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 |
| 10002 | 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. | 18.7 L [Healthy elderly subjects (n = 10, age 65-80 years)] | 139 ml/min [Healthy 65-80 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 | US5180668 | 19-Jan-1993 | 6-Mar-2012 | Treprostinil = increases the risk of bleeding when combined with Lepirudin. | NA | NA | Bayer Healthcare | Bayer Healthcare | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10003 | 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. | 18 L [Renally impaired patients (n = 16, creatinine clearance below 80 mL/min)] | 61 ml/min [renal impaired] | 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 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10004 | 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. | 32.1 L [HIT patients (n = 73)] | 114 ml/min [HIT (Heparin-induced thrombocytopenia)] | 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 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10032 | Th1006 | Bivalirudin | >Th1006_Bivalirudin FPRPGGGGNGDFEEIPEEYL | 2180.285 | C98H138N24O33 | 3.91 | -0.985 | NA | Normal renal function: 0.42 hours (in normal conditions) | 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 [Normal 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 | US7582727 | 1-Sep-2009 | 27-Jul-2028 | Deferasirox, Anticoagulants increase the risk for gastrointestinal ulceration/irritation and/or GI bleeding. If these two agents must be used, patients need to be closely monitored for signs and symptoms of GI toxicity. | Prothrombin | Angiomax | Sandoz Canada Incorporated, The Medicines Company,Cardinal Health, Sandoz Inc | Sandoz Canada Incorporated, The Medicines Company,Cardinal Health, Sandoz Inc | It is used for thinning the blood in patients with unstable angina who are undergoing percutaneous transluminal coronary angioplasty (PTCA) and in patients undergoing percutaneous coronary intervention (PCI). | D-phenylalanyl-L-prolyl-L-arginyl-L-prolyl-glycylglycyl-glycyl-glycyl-L-asparagyl-glycyl-L-aspartyl-L-phenylalanyl-L-glutamyl-L-glutamyl-L-isoleucyl-L-prolyl-L-glutamyl-L-glutamyl-L-tyrosyl-L-leucine trifluoroacetate (salt) hydrate | Each vial contains 250 mg bivalirudin, 125 mg mannitol, and sodium hydroxide to adjust the pH to 5-6 (equivalent of approximately 12.5 mg sodium). When reconstituted with Sterile Water for Injection, the product yields a clear to opalescent, colorless to | Supplied in single-use vials as a white lyophilized cake | Intravenous infusion | Intravenous (IV) bolus dose of 0.75 mg/kg, followed by an infusion of 1.75 mg/kg/h for the duration of the PCI/PTCA procedure. | Allergic and have major active bleeding | Anxiety; back, stomach, or pelvic pain; headache; nausea; nervousness; pain at the injection site; trouble sleeping; upset stomach; vomiting. And severe side effect may include Severe allergic reactions (rash; hives; itching; difficulty breathing. | 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 |
| 10034 | Th1006 | Bivalirudin | >Th1006_Bivalirudin FPRPGGGGNGDFEEIPEEYL | 2180.285 | C98H138N24O33 | 3.91 | -0.985 | NA | Dialysis-dependant patients: 3.5 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 | 2.7 mL/min/kg [moderate 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 | CA2065150 | 14-Dec-1999 | 17-Aug-2010 | Ginkgo biloba, Additive anticoagulant/antiplatelet effects may increase bleed risk. Concomitant therapy should be avoided. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10035 | Th1006 | Bivalirudin | >Th1006_Bivalirudin FPRPGGGGNGDFEEIPEEYL | 2180.285 | C98H138N24O33 | 3.91 | -0.985 | NA | NA | 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 | 2.8 mL/min/kg [severe 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 | NA | NA | NA | Rivaroxaban, Anticoagulants may enhance the anticoagulant effect of rivaroxaban. Avoid concurrent use of rivaroxaban with other anticoagulants whenever possible, other than during transition periods, due to the possible increased for bleeding. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10036 | Th1006 | Bivalirudin | >Th1006_Bivalirudin FPRPGGGGNGDFEEIPEEYL | 2180.285 | C98H138N24O33 | 3.91 | -0.985 | NA | NA | 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 | 1 mL/min/kg [Dialysis-dependent patients] | Amino Acids, Peptides, and Proteins, Anticoagulants, Antithrombins, Blood and Blood Forming Organs, Enzyme Inhibitors, Hematologic Agents, Peptides, Protease Inhibitors, Serine Protease Inhibitors, Thrombin Inhibitors | NA | NA | NA | Treprostinil, The prostacyclin analogue, Treprostinil, increases the risk of bleeding when combined with the anticoagulant, Bivalirudin. Monitor for increased bleeding during concomitant thearpy. