Detailed description page of THPdb

This page displays user query in tabular form.

Th1046 details

Primary information
ID 1327
ThPP ID Th1046
Therapeutic Peptide/Protein Name Abciximab
Sequence H ReoPro-like antibody Heavy Chain 1: EVQLQQSGAELV view full sequnce in fasta
Functional Classification IIa
Molecular Weight 145651.1
Chemical Formula C6462H9964N1690O2049S48
Isoelectric Point 6.16
Hydrophobicity -0.424
Melting Point (℃) 71
Half Life Following intravenous bolus administration, free plasma concentrations of Abciximab decrease rapidly
Description Abciximab is a Fab fragment of the chimeric human-murine monoclonal antibody 7E3. Abciximab binds to the glycoprotein (GP) IIb/IIIa receptor of human platelets and inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules. It also binds to vitronectin (ÃŽÂ±vÃŽÂ²3) receptor found on platelets and vessel wall endothelial and smooth muscle cells.
Indication/Disease Abciximab is indicated as an adjunct to percutaneous coronary intervention for the prevention of cardiac ischemic complications in patients undergoing percutaneous coronary intervention and in patients with unstable angina not responding to conventional medical therapy when percutaneous coronary intervention is planned within 24 hours. Abciximab is intended for use with aspirin and heparin and has been studied only in that setting.
Pharmacodynamics Abciximab inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules to GPIIb/IIIa receptor sites on activated platelets. A single intravenous bolus dose from 0.15 mg/kg to 0.30 mg/kg produced rapid dose-dependent inhibition of platelet function. After two hours post-injection with a dose of 0.25 - 0.30 mg/kg, 80% of the GPIIb/IIIa receptors were blocked and platelet aggregation was prevented. GPIIb/IIIa is the major surface receptor involved in the final pathway of platelet aggregation. Bleeding time increases to over 30 minutes at the aforementioned doses. To compare, baseline values were five minutes.
Mechanism of Action Abciximab binds to the intact platelet GPIIb/IIIa receptor, which is a member of the integrin family of adhesion receptors and the major platelet surface receptor involved in platelet aggregation. This binding is thought to involve steric hindrance and/orconformational alterations which block access of large molecules to the receptor rather than direct interaction with the RGD (arginine-glycine-aspartic acid) binding site of GPIIb/IIIa. By binding to the vitronectin receptor (also known as the ÃŽÂ±vÃŽÂ²3 integrin), abciximab blocks effects mediated by this integrin which include cell adhesion. Furthermore, abciximab blocks Mac-1 receptor on monocytes and neutrophils thus inhibiting monocyte adhesion.
Toxicity N.A.
Metabolism Most likely removed by opsonization via the reticuloendothelial system when bound to platelets, or by human antimurine antibody production. Excreted renally.
Absorption N.A.
Volume of Distribution N.A.
Clearance N.A.
Categories Anticoagulants
Patents Number CA1341357
Date of Issue 07/05/02
Date of Expiry 07/05/19
Drug Interaction Additive anticoagulant/antiplatelet effects may increase bleed risk. Concomitant therapy should be avoided with Ginkgo biloba.
Target Integrin beta-3,Integrin alpha-IIb,Low affinity immunoglobulin gamma Fc region receptor III-B,Complement C1r subcomponent,Complement C1q subcomponent subunit A,Complement C1q subcomponent subunit B,Complement C1q subcomponent subunit C,Low affinity immuno
Information of corresponding available drug in the market
Brand Name ReoPro
Company Eli Lilly and Company
Brand Discription Abciximab, ReoPro, is the Fab fragment of the chimeric human-murine monoclonal antibody 7E3. Abciximab binds to the glycoprotein (GP) IIb/IIIa receptor of human platelets and inhibits platelet aggregation. Abciximab also binds to the vitronectin (_v_3) re
Prescribed for ReoPro is used to lessen the chance of heart attack in people who need percutaneous coronary intervention (PCI), a procedure to open blocked arteries of the heart.
Chemical Name N.A.
Formulation Each single use vial contains 2 mg/mL of Abciximab in a buffered solution (pH 7.2) of 0.01 M sodium phosphate, 0.15 M sodium chloride and 0.001% polysorbate 80 in Water for Injection. No preservatives are added.
Physcial Appearance Clear, colorless, Sterile, non-pyrogenic solution
Route of Administration Intravenous administartion
Recommended Dosage The recommended dosage of Abciximab in adults is a 0.25 mg/kg intravenous bolus administered 10-60 minutes before the start of PCI, followed by a continuous Intravenous infusion of 0.125 _g/kg/min (to a maximum of 10 _g/min) for 12 hours.
Contraindication Active internal bleeding, Recent (within six weeks) gastrointestinal (GI) or genitourinary (GU) bleeding of clinical significance, History of cerebrovascular accident (CVA) within two years, or CVA with a significant residual neurological deficit, Bleeding diathesis; Administration of oral anticoagulants within seven days unless prothrombin time is I 1.2 times control; Thrombocytopenia (< 100,000 cells/pL); Recent (within six weeks) major surgery or trauma; Intracranial neoplasm, arteriovenous malformation, or aneurysm; Severe uncontrolled hypertension; Presumed or documented history of vasculitis; Use of intravenous dextran before percutaneous coronary intervention, or intent to use it during an intervention.
Side Effects Bleeding; blurred vision; confusion; dizziness, faintness, or lightheadedness when getting up from a lying or sitting position suddenly; sweating; unusual tiredness or weakness
Useful Link http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm
PubMed ID 12939213
3-D Structure Th1046 (View) or (Download)

