PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
33887342-0	2021	Clopidogrel in noncarriers of CYP2C19 loss-of-function alleles versus ticagrelor in elderly patients with acute coronary syndrome: A pre-specified sub analysis from the POPular Genetics and POPular Age trials CYP2C19 alleles in elderly patients.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
33887342-1	2021	BACKGROUND: Patients with acute coronary syndrome (ACS) who are carrying CYP2C19 loss-of-function alleles derive less benefit from clopidogrel treatment.	clopidogrel	131-142	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	73-80
33649514-1	2021	Reduced clopidogrel effectiveness in preventing recurrent myocardial ischemia following percutaneous coronary intervention has been demonstrated in CYP2C19 loss-of-function carriers.	clopidogrel	8-19	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	148-155
33649514-8	2021	Caucasian treated with clopidogrel who are homozygote for the CYP2C19 loss-of function allele might be at increased risk for ischemic stroke, and for the composite outcome of ischemic stroke, myocardial infarction and coronary angioplasty.	clopidogrel	23-34	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	62-69
33502028-7	2021	We present evidence suggesting P2RY12, a key microglial gene and target for the anti-thrombotic agent clopidogrel, as the likely driver of a significant Parkinson"s disease association signal on chromosome 3.	clopidogrel	102-113	purinergic receptor P2Y12	Homo sapiens	31-37
33535078-1	2021	BACKGROUND: Patients having CYP2C19 loss-of-function alleles and receiving clopidogrel are at higher risk of adverse cardiovascular outcomes.	clopidogrel	75-86	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
33991548-8	2021	We also show that inhibiting platelet activation with the P2Y12-inhibitor Clopidogrel decreases the number of tumors in a chemically induced mouse model for HCC.	clopidogrel	74-85	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	58-63
33959860-2	2021	Clopidogrel requires bio-activation by cytochrome P450 CYP2C19.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	55-62
33959860-3	2021	Omeprazole may reduce clopidogrel"s antithrombotic efficacy by inhibiting CYP2C19.	clopidogrel	22-33	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	74-81
33753217-2	2021	The method was applied to determine the selectivity of the time-dependent CYP2C8 inhibitors gemfibrozil 1-O-beta-glucuronide and clopidogrel acyl-beta-D-glucuronide.	clopidogrel	129-140	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	74-80
34042199-1	2021	BACKGROUND: The RE-DUAL PCI trial demonstrated that in patients with nonvalvular atrial fibrillation (AF) undergoing percutaneous coronary intervention (PCI), dual therapy with dabigatran and a P2Y12 inhibitor, either clopidogrel or ticagrelor, reduced the risk of bleeding without an increased risk of thromboembolic events as compared to triple therapy with warfarin in addition to a P2Y12 inhibitor and aspirin.	clopidogrel	218-229	purinergic receptor P2Y12	Homo sapiens	194-199
34039032-1	2021	BACKGROUND AND PURPOSE: We performed a systemic review and meta-analysis to elucidate the effectiveness and safety of dual antiplatelet (DAPT) therapy with P2Y12 inhibitors (clopidogrel/ticagrelor) and aspirin versus aspirin monotherapy in patients with mild ischemic stroke or high-risk transient ischemic attack.	clopidogrel	174-185	purinergic receptor P2Y12	Homo sapiens	156-161
33993817-1	2021	INTRODUCTION: Clopidogrel is the most frequently utilized P2Y12 inhibitor and is characterized by broad interindividual response variability resulting in impaired platelet inhibition and increased risk of thrombotic complications in a considerable number of patients.	clopidogrel	14-25	purinergic receptor P2Y12	Homo sapiens	58-63
33993817-3	2021	Genetic variations of the cytochrome P450 (CYP) 2C19 enzyme, a key determinant in clopidogrel metabolism, have been strongly associated with clopidogrel response profiles prompting investigations of genetic-guided selection of antiplatelet therapy.	clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-52
33993817-3	2021	Genetic variations of the cytochrome P450 (CYP) 2C19 enzyme, a key determinant in clopidogrel metabolism, have been strongly associated with clopidogrel response profiles prompting investigations of genetic-guided selection of antiplatelet therapy.	clopidogrel	141-152	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-52
34046471-11	2021	The VerifyNow P2Y12 test showed clopidogrel resistance.	clopidogrel	32-43	purinergic receptor P2Y12	Homo sapiens	14-19
34040417-0	2021	Pharmacogenomics in the United States Community Pharmacy Setting: The Clopidogrel-CYP2C19 Example.	clopidogrel	70-81	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	82-89
34040417-3	2021	The drug-gene pair of clopidogrel-CYP2C19 has been a focus of implementation of PGx in community pharmacy and serves as an example of the evolution of the application of drug-gene interaction information to help optimize drug therapy.	clopidogrel	22-33	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	34-41
34040417-7	2021	The example of clopidogrel-CYP2C19 is discussed and current models of PGx implementation in the community pharmacy in the United States are presented.	clopidogrel	15-26	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	27-34
33931001-2	2021	It is commonly used to reduce the risk of blood coagulation in patients diagnosed with acute coronary syndrome, or ischemic stroke.Area covered: We reviewed published articles in PubMed and Google Scholar that focused on the mutations of CYP2C19, CYP3A4, CYP2C9, CYP2B6, and CYP1A2 genes related to clopidogrel clinical efficacy and safety.Expert opinion: Based on current pharmacogenetic studies, patients carrying CYP2C19*2, CYP2C19*3, CYP2C9*3, and CYP2B6*5 alleles may not respond to clopidogrel due to poor platelet inhibition efficacy revealed among them.	clopidogrel	299-310	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	238-245
33931001-2	2021	It is commonly used to reduce the risk of blood coagulation in patients diagnosed with acute coronary syndrome, or ischemic stroke.Area covered: We reviewed published articles in PubMed and Google Scholar that focused on the mutations of CYP2C19, CYP3A4, CYP2C9, CYP2B6, and CYP1A2 genes related to clopidogrel clinical efficacy and safety.Expert opinion: Based on current pharmacogenetic studies, patients carrying CYP2C19*2, CYP2C19*3, CYP2C9*3, and CYP2B6*5 alleles may not respond to clopidogrel due to poor platelet inhibition efficacy revealed among them.	clopidogrel	488-499	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	238-245
33931001-3	2021	In contrast, carriers of CYP2C19*17, CYP3A4*1G, and CYP1A2*1F alleles showed a more significant antiplatelet effect in clopidogrel users and expected to have a protective role as a genetic factor against cardiovascular events.	clopidogrel	119-130	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
33931001-3	2021	In contrast, carriers of CYP2C19*17, CYP3A4*1G, and CYP1A2*1F alleles showed a more significant antiplatelet effect in clopidogrel users and expected to have a protective role as a genetic factor against cardiovascular events.	clopidogrel	119-130	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	37-43
33931001-3	2021	In contrast, carriers of CYP2C19*17, CYP3A4*1G, and CYP1A2*1F alleles showed a more significant antiplatelet effect in clopidogrel users and expected to have a protective role as a genetic factor against cardiovascular events.	clopidogrel	119-130	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	52-58
33955698-4	2021	Long-term benefit is provided by oral P2Y12 receptor antagonists such as clopidogrel, prasugrel, and ticagrelor.	clopidogrel	73-84	purinergic receptor P2Y12	Homo sapiens	38-43
33953382-2	2021	The most common implementation in practice is CYP2C19 genotyping to predict clopidogrel response and assist in selecting antiplatelet therapy after percutaneous coronary intervention.	clopidogrel	76-87	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	46-53
33831672-1	2021	BACKGROUND AND AIMS: The coprescription of an angiotensin-converting enzyme inhibitor (ACEi) with clopidogrel reportedly increases bleeding risk.	clopidogrel	98-109	angiotensin I converting enzyme	Homo sapiens	46-75
33309519-6	2021	The antagonism of platelet P2Y12 receptors by cangrelor, ticagrelor or active metabolites of the thienopyridine compounds ticlopidine, clopidogrel and prasugrel reduces the ADP-induced platelet aggregation in patients with thrombotic complications of vascular diseases.	clopidogrel	135-146	purinergic receptor P2Y12	Homo sapiens	27-32
32970826-1	2021	This review aimed to evaluate the clinical success of clopidogrel dosing based on CYP2C19 genotype and to identify the relevant additional factors that may be useful for consideration by the clinician when dosing individuals with clopidogrel.	clopidogrel	54-65	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	82-89
32970826-4	2021	Drugs that are CYP2C19 or CYP3A4 inhibitors may reduce the effectiveness of clopidogrel and should be carefully considered during co-administration.	clopidogrel	76-87	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
32970826-4	2021	Drugs that are CYP2C19 or CYP3A4 inhibitors may reduce the effectiveness of clopidogrel and should be carefully considered during co-administration.	clopidogrel	76-87	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	26-32
32970826-5	2021	In particular, as stated in the clopidogrel label, concomitant use with strong or moderate CYP2C19 inhibitors such as omeprazole should be avoided.	clopidogrel	32-43	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	91-98
32970826-8	2021	Recent studies have shown clinically significant increases in exposure to CYP2C8 substrates (repaglinide, dasabuvir, desloratidine) and a CYP2B6 substrate (s-sibutramine) following co-administration with clopidogrel, indicating that therapeutic strategies with clopidogrel should avoid these drugs.	clopidogrel	204-215	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	74-80
32970826-8	2021	Recent studies have shown clinically significant increases in exposure to CYP2C8 substrates (repaglinide, dasabuvir, desloratidine) and a CYP2B6 substrate (s-sibutramine) following co-administration with clopidogrel, indicating that therapeutic strategies with clopidogrel should avoid these drugs.	clopidogrel	204-215	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	138-144
32970826-8	2021	Recent studies have shown clinically significant increases in exposure to CYP2C8 substrates (repaglinide, dasabuvir, desloratidine) and a CYP2B6 substrate (s-sibutramine) following co-administration with clopidogrel, indicating that therapeutic strategies with clopidogrel should avoid these drugs.	clopidogrel	261-272	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	74-80
32970826-8	2021	Recent studies have shown clinically significant increases in exposure to CYP2C8 substrates (repaglinide, dasabuvir, desloratidine) and a CYP2B6 substrate (s-sibutramine) following co-administration with clopidogrel, indicating that therapeutic strategies with clopidogrel should avoid these drugs.	clopidogrel	261-272	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	138-144
33242107-0	2021	Implementation and management outcomes of pharmacogenetic CYP2C19 testing for clopidogrel therapy in clinical practice.	clopidogrel	78-89	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	58-65
33242107-1	2021	PURPOSE: The antiplatelet prodrug clopidogrel is bioactivated by the polymorphic enzyme CYP2C19.	clopidogrel	34-45	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	88-95
33242107-2	2021	Prospective clinical studies demonstrated an association between CYP2C19 loss of function (LoF) variants and an increased risk of thrombotic events under clopidogrel, but pharmacogenetic (PGx) testing is not frequently implemented in clinical practice.	clopidogrel	154-165	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	65-72
33242107-6	2021	The association of recurrent ischemic events under clopidogrel with CYP2C19 LoF variants and other factors was explored in a multivariate case-control analysis.	clopidogrel	51-62	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	68-75
33747159-7	2021	Additionally, CGE pretreatment decreased ROS levels and the protein expression levels of cleaved PARP upon H2O2 treatment, indicating that CGE induced cytoprotective effects against H2O2-induced oxidative stress.	clopidogrel	14-17	poly (ADP-ribose) polymerase family, member 1	Mus musculus	97-101
33455562-0	2021	Association between insulin resistance and aspirin or clopidogrel resistance in Chinese patients with recent ischemic stroke/TIA.	clopidogrel	54-65	insulin	Homo sapiens	20-27
33747159-7	2021	Additionally, CGE pretreatment decreased ROS levels and the protein expression levels of cleaved PARP upon H2O2 treatment, indicating that CGE induced cytoprotective effects against H2O2-induced oxidative stress.	clopidogrel	139-142	poly (ADP-ribose) polymerase family, member 1	Mus musculus	97-101
33877270-2	2021	Dual antiplatelet therapy (DAPT), consisting of aspirin and a P2Y12 inhibitor (clopidogrel, ticagrelor, or prasugrel) reduces cardiovascular event rates after ACS.	clopidogrel	79-90	purinergic receptor P2Y12	Homo sapiens	62-67
33993103-6	2021	To verify our method, we detected ADEs with alanine aminotransferase (ALT) elevation in patients receiving aspirin, clopidogrel and ticlopidine.	clopidogrel	116-127	glutamic--pyruvic transaminase	Homo sapiens	44-68
33877270-10	2021	The newest P2Y12 inhibitors, prasugrel and ticagrelor, are more potent, with high on-treatment residual platelet reactivity of about 3% vs 30% to 40% with clopidogrel and act within 30 minutes compared with 2 hours for clopidogrel.	clopidogrel	155-166	purinergic receptor P2Y12	Homo sapiens	11-16
33744207-11	2021	Ticagrelor and prasugrel compared with clopidogrel resulted in a significant reduction in ischemic events (relative risk: 0.70; 95% confidence interval: 0.59 to 0.83) in CYP2C19 loss-of-function carriers but not in noncarriers (relative risk: 1.0; 95% confidence interval: 0.80 to 1.25).	clopidogrel	39-50	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	170-177
33877270-10	2021	The newest P2Y12 inhibitors, prasugrel and ticagrelor, are more potent, with high on-treatment residual platelet reactivity of about 3% vs 30% to 40% with clopidogrel and act within 30 minutes compared with 2 hours for clopidogrel.	clopidogrel	219-230	purinergic receptor P2Y12	Homo sapiens	11-16
33917717-6	2021	We performed a multicenter prospective observational study and assessed PRI by vasodilator-stimulated phosphoprotein (VASP) index following a loading dose of clopidogrel.	clopidogrel	158-169	vasodilator stimulated phosphoprotein	Homo sapiens	79-116
33917717-6	2021	We performed a multicenter prospective observational study and assessed PRI by vasodilator-stimulated phosphoprotein (VASP) index following a loading dose of clopidogrel.	clopidogrel	158-169	vasodilator stimulated phosphoprotein	Homo sapiens	118-122
32997809-2	2021	Similarly as gemfibrozil, the CYP2C8 inhibitor clopidogrel also increases clopidogrel increased ACT-333679 concentration by 1.9-fold after a single loading dose (300 mg once daily) and 2.7-fold after repeated treatment with the maintenance dose (75 mg once daily) in Europeans.	clopidogrel	47-58	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	30-36
32997809-2	2021	Similarly as gemfibrozil, the CYP2C8 inhibitor clopidogrel also increases clopidogrel increased ACT-333679 concentration by 1.9-fold after a single loading dose (300 mg once daily) and 2.7-fold after repeated treatment with the maintenance dose (75 mg once daily) in Europeans.	clopidogrel	74-85	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	30-36
33531438-7	2021	Clopidogrel ever use was associated with a higher breast cancer risk [HR= 1.30 (1.02-1.68)], restricted to estrogen receptor negative (ER-) tumors [HRER+= 1.14 (0.83-1.57), HRER-= 3.07 (1.64-5.76), Phomogeneity= 0.01].	clopidogrel	0-11	estrogen receptor 1	Homo sapiens	107-124
33531438-7	2021	Clopidogrel ever use was associated with a higher breast cancer risk [HR= 1.30 (1.02-1.68)], restricted to estrogen receptor negative (ER-) tumors [HRER+= 1.14 (0.83-1.57), HRER-= 3.07 (1.64-5.76), Phomogeneity= 0.01].	clopidogrel	0-11	epiregulin	Homo sapiens	135-137
33531438-8	2021	Conclusions Low-dose aspirin was associated with a lower breast cancer risk only after several years of use, while ever use of clopidogrel was associated with a higher ER- breast cancer risk.	clopidogrel	127-138	epiregulin	Homo sapiens	168-170
33722066-0	2021	Clopidogrel Versus Ticagrelor or Prasugrel After Primary Percutaneous Coronary Intervention According to CYP2C19 Genotype: A POPular Genetics Subanalysis.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	105-112
33722066-6	2021	The first assessed the effect of the CYP2C19*17 allele in clopidogrel-treated patients.	clopidogrel	58-69	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-44
33113567-10	2021	The number of CD34+/CD133+/CD45low cells increased in the clopidogrel group (P = 0.008), but not in the prasugrel group.	clopidogrel	58-69	CD34 molecule	Homo sapiens	14-18
33113567-10	2021	The number of CD34+/CD133+/CD45low cells increased in the clopidogrel group (P = 0.008), but not in the prasugrel group.	clopidogrel	58-69	prominin 1	Homo sapiens	20-25
33113567-10	2021	The number of CD34+/CD133+/CD45low cells increased in the clopidogrel group (P = 0.008), but not in the prasugrel group.	clopidogrel	58-69	protein tyrosine phosphatase receptor type C	Homo sapiens	27-31
33067076-12	2021	CONCLUSION: In ACS patients treated with clopidogrel following PCI, high CHADS2 and CHA2DS2-VASc scores correlated with HPR and lower scores correlated with OPR.	clopidogrel	41-52	haptoglobin-related protein	Homo sapiens	120-123
33501709-0	2021	Associations of PER3 polymorphisms with clopidogrel resistance among Chinese Han people treated with clopidogrel.	clopidogrel	40-51	period circadian regulator 3	Homo sapiens	16-20
33501709-0	2021	Associations of PER3 polymorphisms with clopidogrel resistance among Chinese Han people treated with clopidogrel.	clopidogrel	101-112	period circadian regulator 3	Homo sapiens	16-20
33501709-3	2021	Our goal was to evaluate the possible association between the PER3 rs228729 (T/C) polymorphism or PER3 rs2797685(T/C) polymorphism and clopidogrel resistance (CR) and to study the impact of clinical baseline data on clopidogrel resistance.	clopidogrel	135-146	period circadian regulator 3	Homo sapiens	98-102
33501709-8	2021	In patients with albumin values greater than 40 or PCT greater than 0.19, those with the rs228729 TT + TC genotype had an increased risk of clopidogrel resistance compared with those with the CC genotype (albumin>=40, TT+TC:CC, p = 0.01, albumin p = 0.005; PCT >= 0.19, TT+TC:CC, p < 0.001, PCT p = 0.004).	clopidogrel	140-151	albumin	Homo sapiens	17-24
33501709-8	2021	In patients with albumin values greater than 40 or PCT greater than 0.19, those with the rs228729 TT + TC genotype had an increased risk of clopidogrel resistance compared with those with the CC genotype (albumin>=40, TT+TC:CC, p = 0.01, albumin p = 0.005; PCT >= 0.19, TT+TC:CC, p < 0.001, PCT p = 0.004).	clopidogrel	140-151	albumin	Homo sapiens	205-212
33501709-8	2021	In patients with albumin values greater than 40 or PCT greater than 0.19, those with the rs228729 TT + TC genotype had an increased risk of clopidogrel resistance compared with those with the CC genotype (albumin>=40, TT+TC:CC, p = 0.01, albumin p = 0.005; PCT >= 0.19, TT+TC:CC, p < 0.001, PCT p = 0.004).	clopidogrel	140-151	albumin	Homo sapiens	205-212
33501709-9	2021	Logistic regression analysis of clinical baseline data and genotype showed that high albumin is a protective factor against clopidogrel resistance.	clopidogrel	124-135	albumin	Homo sapiens	85-92
33270185-5	2021	METHODS: The effect of CYP2C19, CYP3A4/5, ABCB1 and PON1 genes on the plasma inactive metabolite concentration of clopidogrel and the platelet aggregation was investigated in 155 patients before and after PCI.	clopidogrel	114-125	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	23-30
33270185-5	2021	METHODS: The effect of CYP2C19, CYP3A4/5, ABCB1 and PON1 genes on the plasma inactive metabolite concentration of clopidogrel and the platelet aggregation was investigated in 155 patients before and after PCI.	clopidogrel	114-125	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	32-40
33270185-5	2021	METHODS: The effect of CYP2C19, CYP3A4/5, ABCB1 and PON1 genes on the plasma inactive metabolite concentration of clopidogrel and the platelet aggregation was investigated in 155 patients before and after PCI.	clopidogrel	114-125	ATP binding cassette subfamily B member 1	Homo sapiens	42-47
33270185-5	2021	METHODS: The effect of CYP2C19, CYP3A4/5, ABCB1 and PON1 genes on the plasma inactive metabolite concentration of clopidogrel and the platelet aggregation was investigated in 155 patients before and after PCI.	clopidogrel	114-125	paraoxonase 1	Homo sapiens	52-56
33270185-7	2021	The presence of the A allele at position 2677 in the ABCB1 gene was associated with a significantly lower concentration of inactive metabolite of clopidogrel before PCI.	clopidogrel	146-157	ATP binding cassette subfamily B member 1	Homo sapiens	53-58
33270185-8	2021	CONCLUSION: The CYP2C19*2 allele was associated with decreased platelet reactivity during clopidogrel therapy before and after PCI.	clopidogrel	90-101	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
33641235-0	2021	Increase in the risk of clopidogrel resistance and consequent TIMI flow impairment by DNA hypomethylation of CYP2C19 gene in STEMI patients undergoing primary percutaneous coronary intervention (PPCI).	clopidogrel	24-35	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	109-116
33641235-2	2021	This study aims to investigate the role of CYP2C19 gene DNA methylation as one of the epigenetic factors for the risk of clopidogrel resistance in STEMI patients undergoing PPCI.	clopidogrel	121-132	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	43-50
33641235-11	2021	The lower DNA methylation level of the CYP2C19 gene increases the risk of clopidogrel resistance and subsequent poorer clinical outcome.	clopidogrel	74-85	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	39-46
33758008-9	2021	Among patients receiving clopidogrel, P2Y12 inhibitor monotherapy compared with DAPT showed consistent treatment effects across various subgroups for the primary endpoint.	clopidogrel	25-36	purinergic receptor P2Y12	Homo sapiens	38-43
33727661-1	2021	We investigated the effect of CYP2C19 polymorphisms on the clinical outcomes of clopidogrel therapy in patients after stenting procedure for cerebral artery stenosis in northeast China.	clopidogrel	80-91	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
