CLOPIDOGREL 5-SULFOSALICYLATE

Details

Stereochemistry	ABSOLUTE
Molecular Formula	C16H16ClNO2S.C7H6O6S
Molecular Weight	540.006
Optical Activity	UNSPECIFIED
Defined Stereocenters	1 / 1
E/Z Centers	0
Charge	0

SHOW SMILES / InChI

Structure of CLOPIDOGREL 5-SULFOSALICYLATE

Structure Search

SMILES

OC(=O)C1=C(O)C=CC(=C1)S(O)(=O)=O.COC(=O)[C@@H](N2CCC3=C(C2)C=CS3)C4=CC=CC=C4Cl

InChI

InChIKey=UJDPIKOEIMRDKW-RSAXXLAASA-N

InChI=1S/C16H16ClNO2S.C7H6O6S/c1-20-16(19)15(12-4-2-3-5-13(12)17)18-8-6-14-11(10-18)7-9-21-14;8-6-2-1-4(14(11,12)13)3-5(6)7(9)10/h2-5,7,9,15H,6,8,10H2,1H3;1-3,8H,(H,9,10)(H,11,12,13)/t15-;/m0./s1

HIDE SMILES / InChI

Molecular Formula	C16H16ClNO2S
Molecular Weight	321.822
Charge	0
Count

Stereochemistry	ABSOLUTE
Additional Stereochemistry	No
Defined Stereocenters	1 / 1
E/Z Centers	0
Optical Activity	( + )

Molecular Formula	C7H6O6S
Molecular Weight	218.184
Charge	0
Count

Stereochemistry	ACHIRAL
Additional Stereochemistry	No
Defined Stereocenters	0 / 0
E/Z Centers	0
Optical Activity	NONE

Description
Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2009/020839s044lbl.pdf | https://www.drugbank.ca/drugs/DB00758 | https://www.ncbi.nlm.nih.gov/pubmed/15199474

Clopidogrel, an antiplatelet agent structurally and pharmacologically similar to ticlopidine, is used to inhibit blood clots in a variety of conditions such as peripheral vascular disease, coronary artery disease, and cerebrovascular disease. Clopidogrel is sold under the name Plavix by Sanofi and Bristol-Myers Squibb. Plavix (clopidogrel bisulfate) is an inhibitor of ADP-induced platelet aggregation acting by direct inhibition of adenosine diphosphate (ADP) binding to its receptor and of the subsequent ADPmediated activation of the glycoprotein GPIIb/IIIa complex. Clopidogrel must be metabolized by CYP450 enzymes to produce the active metabolite that inhibits platelet aggregation. The active metabolite of clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADPmediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible. Consequently, platelets exposed to clopidogrel’s active metabolite are affected for the remainder of their lifespan (about 7 to 10 days). Platelet aggregation induced by agonists other than ADP is also inhibited by blocking the amplification of platelet activation by released ADP. Plavix (clopidogrel bisulfate) is indicated for the reduction of atherothrombotic events.

Originator

Approval Year

Targets

Primary Target	Pharmacology	Condition	Potency
Purinergic receptor P2Y12 23 Target ID: CHEMBL2001 Sources: https://www.ncbi.nlm.nih.gov/pubmed/15199474 \| https://www.accessdata.fda.gov/drugsatfda_docs/label/2009/020839s044lbl.pdf \| https://www.drugbank.ca/drugs/DB00758	Antagonist 2849		6.9 null [pKi]
Purinergic receptor P2Y12 23 Target ID: CHEMBL2001 Sources: https://dailymed.nlm.nih.gov/dailymed/fda/fdaDrugXsl.cfm?setid=0078fb3d-3595-4ae1-a059-1d5e81c879cf&type=display\|https://www.ncbi.nlm.nih.gov/pubmed/10446085	Antagonist 2849

