pathway of coagulation and fibrinolysis are inhibited. Its action on plasmin independently slows fibrinolysis. | NA | Aprotinin is slowly degraded by lysosomal enzymes. | 100% (IV) | NA | NA | NA | US5198534 | NA | NA | Captopril- aprotinin infused intravenously in a dose of 2 million KIU over two hours blocked the acute hypotensive effect of 100mg of captopril. | Trypsin-1,Chymotrypsinogen B,Plasminogen,Kallikrein-1 | Trasylol | Bayer Pharmaceuticals | Bayer Pharmaceuticals | Trasylol (aprotinin) is indicated for prophylactic use to reduce perioperative blood loss and the need for blood transfusion in patients undergoing cardiopulmonary bypass in the course of coronary artery bypass graft surgery who are at an increased risk for blood loss and blood transfusion. | NA | Each milliliter contains 10,000 KIU (Kallikrein Inhibitor Units) (1.4 mg/mL) and 9 mg sodium chloride in water for injection. Hydrochloric acid and/or sodium hydroxide is used to adjust the pH to 4.5-6.5. | It is supplied as a clear, colorless, sterile isotonic solution | Intravenous administration | dosage is given as two regimens: Regimen A and Regimen B intial dose is same 1ml (1.4mg or 10000 KIU) but loading dose and PumpPrime dose is 200ml in case of regimen A and 100ml in case of regimen B, and constant infusion rate is 50ml/hr in A and 25ml/hr in B. | Administration of Trasylol (aprotinin) to patients with a known or suspected previous aprotinin exposure during the last 12 months is contraindicated. For patients with known or suspected history of exposure to aprotinin greater than 12 months previously. | Ventricular fibrillation, heart arrest, bradycardia, congestive heart failure, hemorrhage, bundle branch block, myocardial ischemia, ventricular tachycardia, heart block, pericardial effusion, ventricular arrhythmia, shock, pulmonary hypertension. Hyperglycemia, hypokalemia, hypervolemia, acidosis. Arthralgia. Agitation, dizziness, anxiety, convulsion. Pneumonia, apnea, increased cough, lung edema. | 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 |
| 10712 | Th1164 | Antithrombin Alfa | NA | 57,215 | C2191H3451N583O656S19 | NA | NA | NA | 11.6 (84.7) for 50 IU/KG to17.7 (60.9) for 100IU/KG | Antithrombin (Recombinant) and plasma-derived antithrombin both contain six cysteine residues forming three disulphide bridges and 3-4 N-linked carbohydrate moieties. The glycosylation profile of antithrombin (Recombinant) is different from plasma-derived antithrombin, which results in an increased heparin affinity. When assayed in the presence of excess of heparin the potency of the recombinant product is not different from that of plasma-derived product. | Indicated for the prevention of peri-operative and peri-partum thromboembolic events in hereditary antithrombin deficient patients | Hereditary AT deficiency causes an increased risk of venous thromboembolism (VTE). During high-risk situations such as surgery or trauma or for pregnant women, during the peripartum period, the risk of development of VTEs as compared to the normal population in these situations is increased by a factor 10 to 506,7. In hereditary antithrombin deficient patients ATryn restores (normalizes) plasma AT activity levels during peri-operative and peri-partum periods. | Antithrombin (AT) plays a central role in the regulation of hemostasis. AT is the principal inhibitor of thrombin and Factor Xa5, the serine proteases that play pivotal roles in blood coagulation. AT neutralizes the activity of thrombin and Factor Xa by forming a complex which is rapidly removed from the circulation. The ability of antithrombin to inhibit thrombin and Factor Xa can be enhanced by greater than 300 to 1000 fold when AT is bound to heparin. | Highest dose tested was 360mg/kg/day in rats resulted in transient limb swelling. | Not metabolized. | Given IV so not absorbed. | Dose of: 50IU/kg: 126.2 ml/kg 100IU/kg: 156.1 ml/kg Vd in hereditary deficient pregnant women in high risk situations had increased Vd of 14.3L. | Dose of: 50IU/kg: 9.6 ml/hr/kg 100IU/kg: 7.2 ml/hr/kg Cl in hereditary deficient pregnant women in high risk situations had increased Cl of 1.38L/h. | Anticoagulants,Decreased Coagulation Factor Activity,Factor Xa Inhibitors,Recombinant Antithrombin,Thrombin Inhibitors | NA | NA | NA | NA | Prothrombin,Coagulation factor X | Atryn | Gtc Biotherapeutics, Inc. | Gtc Biotherapeutics, Inc. | It is indicated for the prevention of peri-operative and peri-partum thromboembolic events in hereditary antithrombin deficient patients | NA | 1750 [iU]/1 | injection, powder, lyophilized, for solution | IV | The dosage is to be individualized based on the patient's pre-treatment functional AT activity level (expressed in percent of normal) and body weight (expressed in kilograms) and using therapeutic drug monitoring | NA | Hemorrhage (intra-abdominal, hemarthrosis and post procedural) | Link | NA | NA |
| 10713 | Th1164 | Antithrombin Alfa | NA | 57,215 | C2191H3451N583O656S20 | NA | NA | NA | 11.6 (84.7) for 50 IU/KG to17.7 (60.9) for 100IU/KG | Antithrombin (Recombinant) and plasma-derived antithrombin both contain six cysteine residues forming three disulphide bridges and 3-4 N-linked carbohydrate moieties. The glycosylation profile of antithrombin (Recombinant) is different from plasma-derived antithrombin, which results in an increased heparin affinity. When assayed in the presence of excess of heparin the potency of the recombinant product is not different from that of plasma-derived product. | Indicated for the prevention of peri-operative and peri-partum thromboembolic events in hereditary antithrombin deficient patients | Hereditary AT deficiency causes an increased risk of venous thromboembolism (VTE). During high-risk situations such as surgery or trauma or for pregnant women, during the peripartum period, the risk of development of VTEs as compared to the normal population in these situations is increased by a factor 10 to 506,7. In hereditary antithrombin deficient patients ATryn restores (normalizes) plasma AT activity levels during peri-operative and peri-partum periods. | Antithrombin (AT) plays a central role in the regulation of hemostasis. AT is the principal inhibitor of thrombin and Factor Xa5, the serine proteases that play pivotal roles in blood coagulation. AT neutralizes the activity of thrombin and Factor Xa by forming a complex which is rapidly removed from the circulation. The ability of antithrombin to inhibit thrombin and Factor Xa can be enhanced by greater than 300 to 1000 fold when AT is bound to heparin. | Highest dose tested was 360mg/kg/day in rats resulted in transient limb swelling. | Not metabolized. | Given IV so not absorbed. | Dose of: 50IU/kg: 126.2 ml/kg 100IU/kg: 156.1 ml/kg Vd in hereditary deficient pregnant women in high risk situations had increased Vd of 14.3L. | Dose of: 50IU/kg: 9.6 ml/hr/kg 100IU/kg: 7.2 ml/hr/kg Cl in hereditary deficient pregnant women in high risk situations had increased Cl of 1.38L/h. | Anticoagulants,Decreased Coagulation Factor Activity,Factor Xa Inhibitors,Recombinant Antithrombin,Thrombin Inhibitors | NA | NA | NA | NA | Prothrombin,Coagulation factor X | Atryn | R Evo Bioloigics, Inc. | R Evo Bioloigics, Inc. | It is indicated for the prevention of peri-operative and peri-partum thromboembolic events in hereditary antithrombin deficient patients | NA | 525 [iU]/mL | injection, powder, lyophilized, for solution | IV | The dosage is to be individualized based on the patient's pre-treatment functional AT activity level (expressed in percent of normal) and body weight (expressed in kilograms) and using therapeutic drug monitoring | NA | Hemorrhage (intra-abdominal, hemarthrosis and post procedural) | Link | NA | NA |
| 10716 | Th1165 | Antithrombin III human | NA | 58000 | NA | NA | NA | NA | 2.5 - 3.8 hs | A plasma alpha 2 glycoprotein that accounts for the major antithrombin activity of normal plasma and also inhibits several other enzymes. It is a member of the serpin superfamily. | Short-term replacement therapy for prevention or treatment of thromboembolism in selected patients with congenital antithrombin III deficiency at high risk for thromboembolism (i.e., those undergoing surgical or obstetrical procedures) or those with thromboembolism | It s the major plasma inhibitor of thrombin. Inactivation of thrombin by AT-III occurs by formation of a covalent bond resulting in an inactive 1:1 stoichiometric complex between the two, involving an interaction of the active serine of thrombin and an arginine reactive site on AT-III. AT-III is also capable of inactivating other components of the coagulation cascade including factors IXa, Xa, XIa, and XIIa, as well as plasmin. | Neutralizes serine proteinases such as thrombin, plasmin, and activated coagulation factors IX, X, XI, and XII; Principally neutralizes thrombin and activated coagulation factor X (Xa); Neutralization of factor Xa prevents thrombin generation (e.g., decreased formation of prothrombin fragment 1.2 [F1 and F2]); Neutralization of thrombin prevents conversion of fibrinogen to fibrin; lowly and irreversibly complexes stoichiometrically with these coagulation factors; such reactions are rapid in presence of endogenous heparin-like proteoglycans or exogenous heparin; Inhibits thrombus formation. | NA | <5% metabolized to low molecular weight breakdown products. | Therapeutic target plasma concentrations in patients with congenital antithrombin III deficiency range from 80–120% of values in healthy adults. At plasma concentrations =70% of normal, increased thrombin generation. Supraphysiologic plasma concentrations (e.g., 150–200% of normal) have increased bleeding risk in patients with sepsis and disseminated intravascular coagulation, not known whether supraphysiologic concentrations increase bleeding risk in patients with congenital antithrombin III deficiency. | Distributed into plasma (39%), extravascular space (49%), and vascular endothelial cells (11%). | NA | Alpha-Globulins,Amino Acids, Peptides, and Proteins,Anticoagulants,Antithrombin III,Antithrombin III, agonists,Antithrombin Proteins,Biological Factors,Blood and Blood Forming Organs,Blood Coagulation Factor Inhibitors,Blood Proteins,Carbohydrates,Drugs that are Mainly Renally Excreted,Enzyme Inhibitors,Globulins,Glycosaminoglycans,Hematologic Agents,Oligosaccharides,Peptides,Polysaccharides,Proteins,Serum Globulins | NA | NA | NA | The anticoagulant effect of heparin is enhanced by concurrent treatment with Antithrombin III (Human), THROMBATE III® (antithrombin) in patients with hereditary AT-III deficiency. Thus, in order to avoid bleeding, reduced dosage of heparin is recommended during treatment with THROMBATE (antithrombin) III. | Antithrombin-III | Thrombate III | Grifols Therapeutics Inc | Grifols Therapeutics Inc | Indicated for the treatment of patients with hereditary antithrombin III deficiency in connection with surgical or obstetrical procedures or when they suffer from thromboembolism. | NA | 500 unit | powder for solution | NA | Dosage should be determined on an individual basis based on the pre-therapy plasma antithrombin III (AT-III) level, in order to increase plasma AT-III levels to the level found in normal human plasma (100%). It is recommended that following an initial dose of THROMBATE (antithrombin) III, plasma levels of AT-III be initially monitored at least every 12 hours and before the next infusion of THROMBATE (antithrombin) III to maintain plasma AT-III levels greater than 80%. | NA | Dizziness, chest tightness, nausea, foul taste, chills, cramps, shortness of breath, chest pain, film over eye, lightheadedness, bowel fullness, hives, fever, oozing, hematoma formation. | NA | NA | NA |
| 10717 | Th1165 | Antithrombin III human | NA | 58000 | NA | NA | NA | NA | 2.5 - 3.8 hs | A plasma alpha 2 glycoprotein that accounts for the major antithrombin activity of normal plasma and also inhibits several other enzymes. It is a member of the serpin superfamily. | Short-term replacement therapy for prevention or treatment of thromboembolism in selected patients with congenital antithrombin III deficiency at high risk for thromboembolism (i.e., those undergoing surgical or obstetrical procedures) or those with thromboembolism | It s the major plasma inhibitor of thrombin. Inactivation of thrombin by AT-III occurs by formation of a covalent bond resulting in an inactive 1:1 stoichiometric complex between the two, involving an interaction of the active serine of thrombin and an arginine reactive site on AT-III. AT-III is also capable of inactivating other components of the coagulation cascade including factors IXa, Xa, XIa, and XIIa, as well as plasmin. | Neutralizes serine proteinases such as thrombin, plasmin, and activated coagulation factors IX, X, XI, and XII; Principally neutralizes thrombin and activated coagulation factor X (Xa); Neutralization of factor Xa prevents thrombin generation (e.g., decreased formation of prothrombin fragment 1.2 [F1 and F2]); Neutralization of thrombin prevents conversion of fibrinogen to fibrin; lowly and irreversibly complexes stoichiometrically with these coagulation factors; such reactions are rapid in presence of endogenous heparin-like proteoglycans or exogenous heparin; Inhibits thrombus formation. | NA | <5% metabolized to low molecular weight breakdown products. | Therapeutic target plasma concentrations in patients with congenital antithrombin III deficiency range from 80–120% of values in healthy adults. At plasma concentrations =70% of normal, increased thrombin generation. Supraphysiologic plasma concentrations (e.g., 150–200% of normal) have increased bleeding risk in patients with sepsis and disseminated intravascular coagulation, not known whether supraphysiologic concentrations increase bleeding risk in patients with congenital antithrombin III deficiency. | Distributed into plasma (39%), extravascular space (49%), and vascular endothelial cells (11%). | NA | Alpha-Globulins,Amino Acids, Peptides, and Proteins,Anticoagulants,Antithrombin III,Antithrombin III, agonists,Antithrombin Proteins,Biological Factors,Blood and Blood Forming Organs,Blood Coagulation Factor Inhibitors,Blood Proteins,Carbohydrates,Drugs that are Mainly Renally Excreted,Enzyme Inhibitors,Globulins,Glycosaminoglycans,Hematologic Agents,Oligosaccharides,Peptides,Polysaccharides,Proteins,Serum Globulins | NA | NA | NA | The anticoagulant effect of heparin is enhanced by concurrent treatment with Antithrombin III (Human), THROMBATE III® (antithrombin) in patients with hereditary AT-III deficiency. Thus, in order to avoid bleeding, reduced dosage of heparin is recommended during treatment with THROMBATE (antithrombin) III. | Antithrombin-III | Thrombate III | Grifols Therapeutics Inc | Grifols Therapeutics Inc | Indicated for the treatment of patients with hereditary antithrombin III deficiency in connection with surgical or obstetrical procedures or when they suffer from thromboembolism. | NA | 1000 unit | powder for solution | NA | Dosage should be determined on an individual basis based on the pre-therapy plasma antithrombin III (AT-III) level, in order to increase plasma AT-III levels to the level found in normal human plasma (100%). It is recommended that following an initial dose of THROMBATE (antithrombin) III, plasma levels of AT-III be initially monitored at least every 12 hours and before the next infusion of THROMBATE (antithrombin) III to maintain plasma AT-III levels greater than 80%. | NA | Dizziness, chest tightness, nausea, foul taste, chills, cramps, shortness of breath, chest pain, film over eye, lightheadedness, bowel fullness, hives, fever, oozing, hematoma formation. | NA | NA | NA |
| 10719 | Th1165 | Antithrombin III human | NA | 58000 | NA | NA | NA | NA | 2.5 - 3.8 hs | A plasma alpha 2 glycoprotein that accounts for the major antithrombin activity of normal plasma and also inhibits several other enzymes. It is a member of the serpin superfamily. | Short-term replacement therapy for prevention or treatment of thromboembolism in selected patients with congenital antithrombin III deficiency at high risk for thromboembolism (i.e., those undergoing surgical or obstetrical procedures) or those with thromboembolism | It s the major plasma inhibitor of thrombin. Inactivation of thrombin by AT-III occurs by formation of a covalent bond resulting in an inactive 1:1 stoichiometric complex between the two, involving an interaction of the active serine of thrombin and an arginine reactive site on AT-III. AT-III is also capable of inactivating other components of the coagulation cascade including factors IXa, Xa, XIa, and XIIa, as well as plasmin. | Neutralizes serine proteinases such as thrombin, plasmin, and activated coagulation factors IX, X, XI, and XII; Principally neutralizes thrombin and activated coagulation factor X (Xa); Neutralization of factor Xa prevents thrombin generation (e.g., decreased formation of prothrombin fragment 1.2 [F1 and F2]); Neutralization of thrombin prevents conversion of fibrinogen to fibrin; lowly and irreversibly complexes stoichiometrically with these coagulation factors; such reactions are rapid in presence of endogenous heparin-like proteoglycans or exogenous heparin; Inhibits thrombus formation. | NA | <5% metabolized to low molecular weight breakdown products. | Therapeutic target plasma concentrations in patients with congenital antithrombin III deficiency range from 80–120% of values in healthy adults. At plasma concentrations =70% of normal, increased thrombin generation. Supraphysiologic plasma concentrations (e.g., 150–200% of normal) have increased bleeding risk in patients with sepsis and disseminated intravascular coagulation, not known whether supraphysiologic concentrations increase bleeding risk in patients with congenital antithrombin III deficiency. | Distributed into plasma (39%), extravascular space (49%), and vascular endothelial cells (11%). | NA | Alpha-Globulins,Amino Acids, Peptides, and Proteins,Anticoagulants,Antithrombin III,Antithrombin III, agonists,Antithrombin Proteins,Biological Factors,Blood and Blood Forming Organs,Blood Coagulation Factor Inhibitors,Blood Proteins,Carbohydrates,Drugs that are Mainly Renally Excreted,Enzyme Inhibitors,Globulins,Glycosaminoglycans,Hematologic Agents,Oligosaccharides,Peptides,Polysaccharides,Proteins,Serum Globulins | NA | NA | NA | The anticoagulant effect of heparin is enhanced by concurrent treatment with Antithrombin III (Human), THROMBATE III® (antithrombin) in patients with hereditary AT-III deficiency. Thus, in order to avoid bleeding, reduced dosage of heparin is recommended during treatment with THROMBATE (antithrombin) III. | Antithrombin-III | Thrombate III Pws IV 1000iu/vial | Miles Inc. Pharmaceutical Division | Miles Inc. Pharmaceutical Division | Indicated for the treatment of patients with hereditary antithrombin III deficiency in connection with surgical or obstetrical procedures or when they suffer from thromboembolism. | NA | 1000 unit | powder for solution | NA | Dosage should be determined on an individual basis based on the pre-therapy plasma antithrombin III (AT-III) level, in order to increase plasma AT-III levels to the level found in normal human plasma (100%). It is recommended that following an initial dose of THROMBATE (antithrombin) III, plasma levels of AT-III be initially monitored at least every 12 hours and before the next infusion of THROMBATE (antithrombin) III to maintain plasma AT-III levels greater than 80%. | NA | Dizziness, chest tightness, nausea, foul taste, chills, cramps, shortness of breath, chest pain, film over eye, lightheadedness, bowel fullness, hives, fever, oozing, hematoma formation. | NA | NA | NA |
| 10720 | Th1165 | Antithrombin III human | NA | 58000 | NA | NA | NA | NA | 2.5 - 3.8 hs | A plasma alpha 2 glycoprotein that accounts for the major antithrombin activity of normal plasma and also inhibits several other enzymes. It is a member of the serpin superfamily. | Short-term replacement therapy for prevention or treatment of thromboembolism in selected patients with congenital antithrombin III deficiency at high risk for thromboembolism (i.e., those undergoing surgical or obstetrical procedures) or those with thromboembolism | It s the major plasma inhibitor of thrombin. Inactivation of thrombin by AT-III occurs by formation of a covalent bond resulting in an inactive 1:1 stoichiometric complex between the two, involving an interaction of the active serine of thrombin and an arginine reactive site on AT-III. AT-III is also capable of inactivating other components of the coagulation cascade including factors IXa, Xa, XIa, and XIIa, as well as plasmin. | Neutralizes serine proteinases such as thrombin, plasmin, and activated coagulation factors IX, X, XI, and XII; Principally neutralizes thrombin and activated coagulation factor X (Xa); Neutralization of factor Xa prevents thrombin generation (e.g., decreased formation of prothrombin fragment 1.2 [F1 and F2]); Neutralization of thrombin prevents conversion of fibrinogen to fibrin; lowly and irreversibly complexes stoichiometrically with these coagulation factors; such reactions are rapid in presence of endogenous heparin-like proteoglycans or exogenous heparin; Inhibits thrombus formation. | NA | <5% metabolized to low molecular weight breakdown products. | Therapeutic target plasma concentrations in patients with congenital antithrombin III deficiency range from 80–120% of values in healthy adults. At plasma concentrations =70% of normal, increased thrombin generation. Supraphysiologic plasma concentrations (e.g., 150–200% of normal) have increased bleeding risk in patients with sepsis and disseminated intravascular coagulation, not known whether supraphysiologic concentrations increase bleeding risk in patients with congenital antithrombin III deficiency. | Distributed into plasma (39%), extravascular space (49%), and vascular endothelial cells (11%). | NA | Alpha-Globulins,Amino Acids, Peptides, and Proteins,Anticoagulants,Antithrombin III,Antithrombin III, agonists,Antithrombin Proteins,Biological Factors,Blood and Blood Forming Organs,Blood Coagulation Factor Inhibitors,Blood Proteins,Carbohydrates,Drugs that are Mainly Renally Excreted,Enzyme Inhibitors,Globulins,Glycosaminoglycans,Hematologic Agents,Oligosaccharides,Peptides,Polysaccharides,Proteins,Serum Globulins | NA | NA | NA | The anticoagulant effect of heparin is enhanced by concurrent treatment with Antithrombin III (Human), THROMBATE III® (antithrombin) in patients with hereditary AT-III deficiency. Thus, in order to avoid bleeding, reduced dosage of heparin is recommended during treatment with THROMBATE (antithrombin) III. | Antithrombin-III | Thrombate III Pws IV 500iu/vial | Miles Inc. Pharmaceutical Division | Miles Inc. Pharmaceutical Division | Indicated for the treatment of patients with hereditary antithrombin III deficiency in connection with surgical or obstetrical procedures or when they suffer from thromboembolism. | NA | 500 unit | powder for solution | NA | Dosage should be determined on an individual basis based on the pre-therapy plasma antithrombin III (AT-III) level, in order to increase plasma AT-III levels to the level found in normal human plasma (100%). It is recommended that following an initial dose of THROMBATE (antithrombin) III, plasma levels of AT-III be initially monitored at least every 12 hours and before the next infusion of THROMBATE (antithrombin) III to maintain plasma AT-III levels greater than 80%. | NA | Dizziness, chest tightness, nausea, foul taste, chills, cramps, shortness of breath, chest pain, film over eye, lightheadedness, bowel fullness, hives, fever, oozing, hematoma formation. | NA | 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 |