33727661-8	2021	Our study verifies that CYP2C19 *2 and *3 have significant impact on the clinical outcomes of clopidogrel therapy in patients with stenting procedure for cerebral artery stenosis in China.	clopidogrel	94-105	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
33690885-0	2021	The Case for Expanding the FDA Box Warning on Clopidogrel to CYP2C19 Intermediate Metabolizers.	clopidogrel	46-57	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	61-68
33674394-3	2021	The purpose of the present study was to investigate the efficacy and feasibility of clopidogrel dose adjustment for active target P2Y12 reaction unit (PRU).	clopidogrel	84-95	purinergic receptor P2Y12	Homo sapiens	130-135
32895853-8	2021	Potent oral P2Y12 inhibitors were associated with a significant increase in major or clinically relevant non-major bleeding compared with clopidogrel (risk ratio [RR] 1.30, 95% confidence interval [CI] 1.06-1.59, p = 0.01; number needed to harm 18, 95% CI 12-36).	clopidogrel	138-149	purinergic receptor P2Y12	Homo sapiens	12-17
33089397-0	2021	Association of FMO3 rs1736557 polymorphism with clopidogrel response in Chinese patients with coronary artery disease.	clopidogrel	48-59	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	15-19
33089397-5	2021	This study aimed to explore the association between FMO3 rs1736557 polymorphism and clopidogrel response.	clopidogrel	84-95	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	52-56
33089397-12	2021	CONCLUSION: The FMO3 rs1736557 AA genotype was related to an increased the antiplatelet potency of clopidogrel in Chinese CAD patients.	clopidogrel	99-110	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	16-20
33279389-4	2021	Indeed, pharmacodynamic and pharmacokinetic studies suggested an interaction through hepatic CYP2C19 between PPIs and clopidogrel, which could translate into clinical inefficacy, leading to higher rates of cardiovascular events.	clopidogrel	118-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	93-100
33658839-0	2021	A Study on the Correlation Between MDR1 Polymorphism and Clopidogrel Resistance in Hui Patients Treated with Percutaneous Coronary Intervention.	clopidogrel	57-68	ATP binding cassette subfamily B member 1	Homo sapiens	35-39
33744207-1	2021	OBJECTIVES: The aim of this study was to examine the effect of CYP2C19 genotype on clinical outcomes in patients with coronary artery disease (CAD) who predominantly underwent percutaneous coronary intervention (PCI), comparing those treated with ticagrelor or prasugrel versus clopidogrel.	clopidogrel	278-289	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	63-70
33360254-8	2021	In patients with stroke or TIA, clopidogrel inhibited ADP-induced platelet aggregation at all concentrations, and significantly inhibited PAR4-AP-induced platelet aggregation at 50 micromol/L of PAR4-AP (p<0.05), especially in 5 patients who showed high reactivity to PAR4-AP.	clopidogrel	32-43	Prader Willi/Angelman region RNA 4	Homo sapiens	138-142
33360254-8	2021	In patients with stroke or TIA, clopidogrel inhibited ADP-induced platelet aggregation at all concentrations, and significantly inhibited PAR4-AP-induced platelet aggregation at 50 micromol/L of PAR4-AP (p<0.05), especially in 5 patients who showed high reactivity to PAR4-AP.	clopidogrel	32-43	Prader Willi/Angelman region RNA 4	Homo sapiens	195-199
33360254-8	2021	In patients with stroke or TIA, clopidogrel inhibited ADP-induced platelet aggregation at all concentrations, and significantly inhibited PAR4-AP-induced platelet aggregation at 50 micromol/L of PAR4-AP (p<0.05), especially in 5 patients who showed high reactivity to PAR4-AP.	clopidogrel	32-43	Prader Willi/Angelman region RNA 4	Homo sapiens	195-199
33360254-10	2021	CONCLUSIONS: We showed significant inhibitory effects on PAR4-AP-induced platelet aggregation by clopidogrel in patients with stroke or TIA who had high reactivity to PAR4-AP.	clopidogrel	97-108	Prader Willi/Angelman region RNA 4	Homo sapiens	57-61
33360254-10	2021	CONCLUSIONS: We showed significant inhibitory effects on PAR4-AP-induced platelet aggregation by clopidogrel in patients with stroke or TIA who had high reactivity to PAR4-AP.	clopidogrel	97-108	Prader Willi/Angelman region RNA 4	Homo sapiens	167-171
33152483-0	2021	The impact of clopidogrel on plasma-soluble CD40 ligand levels in systemic lupus erythematosus patients: the CLOPUS phase I/II pilot study.	clopidogrel	14-25	CD40 molecule	Homo sapiens	44-48
32973115-0	2021	Remote platelet function testing using P-selectin expression in patients with recent cerebral ischaemia on clopidogrel.	clopidogrel	107-118	selectin P	Homo sapiens	39-49
32973115-14	2021	Thirteen (20.6%) patients had a recurrent cerebrovascular event; those with an ischaemic stroke had a non-significantly higher baseline P-selectin using the clopidogrel test as compared with those with no recurrence: 626 [380, 801] versus 406 [265, 609], p=0.08.	clopidogrel	157-168	selectin P	Homo sapiens	136-146
33658839-1	2021	Objective: This study assesses the correlation between MDR1 gene polymorphism and clopidogrel resistance (CR) in Hui patients with coronary heart disease (CHD) who were treated with percutaneous coronary intervention (PCI).	clopidogrel	82-93	ATP binding cassette subfamily B member 1	Homo sapiens	55-59
33611730-0	2022	CYP2C19 Loss-of-Function Associated with First-Time Ischemic Stroke in Non-surgical Asymptomatic Carotid Artery Stenosis During Clopidogrel Therapy.	clopidogrel	128-139	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
33611730-1	2022	This study measures effect of CYP2C19 genotype on ischemic stroke risk during clopidogrel therapy for asymptomatic, extracranial carotid stenosis patients.	clopidogrel	78-89	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
33611730-12	2022	For asymptomatic carotid stenosis patients receiving clopidogrel to prevent ischemic stroke, CYP2C19 loss-of-function allele is associated with 2- to 10-fold increased risk of ischemic stroke.	clopidogrel	53-64	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	93-100
33626394-0	2021	Short-term standard alcohol consumption enhances platelet response to clopidogrel through inhibition of Nrf2/Ces1 pathway and induction of Cyp2c in mice.	clopidogrel	70-81	nuclear factor, erythroid derived 2, like 2	Mus musculus	104-108
33626394-0	2021	Short-term standard alcohol consumption enhances platelet response to clopidogrel through inhibition of Nrf2/Ces1 pathway and induction of Cyp2c in mice.	clopidogrel	70-81	carboxylesterase 1G	Mus musculus	109-113
33626394-5	2021	KEY FINDINGS: Compared with vehicle control, alcohol pretreatment significantly reduced hydrolysis of clopidogrel as a result of significant down-regulation of Nrf2-mediated Ces1 expression (responsible for the formation of clopidogrel carboxylate), increased metabolic activation of clopidogrel due to significant up-regulation of Cyp2c (for the formation of active thiol metabolite H4), and consequently enhanced inhibition of ADP-induced platelet aggregation and activation by clopidogrel.	clopidogrel	224-235	nuclear factor, erythroid derived 2, like 2	Mus musculus	160-164
33626394-5	2021	KEY FINDINGS: Compared with vehicle control, alcohol pretreatment significantly reduced hydrolysis of clopidogrel as a result of significant down-regulation of Nrf2-mediated Ces1 expression (responsible for the formation of clopidogrel carboxylate), increased metabolic activation of clopidogrel due to significant up-regulation of Cyp2c (for the formation of active thiol metabolite H4), and consequently enhanced inhibition of ADP-induced platelet aggregation and activation by clopidogrel.	clopidogrel	224-235	carboxylesterase 1G	Mus musculus	174-178
33626394-5	2021	KEY FINDINGS: Compared with vehicle control, alcohol pretreatment significantly reduced hydrolysis of clopidogrel as a result of significant down-regulation of Nrf2-mediated Ces1 expression (responsible for the formation of clopidogrel carboxylate), increased metabolic activation of clopidogrel due to significant up-regulation of Cyp2c (for the formation of active thiol metabolite H4), and consequently enhanced inhibition of ADP-induced platelet aggregation and activation by clopidogrel.	clopidogrel	224-235	nuclear factor, erythroid derived 2, like 2	Mus musculus	160-164
33626394-5	2021	KEY FINDINGS: Compared with vehicle control, alcohol pretreatment significantly reduced hydrolysis of clopidogrel as a result of significant down-regulation of Nrf2-mediated Ces1 expression (responsible for the formation of clopidogrel carboxylate), increased metabolic activation of clopidogrel due to significant up-regulation of Cyp2c (for the formation of active thiol metabolite H4), and consequently enhanced inhibition of ADP-induced platelet aggregation and activation by clopidogrel.	clopidogrel	224-235	carboxylesterase 1G	Mus musculus	174-178
33626394-6	2021	SIGNIFICANCE: Short-term standard alcohol consumption would significantly enhance suppression of ADP-induced platelet aggregation and activation by clopidogrel through significant inhibition of Nrf2/Ces1 signaling pathway and induction of Cyp2c, suggesting that alcohol may interact with drugs that are predominantly metabolized by CES1 or CYP2C in patient care, including clopidogrel.	clopidogrel	148-159	NFE2 like bZIP transcription factor 2	Homo sapiens	194-198
33626394-6	2021	SIGNIFICANCE: Short-term standard alcohol consumption would significantly enhance suppression of ADP-induced platelet aggregation and activation by clopidogrel through significant inhibition of Nrf2/Ces1 signaling pathway and induction of Cyp2c, suggesting that alcohol may interact with drugs that are predominantly metabolized by CES1 or CYP2C in patient care, including clopidogrel.	clopidogrel	148-159	carboxylesterase 1	Homo sapiens	199-203
33626394-6	2021	SIGNIFICANCE: Short-term standard alcohol consumption would significantly enhance suppression of ADP-induced platelet aggregation and activation by clopidogrel through significant inhibition of Nrf2/Ces1 signaling pathway and induction of Cyp2c, suggesting that alcohol may interact with drugs that are predominantly metabolized by CES1 or CYP2C in patient care, including clopidogrel.	clopidogrel	148-159	carboxylesterase 1	Homo sapiens	332-336
33626394-6	2021	SIGNIFICANCE: Short-term standard alcohol consumption would significantly enhance suppression of ADP-induced platelet aggregation and activation by clopidogrel through significant inhibition of Nrf2/Ces1 signaling pathway and induction of Cyp2c, suggesting that alcohol may interact with drugs that are predominantly metabolized by CES1 or CYP2C in patient care, including clopidogrel.	clopidogrel	148-159	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	340-345
33578832-0	2021	Use of Clopidogrel and Proton Pump Inhibitors Alone or in Combinations in Persons with Diabetes in Denmark; Potential for CYP2C19 Genotype-Guided Drug Therapy.	clopidogrel	7-18	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	122-129
33580476-0	2021	Correction to: Influence of CYP2C19 genotypes for the effect of 1-month dual antiplatelet therapy followed by clopidogrel monotherapy relative to 12-month dual antiplatelet therapy on clinical outcomes after percutaneous coronary intervention: a genetic substudy from the STOPDAPT-2.	clopidogrel	110-121	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
33578542-0	2021	Correlation study of CYP2C19 gene polymorphism and clopidogrel resistance in Han Chinese patients with cerebral infarction in Guizhou region.	clopidogrel	51-62	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
33578542-1	2021	ABSTRACT: This study conducts a correlation exploration of CYP2C19 gene polymorphism and clopidogrel resistance in Han Chinese patients with cerebral infarction in Guizhou Region.A total of 270 Han Chinese patients with cerebral infarction, who were hospitalized in our hospital from January 2016 to January 2018, are selected.	clopidogrel	89-100	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	59-66
33578542-5	2021	The Logisitic regression analysis revealed that the history of diabetes, history of high blood pressure, increase in low density lipoprotein and CYP2C19 mutant gene were independent risk factors of clopidogrel resistance.	clopidogrel	198-209	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	145-152
33578542-6	2021	After treatment, the serum IL-6 level of patients in the resistance group was 17.21 +- 0.98 ng/L, which was significant higher than that of patients in the sensitive group (11.21 +- 0.68 ng/L), and the difference was statistically significant (P < .05).Patients with cerebral infarction in Guizhou region have a higher occurrence rate of clopidogrel resistance.	clopidogrel	338-349	interleukin 6	Homo sapiens	27-31
33578542-7	2021	Clopidogrel resistance not only will weaken the anti-inflammatory action of the drug, but also correlates with the patient"s CYP2C19 mutant gene and blood lipid level.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	125-132
33555916-8	2021	Dual antiplatelet therapy with aspirin and a P2Y12 inhibitor should be given to all patients during the peri-PCI period (during inpatient stay, until time of discharge, up to 1 week after PCI, at the discretion of the treating physician), after which the default strategy is to stop aspirin and continue treatment with a P2Y12 inhibitor, preferably clopidogrel, in combination with a non-vitamin K antagonist oral anticoagulant (ie, double therapy).	clopidogrel	349-360	purinergic receptor P2Y12	Homo sapiens	45-50
33222458-0	2021	Xuesaitong injection (lyophilized) combined with aspirin and clopidogrel protect against focal cerebral ischemic/reperfusion injury in rats by suppressing oxidative stress and inflammation and regulating the NOX2/IL-6/STAT3 pathway.	clopidogrel	61-72	cytochrome b-245 beta chain	Rattus norvegicus	208-212
33222458-0	2021	Xuesaitong injection (lyophilized) combined with aspirin and clopidogrel protect against focal cerebral ischemic/reperfusion injury in rats by suppressing oxidative stress and inflammation and regulating the NOX2/IL-6/STAT3 pathway.	clopidogrel	61-72	interleukin 6	Rattus norvegicus	213-217
33222458-0	2021	Xuesaitong injection (lyophilized) combined with aspirin and clopidogrel protect against focal cerebral ischemic/reperfusion injury in rats by suppressing oxidative stress and inflammation and regulating the NOX2/IL-6/STAT3 pathway.	clopidogrel	61-72	signal transducer and activator of transcription 3	Rattus norvegicus	218-223
33523336-0	2021	Association of CYP2C19 Loss-of-Function Alleles with Major Adverse Cardiovascular Events of Clopidogrel in Stable Coronary Artery Disease Patients Undergoing Percutaneous Coronary Intervention: Meta-analysis.	clopidogrel	92-103	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
33523336-1	2021	PURPOSE: It was aimed to determine the aggregated risk of MACE (major adverse cardiovascular events) in stable CAD patients carrying CYP2C19 LoF alleles taking clopidogrel.	clopidogrel	160-171	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	133-140
32640858-9	2021	The response to Clopidogrel was between 100 and 239 P2Y12 reaction units (VerifyNow) in 13 patients (45%).	clopidogrel	16-27	purinergic receptor P2Y12	Homo sapiens	52-57
33414804-0	2020	Cyp2C19*2 Polymorphism Related to Clopidogrel Resistance in Patients With Coronary Heart Disease, Especially in the Asian Population: A Systematic Review and Meta-Analysis.	clopidogrel	34-45	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
33246208-2	2021	CYP2C19 gene loss-of-function (up to 45% of patients) causes clopidogrel resistance.	clopidogrel	61-72	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
33246208-3	2021	For patients with asymptomatic ICAD and ICAD characterized by transient ischemic attack (TIA), this study measures the effect of CYP2C19 loss-of-function on ischemic stroke risk during clopidogrel therapy.	clopidogrel	185-196	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	129-136
33246208-15	2021	CONCLUSIONS: CYP2C19 loss-of-function was associated with 3-fold increased risk of first-time ischemic stroke for ICAD patients treated with clopidogrel after TIA.	clopidogrel	141-152	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
33968469-9	2021	Respondents favoring CAS more often chose >=2 agents (adjusted odds ratio [aOR] vs CEA: 2.00, 95% confidence interval 1.36-2.95, p = 0.001) or clopidogrel-containing regimens (aOR: 1.77, 1.16-2.70, p = 0.008).	clopidogrel	143-154	BCAR1 scaffold protein, Cas family member	Homo sapiens	21-24
33208005-0	2021	The mechanism of miR-363-3p/DUSP10 signaling pathway involved in the gastric mucosal injury induced by clopidogrel.	clopidogrel	103-114	dual specificity phosphatase 10	Homo sapiens	28-34
33208005-16	2021	DUSP10 inhibited apoptosis in GES-1 cells treated by clopidogrel.	clopidogrel	53-64	dual specificity phosphatase 10	Homo sapiens	0-6
33208005-18	2021	Knockdown of miR-363-3p increased the proliferation and reduced the apoptosis by targeting DUSP10 in GES-1 cells treated by clopidogrel, indicating that miR-363-3p may be a potential therapeutic target for gastric mucosal injury caused by clopidogrel.	clopidogrel	124-135	dual specificity phosphatase 10	Homo sapiens	91-97
33208005-18	2021	Knockdown of miR-363-3p increased the proliferation and reduced the apoptosis by targeting DUSP10 in GES-1 cells treated by clopidogrel, indicating that miR-363-3p may be a potential therapeutic target for gastric mucosal injury caused by clopidogrel.	clopidogrel	239-250	dual specificity phosphatase 10	Homo sapiens	91-97
33455983-5	2021	Genetic testing found that both cytochrome P450 2C19 (CYP2C19) (G681A) and glycoprotein Ia (GPIa) (C807T, G873A) were hybrid mutant types, demonstrating that the patient was possibly resistant to clopidogrel and aspirin simultaneously.	clopidogrel	196-207	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-52
33455983-5	2021	Genetic testing found that both cytochrome P450 2C19 (CYP2C19) (G681A) and glycoprotein Ia (GPIa) (C807T, G873A) were hybrid mutant types, demonstrating that the patient was possibly resistant to clopidogrel and aspirin simultaneously.	clopidogrel	196-207	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	54-61
33455983-5	2021	Genetic testing found that both cytochrome P450 2C19 (CYP2C19) (G681A) and glycoprotein Ia (GPIa) (C807T, G873A) were hybrid mutant types, demonstrating that the patient was possibly resistant to clopidogrel and aspirin simultaneously.	clopidogrel	196-207	multimerin 1	Homo sapiens	75-90
33455983-5	2021	Genetic testing found that both cytochrome P450 2C19 (CYP2C19) (G681A) and glycoprotein Ia (GPIa) (C807T, G873A) were hybrid mutant types, demonstrating that the patient was possibly resistant to clopidogrel and aspirin simultaneously.	clopidogrel	196-207	multimerin 1	Homo sapiens	92-96
33512659-0	2021	Pretreatment of Indobufen and Aspirin and their Combinations with Clopidogrel or Ticagrelor Alleviates Inflammasome Mediated Pyroptosis Via Inhibiting NF-kappaB/NLRP3 Pathway in Ischemic Stroke.	clopidogrel	66-77	NLR family, pyrin domain containing 3	Rattus norvegicus	161-166
33512659-2	2021	In this study, we investigated the protective efficiency of pretreatment of indobufen or aspirin combined with clopidogrel or ticagrelor (IACT) on cerebral ischemic injury via NF-kappaB/NLRP3 pathway.	clopidogrel	111-122	NLR family, pyrin domain containing 3	Rattus norvegicus	186-191
33551797-1	2020	Background: CYP2C19 loss-of-function (LOF) alleles reduce the effectiveness of clopidogrel in patients undergoing percutaneous coronary intervention for acute coronary syndrome.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
33162063-3	2021	We explored the risk of PH associated with standard antiplatelet therapy (sAP: acetylsalicylic acid, and/or clopidogrel) in the context of aneurysmal subarachnoid hemorrhage (aSAH).	clopidogrel	108-119	phenylalanine hydroxylase	Homo sapiens	24-26
33300437-12	2022	By taking a double dose of clopidogrel, patients with a CYP2C19 LOF allele can therefore overcome the reduced efficacy of clopidogrel associated with LOF alleles without increasing the risk of bleeding, which is of guiding significance for the management of antiplatelet therapy on ACS patients after PCI especially considering the CYP2C19 LOF alleles that carry an important predictor for the ischemic events.	clopidogrel	27-38	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	56-63
33300437-12	2022	By taking a double dose of clopidogrel, patients with a CYP2C19 LOF allele can therefore overcome the reduced efficacy of clopidogrel associated with LOF alleles without increasing the risk of bleeding, which is of guiding significance for the management of antiplatelet therapy on ACS patients after PCI especially considering the CYP2C19 LOF alleles that carry an important predictor for the ischemic events.	clopidogrel	27-38	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	332-339
33300437-12	2022	By taking a double dose of clopidogrel, patients with a CYP2C19 LOF allele can therefore overcome the reduced efficacy of clopidogrel associated with LOF alleles without increasing the risk of bleeding, which is of guiding significance for the management of antiplatelet therapy on ACS patients after PCI especially considering the CYP2C19 LOF alleles that carry an important predictor for the ischemic events.	clopidogrel	122-133	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	56-63
33300437-12	2022	By taking a double dose of clopidogrel, patients with a CYP2C19 LOF allele can therefore overcome the reduced efficacy of clopidogrel associated with LOF alleles without increasing the risk of bleeding, which is of guiding significance for the management of antiplatelet therapy on ACS patients after PCI especially considering the CYP2C19 LOF alleles that carry an important predictor for the ischemic events.	clopidogrel	122-133	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	332-339
33429485-0	2021	[Prevalence of CYP2C19 gene mutations in patients with coronary heart disease and its biological activation effect in clopidogrel antiplatelet response].	clopidogrel	118-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
33429485-1	2021	Objective: The purpose of this study was to investigate the effects of CYP2C19 gene mutations on clopidogrel antiplatelet activity in the patients with coronary heart disease treated by percutaneous coronary intervention.	clopidogrel	97-108	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
33429485-16	2021	In vitro functional studies show that CYP2C19 gene mutation M136K, as a gain-of-function gene mutation, can enhance the activation of CYP2C19 enzyme on clopidogrel, thereby inhibiting the platelet aggregation rate.	clopidogrel	152-163	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	38-45