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10037 | Th1006 | Bivalirudin | >Th1006_Bivalirudin FPRPGGGGNGDFEEIPEEYL | 2180.285 | C98H138N24O33 | 3.91 | -0.985 | NA | NA | 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 | NA | Amino Acids, Peptides, and Proteins, Anticoagulants, Antithrombins, Blood and Blood Forming Organs, Enzyme Inhibitors, Hematologic Agents, Peptides, Protease Inhibitors, Serine Protease Inhibitors, Thrombin Inhibitors | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10559 | Th1111 | Defibrotide | >Th1111_Defibrotide NA | NA | NA | NA | NA | NA | t1/2-alpha = minutes (10-20 minutes in rat); t1/2-beta = a few hours | Sodium salt of a mixture of single-stranded oligodeoxyribonucleotides, derived from porcine mucosal DNA. It has been shown to possess antithrombotic, anti-inflammatory and anti-ischemic properties and without the associated disadvantages of significant systemic anticoagulant effects. It is marketed under the brand names Dasovas (FM), Noravid, and Prociclide in a variety of countries, but is currently not approved in the USA. The manufacturer is Gentium. | Defibrotide is used to treat or prevent a failure of normal blood flow (occlusive venous disease, OVD) in the liver of patients who have had bone marrow transplants or received certain drugs such as oral estrogens, mercaptopurine, and many others | Defibrotide is a deoxyribonucleic acid derivative extracted from mammalian organs, which has been developed for the treatment of a number of vascular disorders. It appears to increase fibrinolysis and may possess antithrombotic, antiatherosclerotic and anti-ischaemic actions, probably due to its ability to selectively increase prostaglandin I2 and E2 levels and to increase tissue plasminogen activator and decrease plasminogen activator inhibitor function. Defibrotide is available as an intravenous and intramuscular preparation, and also as an oral formulation for long term use. | The drug appears to prevent the formation of blood clots and to help dissolve blood clots by increasing levels of prostaglandin I2, E2, and prostacyclin, altering platelet activity, increasing tissue plasminogen activator function, and decreasing activity of tissue plasminogen activator inhibitor. Prostaglandin I2 relaxes the smooth muscle of blood vessels and prevents platelets from adhering to each other. Prostaglandin E2 at certain concentrations also inhibits platelet aggregation. Moreover, the drug provides additional beneficial anti-inflammatory and antiischemic activities as recent sudies have shown. It is yet unclear, if the latter effects can be utilized clinically (e.g., treatment of ischemic stroke). | NA | NA | Bioavailability is 58-70% following oral administration, compared to parenteral forms (i.v. and i.m. = 100%). | NA | NA | Antithrombins | NA | NA | NA | NA | Adenosine receptor A1,Adenosine receptor A2a,Adenosine receptor A2b | Noravid | sanofi-aventis | sanofi-aventis | Defibrotide is used to treat or prevent a failure of normal blood flow (occlusive venous disease, OVD) in the liver of patients who have had bone marrow transplants or received certain drugs such as oral estrogens, mercaptopurine, and many others. | Polydeoxyribonucleotides of bovine lung | N. A. | N. A. | NA | 6.25mg/kg body weight every 6 hours (25mg/kg/day) | NA | NA | Link | NA | NA |
| 10560 | Th1111 | Defibrotide | >Th1111_Defibrotide NA | NA | NA | NA | NA | NA | t1/2-alpha = minutes (10-20 minutes in rat); t1/2-beta = a few hours | Sodium salt of a mixture of single-stranded oligodeoxyribonucleotides, derived from porcine mucosal DNA. It has been shown to possess antithrombotic, anti-inflammatory and anti-ischemic properties and without the associated disadvantages of significant systemic anticoagulant effects. It is marketed under the brand names Dasovas (FM), Noravid, and Prociclide in a variety of countries, but is currently not approved in the USA. The manufacturer is Gentium. | Defibrotide is used to treat or prevent a failure of normal blood flow (occlusive venous disease, OVD) in the liver of patients who have had bone marrow transplants or received certain drugs such as oral estrogens, mercaptopurine, and many others | Defibrotide is a deoxyribonucleic acid derivative extracted from mammalian organs, which has been developed for the treatment of a number of vascular disorders. It appears to increase fibrinolysis and may possess antithrombotic, antiatherosclerotic and anti-ischaemic actions, probably due to its ability to selectively increase prostaglandin I2 and E2 levels and to increase tissue plasminogen activator and decrease plasminogen activator inhibitor function. Defibrotide is available as an intravenous and intramuscular preparation, and also as an oral formulation for long term use. | The drug appears to prevent the formation of blood clots and to help dissolve blood clots by increasing levels of prostaglandin