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clopidogrel besylate (Plavid)

✓ Approved

HanAll Biopharma · P2RY12 · 小分子

什么是 clopidogrel besylate？

clopidogrel besylate 是一种小分子，由HanAll Biopharma研发。该药已获批，用于治疗相关适应症，给药途径：Unknown。

药物档案

商品名Plavid
公司HanAll Biopharma
药物类别小分子
分子靶点P2RY12
给药途径Unknown
状态Approved
来源： ClinicalTrials.gov, HanAll Biopharma

作用机制

分子靶点

clopidogrel besylate 作用于 1 个分子靶点：

P2RY12purinergic receptor P2Y12 (P2Y(ADP), P2Y(cyc))
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

clopidogrel besylate 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Vascular disordersThrombosis✓ Approved

相关研究文献

PubMedIndian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion2026-09-09

Association of Cyp2c19 Genotype with Variability in Clopidogrel Response in Coronary Patients.

Yacoub Farah F, Chouchene Saoussen S, Foddha Hajer H, Abderahmene Amani A et al.

The variability of clopidogrel response is due to many factors including polymorphisms affecting CYP2C19. This study aims to assess the impact of the CYP2C19*2(681G > A), CYP2C19*3(636G > A) and CYP2C19*17(-806 C > T) polymorphisms on platelet response to clopidogrel in patients with coronary artery disease. This is a cross-sectional study led on patients treated with clopidogrel (75 mg/day for at least seven days). Platelet reactivity was assessed by the VerifyNow® P2Y12 test and high on treatment platelet reactivity was defined by a PRU ≥ 208. The genotyping of CYP2C19 polymorphisms was performed by PCR- RFLP. The study involved 115 coronary patients with a mean age of 58 ± 10 years. The VerifyNow®P2Y12 test showed that 27.8% were resistant to clopidogrel. The genetic study showed that CYP2C19*2(681G > A) is significantly associated with biological resistance to clopidogrel (G vs. A, OR = 4.713 [95% CI: 1.738-12.780]; p = 0.002), while CYP2C19*17(-806 C > T) is a protective factor against clopidogrel non-responsiveness (C vs. T, OR = 0.413 [95% CI: 0.174-0.981]; p = 0.02). By classifying patients into extensive (*1/*1: 52%), intermediate (*1/*2: 16%) and ultra-rapid metabolizers (*1/*17;*17/*17: 32%), we found that the type of metabolizer had a significant impact on clopidogrel response (p = 0.001). CYP2C19*2 (681G > A) is significantly associated with biological resistance to clopidogrel while CYP2C19*17(-806 C > T) is a protective factor against clopidogrel non-responsiveness.

PMID 42712845
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PubMedClinical neuroradiology2026-09-09

Comparative Safety and Efficacy of Dual Antiplatelet Therapy Regimens in Flow Diversion for Intracranial Aneurysms: a Systematic Review and Network Meta-Analysis.

Frusteri Marco M, Punukollu Anuraag A, Gaviria Zapata Miguel M, Robledo Arias Jhoan Sebastián JS et al.

Dual antiplatelet therapy is required after flow-diverter treatment of intracranial aneurysms, but the comparative safety and efficacy of clopidogrel-, ticagrelor-, and prasugrel-based regimens remain uncertain. Therefore, the purpose of this study was to compare ischemic, hemorrhagic, functional, and mortality outcomes among different P2Y12 inhibitor-based dual antiplatelet therapy regimens after flow diversion for intracranial aneurysms. A systematic review and frequentist random-effects network meta-analysis were performed according to PRISMA guidelines. PubMed, Embase, and CENTRAL were searched from inception through February 2026. Eligible studies included randomized and nonrandomized comparative studies evaluating clopidogrel-, ticagrelor-, or prasugrel-based dual antiplatelet therapy after flow-diverter treatment. Outcomes were expressed as odds ratios with 95% confidence intervals relative to clopidogrel. Heterogeneity, consistency, treatment ranking by P‑scores, risk of bias, publication bias, and certainty of evidence were assessed. Eleven studies including 2267 patients, at least 2285 procedures, and 2502 aneurysms were included. Compared with clopidogrel-based therapy, ticagrelor- and prasugrel-based regimens showed no statistically significant differences in early ischemic or hemorrhagic complications, ischemic or hemorrhagic complications at longest follow-up, or mortality. Ticagrelor was associated with lower odds of a good functional outcome compared with clopidogrel. Prasugrel ranked highest for ischemic outcomes at longest follow-up, hemorrhagic outcomes at longest follow-up, and good functional outcome. Certainty of evidence was low or very low. Current FD-specific evidence is insufficient to establish superiority, inferiority, or equivalence among clopidogrel-, ticagrelor-, and prasugrel-based DAPT regimens across ischemic, hemorrhagic, functional, and survival outcomes. Because treatment allocation was non-random and alternative regimens were preferentially used in patients with suspected clopidogrel hyporesponsiveness, these findings should not be read as supporting a clopidogrel-first hierarchy; regimen selection is likely to remain guided by local pharmacogenetic testing, and cost considerations pending higher-quality comparative data.