| 10743 | Th1171 | C1 Esterase Inhibitor (Human) | NA | 68000 | NA | NA | NA | NA | Following intravenous administration of a single dose, the half-life was 56 ± 36 hours.3 Subcutaneous administration produces a half-life of 199.6 hours | Recombinant human C1 esterase inhibitor is a human protein developed through Pharming’s proprietary technology where the human protein is expressed in milk of transgenic rabbits. Hereditary Angioedema (HAE) is a human genetic disorder caused by a shortage of C1 inhibitor activity and results in an overreaction of the immune system. The disease is characterized by acute attacks of painful and in some cases fatal swelling of several soft tissues (edema), which may last up to five days when untreated. | For routine prophylaxis against angioedema attacks in adolescent and adult patients with Hereditary Angioedema (HAE). | In clinical studies, intravenous administration demonstrated an increase in plasma levels of C1 inhibitor within approximately one hour or less of administration. | C1 inhibitor is a normal constituent of human blood and is one of the serine proteinase inhibitors (serpins). The primary function of C1 inhibitor is to regulate the activation of the complement and intrinsic coagulation (contact system) pathway. C1 inhibitor also regulates the fibrinolytic system. Regulation of these systems is performed through the formation of complexes between the proteinases and the inhibitor, resulting in inactivation of both and consumption of the C1 inhibitor. HAE patients have low levels of endogenous or functional C1 inhibitor. Although the events that induce attacks of angioedema in HAE patients are not well defined, it is thought by some that increased vascular permeability and the clinical manifestation of HAE attacks are primarily mediated through contact system activation. Suppression of contact system activation by C1 inhibitor through the inactivation of plasma kallikrein and factor XIIa is thought to modulate this vascular permeability by preventing the generation of bradykinin1. Administration of C1 Esterase Inhibitor increases plasma levels of C1 inhibitor activity. | NA | NA | NA | NA | NA | NA | NA | NA | NA | Cyproterone acetate may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Danazol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Desogestrel may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Dienogest may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Drospirenone may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Estradiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Estropipate may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Ethinyl Estradiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Ethynodiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Etonogestrel may increase the thrombogenic activities of C1 Esterase Inhibitor (Human). | Plasma protease C1 inhibitor | Berinert 1500 | Csl Behring Canada Inc | Csl Behring Canada Inc | Berinert is a plasma-derived concentrate of C1 Esterase Inhibitor (Human) indicated for the treatment of acute abdominal, facial, or laryngeal attacks of hereditary angioedema (HAE) in adult and adolescent patients. | NA | 1500 unit | kit; powder for solution | IV | Administer Berinert at a dose of 20 International Units (IU) per kg body weight by intravenous injection. Doses lower than 20 IU/kg body weight should not be administered. Berinert is provided as a freeze-dried powder for reconstitution with the Sterile Water for Injection, USP provided. Store the vial in the original carton in order to protect from light. Do not freeze. | Berinert is contraindicated in individuals who have experienced life-threatening hypersensitivity reactions, including anaphylaxis, to C1 esterase inhibitor preparations. | The most serious adverse reaction reported in subjects enrolled in clinical studies who received Berinert was an increase in the severity of pain associated with HAE. The most common adverse reaction reported in greater than 4% of the subjects and greater than placebo among subjects who received Berinert in the placebo-controlled clinical trial was dysgeusia. | Link | NA | NA |
| 10744 | Th1171 | C1 Esterase Inhibitor (Human) | NA | 68000 | NA | NA | NA | NA | Following intravenous administration of a single dose, the half-life was 56 ± 36 hours.3 Subcutaneous administration produces a half-life of 199.6 hours | Recombinant human C1 esterase inhibitor is a human protein developed through Pharming’s proprietary technology where the human protein is expressed in milk of transgenic rabbits. Hereditary Angioedema (HAE) is a human genetic disorder caused by a shortage of C1 inhibitor activity and results in an overreaction of the immune system. The disease is characterized by acute attacks of painful and in some cases fatal swelling of several soft tissues (edema), which may last up to five days when untreated. | For routine prophylaxis against angioedema attacks in adolescent and adult patients with Hereditary Angioedema (HAE). | In clinical studies, intravenous administration demonstrated an increase in plasma levels of C1 inhibitor within approximately one hour or less of administration. | C1 inhibitor is a normal constituent of human blood and is one of the serine proteinase inhibitors (serpins). The primary function of C1 inhibitor is to regulate the activation of the complement and intrinsic coagulation (contact system) pathway. C1 inhibitor also regulates the fibrinolytic system. Regulation of these systems is performed through the formation of complexes between the proteinases and the inhibitor, resulting in inactivation of both and consumption of the C1 inhibitor. HAE patients have low levels of endogenous or functional C1 inhibitor. Although the events that induce attacks of angioedema in HAE patients are not well defined, it is thought by some that increased vascular permeability and the clinical manifestation of HAE attacks are primarily mediated through contact system activation. Suppression of contact system activation by C1 inhibitor through the inactivation of plasma kallikrein and factor XIIa is thought to modulate this vascular permeability by preventing the generation of bradykinin1. Administration of C1 Esterase Inhibitor increases plasma levels of C1 inhibitor activity. | NA | NA | NA | NA | NA | NA | NA | NA | NA | Cyproterone acetate may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Danazol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Desogestrel may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Dienogest may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Drospirenone may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Estradiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Estropipate may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Ethinyl Estradiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Ethynodiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Etonogestrel may increase the thrombogenic activities of C1 Esterase Inhibitor (Human). | Plasma protease C1 inhibitor | Berinert 500 | Csl Behring Canada Inc | Csl Behring Canada Inc | Berinert is a plasma-derived concentrate of C1 Esterase Inhibitor (Human) indicated for the treatment of acute abdominal, facial, or laryngeal attacks of hereditary angioedema (HAE) in adult and adolescent patients. | NA | 500 unit | kit; powder for solution | IV | Administer Berinert at a dose of 20 International Units (IU) per kg body weight by intravenous injection. Doses lower than 20 IU/kg body weight should not be administered. Berinert is provided as a freeze-dried powder for reconstitution with the Sterile Water for Injection, USP provided. Store the vial in the original carton in order to protect from light. Do not freeze. | Berinert is contraindicated in individuals who have experienced life-threatening hypersensitivity reactions, including anaphylaxis, to C1 esterase inhibitor preparations. | The most serious adverse reaction reported in subjects enrolled in clinical studies who received Berinert was an increase in the severity of pain associated with HAE. The most common adverse reaction reported in greater than 4% of the subjects and greater than placebo among subjects who received Berinert in the placebo-controlled clinical trial was dysgeusia. | Link | NA | NA |
| 10745 | Th1171 | C1 Esterase Inhibitor (Human) | NA | 68000 | NA | NA | NA | NA | Following intravenous administration of a single dose, the half-life was 56 ± 36 hours.3 Subcutaneous administration produces a half-life of 199.6 hours | Recombinant human C1 esterase inhibitor is a human protein developed through Pharming’s proprietary technology where the human protein is expressed in milk of transgenic rabbits. Hereditary Angioedema (HAE) is a human genetic disorder caused by a shortage of C1 inhibitor activity and results in an overreaction of the immune system. The disease is characterized by acute attacks of painful and in some cases fatal swelling of several soft tissues (edema), which may last up to five days when untreated. | For routine prophylaxis against angioedema attacks in adolescent and adult patients with Hereditary Angioedema (HAE). | In clinical studies, intravenous administration demonstrated an increase in plasma levels of C1 inhibitor within approximately one hour or less of administration. | C1 inhibitor is a normal constituent of human blood and is one of the serine proteinase inhibitors (serpins). The primary function of C1 inhibitor is to regulate the activation of the complement and intrinsic coagulation (contact system) pathway. C1 inhibitor also regulates the fibrinolytic system. Regulation of these systems is performed through the formation of complexes between the proteinases and the inhibitor, resulting in inactivation of both and consumption of the C1 inhibitor. HAE patients have low levels of endogenous or functional C1 inhibitor. Although the events that induce attacks of angioedema in HAE patients are not well defined, it is thought by some that increased vascular permeability and the clinical manifestation of HAE attacks are primarily mediated through contact system activation. Suppression of contact system activation by C1 inhibitor through the inactivation of plasma kallikrein and factor XIIa is thought to modulate this vascular permeability by preventing the generation of bradykinin1. Administration of C1 Esterase Inhibitor increases plasma levels of C1 inhibitor activity. | NA | NA | NA | NA | NA | NA | NA | NA | NA | Cyproterone acetate may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Danazol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Desogestrel may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Dienogest may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Drospirenone may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Estradiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Estropipate may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Ethinyl Estradiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Ethynodiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Etonogestrel may increase the thrombogenic activities of C1 Esterase Inhibitor (Human). | Plasma protease C1 inhibitor | Cinryze | Viropharma Biologics Inc | Viropharma Biologics Inc | CINRYZE is a C1 esterase inhibitor indicated for routine prophylaxis against angioedema attacks in adolescent and adult patients with Hereditary Angioedema (HAE). | NA | 500 unit | powder for solution | IV | A dose of 1,000 Units CINRYZE can be administered every 3 or 4 days for routine prophylaxis against angioedema attacks in HAE patients. CINRYZE is administered at an injection rate of 1 mL per minute. | CINRYZE is contraindicated in patients who have manifested life-threatening immediate hypersensitivity reactions, including anaphylaxis to the product. | The only serious adverse reaction observed in clinical studies of CINRYZE was cerebrovascular accident. The most common adverse reactions observed were headache, nausea, rash, and vomiting. | Link | NA | NA |
| 10748 | Th1172 | Coagulation Factor XIII A-Subunit (Recombinant) | >Th1172_Coagulation_Factor_XIII_A-Subunit_(Recombinant) MSETSRTAFGGRRAVPPNNSNAAEDDLPTVELQGVVPRGVNLQEFLNVTSVHLFKERWDTNKVDHHTDKYENNKLIVRRGQSFYVQIDFSRPYDPRRDLFRVEYVIGRYPQENKGTYIPVPIVSELQSGKWGAKIVMREDRSVRLSIQSSPKCIVGKFRMYVAVWTPYGVLRTSRNPETDTYILFNPWCEDDAVYLDNEKEREEYVLNDIGVIFYGEVNDIKTRSWSYGQFEDGILDTCLYVMDRAQMDLSGRGNPIKVSRVGSAMVNAKDDEGVLVGSWDNIYAYGVPPSAWTGSVDILLEYRSSENPVRYGQCWVFAGVFNTFLRCLGIPARIVTNYFSAHDNDANLQMDIFLEEDGNVNSKLTKDSVWNYHCWNEAWMTRPDLPVGFGGWQAVDSTPQENSDGMYRCGPASVQAIKHGHVCFQFDAPFVFAEVNSDLIYITAKKDGTHVVENVDATHIGKLIVTKQIGGDGMMDITDTYKFQEGQEEERLALETALMYGAKKPLNTEGVMKSRSNVDMDFEVENAVLGKDFKLSITFRNNSHNRYTITAYLSANITFYTGVPKAEFKKETFDVTLEPLSFKKEAVLIQAGEYMGQLLEQASLHFFVTARINETRDVLAKQKSTVLTIPEIIIKVRGTQVVGSDMTVTVEFTNPLKETLRNVWVHLDGPGVTRPMKKMFREIRPNSTVQWEEVCRPWVSGHRKLIASMSSDSLRHVYGELDVQIQRRPSM | NA | NA | NA | NA | NA | 7.1 days | Coagulation Factor XIII A-Subunit (Recombinant) is a recombinant human factor XIII-A2 homodimer composed of two factor XIII (FXIII) A-subunits. The FXIII A-subunit is a 731 amino acid chain with an acetylated N- terminal serine. When FXIII is activated by thrombin, a 37 amino acid peptide is cleaved from the N-terminus of the A-subunit. Coagulation Factor XIII A-Subunit (Recombinant) is manufactured as an intracellular, soluble protein in yeast (Saccharomyces cerevisiae) production strain containing the episomal expression vector, pD16. It is subsequently isolated by homogenization of cells and purification by several chromatography steps, including hydrophobic interaction and ion exchange chromatography. No human or animal derived products are used in the manufacturing process. | For routine prophylaxis of bleeding in patients with congenital factor XIII A-Subunit deficiency. | A qualitative assay of clot solubility is widely used as an indicator of FXIII deficiency; when performed correctly the test is positive only when the FXIII activity in the sample is close to zero. The results of standard coagulation tests are normal as it is the quality of the clot that is affected. In addition, at present there are no markers that can quantitatively assess the in vivo pharmacodynamics of FXIII. | Coagulation Factor XIII A-Subunit (Recombinant) is a protransglutaminase (rFXIII [rA2] homodimer) and binds to free human FXIII B-subunit resulting in a heterotetramer [rA2B2] with a similar half-life to [A2B2]. rFXIII has been shown to be activated by thrombin in the presence of Ca2+. Activated rFXIII has been shown in dose-dependent manner to increase mechanical strength of fibrin clots, retard fibrinolysis, and rFXIII has been shown to enhance platelet adhesion to the site of injury. After combining with available plasma B-subunits, Coagulation Factor XIII A-subunit (Recombinant) has been shown to have the same pharmacodynamic properties in plasma as endogenous FXIII. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Tretten | Novo Nordisk Canada Inc | Novo Nordisk Canada Inc | TRETTEN, Coagulation Factor XIII A-Subunit (Recombinant), is indicated for routine prophylaxis for bleeding in patients with congenital factor XIII A-subunit deficiency. | NA | 15mg | powder for solution | IV | Treatment should be initiated under the supervision of a physician experienced in the treatment of rare bleeding disorders. The dose for routine prophylaxis for bleeding in patients with congenital factor XIII (FXIII) A-subunit deficiency is 35 international units (IU) per kilogram body weight once monthly to achieve a target trough level of FXIII activity at or above 10% using a validated assay. Consider dose adjustment if adequate coverage is not achieved with the recommended 35 IU/kg dose. | TRETTEN is contraindicated in patients who have known hypersensitivity to the active substance or to any of the excipients | The most common adverse reactions reported in clinical trials ( ≥ 1%), were headache, pain in the extremities, injection site pain, and increase in fibrin D dimer levels. | Link | NA | NA |
| 10750 | Th1173 | Conestat alfa | NA | 67000 | NA | NA | NA | NA | 2.4 to 2.7 hours | Conestat alfa is a recombinant, human C1-inhibitor (rhC1INH), for the treatment of acute attacks of hereditary angioedema (HAE) due to C1 esterase inhibitor deficiency in adults. Conestat alfa was approved in October 2010 in all 27 EU member states plus Norway, Iceland and Liechtenstein. | For the treatment of acute attacks of hereditary angioedema (HAE) due to C1 esterase inhibitor deficiency in adults. | The complement component (protein) C4 is a substrate for activated C1. Patients with HAE have low levels of C4 in the circulation; RUCONEST shows a dose-dependent restoration of complement homeostasis of C4 in HAE patients. A dose of 50 IU/kg of RUCONEST increases plasma C1INH activity levels to greater than 0.7 IU/mL (the lower limit of normal) in HAE patients. | C1INH exerts its inhibitory effect by irreversibly binding several proteases (target proteases) of the contact and complement systems. The effect of RUCONEST on the following target proteases was assessed in vitro: activated C1s, kallikrein, factor XIIa and factor XIa. Inhibition kinetics were found to be comparable with those observed for plasma-derived human C1INH. | The common adverse reactions (= 2%) reported in clinical trials were headache, nausea, and diarrhea. Serious arterial and venous thromboembolic (TE) events have been reported at the recommended dose of plasma derived C1 esterase inhibitor products in patients with risk factors. Risk factors may include the presence of an indwelling venous catheter/access device, prior history of thrombosis, underlying atherosclerosis, use of oral contraceptives or certain androgens, morbid obesity, and immobility. Monitor patients with known risk factors for TE events during and after administration. | NA | Mean Cmax was found to be 1.2 U/mL and Tmax was 0.31 ± 0.10 hr following administration of 50 U/kg. | NA | Clearance was found to be 1207 ± 414 mL/hr following administration of 50 U/kg. | NA | NA | NA | NA | NA | Complement C1r subcomponent,Complement C1s subcomponent,Plasma kallikrein,Coagulation factor XII,Prothrombin,Coagulation factor XI,Tissue-type plasminogen activator | Ruconest | Pharming; Santarus, Inc. | Pharming; Santarus, Inc. | RUCONEST is a C1 esterase inhibitor [recombinant] indicated for the treatment of acute attacks in adult and adolescent patients with hereditary angioedema (HAE). | NA | 2100 U/1 | powder for solution | IV | IV Injection; The recommended dose of RUCONEST is 50 IU per kg with a maximum of 4200 IU to be administered as a slow intravenous injection over approximately 5 minutes. | RUCONEST is contraindicated in patients with a history of allergy to rabbits or rabbit-derived products. RUCONEST is contraindicated in patients with a history of life-threatening immediate hypersensitivity reactions to C1 esterase inhibitor preparations, including anaphylaxis. | The serious adverse reaction in clinical studies of RUCONEST was anaphylaxis. The most common adverse reactions ( ≥ 2%) reported in all clinical trials were headache, nausea, and diarrhea. | Link | NA | NA |
| 10751 | Th1174 | Daratumumab | >Th1174_Daratumumab EVQLLESGGGLVQPGGSLRLSCAVSGFTFNSFAMSWVRQAPGKGLEWVSAISGSGGGTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYFCAKDKILWFGEPVFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145391.7 | C6466H9996N1724O2010S42 | NA | NA | NA | Intravenous daratumumab has a terminal half life of 18 ± 9 days.6 Subcutaneous daratumumab has a half life of 20 days | Daratumumab is an anti-cancer drug indicated for multiple myeloma in patients who have received at least 3 prior treatments. It was granted accelerated approval by the FDA in November 2016. Marketed under the brand name Darzalex by Janssen Biotech, daratumumab is the first monoclonal antibody injection approved for this indication and provides another options for patients with multiple myeloma resistant to other therapies. Daratumumab induces apoptosis of cancer cells by targeting the CD38 epitope, which is highly expressed on haematological malignancies. | For the treatment of patients with multiple myeloma who have received at least three prior lines of therapy (a proteasome inhibitor (PI) and an immunomodulatory agent) or who are double-refractory to a PI and an immunomodulatory agent. This indication was approved by accelerated approval based on response rate. | In preclinical trials, daratumumab showed synergistic activity with other multiple myeloma therapies, notably lenalidomide. Daratumumab also causes lysis in other cells that express CD38: myeloid-derived suppressor cells, a subset of regulatory T-cells, and NK cells. Decreases in absolute count and percentage of NK cells were observed during treatment. CD4+ and CD8+ T cell absolute counts as well the percentage of total lymphocytes increased in peripheral blood and bone marrow during daratumumab treatment. | Daratumumab is an immunoglobulin G1 kappa monoclonal antibody against CD38 antigen. CD38 is a transmembrane glycoprotein of many functions, including receptor mediated adhesion, signaling, and modulation of cyclase and hydrolase activity. CD38 is expressed on many cell types and tissues, and highly expressed in haematological malignancies including multiple myeloma tumor cells. By binding CD38, daratumumab causes inhibition of tumor cell growth and induces broad-spectrum apoptosis in multiple ways: by Fc-mediated cross linking, by immune-mediate tumor cell lysis through complement dependent cytotoxicity, antibody dependent cell cytotoxicity, and antibody dependent cellular phagocytosis. | Data regarding overdoses of daratumumab are not readily available.[L13290,L13296] Patients should be treated with symptomatic and supportive measures.[L13290,L13296] | Monoclonal antibodies are expected to be metabolized to smaller proteins and amino acids by proteolytic enzymes.[A19126] | Subcutaneous daratumumab reaches a Cmax of 592µg/mL compared to intravenous daratumumab, which reaches a Cmax of 688µg/mL.[L13296] The AUC of subcutaneous daratumumab is 4017µg/mL | Daratumumab intravenous monotherapy has a volume of distribution of 4.7 ± 1.3L and the combination therapy has a volume of distribution of 4.4 ± 1.5L.[L13290] Subcutaneous daratumumab has a volume of distribution of the central compartment of 5.2L and a volume of distribution of the peripheral compartment of 3.8L.[L13296] | Intravenous daratumumab has a clearance of 171.4 ± 95.3mL/day.[L13290] Subcutaneous daratumumab has a clearance of 119mL/day.[L13296] | Antineoplastic Agents | NA | NA | NA | NA | ADP-ribosyl cyclase 1 | NA | NA | NA | NA | NA | 100 mg/5mL | Solution, concentrate | IV | Injection | NA | NA | Link | NA | NA |