33429485-16	2021	In vitro functional studies show that CYP2C19 gene mutation M136K, as a gain-of-function gene mutation, can enhance the activation of CYP2C19 enzyme on clopidogrel, thereby inhibiting the platelet aggregation rate.	clopidogrel	152-163	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	134-141
33412611-0	2021	Insights from In Vitro and Clinical Data to Guide Transition from the Novel P2Y12 Antagonist Selatogrel to Clopidogrel, Prasugrel, and Ticagrelor.	clopidogrel	107-118	purinergic receptor P2Y12	Homo sapiens	76-81
33413066-2	2021	Nearly 10 % of absorbed clopidogrel is metabolized by cytochrome P450 (CYP) enzymes in the liver to active forms and 90 % to inactive clopidogrel carboxylate by esterases.	clopidogrel	24-35	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	54-69
33413066-2	2021	Nearly 10 % of absorbed clopidogrel is metabolized by cytochrome P450 (CYP) enzymes in the liver to active forms and 90 % to inactive clopidogrel carboxylate by esterases.	clopidogrel	24-35	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	71-74
33093222-1	2021	OBJECTIVE: To investigate the association between protease-activated receptor-1 (PAR-1) gene F2R polymorphisms and efficacy of clopidogrel for minor stroke or TIA.	clopidogrel	127-138	coagulation factor II thrombin receptor	Homo sapiens	50-79
33093222-1	2021	OBJECTIVE: To investigate the association between protease-activated receptor-1 (PAR-1) gene F2R polymorphisms and efficacy of clopidogrel for minor stroke or TIA.	clopidogrel	127-138	coagulation factor II thrombin receptor	Homo sapiens	81-86
33093222-1	2021	OBJECTIVE: To investigate the association between protease-activated receptor-1 (PAR-1) gene F2R polymorphisms and efficacy of clopidogrel for minor stroke or TIA.	clopidogrel	127-138	coagulation factor II thrombin receptor	Homo sapiens	93-96
33093222-6	2021	The association between F2R IVSn-14 A/T polymorphism and clopidogrel response was present regardless of the carrier status of the CYP2C19 loss-of-function alleles.	clopidogrel	57-68	coagulation factor II thrombin receptor	Homo sapiens	24-27
33093222-8	2021	CONCLUSIONS: Among patients with minor ischemic stroke or TIA who were receiving clopidogrel and aspirin, those carrying the F2R IVSn-14 T allele had a lower rate of recurrent stroke than those who were not.	clopidogrel	81-92	coagulation factor II thrombin receptor	Homo sapiens	125-128
33137324-0	2021	P-glycoprotein deficiency enhances metabolic activation of and platelet response to clopidogrel through marked up-regulation of Cyp3a11 in mice: direct evidence for the interplay between P-glycoprotein and Cyp3a.	clopidogrel	84-95	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	128-135
33137324-0	2021	P-glycoprotein deficiency enhances metabolic activation of and platelet response to clopidogrel through marked up-regulation of Cyp3a11 in mice: direct evidence for the interplay between P-glycoprotein and Cyp3a.	clopidogrel	84-95	phosphoglycolate phosphatase	Mus musculus	0-14
33137324-1	2021	Variability in P-glycoprotein (P-gp) efflux transporting activity was supposed to be involved in altered intestinal absorption and bioavailability of clopidogrel in patients; however, reliable evidence is still lacking.	clopidogrel	150-161	ATP binding cassette subfamily B member 1	Homo sapiens	15-29
33137324-1	2021	Variability in P-glycoprotein (P-gp) efflux transporting activity was supposed to be involved in altered intestinal absorption and bioavailability of clopidogrel in patients; however, reliable evidence is still lacking.	clopidogrel	150-161	ATP binding cassette subfamily B member 1	Homo sapiens	31-35
33137324-2	2021	In this study, we sought to determine whether P-gp could play an important role in the metabolic activation of and platelet response to clopidogrel in mice.	clopidogrel	136-147	phosphoglycolate phosphatase	Mus musculus	46-50
33137324-7	2021	We conclude that although P-gp does not transport clopidogrel and its major metabolites in mice, P-gp-deficient mice exhibit elevated formation of the active metabolite H4 and enhanced antiplatelet effect of clopidogrel through up-regulation of Cyp3a11 and down-regulation of Ces1, suggesting that P-gp activity may correlate inversely with the formation of H4 and antiplatelet efficacy of clopidogrel in clinical settings due to P-gp and CYP3A4 interplay.	clopidogrel	208-219	phosphoglycolate phosphatase	Mus musculus	97-101
33137324-7	2021	We conclude that although P-gp does not transport clopidogrel and its major metabolites in mice, P-gp-deficient mice exhibit elevated formation of the active metabolite H4 and enhanced antiplatelet effect of clopidogrel through up-regulation of Cyp3a11 and down-regulation of Ces1, suggesting that P-gp activity may correlate inversely with the formation of H4 and antiplatelet efficacy of clopidogrel in clinical settings due to P-gp and CYP3A4 interplay.	clopidogrel	208-219	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	245-252
33137324-7	2021	We conclude that although P-gp does not transport clopidogrel and its major metabolites in mice, P-gp-deficient mice exhibit elevated formation of the active metabolite H4 and enhanced antiplatelet effect of clopidogrel through up-regulation of Cyp3a11 and down-regulation of Ces1, suggesting that P-gp activity may correlate inversely with the formation of H4 and antiplatelet efficacy of clopidogrel in clinical settings due to P-gp and CYP3A4 interplay.	clopidogrel	208-219	carboxylesterase 1G	Mus musculus	276-280
33137324-7	2021	We conclude that although P-gp does not transport clopidogrel and its major metabolites in mice, P-gp-deficient mice exhibit elevated formation of the active metabolite H4 and enhanced antiplatelet effect of clopidogrel through up-regulation of Cyp3a11 and down-regulation of Ces1, suggesting that P-gp activity may correlate inversely with the formation of H4 and antiplatelet efficacy of clopidogrel in clinical settings due to P-gp and CYP3A4 interplay.	clopidogrel	208-219	phosphoglycolate phosphatase	Mus musculus	97-101
33137324-7	2021	We conclude that although P-gp does not transport clopidogrel and its major metabolites in mice, P-gp-deficient mice exhibit elevated formation of the active metabolite H4 and enhanced antiplatelet effect of clopidogrel through up-regulation of Cyp3a11 and down-regulation of Ces1, suggesting that P-gp activity may correlate inversely with the formation of H4 and antiplatelet efficacy of clopidogrel in clinical settings due to P-gp and CYP3A4 interplay.	clopidogrel	208-219	phosphoglycolate phosphatase	Mus musculus	97-101
33137324-7	2021	We conclude that although P-gp does not transport clopidogrel and its major metabolites in mice, P-gp-deficient mice exhibit elevated formation of the active metabolite H4 and enhanced antiplatelet effect of clopidogrel through up-regulation of Cyp3a11 and down-regulation of Ces1, suggesting that P-gp activity may correlate inversely with the formation of H4 and antiplatelet efficacy of clopidogrel in clinical settings due to P-gp and CYP3A4 interplay.	clopidogrel	208-219	phosphoglycolate phosphatase	Mus musculus	97-101
33137324-7	2021	We conclude that although P-gp does not transport clopidogrel and its major metabolites in mice, P-gp-deficient mice exhibit elevated formation of the active metabolite H4 and enhanced antiplatelet effect of clopidogrel through up-regulation of Cyp3a11 and down-regulation of Ces1, suggesting that P-gp activity may correlate inversely with the formation of H4 and antiplatelet efficacy of clopidogrel in clinical settings due to P-gp and CYP3A4 interplay.	clopidogrel	208-219	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	245-252
33137324-7	2021	We conclude that although P-gp does not transport clopidogrel and its major metabolites in mice, P-gp-deficient mice exhibit elevated formation of the active metabolite H4 and enhanced antiplatelet effect of clopidogrel through up-regulation of Cyp3a11 and down-regulation of Ces1, suggesting that P-gp activity may correlate inversely with the formation of H4 and antiplatelet efficacy of clopidogrel in clinical settings due to P-gp and CYP3A4 interplay.	clopidogrel	208-219	carboxylesterase 1G	Mus musculus	276-280
33137324-7	2021	We conclude that although P-gp does not transport clopidogrel and its major metabolites in mice, P-gp-deficient mice exhibit elevated formation of the active metabolite H4 and enhanced antiplatelet effect of clopidogrel through up-regulation of Cyp3a11 and down-regulation of Ces1, suggesting that P-gp activity may correlate inversely with the formation of H4 and antiplatelet efficacy of clopidogrel in clinical settings due to P-gp and CYP3A4 interplay.	clopidogrel	208-219	phosphoglycolate phosphatase	Mus musculus	97-101
33137324-7	2021	We conclude that although P-gp does not transport clopidogrel and its major metabolites in mice, P-gp-deficient mice exhibit elevated formation of the active metabolite H4 and enhanced antiplatelet effect of clopidogrel through up-regulation of Cyp3a11 and down-regulation of Ces1, suggesting that P-gp activity may correlate inversely with the formation of H4 and antiplatelet efficacy of clopidogrel in clinical settings due to P-gp and CYP3A4 interplay.	clopidogrel	208-219	phosphoglycolate phosphatase	Mus musculus	97-101
32415684-0	2021	Clopidogrel, a CYP2C8 inhibitor, causes a clinically relevant increase in the systemic exposure to the active metabolite of selexipag in healthy subjects.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	15-21
32415684-3	2021	This study evaluated the interaction of selexipag and clopidogrel, a CYP2C8 inhibitor.	clopidogrel	54-65	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	69-75
33085221-10	2021	The genes CYP2D6 and CYP2C19 were responsible for the majority of treatment modifications, and the medications most often affected were ondansetron, oxycodone, and clopidogrel.	clopidogrel	164-175	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	10-16
33085221-10	2021	The genes CYP2D6 and CYP2C19 were responsible for the majority of treatment modifications, and the medications most often affected were ondansetron, oxycodone, and clopidogrel.	clopidogrel	164-175	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
33976007-0	2021	The CYP2C19 genotypes and its effect on clopidogrel as an anti-platelet drug among the Arab population.	clopidogrel	40-51	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
33414804-8	2020	In conclusion, Cyp2C19*2 gene polymorphism is strongly associated with clopidogrel resistance.	clopidogrel	71-82	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
33376304-9	2020	Results: This study indicated that Clopidogrel significantly induced the gastric ulcers recurrence, severe inflammation and ER stress related apoptosis of the gastric mucosa, suppressed the synthesis of angiogenic markers and eNOS.	clopidogrel	35-46	nitric oxide synthase 3	Rattus norvegicus	226-230
33519456-0	2020	Physiologically-Based Pharmacokinetic-Pharmacodynamics Model Characterizing CYP2C19 Polymorphisms to Predict Clopidogrel Pharmacokinetics and Its Anti-Platelet Aggregation Effect Following Oral Administration to Coronary Artery Disease Patients With or Without Diabetes.	clopidogrel	109-120	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	76-83
33519456-9	2020	Clopidogrel resistance by DM was the integrated effects of altered K t,i, CYP2C19, CYP3A4, CES1 and k irre.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	74-81
33519456-9	2020	Clopidogrel resistance by DM was the integrated effects of altered K t,i, CYP2C19, CYP3A4, CES1 and k irre.	clopidogrel	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	83-89
33519456-9	2020	Clopidogrel resistance by DM was the integrated effects of altered K t,i, CYP2C19, CYP3A4, CES1 and k irre.	clopidogrel	0-11	carboxylesterase 1	Homo sapiens	91-95
33414804-1	2020	In recent years, the relationship between Cyp2C19*2 gene polymorphism and clopidogrel resistance reflected by platelet function assay has been studied extensively, but there is no clear conclusion yet.	clopidogrel	74-85	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	42-49
33414804-2	2020	In order to evaluate the relationship between Cyp2C19*2 gene polymorphism and clopidogrel resistance more accurately, meta-analysis was conducted in this study.	clopidogrel	78-89	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	46-53
33021875-6	2020	For patients with isolated stable PAD may be sufficient a less potent P2Y12 inhibitor as clopidogrel, whereas patients with lower extremity PAD and documented CAD benefit from a more intense and prolonged antithrombotic treatment.	clopidogrel	89-100	purinergic receptor P2Y12	Homo sapiens	70-75
33040624-1	2020	INTRODUCTION: The effects of the ABCB1 C3435T genetic polymorphism on clopidogrel responses are conflicting and inconclusive especially in patients undergoing percutaneous coronary intervention (PCI).	clopidogrel	70-81	ATP binding cassette subfamily B member 1	Homo sapiens	33-38
33040624-2	2020	This study examined the pooled risk of major adverse cardiovascular events (MACE) and bleeding events associated with the ABCB1 C3435T polymorphism in acute coronary syndrome or coronary artery disease patients undergoing PCI and treated with clopidogrel.	clopidogrel	243-254	ATP binding cassette subfamily B member 1	Homo sapiens	122-127
33040624-7	2020	It is suggested that ABCB1 C3435T genotype should be tested for ACS/CAD patients undergoing PCI to ensure optimum therapy of clopidogrel.	clopidogrel	125-136	ATP binding cassette subfamily B member 1	Homo sapiens	21-26
32862511-1	2020	CYP2C19, ABCB1 and PON1 polymorphisms involve in the metabolism and absorption of clopidogrel, which may be associated with interethnic variability of clopidogrel response.	clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
32862511-1	2020	CYP2C19, ABCB1 and PON1 polymorphisms involve in the metabolism and absorption of clopidogrel, which may be associated with interethnic variability of clopidogrel response.	clopidogrel	82-93	ATP binding cassette subfamily B member 1	Homo sapiens	9-14
32862511-1	2020	CYP2C19, ABCB1 and PON1 polymorphisms involve in the metabolism and absorption of clopidogrel, which may be associated with interethnic variability of clopidogrel response.	clopidogrel	82-93	paraoxonase 1	Homo sapiens	19-23
32862511-1	2020	CYP2C19, ABCB1 and PON1 polymorphisms involve in the metabolism and absorption of clopidogrel, which may be associated with interethnic variability of clopidogrel response.	clopidogrel	151-162	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
32862511-1	2020	CYP2C19, ABCB1 and PON1 polymorphisms involve in the metabolism and absorption of clopidogrel, which may be associated with interethnic variability of clopidogrel response.	clopidogrel	151-162	ATP binding cassette subfamily B member 1	Homo sapiens	9-14
32862511-1	2020	CYP2C19, ABCB1 and PON1 polymorphisms involve in the metabolism and absorption of clopidogrel, which may be associated with interethnic variability of clopidogrel response.	clopidogrel	151-162	paraoxonase 1	Homo sapiens	19-23
33215448-0	2020	Prevalence and types of genetic polymorphisms of CYP2C19 and their effects on platelet aggregation inhibition by clopidogrel.	clopidogrel	113-124	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	49-56
32916563-0	2020	Association of fractalkine with functional severity of heart failure and impact on clopidogrel efficacy in patients with ischemic heart disease.	clopidogrel	83-94	C-X3-C motif chemokine ligand 1	Homo sapiens	15-26
32916563-2	2020	Further, fractalkine has been associated with reduced pharmacodynamic (PD) responsiveness to clopidogrel.	clopidogrel	93-104	C-X3-C motif chemokine ligand 1	Homo sapiens	9-20
32916563-3	2020	The aim of this study was to investigate the association of fractalkine with the severity of HF and its impact on platelet activation and clopidogrel response in patients with coronary artery disease (CAD) with and without HF.	clopidogrel	138-149	C-X3-C motif chemokine ligand 1	Homo sapiens	60-71
33091705-7	2020	RESULTS AND CONCLUSIONS: With all 3 pro-aggregants, (1) response to clopidogrel after 4 h, as measured by DeltaADP response, exhibits a strong inverse relationship with on-treatment aggregation, with a similarly inverse relationship between pre-treatment PGE1 response and on-treatment aggregability; (2) there is a weaker inverse relationship between clopidogrel response and pre-treatment platelet aggregability, and a significant inverse relationship between pre-treatment PGE1 response and pre-treatment platelet aggregability.	clopidogrel	68-79	paired box 5	Homo sapiens	30-35
33091705-7	2020	RESULTS AND CONCLUSIONS: With all 3 pro-aggregants, (1) response to clopidogrel after 4 h, as measured by DeltaADP response, exhibits a strong inverse relationship with on-treatment aggregation, with a similarly inverse relationship between pre-treatment PGE1 response and on-treatment aggregability; (2) there is a weaker inverse relationship between clopidogrel response and pre-treatment platelet aggregability, and a significant inverse relationship between pre-treatment PGE1 response and pre-treatment platelet aggregability.	clopidogrel	352-363	paired box 5	Homo sapiens	30-35
33116024-0	2020	Elevated Serum Levels of Alkaline Phosphatase and the Risk of Low Responsiveness to Clopidogrel.	clopidogrel	84-95	alkaline phosphatase, placental	Homo sapiens	25-45
33116024-2	2020	Our study aims at investigating the relationship between the serum ALP and the responsiveness to clopidogrel.	clopidogrel	97-108	alkaline phosphatase, placental	Homo sapiens	67-70
33116024-9	2020	When multiple confounders were adjusted, the highest ALP quartile correlated with an increased risk of low responsiveness to clopidogrel compared to the lowest ALP quartile (OR, 1.423; 95% CI, 1.017-1.991; P = 0.039).	clopidogrel	125-136	alkaline phosphatase, placental	Homo sapiens	53-56
33116024-11	2020	The elevated serum levels of ALP are independently associated with an increased risk of low responsiveness to clopidogrel.	clopidogrel	110-121	alkaline phosphatase, placental	Homo sapiens	29-32
33343644-2	2020	However, previous pharmacodynamic and clinical studies have reported controversial results on the interaction between PPI and the P2Y12 inhibitor clopidogrel.	clopidogrel	146-157	purinergic receptor P2Y12	Homo sapiens	130-135
33242353-10	2021	We used the murine model of sepsis, cecal ligation, and puncture (CLP) and we blocked P2Y12 using the P2Y12 antagonist, clopidogrel.	clopidogrel	120-131	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	86-91
33242353-10	2021	We used the murine model of sepsis, cecal ligation, and puncture (CLP) and we blocked P2Y12 using the P2Y12 antagonist, clopidogrel.	clopidogrel	120-131	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	102-107
33262635-0	2020	Should CYP2C19 Genotyping Be Recommended as a Straight Forward Approach to Optimize Clopidogrel Utilization in Patients with Ischemic Stroke Complicated by Type 2 Diabetes Mellitus?	clopidogrel	84-95	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	7-14
33262635-11	2020	Conclusion: CYP2C19*2 mutant allele was associated with attenuated platelet response to clopidogrel and increased risk of HTPR in IS patients with T2DM, suggesting that CYP2C19*2 polymorphism might be an important predictor of HTPR in this high-risk population.	clopidogrel	88-99	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
33262635-11	2020	Conclusion: CYP2C19*2 mutant allele was associated with attenuated platelet response to clopidogrel and increased risk of HTPR in IS patients with T2DM, suggesting that CYP2C19*2 polymorphism might be an important predictor of HTPR in this high-risk population.	clopidogrel	88-99	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	169-176
33184726-0	2021	Influence of CYP2C19 genotypes for the effect of 1-month dual antiplatelet therapy followed by clopidogrel monotherapy relative to 12-month dual antiplatelet therapy on clinical outcomes after percutaneous coronary intervention: a genetic substudy from the STOPDAPT-2.	clopidogrel	95-106	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
33184726-2	2021	However, CYP2C19 loss-of-function (LOF) alleles have been reported to diminish the effect of clopidogrel, and clopidogrel monotherapy has a concern about the increased ischemic risk for patients with such alleles.	clopidogrel	93-104	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	9-16
33313086-12	2020	MiR-223 may be a novel biomarker for bleeding in cardiac surgery and can help explain the different efficacies of ticagrelor and clopidogrel.	clopidogrel	129-140	microRNA 223	Homo sapiens	0-7
32546030-1	2020	Cytochrome P450 (CYP) 2C19 genotype is closely associated with the metabolism and efficacy of clopidogrel, thereby having an important impact on clinical outcomes of patients with acute coronary syndrome (ACS) or undergoing percutaneous coronary intervention (PCI).	clopidogrel	94-105	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-26
32472697-2	2020	CYP2C19 loss-of-function alleles play an important role in this response, but account for only a small proportion of variability in response to clopidogrel.	clopidogrel	144-155	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
32472697-8	2020	CYP2C19*2 is the strongest genetic determinant of on-clopidogrel platelet reactivity.	clopidogrel	53-64	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
33215448-1	2020	OBJECTIVE:  The current study was conducted to determine the distribution of genetic polymorphisms in CYP2C19 in Iraqi patients and their role in inter-individual variability of clopidogrel efficacy.	clopidogrel	178-189	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	102-109
33215448-8	2020	CONCLUSIONS: In vitro gene analysis and VASP index improve the clinical outcome of a patient candidate to clopidogrel as prophylaxis in cardiovascular events.	clopidogrel	106-117	vasodilator stimulated phosphoprotein	Homo sapiens	40-44
32835535-3	2020	Amongst these, DDIs involving clopidogrel, the most commonly utilized platelet P2Y12 inhibitor, is a topic of potential clinical concern.	clopidogrel	30-41	purinergic receptor P2Y12	Homo sapiens	79-84
32390477-3	2020	The newer P2Y12 inhibitors (prasugrel and ticagrelor) have better efficacy than clopidogrel.	clopidogrel	80-91	purinergic receptor P2Y12	Homo sapiens	10-15
32524842-5	2020	The main factors found to influence uptake of CYP2C19 genotyping test are, convenience of genotyping test (n = 4), physician"s recommendation (n = 11), prior explanation of genetic testing by medical personnel (n = 5) and inclination toward clopidogrel, with three sub-factors; less frequent dosing (n = 3), lower cost (n = 7) and lower risk of bleeding (n = 9).	clopidogrel	241-252	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	46-53
33357650-10	2020	CONCLUSIONS: Genotyping for CYP2C19 variations to assess clopidogrel resistance in patients undergoing PCI and subsequent drug selection helps reduce MACE after coronary intervention.	clopidogrel	57-68	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
