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 |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 10001 | Th1001 | Lepirudin | >Th1001_Lepirudin LTYTDCTESGQNLCLCEGSNVCGQGNKCILGSDGEKNQCVTGEGTPKPQSHNDGDFEEIPEEYLQ | 6979 | C287H440N80O111S6 | 3.7 | -0.777 | 65 | Approximately 1.3 hours | Lepirudin is identical to natural hirudin except for substitution of leucine for isoleucine at the N-terminal end of the molecule and the absence of a sulfate group on the tyrosine at position 63. It is produced via yeast cells. | For the treatment of heparin-induced thrombocytopenia. | Lepirudin is used to break up clots and to reduce thrombocytopenia. It binds to thrombin and prevents thrombus or clot formation. It is a highly potent, selective, and essentially irreversible inhibitor of thrombin and clot-bond thrombin. Lepirudin requires no cofactor for its anticoagulant action. Lepirudin is a recombinant form of hirudin, an endogenous anticoagulant found in medicinal leeches. | Lepirudin forms a stable non-covalent complex with alpha-thrombin, thereby abolishing its ability to cleave fibrinogen and initiate the clotting cascade. The inhibition of thrombin prevents the blood clotting cascade. | In case of overdose (eg, suggested by excessively high aPTT values) the risk of bleeding is increased. | Lepirudin is thought to be metabolized by release of amino acids via catabolic hydrolysis of the parent drug. However, conclusive data are not available. About 48% of the administration dose is excreted in the urine which consists of unchanged drug (35%) | Bioavailability is 100% following injection. | 12.2 L [Healthy young subjects (n = 18, age 18-60 years)] | 164 ml/min [Healthy 18-60 yrs] | Amino Acids, Peptides, and Proteins, Anticoagulants, Antithrombin Proteins, Antithrombins, Blood and Blood Forming Organs, Cardiovascular Agents, Enzyme Inhibitors, Fibrin Modulating Agents, Hematologic Agents, Peptides, Protease Inhibitors, Proteins, Serine Protease Inhibitors, Serpins, Thrombin Inhibitors | CA1339104 | 29-Jul-1997 | 29-Jul-2014 | Ginkgo biloba = may increase bleed risk. | Prothrombin | Refludan | Berlex Labs | Berlex Labs | heparin-induced thrombocytopenia (HIT) and associated thromboembolic disease | [Leu1, Thr2]-63-desulfohirudin | Each vial of REFLUDAN contains 50 mg lepirudin. Other ingre-dients are 40 mg mannitol and sodium hydroxide for adjust-ment of pH to approximately 7 | Sterile, white, freeze-dried powder | Intravenous infusion | Recommended dose is 0.4 mg/kg body weight (up to 110kg) slowly intravenously (eg, over 15 to 20seconds) as a bolus dose, and can be followed by 0.15 mg/kg body weight (up to 110kg)/hour as a continuous Intravenous infusion for 2 to 10 days or longer if CL. | Hypersensitivity | NA | Link | NA | NA |
| 10025 | Th1004 | Denileukin diftitox | >Th1004_Denileukin_diftitox MGADDVVDSSKSFVMENFSSYHGTKPGYVDSIQKGIQKPKSGTQGNYDDDWKGFYSTDNKYDAAGYSVDNENPLSGKAGGVVKVTYPGLTKVLALKVDNAETIKKELGLSLTEPLMEQVGTEEFIKRFGDGASRVVLSLPFAEGSSSVEYINNWEQAKALSVELEINFETRGKRGQDAMYEYMAQACAGNRVRRSVGSSLSCINLDWDVIRDKTKTKIESLKEHGPIKNKMSESPNKTVSEEKAKQYLEEFHQTALEHPELSELKTVTGTNPVFAGANYAAWAVNVAQVIDSETADNLEKTTAALSILPGIGSVMGIADGAVHHNTEEIVAQSIALSSLMVAQAIPLVGELVDIGFAAYNFVESIINLFQVVHNSYNRPAYSPGHKTHAPTSSSTKKTQLQLEHLLLDLQMILNGINNYKNPKLTRMLTFKFYMPKKATELKHLQCLEEELKPLEEVLNLAQSKNFHLRPRDLISNINVIVLELKGSETTFMCEYADETATIVEFLNRWITFCQSIISTLT | 57647.3 | C2560H4042N678O799S17 | 5.45 | -0.301 | NA | 1.16-1.3 hours | A recombinant (using E. coli expression system) DNA-derived cytotoxic protein containing amino acid sequences for diphtheria toxin fragments A and B (Met 1-Thr 387)-His and sequences for interleukin-2 (Ala 1-Thr 133). | Used in the treatment of cutaneous T-cell lymphoma. | Denileukin diftitox (Ontak) uses the cytocidal action of diphtheria toxin on cells which express the IL-2 receptor. The human IL-2 receptor exists in three forms on basis of affinity, low (CD25), intermediate (CD122/CD132) and high (CD25/CD122/CD132). Malignant cells expressing one or more of the subunits of the IL-2 receptor are found in certain leukemias and lymphomas including cutaneous T-cell lymphoma (CTCL). Ontak interacts with the high affinity IL-2 receptor on the cell surface and inhibits cellular protein synthesis, resulting in cell death within hours. | Denileukin diftitox binds to the high-affinity IL-2 receptor. The IL-2 receptor (Tac) subunit is expressed on activated lymphocytes. The diphtheria toxin associated with Ontak selectively kills the IL-2 bearing cells. | NA | NA | NA | 0.06 to 0.09 L/kg | 0.6 - 2.0 mL/min/kg [Lymphoma] | ADP Ribose Transferases, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Bacterial Toxins, Biological Factors, Cancer immunotherapy, CD25-directed Cytotoxin, Cytokines, Enzymes, Enzymes and Coenzymes, Glycosyltransferases, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interleukins, Lymphokines, Narrow Therapeutic Index Drugs, Pentosyltransferases, Peptides, Proteins, Recombinant Proteins, Toxins, Biological, Transferases | NA | NA | NA | Rilonacept decreases effects of toxoids by pharmacodynamic antagonism | Interleukin-2 receptor subunit alpha,Interleukin-2 receptor subunit beta,Cytokine receptor common subunit gamma | Ontak | Eisai Inc. , Hollister-Stier Laboratories LLC , Ligand Pharmaceuticals Inc. | Eisai Inc. , Hollister-Stier Laboratories LLC , Ligand Pharmaceuticals Inc. | Treating leukemia and lymphomas, including cutaneous (of the skin) T-cell lymphoma. | NA | Ontak contains 300 mcg of recombinant denileukin diftitox in a sterile solution of citric acid (20 mM), EDTA (0.05 mM) and polysorbate 20 ( < 1%) in Water for Injection, USP. The solution has a pH range of 6.9-7.2. | Sterile, white, preservative-free, lyophilized powder. | Intravenous (Intravenous) administration | NA | allergic | Common side effects include:headache, dizziness, or nervousness, numbness or tingling, skin itching or rash, runny or stuffy nose; weight gain or loss; mild diarrhea or constipation, or nausea, vomiting, loss of appetite. | Link | NA | NA |
| 10028 | Th1005 | Etanercept | >Th1005_Etanercept LPAQVAFTPYAPEPGSTCRLREYYDQTAQMCCSKCSPGQHAKVFCTKTSDTVCDSCEDSTYTQLWNWVPECLSCGSRCSSDQVETQACTREQNRICTCRPGWYCALSKQEGCRLCAPLRKCRPGFGVARPGTETSDVVCKPCAPGTFSNTTSSTDICRPHQICNVVAIPGNASMDAVCTSTSPTRSMAPGAVHLPQPVSTRSQHTQPTPEPSTAPSTSFLLPMGPSPPAEGSTGDEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 51234.9 | C2224H3475N621O698S36 | 7.89 | -0.529 | 71 | 102 hours in RA patients | It is a dimeric fusion protein (934 amino acids) consisting of extracellular ligand-binding portion of the human 75 kilodalton (p75) tumor necrosis factor receptor (TNFR) linked to Fc portion of human IgG1 produced by recombinant DNA technology in a Chinese hamster ovary (CHO) mammalian cell expression system.. The Fc component of etanercept contains the CH2 domain, the CH3 domain and hinge region, but not the CH1 domain of IgG1. | Used to treat severe rheumatoid arthritis in adults, severe juvenile idiopathic arthritis, ankylosing spondylitis, and severe plaque psoriasis. | TNF, a naturally occurring cytokine is involved in normal inflammatory and immune responses. Elevated levels of TNF are found in tissues and fluids of patients suffering from rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis (AS), and plaque psoriasis. Etanercept binds specifically to tumor necrosis factor (TNF) and blocks its interaction with cell surface TNF receptors. | There are two distinct receptors for TNF (TNFRs), a 55 kilodalton (p55) and a 75 kilodalton receptor (p75). The biological activity of TNF is dependent upon binding to either of the cell surface receptors p75 or p55. Etanercept is a dimeric soluble form of the p75 TNF receptor that can bind to two TNF molecules, thereby effectively removing them from circulation. | NA | NA | NA | NA | 160 ± 80 mL/hr [RA patients] | Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Dermatologicals, Disease-modifying Antirheumatic Agents, Immunoglobulin Constant Regions, Immunoglobulin Fc Fragments, Immunoglobulin Fragments, Immunoglobulin Isotypes, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Membrane Proteins, Peptides, Proteins, Tumor Necrosis Factor Blockers | CA2476934 | 16-Jun-2009 | 27-Feb-2023 | Rilonacept results in increased immunosuppressive effects; increases the risk of infection. | Tumor necrosis factor,Tumor necrosis factor receptor superfamily member 1B,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c,Lymphotoxin-alpha,Low affinity immunoglobulin gamma Fc region receptor III-B | Enbrel | Immunex Corp | Immunex Corp | Used to treat rheumatoid arthritis, psoriatic arthritis, or ankylosing spondylitis, and prevent joint damage caused by these conditions. Enbrel is also used to treat plaque psoriasis in adults and polyarticular juvenile idiopathic arthritis (in children a | NA | Supplied in a multiple-use vial as a sterile, white, preservative-free, lyophilized powder. Reconstitution with 1 mL of the supplied Sterile Bacteriostatic Water for Injection, USP (containing 0.9% benzyl alcohol) yields a multiple-use, clear, and colorle | Lyophilized powder. | Subcutaneous Injection | NA | NA | Signs of infection (fever, chills, sore throat, body aches, confusion, neck stiffness, flu symptoms); shortness of breath with swelling, rapid weight gain; chest pain, ongoing cough, coughing up mucus or blood; signs of skin infection such as itching, sw | Link | NA | NA |
| 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 |
| 10055 | Th1009 | Alteplase | >Th1009_Alteplase SYQVICRDEKTQMIYQQHQSWLRPVLRSNRVEYCWCNSGRAQCHSVPVKSCSEPRCFNGGTCQQALYFSDFVCQCPEGFAGKCCEIDTRATCYEDQGISYRGTWSTAESGAECTNWNSSALAQKPYSGRRPDAIRLGLGNHNYCRNPDRDSKPWCYVFKAGKYSSEFCSTPACSEGNSDCYFGNGSAYRGTHSLTESGASCLPWNSMILIGKVYTAQNPSAQALGLGKHNYCRNPDGDAKPWCHVLKNRRLTWEYCDVPSCSTCGLRQYSQPQFRIKGGLFADIASHPWQAAIFAKHRRSPGERFLCGGILISSCWILSAAHCFQERFPPHHLTVILGRTYRVVPGEEEQKFEVEKYIVHKEFDDDTYDNDIALLQLKSDSSRCAQESSVVRTVCLPPADLQLPDWTECELSGYGKHEALSPFYSERLKEAHVRLYPSSRCTSQHLLNRTVTDNMLCAGDTRSGGPQANLHDACQGDSGGPLVCLNDGRMTLVGIISWGLGCGQKDVPGVYTKVTNYLDWIRDNMRP | 59042.3 | C2569H3928N746O781S40 | 7.61 | -0.516 | 60 | NA | Glycosylated, human tissue plasminogen activator of 527 residues purified from CHO cells. | To manage acute myocardial infarction, acute ischemic stroke and for lysis of acute pulmonary emboli | Alteplase binds to fibrin in a thrombus and converts the entrapped plasminogen to plasmin, thus limited conversion of plasminogen takes place in the absence of fibrin. | Alteplase on binding to fibrin rich clots via the fibronectin finger-like domain and the Kringle 2 domain cleaves (domain) the Arg/Val bond in plasminogen to form plasmin which in turn degrades the fibrin matrix of the thrombus, thereby exerting its thrombolytic action. | NA | NA | NA | NA | NA | Agents causing angioedema, Amino Acids, Peptides, and Proteins, Anticoagulants, Blood and Blood Forming Organs, Blood Proteins, Cardiovascular Agents, Endopeptidases, Enzymes, Enzymes and Coenzymes, Fibrin Modulating Agents, Fibrinolytic Agents, Hematologic Agents, Hydrolases, Ophthalmologicals, Peptide Hydrolases, Plasminogen Activators, Proteins, Sensory Organs, Serine Endopeptidases, Serine Proteases, Tissue Plasminogen Activator, Tissue Plasminogen Activator, antagonists & inhibitors | NA | NA | NA | Ginkgo biloba.Additive anticoagulant/antiplatelet effects may increase bleeding risk. Concomitant therapy should be avoided. | Plasminogen,Fibrinogen alpha chain,Urokinase plasminogen activator surface receptor,Plasminogen activator inhibitor 1 | Activase | Genentech Inc | Genentech Inc | To treat blood clots in the lungs and improve heart function and survival followed by a heart attack. Activase may also be used to improve recovery and reduce disability in certain patients who have suffered from a stroke. | NA | NA | Sterile, white to off-white, lyophilized powder | Intravenous | The recommended dose is not to exceed 100 mg. Patients weighing > 67 kg are recommended a dose of 100 mg as a 15 mg intravenous bolus, followed by 50 mg infused over the next 30 minutes, and then 35 mg infused over the next 60 minutes. | Allergic | Rash; hives; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue. | Link | NA | NA |
| 10057 | Th1009 | Alteplase | >Th1009_Alteplase SYQVICRDEKTQMIYQQHQSWLRPVLRSNRVEYCWCNSGRAQCHSVPVKSCSEPRCFNGGTCQQALYFSDFVCQCPEGFAGKCCEIDTRATCYEDQGISYRGTWSTAESGAECTNWNSSALAQKPYSGRRPDAIRLGLGNHNYCRNPDRDSKPWCYVFKAGKYSSEFCSTPACSEGNSDCYFGNGSAYRGTHSLTESGASCLPWNSMILIGKVYTAQNPSAQALGLGKHNYCRNPDGDAKPWCHVLKNRRLTWEYCDVPSCSTCGLRQYSQPQFRIKGGLFADIASHPWQAAIFAKHRRSPGERFLCGGILISSCWILSAAHCFQERFPPHHLTVILGRTYRVVPGEEEQKFEVEKYIVHKEFDDDTYDNDIALLQLKSDSSRCAQESSVVRTVCLPPADLQLPDWTECELSGYGKHEALSPFYSERLKEAHVRLYPSSRCTSQHLLNRTVTDNMLCAGDTRSGGPQANLHDACQGDSGGPLVCLNDGRMTLVGIISWGLGCGQKDVPGVYTKVTNYLDWIRDNMRP | 59042.3 | C2569H3928N746O781S40 | 7.61 | -0.516 | 60 | NA | Glycosylated, human tissue plasminogen activator of 527 residues purified from CHO cells. | To manage acute myocardial infarction, acute ischemic stroke and for lysis of acute pulmonary emboli | Alteplase binds to fibrin in a thrombus and converts the entrapped plasminogen to plasmin, thus limited conversion of plasminogen takes place in the absence of fibrin. | Alteplase on binding to fibrin rich clots via the fibronectin finger-like domain and the Kringle 2 domain cleaves (domain) the Arg/Val bond in plasminogen to form plasmin which in turn degrades the fibrin matrix of the thrombus, thereby exerting its thrombolytic action. | NA | NA | NA | NA | NA | Agents causing angioedema, Amino Acids, Peptides, and Proteins, Anticoagulants, Blood and Blood Forming Organs, Blood Proteins, Cardiovascular Agents, Endopeptidases, Enzymes, Enzymes and Coenzymes, Fibrin Modulating Agents, Fibrinolytic Agents, Hematologic Agents, Hydrolases, Ophthalmologicals, Peptide Hydrolases, Plasminogen Activators, Proteins, Sensory Organs, Serine Endopeptidases, Serine Proteases, Tissue Plasminogen Activator, Tissue Plasminogen Activator, antagonists & inhibitors | NA | NA | NA | Ticlopidine.Increased bleeding risk. Monitor for signs of bleeding. | NA | Cathflo Activase | Genentech, Inc | Genentech, Inc | Used to treat the symptoms of Acute Myocardial Infarction, Pulmonary Embolism, Acute Ischemic Stroke, and Central Venous Catheter Occlusion | NA | Each vial of Cathflo Activase contains 2.2 mg of Alteplase (which includes a 10% overfill), 77 mg of Larginine, 0.2 mg of polysorbate 80, and phosphoric acid for pH adjustment. Each reconstituted vial will deliver 2 mg of Cathflo Activase, at a pH of approximately 7.3. | sterile, white to pale yellow, lyophilized powder | Injection for intracatheter instillation for restoration of function to central venous access devices following reconstitution with Sterile Water for Injection, USP. | Cathflo® Activase® (Alteplase) is for instillation into the dysfunctional catheter at a concentration of 1 mg/mL. Patients weighing ≥30 kg: 2 mg in 2 mL Patients weighing <30 kg: 110% of the internal lumen volume of the catheter, not to exceed 2 mg in 2 mL | Cathflo Activase should not be administered to patients with known hypersensitivity to Alteplase or any component of the formulation | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, any bleeding that will not stop, sudden headache, weakness, dizziness, bleeding gums, nosebleeds, easy bruising, bleeding from a wound, incision, catheter, or needle injection, bloody or tarry stools, coughing up blood, vomit that looks like coffee grounds, red or pink urine, heavy menstrual periods, abnormal vaginal bleeding, sudden numbness or weakness (especially on one side of the body), slurred speech, problems with vision or balance, chest pain or pressure, pain spreading to the jaw or shoulder, nausea, sweating, general ill feeling, sudden severe back pain, muscle weakness, numbness or loss of feeling in your arms or legs, swelling, rapid weight gain, little or nor urination, severe stomach pain, vomiting, darkening or purple discoloration of your fingers or toes, very slow heartbeats, shortness of breath, lightheadedness, sudden severe back pain, severe headache, blurred vision, pounding in your neck or ears, and anxiety | Link | NA | NA |
| 10067 | Th1012 | Reteplase | >Th1012_Reteplase SYQGNSDCYFGNGSAYRGTHSLTESGASCLPWNSMILIGKVYTAQNPSAQALGLGKHNYCRNPDGDAKPWCHVLKNRRLTWEYCDVPSCSTCGLRQYSQPQFRIKGGLFADIASHPWQAAIFAKHRRSPGERFLCGGILISSCWILSAAHCFQERFPPHHLTVILGRTYRVVPGEEEQKFEVEKYIVHKEFDDDTYDNDIALLQLKSDSSRCAQESSVVRTVCLPPADLQLPDWTECELSGYGKHEALSPFYSERLKEAHVRLYPSSRCTSQHLLNRTVTDNMLCAGDTRSGGPQANLHDACQGDSGGPLVCLNDGRMTLVGIISWGLGCGQKDVPGVYTKVTNYLDWIRDNMRP | 39589.6 | C1736H2671N499O522S22 | 6.86 | -0.435 | 60 | NA | Human tissue plasminogen activator which is glycosylated and purified (355 residues) from CHO cells. Retavase is considered a third-generation thrombolytic agent, genetically engineered to retain and delete certain portions of human tPA. Retavase is a deletion mutein of human tPA formed by deleting various amino acids present in endogenous human tPA. Retavase contains 355 of the 527 amino acids of native human tPA (amino acids 1-3 and 176-527), and retains the activity-related kringle-2 and serine protease domains of human tPA. Three domains are deleted from retavase – kringle-1, finger, and epidermal growth factor (EGF). | For lysis of acute pulmonary emboli, intracoronary emboli and management of myocardial infarction. | Reteplase cleaves Arg/Val bonds in plasminogen to form plasmin. Plasmin in turn degrades the fibrin matrix of the thrombus thereby exerting its thrombolytic action. This helps eliminate blood clots or arterial blockages that further cause myocardial infarction. | Reteplase binds to fibrin rich clots via the fibronectin finger-like domain and the Kringle 2 domain. The protease domain then cleaves the Arg/Val bond in plasminogen to form plasmin. Plasmin in turn degrades the fibrin matrix of the thrombus, thereby exerting its thrombolytic action. | NA | NA | NA | NA | NA | Agents causing angioedema, Amino Acids, Peptides, and Proteins, Anticoagulants, Biological Factors, Blood and Blood Forming Organs, Blood Proteins, Cardiovascular Agents, Endopeptidases, Enzymes, Enzymes and Coenzymes, Fibrin Modulating Agents, Fibrinolytic Agents, Hematologic Agents, Hydrolases, Peptide Hydrolases, Plasminogen Activators, Proteins, Serine Endopeptidases, Serine Proteases, Tissue Plasminogen Activator | CA2107476 | 18-Dec-2007 | 15-Apr-2012 | Additive anticoagulant/antiplatelet effects may increase bleed risk. Concomitant therapy should be avoided with Ginkgo biloba | Plasminogen,Fibrinogen alpha chain,Urokinase plasminogen activator surface receptor,Plasminogen activator inhibitor 1 | Retavase | Centocor | Centocor | Improves heart function and reduces long-term effects of a heart attack. | NA | Each single-use vial contains:Reteplase 18.1 mg, Tranexamic Acid 8.32 mg, Dipotassium Hydrogen Phosphate 136.24 mg, Phosphoric Acid 51.27 mg, Sucrose 364.0 mg, Polysorbate 805.20 mg | Sterile, white, lyophilized powder | Intravenous Injection | Retavase is administered as a 10 + 10 unit double-bolus injection. Two 10 unit bolus injections are required for a complete treatment. Each bolus is administered as an Intravenous infusion over 2 minutes. The second bolus is given 30 minutes after initial one. | Allergic, or you have an aneurysm, heart or blood vessel defects, bleeding disorders | Rash; hives; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue. | 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 |
| 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 |
| 10129 | Th1018 | Secretin | >Th1018_Secretin HSDGTFTSELSRLREGARLQRLLQGLV | 3039.44 | C130H220N44O39 | 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 | Clidinium. Anticholinergic agents such as secretin may diminish the stimulatory effect of secretin. Avoid using drugs with substantial anticholinergic effects in patients receiving secretin whenever possible. If such agents must be used in combina | Secretin receptor | SecreFlo | Repligen Corp | Repligen Corp | Testing for stimulation of pancreatic secretions, including bicarbonate, to aid in the diagnosis of pancreatic exocrine dysfunction. | H-His-Ser-Asp-Gly-Thr-Phe-Thr-Ser-Glu-Leu-Ser-Arg-Leu-Arg-Asp-Ser- Ala-Arg-Leu-Gln-Arg-Leu-Leu-Gln-Gly-Leu-Val-NH2 | NA | Lyophilized white powder | Intravenous infusion | NA | Allergy | Abdominal discomfort, Nausea, Mild bradycardia (reduced heart rate), Decreased blood pressure and Diaphoresis (profuse perspiration) | Link | NA | NA |
| 10130 | Th1018 | Secretin | >Th1018_Secretin HSDGTFTSELSRLREGARLQRLLQGLV | 3039.44 | C130H220N44O40 | 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 | Tiotropium.The stimulatory effect of Secretin may be reduced by anticholinergics such as Tiotropium. Concomitant use of Secretin and drugs with substantial anticholinergic effects should be avoided. | NA | ChiRhoStim | ChiRhoClin, Inc | ChiRhoClin, Inc | Testing for stimulation of gastrin secretion to aid in the diagnosis of gastrinoma. | NA | As a 10 mL single-dose vial which contains 16 mcg of purified synthetic human secretin, 1.5 mg of Lcysteine hydrochloride, 20 mg of mannitol, and 9 mg of sodium chloride. When reconstituted in 8 mL of Sodium Chloride Injection USP, each mL of solution contains 2 mcg synthetic human secretin for intravenous use. The pH of the reconstituted solution has a range of 3 to 6.5. | white lyophilized sterile powder | Intravenous infusion | 0.2 mcg/kg by intravenous injection over 1 minute | NA | Nausea Vomiting Flushing Upset stomach | Link | NA | NA |
| 10135 | Th1019 | Peginterferon alfa-2b | >Th1019_Peginterferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 31000 | C130H219N43O42 | 5.99 | NA | 61 | Approximately 40 hours (range 22 to 60 hours) in patients with HCV infection | Peginterferon alfa-2b is a covalent conjugate of recombinant alfa-2b interferon with monomethoxy polyethylene glycol (PEG). The average molecular weight of the PEG portion of the molecule is 12,000 daltons. The average molecular weight of the PEG-Intron molecule is approximately 31,000 daltons. The specific activity of peginterferon alfa-2b is approximately 0.7 x 108 IU/mg protein. Interferon alfa-2b is a water-soluble protein with a molecular weight of 19,271 daltons produced by recombinant DNA techniques. It is obtained from the bacterial fermentation of a strain of Escherichia coli bearing a genetically engineered plasmid containing an interferon gene from human leukocytes. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | Used for the treatment of chronic hepatitis C in patients not previously treated with interferon alpha who have compensated liver disease and are at least 18 years of age. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds to type I interferon receptors IFNAR1 and IFNAR2c which upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | NA | NA | After a single subcutaneous dose of peginterferon alfa-2b, the mean absorption half-life was 4.6 hours. | NA | Oral cl=22 mL/hr/kg [patients with HCV infection], Renal elimination accounts for 30% of the clearance. | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 CYP2C9 Inducers, Cytochrome P-450 CYP2C9 Inducers (weak), Cytochrome P-450 CYP2D6 Inhibitors, Cytochrome P-450 CYP2D6 Inhibitors (weak), Cytochrome P-450 Enzyme Inducers, Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatitis C, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Macromolecular Substances, Myelosuppressive Agents, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | CA1341567 | 19-Feb-2008 | 19-Feb-2025 | Aminophylline. Interferon increases the effect and toxicity of theophylline | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | PEG-Intron | Schering Corp | Schering Corp | Used to treat chronic hepatitis C in adults. Peginterferon alfa-2b is often used in combination with another medication called ribavirin (Rebetol, Ribasphere) to treat hepatitis C in adults and children who are at least 3 years old. It may be used in comb | NA | Provided in both vials and the REDIPEN. Each vial contains either 74 mcg, 118.4 mcg, 177.6 mcg, or 222 mcg of PegIntron as a white to off-white tablet-like solid that is whole/in pieces or as a loose powder, and 1.11 mg dibasic sodium phosphate anhydrous, | Powder | Subcutaneous Injection | 1.5 mcg/kg/week. The volume of PegIntron to be injected depends on the strength of PegIntron and patient's body weight | Allergic or in case of having autoimmune hepatitis, liver failure, severe kidney disease, a hemoglobin blood cell disorder | Vision problems; fast heart rate, feeling like you might pass out; unusual weakness; high fever with severe stomach pain and bloody diarrhea; pain or burning when you urinate; severe pain in your upper stomach spreading to your back, nausea and vomiting and new or worsening liver symptoms. | Link | NA | NA |
| 10136 | Th1019 | Peginterferon alfa-2b | >Th1019_Peginterferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 31000 | C130H219N43O42 | 5.99 | NA | 61 | Approximately 40 hours (range 22 to 60 hours) in patients with HCV infection | Peginterferon alfa-2b is a covalent conjugate of recombinant alfa-2b interferon with monomethoxy polyethylene glycol (PEG). The average molecular weight of the PEG portion of the molecule is 12,000 daltons. The average molecular weight of the PEG-Intron molecule is approximately 31,000 daltons. The specific activity of peginterferon alfa-2b is approximately 0.7 x 108 IU/mg protein. Interferon alfa-2b is a water-soluble protein with a molecular weight of 19,271 daltons produced by recombinant DNA techniques. It is obtained from the bacterial fermentation of a strain of Escherichia coli bearing a genetically engineered plasmid containing an interferon gene from human leukocytes. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | Used for the treatment of chronic hepatitis C in patients not previously treated with interferon alpha who have compensated liver disease and are at least 18 years of age. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds to type I interferon receptors IFNAR1 and IFNAR2c which upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | NA | NA | After a single subcutaneous dose of peginterferon alfa-2b, the mean absorption half-life was 4.6 hours. | NA | Oral cl=22 mL/hr/kg [patients with HCV infection], Renal elimination accounts for 30% of the clearance. | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 CYP2C9 Inducers, Cytochrome P-450 CYP2C9 Inducers (weak), Cytochrome P-450 CYP2D6 Inhibitors, Cytochrome P-450 CYP2D6 Inhibitors (weak), Cytochrome P-450 Enzyme Inducers, Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatitis C, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Macromolecular Substances, Myelosuppressive Agents, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | CA2329474 | 26-Feb-2002 | 31-Oct-2016 | Dyphylline.Interferon increases the effect and toxicity of theophylline | NA | Sylatron | Merck Sharp & Dohme Corp. | Merck Sharp & Dohme Corp. | SYLATRON™ is an alpha interferon indicated for the adjuvant treatment of melanoma with microscopic or gross nodal involvement within 84 days of definitive surgical resection including complete lymphadenect | NA | NA | sterile, white to off-white lyophilized powder | Subcutaneous Injection | The recommended starting dose is 6 mcg/kg/week subcutaneously for 8 doses, followed by 3 mcg/kg/week subcutaneously for up to 5 years. Premedicate with acetaminophen 500 to 1000 mg orally 30 minutes prior to the first dose of SYLATRON and as needed for subsequent doses. The recommended starting doses of SYLATRON in patients with moderate or severe renal impairment or end-stage renal disease (ESRD) are listed in Table 1 [see Use In Specific Populations]. No dose adjustment is needed for patients with a creatinine clearance (CLcr) > 50 mL/min/1.73m². | SYLATRON is contraindicated in patients with: A history of anaphylaxis to peginterferon alfa-2b or interferon alfa-2b autoimmune hepatitis hepatic decompensation (Child-Pugh score >6 [class B and C]) | Headache, joint or muscle pain; nausea, dry mouth, loss of appetite, weight loss; dizziness, sleep problems (insomnia), feeling mildly anxious, depressed, or irritable; or pain, redness, swelling, or irritation where the medicine was injected. | Link | NA | NA |
| 10139 | Th1019 | Peginterferon alfa-2b | >Th1019_Peginterferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMKEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 31000 | C130H219N43O42 | 5.99 | NA | 61 | Approximately 40 hours (range 22 to 60 hours) in patients with HCV infection | Peginterferon alfa-2b is a covalent conjugate of recombinant alfa-2b interferon with monomethoxy polyethylene glycol (PEG). The average molecular weight of the PEG portion of the molecule is 12,000 daltons. The average molecular weight of the PEG-Intron molecule is approximately 31,000 daltons. The specific activity of peginterferon alfa-2b is approximately 0.7 x 108 IU/mg protein. Interferon alfa-2b is a water-soluble protein with a molecular weight of 19,271 daltons produced by recombinant DNA techniques. It is obtained from the bacterial fermentation of a strain of Escherichia coli bearing a genetically engineered plasmid containing an interferon gene from human leukocytes. The PEG strand protects the molecule in vivo from proteolytic breakdown, substantially increases its in vivo half-life, and reduces immunogenicity by wrapping around and physically hindering access to the protein portion of the molecule. | Used for the treatment of chronic hepatitis C in patients not previously treated with interferon alpha who have compensated liver disease and are at least 18 years of age. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2-5 oligoadenylate synthetase (2-5 A synthetase) and protein kinase R. | It binds to type I interferon receptors IFNAR1 and IFNAR2c which upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | NA | NA | After a single subcutaneous dose of peginterferon alfa-2b, the mean absorption half-life was 4.6 hours. | NA | Oral cl=22 mL/hr/kg [patients with HCV infection], Renal elimination accounts for 30% of the clearance. | Adjuvants, Immunologic, Alcohols, Alfa Interferons, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cancer immunotherapy, Compounds used in a research, industrial, or household setting, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 CYP2C9 Inducers, Cytochrome P-450 CYP2C9 Inducers (weak), Cytochrome P-450 CYP2D6 Inhibitors, Cytochrome P-450 CYP2D6 Inhibitors (weak), Cytochrome P-450 Enzyme Inducers, Cytochrome P-450 Enzyme Inhibitors, Cytokines, Drug Carriers, Ethylene Glycols, Glycols, Hepatitis C, Immunosuppressive Agents, Immunotherapy, Intercellular Signaling Peptides and Proteins, Interferon alpha, Interferon Type I, Interferon-alpha, Interferons, Macromolecular Substances, Myelosuppressive Agents, Pegylated agents, Peptides, Polymers, Proteins, Treatments for Hepatitis C | NA | NA | NA | Aldesleukin | NA | Unitron PEG | Merck Ltd. | Merck Ltd. | It is used to treat chronic hepatitis C (a disease of the liver) for people who cannot tolerate or use the antiviral medication, ribavirin. The most effective treatment of chronic hepatitis C is the combination of an interferon and ribavirin. Unitron Peg | NA | NA | Lyophilized powder | Subcutaneous Injection | Its Subcutaneous injection once a week on the same day of the week for 48 weeks. Dosing is based on body weight. Treatment with this medication should be stopped if no response is noticed after 6 months. | Allergic | Abdominal pain or swelling, anemia (paleness, tiredness, shortness of breath), changes in mood (e.g., irritability, depression, anxiety, aggression), confusion, dizziness, eye pain or swelling of the eye, high blood sugar (increased thirst, hunger, weakness, irritability, trouble concentrating, signs of infection (e.g., chills, fever, cough, sore throat, difficulty or painful urination, difficulty breathing), burning sensation in arms or legs, ulcers in mouth or sore throats. | Link | NA | NA |
| 10142 | Th1020 | Asparaginase | >Th1020_Asparaginase MEFFKKTALAALVMGFSGAALALPNITILATGGTIAGGGDSATKSNYTVGKVGVENLVNAVPQLKDIANVKGEQVVNIGSQDMNDNVWLTLAKKINTDCDKTDGFVITHGTDTMEETAYFLDLTVKCDKPVVMVGAMRPSTSMSADGPFNLYNAVVTAADKASANRGVLVVMNDTVLDGRDVTKTNTTDVATFKSVNYGPLGYIHNGKIDYQRTPARKHTSDTPFDVSKLNELPKVGIVYNYANASDLPAKALVDAGYDGIVSAGVGNGNLYKSVFDTLATAAKTGTAVVRSSRVPTGATTQDAEVDDAKYGFVASGTLNPQKARVLLQLALTQTKDPQQIQQIFNQY | 31731.9 | C1377H2208N382O442S17 | 4.67 | 0.059 | NA | 8-30 hours | L-asparagine amidohydrolase from E. coli | To treat acute lympocytic leukemia and non-Hodgkins lymphoma | In most patients with acute leukemia, the malignant cells are dependent on an exogenous source of asparagine for survival. Normal cells, however, are able to synthesize asparagine and thus are affected less by the rapid depletion produced by treatment with the enzyme asparaginase. Elspar exploits a metabolic defect in asparagine synthesis of some malignant cells. | Asparaginase converts asparagine to aspartic acid and ammonia. It facilitates production of oxalo-acetate which is needed for general cellular metabolism. Some malignant cells lose the ability to produce asparagine and thus the loss of exogenous sources of asparagine leads to cell death. | NA | NA | NA | Apparent volume of distribution was slightly greater than the plasma volume. Asparaginase levels in cerebrospinal fluid were less than 1% of concurrent plasma levels | NA | Amidohydrolases, Antineoplastic Agents, Antineoplastic and Immunomodulating Agents, Asparaginase, Asparagine-specific Enzyme, Enzymes, Enzymes and Coenzymes, Hydrolases, Narrow Therapeutic Index Drugs, Thyroxine-binding globulin inhibitors | NA | NA | NA | Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. | L-asparagine | Elspar | Lundbeck Inc. | Lundbeck Inc. | To treat acute lymphocytic leukemia. It is used along with other cancer medicines. Elspar is an antineoplastic agent that works by decreasing the amount of asparagine in the body, which kills certain leukemia cells | NA | Each vial contains 10,000 International Units of asparaginase and 80 mg of mannitol. | Lyophilized plug or powder | Intravenous or intramuSubcutaneousular. Intravenou | The recommended dose of Elspar is 6,000 International Units/m_ intramuscularly (IM) or intravenously (IV) three times a week. | Allergic | Fever, chills (see flu like symptoms), Nausea and vomiting, Allergic reaction, (sudden onset of wheezing, itching, rash, face swelling, agitation, low blood pressure). You will be monitored closely for this reaction, Poor appetite, Stomach cramping | Link | NA | NA |
| 10145 | Th1021 | Thyrotropin Alfa | >Th1021_Thyrotropin_Alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 | 25 ± 10 hours | Thyrotropin alfa is a recombinant form of thyroid stimulating hormone used in performing certain tests in patients who have or have had thyroid cancer. It is also used along with a radioactive agent to destroy remaining thyroid tissue in certain patients. | For detection of residueal or recurrent thyroid cancer | Binding of thyrotropin alfa to TSH receptors on normal thyroid epithelial cells or on well-differentiated thyroid cancer tissue stimulates iodine uptake and organification. Thyrogen is an exogenous source of human TSH that offers an additional diagnostic tool in the follow-up of patients with a history of well-differentiated thyroid cancer. | Binding of thyrotropin Alfa to the thyrotropin receptors found on any residual thyroid cells or tissues stimulates radioactive iodine uptake for better radiodiagnostic imaging. | NA | NA | Time to peak: Median: 10 hours (range: 3-24 hours) After a single intramuscular injection of 0.9 mg of thyrotropin alfa: Cmax= 116+38mU/L, Tmax=22+8.5 hours. AUC=5088+1728 mU·hr/L. | NA | Through kidney and liver | Agents used to treat hypothyroidism, Anterior Pituitary Lobe Hormones and Analogues, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Pituitary and Hypothalamic Hormones and Analogues, Pituitary Hormones, Pituitary Hormones, Anterior, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | US5840566 | 24-Nov-1998 | 24-Nov-2015 | NA | Thyrotropin receptor | Thyrogen | Genzyme Corporation , Genzyme Europe Bv | Genzyme Corporation , Genzyme Europe Bv | It is used in performing certain tests in patients who have or have had thyroid cancer. It is also used along with a radioactive agent to destroy remaining thyroid tissue in certain patients who have had their thyroid gland removed because of thyroid canc | NA | Each vial of THYROGEN contains 1.1 mg thyrotropin alfa, 36 mg Mannitol, 5.1 mg Sodium Phosphate, and 2.4 mg Sodium Chloride. | Lyophilized powder | IntramuSubcutaneousular preferably the buttocks | A 0.9 mg intramuscular injection to the buttock followed by a second 0.9 mg intramuscular injection to the buttock 24 hours later. | Allergic | Rash; hives; itching; difficulty breathing; tightness in the chest | Link | NA | NA |
| 10148 | 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 | CA2124690 | 11-Sep-2007 | 1-Oct-2013 | NA | Coagulation factor X,Coagulation factor IX,von Willebrand factor,Phytanoyl-CoA dioxygenase, peroxisomal,Asialoglycoprotein receptor 2,78 kDa glucose-regulated protein,Calreticulin,Calnexin,Protein ERGIC-53,Prolow-density lipoprotein receptor-related protein 1,Multiple coagulation factor deficiency protein 2 | Advate | Takeda , Baxalta US Inc. , Takeda Manufacturing Austria Ag , Baxter Healthcare Corporation | Takeda , Baxalta US Inc. , Takeda Manufacturing Austria Ag , Baxter Healthcare Corporation | ADVATE is a medicine used to replace clotting factor that is missing in people with hemophilia A. It is used to prevent and control bleeding in adults and children (0-16 years) with hemophilia A. | NA | NA | Powder form | Intravenous Injection | Dose (IU) = body weight (kg) _ Desired Factor VIII Rise (IU/dL or % of normal) _ 0.5 (IU/kg per IU/dL). So example, assuming assuming patient's baseline Factor VIII level is < 1% of normal = A dose of 1750 IU ADVATE administered to a 70 kg patient should be expected to result in a peak post-infusion Factor VIII increase of 1750 IU × {[2 IU/dL]/[IU/kg]}/[70 kg] = 50 IU/dL (50% of normal). | Patients who have life-threatening hypersensitivity reactions, including anaphylaxis, to mouse or hamster protein or other constituents of the product. | Chest pain; easy bruising, increased bleeding episodes; or bleeding from a wound or where the medicine was injected. | Link | NA | NA |
| 10149 | 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 | CA1339477 | 23-Sep-1997 | 23-Sep-2014 | NA | NA | Adynovate | Baxalta US Inc. | Baxalta US Inc. | used to help treat and control bleeding in children and adults with hemophilia A (congenital Factor VIII deficiency). Your healthcare provider may give you ADYNOVATE when you have surgery. | NA | NA | sterile, non-pyrogenic, white to off-white lyophilized powder | intravenous | NA | ADYNOVATE is contraindicated in patients who have had prior anaphylactic reaction to ADYNOVATE, to the parent molecule (ADVATE), mouse or hamster protein, or excipients of ADYNOVATE (e.g. Tris, mannitol, trehalose, glutathione, and/or polysorbate 80). | Sore throat, cough, runny nose; fever or chills; mild nausea, vomiting; unusual or unpleasant taste in your mouth; skin itching or rash. | Link | NA | NA |
| 10151 | 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 | Alphanate | NA | NA | It is used for preventing and controlling bleeding in adult patients with hemophilia A. It is also used to control certain types of bleeding episodes (eg, due to injury or surgery) in patients with von Willebrand disease. | NA | When reconstituted with the appropriate volume of Sterile Water for Injection, USP, Alphanate contains 0.3 - 0.9 g Albumin (Human)/100 mL; NMT 5 mmol calcium/L; NMT 750 µg glycine/IU FVIIIC; NMT 1.0 U heparin/mL; 10 - 40 mmol histidine/L; NMT 0.1 mg imida | Lyophilized powder | Intravenous Injection | Bodyweight (in kg) X 0.50 lU/kg X Factor VIII Increase Desired (Percent) = Number of Factor VIII:C IU Required. | Contraindicated in patients who have manifested life-threatening immediate hypersensitivity reactions including anaphylaxis to any components of the product. | Rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); back or stomach pain; calf pain, swelling, or tenderness; chest pain; coughing up blood; dark urine; fever or chills; new or worsening bruis | Link | NA | NA |
| 10153 | 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 | Bioclate | Baxter Healthcare Corporation, Hyland Division and Genetics Institute, Inc. | Baxter Healthcare Corporation, Hyland Division and Genetics Institute, Inc. | To treat or prevent bleeding episodes in adults and children with hemophilia A. It is also used to control bleeding related to surgery or dentistry in a person with hemophilia. | NA | Biocolate is available in single-dose bottles which contain nominally 250, 500 and 1000 International Units per bottle.When reconstituted with the appropriate volume of diluent, it contains the following stabilizers in maximum amounts: 12.5 mg/mL Albumin | Sterile, nonpyrogenic, off-white to faint yellow, lyophilized powder | Intravenous infusion | NA | Allergic | Chest pain; easy bruising, increased bleeding episodes; or bleeding from a wound or where the medicine was injected. | Link | NA | NA |
| 10160 | 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 | Kogenate Bayer | Bayer Ag | Bayer Ag | control and prevention of bleeding episodes in adults and children (0-16 years) with hemophilia A. | NA | Each vial of Kogenate FS contains the labeled amount of recombinant factor VIII in international units (IU). One IU, as defined by the World Health Organization standard for blood coagulation factor VIII, human, is approximately equal to the level of factor VIII activity found in 1 mL of fresh pooled human plasma. | sterile, nonpyrogenic, preservative-free, powder | NA | Dosage (units) = body weight (kg) x desired factor VIII rise (IU/dL or % of normal) x 0.5 (IU/kg per IU/dL) OR IU/dL (or % normal)=Total Dose (IU)/body weight (kg) x 2 [IU/dL]/[IU/kg] | Kogenate FS is contraindicated in patients who have manifested life-threatening immediate hypersensitivity reactions, including anaphylaxis, to the product or its components, including mouse or hamster proteins. | The most serious adverse reactions are systemic hypersensitivity reactions including bronchospastic reactions and/or hypotension and anaphylaxis and the development of high-titer inhibitors necessitating alternative treatments to AHF. The most common adverse reactions observed in clinical trials (frequency ≥ 4% of patients) are inhibitor formation in previously untreated patients (PUPs) and minimally treated patients (MTPs), skin-related hypersensitivity reactions (e.g., rash, pruritus), infusion site reactions (e.g., inflammation, pain), and central venous access device (CVAD) line-associated infections in patients requiring a CVAD for intravenous administration. | Link | NA | NA |
| 10161 | 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 | Hyate:C | NA | NA | To treat and prevent serious bleeding episodes in patients with a bleeding problem called hemophilia A. | NA | NA | Powder | Intravenous Injection | NA | Allergic | Fever, changes in facial skin color, chills, fast or irregular breathing, nausea, puffiness or swelling of the eyelids or around the eyes, sensation of burning, warmth, heat, numbness, tightness, or tingling, skin rash, hives, or itching, tightness in the chest, troubled breathing, and unusual tiredness or weakness. | Link | NA | NA |