| 10752 | Th1174 | Daratumumab | >Th1174_Daratumumab EVQLLESGGGLVQPGGSLRLSCAVSGFTFNSFAMSWVRQAPGKGLEWVSAISGSGGGTYYADSVKGRFTISRDNSKNTLYLQMNSLRAEDTAVYFCAKDKILWFGEPVFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145391.7 | C6466H9996N1724O2010S42 | NA | NA | NA | Intravenous daratumumab has a terminal half life of 18 ± 9 days.6 Subcutaneous daratumumab has a half life of 20 days | Daratumumab is an anti-cancer drug indicated for multiple myeloma in patients who have received at least 3 prior treatments. It was granted accelerated approval by the FDA in November 2016. Marketed under the brand name Darzalex by Janssen Biotech, daratumumab is the first monoclonal antibody injection approved for this indication and provides another options for patients with multiple myeloma resistant to other therapies. Daratumumab induces apoptosis of cancer cells by targeting the CD38 epitope, which is highly expressed on haematological malignancies. | For the treatment of patients with multiple myeloma who have received at least three prior lines of therapy (a proteasome inhibitor (PI) and an immunomodulatory agent) or who are double-refractory to a PI and an immunomodulatory agent. This indication was approved by accelerated approval based on response rate. | In preclinical trials, daratumumab showed synergistic activity with other multiple myeloma therapies, notably lenalidomide. Daratumumab also causes lysis in other cells that express CD38: myeloid-derived suppressor cells, a subset of regulatory T-cells, and NK cells. Decreases in absolute count and percentage of NK cells were observed during treatment. CD4+ and CD8+ T cell absolute counts as well the percentage of total lymphocytes increased in peripheral blood and bone marrow during daratumumab treatment. | Daratumumab is an immunoglobulin G1 kappa monoclonal antibody against CD38 antigen. CD38 is a transmembrane glycoprotein of many functions, including receptor mediated adhesion, signaling, and modulation of cyclase and hydrolase activity. CD38 is expressed on many cell types and tissues, and highly expressed in haematological malignancies including multiple myeloma tumor cells. By binding CD38, daratumumab causes inhibition of tumor cell growth and induces broad-spectrum apoptosis in multiple ways: by Fc-mediated cross linking, by immune-mediate tumor cell lysis through complement dependent cytotoxicity, antibody dependent cell cytotoxicity, and antibody dependent cellular phagocytosis. | Data regarding overdoses of daratumumab are not readily available.[L13290,L13296] Patients should be treated with symptomatic and supportive measures.[L13290,L13296] | Monoclonal antibodies are expected to be metabolized to smaller proteins and amino acids by proteolytic enzymes.[A19126] | Subcutaneous daratumumab reaches a Cmax of 592µg/mL compared to intravenous daratumumab, which reaches a Cmax of 688µg/mL.[L13296] The AUC of subcutaneous daratumumab is 4017µg/mL | Daratumumab intravenous monotherapy has a volume of distribution of 4.7 ± 1.3L and the combination therapy has a volume of distribution of 4.4 ± 1.5L.[L13290] Subcutaneous daratumumab has a volume of distribution of the central compartment of 5.2L and a volume of distribution of the peripheral compartment of 3.8L.[L13296] | Intravenous daratumumab has a clearance of 171.4 ± 95.3mL/day.[L13290] Subcutaneous daratumumab has a clearance of 119mL/day.[L13296] | Antineoplastic Agents | NA | NA | NA | NA | ADP-ribosyl cyclase 1 | Darzalex | Janssen Biotech, Inc. | Janssen Biotech, Inc. | DARZALEX is indicated for the treatment of patients with multiple myeloma who have received at least three prior lines of therapy including a proteasome inhibitor (PI) and an immunomodulatory agent or who are double-refractory to a PI and an immunomodulatory agent. | NA | 100 mg/5mL | Solution, concentrate | IV | The recommended dose of DARZALEX is 16 mg/kg body weight administered as an intravenous infusion according to the following dosing schedule. | The dose of DARZALEX at which severe toxicity occurs is not known. | Infusion reactions | 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 |
| 10763 | Th1177 | Elosulfase alfa | >Th1177_Elosulfase_alfa APQPPNILLLLMDDMGWGDLGVYGEPSRETPLCSPSRAALLTGRLPIRNGFYTTNAHARNLLKKAGYVSKIVGKWHLGHRPQFHPLKHGFNIPVYRDWEMVGRYYEEFPINLKTGEANLTFLYWAVDATHAPVYASKPFLGTSQRGRYGDVADNTFVFFTSDNGAALISAPEQGGSNGPFPGHVTAGQVSHQLGSIMDLFTTSLALAGLTLMDRPIFYYRGDTLMAATLGQHKAHFWTWTVTTHNLEDHTKLPLIFHLGRDPGERFPLSFEALVPAQPQLNVCNWAVMNWAPPGCEKLGKPNLDRMAAEGLLFPNFYSANAYTPQEIVGGIPDSEQLLPEDEWFGSPNCHFGPYDNKARPQIYLQEALDFIKRQARHHPFAVREIDDSIGKILELLQDLHLCGKQTTFEGGMREPALAWWPPSDRAIDGLNLLPTLLQGRNSWENFRQGIDFCPGQNVSGASAEYQEALSRITSVVQQHQCLTPPESIPKKCLWSH | 110800 | C5020H7588N1364O1418S34 | NA | NA | NA | week 0: 7.52 min week 22: 35.9 min | Elosulfase alfa is a synthetic version of the enzyme N-acetylgalactosamine-6-sulfatase. It was approved by the FDA in 2014 for the treatment of Morquio syndrome. Elosulfase alfa was developed by BioMarin Pharmaceutical Inc. and is marketed under the brand Vimizimâ„¢. The recommended dose is 2 mg per kg given intravenously over a minimum range of 3.5 to 4.5 hours, based on infusion volume, once every week. | Vimizim is a hydrolytic lysosomal glycosaminoglycan (GAG)-specific enzyme indicated for patients with Mucopolysaccharidosis type IVA (MPS IVA; Morquio A syndrome). | AUC: 238 min x μg/mL, standard deviation 100. | Mucopolysaccharidoses comprise a group of lysosomal storage disorders caused by the deficiency of specific lysosomal enzymes required for the catabolism of glycosaminoglycans (GAG). Mucopolysaccharidosis IVA (MPS IVA, Morquio A Syndrome) is characterized by the absence or marked reduction in N-acetylgalactosamine-6-sulfatase activity. The sulfatase activity deficiency results in the accumulation of the GAG substrates, KS and C6S, in the lysosomal compartment of cells throughout the body. The accumulation leads to widespread cellular, tissue, and organ dysfunction. Vimizim is intended to provide the exogenous enzyme N-acetylgalactosamine-6-sulfatase that will be taken up into the lysosomes and increase the catabolism of the GAGs KS and C6S. Elosulfase alfa uptake by cells into lysosomes is mediated by the binding of mannose-6-phosphate-terminated oligosaccharide chains of elosulfase alfa to mannose-6-phosphate receptors. In the absence of an animal disease model that recapitulates the human disease phenotype, elosulfase alfa pharmacological activity was evaluated using human primary chondrocytes from two MPS IVA patients. Treatment of MPS IVA chondrocytes with elosulfase alfa induced clearance of KS lysosomal storage from the chondrocytes. | NA | NA | Cmax: 1.49 µg/mL, standard deviation 0.534. | 396 mL/kg, standard deviation 316. | 10.0 mL/min/kg. (standard deviation: 3.73). | Enzymes; Alimentary Tract and Metabolism | NA | NA | NA | NA | N-acetylgalactosamine-6-sulfatase | NA | NA | NA | NA | NA | NA | Injection, solution | IV | NA | NA | NA | NA | NA | NA |
| 10764 | Th1177 | Elosulfase alfa | >Th1177_Elosulfase_alfa APQPPNILLLLMDDMGWGDLGVYGEPSRETPLCSPSRAALLTGRLPIRNGFYTTNAHARNLLKKAGYVSKIVGKWHLGHRPQFHPLKHGFNIPVYRDWEMVGRYYEEFPINLKTGEANLTFLYWAVDATHAPVYASKPFLGTSQRGRYGDVADNTFVFFTSDNGAALISAPEQGGSNGPFPGHVTAGQVSHQLGSIMDLFTTSLALAGLTLMDRPIFYYRGDTLMAATLGQHKAHFWTWTVTTHNLEDHTKLPLIFHLGRDPGERFPLSFEALVPAQPQLNVCNWAVMNWAPPGCEKLGKPNLDRMAAEGLLFPNFYSANAYTPQEIVGGIPDSEQLLPEDEWFGSPNCHFGPYDNKARPQIYLQEALDFIKRQARHHPFAVREIDDSIGKILELLQDLHLCGKQTTFEGGMREPALAWWPPSDRAIDGLNLLPTLLQGRNSWENFRQGIDFCPGQNVSGASAEYQEALSRITSVVQQHQCLTPPESIPKKCLWSH | 110800 | C5020H7588N1364O1418S34 | NA | NA | NA | week 0: 7.52 min week 22: 35.9 min | Elosulfase alfa is a synthetic version of the enzyme N-acetylgalactosamine-6-sulfatase. It was approved by the FDA in 2014 for the treatment of Morquio syndrome. Elosulfase alfa was developed by BioMarin Pharmaceutical Inc. and is marketed under the brand Vimizimâ„¢. The recommended dose is 2 mg per kg given intravenously over a minimum range of 3.5 to 4.5 hours, based on infusion volume, once every week. | Vimizim is a hydrolytic lysosomal glycosaminoglycan (GAG)-specific enzyme indicated for patients with Mucopolysaccharidosis type IVA (MPS IVA; Morquio A syndrome). | AUC: 238 min x μg/mL, standard deviation 100. | Mucopolysaccharidoses comprise a group of lysosomal storage disorders caused by the deficiency of specific lysosomal enzymes required for the catabolism of glycosaminoglycans (GAG). Mucopolysaccharidosis IVA (MPS IVA, Morquio A Syndrome) is characterized by the absence or marked reduction in N-acetylgalactosamine-6-sulfatase activity. The sulfatase activity deficiency results in the accumulation of the GAG substrates, KS and C6S, in the lysosomal compartment of cells throughout the body. The accumulation leads to widespread cellular, tissue, and organ dysfunction. Vimizim is intended to provide the exogenous enzyme N-acetylgalactosamine-6-sulfatase that will be taken up into the lysosomes and increase the catabolism of the GAGs KS and C6S. Elosulfase alfa uptake by cells into lysosomes is mediated by the binding of mannose-6-phosphate-terminated oligosaccharide chains of elosulfase alfa to mannose-6-phosphate receptors. In the absence of an animal disease model that recapitulates the human disease phenotype, elosulfase alfa pharmacological activity was evaluated using human primary chondrocytes from two MPS IVA patients. Treatment of MPS IVA chondrocytes with elosulfase alfa induced clearance of KS lysosomal storage from the chondrocytes. | NA | NA | Cmax: 1.49 µg/mL, standard deviation 0.534. | 396 mL/kg, standard deviation 316. | 10.0 mL/min/kg. (standard deviation: 3.73). | Enzymes; Alimentary Tract and Metabolism | NA | NA | NA | NA | N-acetylgalactosamine-6-sulfatase | Vimizim | Biomarin International Limited | Biomarin International Limited | Vimizim (elosulfase alfa) is indicated for patients with Mucopolysaccharidosis type IVA (MPS IVA; Morquio A syndrome). | NA | 1 mg | Solution | IV | The recommended dose is 2 mg per kg given intravenously over a minimum range of 3.5 to 4.5 hours, based on infusion volume, once every week. Pre-treatment with antihistamines with or without antipyretics is recommended 30 to 60 minutes prior to the start of the infusion | NA | Anaphylaxis and hypersensitivity reactions. | NA | NA | NA |
| 10765 | Th1177 | Elosulfase alfa | >Th1177_Elosulfase_alfa APQPPNILLLLMDDMGWGDLGVYGEPSRETPLCSPSRAALLTGRLPIRNGFYTTNAHARNLLKKAGYVSKIVGKWHLGHRPQFHPLKHGFNIPVYRDWEMVGRYYEEFPINLKTGEANLTFLYWAVDATHAPVYASKPFLGTSQRGRYGDVADNTFVFFTSDNGAALISAPEQGGSNGPFPGHVTAGQVSHQLGSIMDLFTTSLALAGLTLMDRPIFYYRGDTLMAATLGQHKAHFWTWTVTTHNLEDHTKLPLIFHLGRDPGERFPLSFEALVPAQPQLNVCNWAVMNWAPPGCEKLGKPNLDRMAAEGLLFPNFYSANAYTPQEIVGGIPDSEQLLPEDEWFGSPNCHFGPYDNKARPQIYLQEALDFIKRQARHHPFAVREIDDSIGKILELLQDLHLCGKQTTFEGGMREPALAWWPPSDRAIDGLNLLPTLLQGRNSWENFRQGIDFCPGQNVSGASAEYQEALSRITSVVQQHQCLTPPESIPKKCLWSH | 110800 | C5020H7588N1364O1418S35 | NA | NA | NA | week 0: 7.52 min week 22: 35.9 min | Elosulfase alfa is a synthetic version of the enzyme N-acetylgalactosamine-6-sulfatase. It was approved by the FDA in 2014 for the treatment of Morquio syndrome. Elosulfase alfa was developed by BioMarin Pharmaceutical Inc. and is marketed under the brand Vimizimâ„¢. The recommended dose is 2 mg per kg given intravenously over a minimum range of 3.5 to 4.5 hours, based on infusion volume, once every week. | Vimizim is a hydrolytic lysosomal glycosaminoglycan (GAG)-specific enzyme indicated for patients with Mucopolysaccharidosis type IVA (MPS IVA; Morquio A syndrome). | AUC: 238 min x μg/mL, standard deviation 100. | Mucopolysaccharidoses comprise a group of lysosomal storage disorders caused by the deficiency of specific lysosomal enzymes required for the catabolism of glycosaminoglycans (GAG). Mucopolysaccharidosis IVA (MPS IVA, Morquio A Syndrome) is characterized by the absence or marked reduction in N-acetylgalactosamine-6-sulfatase activity. The sulfatase activity deficiency results in the accumulation of the GAG substrates, KS and C6S, in the lysosomal compartment of cells throughout the body. The accumulation leads to widespread cellular, tissue, and organ dysfunction. Vimizim is intended to provide the exogenous enzyme N-acetylgalactosamine-6-sulfatase that will be taken up into the lysosomes and increase the catabolism of the GAGs KS and C6S. Elosulfase alfa uptake by cells into lysosomes is mediated by the binding of mannose-6-phosphate-terminated oligosaccharide chains of elosulfase alfa to mannose-6-phosphate receptors. In the absence of an animal disease model that recapitulates the human disease phenotype, elosulfase alfa pharmacological activity was evaluated using human primary chondrocytes from two MPS IVA patients. Treatment of MPS IVA chondrocytes with elosulfase alfa induced clearance of KS lysosomal storage from the chondrocytes. | NA | NA | Cmax: 1.49 µg/mL, standard deviation 0.534. | 396 mL/kg, standard deviation 316. | 10.0 mL/min/kg. (standard deviation: 3.73). | Enzymes; Alimentary Tract and Metabolism | NA | NA | NA | NA | N-acetylgalactosamine-6-sulfatase | Vimizim | Bio Marin Pharmaceutical Inc. | Bio Marin Pharmaceutical Inc. | Vimizim (elosulfase alfa) is indicated for patients with Mucopolysaccharidosis type IVA (MPS IVA; Morquio A syndrome). | NA | 5 mg/5mL | Injection, solution | IV | The recommended dose is 2 mg per kg given intravenously over a minimum range of 3.5 to 4.5 hours, based on infusion volume, once every week. Pre-treatment with antihistamines with or without antipyretics is recommended 30 to 60 minutes prior to the start of the infusion | NA | Anaphylaxis and hypersensitivity reactions. | NA | NA | NA |
| 10766 | Th1178 | Elotuzumab | >Th1178_Elotuzumab EVQLVESGGGLVQPGGSLRLSCAASGFDFSRYWMSWVRQAPGKGLEWIGEINPDSSTINYAPSLKDKFIISRDNAKNSLYLQMNSLRAEDTAVYYCARPDGNYWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148100 | C6476H9982N1714O2016S42 | NA | NA | NA | NA | Elotuzumab is a humanized IgG1 (Immunoglobulin G) monoclonal antibody indicated in combination with lenalidomide and dexamethasone for the treatment of patients with multiple myeloma who have received one to three prior therapies. Elotuzumab targets SLAMF7, also known as Signaling Lymphocytic Activation Molecule Family member 7, a cell surface glycoprotein. Elotuzumab consists of the complementary determining regions (CDR) of the mouse antibody, MuLuc63, grafted onto human IgG1 heavy and kappa light chain frameworks. Elotuzumab is produced in NS0 cells by recombinant DNA technology. Elotuzumab has a theoretical mass of 148.1 kDa for the intact antibody. Elotuzumab was approved on November 30, 2015 by the U.S. Food and Drug Administration. Elotuzumab is marketed under the brand Emplicitiâ„¢ by Bristol-Myers Squibb. | Indicated in combination with lenalidomide and dexamethasone for the treatment of patients with multiple myeloma who have received one to three prior therapies. | It does not prolong the QT interval to any clinically relevant extent in combination with lenalidomide and dexamethasone at the recommended dose or as monotherapy (at a dose 2 times the recommended dose). | Elotuzumab is a humanized IgG1 monoclonal antibody that specifically targets the SLAMF7 (Signaling Lymphocytic Activation Molecule Family member 7) protein. SLAMF7 is expressed on myeloma cells independent of cytogenetic abnormalities. SLAMF7 is also expressed on Natural Killer cells, plasma cells, and at lower levels on specific immune cell subsets of differentiated cells within the hematopoietic lineage. Elotuzumab directly activates Natural Killer cells through both the SLAMF7 pathway and Fc receptors. Elotuzumab also targets SLAMF7 on myeloma cells and facilitates the interaction with Natural Killer cells to mediate the killing of myeloma cells through antibody-dependent cellular cytotoxicity (ADCC). In preclinical models, the combination of elotuzumab and lenalidomide resulted in enhanced activation of Natural Killer cells that was greater than the effects of either agent alone and increased anti-tumor activity in vitro and in vivo. | NA | NA | NA | NA | The clearance of elotuzumab decreased from a geometric mean (CV%) of 17.5 (21.2%) to 5.8 (31%) mL/day/kg with an increase in dose from 0.5 (i.e., 0.05 times the recommended dosage) to 20 mg/kg (i.e., 2 times the recommended dosage). Based on a population PK model, when elotuzumab is given in combination with lenalidomide and dexamethasone, approximately 97% of the maximum steady-state concentration is predicted to be eliminated with a geometric mean (CV%) of 82.4 (48%) days. | NA | US2014055370 | 10-Jan-2012 | 10-Jan-2032 | NA | SLAM family member 7 | NA | NA | NA | NA | NA | 300 mg/1; 400 mg/1 | injection, powder, lyophilized, for solution | IV | NA | NA | NA | NA | NA | NA |
| 10767 | Th1178 | Elotuzumab | >Th1178_Elotuzumab EVQLVESGGGLVQPGGSLRLSCAASGFDFSRYWMSWVRQAPGKGLEWIGEINPDSSTINYAPSLKDKFIISRDNAKNSLYLQMNSLRAEDTAVYYCARPDGNYWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148100 | C6476H9982N1714O2016S43 | NA | NA | NA | NA | Elotuzumab is a humanized IgG1 (Immunoglobulin G) monoclonal antibody indicated in combination with lenalidomide and dexamethasone for the treatment of patients with multiple myeloma who have received one to three prior therapies. Elotuzumab targets SLAMF7, also known as Signaling Lymphocytic Activation Molecule Family member 7, a cell surface glycoprotein. Elotuzumab consists of the complementary determining regions (CDR) of the mouse antibody, MuLuc63, grafted onto human IgG1 heavy and kappa light chain frameworks. Elotuzumab is produced in NS0 cells by recombinant DNA technology. Elotuzumab has a theoretical mass of 148.1 kDa for the intact antibody. Elotuzumab was approved on November 30, 2015 by the U.S. Food and Drug Administration. Elotuzumab is marketed under the brand Emplicitiâ„¢ by Bristol-Myers Squibb. | Indicated in combination with lenalidomide and dexamethasone for the treatment of patients with multiple myeloma who have received one to three prior therapies. | It does not prolong the QT interval to any clinically relevant extent in combination with lenalidomide and dexamethasone at the recommended dose or as monotherapy (at a dose 2 times the recommended dose). | Elotuzumab is a humanized IgG1 monoclonal antibody that specifically targets the SLAMF7 (Signaling Lymphocytic Activation Molecule Family member 7) protein. SLAMF7 is expressed on myeloma cells independent of cytogenetic abnormalities. SLAMF7 is also expressed on Natural Killer cells, plasma cells, and at lower levels on specific immune cell subsets of differentiated cells within the hematopoietic lineage. Elotuzumab directly activates Natural Killer cells through both the SLAMF7 pathway and Fc receptors. Elotuzumab also targets SLAMF7 on myeloma cells and facilitates the interaction with Natural Killer cells to mediate the killing of myeloma cells through antibody-dependent cellular cytotoxicity (ADCC). In preclinical models, the combination of elotuzumab and lenalidomide resulted in enhanced activation of Natural Killer cells that was greater than the effects of either agent alone and increased anti-tumor activity in vitro and in vivo. | NA | NA | NA | NA | The clearance of elotuzumab decreased from a geometric mean (CV%) of 17.5 (21.2%) to 5.8 (31%) mL/day/kg with an increase in dose from 0.5 (i.e., 0.05 times the recommended dosage) to 20 mg/kg (i.e., 2 times the recommended dosage). Based on a population PK model, when elotuzumab is given in combination with lenalidomide and dexamethasone, approximately 97% of the maximum steady-state concentration is predicted to be eliminated with a geometric mean (CV%) of 82.4 (48%) days. | NA | NA | NA | NA | NA | SLAM family member 7 | Empliciti | E.R. Squibb & Sons, L.L.C. | E.R. Squibb & Sons, L.L.C. | EMPLICITI is indicated in combination with lenalidomide and dexamethasone for the treatment of patients with multiple myeloma who have received one to three prior therapies. | NA | 300 mg/1 | Powder lyophilized for solution | IV | The recommended dosage of EMPLICITI is 10 mg/kg administered intravenously every week for the first two cycles and every 2 weeks thereafter in conjunction with the recommended dosing of lenalidomide and low-dose dexamethasone as described below. | There are no contraindications to EMPLICITI. Because EMPLICITI is indicated for use in combination with lenalidomide and dexamethasone, healthcare providers should consult the prescribing information of these products for a complete description of contraindications before starting therapy. | Infusion reaction; Infections; Second Primary Malignancies; Hepatotoxicity; Interference with determination of complete response | Link | NA | NA |
| 10768 | Th1178 | Elotuzumab | >Th1178_Elotuzumab EVQLVESGGGLVQPGGSLRLSCAASGFDFSRYWMSWVRQAPGKGLEWIGEINPDSSTINYAPSLKDKFIISRDNAKNSLYLQMNSLRAEDTAVYYCARPDGNYWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148100 | C6476H9982N1714O2016S44 | NA | NA | NA | NA | Elotuzumab is a humanized IgG1 (Immunoglobulin G) monoclonal antibody indicated in combination with lenalidomide and dexamethasone for the treatment of patients with multiple myeloma who have received one to three prior therapies. Elotuzumab targets SLAMF7, also known as Signaling Lymphocytic Activation Molecule Family member 7, a cell surface glycoprotein. Elotuzumab consists of the complementary determining regions (CDR) of the mouse antibody, MuLuc63, grafted onto human IgG1 heavy and kappa light chain frameworks. Elotuzumab is produced in NS0 cells by recombinant DNA technology. Elotuzumab has a theoretical mass of 148.1 kDa for the intact antibody. Elotuzumab was approved on November 30, 2015 by the U.S. Food and Drug Administration. Elotuzumab is marketed under the brand Emplicitiâ„¢ by Bristol-Myers Squibb. | Indicated in combination with lenalidomide and dexamethasone for the treatment of patients with multiple myeloma who have received one to three prior therapies. | It does not prolong the QT interval to any clinically relevant extent in combination with lenalidomide and dexamethasone at the recommended dose or as monotherapy (at a dose 2 times the recommended dose). | Elotuzumab is a humanized IgG1 monoclonal antibody that specifically targets the SLAMF7 (Signaling Lymphocytic Activation Molecule Family member 7) protein. SLAMF7 is expressed on myeloma cells independent of cytogenetic abnormalities. SLAMF7 is also expressed on Natural Killer cells, plasma cells, and at lower levels on specific immune cell subsets of differentiated cells within the hematopoietic lineage. Elotuzumab directly activates Natural Killer cells through both the SLAMF7 pathway and Fc receptors. Elotuzumab also targets SLAMF7 on myeloma cells and facilitates the interaction with Natural Killer cells to mediate the killing of myeloma cells through antibody-dependent cellular cytotoxicity (ADCC). In preclinical models, the combination of elotuzumab and lenalidomide resulted in enhanced activation of Natural Killer cells that was greater than the effects of either agent alone and increased anti-tumor activity in vitro and in vivo. | NA | NA | NA | NA | The clearance of elotuzumab decreased from a geometric mean (CV%) of 17.5 (21.2%) to 5.8 (31%) mL/day/kg with an increase in dose from 0.5 (i.e., 0.05 times the recommended dosage) to 20 mg/kg (i.e., 2 times the recommended dosage). Based on a population PK model, when elotuzumab is given in combination with lenalidomide and dexamethasone, approximately 97% of the maximum steady-state concentration is predicted to be eliminated with a geometric mean (CV%) of 82.4 (48%) days. | NA | NA | NA | NA | NA | SLAM family member 7 | Empliciti | E.R. Squibb & Sons, L.L.C. | E.R. Squibb & Sons, L.L.C. | EMPLICITI is indicated in combination with lenalidomide and dexamethasone for the treatment of patients with multiple myeloma who have received one to three prior therapies. | NA | 400 mg/1 | Powder lyophilized for solution | IV | The recommended dosage of EMPLICITI is 10 mg/kg administered intravenously every week for the first two cycles and every 2 weeks thereafter in conjunction with the recommended dosing of lenalidomide and low-dose dexamethasone as described below. | There are no contraindications to EMPLICITI. Because EMPLICITI is indicated for use in combination with lenalidomide and dexamethasone, healthcare providers should consult the prescribing information of these products for a complete description of contraindications before starting therapy. | Infusion reaction; Infections; Second Primary Malignancies; Hepatotoxicity; Interference with determination of complete response | 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 |
