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Clopidogrel (SR-25990C) Bisulfate P2 Receptor modulator

Cat.No.S1415

Clopidogrel (SR-25990C) Bisulfate is an oral, thienopyridine class antiplatelet agent.
Clopidogrel (SR-25990C) Bisulfate P2 Receptor modulator Chemical Structure

Chemical Structure

Molecular Weight: 419.9

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Quality Control

Batch: Purity: 99.98%
99.98

Solubility

In vitro
Batch:

DMSO : 83 mg/mL (197.66 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 83 mg/mL

Water : Insoluble

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In vivo
Batch:

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Working concentration: mg/ml;

Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
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Chemical Information, Storage & Stability

Molecular Weight 419.9 Formula

C16H16ClNO2S.H2SO4

Storage (From the date of receipt)
CAS No. 120202-66-6 Download SDF Storage of Stock Solutions

Mechanism of Action

Targets/IC50/Ki
P2Y12
In vitro
Clopidogrel is converted to its active metabolite by cytochrome P450 (CYP) enzymes. Clopidogrel (1 μM) also inhibits EGF-stimulated EGF receptor, PERK expression, and cell proliferation in RGM-1 cells (P<0.05), and causes much less inhibition of EGF-stimulated cell proliferation in EGF receptor over-expressed RGM-1 cells than in RGM-1 cells (22% vs. 32% reduction). Clopidogrel increases blood vessel number, reduces polymorphonuclear count and decreases attachment and bone loss, also decreases osteoclast number in rats submitted or not to periodontal repair. Clopidogrel decreases CXCL4, CXCL12 and PDGF content compared with saline-treated rats, without affecting CXCL5.
In vivo
Clopidogrel (2mg and 10mg/kg/day) significantly decreases ulcer-induced gastric epithelial cell proliferation and ulcer-stimulated expressions of EGF receptor and phosphorylated extracellular signal-regulated kinase (PERK) at the ulcer margin of rats. Clopidogrel improves endothelial function and NO bioavailability in rats with congestive heart failure. Clopidogrel-treated Congestive heart failure (CHF) rat displays enhances phosphorylation of AKT and eNOS. The clopidogrel/aspirin combination shows only additive-type effects on bleeding time prolongation induced by ear transection in the rabbit, therefore showing that combined inhibition of cyclooxygenase and ADP's effects provide a marked enhanced antithrombotic efficacy.
References
  • [4] https://pubmed.ncbi.nlm.nih.gov/21287353/
  • [5] https://pubmed.ncbi.nlm.nih.gov/9759636/

Applications

Methods Biomarkers Images PMID
Western blot ATF2 / ATF3 / ATF4 / ATF6 TRIB3 / CHOP
S1415-WB1
24058556

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2024-05-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT05723926 Not yet recruiting
Atrial Fibrillation|Oral Anticoagulation|Stroke|Implant
Javelin Medical|Population Health Research Institute
January 20 2025 Not Applicable
NCT06047002 Recruiting
Peripheral Arterial Disease
University of Leicester
September 29 2022 --
NCT05166538 Unknown status
Multi Vessel Coronary Artery Disease
Yonsei University
February 1 2022 Phase 4
NCT05162053 Completed
Acute Coronary Syndrome
Jiangsu vcare pharmaceutical technology co. LTD
December 9 2021 Phase 1

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