| 10163 | 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 | Kovaltry | Bayer | Bayer | KOVALTRY, Antihemophilic Factor (Recombinant), is a recombinant, human DNA sequence derived, full length Factor VIII concentrate indicated for use in adults and children with hemophilia A (congenital Factor VIII deficiency) | NA | The active substance in KOVALTRY is the unmodified full length recombinant Factor VIII glycoprotein comprising the human derived amino acid sequence. Post-translational modifications are similar to those of endogenous Factor VIII including glycosylation sites and sulfation of tyrosine sites. Manufacturing and quality controls ensure that both galactose-alpha-1,3-galactose (alpha-Gal) and N-glycolyl neuraminic acid (NGNA) content are below the 1% limit of detection established for each analytical method. | sterile, non-pyrogenic, white to slightly yellow powder | Intravenous Injection | Required dose (IU) = body weight (kg) x desired Factor VIII rise (% of normal or IU/dL) x reciprocal of expected/observed recovery (e.g., 0.5 for a recovery of 2 IU/dL per IU/kg) | KOVALTRY is contraindicated in patients who have a history of hypersensitivity reactions to the active substance, to any of the excipients, or to mouse or hamster proteins | headache fever itching injection site reactions insomnia rash abdominal pain or discomfort indigestion swollen lymph nodes heart palpitations dizziness allergic skin reactions changes in taste hives, and flushing. | Link | NA | NA |
| 10164 | 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 | Koate-HP | NA | NA | To control and prevent bleeding episodes in people with low levels of factor VIII. It is also used in these patients before surgery to prevent bleeding. People with low factor VIII levels are at risk for bleeding longer after an injury/surgery and for ble | NA | NA | Powder | Intravenous Injection | NA | Allergic | Nausea, stomach pain, low fever, loss of appetite, dark urine, clay-colored stools, jaundice (yellowing of the skin or eyes); fever, chills, runny nose, and drowsiness followed about 2 weeks later by a rash and joint pain; fast heart rate, chest pain, troubled breathing and unusual tiredness. | Link | NA | NA |
| 10166 | 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 | Kogenate FS | Bayer | Bayer | Kogenate FS is used to treat or prevent bleeding episodes in adults and children with hemophilia A. It is also used to control bleeding related to surgery or dentistry in a person with hemophilia, and to prevent joint damage in people age 16 or older with | NA | Kogenate FS is formulated with Sucrose ( 0.9- 1.3%), glycine (210-25mg/ml), histidine (18-23 mmol/L) as stablizers and 27-36mEq/L sodium, 2.0-3.0 mmol/L calcium, 32-40 mEq/L chloride, 64-96 _g/mL polysorbate 80, 28 mg/vial sucrose and trace amounts of Imi | Powder | Intravenous Injection | NA | Allergic | Chest pain; easy bruising, increased bleeding episodes; or bleeding from a wound or where the medicine was injected. | Link | NA | NA |
| 10169 | 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 | Monarc-M | NA | NA | To treat and prevent serious bleeding episodes in patients with hemophilia A. | NA | NA | Powder | Intravenous Injection | NA | Allergic | Blurred vision, flushing, headache, nausea, vomiting | 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 |
| 10174 | 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 | ReFacto | NA | NA | To control and prevent hemorrhagic episodes and for surgical prophylaxis in patients with hemophilia A. ReFacto is indicated for short-term routine prophylaxis to reduce the frequency of spontaneous bleeding episodes | NA | It is available in single-use vials containing the labeled amount of factor VIII activity. Each vial contains nominally 250, 500, 1000 or 2000 IU of ReFacto (antihemophilic factor) per vial. The formulated product is a clear colorless solution upon recons | Lyophilized powder | Intravenous Injection | Required units = body weight (kg)x desired factor VIII rise (IU/dL or % of normal)x 0.5 (IU/kg per IU/dL) | Known hypersensitivity to mouse or hamster proteins | Chest pain; easy bruising, increased bleeding episodes; or bleeding from a wound or where the medicine was injected. | Link | NA | NA |
| 10177 | 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 | Xyntha | NA | NA | Xyntha is used to treat or prevent bleeding episodes in adults and children with hemophilia A. It is also used to control bleeding related to surgery or dentistry in a person with hemophilia A. | NA | Each single-use vial contains nominally 250, 500, 1000 or 2000 IU of XYNTHA (antihemophilic factor) . Upon reconstitution, the product is a clear to slightly opalescent, colorless solution that contains sodium chloride, sucrose, L-histidine, calcium chlor | Sterile, nonpyrogenic, preservative-free, freeze-dried powder | Intravenous Injection | Required units = body weight (kg) x desired factor VIII rise (IU/dL or % of normal) x 0.5 (IU/kg per IU/dL) | NA | Chest pain; easy bruising, increased bleeding episodes; or bleeding from a wound or where the medicine was injected. | Link | NA | NA |
| 10201 | Th1026 | Anistreplase | >Th1026_Anistreplase SYQVICRDEKTQMIYQQHQSWLRPVLRSNRVEYCWCNSGRAQCHSVPVKSCSEPRCFNGGTCQQALYFSDFVCQCPEGFAGKCCEIDTRATCYEDQGISYRGTWSTAESGAECTNWNSSALAQKPYSGRRPDAIRLGLGNHNYCRNPDRDSKPWCYVFKAGKYSSEFCSTPACSEGNSDCYFGNGSAYRGTHSLTESGASCLPWNSMILIGKVYTAQNPSAQALGLGKHNYCRNPDGDAKPWCHVLKNRRLTWEYCDVPSCSTCGLRQYSQPQFRIKGGLFADIASHPWQAAIFAKHRRSPGERFLCGGILISSCWILSAAHCFQERFPPHHLTVILGRTYRVVPGEEEQKFEVEKYIVHKEFDDDTYDNDIALLQLKSDSSRCAQESSVVRTVCLPPADLQLPDWTECELSGYGKHEALSPFYSERLKEAHVRLYPSSRCTSQHLLNRTVTDNMLCAGDTRSGGPQANLHDACQGDSGGPLVCLNDGRMTLVGIISWGLGCGQKDVPGVYTKVTNYLDWIRDNMRP | 59042.3 | C2569H3928N746O781S40 | 7.61 | -0.516 | 60 | NA | Human tissue plasminogen activator, purified, glycosylated, 527 residues purified from CHO cells. Eminase is a lyophilized (freeze-dried) formulation of anistreplase, the p-anisoyl derivative of the primary Lys-plasminogen-streptokinase activator complex (a complex of Lys-plasminogen and streptokinase). A p-anisoyl group is chemically conjugated to a complex of bacterial-derived streptokinase and human Plasma-derived Lys-plasminogen proteins. | For lysis of acute pulmonary emboli, intracoronary emboli and management of myocardial infarction | Anistreplase cleaves the Arg/Val bond in plasminogen to form plasmin. Plasmin in turn degrades the fibrin matrix of the thrombus, thereby exerting its thrombolytic action. This helps eliminate blood clots or arterial blockages that cause myocardial infarction. | Anistreplase cleaves the Arg/Val bond in plasminogen to form plasmin. This in turn leads to the degradation of blood clots. | NA | NA | NA | NA | NA | Agents causing angioedema, Amino Acids, Peptides, and Proteins, Anticoagulants, Blood and Blood Forming Organs, Blood Proteins, Cardiovascular Agents, Endopeptidases, Enzymes, Enzymes and Coenzymes, Fibrin Modulating Agents, Fibrinolytic Agents, Hematologic Agents, Hydrolases, Peptide Hydrolases, Plasminogen Activators, Proteins, Serine Endopeptidases, Serine Proteases | NA | NA | NA | The use of anistreplase with other cardioactive drugs has not been studied. In addition to bleeding associated with heparin and vitamin K antagonists, drugs that alter platelet function (such as ASA and dipyridamole) may increase the risk of bleeding | Plasminogen,Fibrinogen alpha chain,Urokinase plasminogen activator surface receptor,Plasminogen activator inhibitor 1 | Eminase | Wulfing Pharma GmbH | Wulfing Pharma GmbH | For use in the management of ( acute myocardial infarction) AMI in adults for the lysis of thrombi obstructing coronary arteries, the reduction of infarct size, the improvement of ventricular function following AMI, and the reduction of mortality associat | NA | Each unit-dose vial of sterile lyophilized, white to off-white powder contains: anistreplase 30 units, dimethylsulfoxide <3 mg, sodium hydroxide <0.2 mg and the following buffers or stabilizers: p-amidinophenyl-p'-anisate (acylating agent) 150 µg, mannito | Dry powder | Intravenous infusion | 30 units of anistreplase administered only by i.v. injection over 2 to 5 minutes into an i.v. line or vein. | Allergic, active internal bleeding; history of cerebrovascular accident (CVA); patients receiving other i.v. thrombolytic agents; recent (within 2 months) intracranial or intraspinal surgery or trauma, intracranial neoplasm, arteriovenous malformation, or | NA | Link | NA | NA |
| 10210 | Th1028 | Tenecteplase | >Th1028_Tenecteplase SYQVICRDEKTQMIYQQHQSWLRPVLRSNRVEYCWCNSGRAQCHSVPVKSCSEPRCFNGGTCQQALYFSDFVCQCPEGFAGKCCEIDTRATCYEDQGISYRGNWSTAESGAECTNWQSSALAQKPYSGRRPDAIRLGLGNHNYCRNPDRDSKPWCYVFKAGKYSSEFCSTPACSEGNSDCYFGNGSAYRGTHSLTESGASCLPWNSMILIGKVYTAQNPSAQALGLGKHNYCRNPDGDAKPWCHVLKNRRLTWEYCDVPSCSTCGLRQYSQPQFRIKGGLFADIASHPWQAAIFAAAAASPGERFLCGGILISSCWILSAAHCFQERFPPHHLTVILGRTYRVVPGEEEQKFEVEKYIVHKEFDDDTYDNDIALLQLKSDSSRCAQESSVVRTVCLPPADLQLPDWTECELSGYGKHEALSPFYSERLKEAHVRLYPSSRCTSQHLLNRTVTDNMLCAGDTRSGGPQANLHDACQGDSGGPLVCLNDGRMTLVGIISWGLGCGQKDVPGVYTKVTNYLDWIRDNMRP | 58951.2 | C2561H3919N747O781S40 | 7.61 | -0.528 | 60 | 1.9 hours (mammalian reticulocytes, in vitro) | Tenecteplase(527 amino acid) is a glycoprotein developed by introducing the following modifications to the complementary DNA for natural human tPA: a substitution of threonine 103 with asparagine, and a substitution of asparagine 117 with glutamine, both within the kringle 1 domain, and a tetra-alanine substitution at amino acids 296-299 in the protease domain. | To treat myocardial infarction and lysis of intracoronary emboli. | Tenecteplase is a fibrin-specific tissue-plasminogen activator. It binds to fibrin rich clots and cleaves the Arg/Val bond in plasminogen to form plasmin. Plasmin in turn degrades the fibrin matrix of the thrombus, thereby exerting its thrombolytic action. This helps eliminate blood clots or arterial blockages that cause myocardial infarction. | Tenecteplase binds to fibrin rich clots via the fibronectin finger-like domain and the Kringle 2 domain. The protease domain then cleaves the Arg/Val bond in plasminogen to form plasmin. Plasmin in turn degrades the fibrin matrix of the thrombus, thereby exerting its thrombolytic action. | NA | NA | NA | NA | 99 - 119 mL/min [acute myocardial infarction patients] | Agents causing angioedema, Amino Acids, Peptides, and Proteins, Anticoagulants, Biological Factors, Blood and Blood Forming Organs, Blood Proteins, Cardiovascular Agents, Endopeptidases, Enzymes, Enzymes and Coenzymes, Fibrin Modulating Agents, Fibrinolytic Agents, Hematologic Agents, Hydrolases, Peptide Hydrolases, Plasminogen Activators, Proteins, Serine Endopeptidases, Serine Proteases, Tissue Plasminogen Activator | CA2129660 | 28-Jun-2005 | 28-May-2013 | Aprotonin may antagonize the effect of Tenecteplase. Monitor for decreased effects of Tenecteplase. | Plasminogen,Fibrinogen alpha chain,Urokinase plasminogen activator surface receptor,Plasminogen activator inhibitor 1,Plasminogen activator inhibitor 2,Tetranectin,Keratin, type II cytoskeletal 8,Annexin A2,Calreticulin,Calnexin,Prolow-density lipoprotein | TNKase | Genentech Inc, Hoffmann La Roche | Genentech Inc, Hoffmann La Roche | To prevent death from a heart attack (acute myocardial infarction). | NA | Each vial of TNKase nominally contains 52.5 mg Tenecteplase, 0.55 g L-arginine, 0.17 g phosphoric acid, and 4.3 mg polysorbate 20, which includes a 5% overfill. Each vial will deliver 50 mg of Tenecteplase. | Sterile, white to off-white, lyophilized powder | Intravenous Injection | The recommended total dose should not exceed 50 mg and is based upon patient weight. For less than 60 kg of body weight recommended dose is 30 mg of TNKase. Similarly 35 mg for 60-70 kg, 40 mg for 70-80 kg, 45 mg for 80-90 kg and 50 mg for more than 90 kg. | Active internal bleeding, History of cerebrovascular accident | Nausea, vomiting; or fever. | Link | NA | NA |
| 10215 | Th1029 | Menotropins | >Th1029_Menotropins APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 23390.3 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | NA | Menotropins contains follicle stimulating hormone and luteinizing hormone purified from the urine of postmenopausal women. It is used as a fertility medication that is injected either subcutaneously or intramuscularly. It is composed of LH with 2 subunit alpha = 92 residues, beta = 121 residues and FSH with 2 subunits, alpha = 92 residues, beta=111 residues. | For the treatment of female infertility | Menotropins is used to treat female infertility, stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Menotropins bind to the LH/hCG/FSH receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Menotropins is a combination drug which binds to the Follicle stimulating hormone receptor (which results in ovulation in the absence of sufficient endogenous Luteinizing hormone)and it also binds to the LH receptor, thereby stimulating proper hormone release. The drug contains both FSH and LH,therefore, it induces ovarian follicular growth and development as well as gonadal steroid production in women who do not have ovarian failure.FSH is the primary driver of follicular recruitment and growth in early folliculogenesis, while LH is important for ovarian steroidogenesis and is involved in the physiological events leading to development of a competent pre-ovulatory follicle. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Products, Complex Mixtures, Fertility Agents, Fertility Agents, Female, Genito Urinary System and Sex Hormones, Gonadotropins, Gonadotropins and Antigonadotropins, Gonadotropins, Pituitary, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Peptides, Pituitary Hormones, Pituitary Hormones, Anterior, Reproductive Control Agents, Sex Hormones and Modulators of the Genital System | NA | NA | NA | Antagon (ganirelix) | Follicle-stimulating hormone receptor,Lutropin-choriogonadotropic hormone receptor | Menopur | Ferring Pharmaceuticals | Ferring Pharmaceuticals | Menotropins are used to stimulate ovulation (the release of an egg) when a woman's ovaries can produce a follicle but hormonal stimulation is deficient. Menotropins are also used to stimulate the development of multiple eggs for in vitro fertilization. Li | NA | Each vial of MENOPUR contains 75 International Units of follicle-stimulating hormone (FSH) activity and 75 International Units of luteinizing hormone (LH) activity, plus 21 mg lactose monohydrate and 0.005 mg Polysorbate 20 and Sodium Phosphate Buffer (So | Sterile, lyophilized powder which is reconstitution with Sterile 0.9% Sodium Chloride Injection. | Subcutaneous Injection | The dosing scheme for patients undergoing IVF follows a stepwise approach and is individualized for each woman. The recommended initial dose of MENOPUR for women who have received a GnRH agonist for pituitary suppression is 225 International Units. MENOPU | Hypersensitivity, high level of FSH indicating primary ovarian failure, cause fetal harm when administerd to prergnant woman, ex hormone dependent tumors of the reproductive tract and accessory organs. | Less than 2% of female patients treated with menotropins develop ovarian hyperstimulation syndrome (OHSS), especially after the first cycle of therapy. Symptoms of OHSS include swelling of the hands or legs, abdominal pain and swelling, shortness of breathing. | Link | NA | NA |
| 10234 | Th1032 | Coagulation factor VIIa | >Th1032_Coagulation_factor_VIIa ANAFLEELRPGSLERECKEEQCSFEEAREIFKDAERTKLFWISYSDGDQCASSPCQNGGSCKDQLQSYICFCLPAFEGRNCETHKDDQLICVNENGGCEQYCSDHTGTKRSCRCHEGYSLLADGVSCTPTVEYPCGKIPILEKRNASKPQGRIVGGKVCPKGECPWQVLLLVNGAQLCGGTLINTIWVVSAAHCFDKIKNWRNLIAVLGEHDLSEHDGDEQSRRVAQVIIPSTYVPGTTNHDIALLRLHQPVVLTDHVVPLCLPERTFSERTLAFVRFSLVSGWGQLLDRGATALELMVLNVPRLMTQDCLQQSRKVGDSPNITEYMFCAGYSDGSKDSCKGDSGGPHATHYRGTWYLTGIVSWGQGCATVGHFGVYTRVSQYIEWLQKLMRSEPRPGVLLRAPFP | 45079.1 | C1972H3076N560O597S28 | 6.09 | -0.311 | 58 | NA | Recombinant human coagulation Factor VIIa is intended for promoting hemostasis by activating the extrinsic pathway of the coagulation cascade. NovoSeven is a vitamin K-dependent glycoprotein consisting of 406 amino acid residues, cloned and expressed in hamster kidney cells, the protein is catalytically active in a two-chain form. | For treatment of hemorrhagic complications in hemophilia A and B. | To treat bleeding episodes in hemophilia A or B. NovoSeven is recombinant Factor VIIa and when complexed with tissue factor can activate coagulation Factor X to Factor Xa, as well as coagulation Factor IX to Factor IXa. Factor Xa, in complex with other factors, then converts prothrombin to thrombin, which leads to the formation of a hemostatic plug by converting fibrinogen to fibrin and thereby inducing local clotting. | NovoSeven activates the coagulation or clotting cascade by cleaving Factor IX and Factor X, which activates them and then leads to activation of thrombin and fibrin. | NA | NA | NA | 121 ± 30 mL/kg [adults] | 33 - 37 mL/h x kg [healthy] | Amino Acids, Peptides, and Proteins, Biological Factors, Blood and Blood Forming Organs, Blood Coagulation Factors, Blood Proteins, Endopeptidases, Enzymes, Enzymes and Coenzymes, Factor VII, Factor VIIa, antagonists & inhibitors, Hemostatics, Hydrolases, Increased Coagulation Factor IX Activity, Increased Coagulation Factor X Activity, Peptide Hydrolases, Proteins, Serine Endopeptidases, Serine Proteases | NA | NA | NA | Autoplex T (anti-inhibitor coagulant complex) | Coagulation factor X,Serine protease hepsin,Tissue factor pathway inhibitor,Vitamin K-dependent gamma-carboxylase,Coagulation factor VII,Tissue factor | NovoSeven | Novo Nordisk | Novo Nordisk | For treatment and prevention of bleeding in surgeries and procedures in adults and children with hemophilia A or B with inhibitors, congenital Factor VII (FVII) deficiency, and people with Glanzmann’s thrombasthenia who have a decreased or absent response | NA | Each vial contains approximately 0. 6 mg/mL NovoSeven (coagulation factor viia recombinant) (corresponding to 600 _g/mL). The reconstituted vials have a pH of approximately 5. 5 in sodium chloride (3 mg/mL), calcium chloride dihydrate (1. 5 mg/mL), glycyl | Sterile, white lyophilized powder | Injection | For bleeding episodes, the recommended dose of NovoSeven (coagulation factor viia (recombinant)) for hemophilia A or B patients with inhibitors is 90 _g/kg given every two hours by bolus infusion until hemostasis is achieved, or until thehemostasis has been acheived. | Hypersensitivity | Rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue; bleeding at the injection site; bloody stools; calf or stomach pain, tenderness, or swelling; chest pain; confusion; dizziness; fainting; numbness. | Link | NA | NA |
| 10235 | Th1032 | Coagulation factor VIIa | >Th1032_Coagulation_factor_VIIa ANAFLEELRPGSLERECKEEQCSFEEAREIFKDAERTKLFWISYSDGDQCASSPCQNGGSCKDQLQSYICFCLPAFEGRNCETHKDDQLICVNENGGCEQYCSDHTGTKRSCRCHEGYSLLADGVSCTPTVEYPCGKIPILEKRNASKPQGRIVGGKVCPKGECPWQVLLLVNGAQLCGGTLINTIWVVSAAHCFDKIKNWRNLIAVLGEHDLSEHDGDEQSRRVAQVIIPSTYVPGTTNHDIALLRLHQPVVLTDHVVPLCLPERTFSERTLAFVRFSLVSGWGQLLDRGATALELMVLNVPRLMTQDCLQQSRKVGDSPNITEYMFCAGYSDGSKDSCKGDSGGPHATHYRGTWYLTGIVSWGQGCATVGHFGVYTRVSQYIEWLQKLMRSEPRPGVLLRAPFP | 45079.1 | C1972H3076N560O597S28 | 6.09 | -0.311 | 58 | NA | Recombinant human coagulation Factor VIIa is intended for promoting hemostasis by activating the extrinsic pathway of the coagulation cascade. NovoSeven is a vitamin K-dependent glycoprotein consisting of 406 amino acid residues, cloned and expressed in hamster kidney cells, the protein is catalytically active in a two-chain form. | For treatment of hemorrhagic complications in hemophilia A and B. | To treat bleeding episodes in hemophilia A or B. NovoSeven is recombinant Factor VIIa and when complexed with tissue factor can activate coagulation Factor X to Factor Xa, as well as coagulation Factor IX to Factor IXa. Factor Xa, in complex with other factors, then converts prothrombin to thrombin, which leads to the formation of a hemostatic plug by converting fibrinogen to fibrin and thereby inducing local clotting. | NovoSeven activates the coagulation or clotting cascade by cleaving Factor IX and Factor X, which activates them and then leads to activation of thrombin and fibrin. | NA | NA | NA | 153 ± 29 mL/kg [children] | 1375 ± 396 mL/hr [severe hemophilia A male children] | Amino Acids, Peptides, and Proteins, Biological Factors, Blood and Blood Forming Organs, Blood Coagulation Factors, Blood Proteins, Endopeptidases, Enzymes, Enzymes and Coenzymes, Factor VII, Factor VIIa, antagonists & inhibitors, Hemostatics, Hydrolases, Increased Coagulation Factor IX Activity, Increased Coagulation Factor X Activity, Peptide Hydrolases, Proteins, Serine Endopeptidases, Serine Proteases | NA | NA | NA | Bebulin VH (factor ix complex) | NA | Sevenfact | Laboratoire Français du Fractionnement et des Biotechnologies Société Anonyme (LFB S.A.) | Laboratoire Français du Fractionnement et des Biotechnologies Société Anonyme (LFB S.A.) | treatment and control of bleeding episodes occurring in adults and adolescents (12 years of age and older) with hemophilia A or B with inhibitors. | NA | SEVENFACT is formulated with arginine, isoleucine, citrate, glycine, lysine and polysorbate 80. It does not contain any antimicrobial preservatives nor human or bovine plasma-derived proteins. | sterile, white to off-white lyophilized powder | intravenous | For mild bleeding: 75 mcg/kg repeated every 3 hours until hemostasis is achieved or Initial dose of 225 mcg/kg. If hemostasis is not achieved within 9 hours, additional 75 mcg/kg doses may be administered every 3 hours as needed to achieve hemostasis For severe Bleeding: 225 mcg/kg initially, followed if necessary 6 hours later with 75 mcg/kg every 2 hours until hemostasis is achieved. | SEVENFACT is contraindicated in known allergy to rabbits or rabbit proteins. Exposure to SEVENFACT in these patients can result in severe hypersensitivity reaction. patients with severe hypersensitivity reaction to SEVENFACT or any of its components. Exposure to SEVENFACT in these patients can result in severe hypersensitivity reaction. | headache, dizziness, infusion-site discomfort, infusion-site bleeding, infusion-related reactions, and fever | Link | NA | NA |
| 10242 | Th1033 | Oprelvekin | >Th1033_Oprelvekin GPPPGPPRVSPDPRAELDSTVLLTRSLLADTRQLAAQLRDKFPADGDHNLDSLPTLAMSAGALGALQLPGVLTRLRADLLSYLRHVQWLRRAGGSSLKTLEPELGTLQARLDRLLRRLQLLMSRLALPQPPPDPPAPPLAPPSSAWGGIRAAHAILGGLHLTLDWAVRGLLLLKTRL | 19047.2 | C854H1411N253O235S2 | 11.16 | -0.07 | NA | 6.9 ± 1.7 hours | Oprelvekin, the active ingredient in Neumega is recombinant Interleukin eleven, which is produced in Escherichia coli by recombinant DNA technology. The protein has a molecular mass of approximately 19,000 daltons, and is non-glycosylated. The polypeptide is 177 amino acids in length (the natural IL-11 has 178). This alteration has not resulted in measurable differences in bioactivity either in vitro or in vivo. The primary hematopoietic activity of Neumega is stimulation of megakaryocytopoiesis and thrombopoiesis. In mice and nonhuman primate studies Neumega has shown potent thrombopoietic activity in compromised hematopoiesis, including moderately to severely myelosuppressed animals. In these studies, Neumega improved platelet nadirs and accelerated platelet recoveries compared to controls. In animal studies Oprelvekin also has non-hematopoetic activities. This includes the regulation of intestinal epithelium growth (enhanced healing of gastrointestinal lesions), the inhibition of adipogenesis, the induction of acute phase protein synthesis (e.g., fibrinogen), and inhibition of macrophageal released pro-inflammatory cytokines. | Increases reduced platelet levels due to chemotherapy. | Oprelvekin is indicated for the prevention of severe thrombocytopenia and the reduction of the need for platelet transfusions following myelosuppressive chemotherapy in adult patients with nonmyeloid malignancies who are at high risk of severe thrombocytopenia. The primary hematopoietic activity of Oprelvekin is stimulation of megakaryocytopoiesis and thrombopoiesis. Oprelvekin has shown potent thrombopoietic activity in individuals with compromised hematopoiesis | Oprelvekin binds to the interleukin 11 receptor which leads to a cascade of signal transduction events. IL-11 is a thrombopoietic growth factor that directly stimulates the proliferation of hematopoietic stem cells and megakaryocyte progenitor cells and induces megakaryocyte maturation resulting in increased platelet production. | NA | NA | Absolute bioavailability is over 80%. | NA | NA | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Cytokines, Intercellular Signaling Peptides and Proteins, Interleukins, Megakaryocyte Growth Factor, Peptides, Proteins | NA | NA | NA | Dihydrocodeine may increase the serum levels of opioid analgesics. It is recommended to monitor therapy for the signs and symptoms of respiratory depression and enhanced sedation. | Interleukin-11 receptor subunit alpha | Neumega | Wyeth Pharmaceuticals | Wyeth Pharmaceuticals | Prevention of severe reductions in the number of blood clotting cells (platelets) caused by some chemotherapy | NA | Neumega is formulated in single-use vials containing 5 mg of oprelvekin (specific activity approximately 8 x 106 Units/mg) as a sterile, lyophilized powder with 23 mg Glycine, USP, 1.6 mg Dibasic Sodium Phosphate Heptahydrate, USP, and 0.55 mg Monobasic S | Sterile, lyophilized powder | It must be Subcutaneous Injection not in the muSub | The recommended dose of Neumega in adults with severe renal impairment(creatinine clearance<30 mL/min) is 25 µg/kg. An estimate of the patient's creatinine clearance(CLcr) in mL/min is required. CLcr in mL/min may be estimated from a spot serum creatinine determination. | In patients with a history of hypersensitivity to Neumega or any component of the product. | Chills; constipation; cough; diarrhea; dizziness; fever; flushing; hair loss; headache; increased cough; indigestion; inflammation or sores of the mouth or lips; joint pain; loss of appetite; mild swelling of the arms and legs; muscle pain; nausea; nervousness. | Link | NA | NA |
| 10246 | Th1034 | Palifermin | >Th1034_Palifermin MSYDYMEGGDIRVRRLFCRTQWYLRIDKRGKVKGTQEMKNNYNIMEIRTVAVGIVAIKGVESEFYLAMNKEGKLYAKKECNEDCNFKELILENHYNTYASAKWTHNGGEMFVALNQKGIPVRGKKTKKEQKTAHFLPMAIT | 16192.7 | C721H1142N202O204S9 | 9.47 | -0.65 | NA | 4.5 hours (range: 3.3-5.7 hours) | Palifermin(140 residues) is a recombinant human keratinocyte growth factor (KGF) produced using E. coli. | For treatment of oral mucositis associated with chemotherapy and radiation therapy. | Used in the prevention or treatment of oral mucoscitis (mouth ulcers arising from chemotherapy), Kepivance binds to the human keratinocyte growth factor (KGF) receptor on buccal cell surfaces. Kepivance acts as both a cell growth and survival factor by stimulating epithelial cell proliferation, differentiation, and migration around the tongue and mouth. The KGF receptor is found on many tissues particularly around the tongue, esophagus, salivary gland and other gastro-intestinal tract organs. | Kepivance binds to the human keratinocyte growth factor (KGF) receptor found on buccal cell surfaces. The binding activates a Ras-MapK (Map kinase) signaling pathway which leads to the transcriptional activation of many proteins important for cell growth and survival. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Factors, Detoxifying Agents for Antineoplastic Treatment, Fibroblast Growth Factors, Increased Epithelial Proliferation, Intercellular Signaling Peptides and Proteins, Mucocutaneous Epithelial Cell Growth Factor, Peptides, Proteins | NA | NA | NA | Increases toxicity of bendamustine. Should not be administered within a 24 hour time period of antineoplastic agent administration. | Fibroblast growth factor receptor 2,Neuropilin-1,Fibroblast growth factor receptor 1,Fibroblast growth factor receptor 4,Fibroblast growth factor receptor 3,Basement membrane-specific heparan sulfate proteoglycan core protein | Kepivance | Amgen Inc, BioVitrum AB | Amgen Inc, BioVitrum AB | Kepivance is used to help prevent or heal mouth sores and ulcers in people being treated with chemotherapy and stem cell treatment. It is used in people receiving chemotherapy to treat blood cancers (Hodgkin's disease, multiple myeloma, leukemia). | NA | NA | Sterile, lyophilized powder | Intravenous infusion | The recommended dose of Kepivance is 60 mcg/kg/day, administered as an intravenous bolus injection for 3 consecutive days before and 3 consecutive days after myelotoxic therapy, for a total of 6 doses. | NA | Fever; swelling or redness of your skin; itching or rash; changes in your sense of taste or sense of touch; unusual or unpleasant sensations in your mouth; numbness in or around your mouth; joint pain; or discolored or thickened tongue. | Link | NA | NA |
| 10252 | Th1035 | Glucagon recombinant | >Th1035_Glucagon_recombinant HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | -1.197 | NA | 0.43 hours for an intramuscular dose | Glucagon is a 29 residue peptide hormone, synthesized in a special non- pathogenic laboratory strain of Escherichia coli bacteria that has been genetically altered by the addition of the gene for glucagons. | Used to treat severe hypoglycemia, also used in gastrointestinal imaging. | Used in the treatment of hypoglycemia and in gastric imaging, glucagon increases blood glucose concentration and is used in the treatment of hypoglycemia. Glucagon acts only on liver glycogen, converting it to glucose through the release of insulin. It also relaxes the smooth muscles of the gastrointestinal tract. | Glucagon binds the glucagon receptor(G protein-coupled receptor located in the plasma membrane) which then initiates a dual signaling pathway using both adenylate cyclase activation and increased intracellular calcium. Adenylate cyclase manufactures cAMP (cyclic AMP), which activates protein kinase A (cAMP-dependent protein kinase). This enzyme, in turn, activates phosphorylase kinase, which, in turn, phosphorylates glycogen phosphorylase, converting into the active form called phosphorylase A. Phosphorylase A is the enzyme responsible for the release of glucose-1-phosphate from glycogen polymers. This yields glucose molecules to be released into the blood. Glucagon receptors are found in the liver, kidney, brain and pancreatic islet cells. The glucagon mediated signals lead to an increase in insulin excretion | atients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium. Phentolamine may be given to control blood pressure. Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia. | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma. | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes. A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes | 0.25 L/kg | 13.5 mL/min/kg [Adults with IV 1 mg] | Amino Acids, Peptides, and Proteins, Antihypoglycemic Agent, Decreased GI Motility, Decreased GI Smooth Muscle Tone, Decreased Glycolysis, Gastrointestinal Agents, Gastrointestinal Hormones, Gastrointestinal Motility Inhibitor, Glucagon, antagonists & inhibitors, Glycogenolytic Agents, Glycogenolytic Hormones, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Increased Gluconeogenesis, Increased Glycogenolysis, Pancreatic Hormones, Peptide Hormones, Peptides, Proglucagon, Protein Precursors, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | NA | NA | NA | NA | Glucagon receptor,Glucagon-like peptide 2 receptor,Glucagon-like peptide 1 receptor | GlucaGen | Novo Nordisk, Boehringer Ingelheim Pharmaceuticals, Inc. | Novo Nordisk, Boehringer Ingelheim Pharmaceuticals, Inc. | GlucaGen is used to treat severe hypoglycemic (low blood sugar) reactions which may occur in patients with diabetes mellitus treated with insulin. It is also used as a diagniostic aid. GlucaGen is indicated for use during radiologic examinations to tempor | NA | The reconstituted solution contains glucagon as hydrochloride 1 mg/mL (1 unit/mL) and lactose monohydrate (107 mg). GlucaGen is supplied at pH 2.5-3.5 and is soluble in water. | Sterile, lyophilized white powder | Subcutaneous, intramuSubcutaneousular, or Intraven | Inject 1 mL (adults and children, weighing more than 55 lbs (25 kg)) or 0.5 mL (children weighing less than 55 lbs (25 kg)) subcutaneously, intramuscularly, or intravenously. If the weight is not known: children younger than 6 years should be given a 0.5 | Hypersensitivity | Severe side effects are very rare, although nausea and vomiting may occur occasionally especially with doses above 1 mg or with rapid injection (less than 1 minute). You may also have rapid heart beat for a short while. | Link | NA | NA |
| 10253 | Th1035 | Glucagon recombinant | >Th1035_Glucagon_recombinant HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | -1.197 | NA | 0.58 hours for glucagon nasal powder | 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 | Baqsimi | Eli Lilly and Company | Eli Lilly and Company | very low blood sugar (severe hypoglycemia) in people with diabetes ages 4 years and above. | C153H225N43O49S | Glucagon is a single-chain polypeptide containing 29 amino acid residues and has a molecular weight of 3483, and is identical to human glucagon. | preservative-free, white powder | intranasal administration in an intranasal device | The recommended dose of BAQSIMI is 3 mg administered as one actuation of the intranasal device into one nostril. If there has been no response after 15 minutes, an additional 3 mg dose of BAQSIMI from a new device may be administered while waiting for emergency assistance. | BAQSIMI is contraindicated in patients with: Pheochromocytoma because of the risk of substantial increase in blood pressure Insulinoma because of the risk of hypoglycemia Known hypersensitivity to glucagon or to any of the excipients in BAQSIMI. Allergic reactions have been reported with glucagon and include anaphylactic shock with breathing difficulties and hypotension | nausea vomiting headache runny nose discomfort in your nose stuffy nose redness in your eyes itchy nose, throat and eyes watery eyes | Link | NA | NA |
| 10255 | Th1035 | Glucagon recombinant | >Th1035_Glucagon_recombinant HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | -1.197 | NA | NA | Glucagon is a 29 residue peptide hormone, synthesized in a special non- pathogenic laboratory strain of Escherichia coli bacteria that has been genetically altered by the addition of the gene for glucagons. | Used to treat severe hypoglycemia, also used in gastrointestinal imaging. | Used in the treatment of hypoglycemia and in gastric imaging, glucagon increases blood glucose concentration and is used in the treatment of hypoglycemia. Glucagon acts only on liver glycogen, converting it to glucose through the release of insulin. It also relaxes the smooth muscles of the gastrointestinal tract. | Glucagon binds the glucagon receptor(G protein-coupled receptor located in the plasma membrane) which then initiates a dual signaling pathway using both adenylate cyclase activation and increased intracellular calcium. Adenylate cyclase manufactures cAMP (cyclic AMP), which activates protein kinase A (cAMP-dependent protein kinase). This enzyme, in turn, activates phosphorylase kinase, which, in turn, phosphorylates glycogen phosphorylase, converting into the active form called phosphorylase A. Phosphorylase A is the enzyme responsible for the release of glucose-1-phosphate from glycogen polymers. This yields glucose molecules to be released into the blood. Glucagon receptors are found in the liver, kidney, brain and pancreatic islet cells. The glucagon mediated signals lead to an increase in insulin excretion | atients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium. Phentolamine may be given to control blood pressure. Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia. | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma. | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes. A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes | 0.25 L/kg | 13.5 mL/min/kg [Adults with IV 1 mg] | Amino Acids, Peptides, and Proteins, Antihypoglycemic Agent, Decreased GI Motility, Decreased GI Smooth Muscle Tone, Decreased Glycolysis, Gastrointestinal Agents, Gastrointestinal Hormones, Gastrointestinal Motility Inhibitor, Glucagon, antagonists & inhibitors, Glycogenolytic Agents, Glycogenolytic Hormones, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Increased Gluconeogenesis, Increased Glycogenolysis, Pancreatic Hormones, Peptide Hormones, Peptides, Proglucagon, Protein Precursors, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | NA | NA | NA | Walfarin- Glucagon may increase the anticoagulant effect of warfarin (Coumadin) and other anticoagulants causing an increase in the slow clotting of blood and a greater risk of developing an episode of bleeding. | NA | Glucagon | Eli Lilly, Fresenius Kabi USA, LLC,TYA Pharmaceuticals, A-S Medication Solutions, Physicians Total Care, Inc. | Eli Lilly, Fresenius Kabi USA, LLC,TYA Pharmaceuticals, A-S Medication Solutions, Physicians Total Care, Inc. | Glucagon is used to increase the blood glucose level in severe hypoglycemia (low blood glucose). Glucagon is a glucose-elevating drug | NA | Glucagon is available as an emergency kit. The kit contains freeze-dried glucagon as a powder for injection 1 ml syringe of diluent. The powder contains 1 mg (1 unit) of glucagon and 49 mg of lactose. The diluent contains 12 mg/ml of glycerine, water for | Powder | Subcutaneously or intramuSubcutaneousularly Inject | Adults and children weighing 44 pounds or more should receive 1mg (1 unit) of glucagon | Allergy | Nausea and vomiting may occur occasionally after injection of glucagon, but this may be a symptom of the hypoglycemia for which glucagon is being given. Rare allergic-type reactions may occur with glucagon including itching, respiratory distress, or low blood pressure. | Link | NA | NA |
| 10265 | Th1038 | Omalizumab | >Th1038_Omalizumab EVQLVESGGGLVQPGGSLRLSCAVSGYSITSGYSWNWIRQAPGKGLEWVASITYDGSTNYADSVKGRFTISRDDSKNTFYLQMNSLRAEDTAVYYCARGSHYFGHWHFAVWGQGTLVTVSSGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 149000 | C6450H9916N1714O2023S38 | 6.6 - 7.2 | -0.432 | 61(FAB fra | 624 hours | A recombinant DNA-derived humanized IgG1k monoclonal antibody that selectively binds to human immunoglobulin E. Xolair is produced by a Chinese hamster ovary cell suspension culture in a nutrient medium containing the antibiotic gentamicin. | For treatment of asthma caused by allergies | Xolair inhibits the binding of IgE to the high-affinity IgE receptor (FceRI) on the surface of mast cells and basophils. Reduction in surface-bound IgE on FceRI-bearing cells limits the degree of release of mediators of the allergic response. Xolair is used to treat severe, persisten asthma. | Xolair binds to IgE (a class of antibodies normally secreted in allergic responses), which prevents their binding to mast cells and basophils. | Anaphylaxis may occur rarely with this agent, either after the first dose or multiple doses | Most likely removed by opsonization via the reticuloendothelial system. | bioavailability of 62% | 78 ± 32 mL/kg | Liver elimination of IgG includes degradation in the liver reticuloendothelial system (RES) and endothelial cells. Intact IgG is also excreted in bile. | Agents to Treat Airway Disease, Amino Acids, Peptides, and Proteins, Anti-Allergic Agents, Anti-Asthmatic Agents, Anti-IgE, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Blood Proteins, Decreased IgE Activity, Globulins, IgE-directed Antibody Interactions, Immunoglobulins, Immunoproteins, Proteins, Respiratory Agents, Miscellaneous, Respiratory System Agents, Serum Globulins | CA2113813 | 12-Apr-2005 | 14-Aug-2012 | NA | High affinity immunoglobulin epsilon receptor subunit alpha and beta | Xolair | Genentech Inc, Novartis Europharm Limited | Genentech Inc, Novartis Europharm Limited | Xolair is used to treat moderate to severe asthma that is caused by allergies, and chronic idiopathic urticaria (a form of chronic hives) in adults and children who are at least 12 years old. Xolair is usually given after other asthma medications have bee | NA | Formulated in a single use vial that is reconstituted with sterile water for injection (SWFI), USP, and administered as a subcutaneous (SC) injection. Each 202.5 mg vial of omalizumab also contains L-histidine (1.8 mg), L-histidine hydrochloride monohydra | Sterile, white, preservative free, lyophilized powder | Subcutaneous Injection | Xolair is administered at 150 to 375 mg by subcutaneous injection every 2 or 4 weeks. Determine doses (mg) and dosing frequency by serum total IgE level (IU/mL), measured before the start of treatment, and body weight (kg) as if serum IgE is less than 30-or >700 IU/mL and <66 or >330 lb, respectively) should not be dosed. | Severe hypersensitivity | Wheezing, tightness in your chest, trouble breathing; hives or skin rash; feeling anxious or light-headed, fainting; warmth or tingling under your skin; or swelling of your face, lips, tongue, or throat. | Link | NA | NA |
| 10300 | Th1042 | Collagenase | >Th1042_Collagenase MKRKCLSKRLMLAITMATIFTVNSTLPIYAAVDKNNATAAVQNESKRYTVSYLKTLNYYDLVDLLVKTEIENLPDLFQYSSDAKEFYGNKTRMSFIMDEIGRRAPQYTEIDHKGIPTLVEVVRAGFYLGFHNKELNEINKRSFKERVIPSILAIQKNPNFKLGTEVQDKIVSATGLLAGNETAPPEVVNNFTPILQDCIKNIDRYALDDLKSKALFNVLAAPTYDITEYLRATKEKPENTPWYGKIDGFINELKKLALYGKINDNNSWIIDNGIYHIAPLGKLHSNNKIGIETLTEVMKVYPYLSMQHLQSADQIKRHYDSKDAEGNKIPLDKFKKEGKEKYCPKTYTFDDGKVIIKAGARVEEEKVKRLYWASKEVNSQFFRVYGIDKPLEEGNPDDILTMVIYNSPEEYKLNSVLYGYDTNNGGMYIEPEGTFFTYEREAQESTYTLEELFRHEYTHYLQGRYAVPGQWGRTKLYDNDRLTWYEEGGAELFAGSTRTSGILPRKSIVSNIHNTTRNNRYKLSDTVHSKYGASFEFYNYACMFMDYMYNKDMGILNKLNDLAKNNDVDGYDNYIRDLSSNYALNDKYQDHMQERIDNYENLTVPFVADDYLVRHAYKNPNEIYSEISEVAKLKDAKSEVKKSQYFSTFTLRGSYTGGASKGKLEDQKAMNKFIDDSLKKLDTYSWSGYKTLTAYFTNYKVDSSNRVTYDVVFHGYLPNEGDSKNSLPYGKINGTYKGTEKEKIKFSSEGSFDPDGKIVSYEWDFGDGNKSNEENPEHSYDKVGTYTVKLKVTDDKGESSVSTTTAEIKDLSENKLPVIYMHVPKSGALNQKVVFYGKGTYDPDGSIAGYQWDFGDGSDFSSEQNPSHVYTKKGEYTVTLRVMDSSGQMSEKTMKIKITDPVYPIGTEKEPNNSKETASGPIVPGIPVSGTIENTSDQDYFYFDVITPGEVKIDINKLGYGGATWVVYDENNNAVSYATDDGQNLSGKFKADKPGRYYIHLYMFNGSYMPYRINIEGSVGR | 112023.2 | C5028H7666N1300O1564S21 | 5.58 | -0.714 | 49-54 | NA | This enzyme is derived from fermentation of Clostridium histolyticum | It promotes debridement of necrotic tissue and helps in the treatment of severe burns and dermal ulcers including decubitus ulcers. | Helps in the treatment of skin ulcers and severe burns, collagenase is able to digest collagen in necrotic tissue at physiological pH by hydrolyzing the peptide bonds of undenatured and denatured collagen. Collagenase thus contributes towards the formation of granulation tissue and subsequent epithelization of dermal ulcers and severely burned areas. The action of collagenase may remove substrates necessary for bacterial proliferation or may permit antibodies, leukocytes, and antibiotics better access to the infected area. | Collagenase is a protease that is specific to collagen. The triple helical region of interstitial collagens is highly resistant to most cell proteinases. However, during remodeling of the connective tissue in such processes as wound healing and metastasis, collagen becomes susceptible to cleavage by collagenases. Collagenase cleaves all 3 alpha helical chains of native Types I, II and III collagens at a single locus by hydrolyzing the peptide bond following the Gly residue of the sequence: Gly 775-(Ile or Leu) 776-(Ala or Leu) 777 located approximately three-fourths of the chain length from each N-terminus. | NA | NA | NA | NA | NA | Collagen-specific Enzyme, Collagenases, Dermatologicals, Endopeptidases, Enzymes, Enzymes and Coenzymes, Hydrolases, Metalloendopeptidases, Metalloproteases, Microbial Collagenase, antagonists & inhibitors, Misc. Skin and Mucous Membrane Agents, Musculo-Skeletal System, Peptide Hydrolases, Preparations for Treatment of Wounds and Ulcers | NA | NA | NA | silver nitrate topical | NA | Qwo | Endo Aesthetics LLC | Endo Aesthetics LLC | used for the treatment of moderate to severe cellulite in the buttocks of adult women. | NA | Each QWO 0.92-mg single-dose vial contains 0.92 mg of collagenase clostridium histolyticumaaes and mannitol (37.7 mg), sucrose (18.9 mg), tromethamine (1.1 mg), and hydrochloric acid as needed to adjust pH. Reconstitution with 4 mL of supplied Diluent for QWO yields a solution containing 0.23 mg/mL collagenase clostridium histolyticum-aaes at a pH of approximately 8.0. Each QWO 1.84-mg single-dose vial contains 1.84 mg of collagenase clostridium histolyticumaaes and mannitol (75.4 mg), sucrose (37.8 mg), tromethamine (2.2 mg), and hydrochloric acid as needed to adjust pH. Reconstitution with 8 mL of supplied Diluent for QWO yields a solution containing 0.23 mg/mL collagenase clostridium histolyticum-aaes at a pH of approximately 8.0. | sterile, preservative-free, lyophilized powder (appearing as a white cake) | injected subcutaneously | A treatment area is defined as a single buttock receiving up to 12 injections, 0.3 mL each (up to a total of 3.6 mL), of QWO. A treatment visit may consist of up to 2 treatment areas. Treatment should be repeated every 21 days for 3 treatment visits. | QWO is contraindicated in: patients with a history of hypersensitivity to collagenase or to any of the excipients. the presence of infection at the injection sites. | hives swollen face trouble breathing chest pain low blood pressure dizziness or fainting | NA | NA | NA |