| 10773 | Th1180 | Fibrinogen Concentrate (Human) | NA | 340000 | NA | NA | NA | NA | 78.7 ± 18.13 (55.73-117.26) hours | Fibrinogen Concentrate (Human) is a heat-treated, lyophilized fibrinogen (coagulation factor I) powder made from pooled human plasma. | For the treatment of acute bleeding episodes in patients with congenital fibrinogen deficiency, including afibrinogenemia and hypofibrinogenemia. | Administration of fibrinogen concentrate (human) for intravenous use to patients with congenital fibrinogen deficiency replaces the missing, or low coagulation factor. Normal levels are in the range of 200 to 450 mg/dL | Fibrinogen (factor I) is a soluble plasma glycoprotein with a molecular weight of about 340 kDa. The native molecule is a dimer and consists of three pairs of polypeptide chains (Aα, Bβ and γ). Fibrinogen is a physiological substrate of three enzymes: thrombin, factor XIIIa, and plasmin. During the coagulation process, thrombin cleaves the Aα and Bβ chains releasing fibrinopeptides A and B (FPA and FPB, respectively).2 FPA is separated rapidly and the remaining molecule is a soluble fibrin monomer (fibrin I). The slower removal of FPB results in formation of fibrin II that is capable of polymerization that occurs by aggregation of fibrin monomers.2 The resulting fbrin is stabilized in the presence of calcium ions and by activated factor XIII, which acts as a transglutaminase. Factor XIIIa-induced cross-linking of fibrin polymers renders the fibrin clot more elastic and more resistant to fibrinolysis.3 Cross-linked fibrin is the end result of the coagulation cascade, and provides tensile strength to a primary hemostatic platelet plug and structure to the vessel wall. | NA | NA | NA | NA | NA | NA | NA | NA | NA | The risk or severity of adverse effects can be increased when Aminocaproic Acid is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Menadione is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Phylloquinone is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Tranexamic Acid is combined with Fibrinogen Concentrate (Human). | NA | Riastap | Csl Behring Gmb H | Csl Behring Gmb H | RiaSTAP™ (fibrinogen concentrate (human) for intravenous use) , Fibrinogen Concentrate (Human) is indicated for the treatment of acute bleeding episodes in patients with congenital fibrinogen deficiency, including afibrinogenemia and hypofibrinogenemia. | NA | Each vial contains 900 to 1300 mg fibrinogen, 400 to 700 mg human albumin, 375 to 660 mg L-arginine hydrochloride, 200 to 350 mg sodium chloride and 50 to 100 mg sodium citrate. Sodium hydroxide and hydrochloric acid may have been used to adjust the pH. | injection, powder, lyophilized, for solution | IV | Dose should be individually calculated for each patient based on the target plasma fibrinogen level based on the type of bleeding, actual measured plasma fibrinogen level and body weight | RiaSTAP (fibrinogen concentrate (human) for intravenous use) is contraindicated in individuals who have manifested severe immediate hypersensitivity reactions, including anaphylaxis to RiaSTAP (fibrinogen concentrate (human) for intravenous use) or its components. | The most serious adverse reactions that have been reported in clinical studies or through postmarketing surveillance following RiaSTAP (fibrinogen concentrate (human) for intravenous use) treatment are allergic-anaphylactic reactions and thromboembolic episodes, including myocardial infarction, pulmonary embolism, deep vein thrombosis, and arterial thrombosis. The most common adverse reactions that have been reported in clinical studies or through postmarketing surveillance following RiaSTAP (fibrinogen concentrate (human) for intravenous use) treatment are allergic reactions and generalized reactions such as chills, fever, nausea, and vomiting. | 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 |
| 10785 | Th1183 | Hepatitis B immune globulin | NA | NA | NA | NA | NA | NA | 22-25 days | Long-term hepatitis B immune globulin (HBIG) has been shown to reduce hepatitis B virus (HBV) reinfection in patients transplanted for hepatitis B. Infection with hepatitis B may lead to hepatocellular carcinoma, a type of liver cancer. Therefore, the hepatitis-B vaccines are cancer-preventing vaccines. According to the Centers for Disease Control and Prevention (CDC), the hepatitis B vaccine was the first anti-cancer vaccine. HBIG is prepared from the plasma of donors who have high antibody levels of the hepatitis B surface antigen. It is extracted from the Cohn fraction II. During the process, viruses are deactivated, and in the final steps, solvents used in the preparation are removed. The preparation is tested for absence of HIV, HCV, herpes virus, and reovirus. | Investigated for use/treatment in hepatitis (viral, B), liver transplant surgery, and pediatric indications. | NA | In countries with high rates of hepatitis B infection, vaccination of newborns has not only reduced the risk of infection, but has also led to marked reduction in liver cancer. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | HBsAg | NA | NA | NA | NA | NA | 220 [iU]/mL, 1560 [iU]/5mL, 312 [iU]/mL - Injections; 312 [iU]/mL, 50 mg/mL - Injections solutions | Injection; Solution | Intra muscular; IV | NA | NA | NA | NA | NA | NA |
| 10786 | Th1183 | Hepatitis B immune globulin | NA | NA | NA | NA | NA | NA | 22-25 days | Long-term hepatitis B immune globulin (HBIG) has been shown to reduce hepatitis B virus (HBV) reinfection in patients transplanted for hepatitis B. Infection with hepatitis B may lead to hepatocellular carcinoma, a type of liver cancer. Therefore, the hepatitis-B vaccines are cancer-preventing vaccines. According to the Centers for Disease Control and Prevention (CDC), the hepatitis B vaccine was the first anti-cancer vaccine. HBIG is prepared from the plasma of donors who have high antibody levels of the hepatitis B surface antigen. It is extracted from the Cohn fraction II. During the process, viruses are deactivated, and in the final steps, solvents used in the preparation are removed. The preparation is tested for absence of HIV, HCV, herpes virus, and reovirus. | Investigated for use/treatment in hepatitis (viral, B), liver transplant surgery, and pediatric indications. | NA | In countries with high rates of hepatitis B infection, vaccination of newborns has not only reduced the risk of infection, but has also led to marked reduction in liver cancer. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | HBsAg | Hepagam B | Cangene Bio Pharma Inc. | Cangene Bio Pharma Inc. | HepaGam Bâ„¢, Hepatitis B Immune Globulin Intravenous (Human), is indicated for the prevention of hepatitis B recurrence following liver transplantation, in HBsAg-positive liver transplant patients. | NA | 50 mg/mL | injection, solution | intramuscular; intravenous | Based upon the HepaGam B (hepatitis b immune globulin (human)) clinical trial, patients should receive 20,000 lU/dose [see Clinical Trials in Liver Transplant Patients]. The volume of each 20,000 IU dose should be calculated from the measured potency of the particular lot of HepaGam Bâ„¢ (Hepatitis B Immune Globulin Intravenous [Human]) as stamped on the vial label. The first dose should be administered concurrently with the grafting of the transplanted liver (the anhepatic phase) with subsequent dosing as recommended | Individuals known to have anaphylactic or severe systematic reactions associated with the parenteral administration of human globulin preparations should not receive HepaGam B (hepatitis b immune globulin (human)) , (Hepatitis B Immune Globulin Intravenous [Human]), or any other human immune globulin. HepaGam B (hepatitis b immune globulin (human)) contains less than 40 micro-grams/mL of IgA. Individuals who are deficient in IgA may have the potential to develop IgA antibodies and have an anaphylactoid reaction. The physician must weigh the potential benefit of treatment with HepaGam B (hepatitis b immune globulin (human)) against the potential for hypersensitivity reactions. For postexposure prophylaxis indications, HepaGam B (hepatitis b immune globulin (human)) must be administered intramuscularly only. In patients who have severe thrombocytopenia or any coagulation disorder that would contraindicate intramuscular injections, HepaGam B (hepatitis b immune globulin (human)) should be given only if the expected benefits outweigh the potential risks. | The most common expected adverse drug reactions for intravenous immune globulins like HepaGam B (hepatitis b immune globulin (human)) are chills, fever, headaches, vomiting, allergic reactions, nausea, arthralgia and moderate low back pain. | Link | NA | NA |
| 10787 | Th1183 | Hepatitis B immune globulin | NA | NA | NA | NA | NA | NA | 22-25 days | Long-term hepatitis B immune globulin (HBIG) has been shown to reduce hepatitis B virus (HBV) reinfection in patients transplanted for hepatitis B. Infection with hepatitis B may lead to hepatocellular carcinoma, a type of liver cancer. Therefore, the hepatitis-B vaccines are cancer-preventing vaccines. According to the Centers for Disease Control and Prevention (CDC), the hepatitis B vaccine was the first anti-cancer vaccine. HBIG is prepared from the plasma of donors who have high antibody levels of the hepatitis B surface antigen. It is extracted from the Cohn fraction II. During the process, viruses are deactivated, and in the final steps, solvents used in the preparation are removed. The preparation is tested for absence of HIV, HCV, herpes virus, and reovirus. | Investigated for use/treatment in hepatitis (viral, B), liver transplant surgery, and pediatric indications. | NA | In countries with high rates of hepatitis B infection, vaccination of newborns has not only reduced the risk of infection, but has also led to marked reduction in liver cancer. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | HBsAg | Hepagam B | Cangene Bio Pharma Inc. | Cangene Bio Pharma Inc. | HepaGam Bâ„¢, Hepatitis B Immune Globulin Intravenous (Human), is indicated for the prevention of hepatitis B recurrence following liver transplantation, in HBsAg-positive liver transplant patients. | NA | 50 mg/mL | injection, solution | intramuscular; intravenous | Based upon the HepaGam B (hepatitis b immune globulin (human)) clinical trial, patients should receive 20,000 lU/dose [see Clinical Trials in Liver Transplant Patients]. The volume of each 20,000 IU dose should be calculated from the measured potency of the particular lot of HepaGam Bâ„¢ (Hepatitis B Immune Globulin Intravenous [Human]) as stamped on the vial label. The first dose should be administered concurrently with the grafting of the transplanted liver (the anhepatic phase) with subsequent dosing as recommended | Individuals known to have anaphylactic or severe systematic reactions associated with the parenteral administration of human globulin preparations should not receive HepaGam B (hepatitis b immune globulin (human)) , (Hepatitis B Immune Globulin Intravenous [Human]), or any other human immune globulin. HepaGam B (hepatitis b immune globulin (human)) contains less than 40 micro-grams/mL of IgA. Individuals who are deficient in IgA may have the potential to develop IgA antibodies and have an anaphylactoid reaction. The physician must weigh the potential benefit of treatment with HepaGam B (hepatitis b immune globulin (human)) against the potential for hypersensitivity reactions. For postexposure prophylaxis indications, HepaGam B (hepatitis b immune globulin (human)) must be administered intramuscularly only. In patients who have severe thrombocytopenia or any coagulation disorder that would contraindicate intramuscular injections, HepaGam B (hepatitis b immune globulin (human)) should be given only if the expected benefits outweigh the potential risks. | The most common expected adverse drug reactions for intravenous immune globulins like HepaGam B (hepatitis b immune globulin (human)) are chills, fever, headaches, vomiting, allergic reactions, nausea, arthralgia and moderate low back pain. | Link | NA | NA |
| 10788 | Th1183 | Hepatitis B immune globulin | NA | NA | NA | NA | NA | NA | 22-25 days | Long-term hepatitis B immune globulin (HBIG) has been shown to reduce hepatitis B virus (HBV) reinfection in patients transplanted for hepatitis B. Infection with hepatitis B may lead to hepatocellular carcinoma, a type of liver cancer. Therefore, the hepatitis-B vaccines are cancer-preventing vaccines. According to the Centers for Disease Control and Prevention (CDC), the hepatitis B vaccine was the first anti-cancer vaccine. HBIG is prepared from the plasma of donors who have high antibody levels of the hepatitis B surface antigen. It is extracted from the Cohn fraction II. During the process, viruses are deactivated, and in the final steps, solvents used in the preparation are removed. The preparation is tested for absence of HIV, HCV, herpes virus, and reovirus. | Investigated for use/treatment in hepatitis (viral, B), liver transplant surgery, and pediatric indications. | NA | In countries with high rates of hepatitis B infection, vaccination of newborns has not only reduced the risk of infection, but has also led to marked reduction in liver cancer. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | HBsAg | Hepagam B | Cangene Bio Pharma Inc. | Cangene Bio Pharma Inc. | HepaGam Bâ„¢, Hepatitis B Immune Globulin Intravenous (Human), is indicated for the prevention of hepatitis B recurrence following liver transplantation, in HBsAg-positive liver transplant patients. | NA | 312 [iU]/mL | injection, solution | intramuscular; intravenous | Based upon the HepaGam B (hepatitis b immune globulin (human)) clinical trial, patients should receive 20,000 lU/dose [see Clinical Trials in Liver Transplant Patients]. The volume of each 20,000 IU dose should be calculated from the measured potency of the particular lot of HepaGam Bâ„¢ (Hepatitis B Immune Globulin Intravenous [Human]) as stamped on the vial label. The first dose should be administered concurrently with the grafting of the transplanted liver (the anhepatic phase) with subsequent dosing as recommended | Individuals known to have anaphylactic or severe systematic reactions associated with the parenteral administration of human globulin preparations should not receive HepaGam B (hepatitis b immune globulin (human)) , (Hepatitis B Immune Globulin Intravenous [Human]), or any other human immune globulin. HepaGam B (hepatitis b immune globulin (human)) contains less than 40 micro-grams/mL of IgA. Individuals who are deficient in IgA may have the potential to develop IgA antibodies and have an anaphylactoid reaction. The physician must weigh the potential benefit of treatment with HepaGam B (hepatitis b immune globulin (human)) against the potential for hypersensitivity reactions. For postexposure prophylaxis indications, HepaGam B (hepatitis b immune globulin (human)) must be administered intramuscularly only. In patients who have severe thrombocytopenia or any coagulation disorder that would contraindicate intramuscular injections, HepaGam B (hepatitis b immune globulin (human)) should be given only if the expected benefits outweigh the potential risks. | The most common expected adverse drug reactions for intravenous immune globulins like HepaGam B (hepatitis b immune globulin (human)) are chills, fever, headaches, vomiting, allergic reactions, nausea, arthralgia and moderate low back pain. | Link | NA | NA |
| 10789 | Th1183 | Hepatitis B immune globulin | NA | NA | NA | NA | NA | NA | 22-25 days | Long-term hepatitis B immune globulin (HBIG) has been shown to reduce hepatitis B virus (HBV) reinfection in patients transplanted for hepatitis B. Infection with hepatitis B may lead to hepatocellular carcinoma, a type of liver cancer. Therefore, the hepatitis-B vaccines are cancer-preventing vaccines. According to the Centers for Disease Control and Prevention (CDC), the hepatitis B vaccine was the first anti-cancer vaccine. HBIG is prepared from the plasma of donors who have high antibody levels of the hepatitis B surface antigen. It is extracted from the Cohn fraction II. During the process, viruses are deactivated, and in the final steps, solvents used in the preparation are removed. The preparation is tested for absence of HIV, HCV, herpes virus, and reovirus. | Investigated for use/treatment in hepatitis (viral, B), liver transplant surgery, and pediatric indications. | NA | In countries with high rates of hepatitis B infection, vaccination of newborns has not only reduced the risk of infection, but has also led to marked reduction in liver cancer. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | HBsAg | Hepagam B | Cangene Bio Pharma Inc. | Cangene Bio Pharma Inc. | HepaGam Bâ„¢, Hepatitis B Immune Globulin Intravenous (Human), is indicated for the prevention of hepatitis B recurrence following liver transplantation, in HBsAg-positive liver transplant patients. | NA | 312 [iU]/mL | injection, solution | intramuscular; intravenous | Based upon the HepaGam B (hepatitis b immune globulin (human)) clinical trial, patients should receive 20,000 lU/dose [see Clinical Trials in Liver Transplant Patients]. The volume of each 20,000 IU dose should be calculated from the measured potency of the particular lot of HepaGam Bâ„¢ (Hepatitis B Immune Globulin Intravenous [Human]) as stamped on the vial label. The first dose should be administered concurrently with the grafting of the transplanted liver (the anhepatic phase) with subsequent dosing as recommended | Individuals known to have anaphylactic or severe systematic reactions associated with the parenteral administration of human globulin preparations should not receive HepaGam B (hepatitis b immune globulin (human)) , (Hepatitis B Immune Globulin Intravenous [Human]), or any other human immune globulin. HepaGam B (hepatitis b immune globulin (human)) contains less than 40 micro-grams/mL of IgA. Individuals who are deficient in IgA may have the potential to develop IgA antibodies and have an anaphylactoid reaction. The physician must weigh the potential benefit of treatment with HepaGam B (hepatitis b immune globulin (human)) against the potential for hypersensitivity reactions. For postexposure prophylaxis indications, HepaGam B (hepatitis b immune globulin (human)) must be administered intramuscularly only. In patients who have severe thrombocytopenia or any coagulation disorder that would contraindicate intramuscular injections, HepaGam B (hepatitis b immune globulin (human)) should be given only if the expected benefits outweigh the potential risks. | The most common expected adverse drug reactions for intravenous immune globulins like HepaGam B (hepatitis b immune globulin (human)) are chills, fever, headaches, vomiting, allergic reactions, nausea, arthralgia and moderate low back pain. | Link | NA | NA |
| 10797 | Th1186 | Human rabies virus immune globulin | NA | NA | NA | NA | NA | NA | NA | NA | It is indicated for individuals suspected of exposure to rabies, particularly severe exposure, with one exception: persons who have been previously immunized with HDCV Rabies Vaccine in a pre-exposure or postexposure treatment series should receive only vaccine. | NA | It provides passive protection by neutralizing the rabies virus when given to individuals exposed to rabies virus. When a rabies immune globulin dose of 20 IU/kg was given simultaneously with the first dose of rabies vaccine, levels of passive anti-rabies antibody were detected 24 hours after injection in all individuals. There was minimal or no interference with the immune response to the initial and subsequent doses of rabies vaccine, including booster doses. | NA | NA | NA | NA | NA | NA | NA | NA | NA | Live virus vaccines, such as measles vaccine, should not be given for four months following Human rabies virus immune globulin administration because antibodies in the immune globulin preparation may interfere with the immune response to the vaccine. | NA | Hyperrab S/d | Grifols Therapeutics Inc | Grifols Therapeutics Inc | Rabies immune globulin is used together with rabies vaccine to prevent infection caused by the rabies virus. | NA | 150 unit | Solution | intramuscular | The recommended dose for HyperRAB S/D is 20 IU/kg (0.133 mL/kg) of body weight given preferably at the time of the first vaccine dose | Hypersensitivity | Fever, pain, soreness, tenderness, or stiffness at the injection site, Skin rash | Link | NA | NA |
| 10799 | Th1186 | Human rabies virus immune globulin | NA | NA | NA | NA | NA | NA | NA | NA | It is indicated for individuals suspected of exposure to rabies, particularly severe exposure, with one exception: persons who have been previously immunized with HDCV Rabies Vaccine in a pre-exposure or postexposure treatment series should receive only vaccine. | NA | It provides passive protection by neutralizing the rabies virus when given to individuals exposed to rabies virus. When a rabies immune globulin dose of 20 IU/kg was given simultaneously with the first dose of rabies vaccine, levels of passive anti-rabies antibody were detected 24 hours after injection in all individuals. There was minimal or no interference with the immune response to the initial and subsequent doses of rabies vaccine, including booster doses. | NA | NA | NA | NA | NA | NA | NA | NA | NA | Live virus vaccines, such as measles vaccine, should not be given for four months following Human rabies virus immune globulin administration because antibodies in the immune globulin preparation may interfere with the immune response to the vaccine. | NA | Imogam Rabies Pasteurized | Sanofi Pasteur Limited | Sanofi Pasteur Limited | It is indicated for post-exposure prophylaxis in persons suspected of exposure to rabies, who have not previously received a complete immunization regimen with a cell culture produced rabies vaccine. | NA | Human proteins (100-160 mg) containing IgG-class human rabies immune globulins with a minimum titre of 150 IU/mL. Supplied in 2 mL vial s (300 IU) and 10 mL vials (1,500 IU). | Solution | intramuscular | The recommended dose of IMOGAM® Rabies Pasteurized is 20 IU/kg (0.133 mL/kg) of body weight at the time of administration of the first dose of rabies vaccine. | IMOGAM® Rabies Pasteurized should not be administered as repeat doses once rabies vaccination has been in itiated. Repeating the dose may interfere with maximum active immunity expected to develop from the rabies vaccine. | Hypotension, Tachycardia, Nausea, Vomiting, Local reaction, Fever, chills, Allergic type reaction, Anaphylactic shock, General prurit, Rash | Link | NA | NA |