PMID 42711420
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PubMedFrontiers in cardiovascular medicine2026-09-08

Metabolism of 2-oxo-clopidogrel to the clopidogrel active H4 metabolite using human liver microsomes and its inhibitory effect on ADP-induced human platelet aggregation ex vivo: a confirmatory, placebo-controlled, parallel-group study.

Schulz Christian C, Braune Steffen S, Mrowietz Christof C, Küpper Jan-Heiner JH et al.

Clopidogrel is a drug that is commonly used to prevent occlusive events after coronary artery interventions. However, the efficacy of clopidogrel varies depending on the CYP2C19 polymorphism, as it is not clopidogrel itself but the H4 metabolite that is responsible for the pharmacological effect. Carriers of the CYP2C19 loss-of-function allele genotype - which can affect up to 50% of patients - exhibited a higher likelihood of experiencing cardiovascular events. Administering the H4 metabolite directly avoids this problem. In the first step, the H4 metabolite was successfully produced in vitro from 2-oxo-clopidogrel using human liver microsomes. Thereafter, human platelet-rich plasma was supplemented with the H4 metabolite and then stimulated with adenosindiphosphate (ADP, 20 µM). The present confirmatory, placebo-controlled, parallel-group ex vivo study showed that the H4 metabolite of clopidogrel metabolized by human liver microsomes significantly and relevantly inhibited ADP-induced platelet aggregation. The study thus showed that the H4 metabolite of clopidogrel produced by human liver microsomes completely overcomes the limitations of clopidogrel, such as high inter-individual variability due to genetic polymorphisms of CYP2C19, a delayed onset of action and inadequate efficacy.

PMID 42707675
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PubMedThe Journal of international medical research2026-09-08

Indobufen-based dual antiplatelet therapy after percutaneous coronary intervention: A systematic review and network meta-analysis.

Gopinath Aparna A, Heo Jungwook J, Fatima Afifa A, Yerrajonna Amarsimha A et al.

ObjectiveIndobufen has been proposed as an aspirin substitute within dual antiplatelet therapy (DAPT) after percutaneous coronary intervention (PCI), but has been compared only with aspirin plus clopidogrel. We aimed to estimate the comparative safety and efficacy of indobufen-based DAPT against contemporary antiplatelet strategies after PCI.MethodsIn a systematic review and frequentist random-effects network meta-analysis, we searched PubMed/MEDLINE, Embase, and CENTRAL from inception to May 2026 for randomised controlled trials of adults undergoing PCI with drug-eluting stents that compared antiplatelet strategies mapping onto seven pre-specified nodes, with aspirin plus clopidogrel as the reference. Crude per-arm event counts were extracted in duplicate. The connected primary safety outcome was major bleeding (Bleeding Academic Research Consortium [BARC] type 3/5); efficacy outcomes (myocardial infarction, stent thrombosis, all-cause death, stroke) were analysed per component. Odds ratios (ORs) with 95% confidence intervals (CIs) and P-scores were estimated.ResultsEleven trials enrolling more than 55, 000 patients were included. Indobufen plus clopidogrel did not differ significantly from aspirin plus clopidogrel for major bleeding (OR 1.05, 95% CI 0.62-1.78), myocardial infarction (0.91, 0.29-2.89), stent thrombosis (1.27, 0.34-4.74), or stroke (0.96, 0.27-3.44). In a disconnected direct comparison, indobufen reduced BARC 2-5 bleeding (OR 0.62, 0.45-0.84). The significant between-strategy differences concerned others: aspirin plus ticagrelor showed higher major bleeding (2.07, 1.46-2.94) and clopidogrel monotherapy lower (0.38, 0.22-0.64). Every comparison across clusters depended on a single bridging trial, and no network contained closed loops, precluding assessment of inconsistency.ConclusionsIndobufen-based DAPT was comparable, not superior, to aspirin plus clopidogrel across bleeding and ischaemic outcomes, with no signal of increased ischaemic risk. Because only one randomised trial has directly tested indobufen and all comparisons with ticagrelor-based or monotherapy strategies rest on a single bridging trial, the findings primarily support indobufen as a reasonable aspirin-sparing alternative within clopidogrel-based DAPT. Its relative position against other contemporary bleeding-reduction strategies remains unproven. These results reinforce the need for individualised antiplatelet therapy guided by patient-specific ischaemic and bleeding risk.INPLASY registration number: INPLASY202680037.