| 10302 | Th1042 | Collagenase | >Th1042_Collagenase MKRKCLSKRLMLAITMATIFTVNSTLPIYAAVDKNNATAAVQNESKRYTVSYLKTLNYYDLVDLLVKTEIENLPDLFQYSSDAKEFYGNKTRMSFIMDEIGRRAPQYTEIDHKGIPTLVEVVRAGFYLGFHNKELNEINKRSFKERVIPSILAIQKNPNFKLGTEVQDKIVSATGLLAGNETAPPEVVNNFTPILQDCIKNIDRYALDDLKSKALFNVLAAPTYDITEYLRATKEKPENTPWYGKIDGFINELKKLALYGKINDNNSWIIDNGIYHIAPLGKLHSNNKIGIETLTEVMKVYPYLSMQHLQSADQIKRHYDSKDAEGNKIPLDKFKKEGKEKYCPKTYTFDDGKVIIKAGARVEEEKVKRLYWASKEVNSQFFRVYGIDKPLEEGNPDDILTMVIYNSPEEYKLNSVLYGYDTNNGGMYIEPEGTFFTYEREAQESTYTLEELFRHEYTHYLQGRYAVPGQWGRTKLYDNDRLTWYEEGGAELFAGSTRTSGILPRKSIVSNIHNTTRNNRYKLSDTVHSKYGASFEFYNYACMFMDYMYNKDMGILNKLNDLAKNNDVDGYDNYIRDLSSNYALNDKYQDHMQERIDNYENLTVPFVADDYLVRHAYKNPNEIYSEISEVAKLKDAKSEVKKSQYFSTFTLRGSYTGGASKGKLEDQKAMNKFIDDSLKKLDTYSWSGYKTLTAYFTNYKVDSSNRVTYDVVFHGYLPNEGDSKNSLPYGKINGTYKGTEKEKIKFSSEGSFDPDGKIVSYEWDFGDGNKSNEENPEHSYDKVGTYTVKLKVTDDKGESSVSTTTAEIKDLSENKLPVIYMHVPKSGALNQKVVFYGKGTYDPDGSIAGYQWDFGDGSDFSSEQNPSHVYTKKGEYTVTLRVMDSSGQMSEKTMKIKITDPVYPIGTEKEPNNSKETASGPIVPGIPVSGTIENTSDQDYFYFDVITPGEVKIDINKLGYGGATWVVYDENNNAVSYATDDGQNLSGKFKADKPGRYYIHLYMFNGSYMPYRINIEGSVGR | 112023.2 | C5028H7666N1300O1564S21 | 5.58 | -0.714 | 49-54 | NA | This enzyme is derived from fermentation of Clostridium histolyticum | It promotes debridement of necrotic tissue and helps in the treatment of severe burns and dermal ulcers including decubitus ulcers. | Helps in the treatment of skin ulcers and severe burns, collagenase is able to digest collagen in necrotic tissue at physiological pH by hydrolyzing the peptide bonds of undenatured and denatured collagen. Collagenase thus contributes towards the formation of granulation tissue and subsequent epithelization of dermal ulcers and severely burned areas. The action of collagenase may remove substrates necessary for bacterial proliferation or may permit antibodies, leukocytes, and antibiotics better access to the infected area. | Collagenase is a protease that is specific to collagen. The triple helical region of interstitial collagens is highly resistant to most cell proteinases. However, during remodeling of the connective tissue in such processes as wound healing and metastasis, collagen becomes susceptible to cleavage by collagenases. Collagenase cleaves all 3 alpha helical chains of native Types I, II and III collagens at a single locus by hydrolyzing the peptide bond following the Gly residue of the sequence: Gly 775-(Ile or Leu) 776-(Ala or Leu) 777 located approximately three-fourths of the chain length from each N-terminus. | NA | NA | NA | NA | NA | Collagen-specific Enzyme, Collagenases, Dermatologicals, Endopeptidases, Enzymes, Enzymes and Coenzymes, Hydrolases, Metalloendopeptidases, Metalloproteases, Microbial Collagenase, antagonists & inhibitors, Misc. Skin and Mucous Membrane Agents, Musculo-Skeletal System, Peptide Hydrolases, Preparations for Treatment of Wounds and Ulcers | NA | NA | NA | NA | NA | Xiaflex | Auxilium, Endo Pharmaceuticals Inc., Swedish Orphan Biovitrum Ab | Auxilium, Endo Pharmaceuticals Inc., Swedish Orphan Biovitrum Ab | XIAFLEX is indicated for the treatment of adult patients with Dupuytren's contracture with a palpable cord. XIAFLEX is also indicated for the treatment of adult men with Peyronie's disease with a palpable plaque and curvature deformity of at least 30 degr | NA | XIAFLEX is available in single-use, glass vials containing 0.9 mg of collagenase clostridium histolyticum. Each vial also contains 0.5 mg of hydrochloric acid, 18.5 mg of sucrose, and 1.1 mg of tromethamine. | Sterile lyophilized powder (white cake) and must be reconstituted with the provided diluent prior to use. | Intralesional Injection | The dose of XIAFLEX is 0.58 mg per injection into a palpable cord with a contracture of a metacarpophalangeal (MP) joint or a proximal interphalangeal (PIP) joint | The treatment of Peyronie's plaques that involve the penile urethra due to potential risk to this structure. | Swelling, bruising, or bleeding where the medicine was injected; mild pain or tenderness in the treated hand; swollen glands in your elbow or underarm; itching, redness, or warmth of the skin; cracked skin; or underarm pain. | Link | NA | NA |
| 10305 | 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 | 110 to 127 mL/kg [pediatric patients] | 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 | CA2175971 | 30-Dec-2003 | 7-May-2016 | amyl nitrite / sodium nitrite / sodium thiosulfate | Uric acid | Elitek | Sanofi-Synthelabo Inc | Sanofi-Synthelabo Inc | Used for preventing high blood levels of uric acid from occurring in patients with certain types of cancer (eg, leukemia, lymphoma, solid malignant tumors) who are receiving cancer chemotherapy treatment. | NA | Elitek is supplied in 3 mL and 10 mL colorless, glass vials containing rasburicase at a concentration of 1.5 mg/mL after reconstitution. Elitek 1.5 mg presentation contains 1.5 mg rasburicase, 10.6 mg mannitol, 15.9 mg L-alanine, between 12.6 and 14.3 mg | Sterile, white to off-white, lyophilized powder | Intravenous administration | The recommended dose of Elitek is 0.2 mg/kg as a 30 minute Intravenous infusion daily for up to 5 days. Dosing beyond 5 days or administration of more than one course is not recommended. | Pateints with history of anaphylaxic or severe 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 |
| 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 |
| 10331 | Th1047 | Alpha-1-proteinase inhibitor | >Th1047_Alpha-1-proteinase_inhibitor EDPQGDAAQKTDTSHHDQDHPTFNKITPNLAEFAFSLYRQLAHQSNSTNIFFSPVSIATAFAMLSLGTKADTHDEILEGLNFNLTEIPEAQIHEGFQELLRTLNQPDSQLQLTTGNGLFLSEGLKLVDKFLEDVKKLYHSEAFTVNFGDTEEAKKQINDYVEKGTQGKIVDLVKELDRDTVFALVNYIFFKGKWERPFEVKDTEEEDFHVDQVTTVKVPMMKRLGMFNIQHCKKLSSWVLLMKYLGNATAIFFLPDEGKLQHLENELTHDIITKFLENEDRRSASLHLPKLSITGTYDLKSVLGQLGITKVFSNGADLSGVTEEAPLKLSKAVHKAVLTIDEKGTEAAGAMFLEAIPMSIPPEVKFNKPFVFLMIEQNTKSPLFMGKVVNPTQK | 44324.5 | C2001H3130N514O601S10 | 5.37 | -0.302 | 59 | NA | Human alpha-1 proteinase inhibitor or alpha-1-antitrypsin, prepared from human plasma via Cohn alcohol fractionation followed by PEG and zinc chloride fractionation. | For treatment of panacinar emphysema. | Prevents excessive accumulation of active neutrophil elastase and consequent proteolysis of elastin tissues in alveolar lung structures. This prevents the development of emphysema. | Alpha-1 proteinase inhibitor is a serine protease inhibitor (Serpin). Its primary mechanism is inhibiting the action of the serine protease called elastase (also plasmin and thrombin) in the lungs. The reactive center loop (RCL) of alpha-1 proteinase inhibitor extends out from the body of the protein and directs binding to the target protease. The protease cleaves the serpin at the reactive site, establishing a covalent linkage between the carboxyl group of the serpin reactive site and the serine hydroxyl of the protease. The resulting inactive serpin-protease complex is highly stable. | NA | NA | NA | 5632 ± 2006 mL [ARALAST NP] | 940 ± 275 mL/day [Patients with congenital deficiency with single IV infusion of 60mg/kg] | Acute-Phase Proteins, Alpha-Globulins, Amino Acids, Peptides, and Proteins, Antifibrinolytic Agents, Blood and Blood Forming Organs, Blood Proteins, Enzyme Inhibitors, Enzymes, Enzymes and Coenzymes, Globulins, Glycoproteins, Hemostatics, Human alpha-1 Proteinase Inhibitor, Peptides, Protease Inhibitors, Proteinase Inhibitors, Proteins, Serine Protease Inhibitors, Serpins, Serum Globulins, Trypsin Inhibitors | NA | NA | NA | NA | Neutrophil elastase | Aralast | Baxter | Baxter | Its used to treat lung problems (emphysema) caused by a certain inherited disease (alpha-1-proteinase inhibitor deficiency). In people with this condition, lung damage is caused by elastase, a natural substance that the body needs to kill bacteria in the | NA | ARALAST NP is available as a lyophilized powder in single dose vials containing 0.5 gram or 1 gram of functional Alpha 1 -Protenase inhibitor | Lyophilized powder | Intravenous infusion | Recommended dose is 60 mg/kg of body weight, administered once in a week. | ARALAST NP is contraindicated in immunoglobulin A deficient patients with antibodies against IgA, due to the risk of severe hypersensitivity. | Fever, chills, body aches, flu symptoms, sores in your mouth and throat; pain or burning when you urinate; wheezing, chest pain or tightness, trouble breathing; or vision changes. | Link | NA | NA |
| 10334 | Th1047 | Alpha-1-proteinase inhibitor | >Th1047_Alpha-1-proteinase_inhibitor EDPQGDAAQKTDTSHHDQDHPTFNKITPNLAEFAFSLYRQLAHQSNSTNIFFSPVSIATAFAMLSLGTKADTHDEILEGLNFNLTEIPEAQIHEGFQELLRTLNQPDSQLQLTTGNGLFLSEGLKLVDKFLEDVKKLYHSEAFTVNFGDTEEAKKQINDYVEKGTQGKIVDLVKELDRDTVFALVNYIFFKGKWERPFEVKDTEEEDFHVDQVTTVKVPMMKRLGMFNIQHCKKLSSWVLLMKYLGNATAIFFLPDEGKLQHLENELTHDIITKFLENEDRRSASLHLPKLSITGTYDLKSVLGQLGITKVFSNGADLSGVTEEAPLKLSKAVHKAVLTIDEKGTEAAGAMFLEAIPMSIPPEVKFNKPFVFLMIEQNTKSPLFMGKVVNPTQK | 44324.5 | C2001H3130N514O601S10 | 5.37 | -0.302 | 59 | NA | Human alpha-1 proteinase inhibitor or alpha-1-antitrypsin, prepared from human plasma via Cohn alcohol fractionation followed by PEG and zinc chloride fractionation. | For treatment of panacinar emphysema. | Prevents excessive accumulation of active neutrophil elastase and consequent proteolysis of elastin tissues in alveolar lung structures. This prevents the development of emphysema. | Alpha-1 proteinase inhibitor is a serine protease inhibitor (Serpin). Its primary mechanism is inhibiting the action of the serine protease called elastase (also plasmin and thrombin) in the lungs. The reactive center loop (RCL) of alpha-1 proteinase inhibitor extends out from the body of the protein and directs binding to the target protease. The protease cleaves the serpin at the reactive site, establishing a covalent linkage between the carboxyl group of the serpin reactive site and the serine hydroxyl of the protease. The resulting inactive serpin-protease complex is highly stable. | NA | NA | NA | NA | 940 ± 275 mL/day [Patients with congenital deficiency with single IV infusion of 60mg/kg] | Acute-Phase Proteins, Alpha-Globulins, Amino Acids, Peptides, and Proteins, Antifibrinolytic Agents, Blood and Blood Forming Organs, Blood Proteins, Enzyme Inhibitors, Enzymes, Enzymes and Coenzymes, Globulins, Glycoproteins, Hemostatics, Human alpha-1 Proteinase Inhibitor, Peptides, Protease Inhibitors, Proteinase Inhibitors, Proteins, Serine Protease Inhibitors, Serpins, Serum Globulins, Trypsin Inhibitors | NA | NA | NA | NA | NA | Prolastin | Talecris Biotherapeutics C formerly Bayer | Talecris Biotherapeutics C formerly Bayer | It is used to treat alpha 1-antitrypsin deficiency in people who have symptoms of emphysema. | NA | The specific activity of Prolastin is _ 0.35 mg functional alpha1-PI/mg protein and when reconstituted as directed, the concentration of alpha1-PI is _ 20 mg/mL. When reconstituted, Prolastin (alpha) has a pH of 6.6_7.4, a sodium content of 100_210 mEq/L, | Lyophilized powder | Intravenous infusion | Prolastin (alpha) may be given at a rate of 0.08 mL/kg/min or greater and must be administered intravenously. The recommended dosage of 60 mg/kg takes approximately 30 minutes to infuse. | Individuals with selective IgA deficiencies who have known antibody against IgA (anti-IgA antibody) should not receive Alpha1-Proteinase Inhibitor (Human), Prolastin (alpha) , since these patients may experience severe reactions, including anaphylaxis, to IgA which may be present. | Fever, chills, body aches, flu symptoms, sores in your mouth and throat; pain or burning when you urinate; wheezing, chest pain or tightness, trouble breathing; or vision changes. | Link | NA | NA |
| 10341 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | CA1341604 | 4-May-2010 | 4-May-2027 | NA | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | Avonex | Biogen Inc | Biogen Inc | Avonex is used to treat relapsing multiple sclerosis (MS). This medication will not cure MS, it will only decrease the frequency of relapse symptoms. | NA | AVONEX is avalible as powder vial, Single used prefillled syringe, single used prefilled autoinjector. Each vial of reconstituted AVONEX contains 30 micrograms of interferon beta-1a; 15 mg Albumin (Human), USP; 5.8 mg Sodium Chloride, USP; 5.7 mg Dibasic | Lyophilized powder vial, Sterile liquid as single used prefilled syringe and also available as single use prefilled autoinjector. | IntramuSubcutaneousular Injection | The recommended dose is 30 micrograms once a week. To reduce the incidence and severity of flu-like symptoms that may occur when initiating AVONEX therapy at a dose of 30 micrograms, AVONEX may be started at a dose of 7.5 micrograms and the dose may beincreased by 7.5 micrograms each week for the next three weeks until the recommended dose of 30 micrograms is achieved. | Hypersensitivity | Stomach pain; headache, drowsiness; or minor irritation where the injection was given. | Link | NA | NA |
| 10344 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | Betaferon | Bayer | Bayer | Betaferon is indicated for the treatment of patients with a single demyelinating event with an active inflammatory process, if it is severe enough to warrant treatment with intravenous corticosteroids, if alternative diagnoses have been excluded, and if t | NA | NA | Powder and solvent that are made upto make solution. | Subcutaneous Injection | NA | People with severe depression or thoughts of suicide. People with severe liver disease. Pregnancy. Breastfeeding. | Flu-like symptoms such as fever,chills, painful joints, malaise, sweating, headache or muscular pain. These symptoms may be reduced by taking paracetamol or steroidal anti-inflammatory medicines such as ibuprofen. | Link | NA | NA |
| 10347 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | Betaseron | Merck | Merck | Betaseron is used to treat relapsing multiple sclerosis (MS). Betaseron will not cure MS, it will only decrease the frequency of relapse symptoms. | NA | Lyophilized Betaseron is a sterile, white to off-white powder, for subcutaneous injection after reconstitution with the diluent supplied (Sodium Chloride, 0.54% Solution). Albumin (Human) USP and Mannitol, USP (15 mg each/vial) are added as stabilizers. | Sterile, white to off-white powder | Subcutaneous Injection | The recommended starting dose is 0.0625 mg (0.25 mL) subcutaneously every other day, with dose increases over a six week period to the recommended dose of 0.25 mg (1 mL) every other day | Betaseron is contraindicated in patients with a history of hypersensitivity to natural or recombinant interferon beta, Albumin (Human). | Depressed mood, anxiety, trouble sleeping, restlessness, or thoughts of suicide or hurting yourself; bruising, swelling, oozing, or skin changes where the injection was given; weight changes, pounding heartbeats, feeling too hot or cold; fever, chills, bo | Link | NA | NA |
| 10351 | Th1049 | Interferon beta-1a | >Th1049_Interferon_beta-1a MSYNLLGFLQRSSNFQCQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20027 | C908H1408N246O252S7 | 8.93 | -0.427 | NA | 10 hours | Human interferon beta (166 residues, glycosylated, MW=22.5kD) is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence of Avonex is identical to that of natural human interferon beta. | For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | NA | 33-55 L/hour [Healthy SC injection of 60 mcg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Anti-Infective Agents, Antineoplastic and Immunomodulating Agents, Antiviral Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | Extavia | Novartis | Novartis | Extavia is used to treat relapsing multiple sclerosis (MS). This medication will not cure MS, it will only decrease the frequency of relapse symptoms. | NA | Each vial contains 0.3 mg of interferon beta-1b. The unit measurement is derived by comparing the antiviral activity of the product to the World Health Organization (WHO) reference standard of recombinant human interferon beta. Mannitol, USP and Albumin ( | Sterile, white to off-white powder | Subcutaneous Injection | The recommended starting dose is 0.0625 mg (0.25 mL) subcutaneously every other day, with dose increases over a six week period to the recommended dose of 0.25 mg (1 mL) every other day. | Extavia is contraindicated in patients with a history of hypersensitivity to natural or recombinant interferon beta, Albumin (Human). | Depressed mood, anxiety, trouble sleeping, restlessness, or thoughts of suicide or hurting yourself; bruising, swelling, oozing, or skin changes where the injection was given; weight changes, pounding heartbeats, feeling too hot or cold; fever, chills, weating, muscle aches and tiredness. | Link | NA | NA |
| 10368 | Th1054 | Infliximab | NA | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | 71 | 9.5 days | Tumor necrosis factor (TNF-alpha) binding antibody (chimeric IgG1). It is composed of human constant and murine variable regions. Infliximab is produced by a recombinant cell line cultured by continuous perfusion. | To manage the signs and symptoms, as well as to induce and maintain clinical remission in adults with moderate to severe active Crohn's disease or ulcerative colitis. Also used to manage signs and symptoms of rheumatoid arthritis (in conjunction with methotrexate), ankylosing spondylitis, psoriatic arthritis, and juvenile arthritis. | Infliximab is a chimeric human-murine anti-human tumor necrosis factor (TNF) monoclonal antibody. It binds to tumor necrosis factor alpha (TNFa) and inhibits binding of TNFa with its receptors. This reduces production of pro-inflammatory cytokines such as interleukins (IL) 1 and 6. This also limits leukocyte migration and expression of adhesion molecules by endothelial cells and leukocytes. Infliximab also limits the activation of neutrophil and eosinophil functional activity, reduces production of tissue degrading enzymes produced by synoviocytes and/or chondrocytes. Infliximab decreases synovitis and joint erosions in collagen-induced arthritis and allows eroded joints to heal. | Infliximab neutralizes the biological activity of TNFa by binding with high affinity to the soluble and transmembrane forms of TNFa and inhibits binding of TNFa with its receptors. Infliximab does not neutralize TNFb (lymphotoxin a), a related cytokine that utilizes the same receptors as TNFa. Neutralization of the biological activity of TNFa leads to an overall reduction in inflammation. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production | NA | NA | In patients with Crohn's disease, the total body clearance (CL) of infliximab following single doses of 5 mg/kg and 10 mg/kg was 18.4 mL/h and 14.3 mL/h, respectively. In a maintenance therapy study, multiple infusions of infliximab (at week 0, 2 and 6) at the same dose of 5 mg/kg and 10 mg/kg resulted in CL of 15.2 mL/h and 15.2 mL/h, respectively. | Agents Causing Muscle Toxicity, Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Dermatologicals, Disease-modifying Antirheumatic Agents, Gastrointestinal Agents, Globulins, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Proteins, Serum Globulins, Tumor Necrosis Factor Blockers, Tumor Necrosis Factor Receptor Blocking Activity | CA2106299 | 6-Feb-2001 | 18-Mar-2012 | Golimumab avoid combination with infliximab due to the potential increased immunosuppression of infliximab | Tumor necrosis factor | REMICADE | Centocor Inc | Centocor Inc | used in crohn disease, Ankylosing pondylitis, Psoriatic Arthritis, Plaque Psoriasis and ulcerative colitis | NA | Each single-use vial contains 100 mg infliximab, 500 mg sucrose, 0.5 mg polysorbate 80, 2.2 mg monobasic sodium phosphate, monohydrate, and 6.1 mg dibasic sodium phosphate, dihydrate. No preservatives are present. | REMICADE is supplied as a Sterile, white, lyophilized powder, Following reconstitution with 10 mL of Sterile Water for Injection, USP, the resulting pH is approximately 7.2. | Intravenous infusion | for crohn disease, Ankylosing pondylitis, Psoriatic Arthritis, Plaque Psoriasis and ulcerative colitis : The recommended dose of REMICADE is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks for rhematoid arthritis: The recommended dose of REMICADE is 3 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks | REMICADE at doses > 5 mg/kg should not be administered to patients with moderate to severe heart failure.; REMICADE should not be re-administered to patients who have experienced a severe hypersensitivity reaction to REMICADE | Hepatotoxicity, Immunogenicity, Nausea, Diarrhea, Dysepsia, Sinusitis, Bronchitis, Phrayngitis, Rash, Fatigue, Fever, urinary tract infections. | Link | NA | NA |
| 10369 | Th1054 | Infliximab | NA | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | 71 | 9.5 days | Tumor necrosis factor (TNF-alpha) binding antibody (chimeric IgG1). It is composed of human constant and murine variable regions. Infliximab is produced by a recombinant cell line cultured by continuous perfusion. | To manage the signs and symptoms, as well as to induce and maintain clinical remission in adults with moderate to severe active Crohn's disease or ulcerative colitis. Also used to manage signs and symptoms of rheumatoid arthritis (in conjunction with methotrexate), ankylosing spondylitis, psoriatic arthritis, and juvenile arthritis. | Infliximab is a chimeric human-murine anti-human tumor necrosis factor (TNF) monoclonal antibody. It binds to tumor necrosis factor alpha (TNFa) and inhibits binding of TNFa with its receptors. This reduces production of pro-inflammatory cytokines such as interleukins (IL) 1 and 6. This also limits leukocyte migration and expression of adhesion molecules by endothelial cells and leukocytes. Infliximab also limits the activation of neutrophil and eosinophil functional activity, reduces production of tissue degrading enzymes produced by synoviocytes and/or chondrocytes. Infliximab decreases synovitis and joint erosions in collagen-induced arthritis and allows eroded joints to heal. | Infliximab neutralizes the biological activity of TNFa by binding with high affinity to the soluble and transmembrane forms of TNFa and inhibits binding of TNFa with its receptors. Infliximab does not neutralize TNFb (lymphotoxin a), a related cytokine that utilizes the same receptors as TNFa. Neutralization of the biological activity of TNFa leads to an overall reduction in inflammation. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production | NA | NA | In patients with rheumatoid arthritis, the CL of infliximab following a single dose infusion of 5 mg/kg, 10 mg/kg and 20 mg/kg were 11±7.5 mL/h, 11.4±5 mL/h, and 11±8.9 mL/h, respectively. | Agents Causing Muscle Toxicity, Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Dermatologicals, Disease-modifying Antirheumatic Agents, Gastrointestinal Agents, Globulins, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Proteins, Serum Globulins, Tumor Necrosis Factor Blockers, Tumor Necrosis Factor Receptor Blocking Activity | NA | NA | NA | Rilonacept results in increased immunosuppressive effects; increases the risk of infection | NA | Avsola | AMGEN INC | AMGEN INC | Rheumatoid Arthritis -adults with moderately to severely active rheumatoid arthritis, along with the medicine methotrexate. Crohn's Disease -children 6 years and older and adults with Crohn's disease who have not responded well to other medicines. Ankylosing Spondylitis. Psoriatic Arthritis. Plaque Psoriasis -adult patients with plaque psoriasis that is chronic (does not go away), severe, extensive, and/or disabling. Ulcerative Colitis -children 6 years and older and adults with moderately to severely active ulcerative colitis who have not responded well to other medicines. | NA | Following reconstitution with 10 mL of Sterile Water for Injection, USP, the resulting pH is approximately 7.2. Each single-dose vial contains 100 mg infliximab-axxq, dibasic sodium phosphate, anhydrous (4.9 mg), monobasic sodium phosphate, monohydrate (2.2 mg), polysorbate 80 (0.5 mg), and sucrose (500 mg). | sterile, white to slightly yellow, lyophilized powder | intravenous infusion. | Crohn's Disease The recommended dose of AVSOLA is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks followed by a maintenance regimen of 5 mg/kg every 8 weeks thereafter for the treatment of adults with moderately to severely active Crohn's disease or fistulizing Crohn's disease. For adult patients who respond and then lose their response, consideration may be given to treatment with 10 mg/kg. Patients who do not respond by Week 14 are unlikely to respond with continued dosing and consideration should be given to discontinue AVSOLA in these patients. Pediatric Crohn's Disease The recommended dose of AVSOLA for pediatric patients 6 years and older with moderately to severely active Crohn's disease is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks followed by a maintenance regimen of 5 mg/kg every 8 weeks. Ulcerative Colitis The recommended dose of AVSOLA is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks followed by a maintenance regimen of 5 mg/kg every 8 weeks thereafter for the treatment of adult patients with moderately to severely active ulcerative colitis. Pediatric Ulcerative Colitis The recommended dose of AVSOLA for pediatric patients 6 years and older with moderately to severely active ulcerative colitis is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks followed by a maintenance regimen of 5 mg/kg every 8 weeks. Rheumatoid Arthritis The recommended dose of AVSOLA is 3 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks followed by a maintenance regimen of 3 mg/kg every 8 weeks thereafter for the treatment of moderately to severely active rheumatoid arthritis. AVSOLA should be given in combination with methotrexate. For patients who have an incomplete response, consideration may be given to adjusting the dose up to 10 mg/kg or treating as often as every 4 weeks bearing in mind that risk of serious infections is increased at higher doses [see ADVERSE REACTIONS]. Ankylosing Spondylitis The recommended dose of AVSOLA is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks followed by a maintenance regimen of 5 mg/kg every 6 weeks thereafter for the treatment of active ankylosing spondylitis. Psoriatic Arthritis The recommended dose of AVSOLA is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks followed by a maintenance regimen of 5 mg/kg every 8 weeks thereafter for the treatment of psoriatic arthritis. AVSOLA can be used with or without methotrexate. Plaque Psoriasis The recommended dose of AVSOLA is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks followed by a maintenance regimen of 5 mg/kg every 8 weeks thereafter for the treatment of chronic severe (i.e., extensive and/or disabling) plaque psoriasis. | AVSOLA at doses >5 mg/kg should not be administered to patients with moderate to severe heart failure. In a randomized study evaluating infliximab in patients with moderate to severe heart failure (New York Heart Association [NYHA] Functional Class III/IV), infliximab treatment at 10 mg/kg was associated with an increased incidence of death and hospitalization due to worsening heart failure. AVSOLA should not be re-administered to patients who have experienced a severe hypersensitivity reaction to infliximab products. Additionally, AVSOLA should not be administered to patients with known hypersensitivity to inactive components of the product or to any murine proteins. | feel unwell tiredness (fatigue) poor appetite fever, skin rash, or joint pain | Link | NA | NA |
| 10371 | Th1054 | Infliximab | NA | 144190.3 | C6428H9912N1694O1987S46 | 8.25 | -0.441 | 71 | 9.5 days | Tumor necrosis factor (TNF-alpha) binding antibody (chimeric IgG1). It is composed of human constant and murine variable regions. Infliximab is produced by a recombinant cell line cultured by continuous perfusion. | To manage the signs and symptoms, as well as to induce and maintain clinical remission in adults with moderate to severe active Crohn's disease or ulcerative colitis. Also used to manage signs and symptoms of rheumatoid arthritis (in conjunction with methotrexate), ankylosing spondylitis, psoriatic arthritis, and juvenile arthritis. | Infliximab is a chimeric human-murine anti-human tumor necrosis factor (TNF) monoclonal antibody. It binds to tumor necrosis factor alpha (TNFa) and inhibits binding of TNFa with its receptors. This reduces production of pro-inflammatory cytokines such as interleukins (IL) 1 and 6. This also limits leukocyte migration and expression of adhesion molecules by endothelial cells and leukocytes. Infliximab also limits the activation of neutrophil and eosinophil functional activity, reduces production of tissue degrading enzymes produced by synoviocytes and/or chondrocytes. Infliximab decreases synovitis and joint erosions in collagen-induced arthritis and allows eroded joints to heal. | Infliximab neutralizes the biological activity of TNFa by binding with high affinity to the soluble and transmembrane forms of TNFa and inhibits binding of TNFa with its receptors. Infliximab does not neutralize TNFb (lymphotoxin a), a related cytokine that utilizes the same receptors as TNFa. Neutralization of the biological activity of TNFa leads to an overall reduction in inflammation. | NA | Most likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production | NA | NA | NA | Agents Causing Muscle Toxicity, Agents reducing cytokine levels, Amino Acids, Peptides, and Proteins, Anti-Inflammatory Agents, Antibodies, Antibodies, Monoclonal, Antineoplastic and Immunomodulating Agents, Antirheumatic Agents, Biological Products, Biologics for Rheumatoid Arthritis Treatment, Blood Proteins, Complex Mixtures, Dermatologicals, Disease-modifying Antirheumatic Agents, Gastrointestinal Agents, Globulins, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, 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 | Inflectra | Pfizer Europe Ma Eeig | Pfizer Europe Ma Eeig | Crohn's Disease | NA | Following reconstitution with 10 mL of Sterile Water for Injection, USP, the resulting pH is approximately 7.2. Each single-use vial contains 100 mg infliximab-dyyb, 500 mg sucrose, 0.5 mg polysorbate 80, 2.2 mg sodium dihydrogen phosphate monohydrate, and 6.1 mg di-Sodium hydrogen phosphate dihydrate. No preservatives are present. | sterile, white, lyophilized powder | intravenous Injection | The recommended dose of INFLECTRA is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks followed by a maintenance regimen of 5 mg/kg every 8 weeks thereafter for the treatment of adults with moderately to severely active Crohn's disease or fistulizing Crohn's disease. For adult patients who respond and then lose their response, consideration may be given to treatment with 10 mg/kg. Patients who do not respond by Week 14 are unlikely to respond with continued dosing and consideration should be given to discontinue INFLECTRA in these patients. | INFLECTRA at doses >5 mg/kg should not be administered to patients with moderate to severe heart failure. In a randomized study evaluating infliximab in patients with moderate to severe heart failure (New York Heart Association [NYHA] Functional Class III/IV), infliximab treatment at 10 mg/kg was associated with an increased incidence of death and hospitalization due to worsening heart failure. INFLECTRA should not be readministered to patients who have experienced a severe hypersensitivity reaction to infliximab products. Additionally, INFLECTRA should not be administered to patients with known hypersensitivity to inactive components of the product or to any murine proteins. | upper respiratory infections sinus infections runny or stuffy nose sore throat cough bronchitis infusion-related reactions headache abdominal pain nausea diarrhea indigestion rash itching fatigue pain fever oral thrush joint pain urinary tract infection, and high blood pressure (hypertension) | Link | NA | NA |
| 10376 | Th1057 | Interferon beta-1b | >Th1057_Interferon_beta-1b SYNLLGFLQRSSNFQSQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20011 | C908H1408N246O253S6 | 9.02 | -0.447 | NA | 10-20 minutes | Human interferon beta (165 residues), cysteine 17 is substituted with serine. Produced in E. coli, no carbohydrates, MW=18.5kD. | Interferon beta-1b is a drug used for the treatment of relapsing/remitting multiple sclerosis. It has been shown to slow the advance of the disease as well as to decrease the frequency of attacks. | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin, neopterin and protein kinase R. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | 0.25 to 2,88 L/kg | 9.4 - 28.9 mL/min/kg [patients with diseases other than MS receiving single intravenous doses up to 2.0 mg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Myelosuppressive Agents, Peptides, Proteins, Recombinant Human Interferon beta | CA1340861 | 28-Dec-1999 | 28-Dec-2016 | NA | Interferon alpha/beta receptor 1,Interferon alpha/beta receptor 2 | Betaseron | Bayer | Bayer | Betaseron is used to treat relapsing multiple sclerosis (MS). Betaseron will not cure MS, it will only decrease the frequency of relapse symptoms. | NA | Each vial contains 0.3 mg of interferon beta-lb. The unit measurement is derived by comparing the antiviral activity of the product to the World Health Organization (WHO) reference standard of recombinant human interferon beta. Mannitol, USP and Albumin (Human), USP (15 mg each/vial) are added as stabilizers. | Sterile, white to off-white powder | Subcutaneous Injection | The recommended starting dose is 0.0625 mg (0.25 mL) subcutaneously every other day, with dose increases over a six week period to the recommended dose of 0.25 mg (1 mL) every other day. | Betaseron is contraindicated in patients with a history of hypersensitivity to natural or recombinant interferon beta, Albumin (Human), | serious side effects: depressed mood, anxiety, trouble sleeping, restlessness, or thoughts of suicide or hurting yourself; bruising, swelling, oozing, or skin changes where the injection was given; weight changes, pounding heartbeats, feeling too hot or cold; fever, chills, body aches, flu symptoms; or nausea, stomach pain, low fever, loss of appetite, dark urine, clay-colored stools, jaundice (yellowing of the skin or eyes). | Link | NA | NA |
| 10377 | Th1057 | Interferon beta-1b | >Th1057_Interferon_beta-1b SYNLLGFLQRSSNFQSQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20011 | C908H1408N246O253S7 | 9.02 | -0.447 | NA | 10-20 minutes | Human interferon beta (165 residues), cysteine 17 is substituted with serine. Produced in E. coli, no carbohydrates, MW=18.5kD. | Interferon beta-1b is a drug used for the treatment of relapsing/remitting multiple sclerosis. It has been shown to slow the advance of the disease as well as to decrease the frequency of attacks. | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin, neopterin and protein kinase R. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | 0.25 to 2,88 L/kg | 9.4 - 28.9 mL/min/kg [patients with diseases other than MS receiving single intravenous doses up to 2.0 mg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Myelosuppressive Agents, Peptides, Proteins, Recombinant Human Interferon beta | CA1339707 | 10-Mar-1998 | 10-Mar-2015 | NA | NA | Betaferon | Bayer | Bayer | Betaferon is indicated for the treatment of patients with a single demyelinating event with an active inflammatory process, if it is severe enough to warrant treatment with intravenous corticosteroids, if alternative diagnoses have been excluded, and if they are determined to be at high risk of developing clinically definite multiple sclerosis; patients with relapsing-remitting multiple sclerosis and two or more relapses within the last two years; patients with secondary progressive multiple sclerosis with active disease, evidenced by relapses. | NA | NA | Powder and solvent that are made upto make solution. | Subcutaneous Injection | NA | People with severe depression or thoughts of suicide; People with severe liver disease; Pregnancy; Breastfeeding. | The most frequently observed side-effects are: Flu-like symptoms- such as fever,chills, painful joints, malaise, sweating, headache or muscular pain. These symptoms may be reduced by taking paracetamol or steroidal anti-inflammatory medicines such as ibuprofen. Injection site reactions. - Symptoms can include redness, swelling, discolouration, inflammation and pain. These may be reduced by the use of an auto-injector device. | Link | NA | NA |
| 10378 | Th1057 | Interferon beta-1b | >Th1057_Interferon_beta-1b SYNLLGFLQRSSNFQSQKLLWQLNGRLEYCLKDRMNFDIPEEIKQLQQFQKEDAALTIYEMLQNIFAIFRQDSSSTGWNETIVENLLANVYHQINHLKTVLEEKLEKEDFTRGKLMSSLHLKRYYGRILHYLKAKEYSHCAWTIVRVEILRNFYFINRLTGYLRN | 20011 | C908H1408N246O253S8 | 9.02 | -0.447 | NA | 10-20 minutes | Human interferon beta (165 residues), cysteine 17 is substituted with serine. Produced in E. coli, no carbohydrates, MW=18.5kD. | Interferon beta-1b is a drug used for the treatment of relapsing/remitting multiple sclerosis. It has been shown to slow the advance of the disease as well as to decrease the frequency of attacks. | Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin, neopterin and protein kinase R. | Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha. | NA | NA | NA | 0.25 to 2,88 L/kg | 9.4 - 28.9 mL/min/kg [patients with diseases other than MS receiving single intravenous doses up to 2.0 mg] | Adjuvants, Immunologic, Amino Acids, Peptides, and Proteins, Antineoplastic and Immunomodulating Agents, Biological Factors, Cytochrome P-450 CYP1A2 Inhibitors, Cytochrome P-450 CYP1A2 Inhibitors (strength unknown), Cytochrome P-450 Enzyme Inhibitors, Cytokines, Immunologic Factors, Immunomodulatory Agents, Immunosuppressive Agents, Intercellular Signaling Peptides and Proteins, Interferon Type I, Interferon-beta, Interferons, Myelosuppressive Agents, Peptides, Proteins, Recombinant Human Interferon beta | NA | NA | NA | NA | NA | Extavia | Novartis | Novartis | Extavia is used to treat relapsing multiple sclerosis (MS). This medication will not cure MS, it will only decrease the frequency of relapse symptoms. | NA | Each vial contains 0.3 mg of interferon beta-1b. The unit measurement is derived by comparing the antiviral activity of the product to the World Health Organization (WHO) reference standard of recombinant human interferon beta. Mannitol, USP and Albumin (Human), USP (15 mg each/vial) are added as stabilizers. | Sterile, white to off-white powder | Subcutaneous Injection | The recommended starting dose is 0.0625 mg (0.25 mL) subcutaneously every other day, with dose increases over a six week period to the recommended dose of 0.25 mg (1 mL) every other day. | Extavia is contraindicated in patients with a history of hypersensitivity to natural or recombinant interferon beta, Albumin (Human), | serious side effects: depressed mood, anxiety, trouble sleeping, restlessness, or thoughts of suicide or hurting yourself; bruising, swelling, oozing, or skin changes where the injection was given; weight changes, pounding heartbeats, feeling too hot or cold; fever, chills, body aches, flu symptoms; or nausea, stomach pain, low fever, loss of appetite, dark urine, clay-colored stools, jaundice (yellowing of the skin or eyes). | Link | NA | NA |
| 10385 | Th1061 | Trastuzumab | >Th1061_Trastuzumab DIQMTQSPSSLSASVGDRVTITCRASQDVNTAVAWYQQKPGKAPKLLIYSASFLYSGVPSRFSGSRSGTDFTLTISSLQPEDFATYYCQQHYTTPPTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 145531.5 | C6470H10012N1726O2013S42 | 8.45 | -0.415 | 71 | average 28.5 days | A recombinant IgG1 kappa, humanized monoclonal antibody that selectively binds with high affinity in a cell-based assay (Kd = 5 nM) to the extracellular domain of the human epidermal growth factor receptor protein. Produced in CHO cell culture. | For treatment of early stage HER2-positive breast cancer, or metastatic breast cancer that substantially overexpress HER2. | Used in the treatment of HER2-positive breast cancer. HER2 protein overexpression is observed in 25%-30% of primary breast cancers.Trastuzumab has been shown, in both in vitro assays and in animals, to inhibit the proliferation of human tumorcells that overexpress HER2. It is a mediator of antibody dependent cellular cytotoxicity, in that the binding of the antibody to HER2 overexpressing cells leads to preferential cell death. | Trastuzumab binds to the HER2 (or c-erbB2) proto-oncogene, an EGF receptor-like protein found on 20-30% of breast cancer cells. The binding leads to antibody mediated (complement mediated) killing of the HER2 positive cells. | Administration of trastuzumab can result in ventricular dysfunction and congestive heart failure. Risk of cardiotocity is especially elevated in patients recieving concurrent anthracycline or cyclophosphamide therapy. | Most likely removed by opsonization via the reticuloendothelial system. | Peak and trough plasma concentrations at steady state (between weeks 16 and 32) were approximately 123 and 79 mcg/mL, respectively. At the highest weekly dose studied (500 mg), mean peak serum concentration was 377 mcg/mL | 44 mL/kg | The predicted steady-state clearance of trastuzumab is 0.173 - 0.337 L/day, dependent primarily on the dosing regimen. The clearance rate for subcutaneously administered trastuzumab, formulated with hyaluronidase for improved subcutaneous absorption, is 0.11 L/day. | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Cardiotoxic antineoplastic agents, Globulins, HER2 Receptor Antagonist, HER2/Neu/cerbB2 Antagonists, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | CA2103059 | 22-Mar-2005 | 15-Jun-2012 | Abciximab may increase the risk of a hypersensitivy reaction to Trastuzumab | Receptor tyrosine-protein kinase erbB-2 | Truxima | Celltrion, Cephalon, Inc. | Celltrion, Cephalon, Inc. | Adjuvant Breast Cancer, Metastatic Breast Cancer, Metastatic Gastric Cancer | NA | Each multi-use vial of Herceptin contains 440 mg trastuzumab, 400 mg a,a-trehalose dihydrate, 9.9 mg L-histidine HCl, 6.4 mg L-histidine, and 1.8 mg polysorbate 20, USP. Reconstitution with 20 mL of the appropriate diluent (BWFI or SWFI) yields a solution containing 21 mg/mL trastuzumab, at a pH of approximately 6 | Herceptin is a sterile, white to pale yellow, preservative-free lyophilized powder |  Intravenous administration | Initial dose of 4mg/kg for 90 minutes and after that 2mg/kg weekly for 30 minutes during chemotherapy for the first 12 weeks incase of breast cancer. Last Dose 6mg/kg for 3 weeks. | None | Cardiomyopathy, Infusion reactions, Embryo-fetal Toxicity, Pulmonary toxicity,Exacerbation of chemotherapy-induced neutropenia, ever, nausea, vomiting, infusion reactions, diarrhea, infections, increased cough, headache, fatigue, dyspnea, rash, neutropenia, anemia, and myalgia. | Link | NA | NA |
