Clinical Pharmacokinetics and Pharmacodynamics of Clopidogrel

Acute coronary syndromes (ACS) remain life-threatening disorders, which are associated with high morbidity and mortality. Dual antiplatelet therapy with aspirin and clopidogrel has been shown to reduce cardiovascular events in patients with ACS. However, there is substantial inter-individual variabi...

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Published inClinical pharmacokinetics Vol. 54; no. 2; pp. 147 - 166
Main Authors Jiang, Xi-Ling, Samant, Snehal, Lesko, Lawrence J., Schmidt, Stephan
Format Journal Article
LanguageEnglish
Published Cham Springer International Publishing 01.02.2015
Springer Nature B.V
Subjects
Acute Coronary Syndrome - drug therapy
Acute Coronary Syndrome - metabolism
Cytochrome P-450 CYP2C19 - genetics
Cytochrome P-450 CYP2C19 - metabolism
Dose-Response Relationship, Drug
Humans
Internal Medicine
Medicine
Medicine & Public Health
Pharmacology/Toxicology
Pharmacotherapy
Polymorphism, Genetic
Precision Medicine
Purinergic P2Y Receptor Antagonists - pharmacokinetics
Purinergic P2Y Receptor Antagonists - pharmacology
Review Article
Ticlopidine - analogs & derivatives
Ticlopidine - pharmacokinetics
Ticlopidine - pharmacology
Acute Coronary Syndrome Patient
Clopidogrel
Constitutive Androstane Receptor
Clopidogrel Therapy
Percutaneous Coronary Intervention
Online AccessGet full text

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Abstract Acute coronary syndromes (ACS) remain life-threatening disorders, which are associated with high morbidity and mortality. Dual antiplatelet therapy with aspirin and clopidogrel has been shown to reduce cardiovascular events in patients with ACS. However, there is substantial inter-individual variability in the response to clopidogrel treatment, in addition to prolonged recovery of platelet reactivity as a result of irreversible binding to P2Y 12 receptors. This high inter-individual variability in treatment response has primarily been associated with genetic polymorphisms in the genes encoding for cytochrome (CYP) 2C19, which affect the pharmacokinetics of clopidogrel. While the US Food and Drug Administration has issued a boxed warning for CYP2C19 poor metabolizers because of potentially reduced efficacy in these patients, results from multivariate analyses suggest that additional factors, including age, sex, obesity, concurrent diseases and drug–drug interactions, may all contribute to the overall between-subject variability in treatment response. However, the extent to which each of these factors contributes to the overall variability, and how they are interrelated, is currently unclear. The objective of this review article is to provide a comprehensive update on the different factors that influence the pharmacokinetics and pharmacodynamics of clopidogrel and how they mechanistically contribute to inter-individual differences in the response to clopidogrel treatment.
AbstractList Acute coronary syndromes (ACS) remain life-threatening disorders that are associated with high morbidity and mortality. Dual-antiplatelet therapy with aspirin and clopidogrel has shown to reduce cardiovascular events in patients with ACS. However, there is substantial inter-individual variability in response to clopidogrel treatment in addition to prolonged recovery of platelet reactivity as a result of irreversible binding to P2Y 12 receptors. This high inter-individual variability in treatment response has primarily been associated with genetic polymorphisms in the genes encoding for cytochrome (CYP) 2C19 that affect clopidogrel’s pharmacokinetics. While FDA has issued a boxed warning for CYP2C19 poor metabolizers due to a potentially reduced efficacy in these patients, results from multivariate analyses suggest that additional factors, including age, sex, obesity, concurrent diseases and drug-drug interactions, may all contribute to the overall between-subject variability in treatment response. However, the extent to which each of these factors contributes to the overall variability and how they are interrelated is currently unclear. The objective of this review article is to provide a comprehensive update on the different factors that influence clopidogrel’s pharmacokinetics and pharmacodynamics and how they mechanistically contribute to inter-individual differences in response to clopidogrel treatment.