Conditions

Condition	Modality	Highest Phase	Product
Atherosclerosis 76 Sources: https://www.drugs.com/pro/clopidogrel.html	Primary	Approved 8583	PLAVIX Approved Use Plavix (clopidogrel bisulfate) is indicated for the reduction of atherothrombotic events as follows: • Recent MI, Recent Stroke or Established Peripheral Arterial Disease For patients with a history of recent myocardial infarction (MI), recent stroke, or established peripheral arterial disease, Plavix has been shown to reduce the rate of a combined endpoint of new ischemic stroke (fatal or not), new MI (fatal or not), and other vascular death. • Acute Coronary Syndrome -For patients with non-ST-segment elevation acute coronary syndrome (unstable angina/nonQ-wave MI) including patients who are to be managed medically and those who are to be managed with percutaneous coronary intervention (with or without stent) or CABG, Plavix has been shown to decrease the rate of a combined endpoint of cardiovascular death, MI, or stroke as well as the rate of a combined endpoint of cardiovascular death, MI, stroke, or refractory ischemia. Plavix (clopidogrel bisulfate) is indicated for the reduction of atherothrombotic events as follows: • Recent MI, Recent Stroke or Established Peripheral Arterial Disease For patients with a history of recent myocardial infarction (MI), recent stroke, or established peripheral arterial disease, Plavix has been shown to reduce the rate of a combined endpoint of new ischemic stroke (fatal or not), new MI (fatal or not), and other vascular death. • Acute Coronary Syndrome -For patients with non-ST-segment elevation acute coronary syndrome (unstable angina/nonQ-wave MI) including patients who are to be managed medically and those who are to be managed with percutaneous coronary intervention (with or without stent) or CABG, Plavix has been shown to decrease the rate of a combined endpoint of cardiovascular death, MI, or stroke as well as the rate of a combined endpoint of cardiovascular death, MI, stroke, or refractory ischemia. Launch Date 1997
Acute coronary syndrome 33 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2009/020839s044lbl.pdf	Primary	Approved 8583	PLAVIX Approved Use Plavix (clopidogrel bisulfate) is indicated for the reduction of atherothrombotic events as follows: • Recent MI, Recent Stroke or Established Peripheral Arterial Disease For patients with a history of recent myocardial infarction (MI), recent stroke, or established peripheral arterial disease, Plavix has been shown to reduce the rate of a combined endpoint of new ischemic stroke (fatal or not), new MI (fatal or not), and other vascular death. • Acute Coronary Syndrome -For patients with non-ST-segment elevation acute coronary syndrome (unstable angina/nonQ-wave MI) including patients who are to be managed medically and those who are to be managed with percutaneous coronary intervention (with or without stent) or CABG, Plavix has been shown to decrease the rate of a combined endpoint of cardiovascular death, MI, or stroke as well as the rate of a combined endpoint of cardiovascular death, MI, stroke, or refractory ischemia. Launch Date 1997
Peripheral arterial disease 22 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2009/020839s044lbl.pdf	Primary	Approved 8583	PLAVIX Approved Use Plavix (clopidogrel bisulfate) is indicated for the reduction of atherothrombotic events as follows: • Recent MI, Recent Stroke or Established Peripheral Arterial Disease For patients with a history of recent myocardial infarction (MI), recent stroke, or established peripheral arterial disease, Plavix has been shown to reduce the rate of a combined endpoint of new ischemic stroke (fatal or not), new MI (fatal or not), and other vascular death. • Acute Coronary Syndrome -For patients with non-ST-segment elevation acute coronary syndrome (unstable angina/nonQ-wave MI) including patients who are to be managed medically and those who are to be managed with percutaneous coronary intervention (with or without stent) or CABG, Plavix has been shown to decrease the rate of a combined endpoint of cardiovascular death, MI, or stroke as well as the rate of a combined endpoint of cardiovascular death, MI, stroke, or refractory ischemia. Launch Date 1997
Myocardial infarction 125 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2009/020839s044lbl.pdf	Preventing	Approved 8583	PLAVIX Approved Use Plavix (clopidogrel bisulfate) is indicated for the reduction of atherothrombotic events as follows: • Recent MI, Recent Stroke or Established Peripheral Arterial Disease For patients with a history of recent myocardial infarction (MI), recent stroke, or established peripheral arterial disease, Plavix has been shown to reduce the rate of a combined endpoint of new ischemic stroke (fatal or not), new MI (fatal or not), and other vascular death. • Acute Coronary Syndrome -For patients with non-ST-segment elevation acute coronary syndrome (unstable angina/nonQ-wave MI) including patients who are to be managed medically and those who are to be managed with percutaneous coronary intervention (with or without stent) or CABG, Plavix has been shown to decrease the rate of a combined endpoint of cardiovascular death, MI, or stroke as well as the rate of a combined endpoint of cardiovascular death, MI, stroke, or refractory ischemia. Launch Date 1997