| 10802 | Th1187 | Human Rho(D) immune globulin | NA | NA | NA | NA | NA | NA | The half life is 16 ± 4 days following IV administration and 18 ± 5 days following IM administration. | Human Rho(D) immune globulin is a medicine given by intramuscular injection that is used to prevent the immunological condition known as Rh disease (or hemolytic disease of newborn). Human Rho(D) immune globulin is produced by an ion-exchange chromatography isolation procedure, using pooled plasma obtained by plasmapheresis of immunized Rh0(D)-negative US donors. | NA | NA | It acts by suppressing the immune response of Rh-negative individuals to Rh-positive red blood cells. The mechanism of action is unknown. RhoGAM, MICRhoGAM and other Rho(D) Immune Globulin (Human) products are not effective in altering the course or consequences of Rh immunization once it has occurred. | Most serious adverse reactions in patients with ITP include intravascular hemolysis, anemia, acute renal insufficiency, and death. In patients treated for Rh isoimmunization suppression, common adverse effects include nausea, dizziness, headache, pain at injection site and malaise. Common adverse effects in patients with ITP include chills, pyrexia, mild extravascular hemolysis and headache. | Rho (D) immune globulin is expected to undergo nonspecific catabolism. | In patients undergoing therapy for Rh isoimmunization suppression, Rho(D) immune globulin titers were detected in all women up to at least 9 weeks following either intravenous or intramuscular administration. Following intravenous administration of a single 1500 IU (300 mcg) dose, peak serum levels of Rh0(D) immune globulin ranged from 62 to 84 ng/mL after first day. The levels ranged from 7 to 46 ng/mL and were achieved between 2 and 7 days following intramuscular injection. The absolute bioavailability achieved following IM administration is 69%. | A single dose of 300ug Rho(D) Immune Globulin through intramuscular injection displays a Vd of 8.59L [L805]. | Mean systemic clearance following IV administration is 0.20 ±0.03 mL/min. Mean apparent clearance following IM administration is 0.29 ± 0.12 mL/min. | NA | NA | NA | NA | NA | Rhesus blood group D antigen | Hyperrho S/d Mini-dose | GRIFOLS USA, LLC | GRIFOLS USA, LLC | NA | NA | 250 [iU]/1 | Solution | Intramuscular | NA | NA | NA | Link | NA | NA |
| 10803 | Th1187 | Human Rho(D) immune globulin | NA | NA | NA | NA | NA | NA | The half life is 16 ± 4 days following IV administration and 18 ± 5 days following IM administration. | Human Rho(D) immune globulin is a medicine given by intramuscular injection that is used to prevent the immunological condition known as Rh disease (or hemolytic disease of newborn). Human Rho(D) immune globulin is produced by an ion-exchange chromatography isolation procedure, using pooled plasma obtained by plasmapheresis of immunized Rh0(D)-negative US donors. | NA | NA | It acts by suppressing the immune response of Rh-negative individuals to Rh-positive red blood cells. The mechanism of action is unknown. RhoGAM, MICRhoGAM and other Rho(D) Immune Globulin (Human) products are not effective in altering the course or consequences of Rh immunization once it has occurred. | Most serious adverse reactions in patients with ITP include intravascular hemolysis, anemia, acute renal insufficiency, and death. In patients treated for Rh isoimmunization suppression, common adverse effects include nausea, dizziness, headache, pain at injection site and malaise. Common adverse effects in patients with ITP include chills, pyrexia, mild extravascular hemolysis and headache. | Rho (D) immune globulin is expected to undergo nonspecific catabolism. | In patients undergoing therapy for Rh isoimmunization suppression, Rho(D) immune globulin titers were detected in all women up to at least 9 weeks following either intravenous or intramuscular administration. Following intravenous administration of a single 1500 IU (300 mcg) dose, peak serum levels of Rh0(D) immune globulin ranged from 62 to 84 ng/mL after first day. The levels ranged from 7 to 46 ng/mL and were achieved between 2 and 7 days following intramuscular injection. The absolute bioavailability achieved following IM administration is 69%. | A single dose of 300ug Rho(D) Immune Globulin through intramuscular injection displays a Vd of 8.59L [L805]. | Mean systemic clearance following IV administration is 0.20 ±0.03 mL/min. Mean apparent clearance following IM administration is 0.29 ± 0.12 mL/min. | NA | NA | NA | NA | NA | Rhesus blood group D antigen | Micrhogam Ultra-filtered Plus | Kedrion Melville, Inc. | Kedrion Melville, Inc. | NA | NA | 50 ug/1 | injection, solution | Intramuscular | NA | NA | NA | Link | NA | NA |
| 10804 | Th1187 | Human Rho(D) immune globulin | NA | NA | NA | NA | NA | NA | The half life is 16 ± 4 days following IV administration and 18 ± 5 days following IM administration. | Human Rho(D) immune globulin is a medicine given by intramuscular injection that is used to prevent the immunological condition known as Rh disease (or hemolytic disease of newborn). Human Rho(D) immune globulin is produced by an ion-exchange chromatography isolation procedure, using pooled plasma obtained by plasmapheresis of immunized Rh0(D)-negative US donors. | NA | NA | It acts by suppressing the immune response of Rh-negative individuals to Rh-positive red blood cells. The mechanism of action is unknown. RhoGAM, MICRhoGAM and other Rho(D) Immune Globulin (Human) products are not effective in altering the course or consequences of Rh immunization once it has occurred. | Most serious adverse reactions in patients with ITP include intravascular hemolysis, anemia, acute renal insufficiency, and death. In patients treated for Rh isoimmunization suppression, common adverse effects include nausea, dizziness, headache, pain at injection site and malaise. Common adverse effects in patients with ITP include chills, pyrexia, mild extravascular hemolysis and headache. | Rho (D) immune globulin is expected to undergo nonspecific catabolism. | In patients undergoing therapy for Rh isoimmunization suppression, Rho(D) immune globulin titers were detected in all women up to at least 9 weeks following either intravenous or intramuscular administration. Following intravenous administration of a single 1500 IU (300 mcg) dose, peak serum levels of Rh0(D) immune globulin ranged from 62 to 84 ng/mL after first day. The levels ranged from 7 to 46 ng/mL and were achieved between 2 and 7 days following intramuscular injection. The absolute bioavailability achieved following IM administration is 69%. | A single dose of 300ug Rho(D) Immune Globulin through intramuscular injection displays a Vd of 8.59L [L805]. | Mean systemic clearance following IV administration is 0.20 ±0.03 mL/min. Mean apparent clearance following IM administration is 0.29 ± 0.12 mL/min. | NA | NA | NA | NA | NA | Rhesus blood group D antigen | Rhogam Ultra-filtered Plus | Kedrion Melville, Inc. | Kedrion Melville, Inc. | NA | NA | 300 ug/1 | injection, solution | Intramuscular | NA | NA | NA | Link | NA | NA |
| 10805 | Th1187 | Human Rho(D) immune globulin | NA | NA | NA | NA | NA | NA | The half life is 16 ± 4 days following IV administration and 18 ± 5 days following IM administration. | Human Rho(D) immune globulin is a medicine given by intramuscular injection that is used to prevent the immunological condition known as Rh disease (or hemolytic disease of newborn). Human Rho(D) immune globulin is produced by an ion-exchange chromatography isolation procedure, using pooled plasma obtained by plasmapheresis of immunized Rh0(D)-negative US donors. | NA | NA | It acts by suppressing the immune response of Rh-negative individuals to Rh-positive red blood cells. The mechanism of action is unknown. RhoGAM, MICRhoGAM and other Rho(D) Immune Globulin (Human) products are not effective in altering the course or consequences of Rh immunization once it has occurred. | Most serious adverse reactions in patients with ITP include intravascular hemolysis, anemia, acute renal insufficiency, and death. In patients treated for Rh isoimmunization suppression, common adverse effects include nausea, dizziness, headache, pain at injection site and malaise. Common adverse effects in patients with ITP include chills, pyrexia, mild extravascular hemolysis and headache. | Rho (D) immune globulin is expected to undergo nonspecific catabolism. | In patients undergoing therapy for Rh isoimmunization suppression, Rho(D) immune globulin titers were detected in all women up to at least 9 weeks following either intravenous or intramuscular administration. Following intravenous administration of a single 1500 IU (300 mcg) dose, peak serum levels of Rh0(D) immune globulin ranged from 62 to 84 ng/mL after first day. The levels ranged from 7 to 46 ng/mL and were achieved between 2 and 7 days following intramuscular injection. The absolute bioavailability achieved following IM administration is 69%. | A single dose of 300ug Rho(D) Immune Globulin through intramuscular injection displays a Vd of 8.59L [L805]. | Mean systemic clearance following IV administration is 0.20 ±0.03 mL/min. Mean apparent clearance following IM administration is 0.29 ± 0.12 mL/min. | NA | NA | NA | NA | NA | Rhesus blood group D antigen | Rhophylac | Csl Behring Ag | Csl Behring Ag | NA | NA | 1500 [iU]/2mL | solution | intramuscular; intravenous | NA | NA | NA | Link | NA | NA |
| 10811 | Th1189 | Idarucizumab | >Th1189_Idarucizumab QVQLQESGPGLVKPSETLSLTCTVSGFSLTSYIVDWIRQPPGKGLEWIGVIWAGGSTGYNSALRSRVSITKDTSKNQFSLKLSSVTAADTAVYYCASAAYYSYYNYDGFAYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSC | 47766 | C2131H3299N555O671S13 | NA | NA | NA | initial half-life: 47 minutes terminal half-life: 10.3 h | Idarucizumab, sold under the brandname Praxbind, is a humanized monoclonal antibody fragment (Fab) derived from an IgG1 isotype molecule, whose target is the direct thrombin inhibitor dabigatran. Using recombinant expression technology, idarucizumab is produced in a well characterized recombinant (mammalian) CHO cell line and is purified using standard technology. Idarucizumab is composed of a light chain of 219 amino acids and a heavy chain fragment of 225 amino acids, covalently linked together by one disulfide bond between cysteine 225 of the heavy chain fragment and cysteine 219 of the light chain, and has an estimated molecular mass of approximately 47,766 Daltons. | For use in patients treated with Dabigatran when reversal of the anticoagulant effects of dabigatran is needed for emergency surgery/urgent procedures and in life-threatening or uncontrolled bleeding. | The primary PD readout for idarucizumab was reversal of dabigatran-induced anticoagulation. | Idarucizumab is a specific reversal agent for dabigatran. It is a humanized monoclonal antibody fragment (Fab) that binds to dabigatran with an affinity 300-fold more potent than the binding affinity of dabigatran for thrombin. The idarucizumab-dabigatran-complex showed a very rapid on-rate and slow off-rate of dabigatran to idarucizumab which results in a half-life of the idarucizumab-dabigatran complex of approximately 260 h. Approximately 20% of the absorbed dose of dabigatran is further metabolised in humans into glucuronides, which have equivalent anticoagulant activity to the parent drug. Idarucizumab also binds and reverses the effects of these acylglucuronides of dabigatran with a similar potency range as for dabigatran. | In healthy volunteers, the most frequently reported adverse reactions in greater than or equal to 5% of subjects treated with idarucizumab was headache. In patients, the most frequently reported adverse reactions in greater than or equal to 5% of patients treated with idarucizumab were hypokalemia, delirium, constipation, pyrexia, and pneumonia. | Several pathways have been described that may contribute to the metabolism of antibodies. All of these pathways involve biodegradation of the antibody to smaller molecules, i.e., small peptides or amino acids which are then reabsorbed and incorporated in the general protein synthesis. | NA | 8.9 L | 47.0 mL/min | Anticoagulant | NA | NA | NA | NA | NA | Praxbind | Boehringer Ingelheim (Canada) Ltd Ltee | Boehringer Ingelheim (Canada) Ltd Ltee | PRAXBIND is indicated in patients treated with Pradaxa when reversal of the anticoagulant effects of dabigatran is needed. For emergency surgery/urgent procedures. In life-threatening or uncontrolled bleeding | NA | 50 mg | Solution | IV | The recommended dose of PRAXBIND is 5 g, provided as two separate vials each containing 2.5 g/50 mL idarucizumab (see Figure 1). There is limited data to support administration of an additional 5 g of PRAXBIND | NA | Thromboembolic Risk; Hypersensitivity Reactions; Risks of Serious Adverse Reactions in Patients with Hereditary Fructose Intolerance due to Sorbitol Excipient. | 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 |
| 10813 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S43 | 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. | Bivigam | Kedrion Biopharma, Inc. | Kedrion Biopharma, Inc. | BIVIGAM is an Immune Globulin Intravenous (Human), 10% Liquid, indicated for the treatment of patients with primary humoral immunodeficiency (PI). | NA | 1 g/10mL | injection, solution | Intravenous | The recommended dose of BIVIGAM for replacement therapy in primary humoral immunodeficiency (PI) is 300 to 800 mg/kg body weight administered every 3 to 4 weeks. The dosage may be adjusted over time to achieve the desired trough levels and clinical response. | BIVIGAM is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. BIVIGAM is contraindicated in IgA deficiency patients with antibodies to IgA and a history of hypersensitivity. | Serious adverse reactions observed in clinical trial subjects receiving BIVIGAM were vomiting and dehydration in one subject. The most common adverse reactions to BIVIGAM (reported in ≥ 5% of clinical study subjects) were headache, fatigue, infusion site reaction, nausea, sinusitis, blood pressure increased, diarrhea, dizziness, and lethargy. | Link | NA | NA |
| 10814 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S44 | 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. | Bivigam | Biotest Pharmaceuticals Corporation | Biotest Pharmaceuticals Corporation | BIVIGAM is an Immune Globulin Intravenous (Human), 10% Liquid, indicated for the treatment of patients with primary humoral immunodeficiency (PI). | NA | 10 g/100mL | injection, solution | Intravenous | The recommended dose of BIVIGAM for replacement therapy in primary humoral immunodeficiency (PI) is 300 to 800 mg/kg body weight administered every 3 to 4 weeks. The dosage may be adjusted over time to achieve the desired trough levels and clinical response. | BIVIGAM is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. BIVIGAM is contraindicated in IgA deficiency patients with antibodies to IgA and a history of hypersensitivity. | Serious adverse reactions observed in clinical trial subjects receiving BIVIGAM were vomiting and dehydration in one subject. The most common adverse reactions to BIVIGAM (reported in ≥ 5% of clinical study subjects) were headache, fatigue, infusion site reaction, nausea, sinusitis, blood pressure increased, diarrhea, dizziness, and lethargy. | Link | NA | NA |
| 10815 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S45 | 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. | Bivigam | Biotest Pharmaceuticals Corporation | Biotest Pharmaceuticals Corporation | BIVIGAM is an Immune Globulin Intravenous (Human), 10% Liquid, indicated for the treatment of patients with primary humoral immunodeficiency (PI). | NA | 11 g/100mL | injection, solution | Intravenous | The recommended dose of BIVIGAM for replacement therapy in primary humoral immunodeficiency (PI) is 300 to 800 mg/kg body weight administered every 3 to 4 weeks. The dosage may be adjusted over time to achieve the desired trough levels and clinical response. | BIVIGAM is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. BIVIGAM is contraindicated in IgA deficiency patients with antibodies to IgA and a history of hypersensitivity. | Serious adverse reactions observed in clinical trial subjects receiving BIVIGAM were vomiting and dehydration in one subject. The most common adverse reactions to BIVIGAM (reported in ≥ 5% of clinical study subjects) were headache, fatigue, infusion site reaction, nausea, sinusitis, blood pressure increased, diarrhea, dizziness, and lethargy. | Link | NA | NA |
| 10816 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S46 | 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. | Carimune Nanofiltered | Csl Behring Ag | Csl Behring Ag | Carimune® NF is indicated for the maintenance treatment of patients with primary immunodeficiencies (PID), e.g., common variable immunodeficiency, X-linked agammaglobulinemia, severe combined immunodeficiency. Carimune® NF is preferable to intramuscular Immune Globulin (Human) preparations in treating patients who require an immediate and large increase in the intravascular immunoglobulin level, in patients with limited muscle mass, and in patients with bleeding tendencies for whom intramuscular injections are contraindicated. | NA | 12 g/1 | injection, powder, lyophilized, for solution | Intravenous | The recommended dose of Carimune® NF in primary immunodeficiency is 0.4 to 0.8 g/kg of body weight administered once every three to four weeks by intravenous infusion. | Carimune® NF is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. Individuals with IgA deficiency, especially those who have known antibody against IgA, or hypersensitivity to immunoglobulins should only receive Carimune® NF with utmost caution due to the risk of severe immediate hypersensitivity reactions including anaphylaxis. | Increases in creatinine and blood urea nitrogen (BUN) have been observed as soon as one to two days following infusion. Progression to oliguria or anuria, requiring dialysis has been observed. Types of severe renal adverse events that have been seen following IGIV therapy include: acute renal failure, acute tubular necrosis, proximal tubular nephropathy and osmotic nephrosis. Inflammatory adverse reactions have been described in agammaglobulinemic and hypogammaglobulinemic patients who have never received immunoglobulin substitution therapy before or in patients whose time from last treatment is greater than 8 weeks and whose initial infusion rate exceeds 2 mg/kg/min. | Link | NA | NA |
| 10817 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S47 | 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. | Carimune Nanofiltered | Csl Behring Ag | Csl Behring Ag | Carimune® NF is indicated for the maintenance treatment of patients with primary immunodeficiencies (PID), e.g., common variable immunodeficiency, X-linked agammaglobulinemia, severe combined immunodeficiency. Carimune® NF is preferable to intramuscular Immune Globulin (Human) preparations in treating patients who require an immediate and large increase in the intravascular immunoglobulin level, in patients with limited muscle mass, and in patients with bleeding tendencies for whom intramuscular injections are contraindicated. | NA | 6 g/1 | injection, powder, lyophilized, for solution | Intravenous | The recommended dose of Carimune® NF in primary immunodeficiency is 0.4 to 0.8 g/kg of body weight administered once every three to four weeks by intravenous infusion. | Carimune® NF is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. Individuals with IgA deficiency, especially those who have known antibody against IgA, or hypersensitivity to immunoglobulins should only receive Carimune® NF with utmost caution due to the risk of severe immediate hypersensitivity reactions including anaphylaxis. | Increases in creatinine and blood urea nitrogen (BUN) have been observed as soon as one to two days following infusion. Progression to oliguria or anuria, requiring dialysis has been observed. Types of severe renal adverse events that have been seen following IGIV therapy include: acute renal failure, acute tubular necrosis, proximal tubular nephropathy and osmotic nephrosis. Inflammatory adverse reactions have been described in agammaglobulinemic and hypogammaglobulinemic patients who have never received immunoglobulin substitution therapy before or in patients whose time from last treatment is greater than 8 weeks and whose initial infusion rate exceeds 2 mg/kg/min. | Link | NA | NA |
| 10818 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S48 | 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. | Carimune Nanofiltered | Csl Behring Ag | Csl Behring Ag | Carimune® NF is indicated for the maintenance treatment of patients with primary immunodeficiencies (PID), e.g., common variable immunodeficiency, X-linked agammaglobulinemia, severe combined immunodeficiency. Carimune® NF is preferable to intramuscular Immune Globulin (Human) preparations in treating patients who require an immediate and large increase in the intravascular immunoglobulin level, in patients with limited muscle mass, and in patients with bleeding tendencies for whom intramuscular injections are contraindicated. | NA | 3 g/1 | injection, powder, lyophilized, for solution | Intravenous | The recommended dose of Carimune® NF in primary immunodeficiency is 0.4 to 0.8 g/kg of body weight administered once every three to four weeks by intravenous infusion. | Carimune® NF is contraindicated in patients who have had an anaphylactic or severe systemic reaction to the administration of human immune globulin. Individuals with IgA deficiency, especially those who have known antibody against IgA, or hypersensitivity to immunoglobulins should only receive Carimune® NF with utmost caution due to the risk of severe immediate hypersensitivity reactions including anaphylaxis. | Increases in creatinine and blood urea nitrogen (BUN) have been observed as soon as one to two days following infusion. Progression to oliguria or anuria, requiring dialysis has been observed. Types of severe renal adverse events that have been seen following IGIV therapy include: acute renal failure, acute tubular necrosis, proximal tubular nephropathy and osmotic nephrosis. Inflammatory adverse reactions have been described in agammaglobulinemic and hypogammaglobulinemic patients who have never received immunoglobulin substitution therapy before or in patients whose time from last treatment is greater than 8 weeks and whose initial infusion rate exceeds 2 mg/kg/min. | Link | NA | NA |
| 10819 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S49 | 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. | Flebogamma Dif | GRIFOLS USA, LLC | GRIFOLS USA, LLC | NA | NA | 5 g/50mL | injection, solution | Intravenous | Primary Immunodeficiency (PI); Chronic Primary Immune Thrombocytopenia (ITP) | Flebogamma 10% DIF is contraindicated in patients who have had a history of anaphylactic or severe systemic hypersensitivity reactions to the administration of human immune globulin. Flebogamma 10% DIF is contraindicated in IgA deficient patients with antibodies to IgA and a history of hypersensitivity. | The most common adverse reactions (reported in ≥ 5% of clinical trial subjects) were: PI: headache, fever/pyrexia, shaking, tachycardia, hypotension, back pain, myalgia, hypertension, chest pain, pain, nausea, infusion site reactions and pain in extremities. ITP: headache, pyrexia, nausea, chills, vomiting, body temperature increased, dizziness, back pain, hypotension, hypertension, heart rate increased and diarrhea. | Link | NA | NA |