Primary information
ID 1328
ThPP ID Th1046
Therapeutic Peptide/Protein Name Abciximab
Sequence H ReoPro-like antibody Heavy Chain 1: EVQLQQSGAELV view full sequnce in fasta
Functional Classification IIa
Molecular Weight 145651.1
Chemical Formula C6462H9964N1690O2049S48
Isoelectric Point 6.16
Hydrophobicity -0.424
Melting Point (℃) 71
Half Life Following intravenous bolus administration, free plasma concentrations of Abciximab decrease rapidly
Description Abciximab is a Fab fragment of the chimeric human-murine monoclonal antibody 7E3. Abciximab binds to the glycoprotein (GP) IIb/IIIa receptor of human platelets and inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules. It also binds to vitronectin (ÃŽÂ±vÃŽÂ²3) receptor found on platelets and vessel wall endothelial and smooth muscle cells.
Indication/Disease Abciximab is indicated as an adjunct to percutaneous coronary intervention for the prevention of cardiac ischemic complications in patients undergoing percutaneous coronary intervention and in patients with unstable angina not responding to conventional medical therapy when percutaneous coronary intervention is planned within 24 hours. Abciximab is intended for use with aspirin and heparin and has been studied only in that setting.
Pharmacodynamics Abciximab inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules to GPIIb/IIIa receptor sites on activated platelets. A single intravenous bolus dose from 0.15 mg/kg to 0.30 mg/kg produced rapid dose-dependent inhibition of platelet function. After two hours post-injection with a dose of 0.25 - 0.30 mg/kg, 80% of the GPIIb/IIIa receptors were blocked and platelet aggregation was prevented. GPIIb/IIIa is the major surface receptor involved in the final pathway of platelet aggregation. Bleeding time increases to over 30 minutes at the aforementioned doses. To compare, baseline values were five minutes.
Mechanism of Action Abciximab binds to the intact platelet GPIIb/IIIa receptor, which is a member of the integrin family of adhesion receptors and the major platelet surface receptor involved in platelet aggregation. This binding is thought to involve steric hindrance and/orconformational alterations which block access of large molecules to the receptor rather than direct interaction with the RGD (arginine-glycine-aspartic acid) binding site of GPIIb/IIIa. By binding to the vitronectin receptor (also known as the ÃŽÂ±vÃŽÂ²3 integrin), abciximab blocks effects mediated by this integrin which include cell adhesion. Furthermore, abciximab blocks Mac-1 receptor on monocytes and neutrophils thus inhibiting monocyte adhesion.
Toxicity N.A.
Metabolism Most likely removed by opsonization via the reticuloendothelial system when bound to platelets, or by human antimurine antibody production. Excreted renally.
Absorption N.A.
Volume of Distribution N.A.
Clearance N.A.
Categories Platelet Aggregation Inhibitors
Patents Number N.A.
Date of Issue N.A.
Date of Expiry N.A.
Drug Interaction Tirofiban has additive effects. Concomitant use is contraindicated.
Target N.A.
Information of corresponding available drug in the market
Brand Name N.A.
Company N.A.
Brand Discription N.A.
Prescribed for N.A.
Chemical Name N.A.
Formulation N.A.
Physcial Appearance N.A.
Route of Administration N.A.
Recommended Dosage N.A.
Contraindication N.A.
Side Effects Black, tarry stools; bleeding gums; blood in urine or stools; pinpoint red spots on skin; unusual bleeding or bruising
Useful Link http://www.drugs.com/reopro.html
PubMed ID 12939213
3-D Structure Th1046 (View) or (Download)