C_max

Value	Dose	Analyte	Population
0.521 ng/mL Clinical Trial https://clinicaltrials.gov/ct2/show/NCT02185534	75 mg single, oral dose: 75 mg route of administration: oral experiment type: single co-administered:	CLOPIDOGREL plasma	Homo sapiens population: healthy age: sex: food status:
15800 pg/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/22128201	300 mg single, oral dose: 300 mg route of administration: Oral experiment type: SINGLE co-administered:	CLOPIDOGREL BISULFATE plasma	Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: FED
4600 pg/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/22128201	300 mg single, oral dose: 300 mg route of administration: Oral experiment type: SINGLE co-administered:	CLOPIDOGREL BISULFATE plasma	Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: FASTED
2520 pg/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/22128201	75 mg 1 times / day multiple, oral dose: 75 mg route of administration: Oral experiment type: MULTIPLE co-administered:	CLOPIDOGREL BISULFATE plasma	Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: FED
1500 pg/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/22128201	75 mg 1 times / day multiple, oral dose: 75 mg route of administration: Oral experiment type: MULTIPLE co-administered:	CLOPIDOGREL BISULFATE plasma	Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: FASTED

AUC

Value	Dose	Analyte	Population
1.09 ng*h/mL Clinical Trial https://clinicaltrials.gov/ct2/show/NCT02185534	75 mg single, oral dose: 75 mg route of administration: oral experiment type: single co-administered:	CLOPIDOGREL plasma	Homo sapiens population: healthy age: sex: food status:
0.767 ng*h/mL Clinical Trial https://clinicaltrials.gov/ct2/show/NCT02185534	75 mg single, oral dose: 75 mg route of administration: oral experiment type: single co-administered:	CLOPIDOGREL plasma	Homo sapiens population: healthy age: sex: food status:
50600 pg × h/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/22128201	300 mg single, oral dose: 300 mg route of administration: Oral experiment type: SINGLE co-administered:	CLOPIDOGREL BISULFATE plasma	Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: FED
9890 pg × h/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/22128201	300 mg single, oral dose: 300 mg route of administration: Oral experiment type: SINGLE co-administered:	CLOPIDOGREL BISULFATE plasma	Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: FASTED
7440 pg × h/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/22128201	75 mg 1 times / day multiple, oral dose: 75 mg route of administration: Oral experiment type: MULTIPLE co-administered:	CLOPIDOGREL BISULFATE plasma	Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: FED
3130 pg × h/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/22128201	75 mg 1 times / day multiple, oral dose: 75 mg route of administration: Oral experiment type: MULTIPLE co-administered:	CLOPIDOGREL BISULFATE plasma	Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: FASTED

T_1/2

Value	Dose	Analyte	Population
5.4 h EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/22128201	300 mg single, oral dose: 300 mg route of administration: Oral experiment type: SINGLE co-administered:	CLOPIDOGREL BISULFATE plasma	Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: FED
7.9 h EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/22128201	300 mg single, oral dose: 300 mg route of administration: Oral experiment type: SINGLE co-administered:	CLOPIDOGREL BISULFATE plasma	Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: FASTED
7.4 h EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/22128201	75 mg 1 times / day multiple, oral dose: 75 mg route of administration: Oral experiment type: MULTIPLE co-administered:	CLOPIDOGREL BISULFATE plasma	Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: FED
8.5 h EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/22128201	75 mg 1 times / day multiple, oral dose: 75 mg route of administration: Oral experiment type: MULTIPLE co-administered:	CLOPIDOGREL BISULFATE plasma	Homo sapiens population: HEALTHY age: ADULT sex: MALE food status: FASTED