32616329-0	2020	Serum interleukin-18 levels as a predictor for patients with genetic dysfunction of cytochrome P450 2C19 in dual antiplatelet therapy with clopidogrel.	clopidogrel	139-150	interleukin 18	Homo sapiens	6-20
32616329-0	2020	Serum interleukin-18 levels as a predictor for patients with genetic dysfunction of cytochrome P450 2C19 in dual antiplatelet therapy with clopidogrel.	clopidogrel	139-150	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	84-104
32616329-1	2020	BACKGROUND: P2Y12 reaction unit (PRU) is an index of platelet activity upon treatment with clopidogrel.	clopidogrel	91-102	purinergic receptor P2Y12	Homo sapiens	12-17
32616329-2	2020	In spite of suitable P2Y12 reactions in dual antiplatelet therapy (DAPT) with clopidogrel after percutaneous coronary intervention (PCI), cardiovascular events actually occur in some patients, possibly due to a genetic dysfunction of cytochrome P450 2C19 (CYP2C19), which is a major metabolic enzyme of clopidogrel.	clopidogrel	78-89	purinergic receptor P2Y12	Homo sapiens	21-26
32616329-2	2020	In spite of suitable P2Y12 reactions in dual antiplatelet therapy (DAPT) with clopidogrel after percutaneous coronary intervention (PCI), cardiovascular events actually occur in some patients, possibly due to a genetic dysfunction of cytochrome P450 2C19 (CYP2C19), which is a major metabolic enzyme of clopidogrel.	clopidogrel	303-314	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	234-254
32616329-8	2020	CONCLUSIONS: The serum levels of interleukin-18 may be a predictor to diagnose patients who receive undesirable DAPT with clopidogrel, possibly due to the genetic dysfunction of CYP2C19 in spite of suitable P2Y12 reactions after PCI.	clopidogrel	122-133	interleukin 18	Homo sapiens	33-47
32616329-8	2020	CONCLUSIONS: The serum levels of interleukin-18 may be a predictor to diagnose patients who receive undesirable DAPT with clopidogrel, possibly due to the genetic dysfunction of CYP2C19 in spite of suitable P2Y12 reactions after PCI.	clopidogrel	122-133	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	178-185
33118441-1	2020	Background: Poor clopidogrel metabolizers, carrying a cytochrome P450 2C19 loss-of-function allele, are more frequent among East Asians than Caucasians/White.	clopidogrel	17-28	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	54-74
33121452-0	2020	Effectiveness and safety of high dose clopidogrel plus aspirin in ischemic stroke patients with the single CYP2C19 loss-of-function allele: a randomized trial.	clopidogrel	38-49	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	107-114
33121452-11	2020	CONCLUSIONS: In patients with ischaemic stroke who had a single CYP2C19 loss-of-function allele and moderate to severe cerebral stenosis, fewer vascular events occurred within 3 months with high dose of clopidogrel and aspirin than with normal dose of clopidogrel and aspirin.	clopidogrel	203-214	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	64-71
33121452-11	2020	CONCLUSIONS: In patients with ischaemic stroke who had a single CYP2C19 loss-of-function allele and moderate to severe cerebral stenosis, fewer vascular events occurred within 3 months with high dose of clopidogrel and aspirin than with normal dose of clopidogrel and aspirin.	clopidogrel	252-263	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	64-71
33121452-13	2020	TRIAL REGISTRATION: Clinical study of clopidogrel in the treatment of patients with symptomatic moderate to severe cerebral artery stenosis with intermediate metabolites of CYP2C19, URL: http://www.chictr.org.cn/ .	clopidogrel	38-49	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	173-180
33107382-1	2022	BACKGROUND: Clopidogrel is the most commonly prescribed P2Y12 inhibitor for acute coronary syndrome (ACS) or stent placement, though ticagrelor or prasugrel may be preferred.	clopidogrel	12-23	purinergic receptor P2Y12	Homo sapiens	56-61
33036613-0	2020	High glycated albumin is an independent predictor of low response to clopidogrel in ACS patients: a cross-sectional study.	clopidogrel	69-80	albumin	Homo sapiens	14-21
33036613-4	2020	In this study, we evaluated the effect of GA on platelet P2Y12 inhibition by clopidogrel in patients with ACS.	clopidogrel	77-88	purinergic receptor P2Y12	Homo sapiens	57-62
32822211-5	2020	The P2Y12R antagonists such as clopidogrel, ticagrelor, and others are the most successful class of purinergic drugs targeting platelets for the treatment of acute coronary syndrome.	clopidogrel	31-42	purinergic receptor P2Y12	Homo sapiens	4-10
32653591-0	2020	Type 2 diabetes mellitus decreases systemic exposure of clopidogrel active metabolite through upregulation of P-glycoprotein in rats.	clopidogrel	56-67	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	110-124
32632713-10	2020	CONCLUSIONS: The patients with high body weight, the CYP2C19 phenotypes, and P2Y12 receptor (52 G >T) variant alleles are at risk of CR during clopidogrel treatment in Chinese IS patients with aspirin intolerance.	clopidogrel	143-154	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-60
31721430-4	2020	All patients underwent platelet function testing with the VerifyNow assay; HPR on clopidogrel was defined as P2Y12 reaction units (PRU) >208.	clopidogrel	82-93	purinergic receptor P2Y12	Homo sapiens	109-114
33155236-18	2020	CONCLUSIONS: (1) Patients with a CYP2C19 loss-of-function (LOF) gene who take double doses of clopidogrel overcome the decreased efficacy of clopidogrel which partly due to CYP2C19 LOF gene, without increasing the risk of hemorrhage.	clopidogrel	94-105	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-40
33155236-18	2020	CONCLUSIONS: (1) Patients with a CYP2C19 loss-of-function (LOF) gene who take double doses of clopidogrel overcome the decreased efficacy of clopidogrel which partly due to CYP2C19 LOF gene, without increasing the risk of hemorrhage.	clopidogrel	94-105	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	173-180
33155236-18	2020	CONCLUSIONS: (1) Patients with a CYP2C19 loss-of-function (LOF) gene who take double doses of clopidogrel overcome the decreased efficacy of clopidogrel which partly due to CYP2C19 LOF gene, without increasing the risk of hemorrhage.	clopidogrel	141-152	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-40
33155236-18	2020	CONCLUSIONS: (1) Patients with a CYP2C19 loss-of-function (LOF) gene who take double doses of clopidogrel overcome the decreased efficacy of clopidogrel which partly due to CYP2C19 LOF gene, without increasing the risk of hemorrhage.	clopidogrel	141-152	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	173-180
32675750-0	2020	Diabetes and CYP2C19 Polymorphism Synergistically Impair the Antiplatelet Activity of Clopidogrel Compared to Ticagrelor in PCI-Treated ACS Patients.	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
32675750-1	2020	Diabetes and CYP2C19 loss of function (LOF) alleles are associated with variable antiplatelet activity of the prodrug clopidogrel.	clopidogrel	118-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
32675750-2	2020	We conducted a randomized trial (NCT03613857) to compare the combined and individualized effects of diabetes and CYP2C19 polymorphisms on the anti-platelet reactivity of clopidogrel vs ticagrelor in ACS patients undergoing percutaneous coronary intervention (PCI).	clopidogrel	170-181	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	113-120
32675750-9	2020	PCI-treated ACS patients with diabetes and CYP2C19 LOF alleles are at a higher risk of recurrent ACS and high PRI/MPA, when treated with clopidogrel VS. ticagrelor, but almost comparable outcomes are recorded in the absence of one or the two risk factors.	clopidogrel	137-148	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	43-50
32152791-1	2020	High on treatment platelet reactivity (HPR) during treatment with clopidogrel has been consistently found to be strong risk factor for recurrent ischemic events after percutaneous coronary intervention (PCI).	clopidogrel	66-77	haptoglobin-related protein	Homo sapiens	39-42
32653591-5	2020	However, in vitro liver microsomes incubated with Clop exhibited increased Clop-AM levels in T2DM rats due to a significant decrease in carboxylesterase (CES)1 expression and activity and a significant increase in the expression or activity of CYP1A2 and CYP3A.	clopidogrel	50-54	carboxylesterase 1E	Rattus norvegicus	136-159
32653591-5	2020	However, in vitro liver microsomes incubated with Clop exhibited increased Clop-AM levels in T2DM rats due to a significant decrease in carboxylesterase (CES)1 expression and activity and a significant increase in the expression or activity of CYP1A2 and CYP3A.	clopidogrel	50-54	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	244-250
32653591-5	2020	However, in vitro liver microsomes incubated with Clop exhibited increased Clop-AM levels in T2DM rats due to a significant decrease in carboxylesterase (CES)1 expression and activity and a significant increase in the expression or activity of CYP1A2 and CYP3A.	clopidogrel	50-54	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	255-260
32653591-11	2020	P-gp might be the key factor causing the reduction of Clop absorption, consequently making less Clop available for Clop-AM formation.	clopidogrel	54-58	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	0-4
32653591-11	2020	P-gp might be the key factor causing the reduction of Clop absorption, consequently making less Clop available for Clop-AM formation.	clopidogrel	96-100	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	0-4
32932966-0	2020	Effect of CYP3A4*22 and PPAR-alpha Genetic Variants on Platelet Reactivity in Patients Treated with Clopidogrel and Lipid-Lowering Drugs Undergoing Elective Percutaneous Coronary Intervention.	clopidogrel	100-111	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	10-16
32932966-0	2020	Effect of CYP3A4*22 and PPAR-alpha Genetic Variants on Platelet Reactivity in Patients Treated with Clopidogrel and Lipid-Lowering Drugs Undergoing Elective Percutaneous Coronary Intervention.	clopidogrel	100-111	peroxisome proliferator activated receptor alpha	Homo sapiens	24-34
32932966-1	2020	This study aims to determine whether genetic variants that influence CYP3A4 expression are associated with platelet reactivity in clopidogrel-treated patients undergoing elective percutaneous coronary intervention (PCI), and to evaluate the influence of statin/fibrate co-medication on these associations.	clopidogrel	130-141	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	69-75
32932966-8	2020	In conclusion, PPAR-alpha G209A and A208G were associated with lower platelet reactivity in patients undergoing elective PCI who were treated with clopidogrel and statin/fibrate co-medication.	clopidogrel	147-158	peroxisome proliferator activated receptor alpha	Homo sapiens	15-25
32892681-11	2021	CYP2C19 gene polymorphism was associated with clopidogrel on-treatment platelet hyperresponsiveness.	clopidogrel	46-57	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
33417661-0	2020	The Impact of Kinase Insert Domain (KDR) Gene Polymorphism rs2305948 on Clopidogrel Resistance in Iraqi Patients Undergoing Elective Percutaneous Coronary Intervention (PCI).	clopidogrel	72-83	kinase insert domain receptor	Homo sapiens	36-39
32504182-0	2020	Age-dependent association of CYP2C19 polymorphisms with clinical outcome of clopidogrel therapy in minor stroke patients with large-artery atherosclerosis.	clopidogrel	76-87	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	29-36
32504182-1	2020	PURPOSE: Previous studies on the association between CYP2C19 polymorphisms and therapeutic outcome of clopidogrel in stroke patients are inconclusive.	clopidogrel	102-113	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-60
32504182-2	2020	We aimed to investigate the impact of CYP2C19 polymorphisms on therapeutic efficacy of clopidogrel in both young and old minor stroke patients associated with large-artery atherosclerosis (LAA).	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	38-45
32504182-8	2020	RESULTS: Sixty years old was identified as the optimal cutoff age for CYP2C19 polymorphisms to affect the clinical outcome of clopidogrel therapy in LAA-associated minor stroke patients (OR = 1.67; 95% CI 1.08-2.58).	clopidogrel	126-137	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	70-77
32504182-12	2020	CONCLUSIONS: Carriage of the CYP2C19 LOF allele may prevent expected clinical outcome during clopidogrel therapy in young LAA-associated minor stroke patients, whereas not in older patients.	clopidogrel	93-104	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	29-36
32338045-1	2020	BACKGROUND: The benefit of cytochrome P450 (CYP450) enzyme system metabolized medications, especially clopidogrel, was reported more pronounced in smoking than nonsmoking patients, but limited evidence was available from Asian patients.	clopidogrel	102-113	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	27-42
31661948-0	2020	The Efficacy of P2Y12 Reactive Unit to Predict the Periprocedural Thromboembolic and Hemorrhagic Complications According to Clopidogrel Responsiveness and Safety of Modification of Dual Antiplatelet Therapy : A Meta-Analysis.	clopidogrel	124-135	purinergic receptor P2Y12	Homo sapiens	16-21
32713878-0	2020	Comparison Between Clopidogrel and Prasugrel Associated With CYP2C19 Genotypes in Patients Receiving Percutaneous Coronary Intervention in a Japanese Population.	clopidogrel	19-30	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	61-68
32713878-1	2020	BACKGROUND: The association between cytochrome P450 (CYP) 2C19 genotypes and adverse events in patients treated with clopidogrel or prasugrel after percutaneous coronary intervention (PCI) in the Japanese population is unclear.Methods and Results:This study consisted of 1,580 patients whoseCYP2C19genotypes were assessed at Shiga University of Medical Science Hospital, and 193 clopidogrel-treated and 217 prasugrel-treated patients who were followed more than 1 year after receiving PCI were analyzed.	clopidogrel	117-128	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	36-62
32840598-1	2020	Importance: After percutaneous coronary intervention (PCI), patients with CYP2C19*2 or *3 loss-of-function (LOF) variants treated with clopidogrel have increased risk of ischemic events.	clopidogrel	135-146	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	74-81
32840598-7	2020	CYP2C19 LOF carriers were prescribed ticagrelor and noncarriers clopidogrel.	clopidogrel	64-75	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
32840598-14	2020	Of 1849 with CYP2C19 LOF variants, 764 of 903 (85%) assigned to genotype-guided therapy received ticagrelor, and 932 of 946 (99%) assigned to conventional therapy received clopidogrel.	clopidogrel	172-183	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
31498157-2	2020	Clopidogrel, the most widely used oral P2Y12 receptor antagonist in ACS, has attracted considerable attention because of significant variability in antiplatelet effect depending on the presence of CYP2C19 allele.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	39-44
31498157-2	2020	Clopidogrel, the most widely used oral P2Y12 receptor antagonist in ACS, has attracted considerable attention because of significant variability in antiplatelet effect depending on the presence of CYP2C19 allele.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	197-204
31498157-7	2020	RESULTS: Presence of specific CYP2C19 allele significantly influences clopidogrel metabolism and associated outcomes in patients with ACS.	clopidogrel	70-81	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
33417661-5	2020	Aim: To study the impact of KDR gene polymorphism rs2305948 on clopidogrel resistance in patients undergoing elective PCI.	clopidogrel	63-74	kinase insert domain receptor	Homo sapiens	28-31
32904459-0	2020	Increased Risk of Clopidogrel-Induced Gastric Mucosal Erosion in Elderly Chinese Men Harboring the ABCB1 3435T Allele.	clopidogrel	18-29	ATP binding cassette subfamily B member 1	Homo sapiens	99-104
32904459-2	2020	This study aimed to evaluate the relationship between ABCB1 C3435T polymorphisms, which could affect the intestinal absorption of clopidogrel, and gastric mucosal erosion in elderly Chinese men who used clopidogrel alone.	clopidogrel	130-141	ATP binding cassette subfamily B member 1	Homo sapiens	54-59
32904459-2	2020	This study aimed to evaluate the relationship between ABCB1 C3435T polymorphisms, which could affect the intestinal absorption of clopidogrel, and gastric mucosal erosion in elderly Chinese men who used clopidogrel alone.	clopidogrel	203-214	ATP binding cassette subfamily B member 1	Homo sapiens	54-59
32904459-6	2020	After adjustments for significant factors were made, ABCB1 3435T allele carrier (OR 2.14, 95% CI 1.43-3.84, p <0.01) was found to be associated with gastric mucosal erosion in people who used clopidogrel alone.	clopidogrel	192-203	ATP binding cassette subfamily B member 1	Homo sapiens	53-58
32617885-1	2020	BACKGROUND: The clinical implications of potential interactions between proton pump inhibitors (PPIs) and clopidogrel have been debated for over a decade.	clopidogrel	106-117	ATPase H+/K+ transporting subunit alpha	Homo sapiens	72-83
32840951-4	2022	We used dispensing claims to examine dispensing of a P2Y12 inhibitor (clopidogrel, prasugrel or ticagrelor) within 30 days of discharge, and multilevel models to identify predictors of post-discharge dispensing and persistence of therapy to one year.	clopidogrel	70-81	purinergic receptor P2Y12	Homo sapiens	53-58
32551860-7	2020	In the experimental arm, background use of a P2Y12 inhibitor was clopidogrel in 2649 (16.5%) and prasugrel or ticagrelor in 13,408 (83.5%) of patients.	clopidogrel	65-76	purinergic receptor P2Y12	Homo sapiens	45-50
32762577-2	2021	The aim of the study was to track the course of thrombopoietic and erythropoietic cells in patients with coronary artery diseases (CAD) after planned and physician-driven cessation of chronic P2Y12-inhibition (clopidogrel 75 mg OD, or prasugrel 10 mg OD, or ticagrelor 90 mg BID).	clopidogrel	210-221	purinergic receptor P2Y12	Homo sapiens	192-197
32904459-7	2020	Conclusion: Carrying the ABCB1 3435T allele may be a useful genetic predictor for clopidogrel-induced gastric mucosal erosion in elderly Chinese men.	clopidogrel	82-93	ATP binding cassette subfamily B member 1	Homo sapiens	25-30
32759249-0	2020	Clopidogrel preventive effect based on cytochrome P450 2C19 genotype in ischaemic stroke: protocol for multicentre observational study.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	39-59
32487324-7	2020	Yet Aspirin and Clopidogrel each comparably lowered CK-MB, AST, MMP-2, MMP-9, and the lipid peroxidation product malondialdehyde (MDA) in the hyperlipidemic animals exposed to AMI.	clopidogrel	16-27	matrix metallopeptidase 2	Mus musculus	64-69
32487324-7	2020	Yet Aspirin and Clopidogrel each comparably lowered CK-MB, AST, MMP-2, MMP-9, and the lipid peroxidation product malondialdehyde (MDA) in the hyperlipidemic animals exposed to AMI.	clopidogrel	16-27	matrix metallopeptidase 9	Mus musculus	71-76
32487324-8	2020	However, the decline in cTn-T, LDH and PTX3 levels was greater after Clopidogrel than Aspirin administration.	clopidogrel	69-80	pentraxin related gene	Mus musculus	39-43
32487324-11	2020	Furthermore, Clopidogrel demonstrated significant antioxidative action in the AMI animals, resulting in diminished MDA production and preserved CAT activity.	clopidogrel	13-24	catalase	Mus musculus	144-147
32764090-2	2020	Reduced responsiveness to clopidogrel among carriers of CYP2C19 variants has been reported in patients with either coronary artery disease (CAD) or acute coronary syndrome (ACS) after the percutaneous coronary intervention (PCI).	clopidogrel	26-37	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	56-63
32759249-2	2020	The genotype of cytochrome P450 2C19 (CYP2C19) differentially affects the liver"s metabolism of clopidogrel, which may influence the drug"s response and efficacy for cardiovascular event prevention.	clopidogrel	96-107	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-36
32320492-0	2020	Efficacy and safety of clopidogrel versus prasugrel and ticagrelor for coronary artery disease treatment in patients with CYP2C19 LoF alleles: A systemic review and meta-analysis.	clopidogrel	23-34	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	122-129
32320492-1	2020	AIM: We performed a systematic review and meta-analysis to compare the efficacy and safety of ticagrelor and prasugrel with those of clopidogrel in CYP2C19 reduced-metabolizers.	clopidogrel	133-144	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	148-155
32759249-2	2020	The genotype of cytochrome P450 2C19 (CYP2C19) differentially affects the liver"s metabolism of clopidogrel, which may influence the drug"s response and efficacy for cardiovascular event prevention.	clopidogrel	96-107	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	38-45
32320492-12	2020	CONCLUSION: CYP2C19 reduced-metabolizers can expect better clinical outcome on using prasugrel or ticagrelor rather than clopidogrel.	clopidogrel	121-132	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
32759249-4	2020	We hypothesise that, among patients who had an acute ischaemic stroke who are prescribed clopidogrel, the patients with a loss-of-function CYP2C19 genotype (poor and intermediate metabolisers) may be at a higher risk of composite cardiovascular events than those who are non-carriers (extensive metabolisers).	clopidogrel	89-100	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	139-146
32968646-8	2020	Potent P2Y12 inhibitor based dual antiplatelet therapy might have prevented this subacute ST, and thus mortality, as the patient was discharged on clopidogrel after PCI.	clopidogrel	147-158	purinergic receptor P2Y12	Homo sapiens	7-12
32352367-10	2020	CONCLUSION: The present case demonstrates that both diabetes mellitus and carriage of CYP2C19*2 allele are associated with a reduced response to clopidogrel in the setting of this standard dose of clopidogrel and a high risk of stent thrombosis.	clopidogrel	145-156	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	86-93
32427413-0	2020	Search for a practical approach for detection of clopidogrel resistance: Comparison of light transmission aggregometry and INNOVANCE  PFA P2Y cartridge and correlation with CYP2C19 variants.	clopidogrel	49-60	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	173-180
32352367-10	2020	CONCLUSION: The present case demonstrates that both diabetes mellitus and carriage of CYP2C19*2 allele are associated with a reduced response to clopidogrel in the setting of this standard dose of clopidogrel and a high risk of stent thrombosis.	clopidogrel	197-208	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	86-93