Primary information
ID 1329
ThPP ID Th1046
Therapeutic Peptide/Protein Name Abciximab
Sequence H ReoPro-like antibody Heavy Chain 1: EVQLQQSGAELV view full sequnce in fasta
Functional Classification IIa
Molecular Weight 145651.1
Chemical Formula C6462H9964N1690O2049S48
Isoelectric Point 6.16
Hydrophobicity -0.424
Melting Point (℃) 71
Half Life Following intravenous bolus administration, free plasma concentrations of Abciximab decrease rapidly
Description Abciximab is a Fab fragment of the chimeric human-murine monoclonal antibody 7E3. Abciximab binds to the glycoprotein (GP) IIb/IIIa receptor of human platelets and inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules. It also binds to vitronectin (ÃŽÂ±vÃŽÂ²3) receptor found on platelets and vessel wall endothelial and smooth muscle cells.
Indication/Disease Abciximab is indicated as an adjunct to percutaneous coronary intervention for the prevention of cardiac ischemic complications in patients undergoing percutaneous coronary intervention and in patients with unstable angina not responding to conventional medical therapy when percutaneous coronary intervention is planned within 24 hours. Abciximab is intended for use with aspirin and heparin and has been studied only in that setting.
Pharmacodynamics Abciximab inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules to GPIIb/IIIa receptor sites on activated platelets. A single intravenous bolus dose from 0.15 mg/kg to 0.30 mg/kg produced rapid dose-dependent inhibition of platelet function. After two hours post-injection with a dose of 0.25 - 0.30 mg/kg, 80% of the GPIIb/IIIa receptors were blocked and platelet aggregation was prevented. GPIIb/IIIa is the major surface receptor involved in the final pathway of platelet aggregation. Bleeding time increases to over 30 minutes at the aforementioned doses. To compare, baseline values were five minutes.
Mechanism of Action Abciximab binds to the intact platelet GPIIb/IIIa receptor, which is a member of the integrin family of adhesion receptors and the major platelet surface receptor involved in platelet aggregation. This binding is thought to involve steric hindrance and/orconformational alterations which block access of large molecules to the receptor rather than direct interaction with the RGD (arginine-glycine-aspartic acid) binding site of GPIIb/IIIa. By binding to the vitronectin receptor (also known as the ÃŽÂ±vÃŽÂ²3 integrin), abciximab blocks effects mediated by this integrin which include cell adhesion. Furthermore, abciximab blocks Mac-1 receptor on monocytes and neutrophils thus inhibiting monocyte adhesion.
Toxicity N.A.
Metabolism Most likely removed by opsonization via the reticuloendothelial system when bound to platelets, or by human antimurine antibody production. Excreted renally.
Absorption N.A.
Volume of Distribution N.A.
Clearance N.A.
Categories N.A.
Patents Number N.A.
Date of Issue N.A.
Date of Expiry N.A.
Drug Interaction Abciximab may increase the risk of a hypersensitivy reaction to Trastuzumab.
Target N.A.
Information of corresponding available drug in the market
Brand Name N.A.
Company N.A.
Brand Discription N.A.
Prescribed for N.A.
Chemical Name N.A.
Formulation N.A.
Physcial Appearance N.A.
Route of Administration N.A.
Recommended Dosage N.A.
Contraindication N.A.
Side Effects Chest pain or discomfort; chills; cough; eye pain; fever; general feeling of illness; headache; pale skin; rapid weight gain; shortness of breath; slow or irregular heartbeat; sneezing; sore throat; swelling of hands, ankles, feet, or lower legs.
Useful Link http://www.rxlist.com/reopro-drug.htm
PubMed ID 12939213
3-D Structure Th1046 (View) or (Download)