F_unbound

Value	Dose	Co-administered	Analyte	Population
2% DRUG LABEL https://www.accessdata.fda.gov/drugsatfda_docs/label/2009/020839s044lbl.pdf	unknown, unknown		CLOPIDOGREL BISULFATE plasma	Homo sapiens population: UNKNOWN age: UNKNOWN sex: UNKNOWN food status: UNKNOWN

Doses

Dose	Population	Adverse events
600 mg 1 times / day multiple, oral Highest studied dose Dose: 600 mg, 1 times / day Route: oral Route: multiple Dose: 600 mg, 1 times / day Sources: https://pubmed.ncbi.nlm.nih.gov/26063503	healthy, 20-45 years Health Status: healthy Age Group: 20-45 years Sex: M Sources: https://pubmed.ncbi.nlm.nih.gov/26063503	Other AEs: Uric acid abnormal... Other AEs: Uric acid abnormal (5 patients) Sources: https://pubmed.ncbi.nlm.nih.gov/26063503
1650 mg single, oral Overdose Dose: 1650 mg Route: oral Route: single Dose: 1650 mg Sources: https://pubmed.ncbi.nlm.nih.gov/17286151	unknown, 49 years Health Status: unknown Age Group: 49 years Sex: M Sources: https://pubmed.ncbi.nlm.nih.gov/17286151	Sources: https://pubmed.ncbi.nlm.nih.gov/17286151
600 mg 1 times / day multiple, oral Dose: 600 mg, 1 times / day Route: oral Route: multiple Dose: 600 mg, 1 times / day Sources: https://pubmed.ncbi.nlm.nih.gov/16878371	unhealthy, 59 years Health Status: unhealthy Age Group: 59 years Sex: F Sources: https://pubmed.ncbi.nlm.nih.gov/16878371	Disc. AE: Transaminases increased, Fever... AEs leading to discontinuation/dose reduction: Transaminases increased (1 patient) Fever (1 patient) Sources: https://pubmed.ncbi.nlm.nih.gov/16878371

AEs

AE	Significance	Dose	Population
Uric acid abnormal	5 patients	600 mg 1 times / day multiple, oral Highest studied dose Dose: 600 mg, 1 times / day Route: oral Route: multiple Dose: 600 mg, 1 times / day Sources: https://pubmed.ncbi.nlm.nih.gov/26063503	healthy, 20-45 years Health Status: healthy Age Group: 20-45 years Sex: M Sources: https://pubmed.ncbi.nlm.nih.gov/26063503
Fever	1 patient Disc. AE	600 mg 1 times / day multiple, oral Dose: 600 mg, 1 times / day Route: oral Route: multiple Dose: 600 mg, 1 times / day Sources: https://pubmed.ncbi.nlm.nih.gov/16878371	unhealthy, 59 years Health Status: unhealthy Age Group: 59 years Sex: F Sources: https://pubmed.ncbi.nlm.nih.gov/16878371
Transaminases increased	1 patient Disc. AE	600 mg 1 times / day multiple, oral Dose: 600 mg, 1 times / day Route: oral Route: multiple Dose: 600 mg, 1 times / day Sources: https://pubmed.ncbi.nlm.nih.gov/16878371	unhealthy, 59 years Health Status: unhealthy Age Group: 59 years Sex: F Sources: https://pubmed.ncbi.nlm.nih.gov/16878371

Overview

CYP3A4	CYP2C9	CYP2D6	hERG
inhibitor 2252 substrate 1946	substrate 1193 inhibitor 2438	substrate 1388 inhibitor 2507

OverviewOther

Other Inhibitor	Other Substrate	Other Inducer
CYP2C19 2057 CYP1A2 2153 OCT1 620 CYP2E1 1060 primateCYP1A 10 CYP2A6 879 OAT1 725 OCT2 779 CYP2C8 1057 OATP1B1 1079	UGT2B17 237 CYP2B6 776 CYP2E1 729 CES1 45 UGT2B4 278 CYP2A6 626 CYP1A2 1197 CYP2C19 1119 UGT2B7 456 OAT1 395 OCT1 393 P-gp 2052 OCT2 434 rCYP1A1/2 10	primateCYP3A 10 primateCYP2E 10