Acute coronary syndromes (ACS) remain life-threatening disorders, which are associated with high morbidity and mortality. Dual antiplatelet therapy with aspirin and clopidogrel has been shown to reduce cardiovascular events in patients with ACS. However, there is substantial inter-individual variability in the response to clopidogrel treatment, in addition to prolonged recovery of platelet reactivity as a result of irreversible binding to P2Y12 receptors. This high inter-individual variability in treatment response has primarily been associated with genetic polymorphisms in the genes encoding for cytochrome (CYP) 2C19, which affect the pharmacokinetics of clopidogrel. While the US Food and Drug Administration has issued a boxed warning for CYP2C19 poor metabolizers because of potentially reduced efficacy in these patients, results from multivariate analyses suggest that additional factors, including age, sex, obesity, concurrent diseases and drug-drug interactions, may all contribute to the overall between-subject variability in treatment response. However, the extent to which each of these factors contributes to the overall variability, and how they are interrelated, is currently unclear. The objective of this review article is to provide a comprehensive update on the different factors that influence the pharmacokinetics and pharmacodynamics of clopidogrel and how they mechanistically contribute to inter-individual differences in the response to clopidogrel treatment.
Acute coronary syndromes (ACS) remain life-threatening disorders, which are associated with high morbidity and mortality. Dual antiplatelet therapy with aspirin and clopidogrel has been shown to reduce cardiovascular events in patients with ACS. However, there is substantial inter-individual variability in the response to clopidogrel treatment, in addition to prolonged recovery of platelet reactivity as a result of irreversible binding to P2Y12 receptors. This high inter-individual variability in treatment response has primarily been associated with genetic polymorphisms in the genes encoding for cytochrome (CYP) 2C19, which affect the pharmacokinetics of clopidogrel. While the US Food and Drug Administration has issued a boxed warning for CYP2C19 poor metabolizers because of potentially reduced efficacy in these patients, results from multivariate analyses suggest that additional factors, including age, sex, obesity, concurrent diseases and drug-drug interactions, may all contribute to the overall between-subject variability in treatment response. However, the extent to which each of these factors contributes to the overall variability, and how they are interrelated, is currently unclear. The objective of this review article is to provide a comprehensive update on the different factors that influence the pharmacokinetics and pharmacodynamics of clopidogrel and how they mechanistically contribute to inter-individual differences in the response to clopidogrel treatment.Acute coronary syndromes (ACS) remain life-threatening disorders, which are associated with high morbidity and mortality. Dual antiplatelet therapy with aspirin and clopidogrel has been shown to reduce cardiovascular events in patients with ACS. However, there is substantial inter-individual variability in the response to clopidogrel treatment, in addition to prolonged recovery of platelet reactivity as a result of irreversible binding to P2Y12 receptors. This high inter-individual variability in treatment response has primarily been associated with genetic polymorphisms in the genes encoding for cytochrome (CYP) 2C19, which affect the pharmacokinetics of clopidogrel. While the US Food and Drug Administration has issued a boxed warning for CYP2C19 poor metabolizers because of potentially reduced efficacy in these patients, results from multivariate analyses suggest that additional factors, including age, sex, obesity, concurrent diseases and drug-drug interactions, may all contribute to the overall between-subject variability in treatment response. However, the extent to which each of these factors contributes to the overall variability, and how they are interrelated, is currently unclear. The objective of this review article is to provide a comprehensive update on the different factors that influence the pharmacokinetics and pharmacodynamics of clopidogrel and how they mechanistically contribute to inter-individual differences in the response to clopidogrel treatment.