Primary information
ID 1330
ThPP ID Th1046
Therapeutic Peptide/Protein Name Abciximab
Sequence H ReoPro-like antibody Heavy Chain 1: EVQLQQSGAELV view full sequnce in fasta
Functional Classification IIa
Molecular Weight 145651.1
Chemical Formula C6462H9964N1690O2049S48
Isoelectric Point 6.16
Hydrophobicity -0.424
Melting Point (℃) 71
Half Life Following intravenous bolus administration, free plasma concentrations of Abciximab decrease rapidly
Description Abciximab is a Fab fragment of the chimeric human-murine monoclonal antibody 7E3. Abciximab binds to the glycoprotein (GP) IIb/IIIa receptor of human platelets and inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules. It also binds to vitronectin (ÃŽÂ±vÃŽÂ²3) receptor found on platelets and vessel wall endothelial and smooth muscle cells.
Indication/Disease Abciximab is indicated as an adjunct to percutaneous coronary intervention for the prevention of cardiac ischemic complications in patients undergoing percutaneous coronary intervention and in patients with unstable angina not responding to conventional medical therapy when percutaneous coronary intervention is planned within 24 hours. Abciximab is intended for use with aspirin and heparin and has been studied only in that setting.
Pharmacodynamics Abciximab inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules to GPIIb/IIIa receptor sites on activated platelets. A single intravenous bolus dose from 0.15 mg/kg to 0.30 mg/kg produced rapid dose-dependent inhibition of platelet function. After two hours post-injection with a dose of 0.25 - 0.30 mg/kg, 80% of the GPIIb/IIIa receptors were blocked and platelet aggregation was prevented. GPIIb/IIIa is the major surface receptor involved in the final pathway of platelet aggregation. Bleeding time increases to over 30 minutes at the aforementioned doses. To compare, baseline values were five minutes.
Mechanism of Action Abciximab binds to the intact platelet GPIIb/IIIa receptor, which is a member of the integrin family of adhesion receptors and the major platelet surface receptor involved in platelet aggregation. This binding is thought to involve steric hindrance and/orconformational alterations which block access of large molecules to the receptor rather than direct interaction with the RGD (arginine-glycine-aspartic acid) binding site of GPIIb/IIIa. By binding to the vitronectin receptor (also known as the ÃŽÂ±vÃŽÂ²3 integrin), abciximab blocks effects mediated by this integrin which include cell adhesion. Furthermore, abciximab blocks Mac-1 receptor on monocytes and neutrophils thus inhibiting monocyte adhesion.
Toxicity N.A.
Metabolism Most likely removed by opsonization via the reticuloendothelial system when bound to platelets, or by human antimurine antibody production. Excreted renally.
Absorption N.A.
Volume of Distribution N.A.
Clearance N.A.
Categories N.A.
Patents Number N.A.
Date of Issue N.A.
Date of Expiry N.A.
Drug Interaction The prostacyclin analogue, Treprostinil, increases the risk of bleeding when combined with the antiplatelet agent, Abciximab. Monitor for increased bleeding during concomitant thearpy.
Target N.A.
Information of corresponding available drug in the market
Brand Name N.A.
Company N.A.
Brand Discription N.A.
Prescribed for N.A.
Chemical Name N.A.
Formulation N.A.
Physcial Appearance N.A.
Route of Administration N.A.
Recommended Dosage N.A.
Contraindication N.A.
Side Effects N.A.
Useful Link N.A.
PubMed ID 12939213
3-D Structure Th1046 (View) or (Download)