Drug as perpetrator

Target	Modality	Activity	Metabolite
CYP1A2 2333	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=169 Page: 169.0	no
CYP1A2 2333	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=91 Page: 91, 169	no	SR26334 10
CYP2A6 911	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=169	no
CYP2A6 911	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=91 Page: 91, 169	no	SR26334 10
CYP2C19 2141	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=169 Page: 169.0	no
CYP2C19 2141	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=91 Page: 91, 169	no	SR26334 10
CYP2D6 2546	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=169 Page: 169.0	no
CYP2D6 2546	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=91 Page: 91, 169	no	SR26334 10
CYP2E1 1146	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=169 Page: 169.0	no
CYP2E1 1146	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=91 Page: 91, 169	no	SR26334 10
CYP3A4 2633	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=169 Page: 169.0	no
CYP3A4 2633	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=91 Page: 91, 169	no	SR26334 10
primateCYP2E 10	inducer 1966 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=74 Page: 74.0	no
OAT1 730	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/24530383/	weak	clopidogrel carboxylic acid 10
OCT2 782	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/24530383/	weak	CLOPIDOGREL CARBOXYLIC ACID 10
OCT1 656	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/24530383/	yes [IC50 0.307 uM]
OCT1 656	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/24530383/	yes [IC50 6.25 uM]	CLOPIDOGREL CARBOXYLIC ACID 10
CYP2C9 2497	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=91 Page: 91, 170	yes [Ki 28 uM]	SR26334 10
CYP2C8 1117	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/27457785/	yes
CYP2C9 2497	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=22 Page: 22.0	yes
OATP1B1 1095	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/27457785/	yes
primateCYP1A 10	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=74 Page: 74.0	yes
primateCYP3A 10	inducer 1966 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=74 Page: 74.0	yes

Drug as victim

Target	Modality	Activity	Metabolite
CYP1A2 1197	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=168 Page: 168.0	likely
CYP2C9 1193	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=168 Page: 168.0	likely
CYP2E1 729	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=168 Page: 168.0	likely
CYP2A6 626	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=168 Page: 168.0	no
CYP2D6 1388	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=168 Page: 168.0	no
OCT1 393	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/24530383/	no
OCT1 393	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/24530383/	no	CLOPIDOGREL CARBOXYLIC ACID 10
OCT2 434	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/24530383/	no
OCT2 434	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/24530383/	no	CLOPIDOGREL CARBOXYLIC ACID 10
UGT2B17 237	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/29138287/	yes [Km 181 uM]	CLOPIDOGREL CARBOXYLIC ACID 10
UGT2B4 278	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/29138287/	yes [Km 19 uM]	CLOPIDOGREL CARBOXYLIC ACID 10
UGT2B7 456	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/29138287/	yes [Km 20.9 uM]	CLOPIDOGREL CARBOXYLIC ACID 10
OAT1 395	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/24530383/	yes [Km 5.61 uM]	CLOPIDOGREL CARBOXYLIC ACID 10
CES1 45	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/29138287/	yes
CYP2B6 776	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=168 Page: 168.0	yes
CYP2C19 1119	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=168 Page: 168.0	yes
CYP3A4 1946	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=168 Page: 168.0	yes
P-gp 2052	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/17112805/	yes
rCYP1A1/2 10	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/pre96/020839_s000.pdf#page=74 Page: 74.0	yes

Sourcing

Vendor/Aggregator	ID	URL
ChEBI	CHEBI:37941	https://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:37941
eMolecules	2735330	https://www.emolecules.com/cgi-bin/more?vid=2735330
MolPort	MolPort-002-885-817	https://www.molport.com/shop/molecule-link/MolPort-002-885-817
ZINC	ZINC000034781704	http://zinc15.docking.org/substances/ZINC000034781704

