Evidence map›Paper›PMID 42060807›Full record

ArticleIndian journal of pharmacology2026

Repurposing piroxicam for antithrombotic and cardiopulmonary protection: Pharmacological rationale and therapeutic potential.

Waseem Khalid, Arif-Ullah Khan

Abstract read
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Article in Indian journal of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Waseem KhalidDepartment of Pharmacology, Riphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad 04405, Pakistan.
Arif-Ullah Khan

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent research indicates that non-steroidal anti-inflammatory drugs may interfere in coagulation process and platelet aggregation. However, the potential of piroxicam in thrombotic and cardiopulmonary disorders remained unexplored.

objectivesTo bridge this knowledge gap, the current study was conducted to assess the potential of piroxicam as antithrombotic and cardiopulmonary protective agent using multi-level approaches. MATERIALS AND

methodsPiroxicam was docked against 16 key proteins involved in thrombotic and cardiopulmonary conditions. Its antiplatelet effect was evaluated by arachidonic acid (AA) and adenosine diphosphate (ADP)-induced aggregation while its effect on coagulation parameters were also evaluated. Cardiopulmonary protective effect in rats was investigated through isoproterenol induced myocardial infarction (MI) and self-embolus induced pulmonary embolism (PE).

resultsStrong binding interactions were identified, with docking energies of ≥-9.0 kcal/mol noted for cyclooxygenase (COX) 1, glycopotein-IIb/IIIa, antithrombin-III, COX-2, and nuclear factor Kappa-B (NFkB). Piroxicam significantly inhibited AA and ADP-induced platelet aggregation (IC50: 0.68 and 24.9 μM) and also prolonged the prothrombin, activated partial thromboplastin, thrombin, and clot lysis time. Piroxicam markedly and in a dose-related manner lowered MI and PE associated serum markers in experimental rats. Piroxicam further safeguarded cardiac and pulmonary tissues from infarction and histopathological injury through the suppression of oxidative imbalance and inflammatory activity. This protective outcome was also due to reduced expression of tissue necrosis factor-α, NFkB, COX-2, NLRP3, and platelet-derived growth factor-β, verified using immunohistochemistry, enzyme-linked immunosorbent assay, and real-time polymerase chain reaction RT-PCR techniques.

conclusionsThese results indicate the prophylactic potential of piroxicam in cardiopulmonary thrombotic disorders.

Indexed as

Cardiotonic AgentsFibrinolytic AgentsMyocardial InfarctionPiroxicamPlatelet Aggregation InhibitorsPulmonary EmbolismAnimalsBlood CoagulationHumansMaleMolecular Docking SimulationPlatelet AggregationRatsCardiotonic AgentsFibrinolytic AgentsPiroxicamPlatelet Aggregation InhibitorsAntiplateletcoagulationmyocardial infarctionpiroxicampulmonary embolism

Identifiers

PMID42060807
PMCPMC13258202

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.