OSDDlinux

Raghava's Group

IMTECH

CSIR

CRDD
CPPSITE 2.0

Primary information
ID	1327
ThPP ID	Th1046
Therapeutic Peptide/Protein Name	Abciximab
Sequence	H ReoPro-like antibody Heavy Chain 1: EVQLQQSGAELV view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	145651.1
Chemical Formula	C6462H9964N1690O2049S48
Isoelectric Point	6.16
Hydrophobicity	-0.424
Melting Point (℃)	71
Half Life	Following intravenous bolus administration, free plasma concentrations of Abciximab decrease rapidly
Description	Abciximab is a Fab fragment of the chimeric human-murine monoclonal antibody 7E3. Abciximab binds to the glycoprotein (GP) IIb/IIIa receptor of human platelets and inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules. It also binds to vitronectin (ÃŽÂ±vÃŽÂ²3) receptor found on platelets and vessel wall endothelial and smooth muscle cells.
Indication/Disease	Abciximab is indicated as an adjunct to percutaneous coronary intervention for the prevention of cardiac ischemic complications in patients undergoing percutaneous coronary intervention and in patients with unstable angina not responding to conventional medical therapy when percutaneous coronary intervention is planned within 24 hours. Abciximab is intended for use with aspirin and heparin and has been studied only in that setting.
Pharmacodynamics	Abciximab inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules to GPIIb/IIIa receptor sites on activated platelets. A single intravenous bolus dose from 0.15 mg/kg to 0.30 mg/kg produced rapid dose-dependent inhibition of platelet function. After two hours post-injection with a dose of 0.25 - 0.30 mg/kg, 80% of the GPIIb/IIIa receptors were blocked and platelet aggregation was prevented. GPIIb/IIIa is the major surface receptor involved in the final pathway of platelet aggregation. Bleeding time increases to over 30 minutes at the aforementioned doses. To compare, baseline values were five minutes.
Mechanism of Action	Abciximab binds to the intact platelet GPIIb/IIIa receptor, which is a member of the integrin family of adhesion receptors and the major platelet surface receptor involved in platelet aggregation. This binding is thought to involve steric hindrance and/orconformational alterations which block access of large molecules to the receptor rather than direct interaction with the RGD (arginine-glycine-aspartic acid) binding site of GPIIb/IIIa. By binding to the vitronectin receptor (also known as the ÃŽÂ±vÃŽÂ²3 integrin), abciximab blocks effects mediated by this integrin which include cell adhesion. Furthermore, abciximab blocks Mac-1 receptor on monocytes and neutrophils thus inhibiting monocyte adhesion.
Toxicity	N.A.
Metabolism	Most likely removed by opsonization via the reticuloendothelial system when bound to platelets, or by human antimurine antibody production. Excreted renally.
Absorption	N.A.
Volume of Distribution	N.A.
Clearance	N.A.
Categories	Anticoagulants
Patents Number	CA1341357
Date of Issue	07/05/02
Date of Expiry	07/05/19
Drug Interaction	Additive anticoagulant/antiplatelet effects may increase bleed risk. Concomitant therapy should be avoided with Ginkgo biloba.
Target	Integrin beta-3,Integrin alpha-IIb,Low affinity immunoglobulin gamma Fc region receptor III-B,Complement C1r subcomponent,Complement C1q subcomponent subunit A,Complement C1q subcomponent subunit B,Complement C1q subcomponent subunit C,Low affinity immuno
Information of corresponding available drug in the market
Brand Name	ReoPro
Company	Eli Lilly and Company
Brand Discription	Abciximab, ReoPro, is the Fab fragment of the chimeric human-murine monoclonal antibody 7E3. Abciximab binds to the glycoprotein (GP) IIb/IIIa receptor of human platelets and inhibits platelet aggregation. Abciximab also binds to the vitronectin (_v_3) re
Prescribed for	ReoPro is used to lessen the chance of heart attack in people who need percutaneous coronary intervention (PCI), a procedure to open blocked arteries of the heart.
Chemical Name	N.A.
Formulation	Each single use vial contains 2 mg/mL of Abciximab in a buffered solution (pH 7.2) of 0.01 M sodium phosphate, 0.15 M sodium chloride and 0.001% polysorbate 80 in Water for Injection. No preservatives are added.
Physcial Appearance	Clear, colorless, Sterile, non-pyrogenic solution
Route of Administration	Intravenous administartion
Recommended Dosage	The recommended dosage of Abciximab in adults is a 0.25 mg/kg intravenous bolus administered 10-60 minutes before the start of PCI, followed by a continuous Intravenous infusion of 0.125 _g/kg/min (to a maximum of 10 _g/min) for 12 hours.
Contraindication	Active internal bleeding, Recent (within six weeks) gastrointestinal (GI) or genitourinary (GU) bleeding of clinical significance, History of cerebrovascular accident (CVA) within two years, or CVA with a significant residual neurological deficit, Bleeding diathesis; Administration of oral anticoagulants within seven days unless prothrombin time is I 1.2 times control; Thrombocytopenia (< 100,000 cells/pL); Recent (within six weeks) major surgery or trauma; Intracranial neoplasm, arteriovenous malformation, or aneurysm; Severe uncontrolled hypertension; Presumed or documented history of vasculitis; Use of intravenous dextran before percutaneous coronary intervention, or intent to use it during an intervention.
Side Effects	Bleeding; blurred vision; confusion; dizziness, faintness, or lightheadedness when getting up from a lying or sitting position suddenly; sweating; unusual tiredness or weakness
Useful Link	http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm
PubMed ID	12939213
3-D Structure	Th1046 (View) or (Download)