PubMed

Title	Date	PubMed
Future perspectives for optimizing oral antiplatelet therapy.	2001	11316919
Management practices in carotid stenting.	2001	11316918
Current oral antiplatelet agents to prevent atherothrombosis.	2001	11316917
Benefit of ADP receptor antagonists in atherothrombotic patients: new evidence.	2001	11316916
Novel platelet inhibitors.	2001	11160773
Antithrombotic drugs for secondary stroke prophylaxis.	2001 Apr	11310519
Ultrasound guided percutaneous thrombin injection of iatrogenic femoral artery pseudoaneurysms after coronary angiography and intervention.	2001 Apr	11250982
Results of CURE trial for acute coronary syndrome.	2001 Apr 11	11308379
[Acute heart attacks. Prognosis can be further improved].	2001 Apr 5	11340908
Management of neurological complications of carotid artery stenting.	2001 Aug	11552726
Deaggregation is an integral component of the response of platelets to ADP in vitro: kinetic studies of literature and original data.	2001 Aug	11487380
Radiation-induced glomerular thrombus formation and nephropathy are not prevented by the ADP receptor antagonist clopidogrel.	2001 Aug 1	11483346
Clopidogrel in invasive management of non-ST-elevation ACS.	2001 Aug 18	11520515
Comparison of effects of clopidogrel versus ticlopidine on platelet function in patients undergoing coronary stent placement.	2001 Feb 1	11165971
Combination therapy with aspirin plus clopidogrel versus aspirin plus ticlopidine for prevention of subacute thrombosis after successful native coronary stenting.	2001 Feb 15	11179539
[Clopidogrel? Known or known?].	2001 Jan	11223636
Stasis ulcers refractory to therapy--accelerated healing by treatment with clopidogrel +/- dalteparin: a preliminary report.	2001 Jan	11190899
[2 platelet inhibitors administered at the same time. Improved prognosis in myocardial infarct?]].	2001 Jan 11	11219401
Identification of the platelet ADP receptor targeted by antithrombotic drugs.	2001 Jan 11	11196645
Superiority of clopidogrel versus aspirin in patients with prior cardiac surgery.	2001 Jan 23	11157686
Localized intracoronary gamma-radiation therapy to inhibit the recurrence of restenosis after stenting.	2001 Jan 25	11172151
Clopidogrel (Plavix): hematological reactions.	2001 Jan 9	11202680
[Can we use clopidogrel in patients with coronary stent?].	2001 Jan-Mar	11488209
ADP receptors of platelets and their inhibition.	2001 Jul	11487010
Current perspectives on British use of adjunctive therapies during coronary interventions.	2001 Jul	11461731
Multiple intracranial aneurysms as delayed complications of an atrial myxoma: case report.	2001 Jul	11440443
Diffuse alveolar hemorrhage after clopidogrel use.	2001 Jul	11435642
Randomized comparison of ticlopidine and clopidogrel after intracoronary stent implantation in a broad patient population.	2001 Jul 31	11479250
Acute coronary syndrome: are intervention and IIb/IIIa platelet inhibitors epiphenomena?	2001 Jul-Aug	11501219
The P2Y12 receptor as a therapeutic target in cardiovascular disease.	2001 Jun	11454254
[Acute coronary syndromes: an update. I. Pathogenesis and drug therapy].	2001 Mar	11349620
[Pharmacy clinics. Medication of the month. Clopidogrel (Plavix)].	2001 Mar	11338792
[New platelet inhibitors].	2001 Mar	11315485
Initial experience with a newer generation coronary stent.	2001 Mar	11231647
What is the optimal medical management of ischemic heart failure?	2001 Mar-Apr	11251129
The inhibition of oxygen radical release from human neutrophils by resting platelets is reversed by administration of acetylsalicylic acid or clopidogrel.	2001 May	11378529
New recommendations from the 1999 American College of Cardiology/American Heart Association acute myocardial infarction guidelines.	2001 May	11346067
Orbofiban: an orally active GPIIb/IIIa platelet receptor antagonist.	2001 May	11301411
Edge stenosis after intracoronary radiotherapy: angiographic, intravascular, and histological findings.	2001 May 1	11331266
P2y(12), a new platelet ADP receptor, target of clopidogrel.	2001 May 4	11327712
Clopidogrel and aplastic anaemia.	2001 May 5	11360950
Coronary stent deployment in situs inversus.	2001 Nov	11602566
Methods and models to evaluate shear-dependent and surface reactivity-dependent antithrombotic efficacy.	2001 Nov 1	11672758
Antiplatelet agents for secondary prevention of ischemic stroke.	2001 Oct	11675854
[Clopidogrel in acute coronary syndromes with non-ST elevation. Clinical implications of the CURE trial].	2001 Oct	11591313
Effects of clopidogrel pretreatment before percutaneous coronary intervention in patients treated with glycoprotein IIb/IIIa inhibitors (abciximab or tirofiban).	2001 Oct 15	11676953
Drug-associated thrombotic thrombocytopenic purpura-hemolytic uremic syndrome.	2001 Sep	11604563
Coronary stent thrombosis: insights from the porcine coronary stent model.	2001 Sep	11583335
Cilostazol for prevention of thrombosis and restenosis after intracoronary stenting.	2001 Sep	11573862
Effects of combining three different antiplatelet agents on platelets and leukocytes in whole blood in vitro.	2001 Sep	11564653