| 10386 | Th1061 | Trastuzumab | >Th1061_Trastuzumab DIQMTQSPSSLSASVGDRVTITCRASQDVNTAVAWYQQKPGKAPKLLIYSASFLYSGVPSRFSGSRSGTDFTLTISSLQPEDFATYYCQQHYTTPPTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 145531.5 | C6470H10012N1726O2013S42 | 8.45 | -0.415 | 71 | average 28.5 days | A recombinant IgG1 kappa, humanized monoclonal antibody that selectively binds with high affinity in a cell-based assay (Kd = 5 nM) to the extracellular domain of the human epidermal growth factor receptor protein. Produced in CHO cell culture. | For treatment of early stage HER2-positive breast cancer, or metastatic breast cancer that substantially overexpress HER2. | Used in the treatment of HER2-positive breast cancer. HER2 protein overexpression is observed in 25%-30% of primary breast cancers.Trastuzumab has been shown, in both in vitro assays and in animals, to inhibit the proliferation of human tumorcells that overexpress HER2. It is a mediator of antibody dependent cellular cytotoxicity, in that the binding of the antibody to HER2 overexpressing cells leads to preferential cell death. | Trastuzumab binds to the HER2 (or c-erbB2) proto-oncogene, an EGF receptor-like protein found on 20-30% of breast cancer cells. The binding leads to antibody mediated (complement mediated) killing of the HER2 positive cells. | Administration of trastuzumab can result in ventricular dysfunction and congestive heart failure. Risk of cardiotocity is especially elevated in patients recieving concurrent anthracycline or cyclophosphamide therapy. | Most likely removed by opsonization via the reticuloendothelial system. | Peak and trough plasma concentrations at steady state (between weeks 16 and 32) were approximately 123 and 79 mcg/mL, respectively. At the highest weekly dose studied (500 mg), mean peak serum concentration was 377 mcg/mL | 45 mL/kg | The predicted steady-state clearance of trastuzumab is 0.173 - 0.337 L/day, dependent primarily on the dosing regimen. The clearance rate for subcutaneously administered trastuzumab, formulated with hyaluronidase for improved subcutaneous absorption, is 0.11 L/day. | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Cardiotoxic antineoplastic agents, Globulins, HER2 Receptor Antagonist, HER2/Neu/cerbB2 Antagonists, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Daunorubicin, Doxorubicin, Epirubicin), Idarubicin, Valrubicin. may increase the cardiotoxicity of drugs with trastuzumab. Signs and symptoms of cardiac dysfunction should be monitored for frequently. Increased risk of heart failure. Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events | NA | Herzuma | Cephalon, Inc., Celltrion Healthcare | Cephalon, Inc., Celltrion Healthcare | to treat the symptoms of Breast Cancer and Gastric Cancer. | NA | HERZUMA (trastuzumab-pkrb) is a humanized IgG1 kappa monoclonal antibody that selectively binds with high affinity to the extracellular domain of the human epidermal growth factor receptor 2 protein, HER2. Trastuzumab-pkrb is produced by recombinant DNA technology in a mammalian cell (Chinese Hamster Ovary) culture. | sterile, white to pale yellow, preservative-free lyophilized powder | intravenous infusion | Initial dose at 8 mg/kg as an intravenous infusion over 90 minutes Subsequent doses at 6 mg/kg as an intravenous infusion over 30–90 minutes every three weeks. Extending adjuvant treatment beyond one year is not recommended | NA | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, dizziness, fatigue, shortness of breath, swelling, chest pain or pressure, fever, sore throat, chills, and fatigue | Link | NA | NA |
| 10387 | Th1061 | Trastuzumab | >Th1061_Trastuzumab DIQMTQSPSSLSASVGDRVTITCRASQDVNTAVAWYQQKPGKAPKLLIYSASFLYSGVPSRFSGSRSGTDFTLTISSLQPEDFATYYCQQHYTTPPTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 145531.5 | C6470H10012N1726O2013S42 | 8.45 | -0.415 | 71 | average 28.5 days | A recombinant IgG1 kappa, humanized monoclonal antibody that selectively binds with high affinity in a cell-based assay (Kd = 5 nM) to the extracellular domain of the human epidermal growth factor receptor protein. Produced in CHO cell culture. | For treatment of early stage HER2-positive breast cancer, or metastatic breast cancer that substantially overexpress HER2. | Used in the treatment of HER2-positive breast cancer. HER2 protein overexpression is observed in 25%-30% of primary breast cancers.Trastuzumab has been shown, in both in vitro assays and in animals, to inhibit the proliferation of human tumorcells that overexpress HER2. It is a mediator of antibody dependent cellular cytotoxicity, in that the binding of the antibody to HER2 overexpressing cells leads to preferential cell death. | Trastuzumab binds to the HER2 (or c-erbB2) proto-oncogene, an EGF receptor-like protein found on 20-30% of breast cancer cells. The binding leads to antibody mediated (complement mediated) killing of the HER2 positive cells. | Administration of trastuzumab can result in ventricular dysfunction and congestive heart failure. Risk of cardiotocity is especially elevated in patients recieving concurrent anthracycline or cyclophosphamide therapy. | Most likely removed by opsonization via the reticuloendothelial system. | Peak and trough plasma concentrations at steady state (between weeks 16 and 32) were approximately 123 and 79 mcg/mL, respectively. At the highest weekly dose studied (500 mg), mean peak serum concentration was 377 mcg/mL | 46 mL/kg | The predicted steady-state clearance of trastuzumab is 0.173 - 0.337 L/day, dependent primarily on the dosing regimen. The clearance rate for subcutaneously administered trastuzumab, formulated with hyaluronidase for improved subcutaneous absorption, is 0.11 L/day. | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Cardiotoxic antineoplastic agents, Globulins, HER2 Receptor Antagonist, HER2/Neu/cerbB2 Antagonists, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Paclitaxel may increase the risk of neutropenia and anemia with trastuzumab. Concomitant therapy may also increase Trastuzumab serum concentration and decrease Paclitaxel serum concentrations. Monitor closely for adverse events and therapeutic response | Insulin receptor,Insulin-like growth factor 1 receptor,Insulin-degrading enzyme,HLA class II histocompatibility antigen, DQ alpha 2 chain,HLA class II histocompatibility antigen, DQ beta 1 chain,Retinoblastoma-associated protein,Cathepsin D,Carboxypeptidase E,Neuroendocrine convertase 2,Neuroendocrine convertase 1,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7,Synaptotagmin-like protein 4 | Kanjinti | AMGEN INC | AMGEN INC | to treat the symptoms of Breast Cancer and Gastric Cancer. | NA | Trastuzumab-anns is a humanized IgG1 kappa monoclonal antibody that selectively binds with high affinity to the extracellular domain of the human epidermal growth factor receptor 2 protein, HER2. Trastuzumab-anns is produced by recombinant DNA technology in a mammalian cell (Chinese Hamster Ovary) culture containing the antibiotic geneticin. Geneticin is not detectable in the final product. | sterile, white to pale yellow, preservative-free lyophilized powder with a cake-like appearance | intravenous administration. | Initial dose of 4 mg/kg as an intravenous infusion over 90 minutes then at 2 mg/kg as an intravenous infusion over 30 minutes weekly during chemotherapy for the first 12 weeks (paclitaxel or docetaxel) or 18 weeks (docetaxel and carboplatin). One week following the last weekly dose of KANJINTI, administer KANJINTI at 6 mg/kg as an intravenous infusion over 30–90 minutes every three weeks. | NA | heart problems, nausea, diarrhea, weight loss, headache, trouble sleeping, tiredness, low blood cell counts, rash, fever, chills, cough, blisters or ulcers in your mouth, red or swollen gums, trouble swallowing, altered sense of taste, stuffy nose, sinus pain, and sore throat | Link | NA | NA |
| 10388 | Th1061 | Trastuzumab | >Th1061_Trastuzumab DIQMTQSPSSLSASVGDRVTITCRASQDVNTAVAWYQQKPGKAPKLLIYSASFLYSGVPSRFSGSRSGTDFTLTISSLQPEDFATYYCQQHYTTPPTFGQGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC | 145531.5 | C6470H10012N1726O2013S42 | 8.45 | -0.415 | 71 | average 28.5 days | A recombinant IgG1 kappa, humanized monoclonal antibody that selectively binds with high affinity in a cell-based assay (Kd = 5 nM) to the extracellular domain of the human epidermal growth factor receptor protein. Produced in CHO cell culture. | For treatment of early stage HER2-positive breast cancer, or metastatic breast cancer that substantially overexpress HER2. | Used in the treatment of HER2-positive breast cancer. HER2 protein overexpression is observed in 25%-30% of primary breast cancers.Trastuzumab has been shown, in both in vitro assays and in animals, to inhibit the proliferation of human tumorcells that overexpress HER2. It is a mediator of antibody dependent cellular cytotoxicity, in that the binding of the antibody to HER2 overexpressing cells leads to preferential cell death. | Trastuzumab binds to the HER2 (or c-erbB2) proto-oncogene, an EGF receptor-like protein found on 20-30% of breast cancer cells. The binding leads to antibody mediated (complement mediated) killing of the HER2 positive cells. | Administration of trastuzumab can result in ventricular dysfunction and congestive heart failure. Risk of cardiotocity is especially elevated in patients recieving concurrent anthracycline or cyclophosphamide therapy. | Most likely removed by opsonization via the reticuloendothelial system. | Peak and trough plasma concentrations at steady state (between weeks 16 and 32) were approximately 123 and 79 mcg/mL, respectively. At the highest weekly dose studied (500 mg), mean peak serum concentration was 377 mcg/mL | 47 mL/kg | The predicted steady-state clearance of trastuzumab is 0.173 - 0.337 L/day, dependent primarily on the dosing regimen. The clearance rate for subcutaneously administered trastuzumab, formulated with hyaluronidase for improved subcutaneous absorption, is 0.11 L/day. | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Antineoplastic Agents, Immunological, Antineoplastic and Immunomodulating Agents, Blood Proteins, Cancer immunotherapy, Cardiotoxic antineoplastic agents, Globulins, HER2 Receptor Antagonist, HER2/Neu/cerbB2 Antagonists, Immunoglobulins, Immunoproteins, Immunosuppressive Agents, Immunotherapy, Narrow Therapeutic Index Drugs, Proteins, Serum Globulins | NA | NA | NA | Abatacept, Adalimumab, Alemtuzumab, Altretamine, Amsacrine, Anakinra, Asparaginase, Azacitidine, Azathioprine, Basiliximab, Betamethasone, Bleomycin, Busulfan, Capecitabine, Carboplatin, Carmustine, Chlorambucil, Cisplatin, Cladribine, Clofarabine, Corticotropin, Cortisone acetate, Cyclophosphamide, Cyclosporine, Cytarabine, Dacarbazine, Daclizumab, Dactinomycin, Denileukin diftitox, Dexamethasone, Docetaxel, Efalizumab, Erlotinib, Estramustine, Etanercept, Etoposide, Floxuridine, Fludarabine, Fludrocortisone, Fluorouracil, Gefitinib, Gemcitabine, Hydrocortisone, Hydroxyurea, Ibritumomab, Ifosfamide, Imatinib, Infliximab, Irinotecan, Lenalidomide, Lomustine, Mechlorethamine, Melphalan, Mercaptopurine, Methotrexate, Methylprednisolone, Mitomycin, Mitoxantrone, Muromonab, Mycophenolate mofetil, Mycophenolic acid, Natalizumab, Nelarabine, Nilotinib, Oxaliplatin, Pegaspargase, Pentostatin, Prednisolone, Prednisone, Procarbazine, Rilonacept, Rituximab, Sirolimus, Sorafenib, Streptozocin, Sunitinib, Tacrolimus, Temozolomide, Temsirolimus, Teniposide, Thalidomide, Thiotepa, Tioguanine, Tofacitinib, Topotecan, Tositumomab, Tretinoin, Triamcinolone, Vinblastine, Vincristine, Vinorelbine may increase the risk of neutropenia and anemia with trastuzumab. Monitor closely for signs and symptoms of adverse events. | NA | Ogivri | Mylan Institutional LLC, Viatris Limited, Bgp Pharma Ulc | Mylan Institutional LLC, Viatris Limited, Bgp Pharma Ulc | treatment of HER2-overexpressing breast cancer, and the treatment of HER2-overexpressing metastatic gastric or gastroesophageal junction adenocarcinoma. | NA | Ogivri (trastuzumab-dkst) is a humanized IgG1 kappa monoclonal antibody that selectively binds with high affinity to the extracellular domain of the human epidermal growth factor receptor 2 protein, HER2. Trastuzumab-dkst is produced by recombinant DNA technology in a mammalian cell (Chinese Hamster Ovary) culture. | sterile, off-white to pale yellow, preservative-free lyophilized powder | intravenous administration. | Initial dose of 4 mg/kg as an intravenous infusion over 90 minutes then at 2 mg/kg as an intravenous infusion over 30 minutes weekly during chemotherapy for the first 12 weeks (paclitaxel or docetaxel) or 18 weeks (docetaxel/carboplatin). One week following the last weekly dose of Ogivri, administer Ogivri at 6 mg/kg as an intravenous infusion over 30 to 90 minutes every three weeks. | NA | headache, diarrhea, nausea, chills, fever, infection, congestive heart failure, insomnia, cough, rash, low white blood cell count (neutropenia), fatigue, anemia, swelling and sores inside the mouth, weight loss, upper respiratory tract infections, low platelet count (thrombocytopenia), mucosal inflammation, runny or stuffy nose, and changes in taste. | Link | NA | NA |
| 10398 | Th1063 | Basiliximab | >Th1063_Basiliximab QVQLQQPGAELVKPGASVKMSCKASGYTFTSYNMHWVKQTPGRGLEWIGAIYPGNGDTSYNQKFKGKATLTADKSSSTAYMQLSSLTSEDSAVYYCARSTYYGGDWYFNVWGAGTTVTVSAASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKAEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 143801.3 | C6378H9844N1698O1997S48 | 8.68 | -0.473 | 71 | 7.2 ± 3.2 days (adults) | A recombinant chimeric (murine/human) monoclonal antibody (IgG1k) that functions as an immunosuppressive agent, specifically binding to and blocking the interleukin-2 receptor a-chain (IL-2R alpha, also known as CD25 antigen) on the surface of activated T-lymphocytes. It is a 144 kDa glycoprotein obtained from fermentation of an established mouse myeloma cell line genetically engineered to express plasmids containing the human heavy and light chain constant region genes and mouse heavy and light chain variable region genes encoding the RFT5 antibody that binds selectively to the IL-2R alpha. | For prophylactic treatment of kidney transplant rejection | Basiliximab functions as an IL-2 receptor antagonist. Specifically it inhibits IL-2-mediated activation of lymphocytes, a critical pathway in the cellular immune response involved in allograft rejection. | Basiliximab binds with high-affinity to the alpha-subunit (CD25) of the high-affinity IL-2 receptor. This inhibits IL-2 binding, which inhibits T-cell activation and prevents the body from mounting an immune response against the foreign kidney. | NA | Most likely removed by opsonization via the reticuloendothelial system. | NA | 7.8 ± 5.1 L [Pediatric] 4.8 ± 2.1 L [Adult] | 41 ± 19 mL/h [Adult patients undergoing first kidney transplantation] 17 ± 6 mL/h [pediatric patients undergoing renal transplantation] 31 ± 19 mL/h [adolescent patients undergoing renal transplantation] | Amino Acids, Peptides, and Proteins, Antibodies, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antineoplastic and Immunomodulating Agents, Blood Proteins, Globulins, Immunoglobulins, Immunologic Factors, Immunoproteins, Immunosuppressive Agents, Interleukin 2 Receptor-directed Antibody Interactions, Interleukin Inhibitors, Interleukin-2 Receptor Antagonist, Interleukin-2 Receptor Blocking Antibody, Proteins, Serum Globulins | CA2038279 | 9-Mar-1999 | 14-Mar-2011 | Canakinumab, Rilonacept results in increased immunosuppressive effects; increases the risk of infection | Interleukin-2 receptor subunit alpha, Interleukin-2 receptor subunit beta | Simulect | Novartis | Novartis | Simulect (basiliximab) is indicated for the prophylaxis of acute organ rejection in patients receiving renal transplantation when used as part of an immunosuppressive regimen that includes cyclosporine, USP (MODIFIED) and corticosteroids. | NA | Each 10-mg vial contains 10 mg basiliximab, 3.61 mg monobasic potassium phosphate, 0.50 mg disodium hydrogen phosphate (anhydrous), 0.80 mg sodium chloride, 10 mg sucrose, 40 mg mannitol and 20 mg glycine, to be reconstituted in 2.5 mL of Sterile Water for Injection, USP. No preservatives are added. Each 20-mg vial contains 20 mg basiliximab, 7.21 mg monobasic potassium phosphate, 0.99 mg disodium hydrogen phosphate (anhydrous), 1.61 mg sodium chloride, 20 mg sucrose, 80 mg mannitol and 40 mg glycine, to be reconstituted in 5 mL of Sterile Water for Injection, USP. No preservatives are added. | Simulect (basiliximab) , is a sterile lyophilisate which is available in 6 mL colorless glass vials and is available in 10 mg and 20 mg strength powder. | intavenous infusion mainly or bolus (if no allerg | In adult patients, the recommended regimen is two doses of 20 mg each. The first 20-mg dose should be given within 2 hours prior to transplantation surgery. The recommended second 20-mg dose should be given 4 days after transplantation. | Simulect (basiliximab) is contraindicated in patients with known hypersensitivity to basiliximab or any other component of the formulation. | Gastrointestinal System: constipation, nausea, abdominal pain, vomiting, diarrhea, dyspepsia; Body as a Whole-General: pain, peripheral edema, fever, viral infection; Metabolic and Nutritional: hyperkalemia, hypokalemia, hyperglycemia, hypercholesterolemia, hypophosphatemia, hyperuricemia; Urinary System: urinary tract infection;Respiratory System: dyspnea, upper respiratory tract infection; Skin and Appendages: surgical wound complications, acne;Cardiovascular Disorders-General: hypertension; Central and Peripheral Nervous System: headache, tremor; Psychiatric: insomnia; Red Blood Cell: anemia. | Link | NA | NA |
| 10403 | Th1065 | Digoxin Immune Fab (Ovine) | >Th1065_Digoxin_Immune_Fab_(Ovine) EVQLQQSGPELVKPGASVRMSCKSSGYIFTDFYMNWVRQSHGKSLDYIGYISPYSGVTGYNQKFKGKATLTVDKSSSTAYMELRSLTSEDSAVYYCAGSSGNKWAMDYWGHGASVTVSSAKTTAPSVYPLAPVCGDTTGSSVTLGCLVKGYFPEPVTLTWNSGSLSSGVHTFPAVLQSDLYTLSSSVTVTSSTWPSQSITCNVAHPASSTKVDKKIEP | 47301.7 | C2085H3223N553O672S16 | 8.01 | -0.343 | 61 (FAB f | 15-20 hrs | Digoxin Immune Fab is a sheep antibody (26-10) FAB fragment from sheep immunized with the digoxin derivative Digoxindicarboxymethylamine. It is used as an antidote for overdose of digoxin. | For treatment of digitoxin overdose or digitalis glycoside toxicity. | DigiFab binds molecules of digoxin, making them unavailable for binding at their site of action on cells in the body. The Fab fragment-digoxin complex accumulates in the blood, from which it is excreted by the kidney. The net effect is to shift the equilibrium away from binding of digoxin to its receptors in the body, thereby reversing its effects. | Binds excess digoxin or digitoxin molecules circulating in the blood. | NA | NA | NA | 0.3 L/kg [DigiFab] 0.4 L/kg [Digibind] | NA | Amino Acids, Peptides, and Proteins, Antidotes, Blood Proteins, Digoxin Binding Activity, Immunoglobulin G, Immunoglobulins, Proteins, Serum, Serum Globulins | NA | NA | NA | Cinitapride can alter the absorption of digoxin as it simulates gastric emptying | Digoxin | DIGIBIND | Galaxo Smith Kline | Galaxo Smith Kline | DIGIBIND, Digoxin Immune Fab (Ovine), is indicated for treatment of potentially life-threatening digoxin intoxication. Although designed specifically to treat life-threatening digoxin overdose, it has also been used successfully to treat life-threatening digitoxin overdose. Since human experience is limited and the consequences of repeated exposures are unknown, DIGIBIND is not indicated for milder cases of digitalis toxicity. | NA | Each vial, which will bind approximately 0.5 mg of digoxin (or digitoxin), contains 38 mg of digoxin-specific Fab fragments derived from sheep plus 75 mg of sorbitol as a stabilizer and 28 mg of sodium chloride. The vial contains no preservatives. | DIGIBIND, Digoxin Immune Fab (Ovine), is a Sterile lyophilized powder of antigen binding fragments (Fab) derived from specific antidigoxin antibodies raised in sheep. | Intravenous infusion after reconstitution with Ste | Each vial of DIGIBIND (digoxin immune fab) contains 38 mg of purified digoxin-specific Fab fragments which will bind approximately 0.5 mg of digoxin (or digitoxin). Dose (in # of vials) = Total digitalis body load in mg / 0.5 mg of digitalis bound/vial | There are no known contraindications to the use of DIGIBIND. | Allergic reactions to DIGIBIND (digoxin immune fab) have been reported rarely. Patients with a history of allergy, especially to antibiotics, appear to be at particular risk. In a few instances, low cardiac output states and congestive heart failure could have been exacerbated by withdrawal of the inotropic effects of digitalis. Hypokalemia may occur from re-activation of (sodium, potassium) ATPase. Patients with atrial fibrillation may develop a rapid ventricular response from withdrawal of the effects of digitalis on the atrioventricular node. | Link | NA | NA |
| 10404 | Th1065 | Digoxin Immune Fab (Ovine) | >Th1065_Digoxin_Immune_Fab_(Ovine) EVQLQQSGPELVKPGASVRMSCKSSGYIFTDFYMNWVRQSHGKSLDYIGYISPYSGVTGYNQKFKGKATLTVDKSSSTAYMELRSLTSEDSAVYYCAGSSGNKWAMDYWGHGASVTVSSAKTTAPSVYPLAPVCGDTTGSSVTLGCLVKGYFPEPVTLTWNSGSLSSGVHTFPAVLQSDLYTLSSSVTVTSSTWPSQSITCNVAHPASSTKVDKKIEP | 47301.7 | C2085H3223N553O672S16 | 8.01 | -0.343 | 61 (FAB f | 15-20 hrs | Digoxin Immune Fab is a sheep antibody (26-10) FAB fragment from sheep immunized with the digoxin derivative Digoxindicarboxymethylamine. It is used as an antidote for overdose of digoxin. | For treatment of digitoxin overdose or digitalis glycoside toxicity. | DigiFab binds molecules of digoxin, making them unavailable for binding at their site of action on cells in the body. The Fab fragment-digoxin complex accumulates in the blood, from which it is excreted by the kidney. The net effect is to shift the equilibrium away from binding of digoxin to its receptors in the body, thereby reversing its effects. | Binds excess digoxin or digitoxin molecules circulating in the blood. | NA | NA | NA | 0.3 L/kg [DigiFab] 0.4 L/kg [Digibind] | NA | Amino Acids, Peptides, and Proteins, Antidotes, Blood Proteins, Digoxin Binding Activity, Immunoglobulin G, Immunoglobulins, Proteins, Serum, Serum Globulins | NA | NA | NA | NA | NA | DigiFab |  Protherics Inc, Btg International Inc, Savage Laboratories a division of Fougera Pharmaceuticals Inc. |  Protherics Inc, Btg International Inc, Savage Laboratories a division of Fougera Pharmaceuticals Inc. | DigiFab is indicated for the treatment of patients with life-threatening or potentially life-threatening digoxin toxicity or overdose. Although designed specifically to treat digoxin overdose, a product very similar to DigiFab (Digibind) has been used successfully to treat life-threatening digitoxin overdose. | NA | Each vial of DigiFab, which will bind approximately 0.5 mg digoxin, contains 40 mg of digoxin immune Fab, 75 mg (approx) of mannitol USP, and 2 mg (approx) sodium acetate USP as a buffering agent. The product contains no preservatives after reconstitution with 4 mL of Sterile Water for Injection USP | DigiFab [Digoxin Immune Fab (Ovine)] is a sterile, purified, lyophilized powdered preparation of digoxin-immune ovine Fab (monovalent) immunoglobulin fragments. | Intravenous administration | For adult patients who are in acute distress or for whom a serum digoxin concentration is not available, 6 vials (240 mg) should be adequate to reverse most cases of toxicity. | There are no known contraindications to the use of DigiFab | Exacerbation of low cardiac output states and congestive heart failure due to the withdrawal of inotropic effect of digitalis. Hypokalemia due to reactivation of the sodium-potassium ATPase. Rapid ventricular response in patients with atrial fibrillation due to withdrawal of the effects of digitalis on the atrioventricular node. Rare allergic reactions Patients with a history of allergy, especially to antibiotics, appear to be at particular risk. | Link | NA | NA |
| 10415 | Th1069 | Pegvisomant | >Th1069_Pegvisomant FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 | 6 days | Pegvisomant is a highly selective growth hormone (GH) receptor antagonist. It is used to treat acromegaly. Unlike dopamine or somatostatin analogs (which inhibit growth hormone secretion), this drug actually blocks the hepatic (GH-mediated) production of insulin like growth factor (IGF-1), which is the main mediator of growth hormone activity. | Pegvisomant is a growth hormone receptor antagonist used for the treatment of acromegaly. | Somavert is used for the treatment of acromegaly, which arises from excessive IGF-1 levels. Somavert selectively binds to growth hormone (GH) receptors on cell surfaces, where it blocks the binding of endogenous GH, and thus interferes with GH signal transduction. Inhibition of GH action results in decreased serum concentrations of insulin-like growth factor-I (IGF-I), and IGF binding protein-3 (IGFBP-3). This reduces the symptoms of acromegaly. | Somavert selectively binds to growth hormone (GH) receptors on cell surfaces, where it blocks the binding of endogenous GH. This leads to the normalization of serum IGF-1 levels. | NA | NA | NA | 7 L | 36 ± 28 mL/h [SC doses ranging from 10 to 20 mg/day] | Acromegaly, Amino Acids, Peptides, and Proteins, Anterior Pituitary Lobe Hormones and Analogues, Cholinesterase Inhibitors, Cytochrome P-450 CYP3A Inducers, Cytochrome P-450 CYP3A4 Inducers, Cytochrome P-450 CYP3A4 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Growth Hormone Receptor Antagonist, Growth Hormone Receptor Antagonists, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Pegylated agents, Peptide Hormones, Peptides, Pituitary and Hypothalamic Hormones and Analogues, Pituitary Hormones, Pituitary Hormones, Anterior, Somatotropin Antagonists, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | US5849535 | 15-Dec-1998 | 25-Mar-2017 | Dihydrocodeine opioids may diminish the therapeutic effect of pegvisomant. It is recommended to monitor therapy | Growth hormone receptor | SOMAVERT | Pfizer | Pfizer | SOMAVERT is indicated for the treatment of acromegaly in patients who have had an inadequate response to surgery or radiation therapy, or for whom these therapies are not appropriate. The goal of treatment is to normalize serum insulin-like growth factor-I (IGF-I) levels. | NA | SOMAVERT is available in single-dose sterile vials containing 10, 15, or 20 mg of pegvisomant protein (approximately 10, 15, and 20 U activity, respectively). Each vial also contains 1.36 mg of glycine, 36.0 mg of mannitol, 1.04 mg of sodium phosphate dibasic anhydrous, and 0.36 mg of sodium phosphate monobasic monohydrate | SOMAVERT for injection is supplied as a Sterile, white lyophilized powder | Subcutaneous Injection | The recommended loading dose of SOMAVERT is 40 mg given subcutaneously, under healthcare provider supervision. Increase the dosage by 5 mg increments every 4-6 weeks if IGF-I concentrations are elevated.Decrease the dosage by 5 mg decrements every 4-6 weeks if IGF-I concentrations are below the normal range. | None. | Hypoglycemia associated with GH lowering in patients with Diabetes Mellitus, Liver test elevations, Cross-reactivity with GH assay, Lipohypertrophy, Systemic hypersensitivity, pain, nausea ,diarrhea, dizziness, Sinusitis | Link | NA | NA |
| 10421 | Th1070 | Botulinum Toxin Type A | >Th1070_Botulinum_Toxin_Type_A MPFVNKQFNYKDPVNGVDIAYIKIPNVGQMQPVKAFKIHNKIWVIPERDTFTNPEEGDLNPPPEAKQVPVSYYDSTYLSTDNEKDNYLKGVTKLFERIYSTDLGRMLLTSIVRGIPFWGGSTIDTELKVIDTNCINVIQPDGSYRSEELNLVIIGPSADIIQFECKSFGHEVLNLTRNGYGSTQYIRFSPDFTFGFEESLEVDTNPLLGAGKFATDPAVTLAHELIHAGHRLYGIAINPNRVFKVNTNAYYEMSGLEVSFEELRTFGGHDAKFIDSLQENEFRLYYYNKFKDIASTLNKAKSIVGTTASLQYMKNVFKEKYLLSEDTSGKFSVDKLKFDKLYKMLTEIYTEDNFVKFFKVLNRKTYLNFDKAVFKINIVPKVNYTIYDGFNLRNTNLAANFNGQNTEINNMNFTKLKNFTGLFEFYKLLCVRGIITSKTKSLDKGYNKALNDLCIKVNNWDLFFSPSEDNFTNDLNKGEEITSDTNIEAAEENISLDLIQQYYLTFNFDNEPENISIENLSSDIIGQLELMPNIERFPNGKKYELDKYTMFHYLRAQEFEHGKSRIALTNSVNEALLNPSRVYTFFSSDYVKKVNKATEAAMFLGWVEQLVYDFTDETSEVSTTDKIADITIIIPYIGPALNIGNMLYKDDFVGALIFSGAVILLEFIPEIAIPVLGTFALVSYIANKVLTVQTIDNALSKRNEKWDEVYKYIVTNWLAKVNTQIDLIRKKMKEALENQAEATKAIINYQYNQYTEEEKNNINFNIDDLSSKLNESINKAMININKFLNQCSVSYLMNSMIPYGVKRLEDFDASLKDALLKYIYDNRGTLIGQVDRLKDKVNNTLSTDIPFQLSKYVDNQRLLSTFTEYIKNIINTSILNLRYESNHLIDLSRYASKINIGSKVNFDPIDKNQIQLFNLESSKIEVILKNAIVYNSMYENFSTSFWIRIPKYFNSISLNNEYTIINCMENNSGWKVSLNYGEIIWTLQDTQEIKQRVVFKYSQMINISDYINRWIFVTITNNRLNNSKIYINGRLIDQKPISNLGNIHASNNIMFKLDGCRDTHRYIWIKYFNLFDKELNEKEIKDLYDNQSNSGILKDFWGDYLQYDKPYYMLNLYDPNKYVDVNNVGIRGYMYLKGPRGSVMTTNIYLNSSLYRGTKFIIKKYASGNKDNIVRNNDRVYINVVVKNKEYRLATNASQAGVEKILSALEIPDVGNLSQVVVMKSKNDQGITNKCKMNLQDNNGNDIGFIGFHQFNNIAKLVASNWYNRQIERSSRTLGCSWEFIPVDDGWGERPL | 900000 | C6760H10447N1743O2010S32 | 5.6 | -0.368 | 85.5-86.7 | 230 to 260 min in a pharmacokinetic study of rats and mice | Purified botulinum toxin from Clostridium botulinum, purified from culture via dialysis and acid precipitation. | For the treatment of cervical dystonia in adults to decrease the severity of abnormal head position and neck pain associated with cervical dystonia. Also for the treatment of severe primary axillary hyperhidrosis that is inadequately managed with topical agents and for the treatment of strabismus and blepharospasm associated with dystonia, including benign essential blepharospasm or VII nerve disorders in patients 12 years of age and above. Also used cosmetically to temporarily improve the appearance of moderate-to-severe frown lines between the eyebrows (glabellar lines) as well as for the treatment of excessive underarm sweating. | A 150 kDa neurotoxic protein produced from fermentation of Hall strain Clostridium botulinum type A grown in a medium containing casein hydrolysate, glucose and yeast extract. It is purified from the culture solution by dialysis and a series of acid precipitations to a complex consisting of the neurotoxin, and several accessory proteins. Botulinum Toxin Type A is not expected to be present in the peripheral blood at measurable levels following IM or intradermal injection at the recommended doses. The recommended quantities of neurotoxin administered at each treatment session are not expected to result in systemic, overt distant clinical effects, i.e. muscle weakness, in patients without other neuromuscular dysfunction. However, sub-clinical systemic effects have been shown by single-fiber electromyography after IM doses of botulinum toxins appropriate to produce clinically observable local muscle weakness. | Botulinum Toxin Type A blocks neuromuscular transmission by binding to acceptor sites on motor or sympathetic nerve terminals, entering the nerve terminals, and inhibiting the release of acetylcholine. This inhibition occurs as the neurotoxin cleaves SNAP-25, a protein integral to the successful docking and release of acetylcholine from vesicles situated within nerve endings. | Based on toxicological studies, it has been estimated that the human LD50 by injection is approximately 2800 Units, equivalent to 28 individual vials of BOTOX (Botulinum Toxin Type A) Purified Neurotoxin Complex (100 Units) for a 70 kg adult. When injected intramuscularly, Botulinum Toxin Type A has been shown to be teratogenic or to have embryocidal effects in some animal species. | NA | The chemical complexity of Botulinum Toxin Type A combined with its extreme potency limits the opportunity to study its pharmacokinetic profile in humans. Therefore, no human pharmacokinetic studies have been performed. Botulinum Toxin Type A is injected directly into the target organ, a skeletal muscle. Thus, bioavailability of the intravenous or oral route is not of clinical relevance. | NA | NA | Acetylcholine Release Inhibitors, Agents that produce neuromuscular block (indirect), Amino Acids, Peptides, and Proteins, Bacterial Proteins, Bacterial Toxins, Biological Factors, Botulinum Toxins, Botulinum Toxins, Type A, Central Nervous System Depressants, Cholinergic Agents, Endopeptidases, Enzymes, Enzymes and Coenzymes, Ganglion Blockers, Hydrolases, Membrane Transport Modulators, Metalloendopeptidases, Metalloproteases, Muscle Relaxants, Muscle Relaxants, Peripherally Acting Agents, Musculo-Skeletal System, Neuromuscular Agents, Neuromuscular Blocking Agents, Neurotoxins, Neurotransmitter Agents, Noxae, Other Miscellaneous Therapeutic Agents, Peptide Hydrolases, Peripheral Nervous System Agents, Proteins, Toxic Actions, Toxins, Biological | NA | NA | NA | NA | NA | Xeomin | MERZ AESTHETICS | MERZ AESTHETICS | Xeomin is indicated in Cervical Dystonia, Blepharospasm, Glabellar Lines | NA | One vial of XEOMIN contains 50 or 100 Units of incobotulinumtoxinA, 1 mg of human albumin, and 4.7 mg sucrose. | XEOMIN is a sterile white to off-white lyophilized powder after reconstitution with preservative-free 0.9% Saline for Injection. | IntramuSubcutaneousular Injection | In Cervical Dystonia: Initial dose of Xeomin is 120 Units given intramuscularly. In Blepharospasm: The total initial dose of XEOMIN in both eyes should not exceed 70 Units (35 Units/eye).In Glabellar Lines: The total recommended XEOMIN dose is 20 Units per treatment session divided into five equal intramuscular injections of 4 Units each. | Known hypersensitivity to the active substance botulinum neurotoxin type A or to any of the excipients and Infection at the proposed injection sites | In Cervical Dystonia: The most commonly observed adverse reactions (≥5% of patients and > placebo) are dysphagia, neck pain, muscle weakness, injection site pain, and musculoskeletal pain. In Blepharospasm: The most commonly observed adverse reactions (≥5% of patients and > placebo) are eyelid ptosis, dry eye, dry mouth, diarrhea, headache, visual impairment, dyspnea, nasopharyngitis, and respiratory tract infection. In Glabellar Lines:The most commonly observed adverse reaction (>1% of patients and > placebo) is headache. | Link | NA | NA |
| 10423 | Th1071 | Pancrelipase | >Th1071_Pancrelipase QYSPNTQQGRTSIVHLFEWRWVDI | 131000 | C5850H8902N1606O1739S49 | 7.44 | NA | 48-50 | Pancrelipase is not significantly absorbed from the gastrointestinal tract and acts locally, so limination half-life is not relevant | Pancrelipase is an enzyme mixture isolated from porcine or bovine pancreas, sometimes called pancreatin. It contains 3 enzymes: amylase, lipase, and a protease (chymotrypsin). Pancrelipase is marketed under several brand names such as Ultresa and Viokace. | For treatment of exocrine pancreatic insufficiency in cystic fibrosis (Ultresa), chronic pancreatitis (Viokace in combination with a proton pump inhibitor), and pancreatectomy (Viokace in combination with a proton pump inhibitor) | Used in the treatment of cystic fibrosis or pancreatic dysfunction, pancrelipase helps improve fat digestion in the small intestine. Specifically, the lipase, protease and amylase components break down fat, protein, and starches, respectively, in the small intestine. Lipase hydrolyzes fats into glycerol and fatty acids. Protease converts proteins into proteoses and derived substances, while amylase converts starches into dextrins and sugars. Pancreatic enzymes are used to correct maldigestion, malabsorption and pain associated with pancreatic insufficiency. The major maldigestion/malabsorption problems arise from incomplete fat digestion. Exogenous pancrelipase reduces the amount of nitrogen and fat excreted in the stool. | The lipase, protease and amylase components of pancrelipase break down fat, protein, and starches, respectively, in the small intestine. Lipase hydrolyzes fats into glycerol and fatty acids. Protease converts proteins into proteoses and derived substances, while amylase converts starches into dextrins and sugars. | Overdose symptoms may include diarrhea or stomach upset. The most common adverse reactions seen are ear, neck, and abdominal pain; headache, nasal congestion, and beta-hemolytic streptococcal infection. | Pancrelipase acts locally, so there is minimal metabolism. | Pancrelipase is not significantly absorbed from the gastrointestinal tract. | NA | Pancrelipase is not significantly absorbed, so there is minimal clearance from the body. | Alimentary Tract and Metabolism, Carboxylic Ester Hydrolases, Complex Mixtures, Digestives, Incl. Enzymes, Enzyme Preparations, Enzymes, Enzymes and Coenzymes, Esterases, Gastrointestinal Agents, Hydrolases, Lipase, Pancreatic Extracts, Tissue Extracts | NA | NA | NA | NA | NA | Viokace | Aptalis Pharma US, Inc. | Aptalis Pharma US, Inc. | VIOKACE (pancrelipase) tablets, in combination with a proton pump inhibitor, is indicated in adults for the treatment of exocrine paencratic insufficiencydue to chronic pancreatitis or pancreatectomy. | NA | 10,440 USP units of lipase; 39,150 USP units of protease; 39,150 USP units of amylase tablets are tan, round biconvex and have VIO9111 engraved on one side and 9111 on the other side.Inactive ingredients in VIOKACE include: colloidal silicon dioxide, crosscarmellose sodium, lactose monohydrate, microcrystalline cellulose, stearic acid and talc. | Pancrelipase is a beige-white amorphous powder. It is miscible in water and practically insoluble in alcohol and converted to tablet form | Oral route | Enzyme dosing should begin with 500 lipase units/kg of body weight per meal to a maximum of 2,500 lipase units/kg of body weight per meal (or less than or equal to 10,000 lipase units/kg of body weight per day), or less than 4,000 lipase units/g fat ingested per day. | None | The most serious adverse reactions reported with different pancreatic enzyme products of the same active ingredient (pancrelipase) that are described elsewhere in the label include fibrosing colonopathy, hyperuricemia and allergic reactions. | Link | NA | NA |
| 10424 | Th1071 | Pancrelipase | >Th1071_Pancrelipase QYSPNTQQGRTSIVHLFEWRWVDI | 131000 | C5850H8902N1606O1739S49 | 8.44 | NA | 48-50 | Pancrelipase is not significantly absorbed from the gastrointestinal tract and acts locally, so limination half-life is not relevant | Pancrelipase is an enzyme mixture isolated from porcine or bovine pancreas, sometimes called pancreatin. It contains 3 enzymes: amylase, lipase, and a protease (chymotrypsin). Pancrelipase is marketed under several brand names such as Ultresa and Viokace. | For treatment of exocrine pancreatic insufficiency in cystic fibrosis (Ultresa), chronic pancreatitis (Viokace in combination with a proton pump inhibitor), and pancreatectomy (Viokace in combination with a proton pump inhibitor) | Used in the treatment of cystic fibrosis or pancreatic dysfunction, pancrelipase helps improve fat digestion in the small intestine. Specifically, the lipase, protease and amylase components break down fat, protein, and starches, respectively, in the small intestine. Lipase hydrolyzes fats into glycerol and fatty acids. Protease converts proteins into proteoses and derived substances, while amylase converts starches into dextrins and sugars. Pancreatic enzymes are used to correct maldigestion, malabsorption and pain associated with pancreatic insufficiency. The major maldigestion/malabsorption problems arise from incomplete fat digestion. Exogenous pancrelipase reduces the amount of nitrogen and fat excreted in the stool. | The lipase, protease and amylase components of pancrelipase break down fat, protein, and starches, respectively, in the small intestine. Lipase hydrolyzes fats into glycerol and fatty acids. Protease converts proteins into proteoses and derived substances, while amylase converts starches into dextrins and sugars. | Overdose symptoms may include diarrhea or stomach upset. The most common adverse reactions seen are ear, neck, and abdominal pain; headache, nasal congestion, and beta-hemolytic streptococcal infection. | Pancrelipase acts locally, so there is minimal metabolism. | Pancrelipase is not significantly absorbed from the gastrointestinal tract. | NA | Pancrelipase is not significantly absorbed, so there is minimal clearance from the body. | Alimentary Tract and Metabolism, Carboxylic Ester Hydrolases, Complex Mixtures, Digestives, Incl. Enzymes, Enzyme Preparations, Enzymes, Enzymes and Coenzymes, Esterases, Gastrointestinal Agents, Hydrolases, Lipase, Pancreatic Extracts, Tissue Extracts | NA | NA | NA | NA | Synaptosomal-associated protein 25,Rho-related GTP-binding protein RhoB | ULTRESA | Aptalis Pharma US, Inc. | Aptalis Pharma US, Inc. | ULTRESA (pancrelipase) is indicated for the treatment of exocrinepancreatic insufficiency due to cystic fibrosis or other conditions. | NA | Each delayed-release capsule for oral administration contains enteric-coatedbeads (1.7 mm in diameter and 1.9 mm thick for 4,000 USP lipase units, approximately 2.0 mm in diameter and 2.0 – 2.4 mm thick for 13,800, 20,700, and 23,000 USP lipase units). it also contains colloidal silicon dioxide, croscarmellose sodium, hydrogenated castor oil, hypromellose phthalate, magnesium stearate, microcrystalline cellulose, talc, and triethyl citrate. | Pancrelipase is a beige-white amorphous powder. It is miscible in water and practically insoluble or insoluble in alcohol and ether and converted to Delayed-Release Capsules | Oral route | Enzyme dosing should begin with 500 lipase units/kg of body weight per meal for those older than age 4 years to a maximum of 2,500 lipase units/kg of body weight per meal (or less than or equal to 10,000 lipase units/kg of body weight per day), or less than 4,000 lipase units/g fat ingested per day. | None | The most serious adverse reactions reported with different pancreatic enzyme products of the same active ingredient (pancrelipase) that are described elsewhere in the label include fibrosing colonopathy,hyperuricemia and allergic reactions. | Link | NA | NA |
| 10425 | Th1071 | Pancrelipase | >Th1071_Pancrelipase QYSPNTQQGRTSIVHLFEWRWVDI | 131000 | C5850H8902N1606O1739S49 | 9.44 | NA | 48-50 | Pancrelipase is not significantly absorbed from the gastrointestinal tract and acts locally, so limination half-life is not relevant | Pancrelipase is an enzyme mixture isolated from porcine or bovine pancreas, sometimes called pancreatin. It contains 3 enzymes: amylase, lipase, and a protease (chymotrypsin). Pancrelipase is marketed under several brand names such as Ultresa and Viokace. | For treatment of exocrine pancreatic insufficiency in cystic fibrosis (Ultresa), chronic pancreatitis (Viokace in combination with a proton pump inhibitor), and pancreatectomy (Viokace in combination with a proton pump inhibitor) | Used in the treatment of cystic fibrosis or pancreatic dysfunction, pancrelipase helps improve fat digestion in the small intestine. Specifically, the lipase, protease and amylase components break down fat, protein, and starches, respectively, in the small intestine. Lipase hydrolyzes fats into glycerol and fatty acids. Protease converts proteins into proteoses and derived substances, while amylase converts starches into dextrins and sugars. Pancreatic enzymes are used to correct maldigestion, malabsorption and pain associated with pancreatic insufficiency. The major maldigestion/malabsorption problems arise from incomplete fat digestion. Exogenous pancrelipase reduces the amount of nitrogen and fat excreted in the stool. | The lipase, protease and amylase components of pancrelipase break down fat, protein, and starches, respectively, in the small intestine. Lipase hydrolyzes fats into glycerol and fatty acids. Protease converts proteins into proteoses and derived substances, while amylase converts starches into dextrins and sugars. | Overdose symptoms may include diarrhea or stomach upset. The most common adverse reactions seen are ear, neck, and abdominal pain; headache, nasal congestion, and beta-hemolytic streptococcal infection. | Pancrelipase acts locally, so there is minimal metabolism. | Pancrelipase is not significantly absorbed from the gastrointestinal tract. | NA | Pancrelipase is not significantly absorbed, so there is minimal clearance from the body. | Alimentary Tract and Metabolism, Carboxylic Ester Hydrolases, Complex Mixtures, Digestives, Incl. Enzymes, Enzyme Preparations, Enzymes, Enzymes and Coenzymes, Esterases, Gastrointestinal Agents, Hydrolases, Lipase, Pancreatic Extracts, Tissue Extracts | NA | NA | NA | NA | NA | PERTZYE | Digestive care US, Inc. | Digestive care US, Inc. | PERTZYE (pancrelipase) is indicated for the treatment of exocrinepancreatic insufficiency due to cystic fibrosis or other conditions. | NA | Each PERTZYE delayed-release capsule for oral administration contains bicarbonatebuffered enteric-coated microspheres ranging in size from 0.8 – 2.2 mm in diameter.8,000 USP units of lipase; 28,750 USP units of protease; 30,250 USP units of amylase. it also contains odium bicarbonate, sodium carbonate, cellulose acetate phthalate, sodium starch glycolate, diethyl phthalate, ursodiol, polyvinylpyrrolidone, and talc and are contained in hard gelatin capsules. | Pancrelipase is a beige-white amorphous powder. It is miscible in water and practically insoluble or insoluble in alcohol and ether PERTZYE delayed-release capsule | Oral route | Enzyme dosing should begin with 500 lipase units/kg of body weight per meal for those older than age 4 years to a maximum of 2,500 lipase units/kg of body weight per meal (or less than or equal to 10,000 lipase units/kg of body weight per day), or less than 4,000 lipase units/g fat ingested per day. | None | The most serious adverse reactions reported with different pancreatic enzyme products of the same active ingredient (pancrelipase) that are described elsewhere in the label include fibrosing colonopathy,hyperuricemia and allergic reactions | Link | NA | NA |