Primary information
ID	1328
ThPP ID	Th1046
Therapeutic Peptide/Protein Name	Abciximab
Sequence	H ReoPro-like antibody Heavy Chain 1: EVQLQQSGAELV view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	145651.1
Chemical Formula	C6462H9964N1690O2049S48
Isoelectric Point	6.16
Hydrophobicity	-0.424
Melting Point (℃)	71
Half Life	Following intravenous bolus administration, free plasma concentrations of Abciximab decrease rapidly
Description	Abciximab is a Fab fragment of the chimeric human-murine monoclonal antibody 7E3. Abciximab binds to the glycoprotein (GP) IIb/IIIa receptor of human platelets and inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules. It also binds to vitronectin (ÃŽÂ±vÃŽÂ²3) receptor found on platelets and vessel wall endothelial and smooth muscle cells.
Indication/Disease	Abciximab is indicated as an adjunct to percutaneous coronary intervention for the prevention of cardiac ischemic complications in patients undergoing percutaneous coronary intervention and in patients with unstable angina not responding to conventional medical therapy when percutaneous coronary intervention is planned within 24 hours. Abciximab is intended for use with aspirin and heparin and has been studied only in that setting.
Pharmacodynamics	Abciximab inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules to GPIIb/IIIa receptor sites on activated platelets. A single intravenous bolus dose from 0.15 mg/kg to 0.30 mg/kg produced rapid dose-dependent inhibition of platelet function. After two hours post-injection with a dose of 0.25 - 0.30 mg/kg, 80% of the GPIIb/IIIa receptors were blocked and platelet aggregation was prevented. GPIIb/IIIa is the major surface receptor involved in the final pathway of platelet aggregation. Bleeding time increases to over 30 minutes at the aforementioned doses. To compare, baseline values were five minutes.
Mechanism of Action	Abciximab binds to the intact platelet GPIIb/IIIa receptor, which is a member of the integrin family of adhesion receptors and the major platelet surface receptor involved in platelet aggregation. This binding is thought to involve steric hindrance and/orconformational alterations which block access of large molecules to the receptor rather than direct interaction with the RGD (arginine-glycine-aspartic acid) binding site of GPIIb/IIIa. By binding to the vitronectin receptor (also known as the ÃŽÂ±vÃŽÂ²3 integrin), abciximab blocks effects mediated by this integrin which include cell adhesion. Furthermore, abciximab blocks Mac-1 receptor on monocytes and neutrophils thus inhibiting monocyte adhesion.
Toxicity	N.A.
Metabolism	Most likely removed by opsonization via the reticuloendothelial system when bound to platelets, or by human antimurine antibody production. Excreted renally.
Absorption	N.A.
Volume of Distribution	N.A.
Clearance	N.A.
Categories	Platelet Aggregation Inhibitors
Patents Number	N.A.
Date of Issue	N.A.
Date of Expiry	N.A.
Drug Interaction	Tirofiban has additive effects. Concomitant use is contraindicated.
Target	N.A.
Information of corresponding available drug in the market
Brand Name	N.A.
Company	N.A.
Brand Discription	N.A.
Prescribed for	N.A.
Chemical Name	N.A.
Formulation	N.A.
Physcial Appearance	N.A.
Route of Administration	N.A.
Recommended Dosage	N.A.
Contraindication	N.A.
Side Effects	Black, tarry stools; bleeding gums; blood in urine or stools; pinpoint red spots on skin; unusual bleeding or bruising
Useful Link	http://www.drugs.com/reopro.html
PubMed ID	12939213
3-D Structure	Th1046 (View) or (Download)