32723143-3	2020	CYP2C19 activates the antiplatelet drug clopidogrel, and polymorphisms in the CYP2C19 gene are known to alter the outcome for patients taking clopidogrel in the context of cardiovascular disease.	clopidogrel	40-51	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
32335777-11	2020	COLC significantly reduced TRAP-induced platelet aggregation in clopidogrel responders and non-responders.	clopidogrel	64-75	TRAP	Homo sapiens	27-31
32474163-11	2020	Besides, clopidogrel significantly reduced AChE activity, TNF-alpha and IL-1beta concentrations, and APP mRNA gene expression in the hippocampi of rats compared to AlCl3 rats.	clopidogrel	9-20	acetylcholinesterase	Rattus norvegicus	43-47
32474163-11	2020	Besides, clopidogrel significantly reduced AChE activity, TNF-alpha and IL-1beta concentrations, and APP mRNA gene expression in the hippocampi of rats compared to AlCl3 rats.	clopidogrel	9-20	tumor necrosis factor	Rattus norvegicus	58-67
32474163-11	2020	Besides, clopidogrel significantly reduced AChE activity, TNF-alpha and IL-1beta concentrations, and APP mRNA gene expression in the hippocampi of rats compared to AlCl3 rats.	clopidogrel	9-20	interleukin 1 alpha	Rattus norvegicus	72-80
32474163-12	2020	The decrease of hippocampal TNF-alpha and IL-1beta concentrations by clopidogrel was significant compared to donepezil co-treated rats.	clopidogrel	69-80	tumor necrosis factor	Rattus norvegicus	28-37
32474163-12	2020	The decrease of hippocampal TNF-alpha and IL-1beta concentrations by clopidogrel was significant compared to donepezil co-treated rats.	clopidogrel	69-80	interleukin 1 alpha	Rattus norvegicus	42-50
32474163-14	2020	CONCLUSION: These findings demonstrate that clopidogrel could alleviate learning and memory deficit induced by AlCl3 in rats and significantly reduced AChE activity.	clopidogrel	44-55	acetylcholinesterase	Rattus norvegicus	151-155
32668483-1	2020	BACKGROUND:  Clopidogrel is currently the only P2Y12 inhibitor with class I recommendation in patients after percutaneous coronary intervention (PCI) for chronic coronary syndromes (CCS).	clopidogrel	13-24	purinergic receptor P2Y12	Homo sapiens	47-52
32723143-3	2020	CYP2C19 activates the antiplatelet drug clopidogrel, and polymorphisms in the CYP2C19 gene are known to alter the outcome for patients taking clopidogrel in the context of cardiovascular disease.	clopidogrel	40-51	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	78-85
32723143-3	2020	CYP2C19 activates the antiplatelet drug clopidogrel, and polymorphisms in the CYP2C19 gene are known to alter the outcome for patients taking clopidogrel in the context of cardiovascular disease.	clopidogrel	142-153	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
32723143-3	2020	CYP2C19 activates the antiplatelet drug clopidogrel, and polymorphisms in the CYP2C19 gene are known to alter the outcome for patients taking clopidogrel in the context of cardiovascular disease.	clopidogrel	142-153	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	78-85
32723143-4	2020	CYP2C19 loss-of-function alleles are specifically associated with increased risk for coronary stent thrombosis and major adverse cardiovascular events in patients taking clopidogrel following percutaneous coronary intervention.	clopidogrel	170-181	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
32821149-3	2020	However, clopidogrel remains the most commonly prescribed P2Y12 inhibitor in the setting of PCI and is also the preferred agent in the treatment and secondary prevention of stroke.	clopidogrel	9-20	purinergic receptor P2Y12	Homo sapiens	58-63
32821149-4	2020	Clopidogrel is a prodrug that requires bioactivation by the CYP2C19 enzyme.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	60-67
32821149-5	2020	It has been shown that clopidogrel use in patients who are CYP2C19 no function allele carriers are associated with impaired antiplatelet inhibition and a higher risk of major adverse cardiovascular and cerebrovascular events.	clopidogrel	23-34	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	59-66
32821149-9	2020	Multiple recent studies have examined the effects of CYP2C19 genotype on clopidogrel outcomes in the setting of stroke and neurointerventional procedures.	clopidogrel	73-84	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-60
31556777-6	2020	In the clopidogrel subgroup, homozygous carriers (AA) of the CYP1A2*1F gene (rs762551, 163C>A) appeared more frequently in smokers than in nonsmokers (45.6% vs 32.7%, p = .035).	clopidogrel	7-18	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	61-67
32821149-1	2020	In patients undergoing percutaneous coronary intervention (PCI), the standard of care is dual antiplatelet therapy with a P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor) and aspirin.	clopidogrel	139-150	purinergic receptor P2Y12	Homo sapiens	122-127
32765043-4	2020	This expansion was led by a multidisciplinary team that developed an evidence-based, structured framework for the guides, oversaw the technical process/build, and pilot tested the first guide, CYP2C19-Clopidogrel Testing Implementation.	clopidogrel	201-212	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	193-200
32765043-5	2020	Results: Sixty-five resources were collected from 12 institutions and categorized according to a seven-step implementation framework for the pilot CYP2C19-Clopidogrel Testing Implementation Guide.	clopidogrel	155-166	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	147-154
32765043-6	2020	Five months after its launch, 96 CYP2C19-Clopidogrel Testing Implementation Guides had been created.	clopidogrel	41-52	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-40
32702814-2	2020	Clopidogrel is the most commonly used medication worldwide in dual antiplatelet therapy for CAD, and the response of clopidogrel is affected by CYP2C19, PON1, and ABCB1 genetic polymorphisms.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	144-151
32702814-2	2020	Clopidogrel is the most commonly used medication worldwide in dual antiplatelet therapy for CAD, and the response of clopidogrel is affected by CYP2C19, PON1, and ABCB1 genetic polymorphisms.	clopidogrel	0-11	paraoxonase 1	Homo sapiens	153-157
32702814-2	2020	Clopidogrel is the most commonly used medication worldwide in dual antiplatelet therapy for CAD, and the response of clopidogrel is affected by CYP2C19, PON1, and ABCB1 genetic polymorphisms.	clopidogrel	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	163-168
32702814-2	2020	Clopidogrel is the most commonly used medication worldwide in dual antiplatelet therapy for CAD, and the response of clopidogrel is affected by CYP2C19, PON1, and ABCB1 genetic polymorphisms.	clopidogrel	117-128	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	144-151
32702814-2	2020	Clopidogrel is the most commonly used medication worldwide in dual antiplatelet therapy for CAD, and the response of clopidogrel is affected by CYP2C19, PON1, and ABCB1 genetic polymorphisms.	clopidogrel	117-128	paraoxonase 1	Homo sapiens	153-157
32702814-2	2020	Clopidogrel is the most commonly used medication worldwide in dual antiplatelet therapy for CAD, and the response of clopidogrel is affected by CYP2C19, PON1, and ABCB1 genetic polymorphisms.	clopidogrel	117-128	ATP binding cassette subfamily B member 1	Homo sapiens	163-168
32492818-0	2020	P2Y12 Inhibitor Monotherapy with Clopidogrel Versus Ticagrelor in Patients with Acute Coronary Syndrome Undergoing Percutaneous Coronary Intervention.	clopidogrel	33-44	purinergic receptor P2Y12	Homo sapiens	0-5
32414579-9	2020	CYP2C19 polymorphisms may potentially influence clopidogrel resistance.	clopidogrel	48-59	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
32568642-0	2020	Efficacy of Clopidogrel for Prevention of Stroke Based on CYP2C19 Allele Status in the POINT Trial.	clopidogrel	12-23	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	58-65
32568642-1	2020	BACKGROUND AND PURPOSE: Clopidogrel is an antiplatelet drug that is metabolized to its active form by the CYP2C19 enzyme.	clopidogrel	24-35	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	106-113
32568642-2	2020	The CHANCE trial (Clopidogrel in High-Risk Patients With Acute Nondisabling Cerebrovascular Events) found a significant interaction between loss-of-function allele status for the CYP2C19 gene and the effect of dual antiplatelet therapy with aspirin and clopidogrel on the rate of early recurrent stroke following acute transient ischemic attack/minor stroke.	clopidogrel	18-29	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	179-186
32568642-2	2020	The CHANCE trial (Clopidogrel in High-Risk Patients With Acute Nondisabling Cerebrovascular Events) found a significant interaction between loss-of-function allele status for the CYP2C19 gene and the effect of dual antiplatelet therapy with aspirin and clopidogrel on the rate of early recurrent stroke following acute transient ischemic attack/minor stroke.	clopidogrel	253-264	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	179-186
32544082-2	2020	We aimed to elucidate the combined impact of BMI and dysglycemia expressed by glycated albumin (GA) on efficacy of clopidogrel-aspirin therapy among minor stroke (MS) or transient ischemic attack (TIA) patients.	clopidogrel	115-126	albumin	Homo sapiens	87-94
32527038-6	2020	The frequency distribution of CYP2C19 differed for the ADR bleeding cases suspected of clopidogrel (p = 0.020).	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
32527038-7	2020	In a logistic regression analysis, higher CYP2C19 activity (OR (95% CI): 4.97 (1.73-14.27)), together with age (1.05 (1.02-1.08)), showed an impact on the clopidogrel-suspecting ADRs, when adjusting for the clinical parameters.	clopidogrel	155-166	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	42-49
32493215-2	2020	Clopidogrel is a prodrug requiring activation by the cytochrome P450 enzyme, CYP2C19.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	77-84
32493215-10	2020	DISCUSSION: The risk of stent thrombosis in PCI patients is usually reduced by dual anti-platelet therapy, comprising aspirin and a P2Y12 inhibitor, such as clopidogrel.	clopidogrel	157-168	purinergic receptor P2Y12	Homo sapiens	132-137
32493215-11	2020	However, clopidogrel requires activation by the cytochrome P450 enzyme, CYP2C19.	clopidogrel	9-20	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	72-79
32268786-1	2020	OBJECTIVE: Clopidogrel is a commonly used P2Y12 inhibitor to treat and prevent arterial thrombotic events.	clopidogrel	11-22	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	42-47
32268786-2	2020	Clopidogrel is a prodrug that requires bioactivation by CYP (cytochrome P450) enzymes to exert antiplatelet activity.	clopidogrel	0-11	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	56-59
32268786-2	2020	Clopidogrel is a prodrug that requires bioactivation by CYP (cytochrome P450) enzymes to exert antiplatelet activity.	clopidogrel	0-11	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	61-76
32268786-7	2020	Wild-type DIO mice exhibited resistance to antiplatelet and antithrombotic effects of clopidogrel that was associated with reduced hepatic expression of CYP genes and reduced generation of the AM.	clopidogrel	86-97	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	153-156
32349534-6	2020	Additionally, CDL decreased the number of lesional LRP1+ alpha-SMA+ cells and the levels of circulating sLRP1 by activating cAMP/PKA/SREBP-2 in apoE-/- mice fed a high-fat diet.	clopidogrel	14-17	low density lipoprotein receptor-related protein 1	Mus musculus	51-55
32349534-6	2020	Additionally, CDL decreased the number of lesional LRP1+ alpha-SMA+ cells and the levels of circulating sLRP1 by activating cAMP/PKA/SREBP-2 in apoE-/- mice fed a high-fat diet.	clopidogrel	14-17	actin alpha 2, smooth muscle, aorta	Mus musculus	57-66
32349534-6	2020	Additionally, CDL decreased the number of lesional LRP1+ alpha-SMA+ cells and the levels of circulating sLRP1 by activating cAMP/PKA/SREBP-2 in apoE-/- mice fed a high-fat diet.	clopidogrel	14-17	sterol regulatory element binding factor 2	Mus musculus	133-140
32349534-6	2020	Additionally, CDL decreased the number of lesional LRP1+ alpha-SMA+ cells and the levels of circulating sLRP1 by activating cAMP/PKA/SREBP-2 in apoE-/- mice fed a high-fat diet.	clopidogrel	14-17	apolipoprotein E	Mus musculus	144-148
32459538-0	2020	IL-1R (Interleukin-1 Receptor) Signaling and Attenuated Hepatic CYP (Cytochrome P450) 2C Expression: Explanation for Higher Rate of Clopidogrel Resistance in Patients With Diabetes Mellitus?	clopidogrel	132-143	interleukin 1 receptor type 1	Homo sapiens	0-5
32459538-0	2020	IL-1R (Interleukin-1 Receptor) Signaling and Attenuated Hepatic CYP (Cytochrome P450) 2C Expression: Explanation for Higher Rate of Clopidogrel Resistance in Patients With Diabetes Mellitus?	clopidogrel	132-143	interleukin 1 receptor type 1	Homo sapiens	7-29
32392440-1	2020	Aim: To determine the differences in the frequencies of polymorphic variants at the rs4244285(*2), rs4986893 (*3), rs12248560 (*17), loci of the CYP2C19 gene, and the rs2305948 locus of the VEGFR-2 gene in patients receiving clopidogrel treatment as part of a 30-day clinical outcome trial in the Russian and Buryat regions of East Siberia.	clopidogrel	225-236	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	145-152
32194270-5	2020	Patients with a P2Y12 reaction unit (PRU) >= 194 were deemed to be clopidogrel hyporesponsive.	clopidogrel	67-78	purinergic receptor P2Y12	Homo sapiens	16-21
32443494-13	2020	Clopidogrel inhibited HGF secretion after partial hepatectomy.	clopidogrel	0-11	hepatocyte growth factor	Mus musculus	22-25
32537460-5	2020	Based on P-VASP and LTA findings, platelet response to ADP was significantly attenuated after 7 days of clopidogrel treatment.	clopidogrel	104-115	vasodilator stimulated phosphoprotein	Felis catus	11-15
32537460-9	2020	Flow cytometry analysis of P-VASP is effective at monitoring the inhibitory effects of clopidogrel on feline platelets.	clopidogrel	87-98	vasodilator stimulated phosphoprotein	Felis catus	29-33
32509173-0	2020	Role of MKP-5-p38/MAPK pathway in Clopidogrel-induced gastric mucosal epithelial cells apoptosis and tight junction dysfunction.	clopidogrel	34-45	dual specificity phosphatase 10	Homo sapiens	8-13
32509173-0	2020	Role of MKP-5-p38/MAPK pathway in Clopidogrel-induced gastric mucosal epithelial cells apoptosis and tight junction dysfunction.	clopidogrel	34-45	mitogen-activated protein kinase 14	Homo sapiens	14-17
32509173-3	2020	This present study aims to further investigate the role of MAP kinase phosphatase 5 (MKP-5), a MKP known to dephosphorylate and inactivate p38/MAPK, in Clopidogrel-induced gastric mucosal injury and the underlying mechanisms.	clopidogrel	152-163	dual specificity phosphatase 10	Homo sapiens	59-83
32509173-3	2020	This present study aims to further investigate the role of MAP kinase phosphatase 5 (MKP-5), a MKP known to dephosphorylate and inactivate p38/MAPK, in Clopidogrel-induced gastric mucosal injury and the underlying mechanisms.	clopidogrel	152-163	dual specificity phosphatase 10	Homo sapiens	85-90
32509173-3	2020	This present study aims to further investigate the role of MAP kinase phosphatase 5 (MKP-5), a MKP known to dephosphorylate and inactivate p38/MAPK, in Clopidogrel-induced gastric mucosal injury and the underlying mechanisms.	clopidogrel	152-163	mitogen-activated protein kinase 14	Homo sapiens	139-142
32509173-4	2020	It shows that MKP-5 is down-regulated at both mRNA and protein levels in the gastric mucosa from bleeding patients who took Clopidogrel over one year.	clopidogrel	124-135	dual specificity phosphatase 10	Homo sapiens	14-19
32509173-6	2020	Overexpression of MKP-5 promotes GES-1 cell proliferation and reduces apoptosis following Clopidogrel exposure.	clopidogrel	90-101	dual specificity phosphatase 10	Homo sapiens	18-23
32509173-9	2020	We conclude that MKP-5 is down-regulated in Clopidogrel-induced gastric mucosa injury in vivo and in vitro via phosphorylation and activation of p38/MAPK signaling pathway.	clopidogrel	44-55	dual specificity phosphatase 10	Homo sapiens	17-22
32509173-9	2020	We conclude that MKP-5 is down-regulated in Clopidogrel-induced gastric mucosa injury in vivo and in vitro via phosphorylation and activation of p38/MAPK signaling pathway.	clopidogrel	44-55	mitogen-activated protein kinase 14	Homo sapiens	145-148
32509173-10	2020	Overexpression of MKP-5 reverses Clopidogrel-induced gastric mucosal injury.	clopidogrel	33-44	dual specificity phosphatase 10	Homo sapiens	18-23
32509173-11	2020	These findings imply that MKP-5 may be a potential therapeutic target in Clopidogrel-induced gastric mucosal injury and bleeding.	clopidogrel	73-84	dual specificity phosphatase 10	Homo sapiens	26-31
32266041-12	2020	Efficacy of clopidogrel was reduced in patients with very slow CYP2C19 genotype while bleeding complications were higher in patients with fast CYP2C19 genotype receiving ticagrelor.	clopidogrel	12-23	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	63-70
32587571-2	2020	However, with varied clopidogrel resistance (often due to CYP2C19 loss-of-function (LOF) alleles), alternatives like ticagrelor have been suggested.	clopidogrel	21-32	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	58-65
32266017-3	2020	Thus, a meta-analysis was conducted to assess the risk of PPB rate in patients on continued clopidogrel therapy.	clopidogrel	92-103	histatin 1	Homo sapiens	58-61
32266017-4	2020	Systemically identified publications were used to compare the rate of PPB in patients on continued clopidogrel therapy with those who had interrupted clopidogrel therapy.	clopidogrel	99-110	histatin 1	Homo sapiens	70-73
32266017-10	2020	There was an increased risk of PPB with continued clopidogrel [P=0.0003; risk ratio (RR), 1.96; 95% confidence interval (CI), 1.36-2.83).	clopidogrel	50-61	histatin 1	Homo sapiens	31-34
32266017-12	2020	The rate of delayed PPB was increased in the continued clopidogrel group (P=0.0008; RR, 3.10; 95%CI, 1.60-5.98).	clopidogrel	55-66	histatin 1	Homo sapiens	20-23
32124868-8	2020	DAPT was applied during 72.12% of interventions: in 49.68% of interventions, the purinergic signaling receptor Y12 (P2Y12) inhibitor used was clopidogrel and in 25.14% of interventions ticagrelor was used (P<0.001).	clopidogrel	142-153	purinergic receptor P2Y12	Homo sapiens	116-121
32334703-19	2020	Clopidogrel could be an alternative P2Y12 inhibitor especially for elderly patients with a higher bleeding risk.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	36-41
32029306-0	2020	Pharmacodynamic study of prasugrel or clopidogrel in non-ST-elevation acute coronary syndrome with CYP2C19 genetic variants undergoing percutaneous coronary intervention (PRAISE-GENE trial).	clopidogrel	38-49	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	99-106
32029306-1	2020	BACKGROUND: The CYP2C19*2 or *3 loss-of-function (LOF) allele is associated with high platelet reactivity (HPR) on clopidogrel treatment.	clopidogrel	115-126	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
32061670-9	2020	Clopidogrel and prasugrel groups showed enhanced BCL2 expression in cardiac fibers and aortic wall.	clopidogrel	0-11	BCL2, apoptosis regulator	Rattus norvegicus	49-53
32140798-1	2020	PURPOSE: To compare the risk of cardiovascular events between patients with two CYP2C19 loss-of-function alleles who were prescribed ticagrelor or clopidogrel after percutaneous coronary intervention (PCI).	clopidogrel	147-158	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	80-87
33224237-0	2020	Association of ABCB1 Gene Polymorphisms and Clopidogrel Responsiveness in Iranian Patients undergoing Percutaneous Coronary Intervention.	clopidogrel	44-55	ATP binding cassette subfamily B member 1	Homo sapiens	15-20
33224237-3	2020	The present study was designed to investigate the potential association of ABCB1 (ATP-Binding Cassette, Subfamily B, member1) gene polymorphism, and clopidogrel responsiveness in Iranian patients after PCI.	clopidogrel	149-160	ATP binding cassette subfamily B member 1	Homo sapiens	75-80
33224237-3	2020	The present study was designed to investigate the potential association of ABCB1 (ATP-Binding Cassette, Subfamily B, member1) gene polymorphism, and clopidogrel responsiveness in Iranian patients after PCI.	clopidogrel	149-160	ATP binding cassette subfamily B member 1	Homo sapiens	82-124
32256366-0	2020	P2Y12 Receptor Antagonist Clopidogrel Attenuates Lung Inflammation Triggered by Silica Particles.	clopidogrel	26-37	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	0-5
32089086-9	2020	Neutrophil depletion or inhibition of the release of neutrophil extracellular traps had little effects, but platelet P2Y12 receptor antagonism with clopidogrel, fibrinolysis with urokinase or DNA digestion with recombinant DNase I all prevented arterial occlusions, GFR loss, and kidney infarction.	clopidogrel	148-159	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	117-122
32206324-2	2020	It has been suggested that the concomitant use of repaglinide with clopidogrel may inhibit repaglinide metabolism, because repaglinide is a substrate of cytochrome P450 2C8 (CYP2C8) and the main metabolite of clopidogrel acyl-beta-D-glucuronide inhibits CYP2C8 activity.	clopidogrel	67-78	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	153-172
32206324-2	2020	It has been suggested that the concomitant use of repaglinide with clopidogrel may inhibit repaglinide metabolism, because repaglinide is a substrate of cytochrome P450 2C8 (CYP2C8) and the main metabolite of clopidogrel acyl-beta-D-glucuronide inhibits CYP2C8 activity.	clopidogrel	67-78	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	174-180
32206324-2	2020	It has been suggested that the concomitant use of repaglinide with clopidogrel may inhibit repaglinide metabolism, because repaglinide is a substrate of cytochrome P450 2C8 (CYP2C8) and the main metabolite of clopidogrel acyl-beta-D-glucuronide inhibits CYP2C8 activity.	clopidogrel	67-78	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	254-260
32183711-8	2020	Compared to the clopidogrel group, third-generation oral P2Y12 inhibitors were associated with an increased risk of dyspnea compared with clopidogrel (RR 2.15, 95% CI 1.59-2.92), which was consistent in the analysis of ticagrelor (RR 2.65, 95% CI 1.87-3.76).	clopidogrel	16-27	purinergic receptor P2Y12	Homo sapiens	57-62
32001263-0	2020	Coding SNPs in hsa-miR-1343-3p and hsa-miR-6783-3p target sites of CYP2C19 modulates clopidogrel response in individuals with cardiovascular diseases.	clopidogrel	85-96	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	67-74
32001263-11	2020	Out of 13 mirSNP"s analyzed, CYP2C19 rs4244285 was associated with clopidogrel drug resistance and clopidogrel carboxylic acid metabolite in urine and plasma.	clopidogrel	67-78	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	29-36