| 10428 | Th1072 | Streptokinase | >Th1072_Streptokinase MKNYLSFGMFALLFALTFGTVNSVQAIAGPEWLLDRPSVNNSQLVVSVAGTVEGTNQDISLKFFEIDLTSRPAHGGKTEQGLSPKSKPFATDSGAMSHKLEKADLLKAIQEQLIANVHSNDDYFEVIDFASDATITDRNGKVYFADKDGSVTLPTQPVQEFLLSGHVRVRPYKEKPIQNQAKSVDVEYTVQFTPLNPDDDFRPGLKDTKLLKTLAIGDTITSQELLAQAQSILNKNHPGYTIYERDSSIVTHDNDIFRTILPMDQEFTYRVKNREQAYRINKKSGLNEEINNTDLISEKYYVLKKGEKPYDPFDRSHLKLFTIKYVDVDTNELLKSEQLLTASERNLDFRDLYDPRDKAKLLYNNLDAFGIMDYTLTGKVEDNHDDTNRIITVYMGKRPEGENASYHLAYDKDRYTEEEREVYSYLRYTGTPIPDNPNDK | 47286.7 | C2100H3278N566O669S4 | 5.12 | -0.728 | NA | NA | Streptokinase, is a sterile, purified preparation of a bacterial protein elaborated by group C (beta) -hemolytic streptococci. | For the treatment of acute evolving transmural myocardial infarction, pulmonary embolism, deep vein thrombosis, arterial thrombosis or emolism and occlusion of arteriovenous cannulae | Streptokinase creates an active complex which promotes the cleavage of the Arg/Val bond in plasminogen to form the proteolytic enzyme plasmin. Plasmin in turn degrades the fibrin matrix of the thrombus, thereby exerting its thrombolytic action. This helps eliminate blood clots or arterial blockages that cause myocardial infarction. | Plasminogen is an inactive molecule that becomes activated to plasmin when the Arg/Val bond is cleaved. Plasmin breaks down fibrin clots created by the blood clotting cascade. Streptokinase forms a highly specific 1:1 enzymatic complex with plasminogen which converts inactive plasminogen molecules into active plasmin. Plasmin degrades fibrin clots as well as fibrinogen and other plasma proteins. This in turn leads to the degradation of blood clots. | NA | NA | NA | NA | NA | Agents causing angioedema,Amino Acids, Peptides, and Proteins,Anticoagulants,Biological Factors,Blood and Blood Forming Organs,Blood Proteins,Cardiovascular Agents,Endopeptidases,Enzymes,Enzymes and Coenzymes,Fibrin Modulating Agents,Fibrinolytic Agents,Hematologic Agents,Hydrolases,Hypotensive Agents,Peptide Hydrolases,Plasminogen Activators,Proteins,Serine Endopeptidases,Serine Proteases,Streptokinase, antagonists & inhibitors | NA | NA | NA | Ticlopidine Increases bleeding risk. Monitor for signs of bleeding | Plasminogen,Proteinase-activated receptor 1 | Streptase | CSL Behring | CSL Behring | Indicated in Acute Evolving Transmural Myocardial Infarction, Pulmonary Embolism, Deep Vein Thrombosis, Arterial Thrombosis or Embolism, Occlusion of Arteriovenous Cannulae | NA | 25 mg cross-linked gelatin polypeptides, 25 mg sodium L-glutamate, sodium hydroxide to adjust pH, and 100 mg Albumin (Human) per vial or infusion bottle as stabilizers. The preparation contains no preservatives | It is Sterile, purified preparation formulated as lypholized powder | Intravenous and intracoronary administration. | In Acute Evolving Transmural Myocardial Infarction,dose for IV-In 1,500,000 IU and IC-In 140,000 IU. For Pulmonary Embolism, Deep Vein Thrombosis, Arterial Thrombosis or Embolism, IV-In: 250,000 IU/30 min | No Information Provided. | Severe internal bleeding involving gastrointestinal  (including hepaticbleeding), genitourinary, retroperitoneal, or intracerebral sites has occurred and has resulted in fatalities. Minor breathing difficulty to bronchospasm, periorbital swelling or angioneurotic edema have been observed rarely. Other milder allergic effects such as urticaria, itching, flushing, nausea, headache and musculoskeletal pain have also been observed, as have delayed hypersensitivity reactions such as vasculitis and interstitial nephritis, Respiratory depression, etc. | Link | NA | NA |
| 10440 | Th1077 | Urofollitropin | >Th1077_Urofollitropin APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 980.162 | C42H65N11O12S2 | 7.5 | -0.33 | 55 | Circulation half life of 3-4 hours, elimination half life of 35-40 hours | Urofollitropin is a purified form of follicle-stimulating hormone (FSH) that is manufactured by extraction from human urine and then purified. It consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Urofollitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Urofollitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). | For treatment of female infertility | Urofollitropin or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of urofollitropin is the primary hormone responsible for follicular recruitment and development. | FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells. | NA | NA | 0.74 | Time to peak in plasma: IM: 17 hours (single dose), 11 hours (multiple doses) SubQ: 21 hours (single dose), 10 hours (multiple doses) | NA | Fertility Agents | US5767067 | 16-Jun-1998 | 16-Jun-2015 | NA | Follicle-stimulating hormone receptor | BRAVELLE | Ferring Pharmaceuticals Inc. | Ferring Pharmaceuticals Inc. | BRAVELLE (urofollitropin for injection, purified) is a gonadotropin indicated for Induction of ovulation in women who have previously received pituitary suppression – intramuscular and subcutaneous administration, Development of multiple follicles as part of an Assisted Reproductive Technology (ART) cycle in ovulatory women who have previously received pituitary suppression | NA | Each vial of BRAVELLE contains 82.5 International Units (IU) of Follicle Stimulating Hormone (FSH) activity, 23 mg Lactose Monohydrate, 0.005 mg Polysorbate 20, and Sodium Phosphate buffer (Sodium Phosphate dibasic, Heptahydrate and Phosphoric acid) for pH adjustments, which, when reconstituted with diluent, will deliver 75 International Units of FSH. BRAVELLE contains up to 2% luteinizing hormone (LH) activity based on bioassay. Human Chorionic Gonadotropin(hCG) is not detected in BRAVELLE. When stored at 3° to 25, up to 40% of the α-subunits may be oxidized. | BRAVELLE is a sterile, lyophilized powder used after reconstitution with Sterile 0.9% Sodium Chloride Injection, USP | IntramuSubcutaneousular and Subcutaneous administr | Initial starting 150 International Units per day for 5 days, administered subcutaneously or intramuscularly in case of ovulation induction. In case of Assisted Reproductive Technology (ART) initial starting dose of the first cycle – 225 International Units per day for 5 days, administered subcutaneously. | RAVELLE is contraindicated in women who exhibits Prior hypersensitivity to BRAVELLE or urofollitropins, High levels of FSH indicating primary ovarian failure, Pregnancy, Presence of uncontrolled non-gonadal endocrinopathies, Sex hormone dependent tumors of the reproductive tract and accessory organ, Tumors of pituitary gland or hypothalamus, Abnormal uterine bleeding of undetermined origin, Ovarian cysts or enlargement of undetermined origin, not due to polycystic ovary syndrome. | The most common adverse reactions (≥5% incidence) in ovulation induction include: headache, hot flashes, OHSS, pain, and respiratory disorder. The most common adverse reactions (≥2% incidence) in ART include: abdominal cramps, abdominal fullness/enlargement, headache, nausea, OHSS, pain, pelvic pain, and post retrieval pain. | Link | NA | NA |
| 10441 | Th1077 | Urofollitropin | >Th1077_Urofollitropin APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 980.162 | C42H65N11O12S2 | 7.5 | -0.33 | 55 | Circulation half life of 3-4 hours, elimination half life of 35-40 hours | Urofollitropin is a purified form of follicle-stimulating hormone (FSH) that is manufactured by extraction from human urine and then purified. It consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Urofollitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Urofollitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). | For treatment of female infertility | Urofollitropin or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of urofollitropin is the primary hormone responsible for follicular recruitment and development. | FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells. | NA | NA | 0.74 | Time to peak in plasma: IM: 17 hours (single dose), 11 hours (multiple doses) SubQ: 21 hours (single dose), 10 hours (multiple doses) | NA | Fertility Agents | NA | NA | NA | NA | Follicle-stimulating hormone receptor | Metrodin | NA | NA | Metrodin (urofollitropin for injection) and hCG given in a sequential manner are indicated for the stimulation of follicular development and the induction ofovulation in patients with polycystic ovary syndrome, and infertility, who have failed to respond or conceive following adequate clomiphene citrate therapy. Metrodin (urofollitropin for injection) and hCG may also be used to stimulate the development of multiple follicles in ovulatory patients undergoing Assisted Reproductive Technologies (ART) such as in vitro fertilization. | NA | Each ampule of Metrodin (urofollitropin for injection) contains 75 or 150 IU of follicle-stimulating hormone (FSH) activity, in not more than 0.83 mg (75 IU) or 1.66 mg (150 IU) of extract, plus 10 mg lactose | Metrodin (urofollitropin for injection) is a sterile, lypholized powder form contains an acidic, water soluble glycoprotein biologically standardized for FSH gonadotropin activity | IntramuSubcutaneousular Injection. | Initial starting 75 International Units per day for 5 days administered intramuscularly in polycystic ovary syndrome. In ART the dose is 150 IU per day. | contraindicated in High levels of FSH indicating primary ovarian failure, Uncontrolled thyroid or adrenal dysfunction, An organic intracranial lesion such as a pituitary tumor, The presence of any cause of infertility other than anovulation, as stated in the Indications unless they are candidates for Assisted Reproductive Technologies, Abnormal bleeding of undetermined origin, Ovarian cysts or enlargement of undetermined origin, Prior hypersensitivity to urofollitropin. | Pulmonary and vascular complications, Ovarian Hyperstimulation Syndrome, Adnexal torsion, Mild to moderate ovarian enlargement, Abdominal pain, Ovarian cysts, nausea, vomiting, diarrhea, abdominal cramps, bloating, Pain, rash, swelling, and/or irritation at the site of injection, Ectopic pregnancy, Congenital abnormalities, dry skin, body rash, hair loss, hives, Headache. | Link | NA | NA |
| 10442 | Th1077 | Urofollitropin | >Th1077_Urofollitropin APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 980.162 | C42H65N11O12S2 | 7.5 | -0.33 | 55 | Circulation half life of 3-4 hours, elimination half life of 35-40 hours | Urofollitropin is a purified form of follicle-stimulating hormone (FSH) that is manufactured by extraction from human urine and then purified. It consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Urofollitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Urofollitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). | For treatment of female infertility | Urofollitropin or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of urofollitropin is the primary hormone responsible for follicular recruitment and development. | FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells. | NA | NA | 0.74 | Time to peak in plasma: IM: 17 hours (single dose), 11 hours (multiple doses) SubQ: 21 hours (single dose), 10 hours (multiple doses) | NA | Fertility Agents | NA | NA | NA | NA | Follicle-stimulating hormone receptor | Fertinex | NA | NA | FertinexTM (urofollitropin for injection, purified) and hCG given in a sequential manner are indicated for the stimulation of follicular recruitment and development and the induction of ovulation in patients with polycystic ovary syndrome and infertility, who have failed to respond or conceive following adequate clomiphene citrate therapy. Fertinex (urofollitropin) TM and hCG may also be used to stimulate the development of multiple follicles in ovulatory patients undergoing Assisted Reproductive Technologies (ART) such as in vitro fertilization. | NA | Each ampule of Fertinex (urofollitropin) TM contains either 75 IU or 150 IU of highly purified FSH and 10 mg lactose. If required, pH is adjusted with 0.1 M hydrochloric acid and/or 0.1 M sodium hydroxide. | Fertinex (urofollitropin) in asterile, lyophilized powder form contains an acidic, water soluble glycoprotein biologically standardized for FSH gonadotropin activity | Subcutaneous Injection. | Initial starting 75 International Units per day for 5 days administered intramuscularly in polycystic ovary syndrome. In ART the dose is 150 IU per day. | contraindicated in High levels of FSH indicating primary ovarian failure, Uncontrolled thyroid or adrenal dysfunction, An organic intracranial lesion such as a pituitary tumor, The presence of any cause of infertility other than anovulation, as stated in the Indications unless they are candidates for Assisted Reproductive Technologies, Abnormal bleeding of undetermined origin, Ovarian cysts or enlargement of undetermined origin, Prior hypersensitivity to urofollitropin. | Pulmonary and vascular complications, Ovarian Hyperstimulation Syndrome, Adnexal torsion, Mild to moderate ovarian enlargement, Abdominal pain, Ovarian cysts, nausea, vomiting, diarrhea, abdominal cramps, bloating, Pain, rash, swelling, and/or irritation at the site of injection, Ectopic pregnancy, Congenital abnormalities, dry skin, body rash, hair loss, hives, Headache. | Link | NA | NA |
| 10443 | Th1078 | Efalizumab | >Th1078_Efalizumab EVQLVESGGGLVQPGGSLRLSCAASGYSFTGHWMNWVRQAPGKGLEWVGIMIHPSDSETRYNQKFKDIRFTISVDKSKNTLYLQMNSLRAEDTAVYYCARIGIYFYGTTYFDYIWGQGTLVTVSS | 150000 | NA | NA | NA | 61 (FAB f | 5 days | Efalizumab is Humanized IgG1 kappa isotype monoclonal antibody that binds to human CD11a. It is produced in a Chinese hamster ovary mammalian cell expression system in a nutrient medium containing the antibiotic gentamicin. | Indcated in treatment of adult patients with moderate to severe chronic plaque psoriasis, who are candidates for phototherapy or systemic therapy. | In psoriatic skin, ICAM-1 cell surface expression is upregulated on endothelium and keratinocytes. Raptiva inhibits the binding of LFA-1 to the intercellular adhesion molecule-1 (ICAM-1), thereby inhibiting the adhesion of leukocytes to other cell types. | Efalizumab binds to CD11a, a subunit of leukocyte function antigen-1 (LFA-1), which is expressed on all leukocytes. As a result efalizumab decreases cell surface expression of CD11a. | NA | NA | Average efalizumab bioavailability following subcutaneous administration was estimated at 30 to 50%. | NA | NA | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antigens, CD11,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,CD11a-directed Antibody Interactions,CD11a-directed Humanized IgG1 Antibody,Cell Migration Inhibition,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Proteins,Selective Immunosuppressants,Serum Globulins | NA | NA | NA | Ergonovine is the antiretroviral agent may increase the ergot derivative | Integrin alpha-L,Integrin alpha-X | RAPTIVA | Genentech, Inc. | Genentech, Inc. | RAPTIVA (efalizumab) is indicated for the treatment of adult patients (18 years or older) with chronic moderate to severe plaque psoriasis who are candidates for systemic therapy or phototherapy. | NA | Each single-use vial of RAPTIVA contains 150 mg of efalizumab, 123.2 mg of sucrose, 6.8 mg of L-histidine hydrochloride monohydrate, 4.3 mg of L-histidine and 3 mg of polysorbate 20 and is designed to deliver 125 mg of efalizumab in 1.25 mL. | RAPTIVA (efalizumab) is supplied as a sterile, white to off-white, lyophilized powder in single-use glass vials | Subcutaneous (Subcutaneous) Injection. | The recommended dose of RAPTIVA (efalizumab) is a single 0.7 mg/kg SCconditioning dose followed by weekly SC doses of 1 mg/kg (maximum single dose not to exceed a total of 200 mg). | RAPTIVA (efalizumab) should not be administered to patients with known hypersensitivity to RAPTIVA (efalizumab) or any of its components. | he most serious adverse reactions observed during treatment with RAPTIVA (efalizumab) are serious infections, including PML, malignancies,thrombocytopenia, hemolytic anemia, arthritis events, psoriasis worsening and variants, and neurologic events. The most common adverse reactions associated with RAPTIVA (efalizumab) were a first dose reaction complex that included headache, chills, fever, nausea, and myalgia. | Link | NA | NA |
| 10469 | Th1083 | Coagulation factor ix | >Th1083_Coagulation_factor_ix YNSGKLEEFVQGNLERECMEEKCSFEEAREVFENTERTTEFWKQYVDGDQCESNPCLNGGSCKDDINSYECWCPFGFEGKNCELDVTCNIKNGRCEQFCKNSADNKVVCSCTEGYRLAENQKSCEPAVPFPCGRVSVSQTSKLTRAEAVFPDVDYVNSTEAETILDNITQSTQSFNDFTRVVGGEDAKPGQFPWQVVLNGKVDAFCGGSIVNEKWIVTAAHCVETGVKITVVAGEHNIEETEHTEQKRNVIRIIPHHNYNAAINKYNHDIALLELDEPLVLNSYVTPICIADKEYTNIFLKFGSGYVSGWGRVFHKGRSALVLQYLRVPLVDRATCLRSTKFTIYNNMFCAGFHEGGRDSCQGDSGGPHVTEVEGTSFLTGIISWGEECAMKGKYGIYTKVSRYVNWIKEKTKLT | 46548.2 | C2041H3136N558O641S25 | 5.2 | -0.431 | 54 | 18.8 ± 5.4 hr | Coagulation Factor IX (Recombinant) is a glycoprotein with an approximate molecular mass of 55,000 Da consisting of single chain of 415 amino acids. Sequence is identical to the A148 allelic form of plasma-derived factor IX. | For treatment of hemophilia (Christmas disease). | Binds vitamin K and factor VIIIa. Cleaves the Arg-Ile bond in factor X to form active factor Xa. Plays a key role in blood coagulation and clotting. Injections of factor IX are used to treat hemophilia B, which is sometimes called Christmas disease. AlphaNine is injected to increase plasma levels of Factor IX and can temporarily correct this coagulation defect. | Coagulation Factor IX is an important protein in the process of hemostasis and normal blood clotting. Factor IX is plays an important intermediate role in the blood coagulation cascade. It is located within the blood plasma as a zymogen, an antecedent to enzymatic function, in its inactivated state. Factor IX is dependent on the presence of Vitamin K, and is activated to a serine protease by the function of Coagulation Factor XIa. Factor XIa cleaves the peptide bond associated with protein activation in Factor IX, leaving Factor IX with two exposed chains, a light chain and a heavy chain. These two chains are held together by several disulfide bonds that reinforce the structure of Factor IX's activated form. After being activated, Factor IX forms a complex with calcium ions, membrane phospholipids and Coagulation Factor VIII to activate Coagulation Factor X. The activation of Factor X then performs a similarly integral step in the blood coagulation cascade. The ultimate result of phenotypically normal coagulation factors is the creation of platelets for normal blood clotting. | NA | NA | NA | NA | 8.62 ± 1.7. | Coagulants and Thrombotic Agents | NA | NA | NA | NA | NA | Alprolix | Biogen Idec Inc., and Genentech USA, Inc | Biogen Idec Inc., and Genentech USA, Inc | adults and children with hemophilia B (congenital Factor IX deficiency) for: Control and prevention of bleeding episodes, Perioperative management, Routine prophylaxis to prevent or reduce the frequency of bleeding episodes | Coagulation Factor IX (Recombinant), Fc Fusion Protein, is a recombinant DNA derived | After reconstitution, the solution has a clear to slightly opalescent appearance and contains the excipients: sucrose, mannitol, sodium chloride, L-histidine and polysorbate 20. ALPROLIX is available in single-use vials containing the labeled amount of Factor IX activity, expressed in international units. Each vial contains nominally 500 IU, 1000 IU, 2000 IU or 3000 IU. | ALPROLIX is a Sterile, non-pyrogenic, preservative-free, white to off-white, lyophilized powder to cake for reconstitution with the provided diluent, for Intravenous infusion | Intravenous | 30-100 IU/dL depending on intensity of bleeding | ALPROLIX is not indicated for induction of immune tolerance in patients with hemophilia B . ALPROLIX may increase the risk of formation of abnormal blood clots in your body, especially if you have risk factors for developing clots/ | hives; difficulty breathing; swelling of your face, lips, tongue, or throat. | Link | NA | NA |
| 10471 | Th1085 | Agalsidase beta | >Th1085_Agalsidase_beta LDNGLARTPTMGWLHWERFMCNLDCQEEPDSCISEKLFMEMAELMVSEGWKDAGYEYLCIDDCWMAPQRDSEGRLQADPQRFPHGIRQLANYVHSKGLKLGIYADVGNKTCAGFPGSFGYYDIDAQTFADWGVDLLKFDGCYCDSLENLADGYKHMSLALNRTGRSIVYSCEWPLYMWPFQKPNYTEIRQYCNHWRNFADIDDSWKSIKSILDWTSFNQERIVDVAGPGGWNDPDMLVIGNFGLSWNQQVTQMALWAIMAAPLFMSNDLRHISPQAKALLQDKDVIAINQDPLGKQGYQLRQGDNFEVWERPLSGLAWAVAMINRQEIGGPRSYTIAVASLGKGVACNPACFITQLLPVKRKLGFYEWTSRLRSHINPTGTVLLQLENTMQMSLKDLL | 45351.6 | C2029H3080N544O587S27 | 5.17 | -0.307 | NA | 67 ± 12 min for a 1 mg/kg dose (mean infusion length = 115 minutes.) | Recombinant human alpha-galactosidase-A produced in CHO cells. The mature protein comprises 2 subunits of 398 residues. | For treatment of Fabry's disease (alpha-galactosidase A deficiency) | Used in the treatment of Fabry disease, an X-linked genetic disorder of glycosphingolipid metabolism. The disease is characterized by a deficiency of the lysosomal enzyme alpha-galactosidase A, which leads to progressive accumulation of glycosphingolipids, predominantly GL-3, in many body tissues. Clinical manifestations of Fabry disease include renal failure, cardiomyopathy, and cerebrovascular accidents. Fabrazyme is intended to provide an exogenous source of alpha-galactosidase A and to limit the accumulation of these glycolipids in the tissues. Studies show unconclusive evidence for the clinical efficacy of either agalasidase alfa or agalasidase beta in preventing morbidity. | Alpha-galactosidase A catalyzes the hydrolysis of globotriaosylceramide (GL-3) and other a-galactyl-terminated neutral glycosphingolipids, such as galabiosylceramide and blood group B substances to ceramide dihexoside and galactose. | Data regarding overdoses of agalsidase beta are not readily available.6 Patients experiencing an overdose of agalsidase beta may experience an increased incidence and severity of adverse effects.6 Overdose can be managed through the use of symptomatic and supportive measures. | Data regarding the metabolism of agalsidase beta is not readily available.6 However, protein drugs are expected to be degraded by proteases and other catalytic enzymes to smaller peptides and amino acids. | A 1 mg/kg dose of agalsidase beta with a mean infusion length of 115 minutes reaches a Cmax 5.0 ± 1.1 µg/mL with an AUC of 496 ± 137 µg*min/mL | A 1 mg/kg dose of agalsidase beta with a mean infusion length of 115 minutes has a VSS of 112 ± 13 mL/kg | A 1 mg/kg dose of agalsidase beta with a mean infusion length of 115 minutes has a clearance of 2.1 ± 0.7 mL/min/kg | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Enzymes,Enzymes and Coenzymes,Galactosidases,Glycoside Hydrolases,Hydrolases,Hydrolytic Lysosomal Neutral Glycosphingolipid-specific Enzyme,Protein Isoforms,Proteins | CA2265464 | 26-Jun-2007 | 12-Sep-2017 | NA | Globotriaosylceramide | Fabrazyme | Genzyme Corp | Genzyme Corp | Routine prophylaxis to prevent or reduce the frequency of bleeding episodes. | NA | Each 5 mg vial contains 5.5 mg of agalsidase beta as well as 33.0 mg mannitol, 3.0 mg sodium phosphate monobasic monohydrate, and 8.8 mg sodium phosphate dibasic heptahydrate. Following reconstitution as directed, 5 mg of agalsidase beta (1 mL) may be extracted from each 5 mg vial. | Sterile, nonpyrogenic, white to off-white, lyophilized cake or powder for reconstitution with Sterile Water for Injection, uSp. Each 35 mg vial contains 37 mg of agalsidase beta as well as 222 mg mannitol, 20.4 mg sodium phosphate monobasic monohydrate, and 59.2 mg sodium phosphate dibasic heptahydr | NA | NA | This is not a complete list of possible side effects. If you notice other effects not listed above, contact your doctor or pharmacist. | difficulty breathing; closing of the throat; hives; rash; itching; fever; shaking; chest tightness; high or low blood pressure; fast heartbeats; muscle pain; stomach pain; nausea or vomiting; dizziness; numbness or tingling; and headache have occurred upon injection of agalsidase beta in many patients. Most patients treated with agalsidase beta develop antibodies to agalsidase beta and many will develop symptoms of an infusion reaction. A slow rate of injection of the medication and pretreatment with other medications may decrease. | Link | NA | NA |
| 10472 | Th1086 | Interferon alfa-2b | >Th1086_Interferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMNEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE | 19271 | C860H1353N229O255S9 | 5.99 | -0.339 | 61 | The elimination half-life following both intramuscular and subcutaneous injections was approximately 2 to 3 hours | Recombinant type-I Interferon alpha 2b (human leukocyte clone hif-sn 206 protein moiety reduced), composed of 165 amino acid residues with R at position 23. It resembles leukocyte secreted interferon. Widely used as an antiviral or antineoplastic agent. | For the treatment of hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma. | Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. | Interferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which upon dimerization activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. | There is limited experience with overdosage. Postmarketing surveillance includes reports of patients receiving a single dose as great as 10 times the recommended dose. In general, the primary effects of an overdose are consistent with the effects seen with therapeutic doses of interferon alfa-2b. Hepatic enzyme abnormalities, renal failure, hemorrhage, and myocardial infarction have been reported with single administration overdoses and/or with longer durations of treatment than prescribed. Toxic effects after ingestion of interferon alfa-2b are not expected because interferons are poorly absorbed orally. | NA | Absorption is high (greater than 80%) when administered intramuscularly or subcutaneously. | NA | NA | Immunosuppressive Agents | CA1341567 | 19-Feb-2008 | 19-Feb-2025 | NA | Interferon alpha/beta receptor 2,Interferon alpha/beta receptor 1 | INTRON A | Merck | Merck | Hairy Cell Leukemia, Malignant Melanoma, Follicular Lymphoma, Condylomata Acuminata, AIDS-Related Kaposi's Sarcoma, Chronic Hepatitis C, Chronic Hepatitis B, | NA | INTRON A Powder for Injection, 10 million IU per vial and Diluent for INTRON A (Sterile Water for Injection USP) 1 mL per vial, INTRON A Solution for Injection, 18 million IU multidose vial (22.8 million IU per 3.8 mL per vial); boxes containing 1 vial of INTRON A Solution for Injection | Powder or solution | IntramuSubcutaneousular, Subcutaneous, Intralesion | Not all dosage forms and strengths are appropriate for some indications. To enhance the tolerability of INTRON A, injections should be administered in the evening when possible; To reduce the incidence of certain adverse reactions, acetaminophen may be administered at the time of injection;The solution should be allowed to come to room temperature before using. | Alpha interferons, including INTRON A, cause or aggravate fatal or life-threatening neuropsychiatric, autoimmune, ischemic, and infectious disorders. Patients should be monitored closely with periodic clinical and laboratory evaluations. Patients with persistently severe or worsening signs or symptoms of these conditions should be withdrawn from therapy. In many but not all cases these disorders resolve after stopping INTRON A therapy. | most frequently reported adverse reactions were “flu-like†symptoms, particularly fever, headache, chills, myalgia, and fatigue. More severe toxicities are observed generally at higher doses and may be difficult for patients to tolerate. | Link | NA | NA |
| 10478 | Th1088 | Enfuvirtide | >Th1088_Enfuvirtide YTSLIHSLIEESQNQQEKNEQELLELDKWASLWNWF | 4491.876 | C204H301N51O64 | 4.3 | -0.875 | NA | 3.8 ± 0.6 hrs | 36 residue, synthetically prepared peptide with N-terminal acetylation and C-terminal amidation. It blocks the fusion of HIV-1 with CD4 cells. | Enfuvirtide is an antiretroviral drug used in combination therapy for the treatment of HIV-1/AIDS. | NA | Enfuvirtide binds to the first heptad-repeat (HR1) in the gp41 subunit of the viral envelope glycoprotein and prevents the conformational changes required for the fusion of viral and cellular membranes. It works by disrupting the HIV-1 molecular machinery at the final stage of fusion with the target cell, preventing uninfected cells from becoming infected. Enfuvirtide is a biomimetic peptide that was rationally designed to mimic components of the HIV-1 fusion machinery and displace them, preventing normal fusion. | NA | Expected to undergo catabolism to its constituent amino acids, with subsequent recycling of the amino acids in the body pool. | After a 90 mg single subcutaneous injection of Enfuvirtide into the abdomen in 12 HIV-1 infected subjects, the mean peak concentration is 4.59±1.5 ug/ml and the median time to peak concentration was 8 hours (ranged from 3 to12 hours). | 5.5 ± 1.1 L | 24.8 +/- 4.1 mL/h/kg [HIV-1 infected adult and pediatric subjects following a 90-mg single SC dose of enfuvirtide] 30.6 +/- 10.6 mL/h/kg [Following 90-mg twice daily dosing of FUZEON SC in combination with other antiretroviral agents in HIV-1 infected subjects] 40 +/- 17 mL/h/kg [pediatric patients in the presence of concomitant medications including antiretroviral agents receiving the 2 mg/kg twice daily dose] | Amino Acids, Peptides, and Proteins,Anti-HIV Agents,Anti-Infective Agents,Anti-Retroviral Agents,Antigens,Antigens, Viral,Antiinfectives for Systemic Use,Antiviral Agents,Antivirals for Systemic Use,Biological Factors,Cytochrome P-450 CYP2C19 Substrates,Cytochrome P-450 CYP2E1 Substrates,Cytochrome P-450 Substrates,Direct Acting Antivirals,env Gene Products, Human Immunodeficiency Virus,Fusion Protein Inhibitors,Gene Products, env,HIV Antigens,HIV Envelope Protein gp41,HIV Fusion Inhibitors,Human Immunodeficiency Virus 1 Fusion Inhibitor,Human Immunodeficiency Virus Proteins,Membrane Fusion Proteins,Membrane Proteins,Peptide Fragments,Peptides,Polyproteins,Proteins,Retroviridae Proteins,Viral Envelope Proteins,Viral Fusion Protein Inhibitors,Viral Fusion Proteins,Viral Proteins,Viral Structural Proteins | US6475491 | 5-Nov-2002 | 7-Jun-2015 | NA | Envelope glycoprotein | FUZEON | Trimeris, Roche | Trimeris, Roche | FUZEON in combination with other antiretroviral agents is indicated for the treatment of HIV-1 infection in treatment experienced patients with evidence of HIV-1 replication despite ongoing antiretroviral therapy. | NA | Each single-use vial contains 108 mg of enfuvirtide for the delivery of 90 mg. Prior to subcutaneous administration, the contents of the vial are reconstituted with 1.1 mL of Sterile Water for Injection giving a volume of approximately 1.2 mL to provide the delivery of 1 mL of the solution. Each 1 mL of the reconstituted solution contains approximately 90 mg of enfuvirtide with approximate amounts of the following excipients: 22.55 mg of mannitol, 2.39 mg of sodium carbonate (anhydrous), and sodium hydroxide and hydrochloric acid for pH adjustment as needed. The reconstituted solution has an approximate pH of 9.0 | White to off-white, sterile, lyophilized powder. Each single-use vial contains 108 mg of enfuvirtide for the delivery of 90 mg. Prior to subcutaneous administration, the contents of the vial are reconstituted with 1.1 mL of Sterile Water for Injection giving a volume of approximately 1.2 mL to provi | Subcutaneous | 90 mg (1 mL) twice daily injected subcutaneously into the upper arm, anterior thigh or abdomen. Each injection should be given at a site different from the preceding injection site, and only where there is no current injection site reaction from an earlier dose. | FUZEON is contraindicated in patients with known hypersensitivity to FUZEON or any of its components | fever, chills, chest congestion, cough with yellow or green mucus, stabbing chest pain, wheezing, feeling short of breath; signs of a new infection such as sore throat, flu symptoms, swollen glands, easy bruising or bleeding. | Link | NA | NA |
| 10503 | Th1097 | Alglucosidase alfa | >Th1097_Alglucosidase_alfa AHPGRPRAVPTQCDVPPNSRFDCAPDKAITQEQCEARGCCYIPAKQGLQGAQMGQPWCFFPPSYPSYKLENLSSSEMGYTATLTRTTPTFFPKDILTLRLDVMMETENRLHFTIKDPANRRYEVPLETPHVHSRAPSPLYSVEFSEEPFGVIVRRQLDGRVLLNTTVAPLFFADQFLQLSTSLPSQYITGLAEHLSPLMLSTSWTRITLWNRDLAPTPGANLYGSHPFYLALEDGGSAHGVFLLNSNAMDVVLQPSPALSWRSTGGILDVYIFLGPEPKSVVQQYLDVVGYPFMPPYWGLGFHLCRWGYSSTAITRQVVENMTRAHFPLDVQWNDLDYMDSRRDFTFNKDGFRDFPAMVQELHQGGRRYMMIVDPAISSSGPAGSYRPYDEGLRRGVFITNETGQPLIGKVWPGSTAFPDFTNPTALAWWEDMVAEFHDQVPFDGMWIDMNEPSNFIRGSEDGCPNNELENPPYVPGVVGGTLQAATICASSHQFLSTHYNLHNLYGLTEAIASHRALVKARGTRPFVISRSTFAGHGRYAGHWTGDVWSSWEQLASSVPEILQFNLLGVPLVGADVCGFLGNTSEELCVRWTQLGAFYPFMRNHNSLLSLPQEPYSFSEPAQQAMRKALTLRYALLPHLYTLFHQAHVAGETVARPLFLEFPKDSSTWTVDHQLLWGEALLITPVLQAGKAEVTGYFPLGTWYDLQTVPVEALGSLPPPPAAPREPAIHSEGQWVTLPAPLDTINVHLRAGYIIPLQGPGLTTTESRQQPMALAVALTKGGEARGELFWDDGESLEVLERGAYTQVIFLARNNTIVNELVRVTSEGAGLQLQKVTVLGVATAPQQVLSNGVPVSNFTYSPDTKVLDICVSLLMGEQFLVSWC | 105270.8 | C4435H6739N1175O1279S32 | NA | NA | NA | 2.3 ± 0.4 hours. | Recombinant (CHO cell derived) form of the human lysosomal enzyme, acid alpha-glucosidase (GAA), which is essential for the degradation of glygogen to glucose. It hydrolyses the alfa-1,4- and alfa-1,6- glycosidic linkages of lysosomal glycogen. The mature polypeptide is 883 residue long with a mass of 98,008 daltons and a total mass of approximately 109,000 daltons of the full-length glycosylated protein | For the treatment of Pompe disease (GAA deficiency) in infants and pediatric patients. | Pompe disease (glycogen storage disease type II, GSD II, glycogenosis type II, acid maltase deficiency) is an inherited disorder of glycogen metabolism caused by the absence or marked deficiency of the lysosomal enzyme GAA. In the infantile-onset form, Pompe disease results in intralysosomal accumulation of glycogen in various tissues, particularly cardiac and skeletal muscles, and hepatic tissues, leading to the development of cardiomyopathy, progressive muscle weakness, and impairment of respiratory function. In the juvenile- and adult-onset forms, intralysosomal accumulation of glycogen is limited primarily to skeletal muscle, resulting in progressive muscle weakness. Death in all forms is usually related to respiratory failure. Alglucosidase alfa provides an exogenous source of GAA. Binding to mannose-6-phosphate receptors on the cell surface has been shown to occur via carbohydrate groups on the GAA molecule, after which it is internalized and transported into lysosomes, where it undergoes proteolytic cleavage that results in increased enzymatic activity. It then exerts enzymatic activity in cleaving glycogen. | Alglucosidase alfa is designed to act as an exogenous source of GAA, acting to correct GAA deficiency that is the hallmark of Pompe disease. Alglucosidase alfa binds to mannose-6-phosphate receptors on the cell surface via carbohydrate groups on the GAA molecule, after which it is internalized and transported into lysosomes, where it undergoes proteolytic cleavage that results in increased enzymatic activity. It then exerts enzymatic activity in cleaving glycogen. Specifically, it hydrolyses alpha-1,4-glucose bonds. | There have been no reports of overdose with alglucosidase alfa. | NA | NA | 96 ± 16 mL/kg [20 mg/kg dose] 119 ± 28 mL/kg [40 mg/kg dose] | 25+/- 4 mL/hr/kg [4-hour IV infusion of 20 mg/kg] | Alimentary Tract and Metabolism,alpha-Glucosidases,Enzymes,Enzymes and Coenzymes,Glucosidases,Glycogen Storage Disease Type II,Glycoside Hydrolases,Hydrolases,Hydrolytic Lysosomal Glycogen-specific Enzyme | CA2416492 | 29-Apr-2008 | 10-Jul-2021 | NA | Cation-dependent mannose-6-phosphate receptor,Glycogen | LUMIZYME | Genzyme | Genzyme | LUMIZYME (alglucosidase alfa) [see DESCRIPTION] is a hydrolytic lysosomal glycogen-specific enzyme indicated for patients with Pompe disease (acid α-glucosidase (GAA) deficiency). | NA | Each 50 mg vial contains 52.5 mg alglucosidase alfa, 210 mg mannitol, 0.5 mg polysorbate 80, 9.9 mg sodium phosphate dibasic heptahydrate, 31.2 mg sodium phosphate monobasic monohydrate. Following reconstitution as directed, each vial contains 10.5 mL reconstituted solution and a total extractable volume of 10 mL at 5 mg/mL alglucosidase alfa. Alglucosidase alfa does not contain preservatives; each vial is for single use only. | Sterile, nonpyrogenic, white to off-white, lyophilized cake or powder for reconstitution with 10.3 Ml Sterile Water for Injection, USP | Intravenous infusion | The recommended dosage of alglucosidase alfa is 20 mg/kg body weight administered every 2 weeks as an Intravenous infusion. | NA | In clinical trials, the most common adverse reactions ( ≥ 5%) following alglucosidase alfa treatment were hypersensitivity reactions, and included anaphylaxis, rash, pyrexia, flushing/feeling hot, urticaria, headache, hyperhidrosis, nausea, cough, decreased oxygen saturation, tachycardia, tachypnea, chest discomfort, dizziness, muscle twitching, agitation, cyanosis, erythema, hypertension/increased blood pressure, pallor, rigors, tremor, vomiting, fatigue, and myalgia. | Link | NA | NA |
| 10506 | Th1098 | Exenatide | >Th1098_Exenatide HGEGTFTSDLSKQMEEEAVRLFIEWLKNGGPSSGAPPPS | 4186.6 | C184H282N50O60S | 4.86 | NA | NA | Mean terminal half-life is 2.4 hours. | Derived from a compound found in the saliva of the Gila monster, a large lizard native to the southwestern United States. It is a functional analog of Glucagon-Like Peptide-1 (GLP-1) peptide. | Indicated as adjunctive therapy to improve glycemic control in patients with Type 2 diabetes mellitus who are taking metformin, a sulfonylurea, or a combination of both, but have not achieved adequate glycemic control. | Exenatide is an incretin mimetic, which has glucoregulatory effects. While it is has blood-sugar lowering actions alone, it can also be combined with other medications such as pioglitazone, metformin, sulfonylureas, and/or insulin to improve glucose control. The approved use of exenatide is with either sulfonylureas, metformin and thiazolinediones. The medication is injected twice per day using a pre-filled pen device. Typical human responses to exenatide plus eating include improvements in the initial rapid release of endogenous insulin, suppression of glucagon release by the pancreas, regulation of gastric empyting and reduced appetite; all behaviors more typical of individuals without blood sugar control problems. Exenatide is self-regulating in that in lowers blood sugar when levels are elevated but does not continue to lower blood sugar when levels return to normal, unlike with sulfonylureas or insulins. | Exenatide is a functional analog of the human incretin Glucagon-Like Peptide-1 (GLP-1). Incretins enhance glucose-dependent insulin secretion and exhibit other antihyperglycemic actions following their release into the circulation from the gut. The GLP-1 system increases insulin secretion only in the presence of elevated plasma glucose levels, avoiding inappropriately high insulin levels during fasting. The drug also moderates peak serum glucagon levels during hyperglycemic periods following meals, but does not interfere with glucagon release in response to hypoglycemia. Secondary effects of drug administration reduces the rate of gastric emptying and decreases food intake, mitigating the potential severity of hyperglycemic events after meals. | In animal studies, exenatide was associated with fetal deformities of ribs and vertebrae as well as slowed growthLabel. In humans, uncontrolled hyperglycemia can be associated with an up to 25% risk of miscarriageLabel. No human studies in pregnancy have been performed with exenatide and so exenatide should only be prescribed in pregnancy if the benefit to the mother and fetus outweigh the risksLabel. In mice, exenatide is excreted in the milk at a concentration 2.5% of the plasma concentration though this data may not be applicable to humansLabel. The effect of exenatide on breastfed infants is also unknown and so the risk and benefit of breastfeeding while taking exenatide must be weighedLabel. There is no data for the use of exenatide in pediatric patientsLabel. Geriatric patients do not have different results for safety and efficacy of exenatide though caution should still be used in this group as they are at higher risk of renal impairment or other comorbidities that may affect the liklihood of adverse effectsLabel. No dosage adjustments are necessary for patients with creatinine clearance ≥50mL/min, though prescribing to patients with creatinine clearance 30-50mL/min should be done cautiouslyLabel. Exenatide is not recommended for patients with creatinine clearance <30mL/minLabel. Hepatic impairment is not expected to affect clearance of exenatide though no studies have been performed to confirm thisLabel. | Exenatide is filtered through the glomerulus before being degraded to smaller peptides and amino acids by dipeptidyl peptidase-4, metalloproteases, endopeptidase 24-11, amino proteases, and serine proteases. It is currently believed that the metalloproteases are responsible for most of the degradation of exenatide3. Exenatide is metabolised to small peptides <3 amino acids in length by enzymes in the kidney | Exenatide reaches a peak plasma concentration in 2.1 hoursLabel. Because exenatide is administerd subcutaneously, the bioavailability is 1 | 28.3 L | Apparent cl=9.1 L/hr | Hypoglycemic Agents | US5424286 | 13-Jun-1995 | 1-Dec-2016 | NA | Glucagon-like peptide 1 receptor | BYDUREON | Amylin Pharmaceuticals | Amylin Pharmaceuticals | BYDUREON is an extended-release formulation of exenatide, administered as an injection once every 7 days (weekly). BYDUREON is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus | NA | Exenatide is incorporated in an extended-release microsphere formulation containing the 50:50 poly(D,L-lactide-co-glycolide) polymer (37.2 mg per dose) along with sucrose (0.8 mg per dose). The powder must be suspended in the diluent prior to injection. The diluent for the BYDUREON vial is supplied in a prefilled syringe within each single-dose tray. The diluent for the BYDUREON Pen is contained within each single-dose pen. Each configuration contains sufficient diluent to deliver 0.65 mL. The diluent is a clear, colorless to pale-yellow solution composed of carboxymethylcellulose sodium (19 mg), polysorbate 20 (0.63 mg), sodium phosphate monobasic monohydrate (0.61 mg), sodium phosphate dibasic heptahydrate (0.51 mg), sodium chloride (4.1 mg), and water for injection. Sodium hydroxide may be added during manufacture of BYDUREON Pen for pH adjustment. | White to off-white powder that is available in a dosage strength of 2 mg exenatide per vial or per pen | NA | BYDUREON (2 mg per dose) should be administered once every 7 days (weekly). The dose can be administered at any time of day, with or without meals. | BYDUREON is not recommended as first-line therapy for patients who have inadequate glycemic control on diet and exercise. BYDUREON is not a substitute for insulin. BYDUREON should not be used in patients with type 1 diabetes or for the treatment of diabetic ketoacidosis, as it would not be effective in these settings. BYDUREON and BYETTA (exenatide) injection both contain the same active ingredient, exenatide, and therefore should not be used together. BYDUREON has not been studied in patients with a history of pancreatitis. It is unknown whether patients with a history of pancreatitis are at increased risk for pancreatitis while using BYDUREON. Other antidiabetic therapies should be considered in patients with a history of pancreatitis. | Possible thyroid tumors, including cancer, Allergic reaction Pancreatitis, Hypoglycemia | Link | NA | NA |