I2, E2, and prostacyclin, altering platelet activity, increasing tissue plasminogen activator function, and decreasing activity of tissue plasminogen activator inhibitor. Prostaglandin I2 relaxes the smooth muscle of blood vessels and prevents platelets from adhering to each other. Prostaglandin E2 at certain concentrations also inhibits platelet aggregation. Moreover, the drug provides additional beneficial anti-inflammatory and antiischemic activities as recent sudies have shown. It is yet unclear, if the latter effects can be utilized clinically (e.g., treatment of ischemic stroke). | NA | NA | Bioavailability is 58-70% following oral administration, compared to parenteral forms (i.v. and i.m. = 100%). | NA | NA | Antithrombins | NA | NA | NA | NA | Adenosine receptor A1,Adenosine receptor A2a,Adenosine receptor A2b | Defitelio | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10577 | Th1118 | Sulodexide | NA | 5000-8000 | NA | NA | NA | NA | elimination half-life was 11.7 ± 2.0 h by IV route | A mixture of glycosaminoglycans (GAGs), composed of dermatan sulfate (DS) and fast moving heparin (FMH). | For the treatment of thrombosis. Also investigated for use/treatment in diabetic kidney disease, and neuropathy (diabetic). | The low molecular weight of both sulodexide fractions allows for extensive oral absorption compared to unfractionated heparin. The pharmacological effects of sulodexide differ substantially from other glycosaminoglycans and are mainly characterized by a prolonged half-life and reduced effect on global coagulation and bleeding parameters. Due to the presence of both glycosaminoglycan fractions, sulodexide potentiates the antiprotease activities of both antithrombin III and heparin cofactor II simultaneously. | Thrombin inhibition produced by sulodexide is due to the additive effect of its components, namely, heparin cofactor II (HCII) catalysis by dermatan sulfate and antithrombin-III catalysis by fast moving heparin (FMH). | Sulodexide seems to be well tolerated. Most adverse effects reported are related to the GI system and seem to be transient in nature. Among others adverse reactions are diarrhea, epigastralgia, dyspepsia, heartburn and dizziness. Allergic reactions, such as skin rash, have also been reported but are very rare. | It is mainly metabolized in the liver. | Sulodexide can be administered via the oral route, IV and IM routes. After oral dosing, the absorption rate being equivalent, the bioavailability is 40-60%. either calculated from the fast-moving heparin fraction or from the dermatan fraction. Bioavailability following IM administration is approximately 90%. After a rapid absorption in the intestine, the dermatan and heparin components start to appear in the plasma. Sulodexide is degraded after ingestion and loses its sulfate groups and both sulfated and unsulfated groups circulate in the blood for up to 24hours. AUC=22.83+/-4.44mg.h/L. | Cmax=516+/-77.54ng/mL, Tmax=1.33+/-0.58h, Vd=71.24+/-14.06L (b phase). Sulodexide reaches high concentrations in the plasma and is widely distributed in the endothelial layer. Binding to endothelial cell receptors in arteries and veins contributes to its rapid distribution profile. | 2.70+/-0.58L/h | Antithrombins and Fibrinolytic Agents and Hypoglycemic Agents and Anticoagulants and Hypolipidemic Agents | NA | NA | NA | NA | Heparin cofactor 2,Antithrombin-III | SULODEXIDE | Syntex S.A | Syntex S.A | Antithrombotic and antithrombin activity is of great pharmacologic interest and makes sulodexide a suitable drug for the prophylaxis and treatment of arterial and venous peripheral diseases | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10711 | Th1164 | Antithrombin Alfa | NA | 57,215 | C2191H3451N583O656S18 | 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 | NA | NA | NA | NA | NA | NA | NA | NA | 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 |
| 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 |
| 10714 | 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 | Enhanced anticoagulant effect; increased risk of bleeding complications with Heparin; Heparin also Decreases half-life of antithrombin III | Antithrombin-III | NA | NA | NA | NA | NA | NA | NA | NA | NA | 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. | Link | NA | NA |
| 10715 | 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 USA, LLC | GRIFOLS USA, LLC | 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 | NA | kit | 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 |
| 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 |
| 10718 | 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 USA, LLC | GRIFOLS USA, LLC | 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 | NA | kit | 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 |