32001263-11	2020	Out of 13 mirSNP"s analyzed, CYP2C19 rs4244285 was associated with clopidogrel drug resistance and clopidogrel carboxylic acid metabolite in urine and plasma.	clopidogrel	99-110	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	29-36
32001263-13	2020	SIGNIFICANCE: We demonstrated the role of coding mirSNP (rs4244285) in the regulation of the CYP2C19 gene through miRNAs and its implications to clopidogrel drug response prediction in the Indian population.	clopidogrel	145-156	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	93-100
32139218-1	2020	OBJECTIVES: The aim of this study was to develop a risk score integrating cytochrome P450 2C19 loss-of-function genotypes with clinical risk factors influencing clopidogrel response that would allow the identification with more precision of subjects at risk for high platelet reactivity (HPR) and adverse clinical outcomes.	clopidogrel	161-172	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	74-94
32139218-2	2020	BACKGROUND: Clopidogrel is the most broadly used platelet P2Y12 inhibitor.	clopidogrel	12-23	purinergic receptor P2Y12	Homo sapiens	58-63
32139218-4	2020	Although carriers of loss-of-function alleles of the cytochrome P450 2C19 enzyme have reduced clopidogrel metabolism leading to increased rates of HPR and thrombotic complications, this explains only a fraction of the pharmacodynamic response to clopidogrel, and a number of clinical factors have also been shown to have contributing roles.	clopidogrel	94-105	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-73
32139218-4	2020	Although carriers of loss-of-function alleles of the cytochrome P450 2C19 enzyme have reduced clopidogrel metabolism leading to increased rates of HPR and thrombotic complications, this explains only a fraction of the pharmacodynamic response to clopidogrel, and a number of clinical factors have also been shown to have contributing roles.	clopidogrel	246-257	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-73
32139220-2	2020	BACKGROUND: Response to clopidogrel differs widely among patients, notably because of CYP2C19 genetic polymorphisms.	clopidogrel	24-35	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	86-93
31957972-11	2020	CONCLUSIONS: In STEMI patients with HPR, identified by vasodilator stimulated phosphoprotein (VASP)-determined PFT, switching clopidogrel to ticagrelor could significantly improve 1-year clinical outcomes without increasing the risk of bleeding.	clopidogrel	126-137	vasodilator stimulated phosphoprotein	Homo sapiens	55-92
32186937-5	2020	Results: The developed methods demonstrated limits of detection ranging from 0.67 to 1.09 mug/ml-1 for CPS and 0.49 to 0.71 mug.ml-1 for ASP.	clopidogrel	103-106	interleukin 17F	Homo sapiens	94-98
32100736-4	2020	Indeed, pharmacodynamic and pharmacokinetic studies suggested an interaction through CYP2C19 between PPIs and clopidogrel, which could translate into clinical inefficacy, leading to higher rates of cardiovascular events.	clopidogrel	110-121	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	85-92
31039046-0	2020	Inhibition of carboxylesterase-1 alters clopidogrel metabolism and disposition.	clopidogrel	40-51	carboxylesterase 1	Homo sapiens	14-32
31039046-2	2020	Most research has focused on the role of hepatic CYP450 metabolism as the primary source of response variability despite 85-90% of clopidogrel being hydrolyzed by human carboxylesterase-1 (CES1).	clopidogrel	131-142	carboxylesterase 1	Homo sapiens	169-187
31039046-2	2020	Most research has focused on the role of hepatic CYP450 metabolism as the primary source of response variability despite 85-90% of clopidogrel being hydrolyzed by human carboxylesterase-1 (CES1).	clopidogrel	131-142	carboxylesterase 1	Homo sapiens	189-193
31039046-3	2020	The purpose of this study is to determine the effects of the known CES1 inhibitor alcohol on clopidogrel metabolism: (1) in vitro in human recombinant CES1 and human liver S9 (HLS9) fractions and (2) in a plasma carboxylesterase deficient mouse (Es1e) strain administered 25 mg/kg oral clopidogrel alone and with 3 g/kg alcohol.	clopidogrel	93-104	carboxylesterase 1	Homo sapiens	67-71
31039046-3	2020	The purpose of this study is to determine the effects of the known CES1 inhibitor alcohol on clopidogrel metabolism: (1) in vitro in human recombinant CES1 and human liver S9 (HLS9) fractions and (2) in a plasma carboxylesterase deficient mouse (Es1e) strain administered 25 mg/kg oral clopidogrel alone and with 3 g/kg alcohol.	clopidogrel	286-297	carboxylesterase 1	Homo sapiens	67-71
31039046-7	2020	Clopidogrel metabolism is highly sensitive to alterations in CES1 activity.	clopidogrel	0-11	carboxylesterase 1	Homo sapiens	61-65
32109992-10	2020	Conclusion: Increased dose of clopidogrel may reduce the risk of ISR after PCI in CYP2C19 LOF allele(s) carriers.	clopidogrel	30-41	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	82-89
32109992-11	2020	The presence of CYP2C19 LOF allele(s) increases the risk of ISR after stenting, which could be counteracted by the increased dose of clopidogrel.	clopidogrel	133-144	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
32067582-10	2020	With the availability of new P2Y12 inhibitors, a deeper platelet inhibition (46+-17%) and similar survival to the optimal platelet reactivity group were achieved in patients with HPR on clopidogrel therapy after escalation.	clopidogrel	186-197	purinergic receptor P2Y12	Homo sapiens	29-34
31735472-7	2020	Further study demonstrated that XQ-1H combined with clopidogrel lessened TUNEL positive cells, up-regulated bcl-2 expression notably and down-regulated bax expression as compared to both XQ-1H and clopidogrel individually.	clopidogrel	52-63	BCL2, apoptosis regulator	Rattus norvegicus	108-113
31735472-7	2020	Further study demonstrated that XQ-1H combined with clopidogrel lessened TUNEL positive cells, up-regulated bcl-2 expression notably and down-regulated bax expression as compared to both XQ-1H and clopidogrel individually.	clopidogrel	52-63	BCL2 associated X, apoptosis regulator	Rattus norvegicus	152-155
32176040-0	2020	The correlation between recurrent risk and CYP2C19 gene polymorphisms in patients with ischemic stroke treated with clopidogrel for prevention.	clopidogrel	116-127	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	43-50
32176040-1	2020	BACKGROUND: To explore the correlation between recurrent risk and CYP2C19 gene polymorphisms in patients with ischemic stroke (IS) treated with clopidogrel for prevention.	clopidogrel	144-155	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	66-73
32176040-3	2020	The correlation between CYP2C19 gene polymorphism and stroke recurrence in patients taking clopidogrel regularly was analyzed.	clopidogrel	91-102	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
32106619-6	2020	In patients treated with ticagrelor or clopidogrel, we observed a negative correlation among changes in both SIRT1 and HES1 mRNA and serum levels of Epidermal Growth Factor (EGF), a marker of endothelial dysfunction found to be reduced by ticagrelor treatment in our previous study.	clopidogrel	39-50	sirtuin 1	Homo sapiens	109-114
32106619-6	2020	In patients treated with ticagrelor or clopidogrel, we observed a negative correlation among changes in both SIRT1 and HES1 mRNA and serum levels of Epidermal Growth Factor (EGF), a marker of endothelial dysfunction found to be reduced by ticagrelor treatment in our previous study.	clopidogrel	39-50	hes family bHLH transcription factor 1	Homo sapiens	119-123
32106619-6	2020	In patients treated with ticagrelor or clopidogrel, we observed a negative correlation among changes in both SIRT1 and HES1 mRNA and serum levels of Epidermal Growth Factor (EGF), a marker of endothelial dysfunction found to be reduced by ticagrelor treatment in our previous study.	clopidogrel	39-50	epidermal growth factor	Homo sapiens	149-172
32106619-6	2020	In patients treated with ticagrelor or clopidogrel, we observed a negative correlation among changes in both SIRT1 and HES1 mRNA and serum levels of Epidermal Growth Factor (EGF), a marker of endothelial dysfunction found to be reduced by ticagrelor treatment in our previous study.	clopidogrel	39-50	epidermal growth factor	Homo sapiens	174-177
31957972-11	2020	CONCLUSIONS: In STEMI patients with HPR, identified by vasodilator stimulated phosphoprotein (VASP)-determined PFT, switching clopidogrel to ticagrelor could significantly improve 1-year clinical outcomes without increasing the risk of bleeding.	clopidogrel	126-137	vasodilator stimulated phosphoprotein	Homo sapiens	94-98
32461931-0	2020	Comparison of Efficacy between Clopidogrel and Ticagrelor in Patients with Acute Coronary Syndrome after Interventional Treatment and Their Effects on IL-6.	clopidogrel	31-42	interleukin 6	Homo sapiens	151-155
32461931-1	2020	Background: We aimed to compare the efficacy between clopidogrel and ticagrelor in patients with acute coronary syndrome (ACS) after percutaneous coronary intervention (PCI) and their effects on IL-6.	clopidogrel	53-64	interleukin 6	Homo sapiens	195-199
32023226-0	2020	Impact of Continuous P2Y12 Inhibition Tailoring in Acute Coronary Syndrome and Genetically Impaired Clopidogrel Absorption.	clopidogrel	100-111	purinergic receptor P2Y12	Homo sapiens	21-26
32023226-1	2020	Clopidogrel is still widely used in acute coronary syndrome despite the development of more potent P2Y12 inhibitors.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	99-104
31764002-7	2020	The mechanism by which a thrombin-like enzyme VLCV (thrombin-like enzyme)-induced platelet aggregation was explored in presence of ticlopidin, clopidogrel and aspirin.	clopidogrel	143-154	coagulation factor II, thrombin	Homo sapiens	25-33
31981452-6	2020	Platelet antiaggregation point for clopidogrel was measured using VerifyNow P2Y12.	clopidogrel	35-46	purinergic receptor P2Y12	Homo sapiens	76-81
31981452-13	2020	The hypothesis that omeprazole may reduce the antiaggregation effect of clopidogrel as shown by the increase in PRU above the cutoff points >208 PRU (HPR) was not proven.	clopidogrel	72-83	haptoglobin-related protein	Homo sapiens	150-153
32158254-0	2020	CYP2C19*17 May Increase the Risk of Death Among Patients with an Acute Coronary Syndrome and Non-Valvular Atrial Fibrillation Who Receive Clopidogrel and Rivaroxaban.	clopidogrel	138-149	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
32158254-6	2020	Conclusion: In situations of double or triple antithrombotic rivaroxaban and clopidogrel therapy among patients with atrial fibrillation and acute coronary syndrome, the genetic factors associated with bleeding complications risk (CYP2C19*17) may prove to be clinically relevant.	clopidogrel	77-88	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	231-238
31764002-7	2020	The mechanism by which a thrombin-like enzyme VLCV (thrombin-like enzyme)-induced platelet aggregation was explored in presence of ticlopidin, clopidogrel and aspirin.	clopidogrel	143-154	coagulation factor II, thrombin	Homo sapiens	52-60
32736893-0	2020	Effect of clopidogrel vs. aspirin on pro-atherosclerotic NLRP1 inflammasome expression in endothelial cells.	clopidogrel	10-21	NLR family pyrin domain containing 1	Homo sapiens	57-62
31511896-9	2020	At Cox multivariable analysis, potent P2Y12 inhibitors significantly reduced the mortality rate (HR 0.82, 95% CI 0.54-0.96, p = 0.006) and the risk of reinfarction (HR 0.53, 95% CI 0.30-0.95, p = 0.033) in CKD patients as compared to clopidogrel.	clopidogrel	234-245	purinergic receptor P2Y12	Homo sapiens	38-43
33115391-3	2020	CYP2C19 metabolizes very important drug such as antiulcer drug omeprazole, the antiplatelet drug clopidogrel and anticonvulsant mephenytoin.	clopidogrel	97-108	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
31468659-9	2020	The effect of aleglitazar compared to placebo on HbA1c, hemoglobin, serum creatinine and adiponectin was modified by concomitant clopidogrel use (p for interaction 0.007, 0.002, &lt;0.001 and &lt;0.001 respectively).	clopidogrel	129-140	adiponectin, C1Q and collagen domain containing	Homo sapiens	89-100
31468659-11	2020	Patients using clopidogrel demonstrated an additional lowering of HbA1c, at the expense of an additional decrease in hemoglobin and increase in serum creatinine and adiponectin.	clopidogrel	15-26	adiponectin, C1Q and collagen domain containing	Homo sapiens	165-176
31468659-12	2020	Clopidogrel is a moderate inhibitor of CYP2C8.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	39-45
31643039-11	2020	CYP2C19 polymorphisms may have reduced clopidogrel-induced IPA.	clopidogrel	39-50	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
31726963-2	2020	We aimed to determine whether the efficacy of clopidogrel-aspirin therapy among patients with minor stroke / transient ischemic attack was influenced by the stratification of CYP2C19 genotype and body mass index (BMI).	clopidogrel	46-57	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	175-182
31726963-9	2020	Our study suggests that BMI significantly influences the correlation between CYP2C19 genotype and efficacy of clopidogrel-aspirin therapy.	clopidogrel	110-121	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	77-84
31778598-5	2019	OBJECTIVES: The aim of the study was to assess the incidence of polymorphisms of the ABCB1 and CYPC19 genes that encode proteins involved in the absorption and metabolism of clopidogrel.	clopidogrel	174-185	ATP binding cassette subfamily B member 1	Homo sapiens	85-90
31888640-0	2019	Ticagrelor and clopidogrel suppress NF-kappaB signaling pathway to alleviate LPS-induced dysfunction in vein endothelial cells.	clopidogrel	15-26	nuclear factor kappa B subunit 1	Homo sapiens	36-45
31888640-3	2019	Thus, we suspected that ticagrelor and clopidogrel are involved in the regulation of the NF-KappaB signaling pathway.	clopidogrel	39-50	nuclear factor kappa B subunit 1	Homo sapiens	89-98
31888640-7	2019	RESULTS: Ticagrelor and clopidogrel can inhibit the degradation of IKBalpha and phosphorylation of p65, prevent p65 from entering the nucleus, reduce the production of TNFalpha, IL-1, IL-8, IL-6 and IL-2, and alleviate the decrease in cell viability, cell migration and angiogenesis, the changes of cell cycle and apoptosis induced by LPS.	clopidogrel	24-35	NFKB inhibitor alpha	Homo sapiens	67-75
31888640-7	2019	RESULTS: Ticagrelor and clopidogrel can inhibit the degradation of IKBalpha and phosphorylation of p65, prevent p65 from entering the nucleus, reduce the production of TNFalpha, IL-1, IL-8, IL-6 and IL-2, and alleviate the decrease in cell viability, cell migration and angiogenesis, the changes of cell cycle and apoptosis induced by LPS.	clopidogrel	24-35	RELA proto-oncogene, NF-kB subunit	Homo sapiens	99-102
31888640-7	2019	RESULTS: Ticagrelor and clopidogrel can inhibit the degradation of IKBalpha and phosphorylation of p65, prevent p65 from entering the nucleus, reduce the production of TNFalpha, IL-1, IL-8, IL-6 and IL-2, and alleviate the decrease in cell viability, cell migration and angiogenesis, the changes of cell cycle and apoptosis induced by LPS.	clopidogrel	24-35	RELA proto-oncogene, NF-kB subunit	Homo sapiens	112-115
31888640-7	2019	RESULTS: Ticagrelor and clopidogrel can inhibit the degradation of IKBalpha and phosphorylation of p65, prevent p65 from entering the nucleus, reduce the production of TNFalpha, IL-1, IL-8, IL-6 and IL-2, and alleviate the decrease in cell viability, cell migration and angiogenesis, the changes of cell cycle and apoptosis induced by LPS.	clopidogrel	24-35	tumor necrosis factor	Homo sapiens	168-176
31888640-7	2019	RESULTS: Ticagrelor and clopidogrel can inhibit the degradation of IKBalpha and phosphorylation of p65, prevent p65 from entering the nucleus, reduce the production of TNFalpha, IL-1, IL-8, IL-6 and IL-2, and alleviate the decrease in cell viability, cell migration and angiogenesis, the changes of cell cycle and apoptosis induced by LPS.	clopidogrel	24-35	interleukin 1 alpha	Homo sapiens	178-182
31888640-7	2019	RESULTS: Ticagrelor and clopidogrel can inhibit the degradation of IKBalpha and phosphorylation of p65, prevent p65 from entering the nucleus, reduce the production of TNFalpha, IL-1, IL-8, IL-6 and IL-2, and alleviate the decrease in cell viability, cell migration and angiogenesis, the changes of cell cycle and apoptosis induced by LPS.	clopidogrel	24-35	C-X-C motif chemokine ligand 8	Homo sapiens	184-188
31888640-7	2019	RESULTS: Ticagrelor and clopidogrel can inhibit the degradation of IKBalpha and phosphorylation of p65, prevent p65 from entering the nucleus, reduce the production of TNFalpha, IL-1, IL-8, IL-6 and IL-2, and alleviate the decrease in cell viability, cell migration and angiogenesis, the changes of cell cycle and apoptosis induced by LPS.	clopidogrel	24-35	interleukin 6	Homo sapiens	190-194
31888640-7	2019	RESULTS: Ticagrelor and clopidogrel can inhibit the degradation of IKBalpha and phosphorylation of p65, prevent p65 from entering the nucleus, reduce the production of TNFalpha, IL-1, IL-8, IL-6 and IL-2, and alleviate the decrease in cell viability, cell migration and angiogenesis, the changes of cell cycle and apoptosis induced by LPS.	clopidogrel	24-35	interleukin 2	Homo sapiens	199-203
31888640-8	2019	CONCLUSIONS: Ticagrelor and clopidogrel alleviate cellular dysfunction through suppressing NF-KappaB signaling pathway.	clopidogrel	28-39	nuclear factor kappa B subunit 1	Homo sapiens	91-100
30873882-2	2019	Variants in the CYP2C19 gene influence the clinical response of clopidogrel.	clopidogrel	64-75	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
30873882-11	2019	This method provides a new way in the clinical application of CYP2C19 genotyping to guide the clopidogrel medication.	clopidogrel	94-105	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	62-69
31722730-13	2019	MRS2395 and clopidogrel attenuated the development of tactile allodynia and suppressed the expression of CGRP, c-fos, and GTP-RhoA/ROCK2 in the TNC.	clopidogrel	12-23	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	105-109
30916611-0	2019	Comparison between MassARRAY and pyrosequencing for CYP2C19 and ABCB1 gene variants of clopidogrel efficiency genotyping.	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	52-59
30916611-0	2019	Comparison between MassARRAY and pyrosequencing for CYP2C19 and ABCB1 gene variants of clopidogrel efficiency genotyping.	clopidogrel	87-98	ATP binding cassette subfamily B member 1	Homo sapiens	64-69
31062487-4	2019	Preprocedure clopidogrel load >=300 mg or maintenance P2Y12 inhibitor therapy defined preprocedural P2Y12 inhibition.	clopidogrel	13-24	purinergic receptor P2Y12	Homo sapiens	100-105
31722730-13	2019	MRS2395 and clopidogrel attenuated the development of tactile allodynia and suppressed the expression of CGRP, c-fos, and GTP-RhoA/ROCK2 in the TNC.	clopidogrel	12-23	FBJ osteosarcoma oncogene	Mus musculus	111-116
31722730-13	2019	MRS2395 and clopidogrel attenuated the development of tactile allodynia and suppressed the expression of CGRP, c-fos, and GTP-RhoA/ROCK2 in the TNC.	clopidogrel	12-23	ras homolog family member A	Mus musculus	126-130
31722730-13	2019	MRS2395 and clopidogrel attenuated the development of tactile allodynia and suppressed the expression of CGRP, c-fos, and GTP-RhoA/ROCK2 in the TNC.	clopidogrel	12-23	Rho-associated coiled-coil containing protein kinase 2	Mus musculus	131-136
30834895-1	2019	AIMS: Clopidogrel is the P2Y12 inhibitor of choice in patients who undergo PCI and have an indication for oral anticoagulation (OAC).	clopidogrel	6-17	purinergic receptor P2Y12	Homo sapiens	25-30
31418753-4	2019	The smoker"s paradox may be due to enhanced platelet response to clopidogrel therapy in active smokers as compared with nonsmokers caused by hepatic cytochrome P450 activation resulting in an increased generation of clopidogrel active metabolite.	clopidogrel	65-76	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	149-164
31418753-4	2019	The smoker"s paradox may be due to enhanced platelet response to clopidogrel therapy in active smokers as compared with nonsmokers caused by hepatic cytochrome P450 activation resulting in an increased generation of clopidogrel active metabolite.	clopidogrel	216-227	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	149-164
32159124-10	2019	Use of P2Y12 inhibitors was higher in patients who underwent PCI (primarily ticagrelor) compared with patients who underwent CABG (primarily clopidogrel) (99% vs 26%, P < 0.01).	clopidogrel	141-152	purinergic receptor P2Y12	Homo sapiens	7-12
31367811-11	2019	CONCLUSION: Cost-effective strategies to personalize P2Y12 inhibition in ACS include clopidogrel +phenotype and genotype + liberal ticagrelor.	clopidogrel	85-96	purinergic receptor P2Y12	Homo sapiens	53-58
31267433-4	2019	A low response to aspirin and clopidogrel was defined in terms of aspirin reaction units > 550 and P2Y12 reaction units >= 230, respectively, by VerifyNow assay.	clopidogrel	30-41	purinergic receptor P2Y12	Homo sapiens	99-104
31267433-8	2019	The mean P2Y12 reaction unit was 220.0 +- 64.4 in the lansoprazole group, and 174.5 +- 65.0 in the esomeprazole group; there was a significant difference in the clopidogrel response of patient treated with lansoprazole or esomeprazole (p = 0.005).	clopidogrel	161-172	purinergic receptor P2Y12	Homo sapiens	9-14
30993551-1	2019	BACKGROUND AND OBJECTIVES: A recent report indicated that the pharmacodynamic interaction between clopidogrel and vonoprazan leading to attenuation of the anti-platelet effect of clopidogrel was unlikely to be caused by the inhibition of cytochrome P450 (CYP) 2B6, CYP2C19, or CYP3A4/5 by vonoprazan, based on in vitro CYP inhibition data.	clopidogrel	98-109	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	238-263
30993551-1	2019	BACKGROUND AND OBJECTIVES: A recent report indicated that the pharmacodynamic interaction between clopidogrel and vonoprazan leading to attenuation of the anti-platelet effect of clopidogrel was unlikely to be caused by the inhibition of cytochrome P450 (CYP) 2B6, CYP2C19, or CYP3A4/5 by vonoprazan, based on in vitro CYP inhibition data.	clopidogrel	98-109	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	265-272
30993551-1	2019	BACKGROUND AND OBJECTIVES: A recent report indicated that the pharmacodynamic interaction between clopidogrel and vonoprazan leading to attenuation of the anti-platelet effect of clopidogrel was unlikely to be caused by the inhibition of cytochrome P450 (CYP) 2B6, CYP2C19, or CYP3A4/5 by vonoprazan, based on in vitro CYP inhibition data.	clopidogrel	98-109	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	277-285
31445718-2	2019	The oral P2Y12 inhibitors comprise clopidogrel, prasugrel, and ticagrelor.	clopidogrel	35-46	purinergic receptor P2Y12	Homo sapiens	9-14
31385867-0	2019	CYP2C19 loss-of-function alleles: A common but overlooked problem associated with clopidogrel resistance.	clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