Patents

Sample Use Guides

In Vivo Use Guide

Recent MI, Recent Stroke, or Established Peripheral Arterial Disease The recommended daily dose of is 75 mg once daily.

Route of Administration: Oral

In Vitro Use Guide

Incubation of human washed platelets with clopidogrel resulted in a time- (maximum effects after 30 min) and concentration-dependent (IC50 1.9+/-0.3 uM) inhibition of ADP (6 uM)-induced platelet aggregation. Clopidogrel (30 uM) did not inhibit collagen (2.5 ug ml(-1))-, U46619 (1 uM)- or thrombin (0.1 u ml(-1))-induced platelet aggregation.

Substance Class	Chemical Created by `admin` on `Wed Apr 02 12:06:25 GMT 2025` Edited by `admin` on `Wed Apr 02 12:06:25 GMT 2025`
Record UNII	YEU2DVE4SQ
Record Status	`Validated (UNII)`
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Name

Type

Language

THIENO(3,2-C)PYRIDINE-5(4H)-ACETIC ACID, .ALPHA.-(2-CHLOROPHENYL)-6,7-DIHYDRO-, METHYL ESTER, (.ALPHA.S)-, 2-HYDROXY-5-SULFOBENZOATE (1:1)

Preferred Name

English

CLOPIDOGREL 5-SULFOSALICYLATE

Common Name

English

Code System Code Type Description

CAS

1010080-15-5

Created by admin on Wed Apr 02 12:06:25 GMT 2025 , Edited by admin on Wed Apr 02 12:06:25 GMT 2025

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FDA UNII

YEU2DVE4SQ

Created by admin on Wed Apr 02 12:06:25 GMT 2025 , Edited by admin on Wed Apr 02 12:06:25 GMT 2025

PRIMARY

SMS_ID

100000175200

Created by admin on Wed Apr 02 12:06:25 GMT 2025 , Edited by admin on Wed Apr 02 12:06:25 GMT 2025

PRIMARY

PUBCHEM

87203050

Created by admin on Wed Apr 02 12:06:25 GMT 2025 , Edited by admin on Wed Apr 02 12:06:25 GMT 2025

PRIMARY

Related Record Type Details


					A74586SNO7

CLOPIDOGREL

PARENT -> SALT/SOLVATE

Amount:

Related Record Type Details


					A74586SNO7

CLOPIDOGREL

ACTIVE MOIETY

Amount:

Details

SMILES

InChI

DescriptionSources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2009/020839s044lbl.pdf | https://www.drugbank.ca/drugs/DB00758 | https://www.ncbi.nlm.nih.gov/pubmed/15199474

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OverviewOther

Drug as perpetrator​

Drug as victim

Sourcing

PubMed

Patents

Sample Use Guides

Description
Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2009/020839s044lbl.pdf | https://www.drugbank.ca/drugs/DB00758 | https://www.ncbi.nlm.nih.gov/pubmed/15199474

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Drug as perpetrator