| 10522 | Th1102 | Abatacept | >Th1102_Abatacept MHVAQPAVVLASSRGIASFVCEYASPGKATEVRVTVLRQADSQVTEVCAATYMMGNELTFLDDSICTGTSSGNQVNLTIQGLRAMDTGLYICKVELMYPPPYYLGIGNGTQIYVIDPEPCPDSDQEPKSSDKTHTSPPSPAPELLGGSSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 92300 | C3498H5458N922O1090S32 | NA | NA | NA | 16.7 (12-23) days in healthy subjects | Recombinant (CHO cell derived), soluble fusion protein that links the extracellular domain of human cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), to the modified Fc (hinge, CH2, and CH3 domains) portion of human IgG1. Abatacept is a glycosylated fusion protein with molecular weight of 92,300 Da and it is a homodimer of two polypeptide chains of 357 amino acids. The drug has activity as a selective co-stimulation modulator with inhibitory activity on T lymphocytes. | For the management of the signs and symptoms of moderate-to-severe active rheumatoid arthritis, inducing major clinical response, slowing the progression of structural damage, and improving physical function in adult patients. It is indicated both as a monotherapy and for use in combination with a continued regimen of DMARDs (not including TNF antagonists). Also used for the management of the signs and symptoms of moderately to severely active polyarticular juvenile idiopathic arthritis in children. | Abatacept is the first in a new class of drugs known as Selective Co-stimulation Modulators. Known as a recombinant fusion protein, the drug consists of the extracellular domain of human cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) linked to a modified Fc portion of human immunoglobulin G1 (IgG1. The Fc portion of the drug consists of the hinge region, the CH2 domain, and the CH3 domain of IgG1. Although there are multiple pathways and cell types involved in the pathogenesis of rheumatoid arthritis, evidence suggests that T-cell activation may play an important role in the immunopathology of the disease. Ordinarily, full T-cell activation requires binding of the T-cell receptor to an antigen-MHC complex on the antigen-presenting cell as well as a co-stimulatory signal provided by the binding of the CD28 protein on the surface of the T-cell with the CD80/86 proteins on the surface of the antigen-presenting cell. CTLA4 is a naturally occurring protein which is expressed on the surface of T-cells some hours or days after full T-cell activation and is capable of binding to CD80/86 on antigen-presenting cells with much greater affinity than CD28. Binding of CTLA4-Ig to CD80/86 provides a negative feedback mechanism which results in T-cell deactivation. Abatacept was developed by Bristol-Myers-Squibb and is licensed in the US for the treatment of Rheumatoid Arthritis in the case of inadequate response to anti-TNF-alpha therapy. | Abatacept is a selective costimulation modulator, like CTLA-4, the drug has shown to inhibit T-cell (T lymphocyte) activation by binding to CD80 and CD86, thereby blocking interaction with CD28. Blockade of this interaction has been shown to inhibit the delivery of the second co-stimulatory signal required for optimal activation of T-cells. This results in the inhibition of autoimmune T-Cell activation that has been implcated in the pathogenesis of rheumatoid arthritis. | Most common adverse events (≥10%) are headache, upper respiratory tract infection, nasopharyngitis, and nausea. Doses up to 50 mg/kg have been administered without apparent toxic effect. | NA | When a single 10 mg/kg Intravenous infusion of abatacept is administered in healthy subjects, the peak plasma concentration (Cmax) was 292 mcg/mL. When multiple doses of 10 mg/kg was given to rheumatoid arthritis (RA) patients, the Cmax was 295 mcg/mL. The bioavailability of abatacept following subcutaneous administration relative to intravenous administration is 78.6%. | 0.07 L/kg [RA Patients, IV administration] 0.09 L/kg [Healthy Subjects, IV administration] 0.11 L/kg [RA patients, subcutaneous administration] | 0.23 mL/h/kg [Healthy Subjects after 10 mg/kg Intravenous infusion 0.22 mL/h/kg [RA Patients after multiple 10 mg/kg Intravenous infusions] 0.4 mL/h/kg [juvenile idiopathic arthritis patients].The mean systemic clearance is 0.28 mL/h/kg when a subcutaneously administered to adult RA patients.The clearance of abatacept increases with increasing body weight. | Antirheumatic Agents and Immunosuppressive Agents | CA2110518 | 22-May-2007 | 16-Jun-2012 | NA | T-lymphocyte activation antigen CD80,T-lymphocyte activation antigen CD86 | ORENCIA | Bristol-Myers Squibb | Bristol-Myers Squibb | Adult Rheumatoid Arthritis (RA): ORENCIA is indicated for reducing signs and symptoms, inducing major clinical response, inhibiting the progression of structural damage, and improving physical function in adult patients with moderately to severely active rheumatoid arthritis. ORENCIA may be used as monotherapy or concomitantly with disease-modifying antirheumatic drugs (DMARDs) other than tumor necrosis factor (TNF) antagonists.; Juvenile Idiopathic Arthritis: ORENCIA is indicated for reducing signs and symptoms in pediatric patients 6 years of age and older with moderately to severely active polyarticular juvenile idiopathic arthritis. ORENCIA may be used as monotherapy or concomitantly with methotrexate | NA | Following reconstitution of the lyophilized powder with 10 mL of Sterile Water for Injection, USP, the solution of ORENCIA is clear, colorless to pale yellow, with a pH range of 7.2 to 7.8. Each single-use vial of ORENCIA provides 250 mg abatacept, maltose (500 mg), monobasic sodium phosphate (17.2 mg), and sodium chloride (14.6 mg) for administration. | Lyophilized powder for Intravenous infusion is supplied as a Sterile, white, preservative-free, lyophilized powder for intravenous administration | Intravenous infusion, Subcutaneous Injection | Adult Rheumatoid Arthritis, For adult patients with RA, ORENCIA may be administered as an Intravenous infusion or a subcutaneous injection. ORENCIA may be used as monotherapy or concomitantly with DMARDs other than TNF antagonists. For pediatric juvenile idiopathic arthritis, a dose calculated based on each patient's body weight is used. Intravenous Dosing Regimen; ORENCIA intravenous should be administered as a 30-minute Intravenous infusion utilizing the weight range-based dosing specified in Table 1. Following the initial intravenous administration, an Intravenous infusion should be given at 2 and 4 weeks after the first infusion and every 4 weeks thereafter. | NA | The most serious adverse reactions were serious infections and malignancies. The most commonly reported adverse events (occurring in ≥ 10% of patients treated with ORENCIA) were headache, upper respiratory tract infection, nasopharyngitis, and nausea. | Link | NA | NA |
| 10565 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | ILARIS | Novartis Pharmaceuticals | Novartis Pharmaceuticals | Cryopyrin-Associated Periodic Syndromes (CAPS), Familial Cold Autoinflammatory Syndrome (FCAS), Muckle-Wells Syndrome (MWS), Systemic Juvenile Idiopathic Arthritis (SJIA) | NA | Reconstitution with 1 mL of preservative-free Sterile Water for Injection is required prior to subcutaneous administration of the drug. The reconstituted canakinumab is a 150 mg/mL solution essentially free of particulates, clear to slightly opalescent, and is colorless or may have a slightly brownish-yellow tint. A volume of up to 1 mL can be withdrawn for delivery of 150 mg/mL canakinumab for subcutaneous administration. Each reconstituted vial contains 180 mg canakinumab, sucrose, L-histidine, L-histidine HCL monohydrate, polysorbate 80 and Sterile Water for Injection. No preservatives are present. | 180 mg of canakinumab as a white, preservative-free, lyophilized powder | Subcutaneous | Cryopyrin-Associated Periodic Syndromes (CAPS): The recommended dose of ILARIS is 150 mg for CAPS patients with body weight greater than 40 kg. For CAPS patients with body weight greater than or equal to 15 kg and less than or equal to 40 kg, the recommended dose is 2 mg/kg. For children 15 to 40 kg with an inadequate response, the dose can be increased to 3 mg/kg. Systemic Juvenile Idiopathic Arthritis (SJIA): The recommended dose of ILARIS for SJIA patients with a body weight greater than or equal to 7.5 kg is 4mg/kg (with a maximum of 300 mg) administered every four weeks via subcutaneous injection. | Confirmed hypersensitivity to the active substance or to any of the excipients. | ILARIS has been associated with an increased risk of serious infections, Immunosuppression, Hypersensitivity , Live vaccines should not be given concurrently with ILARIS. | Link | NA | NA |
| 10566 | Th1116 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 (deglycosylated) | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant (from murine Sp2/0-Ag14 cell line), human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It comprises of two 447- or 448-residue heavy chains and two 214-residue light chains. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at N298. It binds to human IL-1β, thereby neutralizing its inflammatory activity by preventing its interaction with IL-1 receptors. However it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). It is marketed under the brand name Ilaris. | For the treatment of patients aged 4 years and older, to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS). It is also used to treat systemic juvenile idiopathic arthritis (SJIA) in patients pf age 2 years and older . It can be effectively afe and effective, offerin and is therefore considered a significantly better option cted daily and which is often poorly tolerated by the young patients | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α± or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | 6.01 L [typical CAPS patient weighing 70 kg] | 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | NA | Interleukin-1 beta | Ilaris | Novartis Pharmaceuticals Corporation | Novartis Pharmaceuticals Corporation | NA | NA | NA | Injection, powder, lyophilized, for solution | Subcutaneous | 150 mg/1mL | NA | NA | NA | NA | NA |
| 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 |
| 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 |
| 10590 | Th1122 | Rilonacept | >Th1122_Rilonacept SERCDDWGLDTMRQIQVFEDEPARIKCPLFEHFLKFNYSTAHSAGLTLIWYWTRQDRDLEEPINFRLPENRISKEKDVLWFRPTLLNDTGNYTCMLRNTTYCSKVAFPLEVVQKDSCFNSPMKLPVHKLYIEYGIQRITCPNVDGYFPSSVKPTITWYMGCYKIQNFNNVIPEGMNLSFLIALISNNGNYTCVVTYPENGRTFHLTRTLTVKVVGSPKNAVPPVIHSPNDHVVYEKEPGEELLIPCTVYFSFLMDSRNEVWWTIDGKKPDDITIDVTINESISHSRTEDETRTQILSIKKVTSEDLKRSYVCHARSAKGEVAKAAKVKQKVPAPRYTVEKCKEREEKIILVSSANEIDVRPCPLNPNEHKGTITWYKDDSKTPVSTEQASRIHQHKEKLWFVPAKVEDSGHYYCVVRNSSYCLRIKISAKFVENEPNLCYNAQAIFKQKLPVAGDGGLVCPYMEFFKNENNELPKLQWYKDCKPLLLDNIHFSGVKDRLIVMNVAEKHRGNYTCHASYTYLGKQYPITRVIEFITLEENKPTRPVIVSPANETMEVDLGSQIQLICNVTGQLSDIAYWKWNGSVIDEDDPVLGEDYYSVENPANKRRSTLITVLNISEIESRFYKHPFTCFAKNTHGIDAAYIQLIYPVTNSGDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 251000 | C9030H13932N2400O2670S74 | NA | NA | NA | 8.6 days | Dimeric fusion protein consisting of portions of IL-1R and the IL-1R accessory protein, linked to the Fc portion of immunoglobulin G1. It inhibits interleukin 1 and is used in the treatment of cryopyrin-associated periodic syndromes (CAPS), in adults and children overr than 12 of ageold. | Rilonacept is currently used in the treatment of cryopyrin-associated periodic syndrome. In May 2012, an advisory panel for the FDA voted 11-0 against the use of Rilonacept for the treatment of gout. | Treatment with Rilonacept resulted in decreased levels of mean C-Reactive Protein (CRP) and Serum Amyloid A (SAA). Higher levels of CRP and SAA are associated with inflammatory disease activity found in patients with Cryopyrin-Associated Periodic Syndromes. | CAPS refer to rare genetic syndromes generally caused by mutations in the NLRP-3 [Nucleotide-binding domain, leucine rich family (NLR), pyrin domain containing 3] gene (also known as Cold-Induced Auto-inflammatory Syndtrome-1 [CIAS1]). CAPS disorders are inherited in an autosomal dominant pattern with male and female offspring equally affected. Fever, urticaria-like rash, arthralgia, myalgia, fatigue, and conjunctivitis are features common to all disorders. In most cases, inflammation in CAPS is associated with mutations in the NLRP-3 gene which encodes the protein cryopyrin, an important component of the inflammasome. Cryopyrin regulates the protease caspase-1 and controls the activation of interleukin-1 beta (IL-1β). Mutations in NLRP-3 result in an overactive inflammasome resulting in excessive release of activated IL-1β that drives inflammation. Rilonacept blocks IL-1β signaling by acting as a soluble decoy receptor that binds IL-1β and prevents its interaction with cell surface receptors. Rilonacept also binds IL-1α and IL-1 receptor antagonist (IL-1ra) with reduced affinity. By binding IL-1, rilonacept prevents the activation of IL-1 receptors, thus reducing inflammatory responses and other effects related to an excess of IL-1. | NA | NA | NA | NA | NA | Agents reducing cytokine levels,Amino Acids, Peptides, and Proteins,Anti-Inflammatory Agents,Antineoplastic and Immunomodulating Agents,Immunosuppressive Agents,Immunotherapy,Interleukin Inhibitors,Interleukin-1 Receptor Accessory Protein,Proteins,Receptors, Interleukin-1 Type I,Recombinant Proteins | US5844099 | 12-Jan-1998 | 1-Jan-2020 | NA | Interleukin-1 beta,Interleukin-1 alpha,Interleukin-1 receptor antagonist protein | Arcalyst | Regeneron Pharmaceuticals | Regeneron Pharmaceuticals | ARCALYST (rilonacept) is an interleukin-1 blocker indicated for the treatment of Cryopyrin-Associated Periodic Syndromes (CAPS), including Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS) in adults and children 12 and older. | NA | Each vial of ARCALYST (rilonacept) is to be reconstituted with 2.3 mL of Sterile Water for Injection. A volume of up to 2 mL can be withdrawn, which is designed to deliver 160 mg for subcutaneous administration only. The resulting solution is viscous, clear, colorless to pale yellow, and essentially free from particulates. Each vial contains 220 mg rilonacept (80 mg/ 1mL after reconstitution), histidine, arginine, polyethylene glycol 3350, sucrose, and glycine at a pH of 6.5±0.3. No preservatives are present | Sterile, white to off-white, lyophilized powder | Subcutaneous | Adult patients 18 years and older: Treatment should be initiated with a loading dose of 320 mg delivered as two, 2 mL, subcutaneous injections of 160 mgeach given on the same day at two different sites. Dosing should be continued with a once-weekly injection of 160 mg administered as a single, 2-mL, subcutaneous injection. ARCALYST (rilonacept) should not be given more often than once weekly. Dosage modification is not required based on advanced age or gender. Paediatric patients aged 12 to 17 years: Treatment should be initiated with a loading dose of 4.4mg/kg, up to amaximum of 320 mg, delivered as one or two subcutaneous injections with a maximum single-injection volume of 2mL.Dosing should be continued with a once-weekly injection of 2.2 mg/kg, up to a maximum of 160 mg, administered as a single subcutaneous injection, up to 2 mL. If the initial dose is given as two injections, they should be given on the same day at two different sites. ARCALYST (rilonacept) should not be given more often than once weekly. | Certain type of bulging blood vessel (aneurysm), have a heart attack or blood clot in the lung and you also have had recent brain or spinal injury. | Six serious adverse reactions These serious adverse reactions were Mycobacterium intracellular infection; gastrointestinal bleeding and colitis; sinusitis and bronchitis; and Streptococcus pneumoniae meningitis. | Link | NA | NA |
| 10624 | Th1126 | Belatacept | >Th1126_Belatacept MHVAQPAVVLASSRGIASFVCEYASPGKYTEVRVTVLRQADSQVTEVCAATYMMGNELTFLDDSICTGTSSGNQVNLTIQGLRAMDTGLYICKVELMYPPPYYEGIGNGTQIYVIDPEPCPDSDQEPKSSDKTHTSPPSPAPELLGGSSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 92300 | C3508H5440N922O1096S32 | NA | NA | NA | Mean terminal elimination half-life: 10 mg/kg, kidney transplant recipients= 9.8 days; 5 mg/kg, kidney transplant recipient = 8.2 days | Belatacept is a recombinant (CHO cells derived) soluble fusion protein, which links the extracellular domain of human cytotoxic CTLA-4 to the modified Fc portion of human IgG1, thereby selectively blocking the process of T-cell activation. It is a glycosylated fusion protein, which is a homodimer of two homologous polypeptide chains of 357 amino acids each. The drug acts as a selective co-stimulation modulator with inhibitory activity on T lymphocytes. It differs from abatacept (Orencia) by only 2 amino acids. It is approved for the treatment of rheumatoid arthritis. It was developed by Bristol-Myers-Squibb. FDA approved on June 15, 2011. | For prophylaxis of organ rejection. It is also used concomitantly with basiliximumab for induction therapy, mycophenolate, and corticosteriods in kidney transplant recepients that are seropositive for the Epstein-Barr virus. | Belatacept binds to CD86 with a 4-fold higher affinity than abatacept. It also binds to CD80 with a 2-fold higher affinity than abatacept. It was observed in non-human primates that belatacept prolongs graft survival due to a decrease in antibody production against the donor organ. Furthermore, belatacept also inhibits the primary humoral immune response which is indicated by the decrease in post-transplant levels of IgG, IgM, and IgA. The magnitude of this effect is more significant in belatacept than it is in cyclosporine. | Belatacept is a fusion protein in which the Fc portion of human IgG1 is attached onto the extracellular portion of human CTLA-4 (CD152). Belatacept specifically binds to CD80 and CD86 receptors that are found on the antigen-presenting cell (B cells, macrophages, dendritic cells) to block selective T-cell lymphocyte costimulation. CD80 and CD86 would normally act as the ligands to the CD28 receptor T-cells in which this interaction triggers the activation of T lymphocytes. However in the presence of belatacept, because the extracellular CTLA-4 component binds to CD28 with higher affinity than CD80 or CD86, T lymphyocyte anergy, a state of antigen specific tolerance, occurs instead. The T cell is also no longer able to respond to their antigen. | NA | The cytochrome P450 enzyme system or uridine diphosphate-glucuronosyltransferases are not expected to be involved with the metabolism of belatacept. Because the drug is a protein, belatacept is degraded into smaller peptides and amino acids by proteolytic enzymes. | Following multiple intravenous doses of an initial 10 mg/kg dose and followed by a maintenance dose of 5 mg/kg in kidney transplant recipients, these are the following pharmacokinetic parameters: Cmax, 10 mg/kg = 247 µg/mL; Cmax, 5 mg/kg = 139 µg/mL; AUC, 10 mg/kg = 22,252 µg · h/mL; AUC, 5 mg/kg = 14,090 µg · h/mL; Belatacept had linear and dose-dependent pharmacokinetic profile. | Vd, steady state, transplant patients, 10 mg/kg = 0.11 L/kg; Vd, steady state, transplant patients, 5 mg/kg = 0.12 L/kg | Increased body weight may increase the clearance rate of belatacept. Mean systemic clearance: 10 mg/kg, kidney transplant recipients= 0.49 mL/h/kg; 5 mg/kg, kidney transplant recipient = 0.51 mL/h/kg. | Antirheumatic Agents and Immunosuppressive Agents | NA | NA | NA | NA | T-lymphocyte activation antigen CD86,T-lymphocyte activation antigen CD80 | Nulojix | Bristol-Myers Squibb | Bristol-Myers Squibb | NULOJIX (belatacept) is indicated for prophylaxis of organ rejection in adult patients receiving a kidney transplant. NULOJIX is to be used in combination with basiliximab induction, mycophenolate mofetil, and corticosteroids. | NA | Prior to use, the lyophile is reconstituted with a suitable fluid to obtain a clear to slightly opalescent, colorless to pale yellow solution, with a pH in the range of 7.2 to 7.8. Suitable fluids for constitution of the lyophile include SWFI, 0.9% NS, or D5W. Each 250 mg single-use vial of NULOJIX also contains: monobasic sodium phosphate (34.5 mg), sodium chloride (5.8 mg), and sucrose (500 mg). | NULOJIX is supplied as a sterile, white or off-white lyophilized powder for intravenous administration. | Intravenous Injection | NA | Epstein-Barr virus (EBV) seronegative or with unknown EBV serostatus | PTLD, predominantly CNS PTLD, and other malignancies, EBV Seropositive Subpopulation, Progressive Multifocal Leukoencephalopathy, Bacterial, Mycobacterial, Viral, and Fungal Infections, Proteinuria, Immunogenicity, New-Onset Diabetes After Transplantation, Hypertension, Dyslipidemia | Link | NA | NA |
| 10630 | Th1128 | Velaglucerase alfa | >Th1128_Velaglucerase_alfa ARPCIPKSFGYSSVVCVCNATYCDSFDPPTFPALGTFSRYESTRSGRRMELSMGPIQANHTGTGLLLTLQPEQKFQKVKGFGGAMTDAAALNILALSPPAQNLLLKSYFSEEGIGYNIIRVPMASCDFSIRTYTYADTPDDFQLHNFSLPEEDTKLKIPLIHRALQLAQRPVSLLASPWTSPTWLKTNGAVNGKGSLKGQPGDIYHQTWARYFVKFLDAYAEHKLQFWAVTAENEPSAGLLSGYPFQCLGFTPEHQRDFIARDLGPTLANSTHHNVRLLMLDDQRLLLPHWAKVVLTDPEAAKYVHGIAVHWYLDFLAPAKATLGETHRLFPNTMLFASEACVGSKFWEQSVRLGSWDRGMQYSHSIITNLLYHVVGWTDWNLALNPEGGPNWVRNFVDSPIIVDITKDTFYKQPMFYHLGHFSKFIPEGSQRVGLVASQKNDLDAVALMHPDGSAVVVVLNRSSKDVPLTIKDPAVGFLETISPGYSIHTYLWRRQ | 63000 | C2532H3850N672O711S16 | NA | NA | NA | 11-12 Minutes | Gene-activated human recombinant glucocerebrosidase. It is used to treat Type 1 Gaucher disease, caused by a deficiency of the lysosomal enzyme glucocerebrosidase. Additionally, Velaglucerase alfa has also been investigated for use in Type 3 Gaucher disease. | Velaglucerase alfa is a hydrolytic lysosomal glucocerebroside-specific enzyme indicated for long-term enzyme replacement therapy for pediatric and adult patients with type 1 Gaucher disease. | NA | Velaglucerase alfa catalyzes the hydrolysis of glucocerebroside, reducing the amount of accumulated glucocerebroside. | NA | NA | NA | The mean volume of distribution at steady state ranges from 82 to 108 mL/kg (8.2% to 10.8% of body weight). | Mean clearance ranges from 6.72 to 7.56 mL/min/kg. | Enzymes | US7138262 | 21-11-2006 | 18-08-2020 | NA | Glucosylceramidase | VPRIV | Shire | Shire | long-term enzyme replacement therapy (ERT) for pediatric and adult patients with type 1 Gaucher disease. | NA | velaglucerase alfa (400 Units), citric acid, monohydrate (5.04 mg), polysorbate 20(0.44 mg), sodium citrate, dihydrate (51.76 mg), sucrose (200 mg) | VPRIV is supplied as a sterile, preservative free, lyophilized powder | Intravenous infusion | The recommended dose is 60 Units/kg administered every other week as a 60-minute Intravenous infusion. | NA | Headache, Dizziness, Abdominal pain, Nausea, Back pain, Joint pain (knee), Upper respiratory tract infection, Activated partial thromboplastin time prolonged, Infusion-related reaction*, Pyrexia, Asthenia/Fatigue | Link | NA | NA |
| 10631 | Th1129 | Tesamorelin | >Th1129_Tesamorelin YADAIFTNSYRKVLGQLSARKLLQDIMSRQQGESNQERGARARL | 5005.76 | C216H360N72O63S | NA | NA | NA | 26 and 38 minutes in healthy subjects and HIV-infected patients, respectively. | Stabilized synthetic peptide analogue of Growth Hormone Releasing Hormone (GHRH). It is used to treat excess abdominal fat in HIV-infected patients with lipodystrophy. It is a metabolic condition characterized by insulin resistance, fat redistribution and hyperlipidemia associated with antiretroviral therapy for HIV infection. | Tesamorelin acetate is a synthetic analogue of human hypothalamic Growth Hormone Releasing Factor (hGRF) indicated to induce and maintain a reduction of excess abdominal fat in HIV-infected patients with lipodystrophy. | Tesamorelin stimulates growth hormone secretion, and subsequently increases IGF-1 and IGFBP-3 levels. | By acting on the pituitary cells in the brain, tesamorelin stimulates production and release of the endogenous hormone (hGRF). Tesamorelin therapy predisposes the patient to glucose intolerance and can also increase the risk of type 2 diabetes, so the drug is contraindicated in pregnancy. | NA | NA | NA | NA | NA | NA | US5861379 | 19-01-1999 | 26-05-2020 | NA | Growth hormone-releasing hormone receptor | Egrifta | Theratechnologies | Theratechnologies | excess abdominal fat in HIV-infected patients with lipodystrophy | NA | After reconstitution with the supplied diluent (Sterile Water for Injection, USP), a solution of EGRIFTA is clear and colorless. Each single-use vial of EGRIFTA contains 2 mg of tesamorelin as the free base (2.2 mg tesamorelin acetate, anhydrous) and the following inactive ingredient: 100 mg mannitol, USP. | EGRIFTA is a sterile, white to off-white, preservative-free lyophilized powder for subcutaneous injection | Subcutaneous | The recommended dose of EGRIFTA is 2 mg injected subcutaneously once a day. | Disruption of the Hypothalamic-pituitary Axis, Active Malignancy, Hypersensitivity and Pregnancy | rash, urticaria, arthralgia, extremity pain, peripheral edema, hyperglycemia, carpal tunnel syndrome, erythema, pruritis, pain, urticaria, irritation, swelling, hemorrhage | Link | NA | NA |
| 10632 | Th1130 | Brentuximab vedotin | >Th1130_Brentuximab_vedotin QIQLQQSGPEVVKPGASVKISCKASGYTFTDYYITWVK | 149200-151800 | C6476H9930N1690O2030S40 | NA | NA | NA | Terminal half-life is 4-6 days | Brentuximag vedotin or Adcetris is an antibody-drug conjugate that combines an anti-CD30 antibody and the drug monomethyl auristatin E (MMAE). It is an anti-cancer drug used to treat Hodgkin lymphoma and systemic anaplastic large cell lymphoma. It was approved in 2011 but in January 2012, the drug label was revised to include a boxed warning of progressive multifocal leukoencephalopathy and death following JC virus infection. | Used in the treatment of Hodgkin lymphoma and systemic anaplastic large cell lymphoma. | Brentuximag vedotin causes apoptosis of tumor cells by preventing cell cycle progression of the G2 to M phase through disruption of the cytosolic mictrotuble network. | Brentuximab vedotin is composed of 3 parts: a chimeric human-murine IgG1 that targets CD30, monomethyl auristatin E (MMAE),which is a microtubule disrupting agent, and a protease-susceptible linker that covalently links the antibody and MMAE. The IgG1 antibody enables brentuximab vedotin to target tumor cells expressing CD30 on their cell surface then brentuximab vedotin gets internalized into the cell. Once inside, the linker is cleaved releasing MMAE which binds disrupts the microtuble network. | The most severe toxic reaction seen in patients is progressive multifocal leukoencephalopathy [FDA label]. Progressive multifocal leukoencephalopathy (PML) follows infection by the JC virus (which is not related to Creutzfeldt-Jakob disease). Symptoms of this condition begin insidiously and usually worsen progressively. The symptoms vary depending on which region of the brain is infected. In about two out of three patients, mental function deteriorates rapidly, leading to dementia. Speaking and walking may become increasingly difficult. Vision may be impaired, and total blindness may occur. Rarely, headaches and seizures can occur, mainly in immunocompromised patients. The most serious sequela of this condition is death [L1743]. Common adverse effects of Adcetris may include: neutropenia, anemia, peripheral neuropathy, nausea, fatigue, constipation, diarrhea, vomiting, and fever. In one trial, neutropenia occurred in 91 percent of patients treated with Adcetris plus chemotherapy, which was associated with a 19 percent rate of febrile neutropenia (neutropenia and fever) [L1737]. Preventive treatment with G-CSF, a growth factor for the bone marrow to produce white blood cells, is recommended with Adcetris plus chemotherapy for the first-line treatment of Stage III or IV cHL [L1737]. Adcetris has a boxed warning that emphasizes the risk of John Cunningham virus infection leading to progressive multifocal leukoencephalopathy, or PML, a rare but serious brain infection that may be lethal. Serious risks of Adcetris include peripheral neuropathy; severe allergic (anaphylaxis) or infusion-site reactions; damage to the blood, lungs and liver (hematologic, pulmonary and hepato-toxicities); severe/opportunistic infections; metabolic abnormalities (tumor lysis syndrome); dermatologic reactions and gastrointestinal complications. Adcetris may cause harm to the fetus and newborn baby; women should be warned of the potential risk to the fetus and to use effective contraception, and to avoid breastfeeding while taking Adcetris [L1737]. MMAE was found to be genotoxic in the rat bone marrow micronucleus study through an aneugenic mechanism. This effect is consistent with the pharmacological effect of MMAE as a microtubule-disrupting drug. Fertility studies with Brentuximab vedotin or MMAE have not been conducted. Despite this, results of repeat-dose toxicity studies in rats suggest the potential for Brentuximab vedotin to have a negative effect on male reproductive function and fertility. In a 4-week repeated-dose toxicity study in rats with weekly dosing at 0.5, 5 or 10 mg/kg brentuximab vedotin, seminiferous tubule degeneration, Sertoli cell vacuolation, reduced spermatogenesis, and aspermia were observed [L1737]. Effects in animals were seen mostly at 5 and 10 mg/kg doses of brentuximab vedotin. These dosages are approximately 3 and 6-fold the human recommended dose of 1.8 mg/kg, respectively, based on individual body weight [FDA label]. | Data in both animals and humans suggest that only a small fraction of MMAE released from brentuximab vedotin is metabolized. In vitro data indicate that the MMAE metabolism that occurs is primarily via oxidation by CYP3A4/5. In vitro studies using human liver microsomes indicate that MMAE inhibits CYP3A4/5 but not other CYP isoforms. MMAE did not induce any major CYP450 enzymes in primary cultures of human hepatocytes [FDA LABEL]. | Steady-state of the ADC is achieved within 21 days with every 3-week dosing of Adcetris. Minimal to no accumulation of ADC is observed with multiple doses at the every 3-week schedule. The time to maximum concentration for MMAE ranges from approximately 1 to 3 days. Similar to the ADC, steady-state of MMAE is achieved within 21 days with every 3-week dosing of Adcetris. MMAE exposures decrease with continued administration of Adcetris with about 50% to 80% of the exposure of the first dose being observed at future doses. The AUC of MMAE was measured to be approximately 2.2-fold higher in patients with hepatic impairment in comparison with patients with normal hepatic function [FDA label]. | MMAE is unlikely to displace or to be displaced by highly protein-bound drugs. In vitro studies show that MMAE is a substrate of P-gp and was not a potent inhibitor of P-gp [FDA label]. | The liver is the primary route of clearance for MMAE. The pharmacokinetics and safety of Brentuximab vedotin and MMAE were examined after the administration of 1.2 mg/kg of Adcetris to patients with mild, moderate, and severe hepatic impairment. In patients with moderate and severe hepatic impairment, the rate of =Grade 3 adverse reactions was 6/6 (100%) compared to 3/8 (38%) in patients with normal hepatic function [FDA label]. It is recommended to avoid use in patients with severe renal impairment (CrCl <30mL/min) [L1742]. | NA | NA | NA | NA | NA | Tumor necrosis factor receptor superfamily member 8 | Adcetris | Seattle Genetics | Seattle Genetics | Hodgkin lymphoma (HL) after failure of autologous stem cell transplant (ASCT) or after failure of at least two prior multi-agent chemotherapy regimens in patients who are not ASCT candidates. | NA | Following reconstitution with 10.5 mL Sterile Water for Injection, USP, a solution containing 5 mg/mL brentuximab vedotin is produced. The reconstituted product contains 70 mg/mL trehalose dihydrate, 5.6 mg/mL sodium citrate dihydrate, 0.21 mg/mL citric acid monohydrate, and 0.20 mg/mL polysorbate 80 and water for injection. The pH is approximately 6.6. | ADCETRIS (brentuximab vedotin) for Injection is supplied as a sterile, white to off-white, preservative-free lyophilized cake or powder in single-use vials. | Intravenous infusion | Normal renal and hepatic function (1.8 mg/kg up to 180 mg), Mild (creatinine clearance > 50-80 mL/min) or moderate (creatinine clearance 30-50 mL/min) (1.8 mg/kg up to 180 mg), Severe (creatinine clearance less than 30 mL/min) (Avoid use), Mild (Child-Pugh A) (1.2 mg/kg up to 120 mg), Moderate (Child-Pugh B) or severe (Child-Pugh C) (Avoid use). | concomitant bleomycin due to pulmonary toxicity | Peripheral neuropathy, Anaphylaxis and Infusion Reactions, Hematologic Toxicities, Serious Infections and Opportunistic Infections, Tumor Lysis Syndrome, Increased Toxicity in the Presence of Severe Renal Impairment, Increased Toxicity in the Presence of Moderate or Severe Hepatic Impairment, Hepatotoxicity, Progressive Multifocal Leukoencephalopathy, Serious Dermatologic Reactions, Embryo-Fetal Toxicity | Link | NA | NA |
| 10636 | Th1131 | Taliglucerase alfa | >Th1131_Taliglucerase_alfa EFARPCIPKSFGYSSVVCVCNATYCDSFDPPTFPALGTFSRYESTRSGRR | 56637.94 | C2580H3918N680O727S17 | 10.54 | NA | NA | between 18.9 to 28.7 min. | Recombinant human glucocerebrosidase (a lysosomal enzyme) . Elelyso used in patients with type 1 Gaucher's disease | For the treatment of adult Type 1 Gaucher disease. | Patient's with Type 1 Gaucher disease have a long-term deficiency in the enzyme, glucocerebrosidase. Taliglucerase alfa is a modified form of glucocerebrosidase and is provided to counter this enzyme deficiency, resulting in smaller liver and spleen size, and improved thrombocytopenia and anemia. | Taliglucerase alfa is different from human glucocerebrosidase by two amino acids at the N terminal and up to 7 amino acids at the C terminal. This recombinant enzyme allows the hydrolysis reaction of glucocerebroside to glucose and ceramide that naturally occurs in healthy individuals. | The most common toxic reaction seen was infusion reactions such as urticaria, arthralgia, headache, and chest pain due to IV administration. | Metabolism was not determined. | Taliglucerase alfa is administered IV so absorption is 100%. | The steady state volume of distribution is between 7.30 to 11.7 L. | The systemic clearance was approximately 30 L/hr and 20 L/hr for 30 and 60 units/kg, respectively. | Enzymes | NA | NA | NA | NA | Glucocerebroside | Elelyso | Pfizer | Pfizer | long-term enzyme replacement therapy (ERT) for adult and pediatric patients with a confirmed diagnosis of Type 1 Gaucher disease. | NA | The quantitative composition of each 200 unit vial is D-mannitol (206.7 mg), polysorbate 80 (0.56 mg), sodium citrate (30.4 mg), and taliglucerase alfa (212 units). Citric acid may be added to adjust the pH at the time of manufacture. | ELELYSO is supplied as a sterile, non-pyrogenic, lyophilized powder. | Intravenous infusion | 60 units per kg of body weight | NA | pruritus, flushing, headache, arthralgia, pain in extremity, abdominal pain, vomiting, fatigue, back pain, dizziness, nausea, and rash. | Link | NA | NA |
| 10637 | Th1132 | Belimumab | NA | 147000 | C 6358 H 9904 N 1728 O 2010 S 44 | NA | NA | NA | Elimination half life- 19.4 days, Distribution half life- 1.75 days | RAV12 is a monoclonal antibody that is being studied in the treatment of certain cancers.It binds to a carbohydrate molecule found on gastric, colon, pancreatic, prostate, ovarian, breast, and kidney cancer cells. Administering RAV12 along with gemcitabine may kill more tumor cells than either one alone. | Adjunct treatment for auto-antibody-positive active systemic lupus erythematosus. | By the 52nd week of treatment with belimumab, a reduction in CD19+, CD20+, naive and activated B cells, plasma cells, plasmacytoid cells, and SLE B-cell subset can be observed. Reductions in plasma cells and SLE B-cell subset can be seen by the eighth week and these levels were maintained to week 52. Belimumab also reduced levels of IgG and anti-dsDNA. | Belimumab selectively binds to soluble human B lymphocyte stimulator protein (BLyS) so that BLyS is unable to bind to receptors on B lymphocytes. The binding of BLyS to its receptor is essential for the survival of B lymphocytes. Consequently, belimumab reduces B-cell mediated immunity and the autoimmune response. | The most commonly-reported adverse reactions, occurring in =5% of patients in clinical trials were nausea, diarrhea, pyrexia, nasopharyngitis, bronchitis, insomnia, pain in extremity, depression, migraine, and pharyngitis. The most common serious adverse reactions were serious infections. | Because belimumab is a protein, it is expected that it is degraded into peptides and amino acids by proteolytic enzymes. | Cmax, 10 mg/kg, SLE patients = 313 µg/mL; AUC (0-8), 10 mg/kg, SLE patients = 3083. | Vdss, 10 mg/kg, SLE patients = 5.29 L. | Systemic clearance, 10 mg/kg, SLE patients = 215 mL/day. | Monoclonal antibodies | NA | NA | NA | NA | Tumor necrosis factor ligand superfamily member 13B | Benlysta | GlaxoSmithKline | GlaxoSmithKline | NA | NA | Upon reconstitution with Sterile Water for Injection, USP, each single-use vial delivers 80 mg/mL belimumab in 0.16 mg/mL citric acid, 0.4 mg/mL polysorbate 80, 2.7 mg/mL sodium citrate, and 80 mg/mL sucrose, with a pH of 6.5. | BENLYSTA is supplied as a sterile, white to off-white, preservative-free, lyophilized powder for Intravenous infusion | Intravenous infusion | 10 mg/kg at 2-week intervals for the first 3 doses and at 4-week intervals thereafter. Reconstitute, dilute, and administer as an Intravenous infusion only, over a period of 1 hour. | anaphylaxis with belimumab | Mortality, Serious Infections, Malignancy, Hypersensitivity Reactions, Including Anaphylaxis, Infusion Reactions, Depression | Link | NA | NA |
| 10649 | Th1134 | Asparaginase erwinia chrysanthemi | >Th1134_Asparaginase_erwinia_chrysanthemi ADKLPNIVILATGGTIAGSAATGTQTTGYKAGALGVDTLINAVPEVKKLANVKGEQFSNMASENMTGDVVLKLSQRVNELLARDDVDGVVITHGTDTVEESAYFLHLTVKSDKPVVFVAAMRPATAISADGPMNLLEAVRVAGDKQSRGRGVMVVLNDRIGSARYITKTNASTLDTFKANEEGYLGVIIGNRIYYQNRIDKLHTTRSVFDVRGLTSLPKVDILYGYQDDPEYLYDAAIQHGVKGIVYAGMGAGSVSVRGIAGMRKAMEKGVVVIRSTRTGNGIVPPDEELPGLVSDSLNPAHARILLMLALTRTSDPKVIQEYFHTY | 140000 | C1546H2510N432O476S9 | NA | NA | NA | 18.2 hours | Erwinaze (asparaginase from Erwiniachryanthemi) is an asparaginase specific enzyme derived from Erwiniachrysanthemi. L-asparaginase is a homo-tetramer with each subnuit having a molecular weight of about 35 kDa. It is an antineoplastic agent and was FDA approved in November 19, 2011. | Asparaginase Erwinia chryanthemi is for the treatment of patients with acute lymphoblastic leukemia (ALL) that have developed a hypersensitivity to Escherichia coli-derivied asparaginase. It is a component of a multi-agent chemotherpeutic regimen for the treatment of the aforementioned disease and is considered second- or third- line treatment in European and American protocols. | NA | Asparaginase Erwinia chrysanthemi catalyzes the deamidation of asparagine to aspartic acid and ammonia, resulting in a reduction in circulating levels of asparagine in the plasma. The mechanism of action of Erwinaze is thought to be based on the inability of leukemic cells to synthesize asparagine due to lack of asparagine synthetase activity, resulting in cytotoxicity specific for leukemic cells that depend on an exogenous source of the amino acid asparagine for their protein metabolism and survival. | There are no known cases of overdose with asparaginase _Erwinia chrysanthemi_.[L149] In clinical trials, the most common adverse effects were hypersensitivity reactions, pancreatic toxicity, blood clots, hemorrhage, and liver toxicity.[L34714] Pancreatitis occurs in 8-14% of pediatric patients, with adolescents at the highest risk for developing this adverse event. Pancreatitis typically occurs after the first few weeks of asparaginase administration, which suggests this complication occurs from an underlying predisposition rather than a cumulative drug effect.[A7464] | Metabolism of asparaginase _Erwinia chrysanthemi_ has not been fully characterized; however, it is suspected to be metabolized into small peptides by catabolic pathways.[L34719] | In patients two to 80 years of age, intramuscular administration of asparaginase _Erwinia chrysanthemi_ 25,000 International Units (IU)/m2 resulted in serum trough asparaginase concentrations = 0.1 IU/mL at either 48-hour (n=35) or 72-hour (n=13) post third dose. 80% of patients evaluted at 48 hours and 38% of patients evaluated at 72 hours had serum asparaginase activity levels > 0.4 IU/mL.[L149] For asparaginase _Erwinia chrysanthemi_ (recombinant)-rywn, the median tmax is 10 hours and the mean absolute bioavailability is 37% in healthy subjects.[L34719] | The volume of distribution of asparaginase _Erwinia chrysanthemi_ can be up to 5 L/m2.[L1448] The geometric mean (%CV) apparent volume of distribution of asparaginase _Erwinia chrysanthemi_ (recombinant)-rywn was 1.48 L/m2 (49%).[L34719] While asparaginases are not detectable in cerebrospinal fluid, asparagine in cerebrospinal fluid is depleted with systemic administration of any formulation of asparaginases.[L1448] | The geometric mean (%CV) apparent clearance of asparaginase _Erwinia chrysanthemi_ (recombinant)-rywn is 0.31 L/hour/m2 (36%).[L34719] | Amidohydrolases,Antineoplastic Agents,Asparaginase,Asparagine-specific Enzyme,Enzymes,Enzymes and Coenzymes,Hepatotoxic Agents,Hydrolases,Narrow Therapeutic Index Drugs,Thyroxine-binding globulin inhibitors | NA | NA | NA | NA | NA | Erwinaze | EUSA Pharma | EUSA Pharma | acute lymphoblastic leukemia | NA | Each vial contains 10,000 International Units of asparaginase Erwinia chrysanthemi, and the following inactive ingredients: glucose monohydrate (5.0 mg), sodium chloride (0.5 mg). | ERWINAZE is supplied as a Sterile, lyophilized, white powder in vials. | Intramuscular | 25,000 International Units/m² | Hypersensitivity reactions to ERWINAZE, including anaphylaxis., pancreatitis with prior L-asparaginase therapy, thrombosis with prior L-asparaginase therapy, hemorrhagic events with prior L-asparaginase therapy. | Hypersensitivity reactions, Pancreatitis, Glucose intolerance, Thrombosis and hemorrhage | Link | NA | NA |
| 10651 | Th1136 | Glucarpidase | >Th1136_Glucarpidase MRPSIHRTAIAAVLATAFVAGTALAQKRDNVLFQAATDEQPAVIKTLEKLVNIETGTGDAEGIAAAGNFLEAELKNLGFTVTRSKSAGLVVGDNIVGKIKGRGGKNLLLMSHMDTVYLKGILAKAPFRVEGDKAYGPGIADDKGGNAVILHTLKLLKEYGVRDYGTITVLFNTDEEKGSFGSRDLIQEEAKLADYVLSFEPTSAGDEKLSLGTSGIAYVQVNITGKASHAGAAPELGVNALVEASDLVLRTMNIDDKAKNLRFNWTIAKAGNVSNIIPASATLNADVRYARNEDFDAAMKTLEERAQQKKLPEADVKVIVTRGRPAFNAGEGGKKLVDKAVAYYKEAGGTLGVEERTGGGTDAAYAALSGKPVIESLGLPGFGYHSDKAEYVDISAIPRRLYMARRLIMDLGAGK | 83000 | C3670H5926N10114O1140S12 | NA | NA | NA | Elimination half-life of 5.6 hours | Recombinant (E. Coli derived) form of the Pseudomonas sp. (strain RS-16) enzyme, carboxypeptidase G2. It inactivates methotrexate and other antifolates by hydrolyzing glutamate on the carboxyl terminal of these compounds. Since methotrexate is eliminated enzymatically and not by the kidneys, glucarpidase is indicated in patients on methotrexate treatment who have kidney dysfunction, and are experiencing an abnormally high plasma concentration of methotrexate (>1 micromole per liter). | Used in patients on methotrexate treatment who have kidney dysfunction, and are experiencing an abnormally high plasma concentration of methotrexate (> 1 micromole per liter). | Glucarpidase acts as an antidote to toxic methotrexate levels by elminating methotrexate by a non-kidney route. | Glucarpidase inactivates methotrexate, and other antifolates, by hydrolyzing glutamate on the carboxyl terminal of these compounds. For methotrexate specifically, it is hydrolyzed to the inactive metabolites glutamate and 4-deoxy-4-amino-N10-methylpteroic acid (DAMPA). | Most common adverse reactions include hypotension, flushing, nausea, vomiting, headache, and paresthesia. | Metabolism was not determined. | In healthy patients not taking methotrexate, the average maximum concentration for glucarpidase was 3.3 µg/mL. | Glucarpidase is likely limited to the plasma volume since its volume of distribution is 3.6 L. | In healthy patients not taking methotrexate, glucarpidase has a clearance of 7.5 mL/min. | Enzymes | NA | NA | NA | NA | Methotrexate | Voraxaze | BTG International | BTG International | toxic plasma methotrexate concentrations | NA | Each vial contains 1,000 Units of glucarpidase, lactose monohydrate (10 mg), Tris-HCl (0.6 mg) and zinc acetate dihydrate (0.002 mg). | VORAXAZE is supplied as a Sterile, preservative-free, white lyophilized powder in single-use vials | Intravenous Injection | 50 Units per kg | NA | paraesthesias, flushing, nausea and/or vomiting, hypotension, and headache | 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 |
