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clopidogrel napadisilate (Pidogle / Pidogul)

✓ Approved

Hanmi Pharmaceutical · P2RY12 · Small Molecule

What is clopidogrel napadisilate?

clopidogrel napadisilate is a small molecule developed by Hanmi Pharmaceutical. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesPidogle, Pidogul
CompanyHanmi Pharmaceutical
Drug ClassSmall Molecule
Molecular TargetP2RY12
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Hanmi Pharmaceutical

Mechanism of Action

Molecular Targets

clopidogrel napadisilate acts on 1 molecular target:

P2RY12purinergic receptor P2Y12 (P2Y(ADP), P2Y(cyc))
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

clopidogrel napadisilate is developed for 4 unique indications across 3 therapeutic areas.

Therapeutic AreaConditionPhase
Cardiac disordersMyocardial infarction✓ Approved
Vascular disordersPeripheral vascular disorder✓ Approved
Cardiac disordersAcute coronary syndrome✓ Approved
Nervous system disordersDelayed ischaemic neurological deficit✓ Approved

Related Research Articles

PubMedCurrent pharmaceutical design2026-11-11

Clopidogrel in the Contemporary Management of Coronary and Cerebrovascular Events: Efficacy, Safety, and Decision-making Pathways.

Akman Canan C, Ucar Asli Bahar AB, Inci Ozlem O, Unaldi Mehmet M et al.

Clopidogrel (CLP) remains a cornerstone of antiplatelet therapy in the management of atherothrombotic events affecting the coronary and cerebrovascular circulations. As an irreversible thienopyridine inhibitor of the platelet P2Y12 adenosine diphosphate (ADP) receptor, CLP reduces platelet aggregation by preventing downstream activation of the glycoprotein IIb/IIIa receptor complex. It is a prodrug that requires hepatic bioactivation primarily via CYP2C19, resulting in susceptibility to pharmacogenomic variability and clinically significant drug-drug interactions. Current guidelines from the European Society of Cardiology (2023) and the American College of Cardiology/American Heart Association (2025) recommend potent P2Y12 inhibitors - ticagrelor and prasugrel - in preference to CLP for most patients with acute coronary syndromes (ACS) undergoing percutaneous coronary intervention (PCI); however, CLP retains a pivotal role when potent agents are contraindicated, in elderly patients at high bleeding risk (HBR), in cerebrovascular events, and as a de-escalation target following initial potent P2Y12 inhibition. In acute ischaemic stroke and high-risk TIA, short-course DAPT with CLP and aspirin for 21 days (not prolonged beyond this period) is the evidence-based standard of care. Major clinical trials - including CAPRIE, CURE, CHANCE, POINT, and the landmark CHANCE-2 - have defined the therapeutic boundaries and limitations of CLP-based dual antiplatelet therapy (DAPT). Bleeding remains the most clinically significant adverse effect, with gastrointestinal haemorrhage the most frequent site and intracranial haemorrhage the most feared complication. This review synthesises current evidence, incorporating recent meta-analyses and guideline updates, to provide a practical, evidence-based framework for clinicians regarding the use of CLP and comparator P2Y12 inhibitors in coronary and cerebrovascular disease.

PMID 43012287
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PubMedMedicine2026-11-11

Treatment outcomes and associated factors among acute coronary syndrome patients admitted to Jimma University Medical Centre, Jimma, Ethiopia: A 5-year retrospective study.

Tegene Elsah E, Bekele Gashahun G, Mecha Mohammed M, Godebo Tamirat T et al.

In developing countries, acute coronary syndrome (ACS) is becoming a more common cause of cardiovascular death. Although thrombolytic treatments and limited percutaneous coronary intervention have been introduced, in-hospital mortality from ACS is still high in sub-Saharan countries. This study aimed to evaluate the treatment outcome of ACS and its associated factors among patients attending Jimma University Medical Center, Jimma, Ethiopia. A retrospective hospital-based cross-sectional study was conducted among 300 ACS patients. Patient records from admissions between November 1st, 2017, and October 31st, 2022 were reviewed, with data collected between December 1st and 31st, 2022. Data were collected using a structured checklist, entered, and analyzed using Statistical Package for Social science version 26. Descriptive analysis was used to summarize baseline characteristics and determine treatment outcomes. Bivariable and multivariable regression analyses were employed to determine factors affecting poor treatment outcomes. The odds ratio with a 95% confidence interval was computed, and a P value < .05 was considered significant. Among the 300 ACS patients included in our study, 35.3% died during hospitalization. Hypertension was the most common risk factor, present in 88.3% of the patients. In addition, 20.3% were classified as Killip class III or IV. 20.7% had a left ventricular ejection fraction (LVEF) of less than or equal to 30%, and 79.3% had an LVEF > 30%. Regarding treatment, an aspirin loading dose, clopidogrel loading dose, beta-blockers, statins, morphine, and nitrates were given to 284 (94.7%), 286 (95.3%), 227 (75.7%), 283 (94.3%), 109 (36.3%), and 80 (26.7%) patients, respectively. Factors significantly associated with in-hospital mortality were older age (P ≤ .001), history of diabetes (P = .004), ST-segment elevation myocardial infarction diagnosis (P = .003), and Killip class III and IV (P ≤ .001), whereas LVEF > 30% was associated with significantly lower odds of in-hospital death (P < .001). The proportion of in-hospital mortality attributable to ACS was found to be high. As a result, timely evidence-based therapy should be included in the setup.

PMID 43012815
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PubMedClinical Medicine Insights. Cardiology2026-11-10

Evaluation of Neointimal Coverage After Guiding De-escalation of Antiplatelet Treatment in Patients with ST-elevation Myocardial Infarction Undergoing Percutaneous Coronary Intervention by Optical Coherence Tomography or Angiography: Rationale and Design of the DAPT-OCT Study.

Li Yang Y, Ma Chaoqun C, Xu Kai K, Qiu Miaohan M et al.

Dual antiplatelet therapy (DAPT) de-escalation strategies including early switching from a potent P2Y12 inhibitor to clopidogrel become attractive for patients with ST-elevation Myocardial Infarction (STEMI). It is unclear whether DAPT de-escalation after optical coherence tomography (OCT)- or angiography-guided percutaneous coronary intervention (PCI) improves neointimal coverage in STEMI patients who have completed 1-month DAPT with aspirin plus ticagrelor. This report describes the design of a randomized study evaluating the neointimal coverage in STEMI patients after guiding de-escalation of DAPT from aspirin plus ticagrelor to aspirin plus clopidogrel at 1 month after PCI with drug eluting stent implantation by OCT or angiography and 1-month DAPT with aspirin plus ticagrelor. Eighty patients who meet the inclusion criteria and none of the exclusion criteria will be randomly assigned in a 1:1 fashion to the OCT- or angiography-guided group (first randomization). All patients will receive open label ticagrelor plus aspirin for 1 month after the index PCI. At 30 ± 7 days after the index PCI, patients with no major adverse cardiovascular and cerebrovascular events (MACCE) or major bleeding (⩾Bleeding Academic Research Consortium [BARC] 3a) will be randomized in a 1:1 fashion to either the ticagrelor plus aspirin group or clopidogrel plus aspirin group for an additional 11 months (second randomization). The primary endpoint is the stent-strut neointimal thickness by OCT assessment at 12-month follow up. The data obtained from DAPT-OCT study will explore the neointimal coverage after guiding de-escalation of antiplatelet treatment in STEMI patients undergoing PCI by OCT. ClinicalTrials.gov identifier: NCT06339021.

PMID 43005498
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PubMedEuropean journal of pharmacology2026-11-09

Prostaglandin-Endoperoxide Synthase 1 Regulatory Variants Link Aspirin-Treated Cardiovascular Outcomes to Multicellular Cyclooxygenase-1 Expression and Activity Beyond Platelet-Derived Cyclooxygenase-1 Inhibition.

Li Xiao-Li XL, Wang Yu-Zhe YZ, Wang Qiang Q, Hu Xiao-Xiang XX et al.

Prostaglandin-endoperoxide synthase 1 (PTGS1) encodes cyclooxygenase-1 (COX-1). Aspirin inhibits platelet COX-1/thromboxane A2 (TXA2)-dependent aggregation to prevent major adverse cardiovascular events (MACE). However, relationships of low aspirin response, namely laboratory aspirin resistance (LAR) and MACE, with PTGS1 variants remain uncertain. In total, 486 cardiovascular patients, 454 on mono-antiplatelet therapy (MAPT), 32 on dual antiplatelet therapy (DAPT, aspirin plus clopidogrel), had complete data including COX-1-specific platelet function and median 4.75-year follow-up. MACE comprised acute myocardial infarction, acute stroke, and ischemia-driven revascularization. Eighteen bioinformatically annotated PTGS1 regulatory variants were genotyped. Smoking and clopidogrel exposure significantly modified LAR. Kaplan-Meier analysis linked LAR to higher crude MACE odds in MAPT and MAPT+DAPT groups (log-rank P < 0.05). Genetic analyses clarified gene-LAR, gene-MACE, gene-LAR-MACE interrelationships. Promoter rs1330344 showed lower LAR odds, with unchanged MACE odds, consistent with mild COX-1 modulation. Intronic rs7866582 conferred higher MACE odds alone, consistent with leukocyte COX-1/proinflammatory prostaglandin elevation. 3'-untranslated region (3'-UTR) rs10306190 exhibited marginally higher LAR odds yet lower MACE odds, consistent with variant-mediated COX-1 upregulation and marked vascular COX-1/PGI2 elevation counteracting residual TXA2 under aspirin. 3'-UTR rs10306196 displayed higher MACE odds alone, consistent with marked vascular COX-1/PGI2 reduction (nominal Firth P < 0.05, except for rs10306190-LAR). However, after multiple testing correction, no significant associations were observed (all BH-FDR Q > 0.05). LAR and PTGS1 variants lack population-level value for MACE prediction. This study links aspirin-treated MACE to multicellular COX-1 actions beyond platelets.

PMID 43003331
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PubMedEuropean journal of pharmacology2026-11-08

Extended Clopidogrel Monotherapy versus Dual Antiplatelet Therapy in Acute Coronary Syndrome Patients With and Without Heart Failure: A Prespecified Subgroup Analysis of the OPT-BIRISK Trial.

Jiang Zaixin Z, Li Yi Y, Li Jing J, Wang Bin B et al.

The optimal extended antiplatelet strategy after percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS) in patients with heart failure (HF) remains uncertain. In OPT-BIRISK, patients at high ischemic and bleeding risk who completed 9-12 months of dual antiplatelet therapy (DAPT) were randomized to clopidogrel plus placebo or aspirin for 9 months. This analysis compared treatments by recorded HF history. The primary endpoint was Bleeding Academic Research Consortium (BARC) types 2, 3, or 5 bleeding; the key secondary endpoint was major adverse cardiac and cerebral events (MACCE). Of 7,758 patients, 653 (8.4%) had HF history. Without HF, bleeding occurred in 83/3,565 (2.3%) monotherapy recipients and 118/3,540 (3.3%) DAPT recipients (HR 0.70, 95% CI 0.53-0.92). With HF, bleeding occurred in 12/308 (3.9%) and 9/345 (2.6%), respectively (HR 1.49, 95% CI 0.63-3.53). MACCE occurred in 90/3,565 (2.5%) versus 120/3,540 (3.4%) patients without HF (HR 0.74, 95% CI 0.57-0.98) and 11/308 (3.6%) versus 16/345 (4.6%) patients with HF (HR 0.77, 95% CI 0.36-1.66). Interaction P values were 0.1021 for bleeding and 0.9345 for MACCE. Extended clopidogrel monotherapy reduced clinically relevant bleeding in patients without a history of HF after PCI for ACS. No statistically significant treatment-by-HF interaction was observed for bleeding or MACCE, although HF-specific treatment effects remain inconclusive because of limited events.

PMID 42998742
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PubMedQuantitative imaging in medicine and surgery2026-11-08

Mitral regurgitation and left atrial phasic function and atrioventricular coupling in patients with myocardial infarction: a cardiac magnetic resonance imaging study.

Wen Xiao-Ling XL, Guo Ying-Kun YK, Gao Yue Y, Yang Zhi-Gang ZG

Mitral regurgitation (MR) after myocardial infarction (MI) may increase left atrial (LA) pressure and contribute to cardiac dysfunction. This study evaluated the incremental association of MR with LA phasic function and strain and identified independent factors associated with LA deformation in patients with MI. This retrospective study included 189 patients with MI (111 without MR and 78 with MR: mild, 27; moderate, 33; severe, 18) and 86 normal controls who underwent 3.0-T cardiac magnetic resonance (CMR). MR severity was graded by the CMR-derived MR fraction: mild <30%, moderate 30% to <50%, and severe ≥50%. CMR-derived LA phasic function and strain (reservoir strain, epsilon-s; booster strain, epsilon-a; conduit strain, epsilon-e), left ventricular (LV) function and strain, infarct size, and MR fraction were measured. Between-group comparisons were performed using one-way analysis of variance or the Kruskal-Wallis test with post hoc correction, and multivariable linear regression was used to identify independent factors associated with LA strain. A two-sided P<0.05 was considered statistically significant. Patients with MI and MR had lower LA reservoir strains [22.14%±10.91% vs. 28.65% (22.78%, 38.30%) vs. 41.70% (36.15%, 53.15%)], booster strains [11.52%±6.19% vs. 13.80% (10.20%, 19.80%) vs. 19.25% (15.10%, 24.05%)], and conduit strains [9.40% (6.03%, 14.85%) vs. 14.60% (9.60%, 20.50%) vs. 22.55% (17.75%, 30.43%)] than patients with MI without MR and controls (all P<0.05). They also had higher LA maximum volume [68.43 (57.44, 91.51) mL] and minimum volume [35.93 (24.43, 61.15) mL] and lower LA total ejection fraction (45.39%±14.97%) than the other groups (all P<0.05). In multivariable analysis, MR degree was independently associated with reservoir strain (β=-0.194, P=0.048) and conduit strain (β=-0.208, P=0.038). Anterior wall MI (reservoir strain: β=-0.245, P=0.014; booster strain: β=-0.231, P=0.028; conduit strain: β=-0.224, P=0.027) and posteromedial papillary muscle infarction (reservoir strain: β=-0.329, P=0.004; booster strain: β=-0.370, P=0.003) were also independently associated with LA strain. MR was associated with further deterioration of LA myocardial strain in patients with MI. Posteromedial papillary muscle infarction, anterior wall MI, beta-blocker use, and dual antiplatelet therapy with aspirin plus clopidogrel were independently associated with LA strain. CMR-derived functional and strain parameters may help characterize LV-LA coupling and support risk stratification in this population.

PMID 42997940
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