Primary information
ID	1329
ThPP ID	Th1046
Therapeutic Peptide/Protein Name	Abciximab
Sequence	H ReoPro-like antibody Heavy Chain 1: EVQLQQSGAELV view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	145651.1
Chemical Formula	C6462H9964N1690O2049S48
Isoelectric Point	6.16
Hydrophobicity	-0.424
Melting Point (℃)	71
Half Life	Following intravenous bolus administration, free plasma concentrations of Abciximab decrease rapidly
Description	Abciximab is a Fab fragment of the chimeric human-murine monoclonal antibody 7E3. Abciximab binds to the glycoprotein (GP) IIb/IIIa receptor of human platelets and inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules. It also binds to vitronectin (ÃŽÂ±vÃŽÂ²3) receptor found on platelets and vessel wall endothelial and smooth muscle cells.
Indication/Disease	Abciximab is indicated as an adjunct to percutaneous coronary intervention for the prevention of cardiac ischemic complications in patients undergoing percutaneous coronary intervention and in patients with unstable angina not responding to conventional medical therapy when percutaneous coronary intervention is planned within 24 hours. Abciximab is intended for use with aspirin and heparin and has been studied only in that setting.
Pharmacodynamics	Abciximab inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules to GPIIb/IIIa receptor sites on activated platelets. A single intravenous bolus dose from 0.15 mg/kg to 0.30 mg/kg produced rapid dose-dependent inhibition of platelet function. After two hours post-injection with a dose of 0.25 - 0.30 mg/kg, 80% of the GPIIb/IIIa receptors were blocked and platelet aggregation was prevented. GPIIb/IIIa is the major surface receptor involved in the final pathway of platelet aggregation. Bleeding time increases to over 30 minutes at the aforementioned doses. To compare, baseline values were five minutes.
Mechanism of Action	Abciximab binds to the intact platelet GPIIb/IIIa receptor, which is a member of the integrin family of adhesion receptors and the major platelet surface receptor involved in platelet aggregation. This binding is thought to involve steric hindrance and/orconformational alterations which block access of large molecules to the receptor rather than direct interaction with the RGD (arginine-glycine-aspartic acid) binding site of GPIIb/IIIa. By binding to the vitronectin receptor (also known as the ÃŽÂ±vÃŽÂ²3 integrin), abciximab blocks effects mediated by this integrin which include cell adhesion. Furthermore, abciximab blocks Mac-1 receptor on monocytes and neutrophils thus inhibiting monocyte adhesion.
Toxicity	N.A.
Metabolism	Most likely removed by opsonization via the reticuloendothelial system when bound to platelets, or by human antimurine antibody production. Excreted renally.
Absorption	N.A.
Volume of Distribution	N.A.
Clearance	N.A.
Categories	N.A.
Patents Number	N.A.
Date of Issue	N.A.
Date of Expiry	N.A.
Drug Interaction	Abciximab may increase the risk of a hypersensitivy reaction to Trastuzumab.
Target	N.A.
Information of corresponding available drug in the market
Brand Name	N.A.
Company	N.A.
Brand Discription	N.A.
Prescribed for	N.A.
Chemical Name	N.A.
Formulation	N.A.
Physcial Appearance	N.A.
Route of Administration	N.A.
Recommended Dosage	N.A.
Contraindication	N.A.
Side Effects	Chest pain or discomfort; chills; cough; eye pain; fever; general feeling of illness; headache; pale skin; rapid weight gain; shortness of breath; slow or irregular heartbeat; sneezing; sore throat; swelling of hands, ankles, feet, or lower legs.
Useful Link	http://www.rxlist.com/reopro-drug.htm
PubMed ID	12939213
3-D Structure	Th1046 (View) or (Download)