| 10820 | Th1190 | Immune Globulin Human | >Th1190_Immune_Globulin_Human PSALTQPPSASGSLGQSVTISCTGTSSDVGGYNYVSWYQQHAGKAPKVIIYEVNKRPSGVPDRFSGSKSGNTASLTVSGLQAEDEADYYCSSYEGSDNFVFGTGTKVTVLGQPKANPTVTLFPPSSEELQANKATEVCLISDFYPGAVTVAWKADGSPVKAGVETTKPSKQSNNKYAASSYLSLTPEQWKSHRSYSCQVTHEGSTVEKTVAPTECSPLVLQESGPGLVKPSEALSLTCTVSGDSINTILYYWSWIRQPPGKGLEWIGYIYYSGSTYGNPSLKSRVTISVNTSKNQFYSKLSSVTAADTAVYYCARVPLVVNPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPQPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSL | 142682.3 | C6332H9826N1692O1980S50 | 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. | Flebogamma Dif | GRIFOLS USA, LLC | GRIFOLS USA, LLC | NA | NA | .05 g/mL | injection, solution | Intravenous | Primary Immunodeficiency (PI); Chronic Primary Immune Thrombocytopenia (ITP) | Flebogamma 10% DIF is contraindicated in patients who have had a history of anaphylactic or severe systemic hypersensitivity reactions to the administration of human immune globulin. Flebogamma 10% DIF is contraindicated in IgA deficient patients with antibodies to IgA and a history of hypersensitivity. | The most common adverse reactions (reported in ≥ 5% of clinical trial subjects) were: PI: headache, fever/pyrexia, shaking, tachycardia, hypotension, back pain, myalgia, hypertension, chest pain, pain, nausea, infusion site reactions and pain in extremities. ITP: headache, pyrexia, nausea, chills, vomiting, body temperature increased, dizziness, back pain, hypotension, hypertension, heart rate increased and diarrhea. | Link | NA | NA |
| 10825 | Th1191 | Vedolizumab | >Th1191_Vedolizumab QVQLVQSGAEVKKPGASVKVSCKGSGYTFTSYWMHWVRQAPGQRLEWIGEIDPSESNTNYNQKFKGRVTLTVDISASTAYMELSSLRSEDTAVYYCARGGYDGWDYAIDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELAGAPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 146837 | C6528H10072N1732O2042S42 | 7.6 | NA | NA | 336 to 362 hr. | Vedolizumab is a recombinant humanized IgG1 monoclonal antibody directed against the human lymphocyte α4β7 integrin, a key mediator of gastrointestinal inflammation. It is used in the treatment of moderate to severe active ulcerative colitis and Crohn’s disease for patients who have had an inadequate response with, lost response to, or were intolerant to inhibitors of tumor necrosis factor-alpha (TNF-alpha) or other conventional therapies. By blocking its primary target, α4β7 integrin, vedolizumab reduces inflammation in the gut. | It is indicated for adult patients with moderately to severely active UC or CD who have had an inadequate response with, lost response to, or were intolerant to a tumor necrosis factor (TNF) blocker or immunomodulator; or had an inadequate response with, were intolerant to, or demonstrated dependence on corticosteroids. | Non-clinical studies have shown that the pharmacodynamic effects of vedolizumab are reversible upon removal of the antibody: pharmacologic activity of cells inhibited by vedolizumab could be partially restored within 24 hours after removal, with near complete restoration within 4 days. There are no known drug interactions as vedolizumab is a humanized antibody and does not modulate production of cytokines, which is known to affect drug metabolism | Vedolizumab binds to α4β7 integrin, a key mediator of gastrointestinal inflammation expressed on the surfaces of T and B lymphocytes. By selectively inhibiting the α4β7 integrin, vedolizumab inhibits adhesion of lymphocytes to its natural ligand, mucosal addressin cell adhesion molecule-1 (MAdCAM-1), thereby preventing lymphocytic cells from entering the gut lamina propria and gut-associated lymphoid tissue (GALT). Specifically inhibiting this pathway alleviates GI inflammation without impairing systemic immune responses. | Long-term studies in animals have not been performed to evaluate the carcinogenic potential, mutagenicity, or possible impairments to fertility. Elevated transaminase levels with or without elevated bilirubin has occurred in patients who have received this drug. Progressive multifocal leukoencephalopathy (PML) has not been reported with use of this drug, however it has occurred in patients who have received different integrin receptor antagonists and is therefore considered a risk for this product. Use of vedolizumab may increase risk of developing infections, and one study found that nasopharyngitis occurs more frequently with vedolizumab than with placebo for CD patients (Wang et al, 2014). | The expected consequence of metabolism is proteolytic degradation to small peptides and individual amino acids, and receptor-mediated clearance. | The intended route of administration is intravenous, therefore there is no absorption data and bioavailability is expected to be 100%. | Serum apparent volume of distribution at steady-state has been found to be moderately greater than the serum volume. It is therefore expected to be confined to the systemic circulation, as expected for a high molecular weight protein. | Vedolizumab has a low clearance of 0.180 to 0.266 ml/hr/kg. | Immunosupressive agent, Antineoplastic agent | US2012151248 | 5-Feb-2012 | 5-Feb-2032 | Adalimumab, Belimumab, Certolizumab pegol, Denosumab, Etanercept, Golimumab, Infliximab, Leflunomide, Lenalidomide, Natalizumab, Tacrolimus, Thalidomide, Belimumab, Leflunomide, Natalizumab, Sipuleucel-T, Trastuzumab and Tofacitinib | Integrin alpha-4,Integrin beta-7 | Entyvio | Takeda Pharmaceuticals America, Inc. | Takeda Pharmaceuticals America, Inc. | It is indicated for Adult Ulcerative Colitis and Adult Crohn's Disease | NA | Each single-use vial contains 300 mg vedolizumab, 23 mg L-histidine, 21.4 mg L-histidine monohydrochloride, 131.7 mg L-arginine hydrochloride, 500 mg sucrose and 3 mg polysorbate 80 | Injection, powder, lyophilized, for solution | Intravenous | The recommended dosage of ENTYVIO in adults with ulcerative colitis or Crohn's disease is 300 mg administered by intravenous infusion at zero, two and six weeks and then every eight weeks thereafter | In patients who have had a known serious or severe hypersensitivity reaction to ENTYVIO or any of its excipients (such as dyspnea, bronchospasm, urticaria, flushing, rash and increased heart rate) | The most common adverse reactions were nasopharyngitis, headache, arthralgia, nausea, pyrexia, upper respiratory tract infection, fatigue, cough, bronchitis, influenza, back pain, rash, pruritus, sinusitis, oropharyngeal pain and pain in extremities. | Link | 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 |
| 10828 | Th1194 | Tuberculin Purified Protein Derivative | NA | NA | NA | NA | NA | NA | NA | Aplisol (tuberculin PPD, diluted) is a sterile aqueous solution of a purified protein fraction for intradermal administration as an aid in the diagnosis of tuberculosis. The solution is stabilized with polysorbate (Tween) 80, buffered with potassium and sodium phosphates and contains 0.25% phenol as a preservative. The purified protein fraction is isolated from culture media filtrates of a human strain of Mycobacterium tuberculosis. | Used in the detection of infection with Mycobacterium tuberculosis. | NA | NA | Some adverse effects at the injection site include pain, discomfort, pyrexia, and erythema, rash, hemorrhage, hematoma and rarely ulcer and necrosis. Other unwanted effects include severe hypersensitivity reactions, dyspnea, generalized rash and syncope. | NA | NA | NA | NA | Antigens,Antigens, Bacterial,Antihistamine Drugs,Biological Factors,Cell-mediated Immunity,Compounds used in a research, industrial, or household setting,Indicators and Reagents,Laboratory Chemicals,Skin Test Antigen,Tuberculin,Tuberculosis,Tuberculosis Skin Test | NA | NA | NA | NA | Toll-like receptor 2 | Aplisol | Par Pharmaceutical, Inc. | Par Pharmaceutical, Inc. | Detecting tuberculosis (TB) infection. | NA | The solution is stabilized with polysorbate (Tween) 80, buffered with potassium and sodium phosphates and contains approximately 0.35% phenol as a preservative. | solution for injection | intradermal | Diagnosis: Mantoux test, inject 0.1 mL (5 tuberculin units) intradermally; the result is read 48 to 72 hours after administration | Previous positive tuberculin skin test responsiveness suppressed within 6 weeks of viral infection, inactive TB, immunosuppression, geriatric | Commonside effect include Pain, itching, or redness at the injection site. Sever side effect mmay occur Severe allergic reactions (rash; hives; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); blisters; open sores. | Link | NA | NA |
| 10829 | Th1195 | Simoctocog Alfa | NA | 170000 | NA | NA | NA | NA | 14.05 ± 4.70 h | Simoctocog Alfa is a recombinant B-domain deleted (BDD) rFVIII produced in genetically modified human embryonic kidney (HEK) 293F cells. The harvested product is concentrated and purified by a series of chromatography steps. No animal proteins are used in the purification process and no human albumin is used as a stabiliser in the manufacture of Human-cl rhFVIII. Simoctocog Alfa is a glycoprotein consisting of 1440 amino acids with an approximate molecular mass of 170 kDa, comprising the FVIII domains A1-A2 + A3-C1-C2 whereas the B-domain, present in the full-length plasma-derived FVIII, has been deleted and replaced by a 16 amino acid linker. | Treatment and prophylaxis of bleeding in patients with haemophilia A (congenital factor VIII deficiency). | The factor VIII/von Willebrand factor complex consists of two molecules (factor VIII and von Willebrand factor) with different physiological functions. When infused into a haemophiliac patient, factor VIII binds to von Willebrand factor in the patient’s circulation. Activated factor VIII acts as a cofactor for activated factor IX, accelerating the conversion of factor X to activated factor X. Activated factor X converts prothrombin into thrombin. Thrombin then converts fibrinogen into fibrin and a clot can be formed. Haemophilia A is a sex-linked hereditary disorder of blood coagulation due to decreased levels of factor VIII:C and results in profuse bleeding into joints, muscles or internal organs, either spontaneously or as results of accidental or surgical trauma. By replacement therapy the plasma levels of factor VIII are increased, thereby temporarily enabling a correction of the factor VIII deficiency and correction of the bleeding tendencies. | NA | Simoctocog alfa is not expected to cause any adverse effects on the human reproductive functions or the human fetus. As genotoxicity studies and carcinogenicity studies are not applicable for recombinant products, such studies were not performed. According to the single-dose toxicity study in rats, there were no deaths or notable life-threatening changes to the treatment and the highest non-lethal intravenous dose was determined to be < 10,000 IU/kg [L1115]. In a repeated-dose toxicity study in monkeys, there was no evidence of systemic toxicity. There were no observable local reactions at the injection sites based on the findings of a rabbit local tolerance study [L1115]. Although the formation of neutralizing antibodies (inhibitors) to FVIII is a specified warning/precaution of simoctocog alfa treatment, there have been no cases of inhibitior development throughout clinical studies [L1115]. No cases of overdose have been reported with simoctocog alfa [L1115]. | NA | At initial assessment following administration of 50 IU/kg simoctocog alfa in adolescent or adult patients with severe haemophilia A, the mean ± SD AUC (FVIII:C) was 17.95 ± 5.57 h·IU/mL/(IU/kg) [L1115]. The mean ± SD maximum plasma concentration divided by the dose (Cmaxnorm) was 0.022 ± 0.003 IU/mL/(IU/kg) [L1115]. The values of mean ± SD AUC (FVIII:C) and Cmaxnorm in pediatric patients were 10.92 ± 3.80 h·IU/mL/(IU/kg) and 0.017 ± 0.003 IU/mL/(IU/kg), respectively [L1115]. At 6-month assessment in adolescent or adult patients with the same dose, the mean ± SD AUC (FVIII:C) and Cmaxnorm were 16.86 ± 6.12 h·IU/mL/(IU/kg) and 0.021 ± 0.003 IU/mL/(IU/kg), respectively [L1115]. | It is observed that simoctocog alfa is mainly distributed in the intravascular compartment. At initial assessment following administration of 50 IU/kg simoctocog alfa in adolescent or adult patients with severe haemophilia A, the mean ± SD volume of distribution at steady state is 59.75 ± 19.76 mL/kg [L1115]. The value in pediatric patients was 67.18 ± 13.27 mL/kg [L1115]. At 6-month assessment in adolescent or adult patients with the same dose, the value was 56.90 ± 9.07 mL/kg [L1115]. | At initial assessment following administration of 50 IU/kg simoctocog alfa in adolescent or adult patients with severe haemophilia A, the mean clearance rate (CL) was 2.96 ± 0.97 mL/h/kg [L1115]. The mean CL in pediatric patients was 4.73 ± 1.87 mL/h/kg [L1115]. At 6-month assessment in adolescent or adult patients with the same dose, the value was 3.39 ± 1.42 mL/h/kg [L1115]. | Antihaemorrhagics: blood coagulation factor VIII | NA | NA | NA | NA | von Willebrand factor | Nuwiq | Octapharma Pharmazeutika Produktionsges M B H | Octapharma Pharmazeutika Produktionsges M B H | NA | human coagulation factor VIII | 250 IU | Powder and solvent for solution | Intravenous infusion | The calculation of the required dose of factor VIII is based on the empirical finding that 1 International Unit (IU) factor VIII per kg body weight raises the plasma factor VIII activity by approximately 2% of normal activity or 2 IU/dl. | Hypersensitivity to the active substance or to any of the excipients listed in section | Hypersensitivity which may include angiooedema, burning and stinging at the infusion site, chills, flushing, generalised urticaria, headache, hives, hypotension, lethargy, nausea, restlessness, tachycardia, tightness of the chest, tingling, vomiting, wheezing | Link | NA | NA |
| 10831 | Th1197 | Sebelipase alfa | >Th1197_Sebelipase_alfa SGGKLTAVDPETNMNVSEIISYWGFPSEEYLVETEDGYILCLNRIPHGRKNHSDKGPKPVVFLQHGLLADSSNWVTNLANSSLGFILADAGFDVWMGNSRGNTWSRKHKTLSVSQDEFWAFSYDEMAKYDLPASINFILNKTGQEQVYYVGHSQGTTIGFIAFSQIPELAKRIKMFFALGPVASVAFCTSPMAKLGRLPDHLIKDLFGDKEFLPQSAFLKWLGTHVCTHVILKELCGNLCFLLCGFNERNLNMSRVDVYTTHSPAGTSVQNMLHWSQAVKFQKFQAFDWGSSAKNYFHYNQSYPPTYNVKDMLVPTAVWSGGHDWLADVYDVNILLTQITNLVFHESIPEWEHLDFIWGLDAPWRLYNKIINLMRKYQ | 55000 | C1968H2945N507O551S15 | NA | NA | NA | 5.4-6.6 mins | Sebelipase alfa is a recombinant form of the enzyme lysosomal acid lipase (LAL) approved for the treatment of lysosomal acid lipase deficiency (LAL-D). The amino acid sequence for sebelipase alfa is the same as the amino acid sequence for human LAL. Sebelipase alfa is an orphan drug which is expected to cost about $310,000 for annual treatment in the United States. Sebelipase alfa is marketed under the brand name Kanumaâ„¢ by Alexion Pharmaceuticals, Inc. | Sebelipase alfa is a hydrolytic lysosomal cholesteryl ester and triacylglycerol-specific enzyme indicated for the treatment of patients with a diagnosis of Lysosomal Acid Lipase (LAL) deficiency. | In clinical trials, after initiation of dosing with KANUMA, breakdown of accumulated lysosomal lipid led to initial increases in LDL-c and triglycerides within the first 2 to 4 weeks of treatment. In general, following increases in LDL-c and triglycerides, these parameters decreased to below pre-treatment values within 8 weeks of treatment with KANUMA. | LAL deficiency is an autosomal recessive lysosomal storage disorder characterized by a genetic defect resulting in a marked decrease or loss in activity of the lysosomal acid lipase (LAL) enzyme. The primary site of action of the LAL enzyme is the lysosome, where the enzyme normally causes the breakdown of lipid particles including LDL-c. Deficient LAL enzyme activity results in progressive complications due to the lysosomal accumulation of cholesteryl esters and triglycerides in multiple organs, including the liver, spleen, intestine, and the walls of blood vessels. The resulting lipid accumulation in the liver may lead to increased liver fat content and progression of liver disease, including fibrosis and cirrhosis. Lipid accumulation in the intestinal wall leads to malabsorption and growth failure. In parallel, dyslipidemia due to impaired degradation of lysosomal lipid is common with elevated LDL-c and triglycerides and low HDL-cholesterol (HDL-c). Sebelipase alfa binds to cell surface receptors via glycans expressed on the protein and is subsequently internalized into lysosomes. Sebelipase alfa catalyzes the lysosomal hydrolysis of cholesteryl esters and triglycerides to free cholesterol, glycerol and free fatty acids. | There are no data regarding overdose with sebelipase alfa. Patients in clinical trials were exposed to doses as high as 7.5 mg/kg once weekly with no specific adverse effects observed.[L39342] | As with other therapeutic proteins, the metabolism of sebelipase alfa likely occurs via catabolism to smaller peptides and amino acids. | In patients 4-11 years old, the AUC and Cmax of sebelipase alfa following intravenous administration of 1 mg/kg every other week were 942 ng.hr/mL and 490 ng/mL, respectively.[L39337] In patients =12 years old, the AUC and Cmax ranged between 1454-1861 ng.hr/mL and 784-957 ng/mL, respectively.[L39337] The approximate Tmax of sebelipase alfa was similar across all age groups tested and ranged between 1.1-1.3 hours.[L39337] | In patients 4-11 years old, the central volume of distribution was approximately 3.6 L.[L39337] In patients =12 years old, the central volume of distribution ranged from approximately 5.3 to 5.4 L.[L39337] | Across all age groups included in pharmacokinetic testing, the mean clearance of sebelipase alpha following intravenous administration of 1 mg/kg every other week ranged from 31.1 - 38.2 L/h.[L39337] | Enzymes | NA | NA | NA | NA | NA | Kanuma | Alexion Pharmaceuticals, Inc. | Alexion Pharmaceuticals, Inc. | KANUMAâ„¢ is indicated for the treatment of patients with a diagnosis of Lysosomal Acid Lipase (LAL) deficiency. | NA | 20 mg/10 mL | Aqueous solution | Intravenous infusion | The recommended starting dosage is 1 mg/kg administered once weekly as an intravenous infusion. For patients who do not achieve an optimal clinical response, increase to 3 mg/kg once weekly. | NA | Diarrhea, vomiting, fever, rhinitis, anemia, cough, nasopharyngitis, urticaria. | Link | NA | NA |
| 10832 | Th1198 | Sacrosidase | NA | 100000 | NA | NA | NA | NA | NA | Sacrosidase is a liquid enzyme preparation from S.cerevisiae used for the treatment of congenital sucrose-isomaltase deficiency (CSID). People with CSID have variable amounts of sucrose-isomaltase enzyme activity and therefore have issues metabolizing dietary disaccharide sucrose causing chronic or intermittent watery diarrhea in infants and children. Treatment options for these patients are limited and usually consists of a lifelong sucrose-free diet; therefore, sacrosidase offers a potential alternative for symptom relief. | For the treatment of congenital sucrose-isomaltase deficiency (CSID). | Sucrase is naturally produced in the brush border of the small intestine, primarily the distal duodenum and jejunum. Sucrase hydrolyzes the disaccharide sucrose into its component monosaccharides, glucose and fructose. Isomaltase breaks down disaccharides from starch into simple sugars. SUCRAID does not contain isomaltase. | Sacrosidase is a [beta]-fructofuranoside fructohydrolase that hydrolyzes sucrose. Unlike human intestinal sucrase-isomaltase, it has no activity with oligosaccharides containing 1,6 glucosyl bonds. | NA | NA | It has been suggested that sucrose is better absorbed (and sacrosidase activity preserved) when patients were given milk before sacrosidase rather than consuming the enzyme product alone. Therefore, it has been recommended to take half dose of sacrosidase just after a protein-containing meal, and the other half of the dose approximately half-way through the meal. | NA | NA | Alimentary Tract and Metabolism,Enzymes,Enzymes and Coenzymes,Glycoside Hydrolases,Hydrolases,Sucrose-specific Enzyme | NA | NA | NA | NA | NA | Sucraid | QOL Medical, LLC | QOL Medical, LLC | NA | ß,D-fructofuranoside fructohydrolase | NA | Solution | Oral | The recommended dosage is 1 or 2 mL (8,500 to 17,000 I.U.) or 1 or 2 full measuring scoops (each full measuring scoop equals 1mL; 28 drops from the SUCRAID container tip equals 1mL) taken orally with each meal or snack diluted with 2 to 4 ounces of water, milk or infant formula. The beverage or infant formula should be served cold or at room temperature. The beverage or infant formula should not be warmed or heated before or after addition of SUCRAID because heating is likely to decrease potency. SUCRAID should not be reconstituted or consumed with fruit juice since its acidity may reduce the enzyme activity. It is recommended that approximately half of the dosage be taken at the beginning of the meal or snack and the remainder be taken during the meal or snack. | Patients known to be hypersensitive to yeast, yeast products, glycerin (glycerol), or papain. | Abdominal pain, vomiting; nausea; diarrhea; constipation; insomnia; headache; nervousness and dehydration. | Link | NA | NA |
| 10833 | Th1199 | Ramucirumab | >Th1199_Ramucirumab EVQLVQSGGGLVKPGGSLRLSCAASGFTFSSYSMNWVRQAPGKGLEWVSSISSSSSYIYYADSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCARVTDAFDIWGQGTMVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143600 | C6374H9864N1692O1996S46 | NA | NA | NA | 15 days | Ramucirumab is a human monoclonal antibody (IgG1) against vascular endothelial growth factor receptor 2 (VEGFR2), a type II trans-membrane tyrosine kinase receptor expressed on endothelial cells. By binding to VEGFR2, ramucirumab prevents binding of its ligands (VEGF-A, VEGF-C, and VEGF-D), thereby preventing VEGF-stimulated receptor phosphorylation and downstream ligand-induced proliferation, permeability, and migration of human endothelial cells. VEGFR stimulation also mediates downstream signalling required for angiogenesis and is postulated to be heavily involved in cancer progression, making it a highly likely drug target. In contrast to other agents directed against VEGFR-2, ramucirumab binds a specific epitope on the extracellular domain of VEGFR-2, thereby blocking all VEGF ligands from binding to it. Ramucirumab is indicated for us in advanced gastric or gastro-esophageal junction adenocarcinoma as a single agent or in combination with paclitaxel after prior fluoropyrimidine- or platinum-containing chemotherapy. | For use in advanced gastric or gastro-esophageal junction adenocarcinoma as a single agent or in combination with paclitaxel after prior fluoropyrimidine- or platinum-containing chemotherapy. | Ramucirumab inhibits ligandstimulated activation of VEGF Receptor 2, thereby inhibiting ligand-induced proliferation, and migration of human endothelial cells. Ramucirumab inhibited angiogenesis in an in vivo animal model. | Ramucirumab is a human monoclonal antibody (IgG1) against vascular endothelial growth factor receptor 2 (VEGFR2), a type II trans-membrane tyrosine kinase receptor expressed on endothelial cells. By binding to VEGFR2, ramucirumab prevents binding of its ligands (VEGF-A, VEGF-C, and VEGF-D), thereby preventing VEGF-stimulated receptor phosphorylation and downstream ligand-induced proliferation, permeability, and migration of human endothelial cells. | Ramucirumab packaging includes warnings for arterial thromboembolic events, hypertension, infusion-related reactions, gastrointestinal perforation, clinical deterioration in patients with cirrhosis, and reversible posterior leukoencephalopathy syndrome. The most common reactions observed in single-agent-treated patients at a rate of >10% and >2% higher than placebo were hypertension and diarrhea. The most common adverse reactions observed in patients treated with ramucirumab plus paclitaxel at a rate of of >30% and >2% higher than placebo plus paclitaxel were fatigue, neutropenia, diarrhea, and epistaxis. | NA | NA | 5.5 L | 0.014 L/hour | Antineoplastic and Immunomodulating Agents | US2013067098 | 11-Feb-2011 | 11-Feb-2031 | Belimumab, Pamidronate | Vascular endothelial growth factor receptor 2 | Cyramza | Eli Lilly and Company | Eli Lilly and Company | CYRAMZA®as a single agent, or in combination with paclitaxel, is indicated for the treatment of patients with advanced or metastatic, gastric or gastro-esophageal junction adenocarcinoma with disease progression on or after prior fluoropyrimidine-or platinum-containing chemotherapy. | NA | 10 mg/mL | Solution | Intravenous | Either 8mg/kg or 10 mg/kg every 2 weeks | NA | Hemorrhage; Arterial Thromboembolic Events; Hypertension; Infusion-Related Reactions; Gastrointestinal Perforation; Impaired Wound Healing; Patients with Child-Pugh B or C Cirrhosis; Reversible Posterior Leukoencephalopathy Syndrome; Proteinuria Including Nephrotic Syndrome; Thyroid Dysfunction. | Link | NA | NA |