Acute coronary syndromes (ACS) remain life-threatening disorders, which are associated with high morbidity and mortality. Dual antiplatelet therapy with aspirin and clopidogrel has been shown to reduce cardiovascular events in patients with ACS. However, there is substantial inter-individual variability in the response to clopidogrel treatment, in addition to prolonged recovery of platelet reactivity as a result of irreversible binding to P2Y 12 receptors. This high inter-individual variability in treatment response has primarily been associated with genetic polymorphisms in the genes encoding for cytochrome (CYP) 2C19, which affect the pharmacokinetics of clopidogrel. While the US Food and Drug Administration has issued a boxed warning for CYP2C19 poor metabolizers because of potentially reduced efficacy in these patients, results from multivariate analyses suggest that additional factors, including age, sex, obesity, concurrent diseases and drug–drug interactions, may all contribute to the overall between-subject variability in treatment response. However, the extent to which each of these factors contributes to the overall variability, and how they are interrelated, is currently unclear. The objective of this review article is to provide a comprehensive update on the different factors that influence the pharmacokinetics and pharmacodynamics of clopidogrel and how they mechanistically contribute to inter-individual differences in the response to clopidogrel treatment.
Author Jiang, Xi-Ling
Samant, Snehal
Lesko, Lawrence J.
Schmidt, Stephan
Author_xml – sequence: 1
  givenname: Xi-Ling
  surname: Jiang
  fullname: Jiang, Xi-Ling
  organization: Department of Pharmaceutics, Center for Pharmacometrics and Systems Pharmacology, University of Florida at Lake Nona (Orlando)
– sequence: 2
  givenname: Snehal
  surname: Samant
  fullname: Samant, Snehal
  organization: Department of Pharmaceutics, Center for Pharmacometrics and Systems Pharmacology, University of Florida at Lake Nona (Orlando)
– sequence: 3
  givenname: Lawrence J.
  surname: Lesko
  fullname: Lesko, Lawrence J.
  organization: Department of Pharmaceutics, Center for Pharmacometrics and Systems Pharmacology, University of Florida at Lake Nona (Orlando)
– sequence: 4
  givenname: Stephan
  surname: Schmidt
  fullname: Schmidt, Stephan
  email: sschmidt@cop.ufl.edu
  organization: Department of Pharmaceutics, Center for Pharmacometrics and Systems Pharmacology, University of Florida at Lake Nona (Orlando)
BackLink https://www.ncbi.nlm.nih.gov/pubmed/25559342$$D View this record in MEDLINE/PubMed
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Keywords Acute Coronary Syndrome Patient
Clopidogrel
Constitutive Androstane Receptor
Clopidogrel Therapy
Percutaneous Coronary Intervention
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Snippet Acute coronary syndromes (ACS) remain life-threatening disorders, which are associated with high morbidity and mortality. Dual antiplatelet therapy with...
Acute coronary syndromes (ACS) remain life-threatening disorders that are associated with high morbidity and mortality. Dual-antiplatelet therapy with aspirin...
SourceID pubmedcentral
proquest
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crossref
springer
SourceType Open Access Repository
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StartPage 147
SubjectTerms Acute Coronary Syndrome - drug therapy
Acute Coronary Syndrome - metabolism
Cytochrome P-450 CYP2C19 - genetics
Cytochrome P-450 CYP2C19 - metabolism
Dose-Response Relationship, Drug
Humans
Internal Medicine
Medicine
Medicine & Public Health
Pharmacology/Toxicology
Pharmacotherapy
Polymorphism, Genetic
Precision Medicine
Purinergic P2Y Receptor Antagonists - pharmacokinetics
Purinergic P2Y Receptor Antagonists - pharmacology
Review Article
Ticlopidine - analogs & derivatives
Ticlopidine - pharmacokinetics
Ticlopidine - pharmacology
Title Clinical Pharmacokinetics and Pharmacodynamics of Clopidogrel
URI https://link.springer.com/article/10.1007/s40262-014-0230-6
https://www.ncbi.nlm.nih.gov/pubmed/25559342
https://www.proquest.com/docview/1672598495
https://www.proquest.com/docview/1652412534
https://pubmed.ncbi.nlm.nih.gov/PMC5677184
Volume 54
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