30169782-0	2019	Precision of VerifyNow P2Y12 Assessment of Clopidogrel Response in Patients Undergoing Cerebral Aneurysm Flow Diversion.	clopidogrel	43-54	purinergic receptor P2Y12	Homo sapiens	23-28
30169782-3	2019	OBJECTIVE: To investigate the real-world precision of VerifyNow P2Y12 assessment (Accumetrics, San Diego, California) of Clopidogrel response.	clopidogrel	121-132	purinergic receptor P2Y12	Homo sapiens	64-69
31560647-0	2019	Effects of the rs2244613 polymorphism of the CES1 gene on the antiplatelet effect of the receptor P2Y12 blocker clopidogrel.	clopidogrel	112-123	carboxylesterase 1	Homo sapiens	45-49
31560647-0	2019	Effects of the rs2244613 polymorphism of the CES1 gene on the antiplatelet effect of the receptor P2Y12 blocker clopidogrel.	clopidogrel	112-123	purinergic receptor P2Y12	Homo sapiens	98-103
31560647-1	2019	Background The aim of this study was to evaluate the association of the carriage of the rs2244613 polymorphism of the CES1 gene with clopidogrel resistance as well as to evaluate the effectiveness of antiplatelet therapy in the carriers of this marker who have had acute coronary syndrome (ACS).	clopidogrel	133-144	carboxylesterase 1	Homo sapiens	118-122
31632514-8	2019	According to LTA, VASP assay and CD62P test results, 65%, 71% and 0% of patients, respectively, had a low response to clopidogrel, indicating poor agreement between these assays.	clopidogrel	118-129	vasodilator stimulated phosphoprotein	Homo sapiens	18-22
31632514-8	2019	According to LTA, VASP assay and CD62P test results, 65%, 71% and 0% of patients, respectively, had a low response to clopidogrel, indicating poor agreement between these assays.	clopidogrel	118-129	selectin P	Homo sapiens	33-38
31242837-1	2019	BACKGROUND: Dual antiplatelet therapy (DAPT) with aspirin and one of inhibitors of P2Y12 receptors (clopidogrel, ticagrelor, prasugrel) is an international standard of receptors (clopidogrel, ticagrelor, prasugrel) is an international standard of is an international standard of treatment strategy in patients with acute coronary syndrome (ACS).	clopidogrel	179-190	purinergic receptor P2Y12	Homo sapiens	83-88
30828769-1	2019	BACKGROUND: The newer P2Y12 inhibitors have better efficacy than clopidogrel.	clopidogrel	65-76	p2y12	None	22-27
31372962-10	2019	MAthrombin and fibrinogen were meaningful mediators for the significant positive association of the number of narrowed vessels and HRPR on clopidogrel, which were enhanced by around 30% and 43%, respectively, for this effect.	clopidogrel	139-150	fibrinogen beta chain	Homo sapiens	15-25
31237713-0	2019	Efficacy of clopidogrel for stroke depends on CYP2C19 genotype and risk profile.	clopidogrel	12-23	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	46-53
31237713-11	2019	The benefit of clopidogrel in Chinese MS/TIA patients depends on CYP2C19 genotype and risk profile.	clopidogrel	15-26	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	65-72
30922852-5	2019	The nucleoside analogue ticagrelor and active metabolites of the thienopyridine compounds ticlopidine, clopidogrel and prasugrel inhibit platelet P2Y12 receptors and reduce thereby platelet aggregation.	clopidogrel	103-114	purinergic receptor P2Y12	Homo sapiens	146-151
28403626-10	2019	In patients with ACS treated with aspirin and clopidogrel, residual platelet aggregation was significantly reduced 20 min after intravenous bolus of 1 mg/kg pegnivacogin (100% versus 43.21+-8.23%, p=0.020).	clopidogrel	46-57	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	17-20
30974489-2	2019	However, whether it influences the association between CYP2C19 genetic variants and clopidogrel efficacy is not clear.	clopidogrel	84-95	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	55-62
30974489-4	2019	The Cox proportional risk regression model was used to evaluate the interactions between CYP2C19*2 and CYP2C19*3 carrier status and clopidogrel efficacy stratified by smoking status.	clopidogrel	132-143	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	89-96
30974489-9	2019	CONCLUSIONS: Amongst patients with minor stroke or transient ischaemic attack, marginal significant interactions between CYP2C19*2 and CYP2C19*3 allele carrier status and clopidogrel efficacy were found in smokers but not in non-smokers.	clopidogrel	171-182	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	121-128
30974489-9	2019	CONCLUSIONS: Amongst patients with minor stroke or transient ischaemic attack, marginal significant interactions between CYP2C19*2 and CYP2C19*3 allele carrier status and clopidogrel efficacy were found in smokers but not in non-smokers.	clopidogrel	171-182	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	135-142
31395432-0	2019	CYP2C19 Polymorphism is Associated With Amputation Rates in Patients Taking Clopidogrel After Endovascular Intervention for Critical Limb Ischaemia.	clopidogrel	76-87	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
31395432-1	2019	OBJECTIVE: Clopidogrel is a pro-drug requiring cytochrome P450 (CYP) 2C19 enzyme to be oxidised to its active form.	clopidogrel	11-22	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	47-73
31395432-2	2019	This study evaluated the association between the CYP 2C19 genetic polymorphism and clinical outcomes in patients with critical limb ischaemia (CLI) taking clopidogrel after endovascular therapy (EVT).	clopidogrel	155-166	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	49-57
31395432-11	2019	Carriers of at least one CYP2C19 LOF allele (44.9%, 125/278) had diminished pharmacodynamic responses to clopidogrel as measured using VerifyNow (174 +- 27 platelet reactivity units (PRU), 216 +- 21 PRU, and 245 +- 35 PRU for patients with EM, IM, and PM CYP2C19 profiles, respectively; EM vs. IM, p &lt; .0001 and EM vs. PM, p &lt; .0001).	clopidogrel	105-116	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
31395432-15	2019	CONCLUSION: CYP2C19 genetic profiles can significantly influence clinical outcomes (in both amputation free survival and all cause mortality) in CLI patients who are taking only clopidogrel after EVT.	clopidogrel	178-189	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
31175950-1	2019	Human carboxylesterase 1 (CES1), primarily expressed in the liver and adipocytes, is responsible for the hydrolysis of endogenous esters (such as cholesteryl esters and triacylglycerols) and the metabolism of xenobiotic esters (such as clopidogrel and oseltamivir), thus participates in physiological and pathological processes.	clopidogrel	236-247	carboxylesterase 1	Homo sapiens	6-24
31175950-1	2019	Human carboxylesterase 1 (CES1), primarily expressed in the liver and adipocytes, is responsible for the hydrolysis of endogenous esters (such as cholesteryl esters and triacylglycerols) and the metabolism of xenobiotic esters (such as clopidogrel and oseltamivir), thus participates in physiological and pathological processes.	clopidogrel	236-247	carboxylesterase 1	Homo sapiens	26-30
31387163-5	2019	Clopidogrel resistance was defined as P2Y12 inhibition &lt;40%.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	38-43
31484595-0	2019	The activation of high mobility group Box1 and toll-like receptor 4 is involved in clopidogrel-induced gastric injury through p38 MAPK.	clopidogrel	83-94	toll like receptor 4	Homo sapiens	47-67
31484595-0	2019	The activation of high mobility group Box1 and toll-like receptor 4 is involved in clopidogrel-induced gastric injury through p38 MAPK.	clopidogrel	83-94	mitogen-activated protein kinase 14	Homo sapiens	126-129
31484595-3	2019	This study aimed to investigate the role of high mobility group box protein 1 (HMGB1) and the toll-like receptor 4 (TLR4) pathway in normal human gastric epithelial (GES-1) cells under clopidogrel exposure.	clopidogrel	185-196	high mobility group box 1	Homo sapiens	44-77
31484595-3	2019	This study aimed to investigate the role of high mobility group box protein 1 (HMGB1) and the toll-like receptor 4 (TLR4) pathway in normal human gastric epithelial (GES-1) cells under clopidogrel exposure.	clopidogrel	185-196	high mobility group box 1	Homo sapiens	79-84
31484595-3	2019	This study aimed to investigate the role of high mobility group box protein 1 (HMGB1) and the toll-like receptor 4 (TLR4) pathway in normal human gastric epithelial (GES-1) cells under clopidogrel exposure.	clopidogrel	185-196	toll like receptor 4	Homo sapiens	94-114
31484595-3	2019	This study aimed to investigate the role of high mobility group box protein 1 (HMGB1) and the toll-like receptor 4 (TLR4) pathway in normal human gastric epithelial (GES-1) cells under clopidogrel exposure.	clopidogrel	185-196	toll like receptor 4	Homo sapiens	116-120
31484595-5	2019	A laser scanning confocal microscope was used to determine the distribution of HMGB1 and TLR4 in clopidogrel-induced injury.	clopidogrel	97-108	high mobility group box 1	Homo sapiens	79-84
31484595-5	2019	A laser scanning confocal microscope was used to determine the distribution of HMGB1 and TLR4 in clopidogrel-induced injury.	clopidogrel	97-108	toll like receptor 4	Homo sapiens	89-93
31484595-8	2019	We found the expression of HMGB1 and TLR4 in the cytoplasm increased after clopidogrel administration.	clopidogrel	75-86	high mobility group box 1	Homo sapiens	27-32
31484595-8	2019	We found the expression of HMGB1 and TLR4 in the cytoplasm increased after clopidogrel administration.	clopidogrel	75-86	toll like receptor 4	Homo sapiens	37-41
31484595-9	2019	Besides, inhibited TLR4, which is a receptor of HMGB1, prevented the injury and occludin reducing caused by clopidogrel challenge.	clopidogrel	108-119	toll like receptor 4	Homo sapiens	19-23
31484595-9	2019	Besides, inhibited TLR4, which is a receptor of HMGB1, prevented the injury and occludin reducing caused by clopidogrel challenge.	clopidogrel	108-119	high mobility group box 1	Homo sapiens	48-53
31484595-9	2019	Besides, inhibited TLR4, which is a receptor of HMGB1, prevented the injury and occludin reducing caused by clopidogrel challenge.	clopidogrel	108-119	occludin	Homo sapiens	80-88
31484595-11	2019	Gastric mucosal damages observed by clopidogrel challenge are associated with HMGB1, TLR4, through p38MAPK signal pathway.	clopidogrel	36-47	high mobility group box 1	Homo sapiens	78-83
31484595-11	2019	Gastric mucosal damages observed by clopidogrel challenge are associated with HMGB1, TLR4, through p38MAPK signal pathway.	clopidogrel	36-47	toll like receptor 4	Homo sapiens	85-89
31484595-11	2019	Gastric mucosal damages observed by clopidogrel challenge are associated with HMGB1, TLR4, through p38MAPK signal pathway.	clopidogrel	36-47	mitogen-activated protein kinase 14	Homo sapiens	99-102
31202949-2	2019	The availability of different P2Y12 receptor inhibitors (clopidogrel, prasugrel, ticagrelor) with varying levels of potency has enabled physicians to contemplate individualized treatment regimens, which may include escalation or de-escalation of P2Y12-inhibiting therapy.	clopidogrel	57-68	purinergic receptor P2Y12	Homo sapiens	30-35
31134829-9	2019	CYP2C19 metabolizer status is closely related to the clinical efficacy of clopidogrel.	clopidogrel	74-85	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
30648733-1	2019	Simultaneous competition for cytochrome P450 (CYP) 2C19 and CYP3A4 might diminish clopidogrel"s antiplatelet effect by impacting its metabolic activation.	clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	29-55
30648733-1	2019	Simultaneous competition for cytochrome P450 (CYP) 2C19 and CYP3A4 might diminish clopidogrel"s antiplatelet effect by impacting its metabolic activation.	clopidogrel	82-93	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	60-66
30648733-2	2019	This pharmacoepidemiologic study investigated whether proton pump inhibitors (PPIs) and CYP3A4-metabolized statins individually and jointly increase thrombotic events by attenuating clopidogrel"s effectiveness.	clopidogrel	182-193	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	88-94
31571629-1	2019	Background & objectives: Cytochrome P450, P2Y 12, cyclooxygenase-1 (COX1) and glycoprotein V1 (GPVI) gene polymorphisms are known to affect patient responsiveness towards aspirin and clopidogrel dual antiplatelet therapy (DAPT).	clopidogrel	183-194	prostaglandin-endoperoxide synthase 1	Homo sapiens	50-66
31571629-1	2019	Background & objectives: Cytochrome P450, P2Y 12, cyclooxygenase-1 (COX1) and glycoprotein V1 (GPVI) gene polymorphisms are known to affect patient responsiveness towards aspirin and clopidogrel dual antiplatelet therapy (DAPT).	clopidogrel	183-194	prostaglandin-endoperoxide synthase 1	Homo sapiens	68-72
31571629-1	2019	Background & objectives: Cytochrome P450, P2Y 12, cyclooxygenase-1 (COX1) and glycoprotein V1 (GPVI) gene polymorphisms are known to affect patient responsiveness towards aspirin and clopidogrel dual antiplatelet therapy (DAPT).	clopidogrel	183-194	glycoprotein VI platelet	Homo sapiens	95-99
31141104-0	2019	P2Y12 Inhibitor Switching in Response to Routine Notification of CYP2C19 Clopidogrel Metabolizer Status Following Acute Coronary Syndromes.	clopidogrel	73-84	purinergic receptor P2Y12	Homo sapiens	0-5
31141104-0	2019	P2Y12 Inhibitor Switching in Response to Routine Notification of CYP2C19 Clopidogrel Metabolizer Status Following Acute Coronary Syndromes.	clopidogrel	73-84	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	65-72
31141104-1	2019	Importance: Physician behavior in response to knowledge of a patient"s CYP2C19 clopidogrel metabolizer status is unknown.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
31141104-10	2019	Investigators prestipulated that they would use CYP2C19 metabolizer status to change P2Y12 inhibitor in 48.5% of genotyped clopidogrel-treated patients (n = 642 of 1324) and 5.5% of genotyped ticagrelor-treated patients (n = 93 of 1692).	clopidogrel	123-134	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	48-55
31141104-10	2019	Investigators prestipulated that they would use CYP2C19 metabolizer status to change P2Y12 inhibitor in 48.5% of genotyped clopidogrel-treated patients (n = 642 of 1324) and 5.5% of genotyped ticagrelor-treated patients (n = 93 of 1692).	clopidogrel	123-134	purinergic receptor P2Y12	Homo sapiens	85-90
31141104-15	2019	Conclusions and Relevance: Physicians were evenly split on how to respond to knowledge of CYP2C19 metabolizer status in clopidogrel-treated patients.	clopidogrel	120-131	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	90-97
31082751-6	2019	All patients were on dual antiplatelet therapy; aspirin plus a P2Y12 inhibitor (clopidogrel or ticagrelor).	clopidogrel	80-91	purinergic receptor P2Y12	Homo sapiens	63-68
31242837-1	2019	BACKGROUND: Dual antiplatelet therapy (DAPT) with aspirin and one of inhibitors of P2Y12 receptors (clopidogrel, ticagrelor, prasugrel) is an international standard of receptors (clopidogrel, ticagrelor, prasugrel) is an international standard of is an international standard of treatment strategy in patients with acute coronary syndrome (ACS).	clopidogrel	100-111	purinergic receptor P2Y12	Homo sapiens	83-88
31675507-4	2019	This study aimed to evaluate the in vitro effects of different contrast agents on the antiaggregant activity of P2Y12 inhibitors (clopidogrel, ticagrelor and prasugrel).	clopidogrel	130-141	purinergic receptor P2Y12	Homo sapiens	112-117
30974489-10	2019	Amongst smokers, clopidogrel plus aspirin might decrease the recurrence rate of stroke in non-carriers of *2 and *3 alleles of CYP2C19 compared with aspirin alone.	clopidogrel	17-28	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	127-134
31073846-0	2019	Did Generic Clopidogrel Commercialization Affect Trends of ER Consultations and Hospitalizations in the Population Treated with Clopidogrel?	clopidogrel	12-23	epiregulin	Homo sapiens	59-61
31073846-0	2019	Did Generic Clopidogrel Commercialization Affect Trends of ER Consultations and Hospitalizations in the Population Treated with Clopidogrel?	clopidogrel	128-139	epiregulin	Homo sapiens	59-61
31073846-14	2019	CONCLUSIONS: The population treated with clopidogrel had similar rates of hospitalizations or ER consultations before and after generics commercialization.	clopidogrel	41-52	epiregulin	Homo sapiens	94-96
31073846-15	2019	However, differences in rates of hospitalizations or ER consultations between generic and brand-name clopidogrel users may represent a drug safety signal which remains to be validated.	clopidogrel	101-112	epiregulin	Homo sapiens	53-55
31092394-0	2019	Enhanced Platelet Response to Clopidogrel in Zucker Diabetic Fatty Rats due to Impaired Clopidogrel Inactivation by Carboxylesterase 1 and Increased Exposure to Active Metabolite.	clopidogrel	30-41	carboxylesterase 1E	Rattus norvegicus	116-134
31092394-0	2019	Enhanced Platelet Response to Clopidogrel in Zucker Diabetic Fatty Rats due to Impaired Clopidogrel Inactivation by Carboxylesterase 1 and Increased Exposure to Active Metabolite.	clopidogrel	88-99	carboxylesterase 1E	Rattus norvegicus	116-134
31092394-1	2019	Clopidogrel (Clop), a thienopyridine antiplatelet prodrug, is metabolized by cytochrome P450s (CYPs) to an active metabolite, Clop-AM, and hydrolyzed by carboxylesterase (CES)1 to the inactive Clop-acid.	clopidogrel	0-11	carboxylesterase 1E	Rattus norvegicus	153-176
31092394-1	2019	Clopidogrel (Clop), a thienopyridine antiplatelet prodrug, is metabolized by cytochrome P450s (CYPs) to an active metabolite, Clop-AM, and hydrolyzed by carboxylesterase (CES)1 to the inactive Clop-acid.	clopidogrel	0-4	carboxylesterase 1E	Rattus norvegicus	153-176
31092394-4	2019	In this work, we compared ZDF and control rats for hepatic CES1- and CYP-mediated Clop metabolism; pharmacokinetics of Clop, Clop-AM, and Clop-acid; and the antiplatelet efficacy of Clop.	clopidogrel	82-86	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	69-72
31092394-8	2019	These results suggest that the reduction in CES1-based Clop inactivation indirectly enhances Clop efficacy in ZDF rats by making more Clop available for CYP-mediated Clop-AM formation.	clopidogrel	55-59	carboxylesterase 1E	Rattus norvegicus	44-48
31092394-8	2019	These results suggest that the reduction in CES1-based Clop inactivation indirectly enhances Clop efficacy in ZDF rats by making more Clop available for CYP-mediated Clop-AM formation.	clopidogrel	55-59	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	153-156
31092394-8	2019	These results suggest that the reduction in CES1-based Clop inactivation indirectly enhances Clop efficacy in ZDF rats by making more Clop available for CYP-mediated Clop-AM formation.	clopidogrel	93-97	carboxylesterase 1E	Rattus norvegicus	44-48
31092394-8	2019	These results suggest that the reduction in CES1-based Clop inactivation indirectly enhances Clop efficacy in ZDF rats by making more Clop available for CYP-mediated Clop-AM formation.	clopidogrel	93-97	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	153-156
31102151-1	2019	The objective of this study was to determine the impact of polymorphism of CYP3A subfamily isoenzymes (allelic variants of CYP3A4*22 and CYP3A5*3) on the efficacy clopidogrel in patients with an acute coronary syndrome (ACS), who have undergone percutaneous coronary intervention (PCI).	clopidogrel	163-174	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	123-129
31102151-1	2019	The objective of this study was to determine the impact of polymorphism of CYP3A subfamily isoenzymes (allelic variants of CYP3A4*22 and CYP3A5*3) on the efficacy clopidogrel in patients with an acute coronary syndrome (ACS), who have undergone percutaneous coronary intervention (PCI).	clopidogrel	163-174	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	137-143
30487649-0	2019	Influences of an NR1I2 polymorphism on heterogeneous antiplatelet reactivity responses to clopidogrel and clinical outcomes in acute ischemic stroke patients.	clopidogrel	90-101	nuclear receptor subfamily 1 group I member 2	Homo sapiens	17-22
30487649-1	2019	Pregnane X receptor (PXR) is a member of nuclear receptor subfamily 1 (NR1I2) that is a transcriptional regulator of several metabolic enzymes involved in clopidogrel metabolism.	clopidogrel	155-166	nuclear receptor subfamily 1 group I member 2	Homo sapiens	0-19
30487649-1	2019	Pregnane X receptor (PXR) is a member of nuclear receptor subfamily 1 (NR1I2) that is a transcriptional regulator of several metabolic enzymes involved in clopidogrel metabolism.	clopidogrel	155-166	nuclear receptor subfamily 1 group I member 2	Homo sapiens	21-24
30487649-1	2019	Pregnane X receptor (PXR) is a member of nuclear receptor subfamily 1 (NR1I2) that is a transcriptional regulator of several metabolic enzymes involved in clopidogrel metabolism.	clopidogrel	155-166	nuclear receptor subfamily 1 group I member 2	Homo sapiens	71-76
30487649-2	2019	In this study we identified and evaluated the contributions of single nucleotide polymorphisms (SNPs) in NR1I2 and cytochrome P450 (CYP) 2C19 alleles to clopidogrel resistance (CR) and long-term clinical outcomes in acute ischemic stroke (IS) patients.	clopidogrel	153-164	nuclear receptor subfamily 1 group I member 2	Homo sapiens	105-110
30825385-2	2019	There is limited evidence indicating that exogenous IL-10 suppresses CYP3A4 activity in healthy subjects and that IL-10 knockout (KO) mice exhibit increased clopidogrel bioactivation compared with wild-type (WT) mice.	clopidogrel	157-168	interleukin 10	Mus musculus	114-119
31128980-0	2019	Influence of CYP450 Enzymes, CES1, PON1, ABCB1, and P2RY12 Polymorphisms on Clopidogrel Response in Patients Subjected to a Percutaneous Neurointervention.	clopidogrel	76-87	purinergic receptor P2Y12	Homo sapiens	52-58
31128980-3	2019	The influence of cytochrome P-450 (CYP) 2C19 on the response to clopidogrel has been widely studied; however, the effect of other genes involved in clopidogrel absorption and metabolism has not been established in this cohort of patients.	clopidogrel	64-75	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-44
31128980-7	2019	FINDINGS: We confirmed that CYP2C19 is the most important enzyme involved in clopidogrel response.	clopidogrel	77-88	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
31128980-8	2019	The carriage of the CYP2C19*2 allele was strongly associated with hyporesponse to clopidogrel, while the CYP2C19*17 allele was a protective factor for the development of ischemic events (odds ratio = 0.149; P = 0.002) but a risk factor for bleeding (odds ratio = 3.60; P = 0.038).	clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	20-27
31128980-9	2019	Patients carrying ABCB1 mutated alleles showed lower aggregation values, suggesting that clopidogrel absorption is influenced by P-glycoprotein.	clopidogrel	89-100	ATP binding cassette subfamily B member 1	Homo sapiens	18-23
31128980-14	2019	This is the first study to carry out a joint analysis of CYP2C19 and other genes involved in clopidogrel treatment in patients receiving percutaneous neurointervention.	clopidogrel	93-104	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	57-64