| 10837 | Th1200 | Prothrombin complex concentrate | NA | NA | NA | NA | NA | NA | Factor II - 48-60 hrs; factor VII - 1.5-6 hrs; factor IX - 20-24 hrs and factor X - 24 - 48 hrs. | Anti-inhibitor coagulant complex, also known as activated prothrombin complex concentrate (APCC) is a preparation containing precursor and activated forms of blood coagulation factors II, VII, IX, and X derived from pooled human venous plasma. | For use in hemophilia A and B patients with inhibitors for: 1) control and prevention of bleeding episodes; 2) perioperative management; and 3) Routine prophylaxis to prevent or reduce the frequency of bleeding episodes. | The administration of human prothrombin complex provides an increase in plasma levels of the vitamin K dependent coagulation factors, and can temporarily correct the coagulation defect of patients with deficiency of one or several of these factors. | They act by reversal of anticoagulants | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Octaplex | Octapharma | Octapharma | Treatment of bleeding and perioperative prophylaxis of bleeding in acquired deficiency of the prothrombin complex coagulation factors, such as deficiency caused by treatment with vitamin K antagonists, or in case of overdose of vitamin K antagonists, when rapid correction of the deficiency is required. Treatment of bleeding and perioperative prophylaxis in congenital deficiency of the vitamin K dependent coagulation factors II and X when purified specific coagulation factor product is not available. | NA | NA | Powder and solvent for solution | Intravenous | The dose will depend on the INR before treatment and the targeted INR. In the following table approximate doses (ml/kg body weight of the reconstituted product) required for normalisation of INR (≤ 1.2 within 1 hour) at different initial INR levels are given | In patients with acquired deficiency of the vitamin K dependent coagulation factors (e.g. as induced by treatment with vitamin K antagonists), Octaplex should only be used when rapid correction of prothrombin complex levels is necessary, such as major bleeding or emergency surgery. In other cases, reduction of the dose of the vitamin K antagonist and/or administration of vitamin K is usually sufficient. Patients receiving a vitamin K antagonist may have an underlying hypercoaguable state and infusion of prothrombin complex concentrate may exacerbate this. In congenital deficiency of any of the vitamin K dependent factors, specific coagulation factor product should be used when available. If allergic or anaphylactic-type reactions occur, the infusion should be stopped immediately. In case of shock, standard medical treatment for shock should be implemented. | Immune system disorders; General disorders and administration site conditions; Vascular disorders; Nervous system disorders; | 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 |
| 10844 | Th1207 | Necitumumab | >Th1207_Necitumumab QVQLQESGPGLVKPSQTLSLTCTVSGGSISSGDYYWSWIRQPPGKGLEWIGYIYYSGSTDYNPSLKSRVTMSVDTSKNQFSLKVNSVTAADTAVYYCARVSIFGVGTFDYWGQGTLVTVSSASTKGPSVLPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 144844.9 | C6436H9958N1702O2020S42 | NA | NA | NA | Approx 14 days | Necitumumab is an intravenously administered recombinant monoclonal IgG1 antibody used in the treatment of non-small cell lung cancer (NSCLC) as an EGFR antagonist. It functions by binding to epidermal growth factor receptor (EGFR) and prevents binding of its ligands, a process that is involved in cell proliferation, metastasis, angiogenesis, and malignant progression. Binding of necitumumab to EGFR induces receptor internalization and degradation, thereby preventing further activation of EGFR which is beneficial in NSCLC as many patients have increased protein expression of EGFR. Necitumumab is approved for use in combination with cisplatin and gemcitabine as a first-line treatment for metastatic squamous non-small cell lung cancer (NSCLC). | Necitumumab is approved for use in combination with cisplatin and gemcitabine as a first-line treatment for metastatic squamous non-small cell lung cancer (NSCLC). It is not indicated for treatment of non-squamous NSCLC. | In animal models administration of necitumumab to implanted mice resulted in increased antitumor activity in combination with gemcitabine and cisplatin as compared to mice receiving gemcitabine and cisplatin alone. | Necitumumab is a recombinant human lgG1 monoclonal antibody that binds to the human epidermal growth factor receptor (EGFR) and blocks the binding of EGFR to its ligands. Expression and activation of EGFR has been correlated with malignant progression, induction of angiogenesis, and inhibition of apoptosis. Binding of necitumumab induces EGFR internalization and degradation in vitro. In vitro, binding of necitumumab also led to antibody-dependent cellular cytotoxicity (ADCC) in EGFR-expressing cells. | The poor safety profile of necitumumab has been one of the major limitations of its use. Rigorous monitoring of the following adverse events is recommended for the use of this drug: cardiopulmonary arrest, hypomagnesia, venous and arterial thromboembolic events, dermatologic toxicities, and infusion-related reactions. Due to observations of increased toxicity and mortality in treatment of non-squamous NSCLC, necitumumab is only recommended for the treatment of squamous NSCLC in combination with cisplatin and gemcitabine. Animal studies suggest potential embryo-fetal toxicity. | NA | NA | Steady state volume of distribution is 7.0 L. | 14.1 mL/h | NA | NA | NA | NA | NA | Epidermal growth factor receptor | Portrazza | Eli Lilly and Company | Eli Lilly and Company | PORTRAZZAâ„¢ is indicated, in combination with gemcitabine and cisplatin, for first-line treatment of patients with metastatic squamous non-small cell lung cancer. | NA | Each vial contains 800 mg PORTRAZZA in 50 mL (16 mg/mL) | Sterile, preservative free, clear to slightly opalescent and colorless to slightly yellow solution | intravenous | The recommended dose of PORTRAZZA is 800 mg administered as an intravenous infusion over 60 minutes on Days 1 and 8 of each 3-week cycle prior to gemcitabine and cisplatin infusion. Continue PORTRAZZA until disease progression or unacceptable toxicity. | NA | Cardiopulmonary Arrest; Hypomagnesemia; Venous and Arterial Thromboembolic Events; Dermatologic Toxicities; nfusion-Related Reactions; Non-Squamous NSCLC - Increased Toxicity and Increased Mortality . | 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 |
| 10846 | Th1209 | Methoxy polyethylene glycol-epoetin beta | NA | 60,000 | NA | NA | NA | NA | In CKD patients on peritoneal dialysis with IV administration: 134 ± 65 hours In CKD patients on peritoneal dialysis with SC administration: 139 ± 67 hours | Methoxy polyethylene glycol-epoetin beta is a chemically synthesised Erythropoiesis Stimulating Agent (ESA) with a much longer half-life than erythropoietin. It is produced by recombinant DNA technology in Chinese Hamster Ovary (CHO) cells and differs from erythropoietin through the integration of an amide bond between either the N- terminal amino group or the ε-amino group of lysine, predominantly Lys52 and Lys45 and methoxy polyethylene glycol butanoic acid. This results in a molecular weight of approximately 60 kDa with the polyethylene glycol-moiety having an approximate molecular weight of 30 kDa. The dosage strength in μg indicates the quantity of the protein moiety of the methoxy polyethylene glycol-epoetin beta molecule without consideration of glycosylation. Methoxy polyethylene glycol-epoetin beta was approved (as Mircera) for use in Europe in July 2007 by the European Commission, in September 2007 by the Swissmedic, and in November 2007 by the U.S. Food and Drug Administration for use in the United States. | For the treatment of patients with anaemia associated with chronic kidney disease. | Following a single-dose of Mircera in CKD patients, the onset of hemoglobin increase (defined as an increase > 0.4 g/dL from baseline) was observed 7 to 15 days following initial dose administration | Mircera is an erythropoietin receptor activator with greater activity in vivo as well as increased half-life, in contrast to erythropoietin. A primary growth factor for erythroid development, erythropoietin is produced in the kidney and released into the bloodstream in response to hypoxia. In responding to hypoxia, erythropoietin interacts with erythroid progenitor cells to increase red cell production. Production of endogenous erythropoietin is impaired in patients with CKD and erythropoietin deficiency is the primary cause of their anemia. | Overdosage can cause severe hypertension. | Not metabolized. | Administered parenterally (subcutaneous or IV) therefore not absorbed. | ~94.74 ml/kg | In CKD patients on peritoneal dialysis : 0.49 ± 0.18 mL/hr/kg | NA | NA | NA | NA | Lenalidomide, Nandrolone phenpropionate, Thalidomide | Erythropoietin receptor | Mircera | Genentech, Inc. | Genentech, Inc. | Mircera is indicated for the treatment of anemia associated with chronic kidney disease (CKD) in adult patients on dialysis and patients not on dialysis. | NA | 30 mcg, 50 mcg, 75 mcg, 100 mcg, 120 mcg, 150 mcg, 200 mcg, or 250 mcg in 0.3 mL | solution for injection | Intravenous | Individualize dosing and use the lowest dose of Mircera sufficient to reduce the need for RBC transfusions | Uncontrolled hypertension; Pure red cell aplasia (PRCA) that begins after treatment with Mircera or other erythropoietin protein drugs; History of serious or severe allergic reactions to Mircera (e.g. anaphylactic reactions, angioedema, bronchospasm, skin rash, and urticaria). | Increased Mortality, Myocardial Infarction, Stroke, and Thromboembolism; Increased mortality and/or tumor progression in patients with cancer; Hypertension; Seizures; Pure red cell aplasia; Serious allergic reactions. | 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 |
| 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 |
| 10857 | Th1219 | Anti-thymocyte Globulin (Rabbit) | NA | NA | NA | NA | NA | 61 °C (FA | 2-3 days, may increase after multiple doses administration | Rabbit anti-thymocyte globulin. Thymoglobulin is a polyclonal antibody that suppresses certain types of immune cells responsible for acute organ rejection in transplant patients. Thymoglobulin is a mixture of antibodies intended to bind to various cell surface antigens. The most common mode of action of Thymoglobulin is via selective depletion of T-cells. | For prevention of renal transplant rejection | Antithymocyte Globulin (ATG) is a concentrated anti-human T-lymphocyte immunoglobulin preparation derived from rabbits after immunization with a T-lympoblast cell line. ATG is an immunosuppressive product for the prevention and treatment of acute rejection following organ transplantation. ATG reduces the host immune response against tissue transplants or organ allografts. | Binds to multiple, T-cell specific antigens leading to T-lymphocyte cell death via complement mediated cytotoxicity or apoptosis. | NA | NA | NA | NA | NA | Antibody | 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. | T-cell surface glycoprotein CD1a, Major histocompatibility complex class I-related gene protein, Integrin alpha-L, T-lymphocyte activation antigen CD86, Low affinity immunoglobulin gamma Fc region receptor II-b, T-cell surface glycoprotein CD4, Integrin beta-1, Integrin alpha-V, Integrin beta-3 | ATG-Fresenius | Genzyme Inc. | Genzyme Inc. | ATG-Freseniusis usually used in combination with other immunosuppressive drugs(corticosteroids,azathioprine,cyclosporineA,etc.) to suppress the immune system and thus preventing rejection following organ transplantation. | NA | One ml of the concentrate contains 20 mg anti-human T-lymphocyte immunoglobulin from rabbits | Concentrate for solution for infusion. | Intravenous | One ml of the concentrate contains 20 mg anti-human T-ddiThe recommended dose range is 2 to 5 mg/kg/d ATG - Fresenius S. The most common doses are in the range of 3 to 4 mg/kg/ dlymphocyte immunoglobulin from rabbits | Hypersensitivity to the active substance or to any of the excipients | bladder pain,chest pain,chills | 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 |
| 10859 | Th1221 | C1 Esterase Inhibitor (Recombinant) | NA | 67000 | NA | NA | NA | NA | 2.4-2.7 hr | C1 Esterase Inhibitor (Recombinant) is a recombinant analogue of endogenous complement component-1 esterase inhibitor (rhC1INH), purified from the milk of transgenic rabbits. The primary function of endogenous C1INH is to regulate the activation of the complement and contact system pathways. It does this through inhibition of several target proteases within these pathways including activated C1s, kallikrein, factor XIIa and factor XIa. C1 esterase inhibitor has also been shown to inhibit the action of thrombin within the coagulation pathway, and tPA and plasmin within the fibrinolytic pathway. Deficiency of C1-inhibitor permits plasma kallikrein activation, which leads to the production of the vasoactive peptide bradykinin. Additionally, C4 and C2 cleavage goes unchecked, resulting in auto-activation of the complement system. Down-stream effects of the lack of enzyme inhibition by C1 esterase inhibitor results in swelling due to leakage of fluid from blood vessels into connective tissue and consequently the presentation of hereditary angioedema (HAE). Marketed as the product Ruconest (FDA), this drug is indicated for the treatment of acute attacks of hereditary angioedema (HAE) due to C1 esterase inhibitor deficiency in adults. Intravenous replacement of C1 esterase inhibitor results in reversal of acute symptoms of HAE. | For the treatment of acute attacks of hereditary angioedema (HAE) due to C1 esterase inhibitor deficiency in adults. | A dose of 50 U/kg of Ruconest increases plasma C1INH activity levels to greater than 0.7 U/mL (the lower limit of normal) in HAE patients. | The primary function of endogenous C1INH is to regulate the activation of the complement and contact system pathways. It does this through inhibition of several target proteases within these pathways including activated C1s, kallikrein, factor XIIa and factor XIa. C1 esterase inhibitor has also been shown to inhibit the action of thrombin within the coagulation pathway, and tPA and plasmin within the fibrinolytic pathway. Deficiency of C1-inhibitor permits plasma kallikrein activation, which leads to the production of the vasoactive peptide bradykinin. Additionally, C4 and C2 cleavage goes unchecked, resulting in auto-activation of the complement system. Down-stream effects of the lack of enzyme inhibition by C1 esterase inhibitor results in swelling due to leakage of fluid from blood vessels into connective tissue and consequently the presentation of hereditary angioedema (HAE). Replacement of C1 esterase inhibitor results in a reversal of these effects. | NA | NA | NA | NA | NA | Blood and Blood Forming Organs | NA | NA | NA | Allylestrenol, Altrenogest, Bazedoxifene, Chlorotrianisene, Conjugated Equine Estrogens, Desogestrel, Dienestrol, Dienogest, Diethylstilbestrol, Dihydrotestosterone may increase the thrombogenic activities of C1 Esterase Inhibitor (Recombinant). | Complement C1r subcomponent, Complement C1s subcomponent, Plasma kallikrein, Coagulation factor XII, Prothrombin, Coagulation factor XI, Tissue-type plasminogen activator | Ruconest | Tjoapack Netherlands Bv | Tjoapack Netherlands Bv | Indicated for treatment of acute attacks in adult and adolescent patients with hereditary angioedema (HAE) | NA | NA | Powder and liquid for solution | Intravenous | <84 kg: 50 IU/kg infused over 5 minutes; not to exceed 4200 IU/dose | History of life-threatening immediate hypersensitivity reactions to C1 esterase inhibitor preparations, including anaphylaxis | Severe hypersensitivity reactions may occur during or after injection; signs and symptoms include hives, generalized urticaria, tightness of the chest, wheezing, hypotension, and/or anaphylaxis | 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 |
| 10864 | Th1225 | Coagulation factor X human | NA | 59000 | NA | NA | NA | NA | Following a single intravenous dose of 25 IU/kg, the mean plasma half-life (CV%) was 30.3 (22.8) hr | NA | NA | The active substance in Coagadex is human factor X isolated from the plasma of blood donors. It replaces the missing factor X, thereby helping the blood to clot and giving temporary control of bleeding. | Patients with hereditary factor X deficiency lack factor X, a protein needed to form the scab (blood clot) that stops wounds from bleeding. In these patients, blood clots do not form properly, resulting in longer bleeding time and poor wound healing. Blood may seep into surrounding tissues, resulting in local pain and swelling. Bleeding may also occur in internal organs. The active substance in Coagadex is human factor X isolated from the plasma of blood donors. It replaces the missing factor X, thereby helping the blood to clot and giving temporary control of bleeding. | NA | NA | Following a single intravenous dose of 25 IU/kg, the mean peak plasma concentration (CV%) was 0.504 (17.2) IU/mL [FDA Label]. | Following a single intravenous dose of 25 IU/kg, the mean volume of distribution at steady state (CV%) was 56.3 (24.0) mL/kg [FDA Label]. | Following a single intravenous dose of 25 IU/kg, the mean total body clearance was 1.35 (21.7) mL/kg/hr [FDA Label]. | Amino Acids, Peptides, and Proteins,Biological Factors,Blood and Blood Forming Organs,Blood Coagulation Factors,Blood Proteins,Factor X,Factor X, agonists,Factor X, antagonists & inhibitors,Hemostatics,Increased Coagulation Activity,Proteins | NA | NA | NA | NA | NA | Coagadex | NA | NA | It is used for the treatment and prevention of bleeding (including during and after an operation) in patients with hereditary factor X deficiency. Factor X deficiency is a bleeding disorder caused by lack of factor X, a protein needed for normal clotting of the blood. | NA | NA | powder and solvent used to make a solution | Intravenous | Dose(IU)=body weight(kg)xdesired factor X rise(IU/dL or % of normal)x0.5(IU/kg/(IU/dL) | Hypersensitivity to the active substance | The most common side effects with Coagadex (which may affect up to 1 in 10 people) are pain or redness at the injection site, fatigue (tiredness), and back pain. | Link | NA | NA |
| 10865 | Th1226 | Dinutuximab | NA | 145000 | C6422H9982N1722O2008S48 | NA | NA | NA | The terminal half-life is 10 days | Dinutuximab is an IgG1 monoclonal human/mouse chimeric antibody against GD2, a disialoganglioside expressed on tumors of neuroectodermal origin, including human neuroblastoma and melanoma, with highly restricted expression on normal tissues. It is composed of the variable heavy- and light-chain regions of the murine anti-GD2 mAb 14.18 and the constant regions of human IgG1 heavy-chain and kappa light-chain. By binding to GD2, dinutiximab induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity of tumor cells thereby leading to apoptosis and inhibiting proliferation of the tumour. It is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA), for the treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to prior first-line multiagent, multimodality therapy. Despite a high clinical response seen after first-line treatment, the complete eradication of neuroblastoma is rarely achieved and the majority of patients with advanced disease suffer a relapse. Current strategies for treatment include immunotherapy with drugs such as dinutuximab to target surviving neuroblastoma cells and to prevent relapse. | Dinutuximab is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA), for the treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to prior first-line multiagent, multimodality therapy. Despite a high clinical response seen after first-line treatment, the complete eradication of neuroblastoma is rarely achieved and the majority of patients with advanced disease suffer a relapse. Current strategies for treatment include immunotherapy with drugs such as dinutuximab to target surviving neuroblastoma cells and to prevent relapse. | In vitro dinutuximab binds to neuroblastoma tumour cells and mediates the lysis of tumour cells via cell-mediated and complement-mediated cytotoxicity. | Dinutuximab is an IgG1 monoclonal human/mouse chimeric antibody against GD2, a disialoganglioside expressed on tumors of neuroectodermal origin, including human neuroblastoma and melanoma, with highly restricted expression on normal tissues. It is composed of the variable heavy- and light-chain regions of the murine anti-GD2 mAb 14.18 and the constant regions of human IgG1 heavy-chain and kappa light-chain. By binding to GD2, dinutiximab induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity of tumor cells thereby leading to apoptosis and inhibiting proliferation of the tumour. | The most common (incidence 15 %) grade 3 or 4 treatment-related adverse events in dinutuximab compared with standard therapy recipients were neuropathic pain (52 vs. 6 %), fever without neutropenia (39 vs. 6 %), any in-fection (39 vs. 22 %), hypokalaemia (35 vs. 2 %), hypersensitivity reactions (25 vs. 1 %), hyponatraemia (23 vs. 4 %), elevation of alanine transferase levels (23 vs. 3 %) and hypotension (18 vs. 0 %). Based on its mechanism of action, dinutuximab may cause fetal harm when administered to a pregnant woman however, there are no studies in pregnant women and no reproductive studies in animals to inform the drug-associated risk. Non-clinical studies suggest that dinutuximab-induced neuropathic pain is mediated by binding of the antibody to the GD2 antigen located on the surface of peripheral nerve fibers and myelin and subsequent induction of cell- and complement-mediated cytotoxicity. In clinical trials, 114 (85%) patients treated in the dinutuximab/RA group experienced pain despite pre-treatment with analgesics including morphine sulfate infusion. Severe (Grade 3) pain occurred in 68 (51%) patients in the dinutuximab/RA group compared to 5 (5%) patients in the RA group. Pain typically occurred during the dinutuximab infusion and was most commonly reported as abdominal pain, generalized pain, extremity pain, back pain, neuralgia, musculoskeletal chest pain, and arthralgia. | NA | NA | The mean volume of distribution at steady state (Vdss) is 5.4 L | The clearance is 0.21 L/day and increases with body size | Antibody, Immunosuppresive agent, Antineoplastic agent | US20140170155 | 18-02-2014 | 18-02-2038 | Severity of adverse effect can be increased while combining Dinutuximab with Acebutolol, Acetazolamide, Acetyldigitoxin, Aldesleukin, Aliskiren, Amifostine, Amiloride, Amiodarone, Amlodipine etc | GD2 disialoganglioside | unituxin | NA | NA | Unituxin (dinutuximab) is indicated, in combination with granulocyte- macrophage colony - stimulating factor (GM- CSF), interleukin- 2 (IL- 2) and 13- cis -retinoic acid (RA ), for the treatment of pediatric patients with high- risk neuroblastoma who achieve at least a partial response to prior first -line multiagent, multimodality therapy. | NA | 1 mL of concentrate contains 3.5 mg of dinutuximab | sterile, preservative-free, clear/colorless to slightly opalescent solution | Intravenous | The recommended dose of Unituxin is 17.5 mg/m2/day administered as an intravenous infusion over 10 to 20 hours for 4 consecutive days for a maximum of 5 cycles. | History of anaphylaxis to dinutuximab. | The most common serious adverse reactions (≥ 5%) are infections, infusion reactions, hypokalemia, hypotension, pain, fever, and capillary leak syndrome. | Link | NA | NA |