PMID 42706689
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PubMedEuropean journal of clinical pharmacology2026-09-08

Recent research progress on the mechanisms of clopidogrel resistance.

Wu Chunrong C, Huang Xinyi X, Zhu Guoliang G, Cao Qing Q et al.

To narratively review recent advances in clopidogrel resistance, including genetic determinants, epigenetic regulation, clinical modifiers, and methods of assessment. Particular attention is given to distinguishing laboratory-defined high on-treatment platelet reactivity (HTPR) from clinical treatment failure, with the aim of supporting risk assessment and individualized antiplatelet therapy. PubMed was searched from inception to August 23, 2026, using combinations of "clopidogrel resistance," "high on-treatment platelet reactivity," "CYP2C19," "pharmacogenetics," "epigenetics," "miRNA," "clinical risk factors," "drug interactions," "gut microbiota," and "platelet-function testing." Targeted searches of reference lists and publisher websites identified recent guidelines and online-ahead-of-print articles not yet indexed in PubMed. Peer-reviewed original human studies and relevant experimental studies, guidelines, and foundational reports were included when they addressed clopidogrel pharmacokinetics, pharmacodynamics, biomarkers, or clinical modifiers; duplicates, case reports, conference abstracts, and reports without direct relevance were excluded. As this was a narrative review, no formal risk-of-bias score was applied; evidence was appraised qualitatively by study design, sample size, confounding control, replication, and whether outcomes were laboratory or clinical. CYP2C19 loss-of-function alleles remain the principal pharmacokinetic determinant of reduced clopidogrel responsiveness by impairing two-step bioactivation, although they explain only 12%-20% of interindividual variability. HTPR, defined as residual platelet reactivity above an assay- and study-specific threshold during treatment, has been reported in approximately 20%-45% of clopidogrel-treated patients; this range reflects heterogeneous platforms and cutoffs rather than a harmonized prevalence estimate. In this review, HTPR is treated as a laboratory pharmacodynamic surrogate, whereas clinical treatment failure denotes an adjudicated ischemic event during therapy. Competing CES1-mediated hydrolysis and transporter activity involving ABCB1 and ABCC2 may further modify exposure, whereas P2RY12 and platelet-signaling variants predominantly affect pharmacodynamic responsiveness. Epigenetic mechanisms, inflammation, metabolic comorbidity, concomitant medications, and food interactions may also influence active-metabolite formation or platelet reactivity. Clopidogrel resistance is multifactorial and extends beyond CYP2C19 genotype. Laboratory-defined HTPR should not be equated with clinical treatment failure, because ischemic outcomes also depend on baseline risk, adherence, comorbidity, and concomitant therapy. Integrating validated genetic, laboratory, and clinical information may improve individualized antiplatelet strategies.

PMID 42706349
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PubMedNaunyn-Schmiedeberg's archives of pharmacology2026-09-08

Analysis of marketing authorizations, withdrawals, and refusals by the European Medicines Agency (EMA): trends in approval procedures 1995-2025.

Hitsch Florian F, Seifert Roland R

The European Medicines Agency (EMA) is an institution of the European Union (EU), responsible for the authorization and pharmacovigilance of medicinal products. In our study, we present a systematic analysis of the 1,985 centralized EMA marketing authorization procedures (MAP) between 1995 and 2025. The analysis mainly includes EMA marketing authorizations, withdrawals of marketing authorizations, and revocations of marketing authorizations or refusals of drug applications. With regard to the analysis period, it is evident that the number of marketing authorizations recommended by the EMA increased significantly between 1996 (first fully published evaluation year) and 2025. Among the active substances (International Nonproprietary Names, INNs) in centralized EMA MAPs, clopidogrel and denosumab are the most frequently represented. On the other hand, antineoplastic agents and immunosuppressants are the most common therapeutic subgroups according to the Anatomical Therapeutic Chemical Classification (ATC) in MAPs. Notably, special MAPs for medicines such as generics, biosimilars, and medicines for the treatment of rare diseases (orphan medicines) account for more than 30% of MAPs. Our analysis shows that the development of centralized EMA MAPs is influenced by multiple factors such as medical need, regulatory framework, the economic potential of medicines, and patent law considerations. Our analysis provides a comprehensive overview of these procedures and may help identify potential obstacles and opportunities for their further development.

PMID 42706333
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