| 10666 | Th1144 | Follitropin alpha | >Th1144_Follitropin_alpha APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | NA | NA | 24-53 hours in females, 32-41 hours in males | Recombinant (CHO cell derived) human follicle stimulating hormone (FSH). It consists of two non-covalently linked, non-identical glycoproteins designated as the alpha (92 amino acids)- and beta (111 amino acids)- subunits. The alpha subunit is glycosylated at N51 and N78 while the beta subunit is glycosylated at N7 and N24. Follitropin alpha was the world's first recombinant human FSH preparation. The term “alpha†differentiates it from another recombinant human FSH product that was marketed later as follitropin beta. Follitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). Numerous physio-chemical tests and bioassays indicate that follitropin beta and follitropin alpha are indistinguishable. However, a more recent study showed there is may be a slight clinical difference, with the alpha form tending towards a higher pregnancy rate than beta but with significantly higher estradiol (E2) levels. The amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (FSH). Further, the ogliosaccharide side-chains are very similar, but not completely identical to that of natural FSH. However, these small differences do not affect the bioactivity compared to natural FSH. | In women having been diagnosed with primary ovarian failure, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. In men with hypogonadotrophic hypogonadism, it is used to induce spermatogenesis. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF) | The main pharmacodynamic parameters are serum inhibin, estradiol and total follicular volume with daily injections of follitropin. The quickest response was noticed with serum inhibin, which declined rapidly after discontinuation. Follicular growth showed late response and continued even after discontinuation of the drug and after decline of the serum concentrations. Thus follicular growth was better correlated with serum inhibin and estradiol rather than peal levels of the drug. It should be noted that there is great inter-individual variability | Follitropin is important for spermatogenesis, gonadal steroid production and follicule growth and maturation | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Gonal-F | Serono Laboratories | Serono Laboratories | induction of ovulation and pregnancy anovulatory infertile patients in whom the cause of infertility is functional and not due to primary ovarian failure, for the development of multiple follicles in the ovulatory patient participating in an Assisted Reproductive Technology (ART) program. | NA | Each Gonal-f (follitropin alfa) RFF single-dose vial is filled with 82 IU (6 µg)follitropin alfa to deliver 75 IU (5.5 µg) follitropin alfa and contains 30 mg sucrose, 1.11 mg dibasic sodium phosphate dihydrate, 0.45 mg monobasic sodium phosphate monohydrate, 0.1 mg methionine, and 0.05 mg polysorbate 20. Phosphoric acid and/or sodium hydroxide may be used prior to lyophilization for pH adjustment. Vials are reconstituted with Sterile Water for Injection, USP. | Gonal-f (follitropin alfa) RFF is a sterile, lyophilized powder intended for subcutaneous injection after reconstitution. | Subcutaneous Injection | 300 IU per day | Prior hypersensitivity to recombinant FSH preparations or one of their excipients, High levels of FSH indicating primary ovarian failure., Uncontrolled thyroid or adrenal dysfunction, An organic intracranial lesion such as a pituitary tumor, Abnormal uterine bleeding of undetermined origin, Ovarian cyst or enlargement of undetermined origin, Sex hormone dependent tumors of the reproductive tract and accessory organs, Pregnancy. | headache, ovarian cyst, nausea, and upper respiratory tract infection | Link | NA | NA |
| 10667 | Th1144 | Follitropin alpha | >Th1144_Follitropin_alpha APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | NA | NA | NA | Recombinant (CHO cell derived) human follicle stimulating hormone (FSH). It consists of two non-covalently linked, non-identical glycoproteins designated as the alpha (92 amino acids)- and beta (111 amino acids)- subunits. The alpha subunit is glycosylated at N51 and N78 while the beta subunit is glycosylated at N7 and N24. Follitropin alpha was the world's first recombinant human FSH preparation. The term “alpha†differentiates it from another recombinant human FSH product that was marketed later as follitropin beta. Follitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). Numerous physio-chemical tests and bioassays indicate that follitropin beta and follitropin alpha are indistinguishable. However, a more recent study showed there is may be a slight clinical difference, with the alpha form tending towards a higher pregnancy rate than beta but with significantly higher estradiol (E2) levels. The amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (FSH). Further, the ogliosaccharide side-chains are very similar, but not completely identical to that of natural FSH. However, these small differences do not affect the bioactivity compared to natural FSH. | In women having been diagnosed with primary ovarian failure, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. In men with hypogonadotrophic hypogonadism, it is used to induce spermatogenesis. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF) | The main pharmacodynamic parameters are serum inhibin, estradiol and total follicular volume with daily injections of follitropin. The quickest response was noticed with serum inhibin, which declined rapidly after discontinuation. Follicular growth showed late response and continued even after discontinuation of the drug and after decline of the serum concentrations. Thus follicular growth was better correlated with serum inhibin and estradiol rather than peal levels of the drug. It should be noted that there is great inter-individual variability | Follitropin is important for spermatogenesis, gonadal steroid production and follicule growth and maturation | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Gonal-f RFF | EMD SERONO | EMD SERONO | ovulation and pregnancy in the oligo-anovulatory infertile patient in whom the cause of infertility is functional and not due to primary ovarian failure, development of multiple follicles in the ovulatory patient participating in an Assisted Reproductive Technology (ART) program. | NA | Each Gonal-f RFF single-dose vial is filled with 82 IU (6 µg)follitropin alfa to deliver 75 IU (5.5 µg) follitropin alfa and contains 30 mg sucrose, 1.11 mg dibasic sodium phosphate dihydrate, 0.45 mg monobasic sodium phosphate monohydrate, 0.1 mg methionine, and 0.05 mg polysorbate 20. Phosphoric acid and/or sodium hydroxide may be used prior to lyophilization for pH adjustment. Vials are reconstituted with Sterile Water for Injection, USP. | Gonal-f RFF (follitropin alfa injection) is a sterile, lyophilized powder intended for subcutaneous injection after reconstitution. | Subcutaneous Injection | 300 IU per day | Prior hypersensitivity to recombinant FSH preparations or one of their excipients, High levels of FSH indicating primary ovarian failure., Uncontrolled thyroid or adrenal dysfunction, An organic intracranial lesion such as a pituitary tumor, Sex hormone dependent tumors of the reproductive tract and accessory organs, Abnormal uterine bleeding of undetermined origin, Ovarian cyst or enlargement of undetermined origin, Pregnancy. | Headache, Dizziness, Migraine, Abdominal Pain, Nausea, Flatulence, Diarrhea, Toothache, Dyspepsia, Constipation, Stomatitis Ulcerative, Ovarian Cyst, Reproductive, Female, Ovarian Hyperstimulation, Breast Pain Female, Vaginal Haemorrhage, Gynecological-related pain, Uterine haemorrhage, Sinusitis, Pharyngitis, Rhinitis, Coughing, Injection Site Pain, Injection Site Inflammation, Back Pain, Pain, Fever, Hot Flushes, Malaise, Acne, Micturition Frequency, Cystitis, Infection viral. | Link | NA | NA |
| 10668 | Th1145 | Romiplostim | >Th1145_Romiplostim IEGPTLRQWLAARA | 59000 | C2634H4086N722O790S18 | NA | NA | NA | Immunen thrombocytopenia patients, subQ = 3.5 days (median) (range 1-34 days) | Romiplostim is a thrombopoiesis stimulating dimer Fc-peptide fusion protein (peptibody) to increase platelet production through activation of the thrombopoietin receptor. The peptibody molecule has two identical single-chain subunits, each one is made up of 269 amino acid residues. Each subunit consists of an IgG1 Fc carrier domain that is covalently attached to a polypeptide sequence that contains two binding domains to interact with thrombopoietin receptor c-Mpl. Each domain consists of 14 amino acids. Interestingly, romiplostim's amino acid sequence is not similar to that of endogenous thrombopoietin. Romiplostim is produced by recombinant DNA technology in Escherichia coli. FDA approved on August 22, 2008. | Treatment of chronic immune thrombocytopenic purpura. | Responses to platelet increase varies between patients thus indicating a need for individualization of dose. However, a dose dependent-increase in platelet counts have been observed in clinical trials. Does not affect platelet destruction. | Romiplostim is a thrombopoietin receptor agonist that activates intracellular transcriptional pathways via c-Mpl to increase production of platelets. It also works similarly to thrombopoietin (TPO), an endogenous glycoprotein hormone that regulates the production of platelets in the bone marrow. | The most common adverse reactions (= 5% higher patient incidence in Nplate versus placebo) are arthralgia, dizziness, insomnia, myalgia, pain in extremity, abdominal pain, shoulder pain, dyspepsia, and paresthesia. Headache was the most commonly reported adverse reaction that did not occur at = 5% higher patient incidence in Nplate versus placebo. LD50 = 980 mg/kg. | NA | Cmax, healthy volunteers, subQ = 24-36 hours; Cmax, immune thrombocytopenia patients, subQ = 7-50 hours (median = 14 hours). Not affected by age, weight, or gender. Accumulation does not occur after six weekly doses of 3 mcg/kg romiplostim. | In healthy volunteers, non-linear decrease in Vd with increase IV dose of romiplostim which indicates saturation of c-Mpl receptors. Vd, 0.3 µg/kg = 122 mL/kg Vd, 10 µg/kg = 48.2 mL/kg | NA | Amino Acids, Peptides, and Proteins,Biological Factors,Blood and Blood Forming Organs,Carbohydrates,Colony-Stimulating Factors,Cytokines,Glycoconjugates,Glycoproteins,Hematinics,Hematopoietic Cell Growth Factors,Hemostatics,Increased Megakaryocyte Maturation,Increased Platelet Production,Intercellular Signaling Peptides and Proteins,Membrane Proteins,Peptides,Proteins,Receptors, Thrombopoietin, agonists,Recombinant Proteins,Thrombopoietin Receptor Agonist,Thrombopoietin Receptor Agonists | NA | NA | NA | NA | Thrombopoietin receptor | Nplate | Amgen | Amgen | Nplate is indicated for the treatment of thrombocytopenia in patients with chronic immune thrombocytopenia (ITP) who have had an insufficient response to corticosteroids, immunoglobulins or splenectomy. | NA | Two vial presentations are available, which contain a sufficient amount of active ingredient to provide either 250 mcg or 500 mcg of deliverable romiplostim, respectively. Each single-use 250 mcg vial of Nplate contains the following: 375 mcg romiplostim, 30 mg mannitol, 15 mg sucrose, 1.2 mg L-histidine, 0.03 mg polysorbate 20, and sufficient HCl to adjust the pH to a target of 5.0. Each single-use 500 mcg vial of Nplate contains the following: 625 mcg romiplostim, 50 mg mannitol, 25 mg sucrose, 1.9 mg L-histidine, 0.05 mg polysorbate 20, and sufficient HCl to adjust the pH to a target of 5.0 | Sterile, preservative-free, lyophilized, solid white powder | Subcutaneous Injection | Use the lowest dose of Nplate to achieve and maintain a platelet count ≥ 50 x 109/L as necessary to reduce the risk for bleeding. Administer Nplate as a weekly subcutaneous injection with dose adjustments based upon the platelet count response. The prescribed Nplate dose may consist of a very small volume (eg, 0.15 mL). Administer Nplate only with a syringe that contains 0.01 mL graduations. The initial dose for Nplate is 1 mcg/kg based on actual body weight. Dose AdjustmentsUse the actual body weight at initiation of therapy, then adjust the weekly dose of Nplate by increments of 1 mcg/kg until the patient achieves a platelet count ≥ 50 x 109/L as necessary to reduce the risk for bleeding; do not exceed a maximum weekly dose of 10 mcg/kg. In clinical studies, most patients who responded to Nplate achieved and maintained platelet counts ≥ 50 x 109/L with a median dose of 2 mcg/kg. During Nplate therapy, assess CBCs, including platelet counts, weekly until a stable platelet count ( ≥ 50 x 109/L for at least 4 weeks without dose adjustment) has been achieved. Obtain CBCs, including platelet counts, monthly thereafter. | NA | The following serious adverse reactions: Progression of Myelodysplastic Syndromes, Thrombotic/Thromboembolic Complications, Loss of Response to Nplate, Overdoses due to medication errors have been reported in patients receiving Nplate. In the event of overdose, platelet counts may increase excessively and result in thrombotic/thromboembolic complications. In this case, discontinue Nplate and monitor platelet counts. Reinitiate treatment with Nplate in accordance with dosing and administration recommendations. | Link | NA | NA |
| 10683 | Th1151 | Somatotropin Recombinant | >Th1151_Somatotropin_Recombinant FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 at pH 3 | 21.1 (±5.1) minutes | Somatropin (rDNA origin - nonrefrigerated) is a growth hormone. It works by increasing the flow of water, electrolytes, and nutrients into the bowels. | For treatment of dwarfism, acromegaly and prevention of HIV-induced weight loss | Used in the treatment of dwarfism and growth failure, growth hormone (hGH) stimulates skeletal growth in pediatric patients with growth failure due to a lack of adequate secretion of endogenous GH. Skeletal growth is accomplished at the epiphyseal plates at the ends of a growing bone. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and one of its mediators, IGF-I (insulin-like growth factor). | hGH binds to the human growth hormone receptor (GHR). Upon binding, hGH causes dimerization of GHR, activation of the GHR-associated JAK2 tyrosine kinase, and tyrosyl phosphorylation of both JAK2 and GHR. These events recruit and/or activate a variety of signaling molecules, including MAP kinases, insulin receptor substrates, phosphatidylinositol 3' phosphate kinase, diacylglycerol, protein kinase C, intracellular calcium, and Stat transcription factors. These signaling molecules contribute to the GH-induced changes in enzymatic activity, transport function, and gene expression that ultimately culminate in changes in growth and metabolism. | NA | NA | NA | NA | NA | Hormone Replacement Agents | CA1326439 | 25-01-1994 | 25-01-2011 | NA | Growth hormone receptor | NutropinAQ | Genentech Inc. | Genentech Inc. | Various brands of this medication are used for the treatment of one of the following medical conditions: growth failure, growth hormone deficiency, intestinal disorder (short bowel syndrome) or HIV-related weight loss or wasting. Somatropin is also used to increase height in children with a certain genetic disorder (Noonan syndrome). | Growth hormon (human), r-DNA derived | Nutropin is a sterile, white lyophilized powder intended for subcutaneous administration after reconstitution with Bacteriostatic Water for Injection, USP (benzyl alcohol preserved). The reconstituted product is nearly isotonic at a concentration of 5 mg/mL GH and has a pH of approximately 7.4. | Sterile, white lyophilized powder intended for subcutaneous administration after reconstitution with Bacteriostatic Water | Subcutaneous administration | Not to exceed 0.006 mg/kg/day SC initially for 6 weeks; may increase up to 0.025 mg/kg/day if patient <35 years of age and up to 0.0125 mg/kg/day if patient >35 years | Acute Critical Illness, Prader-Willi Syndrome (PWS) in Children, Active MalignancyIn, Diabetic Retinopathy and Hypersensitivity | Sudden death in pediatric patients with Prader-Willi syndrome (PWS) with risk factors includingsevere obesity, history of upper airway obstruction or sleep apnea and unidentified respiratoryinfection, Intracranial tumors, in particular meningiomas, in teenagers/young adults treated with radiationto the head as children for a first neoplasm and somatropin, Glucose intolerance including impaired glucose tolerance/impaired fasting glucose as well asovert diabetes mellitus, Intracranial hypertension, Unmasking of latent central hypothyroidism, Significant diabetic retinopathy , Slipped capital femoral epiphysis in pediatric patients, Progression of preexisting scoliosis in pediatric patients and Fluid retention manifested by edema, arthralgia, myalgia, nerve compression syndromes including carpal tunnel syndrome/paraesthesias. | Link | NA | NA |
| 10684 | Th1151 | Somatotropin Recombinant | >Th1151_Somatotropin_Recombinant FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 at pH 3 | 21.1 (±5.1) minutes | Somatropin (rDNA origin - nonrefrigerated) is a growth hormone. It works by increasing the flow of water, electrolytes, and nutrients into the bowels. | For treatment of dwarfism, acromegaly and prevention of HIV-induced weight loss | Used in the treatment of dwarfism and growth failure, growth hormone (hGH) stimulates skeletal growth in pediatric patients with growth failure due to a lack of adequate secretion of endogenous GH. Skeletal growth is accomplished at the epiphyseal plates at the ends of a growing bone. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and one of its mediators, IGF-I (insulin-like growth factor). | hGH binds to the human growth hormone receptor (GHR). Upon binding, hGH causes dimerization of GHR, activation of the GHR-associated JAK2 tyrosine kinase, and tyrosyl phosphorylation of both JAK2 and GHR. These events recruit and/or activate a variety of signaling molecules, including MAP kinases, insulin receptor substrates, phosphatidylinositol 3' phosphate kinase, diacylglycerol, protein kinase C, intracellular calcium, and Stat transcription factors. These signaling molecules contribute to the GH-induced changes in enzymatic activity, transport function, and gene expression that ultimately culminate in changes in growth and metabolism. | NA | NA | NA | NA | NA | Hormone Replacement Agents | CA2252535 | 23-06-2009 | 24-04-2017 | NA | Growth hormone receptor | BioTropin | Bio-Technology General (Israel) Ltd. | Bio-Technology General (Israel) Ltd. | Various brands of this medication are used for the treatment of one of the following medical conditions: growth failure, growth hormone deficiency, intestinal disorder (short bowel syndrome) or HIV-related weight loss or wasting. Somatropin is also used to increase height in children with a certain genetic disorder (Noonan syndrome). | Growth hormon (human), r-DNA derived | Bio-Tropin is provided as a sterile, white, lyophilized powder, available 4 mg presentations. It is intended for subcutaneous administration after reconstitution with bacteriostatic sodium chloride injection, USP, (benzyl alcohol preserved).The diluent for the 4 mg presentation contains solution of 0.9% sodium chloride in water for injection and 0.9% benzyl alcohol as a preservative (bacteriostatic normal saline, USP). A 5 ml vial of the diluent is provided with each dispensed vial of Bio-Tropin. | Sterile, white, lyophilized powder | Subcutaneous administration | Growth hormone insufficiency:25-35 µg/kg/day or 0.7-1.0 mg/m2/day, Turner syndrome:50 µg/kg/day or 1.4 mg/m2/day, Chronic Renal Disease:50 µg/kg/day or 1.4 mg/m2/day, In children born small for gestational age (SGA):35 microgram/kg/day or 1 mg/m2/day. A dose of 0.035 mg/kg/day is usually recommended until final height is reached. Treatment should be discontinued after the first year of treatment, if the height velocity SDS is below +1. Treatment should be discontinued if height velocity is < 2cm/year and, if confirmation is required, bone age is>14 years (girls) or >16 years (boys), corresponding to closure of the epiphyseal growth plates. | Bio-Tropin should not be used in subjects with closed epiphyses.Patients with evidence of progression of an underlying intracranial lesion should not receive Bio-Tropin. Prior to the initiation of the therapy with Bio-Tropin, intracranial tumors must be inactive and antitumor therapy, including a reasonable period of observation, should be completed. Bio-Tropin should be discontinued if there is evidence of recurrent tumor growth. Bio-Tropin reconstituted with bacteriostatic sodium chloride injection, USP (benzyl alcohol preserved) should not be administered to patients with a known sensitivity to benzyl alcohol. Bio-Tropin is not indicated for the treatment of short stature in genetically confirmed Prader-Willi syndrome. | Irritability, Mental Disorder, Insomnia, Depression, Asocial Behaviour, Aggression, Nephrotic Syndrome, Blood Cholesterol Increased | Link | NA | NA |
| 10685 | Th1151 | Somatotropin Recombinant | >Th1151_Somatotropin_Recombinant FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 at pH 3 | 21.1 (±5.1) minutes | Somatropin (rDNA origin - nonrefrigerated) is a growth hormone. It works by increasing the flow of water, electrolytes, and nutrients into the bowels. | For treatment of dwarfism, acromegaly and prevention of HIV-induced weight loss | Used in the treatment of dwarfism and growth failure, growth hormone (hGH) stimulates skeletal growth in pediatric patients with growth failure due to a lack of adequate secretion of endogenous GH. Skeletal growth is accomplished at the epiphyseal plates at the ends of a growing bone. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and one of its mediators, IGF-I (insulin-like growth factor). | hGH binds to the human growth hormone receptor (GHR). Upon binding, hGH causes dimerization of GHR, activation of the GHR-associated JAK2 tyrosine kinase, and tyrosyl phosphorylation of both JAK2 and GHR. These events recruit and/or activate a variety of signaling molecules, including MAP kinases, insulin receptor substrates, phosphatidylinositol 3' phosphate kinase, diacylglycerol, protein kinase C, intracellular calcium, and Stat transcription factors. These signaling molecules contribute to the GH-induced changes in enzymatic activity, transport function, and gene expression that ultimately culminate in changes in growth and metabolism. | NA | NA | NA | NA | NA | Hormone Replacement Agents | US5288703 | 22-02-1994 | 10-Jul-2011 | Concomitant glucocorticoid therapy may inhibit the growth promoting effect of Protropin (somatrem) . If glucocorticoid replacement is required, the dose should be carefully adjusted. | Growth hormone receptor | Protropin | Genentech Inc. | Genentech Inc. | Protropin is indicated only for the long- term treatment of children who have growth failure due to a lack of adequateendogenous growth hormone secretion. Other etiologies of short stature should be excluded. | Growth hormon (human), r-DNA derived | Each 5 mg Protropin vial contains 5 mg (approximately 15 IU) somatrem, lyophilized with 40 mg mannitol, and 1.7 mg sodium phosphates (0.1 mg sodium phosphate monobasic and 1.6 mg sodium phosphate dibasic). | Protropin (somatrem) is a sterile, white, lyophilized powder intended forintramuscular or subcutaneous administration after reconstitution withBacteriostatic Water for Injection, USP (benzyl alcohol preserved). | Intramuscular or subcutaneous administration | A weekly dosage of 0.30 mg/kg (approximately 0.90 IU/kg) of body weight administered by daily intramuscular or subcutaneous injection is recommended. | Protropin (somatrem for injection) should not be used in subjects with closed epiphyses, protropin should not be used in patients with active neoplasia. Growth hormone therapy should be discontinued if evidence of neoplasia develops and when reconstituted with Bacteriostatic Water for Injection, USP (benzyl alcohol preserved) should not be used in patients with a known sensitivity to benzyl alcohol. | As with all protein pharmaceuticals, a small percentage of patients may develop antibodies to the protein. Growth hormone antibody binding capacities below 2 mg/L have not been associated with growth attenuation. In some cases when binding capacity exceeds 2 mg/L, growth attenuation has been observed. Common side effects include headache, fatigue, or muscle pain. | Link | NA | NA |
| 10687 | Th1152 | Drotrecogin alfa | >Th1152_Drotrecogin_alfa LIDGKMTRRGDSPWQVVLLDSKKKLACGAVLIHPSWVLTAAHCMDESKKLLVRLGEYDLRRWEKWELDLDIKEVFVHPNYSKSTTDNDIALLHLAQPATLSQTIVPICLPDSGLAERELNQAGQETLVTGWGYHSSREKEAKRNRTFVLNFIKIPVVPHNECSEVMSNMVSENMLCAGILGDRQDACEGDSGGPMVASFHGTWFLVGLVSWGEGCGLLHNYGVYTKVSRYLDWIHGHIRDKEAPQKSWAP | 55000 | C1786H2779N509O519S29 | 6.78 | -0.291 | NA | 5.5 Hrs (Mammalian reticulocytes,in vitro | Drotrecogin alfa is activated human protein C that is synthesized by recombinant DNA technology. It is a glycoprotein of approximately 55 kilodalton molecular weight, consisting of a heavy chain and a light chain linked by a disulfide bond. Drotrecogin alfa was withdrawn from the market after a major study indicated that it was not effective in improving outcomes in patients with sepsis. | For reduction of mortality in patients with severe sepsis. | Drotrecogin alfa is activated human protein C that is synthesized by recombinant DNA technology. It is a glycoprotein of approximately 55 kilodalton molecular weight, consisting of a heavy chain and a light chain linked by a disulfide bond. Drotrecogin alfa inhibits factor Va and VIIIa, thereby reducing the coagulability of blood. | Activated protein C combines with protein S on platelet surfaces and then degrades factor Va and factor VIIIa, thereby reducing blood coagulability. | NA | NA | NA | NA | * 40 L/hr [severe sepsis adults] * 30 +/- 8 L/hr [patients without sepsis undergoing hemodialysis] * 28 +/- 9 L/hr [heathy] | Amino Acids, Peptides, and Proteins,Anti-Infective Agents,Anticoagulants,Biological Factors,Blood and Blood Forming Organs,Blood Coagulation Factor Inhibitors,Blood Proteins,Carbohydrates,Enzyme Precursors,Enzymes,Enzymes and Coenzymes,Fibrinolytic Agents,Glycoconjugates,Glycoproteins,Proteins,Recombinant Activated Protein C | CA2036894 | 15-01-2002 | 22-02-2011 | Clopidogrel, Enoxaprin, Dalteparin, Fondaparinux, Tinzaparin, enhance the adverse or toxic effect of drotrecogin alfa | Coagulation factor VIII,Coagulation factor V,Plasminogen activator inhibitor 1,Thrombomodulin,Vitamin K-dependent protein S,Prothrombin,Platelet factor 4,Plasma serine protease inhibitor,Serpin B6,Endothelial protein C receptor | Xigris | Eli Lilly and Company | Eli Lilly and Company | Xigris (drotrecogin alfa) is indicated for the reduction of mortality in adult patients with severe sepsis (sepsis associated with acute organ dysfunction) who have a high risk of death | NA | The 5 and 20 mg vials of Xigris contain 5.3 mg and 20.8 mg of drotrecogin alfa (activated), respectively. The 5 and 20 mg vials of Xigris (drotrecogin alfa) also contain 40.3 and 158.1 mg of sodium chloride, 10.9 and 42.9 mg of sodium citrate, and 31.8 and 124.9 mg of sucrose, respectively. | Xigris (drotrecogin alfa) is supplied as a sterile, lyophilized, white to off-white powder | Intravenous Infusion | Xigris (drotrecogin alfa) should be administered intravenously at an infusion rate of 24 mcg/kg/hr (based on actual body weight) for a total duration of infusion of 96 hours. Dose adjustment based on clinical or laboratory | Xigris (drotrecogin alfa) increases the risk of bleeding. Xigris (drotrecogin alfa) is contraindicated in the active internal bleeding, hemorraghic stroke, intracranial surgery, Trauma, Intracranial neospasm | Bleeding is the most commonly reported adverse reaction in patients receiving Xigris therapy | Link | NA | NA |
| 10689 | Th1153 | Alefacept | >Th1153_Alefacept CFSQQIYGVVYGNVTFHVPSNVPLKEVLWKKQKDKVAELENSEFRAFSSFKNRVYLDTVSGSLTIYNLTSSDEDEYEMESPNITDTMKFFLYVLESLPSPTLTCALTNGSIEVQCMIPEHYNSHRGLIMYSWDCPMEQCKRNSTSIYFKMENDLPQKIQCTLSNPLFNTTSSIILTTCIPSSGHSRHRYALIPIPLAVITTCIVLYMNGILKCDRKPDRTNSNRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPQVKFNWYVDGVQVHNAKTKPREQQYNSTYRVVSVLTVLHQNWLDGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 51801.1 | C2306H3594N610O694S26 | 7.86 | -0.432 | NA | 270 hrs | Immunosuppressive dimeric fusion protein that consists of the extracellular CD2-binding portion of the human leukocyte function antigen-3 (LFA-3) linked to the Fc (hinge, CH2 and CH3 domains) portion of human IgG1. Produced by CHO cells, mW is 91.4 kD. | As an immunosuppressive drug, Alefacept can be used for treatment of moderate to severe chronic plaque psoriasis | Interferes with lymphocyte activation by specifically binding to the lymphocyte antigen, CD2, and inhibiting LFA-3/CD2 interaction. Activation of T lymphocytes involving the interaction between LFA-3 on antigen-presenting cells and CD2 on T lymphocytes plays a role in the pathophysiology of chronic plaque psoriasis. Also causes a reduction in subsets of CD2+ T lymphocytes as well as CD4+ and CD8+ T lymphocytes. | Inhibits T-lymphocyte activation and production by binding to the CD2 lymphocyte antigen. | While it has been found to cross the placenta in monkeys, it is not yet known if it also diffuses into breast milk. | NA | Bioavailability after IM administration is 63%. | NA | NA | Dermatologic and Immunosupressive agents | NA | NA | NA | Canakinumab, Rilonacept- Increases immunosupressive effects | T-cell surface antigen CD2,Low affinity immunoglobulin gamma Fc region receptor III-A,Low affinity immunoglobulin gamma Fc region receptor III-B | Amevive | Astellas Pharma Inc. | Astellas Pharma Inc. | AMEVIVE is indicated for the treatment of adult patients with moderate to severe chronic plaque psoriasis who are candidates for systemic therapy or phototherapy. | NA | It contains alefacept (15 mg), citric acid monohydrate (0.06 mg), glycine (5 mg), sodium citrate dehydrate (3.6 mg), and sucrose (12.5 mg) per 0.5 mL of reconstituted solution. | AMEVIVE is supplied as a sterile, white-to-off-white, preservative-free, lyophilized powder | Intramuscular Injection | The recommended dose of AMEVIVE® is 15 mg intramuscularly once weekly for 12 weeks. The CD4+ T lymphocyte counts should be measured before initiating dosing. | AMEVIVE should not be administered to patients infected with HIV. AMEVIVE reduces CD4+ T lymphocyte counts, which might accelerate disease progression or increase complications of disease in these patients | Lymphopenia, Malignancies, Serious Infections reuiring hospitalization, Hypersenstivity reactions. | Link | NA | NA |
| 10691 | Th1155 | Urokinase | >Th1155_Urokinase KPSSPPEELKFQCGQKTLRPRFKIIGGEFTTIENQPWFAAIYRRHRGGSVTYVCGGSLMSPCWVISATHCFIDYPKKEDYIVYLGRSRLNSNTQGEMKFEVENLILHKDYSADTLAHHNDIALLKIRSKEGRCAQPSRTIQTICLPSMYNDPQFGTSCEITGFGKENSTDYLYPEQLKMTVVKLISHRECQQPHYYGSEVTTKMLCAADPQWKTDSCQGDSGGPLVCSLQGRMTLTGIVSWGRGCALKDKPGVYTRVSHFLPWIRSHTKEENGLAL | 31126.5 | C1376H2145N383O406S18 | 8.66 | -0.466 | 76°C | 12.6±6.2 minutes | Low molecular weight form of human urokinase, that consists of an A chain of 2,000 daltons linked by a sulfhydryl bond to a B chain of 30,400 daltons. Recombinant urokinase plasminogen activator | Urokinase can be used for the treatment of pulminary embolism, coronary artery thrombosis, IV catheter clearance, and venous and arterial blood clots. | Urokinase is used for the treatment of pulmonary embolisms. The low molecular weight form of human urokinase consists of an A chain of 2,000 daltons linked by a sulfhydryl bond to a B chain of 30,400 daltons. Urokinase is an enzyme (protein) produced by the kidney, and found in the urine. There are two forms of urokinase which differ in molecular weight but have similar clinical effects. Urokinase is the low molecular weight form. Urokinase acts on the endogenous fibrinolytic system. It converts plasminogen to the enzyme plasmin. Plasmin degrades fibrin clots as well as fibrinogen and some other plasma proteins. | Urokinase acts on the endogenous fibrinolytic system. It cleaves the Arg-Val bond in plasminogen to produce active plasmin. Plasmin degrades fibrin clots as well as fibrinogen and other plasma proteins. | Patients experiencing an overdose may present with bleeding.[L12141] Treat patients with symptomatic and supportive measures which may include application of local pressure, administration of whole blood or plasma, and administration of aminocaproic acid.[L12141] | Because urokinase is a protein, it is expected to be metabolized by proteases to smaller proteins and amino acids. | Urokinase is delivered intravenously, so the bioavailability is high. | The volume of distribution of urokinase is 11.5L.[L12138] | Data regarding the clearance of urokinase is not readily available. | Agents causing angioedema,Amino Acids, Peptides, and Proteins,Anticoagulants,Biological Factors,Blood and Blood Forming Organs,Blood Proteins,Endopeptidases,Enzymes,Enzymes and Coenzymes,Fibrinolytic Agents,Hydrolases,Increased Thrombolysis,Peptide Hydrolases,Plasminogen Activators,Proteins,Serine Endopeptidases,Serine Proteases,Urokinase-Type Plasminogen Activator, antagonists & inhibitors | US4258030 | NA | NA | Drotrecogin alfa, Gingko biloba, Ginseng increases risk of bleeding. | Plasminogen,Urokinase plasminogen activator surface receptor,Plasminogen activator inhibitor 1,Plasminogen activator inhibitor 2,Plasma serine protease inhibitor,Low-density lipoprotein receptor-related protein 2,Suppressor of tumorigenicity 14 protein,Nidogen-1 | Kinlytic | NA | NA | For the lysis of acute massive pulmonary emboli, defined as obstruction of blood flow to a lobe or multiple segments; For the lysis of pulmonary emboli accompanied by unstable hemodynamics, i.e., failure to maintain blood pressure without supportive measures. | NA | Each mL contains 50,000 international units of urokinase activity, 0.5% mannitol, 5% Albumin (Human), and 1% sodium chloride (pH range 6.0 to 7.5). | Kinlytic (urokinase injection) is supplied as a sterile lyophilized white powder | Intravenous infusion | The loading dose of 4,400 international units per kilogram of Kinlyticâ„¢ (urokinase injection) is given at a rate of 90 mL per hour over a period of 10 minutes. | The use of Kinlytic (urokinase injection) is contraindicated in patients with a history of hypersensitivity to the product. It is also containdicated in stages like active internal bleeding, cardiopulmonary resustication, intracranial surgery. | hypoxia, cyanosis, dyspnea, tachycardia, hypotension, hypertension, acidosis, fever and/or chills/rigors, back pain, vomiting, and nausea. | Link | NA | NA |
| 10692 | Th1156 | Abarelix | >Th1156_Abarelix XXXSYNLXPA | 1416.063 | C72H95ClN14O14 | NA | NA | NA | 13.2 ± 3.2 days | Synthetic decapeptide antagonist to gonadotropin releasing hormone (GnRH). It is marketed by Praecis Pharmaceuticals as Plenaxis. Praecis announced in June 2006 that it was voluntarily withdrawing the drug from the market. | For palliative treatment of advanced prostate cancer. | Used in the palliative treatment of advanced prostate cancer. Abarelix is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis | Abarelix binds to the gonadotropin releasing hormone receptor and acts as a potent inhibitor of gonadotropin secretion | NA | NA | NA | NA | NA | Anti-Testosterone Agents | US5968895 | 19-10-1999 | 12-Nov-2016 | Tacrolimus, Thiothixene, Toremifene, Trimipramine, Voriconazole, Vorinostat, Ziprasidone, Zuclopenthixol- All above drugs cause Additive QTc Prolongation and increases the risk of severe ventricular arrythmias | Gonadotropin-releasing hormone receptor | Plenaxis | Speciality european pharma | Speciality european pharma | Plenaxis is indicated for the palliative treatment of men with advanced symptomatic prostate cancer, in whom LHRH agonist therapy is not appropriate and who refuse surgical castration, and have one or more of the following: (1) risk of neurological compromise due to metastases, (2) ureteral or bladder outlet obstruction due to local encroachment or metastatic disease, or (3) severe bone pain from skeletal metastases persisting on narcotic analgesia. | Abarelix is chemically described as acetyl-D-β-naphthylalanyl-D-4-chlorophenylalanyl- D-3-pyridylalanyl-L-seryl-L-N-methyl-tyrosyl-D-asparagyl-L-leucyl-L-N(ε)-isopropyllysyl- L-prolyl-D-alanyl-amide. | The single-dose vial contains 113 mg of anhydrous free base abarelix peptide (net) supplied in an abarelix CMC complex. This complex also contains 19.1 to 31 mg of CMC. After the vial is reconstituted with 2.2 mL of 0.9% sodium chloride injection | Abarelix for injectable suspension is supplied as a white to off-white sterile dry powder | Intramuscular Injection | The recommended dose of Plenaxis is 100 mg administered intramuscularly to the buttock on Day 1, 15, 29 (week 4) and every 4 weeks thereafter. | Plenaxis is not indicated in women or pediatric patients. In addition, Plenaxis may cause fetal harm if administered to a pregnant woman. | Diarrhea, Dizziness, Flushing of Skin, Headache, Constipation, Sleep Disturbance | Link | NA | NA |
| 10694 | Th1157 | Sermorelin | >Th1157_Sermorelin YADAIFTNSYRKVLGQLSARKLLQDIMSRQ | 3357.882 | C149H246N44O42S | 9.99 | -0.33 | NA | 11-12 minutes | Sermorelin acetate is the acetate salt of an amidated synthetic 29-amino acid peptide (GRF 1-29 NH 2 ) that corresponds to the amino-terminal segment of the naturally occurring human growth hormone-releasing hormone (GHRH or GRF) consisting of 44 amino acid residues. | For the treatment of dwarfism, prevention of HIV-induced weight loss | Sermorelin is used in the treatment of children with growth hormone deficiency or growth failure. Geref increases plasma growth hormone (GH) concentration by stimulating the pituitary gland to release GH. Geref is similar to the full-length native hormone (44 residues) in its ability to stimulate GH secretion in humans. | Sermorelin binds to the growth hormone releasing hormone receptor and mimics native GRF in its ability to stimulate growth hormone secretion. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins,Anterior Pituitary Lobe Hormones and Analogues,Diagnostic Agents,Growth Hormone-Releasing Hormone,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypothalamic Hormones,Nerve Tissue Proteins,Neuropeptides,Peptide Hormones,Peptides,Pituitary and Hypothalamic Hormones and Analogues,Pituitary Hormone-Releasing Hormones,Somatropin and Somatropin Agonists,Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins,Tests for Pituitary Function | NA | NA | NA | NA | Growth hormone-releasing hormone receptor | Sermorelin acetate | Emd serono inc | Emd serono inc | Sermorelin is approved for diagnostic evaluation of pituitary function and also for increasing growth in children. Off label usage may include acute or age-related growth hormone insufficiency | NA | Two vial presentations are available, Each vial contains 0.5 mg sermorelin (as the acetate) and 5 mg mannitol. The pH is adjusted with dibasic sodium phosphate and monobasic sodium phosphate buffer. Each vial contains 3.0 mg sermorelin (as the acetate) and 5 mg mannitol. The pH is adjusted with dibasic sodium phosphate and monobasic sodium phosphate buffer. | Sermorelin is a sterile, non-pyrogenic, lyophilized powder | Subcutaneous Injection | A dosage of 0.2 - 0.3 mcg once daily at bedtime by subcutaneous injection is recommended. It is also recommended that subcutaneous injection sites be periodically rotated. | Sermorelin should not be used by patients with a known sensitivity to sermorelin or any of the excipients | The most common treatment-related adverse event (occurring in about 1 patient in 6) is local injection reaction characterized by pain, swelling or redness. Other treatment-related adverse events had individual occurrence rates of less than 1% and include: headache, flushing, dysphagia, dizziness, hyperactivity, somnolence and urticaria. | Link | NA | NA |
| 10699 | Th1159 | Gemtuzumab ozogamicin | >Th1159_Gemtuzumab_ozogamicin EVQLVQSGAEVKKPGSSVKVSCKASGYTITDSNIHWVRQAPGQSLEWIGYIYPYNGGTDYNQKFKNRATLTVDNPTNTAYMELSSLRSEDTAFYYCVNGNPWLAYWGQGTLVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 151000 to 153000 | NA | NA | NA | 61 (FAB fr | 64±44 h | Recombinant humanized IgG4, kappa antibody conjugated with a cytotoxic antitumor antibiotic, calicheamicin, isolated from fermentation of a bacterium, Micromonospora echinospora ssp. calichensis. The antibody portion of Mylotarg binds specifically to the CD33 antigen, The anti-CD33 hP67.6 antibody is produced by mammalian cell suspension culture using a myeloma NS0 cell line. | For treatment of CD33-positive acute myeloid leukemia in patients 60 and over who are not candidates for other chemotherapy. | Used for the treatment of acute myeloid leukemia (AML), mylotarg binds to the CD33 antigen, which is expressed on the surface of leukemic cells in more than 80% of patients with AML. The CD33 antigen is not expressed on pluripotent hematopoietic stem cells or nonhematopoietic cells. This gives mylotarg the selectivity needed to target leukemic cells. | Mylotarg is directed against the CD33 antigen expressed by hematopoietic cells. Binding of the anti-CD33 antibody portion of Mylotarg with the CD33 antigen results in the formation of a complex that is internalized. Upon internalization, the calicheamicin derivative is released inside the lysosomes of the myeloid cell. The released calicheamicin derivative binds to DNA in the minor groove resulting in DNA double strand breaks and cell death. | The most frequently reported toxicities are myelosuppression and hepatic veno-occlusive disorder. | Metabolic studies indicate hydrolytic release of the calicheamicin derivative from gemtuzumab ozogamicin. The drug is most likely removed by opsonization via the reticuloendothelial system. | In pediatric patients receiving a dose level of 9mg/m^2, the peak plasma concentration (Cmax) was approximately 3.47±1.04 mg/L with the AUC of 136 ±107 mg * h/L [A20377]. | The volume of distribution at steady state (Vss) was approximately 6.5 ± 5.5 L in pediatric patients receiving a dose level of 9mg/m^2 [A20377]. | The mean clearance rate was approximately 0.12±0.15 L/h/m^2 in pediatric patients receiving a dose level of 9mg/m^2 [A20377]. | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,Carbohydrates,CD33-directed Antibody Interactions,CD33-directed Cytotoxin,Globulins,Glycosides,Hepatotoxic Agents,Immunoconjugates,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Immunotoxins,Myelosuppressive Agents,Narrow Therapeutic Index Drugs,Noxae,Proteins,Serum Globulins,Toxic Actions | US5585089 | 17-12-1996 | 17-12-2013 | Belizumab, Clozapine, Denosumab, Leflunomide, Natalizumab due to adverse effects of these drugs with Gemtuzumab; Pimecrolimus, Roflumilast, Sipuleucel-T, Tacrolimus, Tofacitinib, Trastuzumab due to adverse effects of above immmunosupressants | Myeloid cell surface antigen CD33,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 | Mylotarg | Wyeth pharmaceuticals inc | Wyeth pharmaceuticals inc | Mylotarg (gemtuzumab ozogamicin for injection) is indicated for the treatment of patients with CD33 positive acute myeloid leukemia | NA | 5 mg of drug conjugate (protein equivalent) in an amber vial. The inactive ingredients are: dextran 40; sucrose; sodium chloride; monobasic and dibasic sodium phosphate. | Mylotarg (gemtuzumab ozogamicin for injection) is a sterile, white, preservative-free lyophilized powder | Intravenous infusion | The recommended dose of Mylotarg (gemtuzumab ozogamicin for injection) is 9 mg/m² , infused over a 2-hour period. | Mylotarg (gemtuzumab ozogamicin for injection) is contraindicated in patients with a known hypersensitivity to gemtuzumab ozogamicin or any of its components: anti-CD33 antibody (hP67.6), calicheamicin derivatives, or inactive ingredients. Mylotarg is contraindicated in lactating mothers. | Fever, Nausea, Chills, Vomiting, Headache,Dyspnea, Hypotension, Hypertension, Hypoxia | 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 |