Primary information
ID	1330
ThPP ID	Th1046
Therapeutic Peptide/Protein Name	Abciximab
Sequence	H ReoPro-like antibody Heavy Chain 1: EVQLQQSGAELV view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	145651.1
Chemical Formula	C6462H9964N1690O2049S48
Isoelectric Point	6.16
Hydrophobicity	-0.424
Melting Point (℃)	71
Half Life	Following intravenous bolus administration, free plasma concentrations of Abciximab decrease rapidly
Description	Abciximab is a Fab fragment of the chimeric human-murine monoclonal antibody 7E3. Abciximab binds to the glycoprotein (GP) IIb/IIIa receptor of human platelets and inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules. It also binds to vitronectin (ÃŽÂ±vÃŽÂ²3) receptor found on platelets and vessel wall endothelial and smooth muscle cells.
Indication/Disease	Abciximab is indicated as an adjunct to percutaneous coronary intervention for the prevention of cardiac ischemic complications in patients undergoing percutaneous coronary intervention and in patients with unstable angina not responding to conventional medical therapy when percutaneous coronary intervention is planned within 24 hours. Abciximab is intended for use with aspirin and heparin and has been studied only in that setting.
Pharmacodynamics	Abciximab inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules to GPIIb/IIIa receptor sites on activated platelets. A single intravenous bolus dose from 0.15 mg/kg to 0.30 mg/kg produced rapid dose-dependent inhibition of platelet function. After two hours post-injection with a dose of 0.25 - 0.30 mg/kg, 80% of the GPIIb/IIIa receptors were blocked and platelet aggregation was prevented. GPIIb/IIIa is the major surface receptor involved in the final pathway of platelet aggregation. Bleeding time increases to over 30 minutes at the aforementioned doses. To compare, baseline values were five minutes.
Mechanism of Action	Abciximab binds to the intact platelet GPIIb/IIIa receptor, which is a member of the integrin family of adhesion receptors and the major platelet surface receptor involved in platelet aggregation. This binding is thought to involve steric hindrance and/orconformational alterations which block access of large molecules to the receptor rather than direct interaction with the RGD (arginine-glycine-aspartic acid) binding site of GPIIb/IIIa. By binding to the vitronectin receptor (also known as the ÃŽÂ±vÃŽÂ²3 integrin), abciximab blocks effects mediated by this integrin which include cell adhesion. Furthermore, abciximab blocks Mac-1 receptor on monocytes and neutrophils thus inhibiting monocyte adhesion.
Toxicity	N.A.
Metabolism	Most likely removed by opsonization via the reticuloendothelial system when bound to platelets, or by human antimurine antibody production. Excreted renally.
Absorption	N.A.
Volume of Distribution	N.A.
Clearance	N.A.
Categories	N.A.
Patents Number	N.A.
Date of Issue	N.A.
Date of Expiry	N.A.
Drug Interaction	The prostacyclin analogue, Treprostinil, increases the risk of bleeding when combined with the antiplatelet agent, Abciximab. Monitor for increased bleeding during concomitant thearpy.
Target	N.A.
Information of corresponding available drug in the market
Brand Name	N.A.
Company	N.A.
Brand Discription	N.A.
Prescribed for	N.A.
Chemical Name	N.A.
Formulation	N.A.
Physcial Appearance	N.A.
Route of Administration	N.A.
Recommended Dosage	N.A.
Contraindication	N.A.
Side Effects	N.A.
Useful Link	N.A.
PubMed ID	12939213
3-D Structure	Th1046 (View) or (Download)

Updated version of this database is available at ThpDB2

Detailed description page of THPdb