research use only
Cat.No.S1415
| Related Targets | Adrenergic Receptor AChR 5-HT Receptor COX Calcium Channel Histamine Receptor Dopamine Receptor GABA Receptor TRP Channel Cholinesterase (ChE) |
|---|---|
| Other P2 Receptor Inhibitors | A-438079 Hydrochloride A-804598 MRS 2578 AF-353 A-740003 5-BDBD Aurintricarboxylic acid A-317491 Gefapixant JNJ-47965567 |
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In vitro |
DMSO
: 83 mg/mL
(197.66 mM)
Ethanol : 83 mg/mL Water : Insoluble |
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In vivo |
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| Molecular Weight | 419.9 | Formula | C16H16ClNO2S.H2SO4 |
Storage (From the date of receipt) | |
|---|---|---|---|---|---|
| CAS No. | 120202-66-6 | Download SDF | Storage of Stock Solutions |
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Read more about storage stability stock solution CAS number SMILES
| Targets/IC50/Ki |
P2Y12
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|---|---|
| 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.
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| 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.
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References |
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| Methods | Biomarkers | Images | PMID |
|---|---|---|---|
| Western blot | ATF2 / ATF3 / ATF4 / ATF6 TRIB3 / CHOP |
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24058556 |
(data from https://clinicaltrials.gov, updated on 2026-07-06)
| NCT Number | Recruitment | Conditions | Sponsor/Collaborators | Start Date | Phases |
|---|---|---|---|---|---|
| NCT07683923 | NOT_YET_RECRUITING | SCAD; ACS (Acute Coronary Syndrome) |
Universitätsklinikum Hamburg-Eppendorf |
2027-03-01 | PHASE4 |
| NCT07572747 | NOT_YET_RECRUITING | Chronic Coronary Syndrome |
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2027-04-01 | PHASE3 |
| NCT07583784 | RECRUITING | Myocardial Infarction (MI); ST-Segment Elevation Myocardial Infarction(STEMI); NSTEMI - Non-ST-Segment Elevation Myocardial Infarction; AF - Atrial Fibrillation |
Chonnam National University Hospital |
2026-08-26 | |
| NCT07744191 | NOT_YET_RECRUITING | Psoriasis (PsO); Psoriatic Arthritis (PsA) |
NYU Langone Health |
2026-09 | PHASE4 |
| NCT07384702 | NOT_YET_RECRUITING | Bacteremia Due to Staphylococcus Aureus |
Fundación Pública Andaluza para la gestión de la Investigación en Sevilla |
2026-06 | PHASE2 |
| NCT06650488 | RECRUITING | Staphylococcus Aureus Endocarditis; Staphylococcus Aureus Septicemia; Staphylococcus Aureus Bloodstream Infection |
Todd C. Lee MD MPH FIDSA |
2026-01-15 | PHASE4 |
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