| 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 |
| 10736 | Th1170 | Blinatumomab | >Th1170_Blinatumomab DIQLTQSPASLAVSLGQRATISCKASQSVDYDGDSYLNWYQQIPGQPPKLLIYDASNLVSGIPPRFSGSGSGTDFTLNIHPVEKVDAATYHCQQSTEDPWTFGGGTKLEIKGGGGSGGGGSGGGGSQVQLQQSGAELVRPGSSVKISCKASGYAFSSYWMNWVKQRPGQGLEWIGQIWPGDGDTNYNGKFKGKATLTADESSSTAYMQLSSLASEDSAVYFCARRETTTVGRYYYAMDYWGQGTTVTVSSGGGGSDIKLQQSGAELARPGASVKMSCKTSGYTFTRYTMHWVKQRPGQGLEWIGYINPSRGYTNYNQKFKDKATLTTDKSSSTAYMQLSSLTSEDSAVYYCARYYDDHYCLDYWGQGTTLTVSSVEGGSGGSGGSGGSGGVDDIQLTQSPAIMSASPGEKVTMTCRASSSVSYMNWYQQKSGTSPKRWIYDTSKVASGVPYRFSGSGSGTSYSLTISSMEAEDAATYYCQQWSSNPLTFGAGTKLELKHHHHHH | 54100 | C2367H3577N649O772S19 | NA | NA | NA | 2.11 hours, standard deviation 1.42. | Blinatumomab is a BiTE-class (bi-specific T-cell engagers) constructed monoclonal antibody indicated for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). Blinatumomab is manufactured by Amgen Inc. and marketed under the brand Blincyto™. A full treatment regimen consisting of two cycles of four weeks each, is priced at $178 000 USD. Blinatumomab was approved in December 2014 under the FDA’s accelerated approval program, which allows approval of a drug to treat a serious or life-threatening disease based on clinical data showing the drug has an effect on a surrogate endpoint reasonably likely to predict clinical benefit to patients. | Indicated for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). | NA | Blinatumomab is a bispecific CD19-directed CD3 T-cell engager that binds to CD19 expressed on the surface of cells of B-lineage origin and CD3 expressed on the surface of T cells. It activates endogenous T cells by connecting CD3 in the T-cell receptor (TCR) complex with CD19 on benign and malignant B cells. Blinatumomab mediates the formation of a synapse between the T cell and the tumor cell, upregulation of cell adhesion molecules, production of cytolytic proteins, release of inflammatory cytokines, and proliferation of T cells, which result in redirected lysis of CD19+ cells. | - Cytokine Release Syndrome (CRS), which may be life-threatening or fatal, occurred in patients receiving blinatumomab. Interrupt or discontinue blinatumomab as recommended. - Neurological toxicities, which may be severe, life-threatening, or fatal, occurred in patients receiving blinatumomab. Interrupt or discontinue blinatumomab as recommended. - In patients receiving blinatumomab in clinical trials, serious infections such as sepsis, pneumonia, bacteremia, opportunistic infections, and catheter-site infections were observed in approximately 25% of patients, some of which were life-threatening or fatal. - Tumor lysis syndrome (TLS), which may be life-threatening or fatal, has been observed in patients. - Neutropenia and febrile neutropenia, including life-threatening cases, have been observed in patients. - Treatment with blinatumomab was associated with transient elevations in liver enzymes. - Cranial magnetic resonance imaging (MRI) changes showing leukoencephalopathy have been observed in patients receiving blinatumomab, especially in patients with prior treatment with cranial irradiation and antileukemic chemotherapy (including systemic high-dose methotrexate or intrathecal cytarabine). | The metabolic pathway of blinatumomab has not been characterized. Like other protein therapeutics, blinatumomab is expected to be degraded into small peptides and amino acids via catabolic pathways. | NA | 4.52 L, standard deviation 2.89. | 2.92 L/hour, standard deviation 2.83. | Amides,Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antineoplastic Agents,Antineoplastic and Immunomodulating Agents,Bispecific CD19-directed CD3-directed T Cell Engager,Blood Proteins,Cancer immunotherapy,CD19-directed Antibody Interactions,CD3 Receptor Agonists,CD3-directed Antibody Interactions,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Monoterpenes,Myelosuppressive Agents,Narrow Therapeutic Index Drugs,Norbornanes,Proteins,Serum Globulins,Sulfones,Sulfur Compounds,Terpenes | US20120328618 | 27-10-2009 | 27-10-2029 | The risk or severity of adverse effects can be increased when Blinatumomab is combined with Clozapine; The risk or severity of adverse effects can be increased when Denosumab is combined with Blinatumomab; The risk or severity of adverse effects can be increased when Blinatumomab is combined with Leflunomide; The risk or severity of adverse effects can be increased when Metamizole is combined with Blinatumomab; The risk or severity of adverse effects can be increased when Blinatumomab is combined with Natalizumab; The risk or severity of adverse effects can be increased when Pimecrolimus is combined with Blinatumomab; Roflumilast may increase the immunosuppressive activities of Blinatumomab; The therapeutic efficacy of Sipuleucel-T can be decreased when used in combination with Blinatumomab; The risk or severity of adverse effects can be increased when Tacrolimus is combined with Blinatumomab; Blinatumomab may increase the immunosuppressive activities of Tofacitinib. | B-lymphocyte antigen CD19,T-cell surface glycoprotein CD3 delta chain | Blincyto | AMGEN | AMGEN | BLINCYTO is indicated for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). | NA | 12.5 mcg/mL | lyophilized powder for intravenous administration | Intravenous | A single cycle of treatment of BLINCYTO consists of 4 weeks of continuous intravenous infusion followed by a 2-week treatment-free interval. For patients at least 45 kg in weight: In Cycle 1, administer BLINCYTO at 9 mcg/day on Days 1–7 and at 28 mcg/day on Days 8–28. For subsequent cycles, administer BLINCYTO at 28 mcg/day on Days 1–28. Allow for at least 2 weeks treatment-free between cycles of BLINCYTO. A treatment course consists of up to 2 cycles of BLINCYTO for induction followed by 3 additional cycles for consolidation treatment (up to a total of 5 cycles). | BLINCYTO is contraindicated in patients with known hypersensitivity to blinatumomab or to any component of the product formulation. | Cytokine Release Syndrome; Neurological Toxicities; Infections; Tumor Lysis Syndrome; Neutropenia and Febrile Neutropenia; Effects on Ability to Drive and Use Machines; Elevated Liver Enzymes; Leukoencephalopathy; Preparation and Administration Errors. | 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 |
| 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 |
| 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 |
| 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 |
| 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 |
| 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 |
| 10827 | Th1193 | Turoctocog alfa | >Th1193_Turoctocog_alfa ATRRYYLGAVELSWDYMQSDLGELPVDARFPPRVPKSFPFNTSVVYKKTLFVEFTDHLFNIAKPRPPWMGLLGPTIQAEVYDTVVITLKNMASHPVSLHAVGVSYWKASEGAEYDDQTSQREKEDDKVFPGGSHTYVWQVLKENGPMASDPLCLTYSYLSHVDLVKDLNSGLIGALLVCREGSLAKEKTQTLHKFILLFAVFDEGKSWHSETKNSLMQDRDAASARAWPKMHTVNGYVNRSLPGLIGCHRKSVYWHVIGMGTTPEVHSIFLEGHTFLVRNHRQASLEISPITFLTAQTLLMDLGQFLLFCHISSHQHDGMEAYVKVDSCPEEPQLRMKNNEEAEDYDDDLTDSEMDVVRFDDDNSPSFIQIRSVAKKHPKTWVHYIAAEEEDWDYAPLVLAPDDRSYKSQYLNNGPQRIGRKYKKVRFMAYTDETFKTREAIQHESGILGPLLYGEVGDTLLIIFKNQASRPYNIYPHGITDVRPLYSRRLPKGVKHLKDFPILPGEIFKYKWTVTVEDGPTKSDPRCLTRYYSSFVNMERDLASGLIGPLLICYKESVDQRGNQIMSDKRNVILFSVFDENRSWYLTENIQRFLPNPAGVQLEDPEFQASNIMHSINGYVFDSLQLSVCLHEVAYWYILSIGAQTDFLSVFFSGYTFKHKMVYEDTLTLFPFSGETVFMSMENPGLWILGCHNSDFRNRGMTALLKVSSCDKNTGDYYEDSYEDISAYLLSKNNAIEPRSFSQNSRHPSQNPPVLKRHQR | 166000 | C7480H11379N1999O2194S68 | NA | NA | NA | 16 hours | Turoctocog alfa is a recombinant factor VIII (rFVIII) with a truncated B-domain made from the sequence coding for 10 amino acids from the N-terminus and 11 amino acids from the C-terminus of the naturally occurring B-domain. Turoctocog alfa is produced in Chinese hamster ovary (CHO) cells without addition of any human- or animal-derived materials. During secretion, some rFVIII molecules are cleaved at the C-terminal of the heavy chain (HC) at amino acid 720, and a monoclonal antibody binding C-terminal to this position is used in the purification process allowing isolation of the intact rFVIII. It was first launched in Germany in January 2014 and has been approved in the US, EU and Japan | In the safety and efficacy trial for prevention and treatment of bleeds, in hemophilia patients | NA | NA | In preclinical safety studies, there was a change in reported systolic pressure after 2-weeks of multiple dosing.[L1107] Thrombus formation, cardiovascular, neurological or respiratory effects are not expected to be a safety concern.[L1108] | Turoctocog alfa is expected to be cleaved by proteolysis into small individual aminoacids that constitute them after receptor mediated cell endocytosis.[L1108] | In pre-clinical studies, the absorption half-life was reported wot be 5.4 hours.[A31506] The absorption profile varies depending on the age of the patient where the AUC is 9.92, 11.09 and 15.26 IU hour/ml for the age range of 0-6 years, 6-12 years and over 12 years old respectively. The Cmax according to the different age groups is 1, 1.07 and 1.226 IU/ml for the age range of 0-6 years, 6-12 years and over 12 years old respectively.[L1107] | In pre-clinical studies, turoctocog distribution was studied based on a two model compartment and it resulted in 59 ml/kg in the central compartment and 13 ml/kg in the peripheral compartment. It also presented an inter-compartmental flow of 0.66 ml/hour kg.[A31506] | In pre-clinical studies, turoctocog clearance was reported to be 6.5 ml/hour kg.[A31506] | Amino Acids, Peptides, and Proteins,Biological Factors,Blood Coagulation Factors,Blood Proteins,Hemostatics,Proteins,Recombinant Proteins | NA | NA | NA | NA | Coagulation factor IX,Coagulation factor X,Prothrombin | Zonovate | Novo Nordisk Canada Inc | Novo Nordisk Canada Inc | Treatment and control of bleeding episodes; Perioperative management; Routine prophylaxis to prevent or reduce the frequency of bleeding episodes. | NA | Zonovate®is available in strengths of 250, 500, 1000, 1500, 2000 or 3000 IU/vial. The solvent for reconstitution of Zonovate® is 0.9% sodium chloride solution and is supplied as a clear colorless solutionin a prefilled syringe. | sterile, non-pyrogenic, white or slightly yellow powder | Intravenous | in minor Degree of Hemorrhage 20-40 IU/dl required. Repeat every 12 to 24 hours, at least 1 day, until the bleeding episode as indicated by pain is resolved or healing is achieved. In major Life threatening hemorrhages 60-100 IU/dl required with repeated injection every 8 to 24 hours until threat is resolved | Hypersensitivity | NA | 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 |
| 10830 | Th1196 | Siltuximab | >Th1196_Siltuximab EVQLVESGGKLLKPGGSLKLSCAASGFTFSSFAMSWFRQSPEKRLEWVAEISSGGSYTYYPDTVTGRFTISRDNAKNTLYLEMSSLRSEDTAMYYCARGLWGYYALDYWGQGTSVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145000 | C6450H9932N1688O2016S50 | NA | NA | NA | The mean terminal half life after the first intravenous infusion of 11 mg/kg is 20.6 days. | Siltuximab is a chimeric (human-mouse) monoclonal immunoglobulin G1-kappa antibody produced in a Chinese hamster ovary (CHO) cell line by recombinant DNA technology. Siltuximab prevents the binding of IL-6 to soluble and membrane-bound IL-6 receptors by forming high affinity complexes with human interleukin-6 (IL-6). Its use is indicated for the treatment of adult patients with multicentric Castleman’s disease (MCD) who are human immunodeficiency virus (HIV) negative and human herpesvirus-8 (HHV-8) negative. MCD is a rare blood disorder caused by dysregulated IL-6 production, proliferation of lymphocytes, and subsequent enlargement of the lymph nodes. It is administered as a 1 hour intravenous infusion every 3 weeks. | It is indicated for the treatment of patients with multicentric Castleman's disease (MCD) who are human immunodeficiency virus (HIV) negative and human herpesvirus-8 (HHV-8) negative. Siltuximab did not bind to virally produced IL-6 in a nonclinical study and was therefore not studied in patients with MCD who are HIV or HHV-8 positive. | Siltuximab-neutralized antibody-IL-6 complexes interfere with current immunological-based IL-6 quantification methods, therefore measurement of serum or plasma IL-6 concentrations should not be used as a pharmacodynamic marker during treatment. As well, cytochrome P450 enzymes in the liver are down regulated by infection and inflammation stimuli, which includes cytokines such as IL-6. By preventing IL-6 signalling through treatment with siltuximab, CYP450 activity may be increased leading to faster metabolism of drugs that are CYP450 substrates. | Siltuximab complexes with human IL-6 and prevents binding to soluble and membrane-bound IL-6 receptors, thereby inhibiting the proliferation of lymphocytes. | The most common side effects that occurred during siltuximab treatment were pruritis, increased weight, rash, hyperuricemia, and upper respiratory tract infection. Siltuximab should not be administered to patients with severe infections as it may mask signs and symptoms of acute inflammation including suppression of fever and acute phase reactants such as C-reactive protein (CRP). Gastrointestinal perforation has been reported in clinical trials, therefore use with caution in patients who may be at increased risk for GI perforation. | As siltuximab is an antibody, the expected consequence of metabolism is proteolytic degradation to small peptides and individual amino acids, and receptor-mediated clearance. | NA | Based on population pharmacokinetic analysis, the central volume of distribution in a male subject with body weight of 70 kg is 4.5 L. | Body weight was identified as the only statistically significant covariate of siltuximab clearance, therefore body weight based dosing is appropriate. Based on population pharmacokinetic analysis, the clearance of situximab in patients is 0.23 L/day. | Agents reducing cytokine levels,Amino Acids, Peptides, and Proteins,Antibodies,Antineoplastic Agents,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cytochrome P-450 CYP3A Inducers,Cytochrome P-450 CYP3A Inhibitors,Cytochrome P-450 CYP3A4 Inducers,Cytochrome P-450 CYP3A4 Inducers (weak),Cytochrome P-450 CYP3A4 Inhibitors,Cytochrome P-450 CYP3A4 Inhibitors (weak),Cytochrome P-450 Enzyme Inducers,Cytochrome P-450 Enzyme Inhibitors,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Immunotherapy,Interleukin Inhibitors,Interleukin-6 Antagonist,Proteins,Serum Globulins | US7612182 | 11-Mar-2009 | 8-Jan-2027 | Abiraterone, Alfuzosin, Alprazolam, Aminophylline, Amiodarone, Amlodipine, Apixaban, Apremilast, Aprepitant, Aripiprazole, Armodafinil, Atazanavir, Atorvastatin, Avanafil, Axitinib, Bedaquiline, Belimumab, Benzphetamine, Bisoprolol, Boceprevir, Bortezomib, Bosutinib, Brexpiprazole, Buprenorphine, Buspirone, Cabazitaxel, Cabozantinib, Calcitriol, Carbamazepine, Ceritinib, Chlordiazepoxide, Chloroquine, Cilostazol, Citalopram, Clarithromycin, Clonazepam, Clorazepate, Cobicistat, Cobimetinib, Conivaptan, Crizotinib, Cyclosporine, Cyproterone acetate, Daclatasvir, Dantrolene, Dapsone, Darifenacin, Darunavir, Dasatinib, Delavirdine, Denosumab, Dexamethasone, Diazepam, Dienogest, Diltiazem, Disopyramide, Docetaxel, Doxazosin, Doxorubicin, Dronedarone, Efavirenz, Eliglustat, Elvitegravir, Enzalutamide, Eplerenone, Erlotinib, Erythromycin, Escitalopram, Estradiol, Estrone sulfate, Eszopiclone, Ethosuximide, Etoposide, Etravirine, Everolimus, Exemestane, Felbamate, Felodipine, Fesoterodine, Flibanserin, Flunisolide, Flurazepam, Flutamide, Fosamprenavir, Fosaprepitant, Gefitinib, Guanfacine, Haloperidol, Hydrocodone, Hydroxyprogesterone caproate, Ibrutinib, Idelalisib, Imatinib, Indinavir, Irinotecan, Isavuconazonium, Isosorbide, Isosorbide Dinitrate, Isosorbide Mononitrate, Isradipine, Itraconazole, Ivabradine, Ivacaftor, Ixabepilone, Ixazomib, Ketoconazole, Lansoprazole, Lapatinib, Leflunomide, Levonorgestrel, Lidocaine, Lomitapide, Losartan, Lovastatin, Lurasidone, Macitentan, Maraviroc, Medroxyprogesterone acetate, Mefloquine, Methadone, Midazolam, Mifepristone, Mirtazapine, Modafinil, Naloxegol, Natalizumab, Nateglinide, Nefazodone, Nelfinavir, Nevirapine, Nicardipine, Nifedipine, Nilotinib, Nimodipine, Nisoldipine, Norethisterone, Olaparib, Ondansetron, Ospemifene, Oxycodone, Paclitaxel, Palbociclib, Panobinostat, Pazopanib, Perampanel, Pimecrolimus, Pimozide, Pipotiazine, Praziquantel, Primaquine, Progesterone, Quetiapine, Quinidine, Quinine, Rabeprazole, Ranolazine, Regorafenib, Repaglinide, Rifabutin, Rilpivirine, Riociguat, Ritonavir, Rivaroxaban, Roflumilast, Rolapitant, Ruxolitinib, Saquinavir, Sildenafil, Silodosin, Simeprevir, Simvastatin, Sipuleucel-T, Sirolimus, Solifenacin, Sonidegib, Spiramycin, Stiripentol, Sunitinib, Suvorexant, Tacrolimus, Tamoxifen, Tamsulosin, Tasimelteon, Telaprevir, Telithromycin, Temsirolimus, Teniposide, Tetracycline, Theophylline, Tiagabine, Ticagrelor, Ticlopidine, Tipranavir, Tofacitinib, Tolterodine, Tolvaptan, Toremifene, Trabectedin, Tramadol, Trastuzumab, Trazodone, Triazolam, Trimethoprim, Trimipramine, Ulipristal, Vandetanib, Vemurafenib, Venlafaxine, Verapamil, Vilazodone, Vinblastine, Vincristine, Vinorelbine, Vortioxetine, Zolpidem, Zonisamide, Zopiclone | Interleukin-6 | Sylvant | Janssen Inc | Janssen Inc | NA | NA | 100 mg | Lyophilized powder | Intravenous infusion | SYLVANT 11 mg/kg is given over 1 hour as an intravenous infusion administered every 3 weeks until treatment failure. | Severe hypersensitivity reaction to siltuximab or any of the excipients in SYLVANT. | Concurrent active severe infections; Infusion-related reactions and hypersensitivity | 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 |
| 10839 | Th1202 | Pembrolizumab | >Th1202_Pembrolizumab QVQLVQSGVEVKKPGASVKVSCKASGYTFTNYYMYWVRQAPGQGLEWMGGINPSNGGTNFNEKFKNRVTLTTDSSTTTAYMELKSLQFDDTAVYYCARRDYRFDMGFDYWGQGTTVTVSSASTKGPSVFPLAPCSRSTSESTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTKTYTCNVDHKPSNTKVDKRVESKYGPPCPPCPAPEFLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK | 149000 | C6504H10004N1716O2036S46 | 6.8-6.9 | NA | NA | 22 days. | Pembrolizumab is an antibody drug that targets the cell surface receptor programmed cell death protein 1 (PD-1) found on T cells. By preventing the binding of its ligands (PD-L1 and PD-L2), pembrolizumab induces an antitumor immune response. Upregulation of PD-1 ligands occurs in some tumors and signaling through this pathway can contribute to inhibition of active T-cell immune surveillance of tumors. Its use is indicated for the treatment of patients with unresectable or metastatic melanoma and disease progression following therapy with ipilimumab and, if BRAF V600 mutation positive, a BRAF inhibitor. Due to its success in clinical trials, pembrolizumab was approved early to allow quick patient access and was given breakthrough therapy and orphan drug designation. Pembrolizumab (as Keytruda) was approved by the U.S. Food and Drug Administration to treat advanced cases of the most common type of lung malignancy, non-small cell lung cancer (NSCLC) on Oct. 2, 2015. | For the treatment of patients with unresectable or metastatic melanoma and disease progression following therapy with ipilimumab and, if BRAF V600 mutation positive, a BRAF inhibitor. It is also for the treatment of patients with metastatic NSCLC (non-small cell lung cancer) whose tumors express PD-L1 (as determined by an approved test) and who have disease progression on or after platinum-containing chemotherapy. | In syngeneic mouse tumor models, blocking PD-1 activity resulted in decreased tumor growth. | Pembrolizumab is an antibody drug that targets the cell surface receptor programmed cell death protein 1 (PD-1) found on T cells. By preventing the binding of its ligands (PD-L1 and PD-L2), pembrolizumab induces an antitumor immune response. Upregulation of PD-1 ligands is a mechanism for tumours to evade antitumor immune response; when PD-1 binds its ligand, the T cell receives an inhibitory signal leading to T cell anergy and blockade of anti tumour immune response. Instead of directly targeting tumor tissue to induce tumor cell death, pembrolizumab acts as a checkpoint inhibitor to stimulate immune responses to eliminate cancer cells. | There are no data regarding overdosage with pembrolizumab. | Pembrolizumab is catalyzed into smaller peptides and amino acids via general protein degradation.[A18829] | When administered intravenously, pembrolizumab is completely bioavailable. When administered in repeated doses every 3 weeks, the systemic accumulation accounts for a 2.2 fold increase.[A18829] Steady-state is reached after approximately 16 weeks.[L38934] The absorption of pembrolizumab increases proportionally with increased dosage.[L38934] | The steady-state volume of distribution of pembrolizumab is approximately 6 liters.[L38934] | Clearance is moderately lower at steady-state (195 mL/day) than after the first dose (252 mL/day), although this decrease is not clinically significant.[L38934] | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineoplastic Agents,Antineoplastic Agents, Immunological,Antineoplastic and Immunomodulating Agents,Blood Proteins,Cancer immunotherapy,Globulins,Immune Checkpoint Inhibitors,Immunoglobulins,Immunoproteins,Immunotherapy,Programmed Death Receptor-1 Blocking Antibody,Programmed Death Receptor-1-directed Antibody Interactions,Proteins,Serum Globulins | US2012135408 | 29-03-2012 | 29-03-2032 | NA | Programmed cell death protein 1 | Keytruda | Merck Sharp & Dohme Corp. | Merck Sharp & Dohme Corp. | KEYTRUDA® (pembrolizumab) is indicated for the treatment of patients with unresectable or metastatic melanoma. | NA | 100 mg of pembrolizumab in 4 mL of solution. | lyophilized powder | Intravenous infusion | The recommended dose of KEYTRUDA is 2 mg/kg administered as an intravenous infusion over 30 minutes every 3 weeks until disease progression or unacceptable toxicity. | NA | Immune-mediated pneumonitis; Immune-mediated colitis; Immune-mediated hepatitis; Immune-mediated endocrinopathies; Immune-mediated nephritis and renal dysfunction; Other immune-mediated adverse reactions; Infusion-related reactions. | Link | NA | NA |
| 10845 | Th1208 | Metreleptin | >Th1208_Metreleptin MVPIQKVQDDTKTLIKTIVTRINDISHTQSVSSKQKVTGLDFIPGLHPILTLSKMDQTLAVYQQILTSMPSRNVIQISNDLENLRDLLHVLAFSKSCHLPWASGLETLDSLGGVLEASGYSTEVVALSRLQGSLQDMLWQLDLSPGC | 16155.44 | C714H1167N191O221S6 | NA | NA | NA | 3.8 to 4.7 hours | Metreleptin, a recombinant analog of the human hormone leptin, is an orphan drug used to treat complications of leptin deficiency in people with congenital or acquired lipodystrophy. Affecting less than 500 people worldwide, lipodystrophy is characterized by a lack of adipose tissue, fat deposition in the muscles and liver, and metabolic complications such as hypertriglyceridemia, insulin resistance, diabetes mellitus, and fatty liver disease. These metabolic abnormalities are often aggravated by excessive food intake, which is further aggravated by leptin deficiency, a protein secreted by adipose tissue. Administration of Metreleptin results in improvement of metabolic symptoms including improvements in insulin resistance, reduced HbA1c and fasting glucose, reduced triglycerides, and reductions in food intake. Metreleptin is produced in E. coli and differs from native human leptin by the addition of a methionine residue at its amino terminus. It is administered as a once daily subcutaneous injection. On Feb. 24, 2014, Metreleptin was approved by the FDA for the treatment of complications of leptin deficiency, in addition to diet, in patients with congenital generalized or acquired generalized lipodystrophy. Metreleptin is marketed under the brand Myalept® by Aegerion Pharmaceuticals, Inc. | It is indicated as an adjunct to diet as replacement therapy to treat the complications of leptin deficiency in patients with congenital or acquired generalized lipodystrophy. | In patients with leptin deficiency, clinical trials demonstrated that exogenous leptin administration results in weight loss, reduction in mean HbA1c and fasting glucose levels, reduced blood insulin, and reduced triglyceride levels leading to improved insulin sensitivity and reductions in food intake. | Metreleptin functions by binding to and activating the human leptin receptor (ObR), which belongs to the Class I cytokine family of receptors that signals through the JAK/STAT transduction pathway. | The most common adverse events reported for metreleptin use have been headache, hypoglycemia, weight loss, and abdominal pain. A boxed warning states that anti-metreleptin antibodies, serious infections, and worsening metabolic control have been reported in patients taking the drug, and that some patients with acquired generalized lipodystrophy taking metreleptin have developed T-cell lymphoma. Anti-metreleptin antibodies with neutralizing activity have been identified in patients treated with metreleptin which can lead to inhibition of endogenous leptin action and loss of drug efficacy. As part of a Risk Evaluation and Mitigation Strategy (REMS), the FDA has required healthcare providers to be trained in the use of metreleptin before prescribing it and to attest that patients for whom they prescribe metreleptin have a labeled indication for the drug. Metreleptin is classified as category C (no adequate studies in women) for use during pregnancy. Two-year carcinogenicity studies in rodents have not been conducted with metreleptin. No proliferative or preneoplastic lesions were observed in mice or dogs following treatment up to six months. However, leptin is reported in the literature to promote cell proliferation in vitro and tumor progression in some mouse models of cancer. Metreleptin was not mutagenic in the Ames bacterial mutagenicity assay or clastogenic in an in vitro chromosomal aberration assay in Chinese hamster ovary cells and human peripheral blood lymphocytes. Metreleptin was not mutagenic or clastogenic in an in vivo mouse micronucleus assay. In a fertility study in mice, metreleptin had no adverse effects on mating, fertility, or early embryonic development at doses ranging between 7 and 15 times the maximum recommended clinical dose based on body surface area of a 20- and 60-kg patient, respectively. | No formal metabolism studies have been conducted with metreleptin. Nonclinical data indicate renal clearance is the major route of metreleptin elimination, with no apparent contribution of systemic metabolism or degradation. | Peak serum leptin concentration (Cmax) occurred approximately 4.0 to 4.3 hours after subcutaneous administration of single doses ranging from 0.1 to 0.3 mg/kg in healthy subjects. | Following intravenous administration of metreleptin, leptin volume of distribution was approximately 4 to 5 times plasma volume; volumes (mean ± SD) were 370 ± 184 mL/kg, 398 ± 92 mL/kg, and 463 ± 116 mL/kg for 0.3, 1.0, and 3.0 mg/kg/day doses, respectively. | The clearance of metreleptin is expected to be delayed in the presence of leptin antibodies. | Adipokines,Alimentary Tract and Metabolism,Amino Acids and Derivatives,Amino Acids, Peptides, and Proteins,Analogs/Derivatives,Biological Factors,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Intercellular Signaling Peptides and Proteins,Leptin Analog,Obesity, drug therapy,Peptide Hormones,Peptides,Proteins | US20070099836 | 29-11-2006 | 29-11-2026 | Chlorotrianisene, Chlorpropamide, Cyclosporine, Dienogest, Etonogestrel, Gliclazide, Glimepiride, Glipizide, Glyburide, Insulin Aspart, Insulin Degludec, Insulin Detemir, Insulin Glargine, Insulin Glulisine, Insulin Human, Insulin Lispro, Levonorgestrel, Medroxyprogesterone acetate, Norethisterone, Theophylline, Tolazamide, Tolbutamide, Warfarin | Leptin receptor | Myalept | Amylin Pharmaceuticals, LLC | Amylin Pharmaceuticals, LLC | MYALEPT (metreleptin) for injection is indicated as an adjunct to diet as replacement therapy to treat the complications of leptin deficiency in patients with congenital or acquired generalized lipodystrophy. | NA | NA | Lyophilized powder for solution | subcutaneous | The starting daily dose (injection volume) should be 0.06 mg/kg for a baseline weight of less than 40kg. For a weight greater than 40 kg, the starting dose should be 2.5 mg (0.5 mL) for males and 5 mg (1 mL) for females. | MYALEPT is contraindicated in patients with general obesity not associated with congenital leptin deficiency. MYALEPT has not been shown to be effective in treating general obesity, and the development of anti-metreleptin antibodies with neutralizing activity has been reported in obese patients treated with MYALEPT; Also, is contraindicated in patients with prior severe hypersensitivity reactions to metreleptin or to any of the product components. Known hypersensitivity reactions have included urticaria and generalized rash. | As observed from an open-lable single-arm study the most frequesnt reactions were headache, hypoglycaemia, decreased weight, abdominal pain, athralgia, dizziness, ear infection, fatigue, nausea, ovarian cyst, upper respiratory tract infection, anaemia, diarrhea, back pain, paresthesia, proteinuria, pyrexia. | Link | NA | NA |
| 10847 | Th1210 | Mepolizumab | NA | 149000 | NA | NA | NA | NA | 16 to 22 days. | Mepolizumab is a humanized IL-5 antagonist monoclonal antibody produced by recombinant DNA technology in Chinese hamster ovary cells. It has a molecular weight of approximately 149 kDa. It was approved by the FDA in November, 2015 for the treatment of asthma under the brand name Nucala (marketed by GlaxoSmithKline). Mepolizumab has been investigated in the treatment of severe nasal polyposis, among numerous other conditions. | Mepolizumab is indicated for add-on maintenance treatment of severe eosinophilic asthma, as identified by blood eosinophils greater than or equal to 150 cells/μl at initiation of treatment or blood eosinophils greater than or equal to 300 cells/μl in the past 12 months, in patients aged 12 years and older. Mepolizumab has been shown to reduce exacerbations of asthma in patients with an exacerbation history | The pharmacodynamic response (blood eosinophil reduction) following repeat doses of mepolizumab administered subcutaneously or intravenously was evaluated in subjects with asthma and blood eosinophil levels greater than 200 cells/mcL. Subjects received 1 of 4 mepolizumab treatments (administered every 28 days for a total of 3 doses): 12.5 mg SC, 125 mg SC, 250 mg SC, or 75 mg IV. Sixty-six (66) of the 70 randomized subjects completed the trial. Compared with baseline levels, blood eosinophils decreased in a dose-dependent manner. A reduction in blood eosinophil levels was observed in all treatment groups by Day 3. On Day 84 (4 weeks post-last dose), the observed geometric mean reduction from baseline in blood eosinophils was 64%, 78%, 84%, and 90% in the 12.5-mg SC, 75-mg IV, 125-mg SC, and 250-mg SC treatment groups, respectively. The model-predicted SC doses providing 50% and 90% of maximal reduction of blood eosinophils at Day 84 were estimated to be 11 and 99 mg, respectively. These results, along with the clinical efficacy data from the dose-ranging exacerbation trial (Trial 1) supported the evaluation of mepolizumab 75 mg IV and 100 mg SC in the confirmatory trials [see Clinical Studies (14)]. Following SC administration of mepolizumab 100 mg every 4 weeks for 32 weeks (Trial 2), blood eosinophils were reduced to a geometric mean count of 40 cells/mcL, which corresponds to a geometric mean reduction of 84% compared with placebo. This magnitude of reduction was observed within 4 weeks of treatment and was maintained throughout the treatment period | Mepolizumab is an interleukin-5 antagonist (IgG1 kappa). IL-5 is the major cytokine responsible for the growth and differentiation, recruitment, activation, and survival of eosinophils. Mepolizumab binds to IL-5 with a dissociation constant of 100 pM, inhibiting the bioactivity of IL-5 by blocking its binding to the alpha chain of the IL-5 receptor complex expressed on the eosinophil cell surface. Inflammation is an important component in the pathogenesis of asthma. Multiple cell types (e.g., mast cells, eosinophils, neutrophils, macrophages, lymphocytes) and mediators (e.g., histamine, eicosanoids, leukotrienes, cytokines) are involved in inflammation. Mepolizumab, by inhibiting IL-5 signaling, reduces the production and survival of eosinophils; however, the mechanism of mepolizumab action in asthma has not been definitively established. | Toxicity information regarding mepolizumab is not readily available. Patients experiencing an overdose are at an increased risk of severe adverse effects such as newly established or worsening chronic infections, including those caused by helminths, and generalized immune depression. Symptomatic and supportive measures are recommended.[L16518] | As a monoclonal antibody, mepolizumab is subject to proteolytic degradation at sites distributed throughout the body.[L16518] | Mepolizumab is administered subcutaneously and has a bioavailability of approximately 80% based on a 100 mg dose given to both adult and adolescent subjects with asthma. With the recommended four-week dosing schedule, there is an approximately two-fold accumulation of mepolizumab at steady-state.[L16518] | Mepolizumab has a population central volume of distribution of 3.6 L (for a 70 kg individual) in adult asthma patients.[L16518] | Mepolizumab has an estimated apparent population systemic clearance of 0.28 L/day (for a 70-kg individual) in adult and adolescent subjects.[L16518] | Amino Acids, Peptides, and Proteins,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Blood Proteins,Drugs for Obstructive Airway Diseases,Globulins,Immunoglobulins,Immunoproteins,Immunosuppressive Agents,Interleukin-5 Antagonist,Proteins,Serum Globulins | US2008134721 | NA | NA | NA | Interleukin-5 | Nucala | Glaxosmithkline Inc | Glaxosmithkline Inc | NUCALA® is indicated for the add-on maintenance treatment of patients with severe asthma aged 12 years and older, and with an eosinophilic phenotype. | NA | 100 mg/mL | lyophilized powder | subcutaneous | The recommended dose of NUCALA is 100 mg administered once every 4 weeks by subcutaneous injection into the upper arm, thigh, or abdomen. | NUCALA should not be administered to patients with a history of hypersensitivity to mepolizumab or excipients in the formulation. | Hypersensitivity reactions; Opportunistic infections: herpes zoster | Link | NA | NA |
| 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 |
| 10860 | Th1222 | Canakinumab | >Th1116_Canakinumab QVQLVESGGGVVQPGRSLRLSCAASGFTFSVYGMNWVRQAPGKGLEWVAIIWYDGDNQYYADSVKGRFTISRDNSKNTLYLQMNGLRAEDTAVYYCARDLRTGPFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 145200 | C6452H9958N1722O2010S42 | NA | NA | NA | 26 days | Canakinumab is a recombinant, human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It is expressed in a murine Sp2/0-Ag14 cell line and comprised of two 447- (or 448-) residue heavy chains and two 214-residue light chains, with a molecular mass of 145157 Daltons when deglycosylated. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at asparagine 298 (Asn 298). Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). Canakinumab is marketed under the brand name Ilaris and indicated for patients 4 years of age and older to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS) as well as for patients 2 years of age and older to treat systemic juvenile idiopathic arthritis (SJIA). Clinical trials have established the administration of canakinumab every 2 weeks to be safe and effective, offering a considerable advantage over the existing treatment with the human IL-1 receptor antagonist, anakinra, which must be injected daily and which is often poorly tolerated by patients. | Used in patients 4 years of age and older to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS) as well as for patients 2 years of age and older to treat systemic juvenile idiopathic arthritis (SJIA). | Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases. | In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α or IL-1 receptor antagonist (IL-1ra). | The most common adverse reactions involved the central nervous system (headache and vertigo), gastrointestinal system (diarrhea and nausea), neuromuscular and skeletal system (musculoskeletal pain), and respiratory system (rhinitis, nasopharyngitis and bronchitis). Influenza was also reported. | The metabolism of canakinumab is not yet determined. | The absolute bioavailability of subcutaneous canakinumab is estimated to be 70%. | * 6.01 L [typical CAPS patient weighing 70 kg] | * 0.174 L/day [typical CAPS patient weighing 70 kg] | Anti-Inflammatory Agents and Monoclonal antibodies | NA | NA | NA | The risk or severity of adverse effects can be increased when Canakinumab is combined with Adalimumab, Afelimomab, Anakinra, BCG, Certolizumab pegol, Denosumab, Etanercept, Fingolimod, G17DT, GI-5005 etc | Interleukin-1 beta | Ilaris | Novartis | Novartis | Ilaris is used to treat certain types of periodic fever syndromes, sometimes called auto-inflammatory syndromes. | NA | Each vial of sterile, white, preservative-free, lyophilized powder contains canakinumab 150 mg. Nonmedicinal ingredients: sucrose, L-histidine, L-histidine HCL monohydrate, polysorbate 80. | Lyphilized powder | Subcutaneous | The recommended dose of Ilaris is 150 mg for CAPS patients with body weight greater than 40 kg. For CAPS patients with body weight greater than or equal to 15 kg and less than or equal to 40 kg, the recommended dose is 2 mg/kg. For children 15 to 40 kg with an inadequate response, the dose can be increased to 3 mg | Confirmed hypersensitivity to the active substance or to any of the excipients. | The most common adverse reactionsgreater than 10% reported by patients treated with ILARISare nasopharyngitis, diarrhea, influenza, rhinitis, nausea, headache, bronchitis, gastroenteritis, pharyngitis, weight increased, musculoskeletal pain, and vertigo. | Link | NA | NA |
| 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 |
| 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 |
| 10874 | Th1234 | Protamine sulfate | NA | NA | NA | NA | NA | NA | Without heparin in healthy individuals: Median 7.4 minutes. With heparin: Median 4.5 minutes. | Protamine sulfate is a drug that reverses the anticoagulant effects of heparin by binding to it. It was originally isolated from the sperm of salmon and other species of fish but is now produced primarily through recombinant biotechnology. Protamine sulfate was approved for medical use in the United States in 1969. Protamine sulfate (protamine (protamines) s) occurs as fine white or off-white amorphous or crystalline powder. It is sparingly soluble in water. The pH is between 6 and 7. The cationic hydrogenated protamine at a pH of 6.8 to 7.1 reacts with anionic heparin at a pH of 5.0 to 7.5 to form an inactive complex. | Protamine sulfate is usually administered to reverse the large dose of heparin administered during certain surgeries, especially heart surgery. | Protamine sulphate 1% demonstrates activity neutralising anticoagulant properties of heparin, creating the complex heparin/protamine. Activity of protamine (towards heparin) takes place within five minutes after intravenous injection of the preparation. | It is a highly cationic peptide that binds to either heparin or low molecular weight heparin (LMWH) to form a stable ion pair, which does not have anticoagulant activity. The ionic complex is then removed and broken down by the reticuloendothelial system. In large doses, protamine sulfate may also have an independentâ€â€however weakâ€â€anticoagulant effect. | Administration of protamine sulfate intravenously could result in severe drop in blood pressure, dyspnea, bradycardia, pulmonary hypertension and anaphylaxis [F3559, F3562, L5371, L5443]. Systemic hypertension, nausea, vomiting and lassitude were also reported [F3559, F3562, L5371, L5443]. Overdosage of this drug may theoretically result in hemorrhage [F3559, F3562, L5371, L5443]. Nevertheless, any possible carcinogenicity, mutagenicity, effects upon pregnancy, effects on the newborn, on children, elderly individuals and a few other groups at risk have revealed there to be no animal toxicology cited in the literature to indicate that any of these risk factors might be present for protamine sulfate [F3562]. | The metabolic fate of the inactive heparin-protamine complex has not yet been formally elucidated [F3559, F3562, L5371, L5443]. Nevertheless, considering protamine sulfate is itself objectively a mixture of basic protein peptide sulfates prepared from sperm or roe of appropriate species of fish (typically of the families Clupeidae or Salmonidae), the involvement of basic protein catalysis via the participation of endogenous peptidases may presumably play a part in the metabolism of protamine sulfate [F3562]. Moreover, as protamine sulfate specifically reverses the anticoagulant activities of heparin by complexing with it, it has also been proposed that the heparin-protamine complex may be plausibly metabolized in part by the lytic enzyme fibrinolysin - a process which would also free heparin [F3559, L5371, L5443]. | In general, based on data obtained from protamine sulfate administered in healthy humans the AUC demonstrated during the initial infusion is concave [F3562]. Protamine concentrations were less than the limit of detection after twenty minutes or less, although the onset of action had been reported to appear within thirty to sixty seconds after intravenous administration [F3559, F3562, L5371, L5443] It is, however, generally documented that the neutralization of heparin occurs within five minutes after the intravenous administration of protamine sulfate [F3559, L5371, L5443]. Moreover, protamine concentration-versus-time data appears to be substantially different between men and women, where weight-adjusted protamine sulfate dosing ended up in significantly decreased AUC and substantially greater plasma clearance and volume of distribution at steady state in women as compared to men [F3562]. | In a study group of twenty-six patients aged between 26 to 80 years and undergoing a cardiac operation with cardiopulmonary bypass, the volume of distribution of protamine sulfate administered was recorded as being 5.4L (with a range of 0.82 to 34L) [A174952]. | In a study group of twenty-six patients aged between 26 to 80 years and undergoing a cardiac operation with cardiopulmonary bypass, the clearance of protamine sulfate administered was recorded as being 1.4 L/min (with a range of 0.61 to 3.8 L/min) [A174952]. | Heparin Antagonists, Hematologic Agents | NA | NA | NA | NA | Coagulation factor X,Antithrombin-III | Protamine Sulfate Injection, USP | Omega Laboratories Ltd | Omega Laboratories Ltd | Protamine Sulfate (protamine (protamines) s) Injection, USP is indicated in the treatment of heparin overdosage. | NA | Protamine sulfate 10 mg, sodium chloride 9 mg and Water for Injection q.s. Sulfuric acid and/or dibasic sodium phosphate (heptahydrate) may have been added for pH adjustment. | off-white amorphous or crystalline powder | Intravenous | Protamine Sulfate (protamine (protamines) s) Injection,USP should be given by very slow intravenous injection in doses not to exceed 50 mg of protamine sulfate (protamine (protamines) s) in any 10-minute period | Protamine sulfate (protamine (protamines) s) is contraindicated in patients who have shown previous intolerance to the drug. | Intravenous injections of protamine (protamines) may cause a sudden fall in blood pressure, bradycardia, pulmonary hypertension, dyspnea, or transitory flushing and a feeling of warmth. There have been reports of anaphylaxis that resulted in respiratory embarrassment | 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 |