| 10866 | Th1227 | Efmoroctocog alfa | NA | 220000 | C9736H14863N2591O2855S78 | NA | NA | NA | Following a single intravenous dose of 50 IU/kg in previously-treated adult patients with severe haemophilia A, mean half life (t1/2) ranged from 19 to 20.9 h. Mean t1/2 in adolescent patients 12 to 18 years of age ranged from 16 to 17.5 h. Mean t1/2 in pediatric patients < 12 years of age ranged from 12.3 to 15.9 h | Efmoroctocog alfa is a long-acting, fully-recombinant factor VIII Fc fusion protein. | For the treatment of Haemophilia A. | NA | Patients with haemophilia A lack factor VIII, a protein needed for normal clotting of the blood, and as a result, they bleed readily. The active substance in Elocta, efmoroctocog alfa, works in the body in the same way as human factor VIII. It replaces the missing factor VIII, thereby helping the blood to clot and giving temporary control of bleeding. | Based on the findings from acute and repeated dose toxicity studies, efmoroctocog alfa displays no special hazard for humans. Studies to assess the genotoxicity, carcinogenicity, toxicity to reproduction or embryo-foetal development of efmoroctocog alfa have not been conducted. In a placental transfer study, efmoroctocog alfa has been shown to cross the placenta in small amounts in mice [FDA Label]. | There are no detectable metabolites for efmoroctocog alfa. It is presumed to be metabolized via a same degradation pathway as endogenous factor VIII. | Following a single intravenous dose of 50 IU/kg in previously-treated adult patients with severe haemophilia A, mean peak plasma concentrations (Cmax) ranged from 108 to 131 IU/dL. Mean area under the FVIII activity time curve (AUC/Dose) ranged from 47.5 to 51.2 IUxh/dL per IU/kg. Mean AUC/Dose in adolescent patients 12 to 18 years of age ranged from 38.2 to 40.8 IUxh/dL per IU/kg. Mean AUC/Dose in pediatric patients < 12 years of age ranged from 25.9 to 38.4 IUxh/dL per IU/kg [FDA Label]. | Following a single intravenous dose of 50 IU/kg in previously-treated adult patients with severe haemophilia A, mean volume of distribution at steady state (Vss) ranged from 49.1 to 52.6 mL/kg. Mean Vss in adolescent patients 12 to 18 years of age ranged from 57.6 to 59.4mL/kg. Mean Vss in pediatric patients < 12 years of age ranged from 49.5 to 63.1 mL/kg [FDA Label]. | Following a single intravenous dose of 50 IU/kg in previously-treated adult patients with severe haemophilia A, mean clearance (CL) rate ranged from 1.95 to 2.11 mL/h/kg. Mean CL in adolescent patients 12 to 18 years of age ranged from 2.45 to 2.62 mL/h/kg. Mean t1/2 in pediatric patients < 12 years of age ranged from 2.61 to 3.86 mL/h/kg [FDA Label]. | Hemostatics | NA | NA | NA | No interactions of human coagulation factor VIII (rDNA) with other medicinal products have been reported. | von Willebrand factor | ELOCTA | NA | NA | Treatment and prophylaxis of bleeding in patients with haemophilia A (congenital factor VIII deficiency). | NA | 0.6 mmol (or 14 mg) sodium per vial | Powder and solvent for solution for injection | Intravenous | The calculation of the required dose of recombinant factor VIII Fc is based on the empirical finding that 1 International Unit (IU) factor VIII per kg body weight raises the plasma factor VIII activity by 2 IU/dL. The required dose is determined using the following formula: Required units = body weight (kg) x desired factor VIII rise (%) (IU/dL) x 0.5 (IU/kg per IU/dL) | Hypersensitivity to the active substance (recombinant human coagulation factor VIII, and/or Fc domain) | Hypersensitivity or allergic reactions (which may include swelling of the face, rash, hives, tightness of the chest and difficulty breathing, burning and stinging at the infusion site, chills, flushing, generalised urticaria, headache, hypotension, lethargy, nausea, restlessness, tachycardia) have been observed rarely and may in some cases progress to severe anaphylaxis. | Link | NA | NA |
| 10867 | Th1228 | Factor IX Complex (Human) | NA | NA | NA | NA | NA | NA | 11-28 hr | Factor IX Complex is a sterile, lyophilized concentrate composed of a number of Vitamin K-dependent clotting factors found in functioning human plasma. Also known as prothrombin complex concentrate, products containing this complex often include Factor IX (antihemophilic factor B), Factor II (prothrombin), Factor X (Stuart-Prower Factor), and low levels of Factor VII (proconvertin) derived from human plasma. Many commercially available products also contain low levels of other antithrombotic proteins. For example, Kcentra (FDA) also contains the antithrombotic proteins C and S, while Bebulin VH (FDA) contains heparin. Coagulation factors are purified from pooled human plasma and subsequently sterilized and treated. Although Factor IX Complex products contain many different coagulation components, Factor IX is the lead component for potency and efficacy, particularly when used for the treatment of bleeding associated with Hemophilia B (Factor IX deficiency). As the product Kcentra, Factor IX Complex is also indicated for the urgent reversal of acquired coagulation factor deficiency induced by Vitamin K antagonist (VKA, e.g., warfarin) therapy in adult patients experiencing acute major bleeding or requiring rapid reversal of therapy. | Factor IX Complex is indicated for the prevention and control of hemorrhagic episodes in hemophilia B patients. It is also indicated for the urgent reversal of acquired coagulation factor deficiency induced by Vitamin K antagonist (VKA, e.g., warfarin) therapy in adult patients with acute major bleeding or who require rapid reversal of therapy. | NA | Factor IX is a vitamin K-dependent coagulation factor sythesized in the liver; purified FActor IX from human plasma temporarily replace missing clotting factor IX to correct and/or prevent bleeding. | NA | NA | NA | NA | NA | Antihemophilic agent | NA | NA | NA | NA | NA | AlphaNine SD or Mononine | NA | NA | s used to treat or prevent bleeding in people with hemophilia B | NA | NA | Powder and solvent for solution for injection | Intravenous | AlphaNine SD, Mononine: 1 unit/kg x body wt (kg) x desired increase (% of normal) = Number of factor IX units required | NA | NA | Link | NA | NA |
| 10870 | Th1230 | Human Varicella-Zoster Immune Globulin | NA | NA | NA | NA | NA | NA | Human Varicella-Zoster Immunoglobulin has a half-life of about 18-24 days following intravenous administration and 24-30 days following intramuscular administration. | Human Varicella-Zoster Immune Globulin is a solvent/detergent-treated sterile liquid preparation of purified human immune globulin G (IgG) containing antibodies to varicella zoster virus (anti-VZV). | Indicated for reducing the severity of chicken pox (varicella zoster virus) infections in high risk individuals after exposure | Provides passive immunization for nonimmune individuals exposed to varicella zoster virus, thereby reducing the severity of varicella infections | NA | Since the drug was prepared from human plasma pool, it may contain other infectious agents such as viruses and Creutzfeldt-Jakob disease (vCJD) agent. Hypersensitivity reactions such as allergic or anaphylactic reactions may occur. More common adverse effects include pain at injection site, headache, and rash. Rare adverse effects from immune globulin intravenous therapy include thrombotic events, renal dysfunction and acute renal failure, and noncardiogenic pulmonary edema. An LD50 was not determined, as the maximal dose used did not kill any experimental animals. | Immune globulins are metabolized in the reticuloendothelial system. | Intravenous administration of varicella zoster antibodies tends to persist for 6 weeks or longer. Following intramuscular administration of varicella immune globulin products, varicella antibodies are detectable within 2-3 days. The peak levels of varicella antibodies is expected to occur within 3-7 days of VariZIG administration. | Following intravenous administration of varicella zoster VZIG, anti-varicella zoster antibodies are expected to be quickly distributed between plasma and extravascular spaces with complete and immediate bioavailability. Intramuscular administration achieves nearly 100% bioavailability. | NA | Antibody | NA | NA | NA | The passive transfer of antibodies with immune globulin administration may impair the efficacy of live attenuated virus vaccines such as measles, rubella, mumps and varicella | varicella zoster virus | VARIZIG | NA | NA | It is indicated for post-exposure prophylaxis of varicella in high risk individuals. | NA | It is available in a single-use vial of 125 IU. Each 125 IU vial of VARIZIG contains less than 156 milligrams of total protein, mostly human immune globulin G (IgG). VARIZIG contains no preservative | lyophilized powder for solution | Intramuscular | Depending on patient size, divide the IM dose and administer in 2 or more injection sites; not to exceed 3 mL/injection site | Hypersensitivity to human immunoglobulins | The most common adverse drug reactions (reported by ≥ 1% of subjects) observed in clinical trials for all subjects and patients (n=601) are the following:injection site pain (3%),headache (2%),rash (including terms pruritus, rash, rash erythematous, rash vesicular and urticaria) (1%),fatigue (1%),chills (1%),nausea (1%) | Link | NA | NA |
| 10871 | Th1231 | Ibritumomab tiuxetan | >Th1231_Ibritumomab_tiuxetan QAYLQQSGAELVRPGASVKMSCKASGYTFTSYNMHWVKQTPRQGLEWIGAIYPGNGDTSYNQKFKGKATLTVDKSSSTAYMQLSSLTSEDSAVYFCARVVYYSNSYWYFDVWGTGTTVTVSAPSVYPLAPVCGDTTGSSVTLGCLVKGYFPEPVTLTWNSGSLSSGVHTFPAVLQSDLYTLSSSVTVTSSTWPSQSITCNVAHPASSTKVDKKIEPRGPTIKPCPPCKCPAPNLLGGPSVFIFPPKIKDVLMISLSPIVTCVVVDVSEDDPDVQISWFVNNVEVHTAQTQTHREDYNSTLRVVSALPIQHQDWMSGKEFKCKVNNKDLPAPIERTISKPKGSVRAPQVYVLPPPEEEMTKKQVTLTCMVTDFMPEDIYVEWTNNGKTELNYKNTEPVLDSDGSYFMYSKLRVEKKNWVERNSYSCSVVHEGLHNHHTTKSFSR | 143375.5 | C6382H9830N1672O1979S54 | 7.91 | -0.359 | 61 °C (FAB fragment), 71 °C (whole mAb) | 0.8 hours | Indium or yttrium conjugated murine IgG1 kappa monoclonal antibody directed against the CD20 antigen, which is found on the surface of normal and malignant B lymphocytes. Ibritumomab is produced in Chinese hamster ovary cells and is composed of two murine gamma 1 heavy chains of 445 amino acids each and two kappa light chains of 213 amino acids each. | For treatment of non-Hodgkin's lymphoma | Ibritumomab is a murine monoclonal antibody against CD20 that has been radiolabeled with yttrium-90. | The Fab segment of the antibody targets the CD20 epitope on B-cells, allowing the radioactive yttrium to destroy the cell via production of beta particles. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to B cells, or by human antimurine antibody production | NA | Binding observed on lymphoid cells of the bone marrow, lymph node, thymus, red and white pulp of the spleen, lymphoid follicles of the tonsil, and lymphoid nodules of other organs (e.g., large and small intestines) | Approximately 7.2% of injected dose of yttrium Y 90 ibritumomab tiuxetan is excreted in urine within 7 days. | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antigens, CD20,Blood Proteins,Cancer immunotherapy,CD20-directed Antibody Interactions,CD20-directed Radiotherapeutic Antibody,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Lymphoma, B-Cell,Myelosuppressive Agents,Proteins,Radiopharmaceutical Activity,Serum Globulins,Therapeutic Radiopharmaceuticals,Various Therapeutic Radiopharmaceuticals,Yttrium Radioisotopes | CA2149329 | 15-07-2008 | 11-Dec-2013 | The risk or severity of adverse effects can be increased while combining Ibritumomab tiuxetan with Abciximab, Acenocoumarol, Acetylsalicylic acid, Alprostadil, Anagrelide, Ancrod, Antithrombin III human, Apixaban, Ardeparin, Argatroban. | B-lymphocyte antigen CD20 | Zevalin | Spectrum Pharmaceuticals B.V. | Spectrum Pharmaceuticals B.V. | Zevalin is indicated for the treatment of relapsed or refractory, low-grade or follicular B-cell non-Hodgkin's lymphoma (NHL). | NA | 3.2 mg ibritumomab tiuxetan per 2 mL in a single-use vial. The contents of all vials are sterile, pyrogenfree, contain no preservatives, and are not radioactive. | Colourless Solution | Intravenous | nitiate the Zevalin therapeutic regimen following recovery of platelet counts to ≥ 150,000/mm³ at least 6 weeks, but no more than 12 weeks, following the last dose of first-line chemotherapy | None. | Serious Infusion Reactions, Severe Cutaneous and Mucocutaneous Reactions, Prolonged and Severe Cytopeniasmight occur | Link | NA | NA |
| 10876 | Th1236 | Sipuleucel-T | NA | NA | NA | NA | NA | NA | NA | Sipuleucel-T is a personalized, autologous, cellular immunotherapy. Sipuleucel-T is a therapeutic cancer vaccine for prostate cancer. Sipuleucel-T selectively targets the prostate-specific antigen (PSA) known as prostatic acid phosphatase (PAP) that is expressed in around 95% of prostate cancers. It must be prepared specifically for each patient. In metastatic prostate cancer, it has extended survival by median 4.1 months (IMPACT Phase III trial data). Sipuleucel-T is marketed under the brand name Provenge by Dendreon Corporation. Sipuleucel-T was approved by the U.S. Food and Drug Administration (FDA) on April 29, 2010, to treat asymptomatic or minimally symptomatic metastatic Hormone-Refractory Prostate Cancer (HRPC). The treatment initially cost $93,000 at the time of FDA approval, but rose to over $100,000 in 2014. | Sipuleucel-T is an autologous cellular immunotherapy indicated for the treatment of asymptomatic or minimally symptomatic metastatic castrate resistant (hormone refractory) prostate cancer. | NA | Sipuleucel-T is designed to induce an immune response targeted against PAP, an antigen expressed in most prostate cancers. During ex vivo culture with PAP-GM-CSF, APCs take up and process the recombinant target antigen into small peptides that are then displayed on the APC surface. The precise mechanism remains unknown, however. | NA | NA | NA | NA | NA | Antineoplastic and Immunomodulating Agents | US8153120 | 4-Oct-2012 | 22-03-2027 | The therapeutic efficacy of Sipuleucel-T can be decreased when used in combination with 2-Methoxyethanol, 9-(2-phosphonylmethoxyethyl)-2,6-diaminopurine, Abatacept, abetimus, ABR-215757, Acteoside, Adalimumab, Adefovir Dipivoxil, Afelimomab, Alefacept. | Prostatic acid phosphatase | Provenge | NA | NA | Provenge® (sipuleucel-T) is an autologous cellular immunotherapy indicated for the treatment of asymptomatic or minimally symptomatic metastatic castrate resistant (hormone refractory) prostate cancer | NA | NA | Solution | Intravenous | The recommended course of therapy for PROVENGE is 3 complete doses, given at approximately 2-week intervals. In controlled clinical trials, the median dosing interval between infusions was 2 weeks (range 1 to 15 weeks); the maximum dosing interval has not been established | Hypersensitivity to the active substance | fever;gredness, swelling, oozing, or other signs of infection where the IV needle was placed; orgsigns of infection around the veins your cells were collected from. | 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 |
| 10879 | Th1238 | Susoctocog alfa | >Th1238_Susoctocog_alfa AIRRYYLGAVELSWDYRQSELLRELHVDTRFPATAPGALPLGPSVLYKKTVFVEFTDQLFSVARPRPPWMGLLGPTIQAEVYDTVVVTLKNMASHPVSLHAVGVSFWKSSEGAEYEDHTSQREKEDDKVLPGKSQTYVWQVLKENGPTASDPPCLTYSYLSHVDLVKDLNSGLIGALLVCREGSLTRERTQNLHEFVLLFAVFDEGKSWHSARNDSWTRAMDPAPARAQPAMHTVNGYVNRSLPGLIGCHKKSVYWHVIGMGTSPEVHSIFLEGHTFLVRHHRQASLEISPLTFLTAQTFLMDLGQFLLFCHISSHHHGGMEAHVRVESCAEEPQLRRKADEEEDYDDNLYDSDMDVVRLDGDDVSPFIQIRSVAKKHPKTWVHYISAEEEDWDYAPAVPSPSDRSYKSLYLNSGPQRIGRKYKKARFVAYTDVTFKTRKAIPYESGILGPLLYGEVGDTLLIIFKNKASRPYNIYPHGITDVSALHPGRLLKGWKHLKDMPILPGETFKYKWTVTVEDGPTKSDPRCLTRYYSSSINLEKDLASGLIGPLLICYKESVDQRGNQMMSDKRNVILFSVFDENQSWYLAENIQRFLPNPDGLQPQDPEFQASNIMHSINGYVFDSLQLSVCLHEVAYWYILSVGAQTDFLSVFFSGYTFKHKMVYEDTLTLFPFSGETVFMSMENPGLWVLGCHNSDLRNRGMTALLKVYSCDRDIGDYYDNTYEDIPGFLLSGKNVIEPRSFAQNSRPPSASAPKPPVLRRHQRDISLPTFQPEEDKMDYDDIFSTETKGEDFDIYGEDENQDPRSFQKRTRHYFIAAVEQLWDYGMSESPRALRNRAQNGEVPRFKKVVFREFADGSFTQPSYRGELNKHLGLLGPYIRAEVEDNIMVTFKNQASRPYSFYSSLISYPDDQEQGAEPRHNFVQPNETRTYFWKVQHHMAPTEDEFDCKAWAYFSDVDLEKDVHSGLIGPLLICRANTLNAAHGRQVTVQEFALFFTIFDETKSWYFTENVERNCRAPCHLQMEDPTLKENYRFHAINGYVMDTLPGLVMAQNQRIRWYLLSMGSNENIHSIHFSGHVFSVRKKEEYKMAVYNLYPGVFETVEMLPSKVGIWRIECLIGEHLQAGMSTTFLVYSKECQAPLGMASGRIRDFQITASGQYGQWAPKLARLHYSGSINAWSTKDPHSWIKVDLLAPMIIHGIMTQGARQKFSSLYISQFIIMYSLDGRNWQSYRGNSTGTLMVFFGNVDASGIKHNIFNPPIVARYIRLHPTHYSIRSTLRMELMGCDLNSCSMPLGMQNKAISDSQITASSHLSNIFATWSPSQARLHLQGRTNAWRPRVSSAEEWLQVDLQKTVKVTGITTQGVKSLLSSMYVKEFLVSSSQDGRRWTLFLQDGHTKVFQGNQDSSTPVVNALDPPLFTRYLRIHPTSWAQHIALRLEVLGCEAQDLY | 170000 | NA | NA | NA | NA | 2-17 hours | Intravenous susoctocog alfa is a recombinant, B-domain deleted, porcine sequence antihaemophilic factor VIII (FVIII) product that has recently been approved for the treatment of bleeding episodes in adults with acquired haemophilia A (AHA). | For the treatment of Haemophilia A | Immediately after release in the patient’s circulation, Factor VIII binds to von Willebrand factor (vWF). The Factor VIII/von Willebrand factor complex consists of two molecules (Factor VIII and von Willebrand factor) with different physiological functions. Activated Factor VIII acts as a co-factor for activated Factor IX, accelerating the conversion of Factor X to activated Factor X, which ultimately converts prothrombin into thrombin. Thrombin then converts fibrinogen into fibrin and a clot can be formed. | Blood coagulation factor replacements, Factor X stimulants | Long-term studies in animals to evaluate the carcinogenic potential, genotoxicity and effects on fertility have not been performed with susoctocog alfa. In repeated-dose studies, the incidence and severity of glomerulopathy observed in monkeys intravenously administered susoctocog alfa at doses of 75, 225 and 750 U/kg/day tended to increase over time [L1130]. | NA | The time to reach peak plasma concentrations (Tmax) is approximately 26 minutes or 0.42 hour following intravenous administration of 5000U susoctocog alfa in patients with acquired haemophilia in a non-bleeding state [FDA Label]. | Following intravenous dose of 5000U to patients with acquired haemophilia in a non-bleeding state, the volume of distribution at steady state was 30.7 U/% [L1130]. | Following intravenous dose of 5000U to patients with acquired haemophilia in a non-bleeding state, the clearance rate was approximately 4.80 U/% * t [L1130]. | Blood and Blood Forming Organs,Blood Coagulation Factors,Hemostatics | NA | NA | NA | NA | von Willebrand factor | Obizur | NA | NA | It is indicated for the treatment of bleeding episodes in adults with acquired hemophilia A. | NA | Each powder vial contains nominally 500 Units of B domain deleted antihaemophilic Factor VIII (recombinant), porcine sequence, susoctocog alfa. | Powder and solvent for solution for injection. | Intravenous | The recommended initial dose is 200 U per kilogram bodyweight, given by intravenous injection | life-threatening hypersensitivity reactionsto OBIZUR or its components, including hamster protein. | Hypersensitivity reactions, including anaphylaxis, may occur. Should symptoms occur, discontinue OBIZUR and administer appropriate treatment | Link | NA | NA |
| 10880 | Th1239 | Thrombomodulin Alfa | NA | 52124 | C2230-H3357-N633-O718-S50 | NA | NA | NA | 2-3 days after sc injection; 19.82 +/- 2.10 hours after IV injection | Thrombomodulin Alfa is a novel, recombinant and soluble thrombomodulin (ART-123). It is a human protein with both thrombin inhibiting and protein C stimulating activities, for the potential treatment of thromboembolism and blood clotting disorders, such as disseminated intravascular thromboembolism. | Investigated for use/treatment in blood preservative, blood (blood forming organ disorders, unspecified), sepsis and septicemia, and thrombosis. | Thrombomodulin (TM) alfa, a recombinant human soluble TM, enhances activation of pro-carboxypeptidase B2 (pro-CPB2) by thrombin. Activated pro-CPB2 (CPB2) exerts anti-inflammatory and anti-fibrinolytic activities. | Thrombomodulin alfa is a soluble form of recombinant human thrombomodulin comprising all extracellular domains of thrombomodulin. Bound to thrombin, Thrombomodulin alfa inhibits its procoagulant activity and promotes activation of protein C. Thrombomodulin alfa inhibits thrombin generation by the activation of protein C and the subsequent inactivation of factor Va in the presence of protein S. Thrombomodulin alfa attenuates the extension of the clot by inhibiting further thrombin generation on clots, while other anticoagulants inhibit the initiation of clot formation. A higher concentration of Thrombomodulin alfa is needed to affect clotting time and platelet aggregation than thrombin generation. | NA | NA | NA | NA | 7-10 days | Amino Acids, Peptides, and Proteins,Carbohydrates,Glycoconjugates,Glycoproteins,Membrane Glycoproteins,Membrane Proteins,Platelet Membrane Glycoproteins,Proteins,Receptors, G-Protein-Coupled,Receptors, Peptide,Receptors, Proteinase-Activated,Receptors, Thrombin | NA | NA | NA | NA | Prothrombin,Coagulation factor V | Recomodulin (in Japan only) | Asahi Kasei Pharma Corp | Asahi Kasei Pharma Corp | For the treatment of patients with disseminated intravascular cogulation (DIC) | 1-498-thrombomodulin | NA | lyophilized powder for solution | Intravenous | NA | NA | NA | Link | NA | NA |