| 12578 | Th1335 | Caplacizumab | >Th1335_Caplacizumab EVQLVESGGGLVQPGGSLRLSCAASGRTFSYNPMGWFRQAPGKGRELVAAISRTGGSTYYPDSVEGRFTISRDNAKRMVYLQMNSLRAEDTAVYYCAAAGVRAEDGRVRTLPSEYTFWGQGTQVTVSSAAAEVQLVESGGGLVQPGGSLRLSCAASGRTFSYNPMGWFRQAPGKGRELVAAISRTGGSTYYPDSVEGRFTISRDNAKRMVYLQMNSLRAEDTAVYYCAAAGVRAEDGRVRTLPSEYTFWGQGTQVTVSS | 27880 | C1213H1891N357O380S10 | 6.6 - 7.2 | NA | 61 ºC (Fab fragment) | The reported half-life is reported to be in the range of 16-27 hours.[F3457] | Caplacizumab, firstly called ALX-0081, is a humanized single-variable-domain immunoglobulin consisting of two identical humanized building blocks genetically linked by a three-alanine linker. Caplacizumab was developed by Ablynx, a Sanofi company and FDA approved on February 6, 2019,[L5302] and approved previously by the EU in October 2018 as a combination therapy with plasma exchange and immunosuppression.[A174634] | Capacizumab is approved for the treatment of adults experiencing an episode of acquired thrombotic thrombocytopenic purpura (aTTP) in conjunction with plasma exchange and immunosuppression in patients 18 years or older.[A174634, L5302] aTTP is a rare autoimmune condition presented by a disruption of blood clotting order which is translated into systemic microvascular thrombosis leading to profound thrombocytopenia, hemolytic anemia and organ ischemia. It is caused by the production of autoantibodies against ADAMTS-13 which is the protein in charge of cleaving the von-Wilebrand factor. The lack of this process produces the generation of ultra large von Wilebrand multimers that bind to platelets and form microthrombi and causing thromboembolic complications.[A174649] Previously, capacizumab was under review for the prevention of thrombosis in high-risk patients with acute coronary syndrome undergoing percutaneous coronary intervention but this indication was withdrawn.[A174634] | _In vitro_ studies have shown a caplacizumab-driven complete inhibition of platelet aggregation and in phase II clinical trials, it was shown to reduce the activity of the von Willebrand factor by 20% from treatment day 1 until treatment day 30. The level of von Willebrand factor in the plasma was also significantly reduced due to the clearance of the von Willebrand-caplacizumab complex.[A174634] In phase III clinical trials, more than 50% of the tested individuals reached a platelet normal count. In these trials, it was observed as well a significant reduction in the incidence of aTTP[A174634] as well as a significant reduction in the median time to response of about 39%.[A174652] However, as caplacizumab does not target autoimmune response, relapses were observed after treatment discontinuation.[A174643] The last clinical trial prior approval showed production of a platelet count of more than 150,000 per mcl after the cessation of plasma exchange therapy for 5 days as well as a reduction of patient recurrent thrombotic thrombocytopenic purpura and of disease-related death during treatment.[L5302] | Caplacizumab acts by targetting the A1 domain of the ultra-large von Willebrand factor which in order inhibits the interaction with the glycoprotein Ib-IX-V receptor in the platelets. Caplacizumab binds to von Willebrand factor with an affinity of 8.5 nM, thus it is very target specific.[5305] The blockage of the von Willebrand factor prevents the interaction between the von Willebrand factor and the platelets, hence, preventing platelet aggregation.[A174634] | Cases of overdose are represented by an increased risk of bleeding and in these cases, external administration of von Willebrand factor concentrate should be done.[FDA label] To this point, there have not been performed studies regarding the effect on fertility, genotoxicity, or carcinogenicity | Caplacizumab is degraded in the reticuloendothelial system to small peptides and amino acids which can be used for de-novo protein synthesis.[A31470] | After intravenous administration of caplacizumab, the pharmacokinetic profile is non-linear and to follow a non-compartmental model as the pharmacokinetic profile of this drug is dependent on the expression of von Willebrand factor. After administration, caplacizumab is rapidly absorbed with a dose-dependent behavior. The peak concentration was reached after 6-7 hours[A174634] and it presents a very high bioavailability reaching approximately 90%.[F3457] The subcutaneous administration of a dose of 10 mg of caplacizumab produced a peak concentration of 528 ng/ml and an AUC of 7951 ng.h/ml.[L5314] | The reported volume of distribution of caplacizumab is 6.33 L.[A174634] | As the elimination is highly divided among hepatic, target-driven and renal elimination, the calculation of the clearance rate is not significant for drug description. | Antithrombotic Agents, Misc. | NA | NA | NA | NA | von Willebrand factor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |