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clopidogrel besylate (Plavid)

✓ Approved

HanAll Biopharma · P2RY12 · Small Molecule

What is clopidogrel besylate?

clopidogrel besylate is a small molecule developed by HanAll Biopharma. It is approved for therapeutic indications via unknown.

Drug Profile

Brand NamesPlavid
CompanyHanAll Biopharma
Drug ClassSmall Molecule
Molecular TargetP2RY12
RouteUnknown
StatusApproved
Sources: ClinicalTrials.gov, HanAll Biopharma

Mechanism of Action

Molecular Targets

clopidogrel besylate acts on 1 molecular target:

P2RY12purinergic receptor P2Y12 (P2Y(ADP), P2Y(cyc))
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Therapeutic Indications

clopidogrel besylate is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Vascular disordersThrombosis✓ Approved

Related Research Articles

PubMedNature medicine2026-08-30

Dual antithrombotic therapy using potent antiplatelet inhibitors in atrial fibrillation and acute coronary syndrome: a randomized controlled trial.

Rizas Konstantinos D KD, Mourouzis Konstantinos K, Rath Dominik D, Olivier Christoph B CB et al.

The selection of the optimal antithrombotic regimen in patients with atrial fibrillation and acute coronary syndrome remains challenging. Previous trials have demonstrated that dual antithrombotic therapy (DAT), consisting of direct oral anticoagulants (DOACs) plus a P2Y12 inhibitor, reduces bleeding compared to a triple-therapy regimen using vitamin K antagonists. However, subsequent meta-analyses have suggested an increased risk of ischemic events with DAT, particularly within the first month of treatment. Clopidogrel has been the predominant P2Y12 inhibitor used across these studies, despite the risk of high on-treatment platelet reactivity when using this drug. In this study, we conducted an open-label, randomized controlled trial (EPIDAURUS) in patients with atrial fibrillation and acute coronary syndrome, designed to assess the efficacy and safety of a 1-month regimen of DOAC plus potent P2Y12 inhibitor (prasugrel or ticagrelor) compared to DOAC plus clopidogrel and in-hospital aspirin. The primary outcomes of the trial were an efficacy endpoint, recurrent ischemic events and safety endpoints, including death and major bleeding, which were evaluated 6 weeks after randomization using separate win-loss ratio analyses. The study was prematurely terminated after enrollment of 602 patients (154 female) of an expected 1,474 patients, owing to safety concerns raised by the Data and Safety Monitoring Board. Exploratory analyses of secondary safety endpoints, including bleeding type ≥2 and ≥3 according to the Bleeding Academic Research Consortium scale, revealed that, compared to clopidogrel and in-hospital aspirin, treatment with a potent P2Y12 inhibitor was associated with higher bleeding rates without a clear reduction in the risk of ischemic complications. These findings do not support the routine use of potent P2Y12 inhibitors in combination with DOACs in this patient population. ClinicalTrials.gov identifier: NCT04981041 .

PMID 42668287
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PubMedJournal of visualized experiments : JoVE2026-08-29

Clopidogrel-Induced Gastric Mucosal Injury Associated with Endoplasmic Reticulum Stress in Rats.

Li Zhenwei Z, Han Fengzheng F, Liu Wenxia W, Wu Xuan X et al.

Clopidogrel is widely used as an antiplatelet agent for the prevention and treatment of arterial thrombotic diseases, but its clinical application may be limited by gastrointestinal adverse effects, including gastric mucosal injury. Because epithelial cell survival is essential for maintaining gastric mucosal integrity, we hypothesized that clopidogrel-induced gastric epithelial injury would be accompanied by alterations in ER stress- and apoptosis-related markers. To test this hypothesis, GES-1 human gastric epithelial cells were treated with different concentrations of clopidogrel, and cell viability, apoptosis, cell cycle distribution, and molecular changes were evaluated using the Cell Counting Kit-8 (CCK-8) assay, flow cytometry, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blotting. In parallel, Sprague-Dawley rats were administered clopidogrel by gavage to establish an in vivo gastric injury model. Gastric mucosal pathological changes were assessed by hematoxylin and eosin staining, and serum inflammatory cytokine levels were measured using enzyme-linked immunosorbent assay (ELISA). Clopidogrel reduced GES-1 cell viability, promoted apoptosis, and altered cell cycle progression. In rats, clopidogrel induced gastric mucosal erosion, edema, and inflammatory cell infiltration, accompanied by increased serum interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) levels. Clopidogrel also increased the expression of the ER stress markers C/EBP homologous protein (CHOP) and activating transcription factor 5 (ATF5), increased Bcl-2-associated X protein (Bax) expression, decreased B-cell lymphoma 2 (Bcl-2) expression, and elevated the Bax/Bcl-2 ratio in both gastric tissues and GES-1 cells. These findings suggest that clopidogrel-induced gastric mucosal injury is associated with increased ER stress-related marker expression and disruption of the Bax/Bcl-2 balance, although a direct causal ER stress-mitochondrial apoptosis pathway was not established in this study.

PMID 42667183
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PubMedCureus2026-08-29

Flatline Thromboelastography During Massive Intraoperative Bleeding in a Patient With Multiple Myeloma: A Case Report.

Nivedithaa, Neethirajan Soma Ganesh Raja SGR, M Akilandeswari A

Multiple myeloma is a malignant plasma cell disorder associated with complex coagulation abnormalities that may increase the perioperative bleeding risk. We report the case of a 38-year-old man with multiple myeloma, chronic kidney disease on maintenance haemodialysis, thrombocytopenia, and recent clopidogrel use, who underwent posterior spinal decompression and instrumented fusion from C7 to T6 for an epidural abscess. Intraoperatively, he developed massive hemorrhage with an estimated blood loss of 5,000 mL, accompanied by profound hemodynamic instability requiring vasopressor support. Thromboelastography (TEG) showed a flatline tracing, indicating near-complete failure of clot formation. Prompt recognition of the coagulopathy and aggressive goal-directed transfusion with 5 units of packed red blood cells, 10 units of fresh frozen plasma, and 10 units of platelets resulted in successful hemostatic resuscitation and stabilization. The coagulopathy was likely multifactorial, due to a combination of hemostatic dysfunction associated with multiple myeloma, uremic platelet dysfunction, thrombocytopenia, recent antiplatelet therapy, and ongoing surgical bleeding. This case highlights the importance of viscoelastic testing in identifying severe coagulopathy in patients with plasma cell malignancies and guiding perioperative transfusion management.

PMID 42667016
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PubMedNeurosurgery practice2026-08-29

Subtonsillar Approach to a Polylobulated Posterior Inferior Cerebellar Artery Aneurysm: A Case Illustration.

Liu Hongjun H, Bai Junsheng J, Muhammad Sajjad S

Dysplastic and polylobulated aneurysms of the posterior inferior cerebellar artery (PICA) present significant technical challenges because of their irregular geometry and proximity to the lower cranial nerves and brainstem perforators. When endovascular options carry elevated risks, microsurgical clip reconstruction remains a definitive treatment to restore the vascular architecture. A 46-year-old woman presented for the elective surgical management of an unruptured, polylobulated left PICA aneurysm. She had a history of subarachnoid hemorrhage secondary to a ruptured anterior communicating artery aneurysm, which was successfully clipped alongside an unruptured right middle cerebral artery aneurysm in November 2024. Interdisciplinary case discussion considered endovascular treatment, including flow-diverting stents; however, the patient was unwilling to take dual antiplatelet therapy (aspirin and clopidogrel), and digital subtraction angiography demonstrated complex polylobulated morphology with multiple small perforators arising from the aneurysm base, making endovascular therapy high-risk. Microsurgical intervention was chosen because the surgical approach allowed for direct visualization and safe control of the aneurysm and surrounding neurovascular structures. A left medial suboccipital craniotomy with a subtonsillar approach was used. Stepwise reconstruction was performed using 2 straight mini clips (Aesculap No. 710 and 720) under continuous intraoperative neuromonitoring, including somatosensory evoked potentials, motor evoked potentials, and cranial nerve IX-XII electromyography. Multimodal verification, including microvascular Doppler, aneurysm puncture, and indocyanine green videoangiography, confirmed complete aneurysm obliteration and preservation of the parent vessel and perforators. The patient was discharged on postoperative day 4 without neurological deficits. Follow-up at 3 months confirmed favorable clinical and radiological outcome. For complex PICA aneurysms, a systematic approach incorporating subtonsillar exposure and multimodal intraoperative verification helps ensure complete exclusion while protecting the local neurovascular circulation.

PMID 42666764
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PubMedTherapeutic advances in neurological disorders2026-08-28

The impact of concomitant use of rosuvastatin or atorvastatin plus clopidogrel on the platelet inhibition and clinical outcomes in acute large-vessel minor stroke or TIA: A randomized controlled multi-center trial, the ROCATIS-1 trial.

Zeinhom Mohamed G MG, Sayed Ismaiel Mohamed Gamal MG, Khalil Mohamed Fouad Elsayed MFE, Elmesallami Ahmad Galal AG et al.

Although clopidogrel is commonly used for ischemic stroke secondary prevention, 20-50% of patients experienced clopidogrel failure and recurrence of ischemic events. We aimed to evaluate the benefits or hazards of adding atorvastatin or rosuvastatin to clopidogrel on the clopidogrel-induced inhibition of platelet activation and vascular events prevention. Our multi-center, randomized, single-blinded, parallel-group trial was conducted between 10th April 2024 and 10th May 2026. 600 first-ever, large-vessel minor ischemic stroke or TIA patients received 40 mg of atorvastatin or 20 mg of rosuvastatin during the first 24 hours of stroke onset once daily till the 90th day after stroke onset. Both groups received open-label 300 mg loading doses of aspirin and clopidogrel during the first 24 hours after stroke onset, followed by 75 mg clopidogrel and 100 mg aspirin once daily for 3 weeks, then 75 mg clopidogrel only until the end of the follow-up period. We followed up with our patients for 3 months. The change in the percentage of platelet maximum aggregation at 3 months of treatment compared with baseline while using adenosine diphosphate (ADP), 5 µM/L as an agonist was 54.4 (51.0-57.1) in the rosuvastatin group compared with 49.2 (45.5-52.3) in the atorvastatin group with P-value 0.003. 22 (7.3%) patients in the rosuvastatin group and 40 (13.3%) patients in the atorvastatin group experienced a composite of a new stroke, MI, or death due to vascular insults (HR 0.52; 95% CI, 0.33-0.81; P-value= 0.004), moreover, 12 (4.0%) patients in the rosuvastatin group and 19 (6.3%) in the atorvastatin group experienced recurrent stroke either ischemic or hemorrhagic, with (HR 0.60; 95% CI, 0.32-1.10; P-value 0.10). Compared with combining atorvastatin with clopidogrel in African large-vessel minor stroke or TIA, combining rosuvastatin with clopidogrel yielded higher rates of clopidogrel-induced platelet aggregation inhibition, significantly lower rates of a composite of recurrent stroke, MI, and death due to vascular events at three months. There were no significant differences between rosuvastatin and atorvastatin regarding drug-related side effects. Our findings are hypothesis-generating and require confirmation in a double-blinded, multinational randomized trial before they can inform practice.

PMID 42662137
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PubMedPharmacogenomics and personalized medicine2026-08-28

Cost-Effectiveness of Pharmacogenomics-Guided Treatment in Cardiovascular Disease: An Umbrella Review.

Janković Slobodan M SM, Milosavljević Miloš M, Stević Ivana I, Ašić Adna A et al.

Pharmacogenomics-guided prescribing uses patient genetic information to individualize drug selection and dosing and has attracted interest as a strategy to improve outcomes and reduce adverse drug events in cardiovascular diseases. Several systematic reviews have examined its cost-effectiveness, but their findings have not been synthesized across drug classes and healthcare settings. To identify, critically appraise, and synthesize findings from systematic reviews evaluating cost-effectiveness or cost-utility of pharmacogenomics-guided treatment of cardiovascular diseases. This systematic review of systematic reviews was pre-registered in PROSPERO (CRD420261281565). Five databases were searched from inception, without language restrictions. Eligible studies were systematic reviews that summarized cost-effectiveness evidence on pharmacogenomics-guided cardiovascular drug prescribing. Risk of bias was assessed using ROBIS and methodological quality using AMSTAR 2. Findings were synthesized narratively. Ten systematic reviews (2010-2024) were included, encompassing 149 unique primary cost-effectiveness studies. The corrected covered area across reviews was 9.47% (moderate overlap). Most evidence was derived from economic modelling studies and substantial heterogeneity was observed across drug-gene pairs, comparators, and healthcare settings. CYP2C19-guided clopidogrel therapy was frequently reported as cost-effective or cost-saving, although results were less favourable when universal ticagrelor served as comparator. Evidence for CYP2C9/VKORC1-guided coumarin anticoagulation was more heterogeneous with cost-effectiveness varying across contexts. Limited evidence suggested that SLCO1B1-guided statin therapy may be cost-effective, although data were sparse. No review reported pooled incremental cost-effectiveness ratios or net monetary benefit. Risk of bias was low in 7 reviews; AMSTAR 2 confidence was high in 4 and low in 5. Cost-effectiveness of pharmacogenomics-guided cardiovascular treatment seems to vary by drug-gene pair, comparator, healthcare context, and modelling assumptions. Further real-world studies and standardized economic evaluations are needed to clarify broader clinical adoption.

PMID 42662837
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