30962288-9	2019	Additionally, we evaluated whether clopidogrel (CYP2C19 substrate)-induced liver toxicity could be predicted using our model.	clopidogrel	35-46	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	48-55
30962288-11	2019	However, the cell viability in clopidogrel- and ketoconazole (CYP3A4 inhibitor)-treated CYP2C19-KO HLCs was significantly enhanced as compared with that in clopidogrel- and DMSO-treated CYP2C19-KO HLCs.	clopidogrel	31-42	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	88-95
30962288-11	2019	However, the cell viability in clopidogrel- and ketoconazole (CYP3A4 inhibitor)-treated CYP2C19-KO HLCs was significantly enhanced as compared with that in clopidogrel- and DMSO-treated CYP2C19-KO HLCs.	clopidogrel	31-42	holocarboxylase synthetase	Homo sapiens	99-103
30962288-11	2019	However, the cell viability in clopidogrel- and ketoconazole (CYP3A4 inhibitor)-treated CYP2C19-KO HLCs was significantly enhanced as compared with that in clopidogrel- and DMSO-treated CYP2C19-KO HLCs.	clopidogrel	31-42	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	186-193
30962288-11	2019	However, the cell viability in clopidogrel- and ketoconazole (CYP3A4 inhibitor)-treated CYP2C19-KO HLCs was significantly enhanced as compared with that in clopidogrel- and DMSO-treated CYP2C19-KO HLCs.	clopidogrel	31-42	holocarboxylase synthetase	Homo sapiens	197-201
30962288-12	2019	This result suggests that CYP2C19-KO HLCs can predict clopidogrel-induced liver toxicity.	clopidogrel	54-65	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
30962288-12	2019	This result suggests that CYP2C19-KO HLCs can predict clopidogrel-induced liver toxicity.	clopidogrel	54-65	holocarboxylase synthetase	Homo sapiens	37-41
30487649-2	2019	In this study we identified and evaluated the contributions of single nucleotide polymorphisms (SNPs) in NR1I2 and cytochrome P450 (CYP) 2C19 alleles to clopidogrel resistance (CR) and long-term clinical outcomes in acute ischemic stroke (IS) patients.	clopidogrel	153-164	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	115-141
30487649-7	2019	SNP NR1I2 (rs13059232) was identified as an independent risk factor for the long-term clinical outcomes in the clopidogrel cohorts (P &lt; 0.001), but similar results were not observed in a matched aspirin cohort (P &gt; 0.05).	clopidogrel	111-122	nuclear receptor subfamily 1 group I member 2	Homo sapiens	4-9
30487649-8	2019	Our results suggest that NR1I2 variant (rs13059232) could serve as biomarker for clopidogrel therapy and individualized antiplatelet medications in the treatment of acute IS patients.	clopidogrel	81-92	nuclear receptor subfamily 1 group I member 2	Homo sapiens	25-30
30932939-1	2019	BACKGROUND: CYP2C19 loss-of-function single-nucleotide polymorphisms (SNPs) are associated with poor responses of clopidogrel in secondary prevention of ischemic stroke (IS).	clopidogrel	114-125	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
30891852-0	2019	Association of PON1 gene promoter DNA methylation with the risk of Clopidogrel resistance in patients with coronary artery disease.	clopidogrel	67-78	paraoxonase 1	Homo sapiens	15-19
30891852-2	2019	We aimed to study the contribution of promoter DNA methylation of paraoxonase 1 (PON1) to the risk of clopidogrel poor response.	clopidogrel	102-113	paraoxonase 1	Homo sapiens	66-79
30891852-2	2019	We aimed to study the contribution of promoter DNA methylation of paraoxonase 1 (PON1) to the risk of clopidogrel poor response.	clopidogrel	102-113	paraoxonase 1	Homo sapiens	81-85
30891852-7	2019	RESULTS: In the subgroup with dyslipidemia, we discovered that higher CpG4 levels of the PON1 promoter indicated a poorer clopidogrel response (cases versus controls (%): 51.500 +- 14.742 vs 43.308 +- 10.891, P = 0.036), and the PON1 mRNA expression was reduced in CR patients.	clopidogrel	122-133	paraoxonase 1	Homo sapiens	89-93
30891852-9	2019	CONCLUSIONS: The DNA methylation of CpG4 in the PON1 promoter would lead to a low expression of PON1 mRNA, which might induce clopidogrel resistance in the patients with dyslipidemia, and the number of stents might be a risk for CR.	clopidogrel	126-137	paraoxonase 1	Homo sapiens	48-52
30891852-9	2019	CONCLUSIONS: The DNA methylation of CpG4 in the PON1 promoter would lead to a low expression of PON1 mRNA, which might induce clopidogrel resistance in the patients with dyslipidemia, and the number of stents might be a risk for CR.	clopidogrel	126-137	paraoxonase 1	Homo sapiens	96-100
31006731-0	2019	Association of CYP2C19 Polymorphisms With Clopidogrel Reactivity and Clinical Outcomes in Chronic Ischemic Stroke.	clopidogrel	42-53	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
31006731-1	2019	BACKGROUND: CYP2C19variants are associated with the antiplatelet effects of clopidogrel against recurrent cardiovascular events.	clopidogrel	76-87	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
31006731-5	2019	Antiplatelet effects of clopidogrel were assessed by adenosine diphosphate (ADP)-induced platelet aggregation and vasodilator-stimulated phosphoprotein (VASP) phosphorylation.	clopidogrel	24-35	vasodilator stimulated phosphoprotein	Homo sapiens	114-151
31006731-5	2019	Antiplatelet effects of clopidogrel were assessed by adenosine diphosphate (ADP)-induced platelet aggregation and vasodilator-stimulated phosphoprotein (VASP) phosphorylation.	clopidogrel	24-35	vasodilator stimulated phosphoprotein	Homo sapiens	153-157
30826050-1	2019	P2Y12-inhibitor initiation with clopidogrel using a loading dose (LD) versus no LD (NLD) provides more rapid inhibition of platelet activation and reduced risk of ischemic events after coronary stenting.	clopidogrel	32-43	purinergic receptor P2Y12	Homo sapiens	0-5
31198410-3	2019	The most used P2Y12-antagonists are clopidogrel, prasugrel and ticagrelor.	clopidogrel	36-47	purinergic receptor P2Y12	Homo sapiens	14-19
31018667-0	2019	Impact of Platelet Endothelial Aggregation Receptor-1 Genotypes on Platelet Reactivity and Early Cardiovascular Outcomes in Patients Undergoing Percutaneous Coronary Intervention and Treated With Aspirin and Clopidogrel.	clopidogrel	208-219	platelet endothelial aggregation receptor 1	Homo sapiens	10-53
30652301-0	2019	CYP2C19 Ultrarapid Phenotype as a Risk Predictor of Subsequent Events During Clopidogrel Treatment in Patients Undergoing a Percutaneous Neurointervention.	clopidogrel	77-88	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
30061570-1	2019	The effect of dual antiplatelet therapy, clopidogrel combined with aspirin, was influenced by CYP2C19 gene mutation and heterogeneity of population.	clopidogrel	41-52	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	94-101
29335863-2	2019	Translational and evidence-based medical studies show that the CYP2C19 gene mutation (CYP2C19*2 and CYP2C19*3) could affect &gt; 50% of the Chinese population, and that this mutation is closely associated with clopidogrel resistance and an increased risk of major adverse cardiovascular events, particularly stent thrombosis in patients following percutaneous coronary intervention (PCI).	clopidogrel	210-221	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	63-70
29335863-2	2019	Translational and evidence-based medical studies show that the CYP2C19 gene mutation (CYP2C19*2 and CYP2C19*3) could affect &gt; 50% of the Chinese population, and that this mutation is closely associated with clopidogrel resistance and an increased risk of major adverse cardiovascular events, particularly stent thrombosis in patients following percutaneous coronary intervention (PCI).	clopidogrel	210-221	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	86-93
29335863-2	2019	Translational and evidence-based medical studies show that the CYP2C19 gene mutation (CYP2C19*2 and CYP2C19*3) could affect &gt; 50% of the Chinese population, and that this mutation is closely associated with clopidogrel resistance and an increased risk of major adverse cardiovascular events, particularly stent thrombosis in patients following percutaneous coronary intervention (PCI).	clopidogrel	210-221	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	86-93
30789491-6	2019	Primary outcome was adherence to use of P2Y12 inhibitor (clopidogrel or ticagrelor) therapy at 30 days of follow-up.	clopidogrel	57-68	purinergic receptor P2Y12	Homo sapiens	40-45
30795966-0	2019	Platelet Surface CD62p and Serum Vitamin D Levels are Associated with Clopidogrel Resistance in Chinese Patients with Ischemic Stroke.	clopidogrel	70-81	selectin P	Homo sapiens	17-22
30742211-0	2019	Association Between ABCB1 Polymorphisms and Outcomes of Clopidogrel Treatment in Patients With Minor Stroke or Transient Ischemic Attack: Secondary Analysis of a Randomized Clinical Trial.	clopidogrel	56-67	ATP binding cassette subfamily B member 1	Homo sapiens	20-25
30742211-1	2019	Importance: Genetic variants of ABCB1 may affect intestinal absorption of clopidogrel bisulfate.	clopidogrel	74-95	ATP binding cassette subfamily B member 1	Homo sapiens	32-37
30742211-3	2019	Objectives: To investigate the association between ABCB1 polymorphisms and clopidogrel efficacy for minor stroke or TIA.	clopidogrel	75-86	ATP binding cassette subfamily B member 1	Homo sapiens	51-56
30742211-7	2019	The association of ABCB1 genetic variants (-154 TC/CC and 3435 CT/TT) with clopidogrel efficacy was evaluated in the context of CYP2C19 status, another gene associated with clopidogrel efficacy.	clopidogrel	75-86	ATP binding cassette subfamily B member 1	Homo sapiens	19-24
30742211-13	2019	Clopidogrel plus aspirin treatment was associated with reduced risk of new stroke in patients with ABCB1 -154 TT and 3435 CC genotype (hazard ratio [HR], 0.43; 95% CI, 0.26-0.71) but not in those with ABCB1 -154 TC/CC or 3435 CT/TT genotype (HR, 0.78; 95% CI, 0.60-1.03) compared with aspirin (P = .04 for interaction).	clopidogrel	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	99-104
30742211-13	2019	Clopidogrel plus aspirin treatment was associated with reduced risk of new stroke in patients with ABCB1 -154 TT and 3435 CC genotype (hazard ratio [HR], 0.43; 95% CI, 0.26-0.71) but not in those with ABCB1 -154 TC/CC or 3435 CT/TT genotype (HR, 0.78; 95% CI, 0.60-1.03) compared with aspirin (P = .04 for interaction).	clopidogrel	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	201-206
30742211-16	2019	Conclusions and Relevance: The ABCB1 polymorphism was associated with the reduced efficacy of clopidogrel plus aspirin treatment compared with aspirin among patients with minor ischemic stroke or TIA.	clopidogrel	94-105	ATP binding cassette subfamily B member 1	Homo sapiens	31-36
30742211-17	2019	Genetic polymorphism of ABCB1 should be considered when prescribing clopidogrel for these patients.	clopidogrel	68-79	ATP binding cassette subfamily B member 1	Homo sapiens	24-29
31124413-3	2019	Results: Multivariate binary regression analysis demonstrated that aspirin use and CYP4F2 T allele significantly increased odds for bleeding in clopidogrel users (OR: 2.488, 95% CI: 1.452-4.265; p = 0.001 and OR: 1.573, 95% CI: 1.066-2.320; respectively; p = 0.022).	clopidogrel	144-155	cytochrome P450 family 4 subfamily F member 2	Homo sapiens	83-89
31124414-2	2019	While loss-of-function (LOF) alleles in CYP2C19 have been elucidated as contributing to high on treatment platelet reactivity (HTPR) during clopidogrel therapy, genetic variations in the metabolic pathway of prasugrel have not been shown to elicit this same effect.	clopidogrel	140-151	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-47
30876967-1	2019	The pharmacological and clinical differences of the three recommended oral P2Y12 inhibitors (clopidogrel, prasugrel, ticagrelor) enable physicians to switch from one agent to another that it is considered more appropriate in the specific clinical setting.	clopidogrel	93-104	purinergic receptor P2Y12	Homo sapiens	75-80
31060148-3	2019	The mechanism of mucosal injury included free radical injury induced by aspirin and decreased synthesis of vascular endothelial growth factor (VEGF) by clopidogrel.	clopidogrel	152-163	vascular endothelial growth factor A	Rattus norvegicus	107-141
31060148-3	2019	The mechanism of mucosal injury included free radical injury induced by aspirin and decreased synthesis of vascular endothelial growth factor (VEGF) by clopidogrel.	clopidogrel	152-163	vascular endothelial growth factor A	Rattus norvegicus	143-147
31007424-9	2019	The frequency of CYP2C19*2 mutant genotype was significantly higher in clopidogrel nonresponders compared to responders (P = 0.014).	clopidogrel	71-82	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-24
31007424-12	2019	In an interim analysis on 65 Indian patients, a significant association was found between CYP2C19*2 and clopidogrel nonresponsiveness.	clopidogrel	104-115	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	90-97
30760018-2	2019	Although clopidogrel is the most commonly prescribed P2Y12 inhibitor, it is associated with an increased risk of major adverse cardiovascular events in patients carrying loss-of-function CYP2C19 alleles.	clopidogrel	9-20	purinergic receptor P2Y12	Homo sapiens	53-58
30760018-2	2019	Although clopidogrel is the most commonly prescribed P2Y12 inhibitor, it is associated with an increased risk of major adverse cardiovascular events in patients carrying loss-of-function CYP2C19 alleles.	clopidogrel	9-20	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	187-194
30998396-1	2019	Common genetic variation in CYP2C19 (cytochrome P450, family 2, subfamily C, polypeptide 19) *2 and *3 alleles leads to a loss of functional protein, and carriers of these loss-of-function alleles when treated with clopidogrel have significantly reduced clopidogrel active metabolite levels and high on-treatment platelet reactivity resulting in increased risk of major adverse cardiovascular events, especially after percutaneous coronary intervention.	clopidogrel	215-226	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
30998396-1	2019	Common genetic variation in CYP2C19 (cytochrome P450, family 2, subfamily C, polypeptide 19) *2 and *3 alleles leads to a loss of functional protein, and carriers of these loss-of-function alleles when treated with clopidogrel have significantly reduced clopidogrel active metabolite levels and high on-treatment platelet reactivity resulting in increased risk of major adverse cardiovascular events, especially after percutaneous coronary intervention.	clopidogrel	215-226	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	37-62
30998396-1	2019	Common genetic variation in CYP2C19 (cytochrome P450, family 2, subfamily C, polypeptide 19) *2 and *3 alleles leads to a loss of functional protein, and carriers of these loss-of-function alleles when treated with clopidogrel have significantly reduced clopidogrel active metabolite levels and high on-treatment platelet reactivity resulting in increased risk of major adverse cardiovascular events, especially after percutaneous coronary intervention.	clopidogrel	254-265	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
30998396-1	2019	Common genetic variation in CYP2C19 (cytochrome P450, family 2, subfamily C, polypeptide 19) *2 and *3 alleles leads to a loss of functional protein, and carriers of these loss-of-function alleles when treated with clopidogrel have significantly reduced clopidogrel active metabolite levels and high on-treatment platelet reactivity resulting in increased risk of major adverse cardiovascular events, especially after percutaneous coronary intervention.	clopidogrel	254-265	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	37-62
30936195-5	2019	Although variants were reported for all drugs, the highest level of evidence was found in cytochrome P450 (CYP450) genotype variation related to clopidogrel response.	clopidogrel	145-156	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	90-105
30936195-5	2019	Although variants were reported for all drugs, the highest level of evidence was found in cytochrome P450 (CYP450) genotype variation related to clopidogrel response.	clopidogrel	145-156	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	107-113
30630815-0	2019	Clopidogrel and Gemfibrozil Strongly Inhibit the CYP2C8-Dependent Formation of 3-Hydroxydesloratadine and Increase Desloratadine Exposure In Humans.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	49-55
30630815-3	2019	Glucuronide metabolites of clopidogrel and gemfibrozil act as time-dependent inhibitors of CYP2C8, but they have not been compared clinically.	clopidogrel	27-38	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	91-97
30630815-4	2019	We conducted a randomized crossover study in 11 healthy subjects to characterize the involvement of CYP2C8 in desloratadine metabolism and to compare the CYP2C8 inhibitory strength of clopidogrel (300 and 75 mg on two following days) with that of gemfibrozil (600 mg BID for 5 days).	clopidogrel	184-195	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	154-160
30630815-10	2019	Furthermore, the findings corroborate the previous estimates that clinically relevant doses of clopidogrel cause strong CYP2C8 inhibition, whereas those of gemfibrozil almost completely inactivate the enzyme in humans.	clopidogrel	95-106	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	120-126
30361928-0	2019	In Vitro Assessment of Potential for CYP-Inhibition-Based Drug-Drug Interaction Between Vonoprazan and Clopidogrel.	clopidogrel	103-114	peptidylprolyl isomerase G	Homo sapiens	37-40
30361928-1	2019	BACKGROUND AND OBJECTIVES: It was recently proposed that CYP-mediated drug-drug interactions (DDIs) of vonoprazan with clopidogrel and prasugrel can attenuate the antiplatelet actions of the latter two drugs.	clopidogrel	119-130	peptidylprolyl isomerase G	Homo sapiens	57-60
30361928-2	2019	Clopidogrel is metabolized to the pharmacologically active metabolite H4 and its isomers by multiple CYPs, including CYP2C19 and CYP3A4.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	117-124
30361928-2	2019	Clopidogrel is metabolized to the pharmacologically active metabolite H4 and its isomers by multiple CYPs, including CYP2C19 and CYP3A4.	clopidogrel	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	129-135
30537341-8	2019	Clopidogrel pretreatment markedly decreased lung damage, inhibited platelet-neutrophil aggregates and TF expression.	clopidogrel	0-11	coagulation factor III	Mus musculus	102-104
30537341-10	2019	Moreover, clopidogrel also reduced platelet shedding of CD40L and CD62P in endotoxemic mice.	clopidogrel	10-21	CD40 ligand	Mus musculus	56-61
30537341-10	2019	Moreover, clopidogrel also reduced platelet shedding of CD40L and CD62P in endotoxemic mice.	clopidogrel	10-21	selectin, platelet	Mus musculus	66-71
31041128-1	2019	Purpose of review: CYP2C19 is the primary enzyme involved in the activation of clopidogrel, an antiplatelet agent used for secondary stroke prevention.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	19-26
31041128-2	2019	An individual"s CYP2C19 alleles are used to understand their CYP2C19-clopidogrel metabolizer phenotype.	clopidogrel	69-80	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
31041128-2	2019	An individual"s CYP2C19 alleles are used to understand their CYP2C19-clopidogrel metabolizer phenotype.	clopidogrel	69-80	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	61-68
30061570-9	2019	It was found that patients with allele A in CYP2C19*2 and *3 were susceptibility to high PR (OR, 95%CI and P values were 1.34, 1.20-1.50, &lt;0.0001 and 1.42, 1.13-1.79, 0.0029, respectively) after taking clopidogrel.	clopidogrel	205-216	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	44-51
30061570-11	2019	This research suggested that LOF alleles and risk haplotypes in CYP2C19 could significantly attenuate the response to clopidogrel, which resulted in platelet aggregation.	clopidogrel	118-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	64-71
30685502-3	2019	The availability of different oral P2Y12 antagonists (clopidogrel, prasugrel, ticagrelor) along with the introduction of the first intravenous P2Y12 antagonist cangrelor offer an opportunity to individualize antiplatelet therapy according to the changing clinical setting.	clopidogrel	54-65	purinergic receptor P2Y12	Homo sapiens	35-40
30738371-4	2019	MATERIALS AND METHODS: This PD study included 988 patients with acute coronary syndromes (ACS) undergoing percutaneous coronary intervention (PCI) and receiving dual therapy with aspirin and a P2Y12 inhibitor (clopidogrel, prasugrel or ticagrelor).	clopidogrel	210-221	purinergic receptor P2Y12	Homo sapiens	193-198
30760018-1	2019	Current guidelines recommend dual antiplatelet therapy-a P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor) and aspirin-for patients undergoing percutaneous coronary intervention.	clopidogrel	74-85	purinergic receptor P2Y12	Homo sapiens	57-62
29536505-0	2019	Influence of CYP2C19 Phenotype on the Effect of Clopidogrel in Patients Undergoing a Percutaneous Neurointervention Procedure.	clopidogrel	48-59	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
29536505-1	2019	This observational retrospective study assessed the antiplatelet response and clinical events after clopidogrel treatment in patients who underwent percutaneous neurointervention, related to CYP2C19 metabolizer status (normal (NM), intermediate/poor (IM-PM), and ultrarapid (UM); inferred from *2, *3, and *17 allele determination).	clopidogrel	100-111	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	191-198
29536505-5	2019	CYP2C19 no-function and increased function alleles defined the clopidogrel response.	clopidogrel	63-74	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
30723937-2	2019	The combination of aspirin and a P2Y12 inhibitor such as clopidogrel is often initiated days before elective procedures or as loading doses for emergent procedures; however, some patients may still experience thrombotic complications.	clopidogrel	57-68	purinergic receptor P2Y12	Homo sapiens	33-38
30778044-5	2019	Injections of P2Y12 antagonists (MRS2395 or clopidogrel) attenuated microglia activation and increased the paw withdrawal latency in response to thermal stimuli on the ipsilateral side without affecting the basal threshold on the contralateral side.	clopidogrel	44-55	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	14-19
30839367-5	2019	Rivaroxaban 2.5 mg BID in triple therapy with DAPT, rivaroxaban 15 mg, or dabigatran 110/150 mg BID in dual therapy with P2Y12 inhibitor (mainly clopidogrel) is safer in terms of bleeding risk than triple therapy with VKA plus DAPT.	clopidogrel	145-156	BH3 interacting domain death agonist	Homo sapiens	19-22
30839367-7	2019	Ongoing trials with apixaban and edoxaban could clarify whether dual therapy NOACs with P2Y12 inhibitor sufficiently protect against stent thrombosis or myocardial infarction and are safer in terms of bleeding risk than a dual therapy with a VKA and clopidogrel.	clopidogrel	250-261	purinergic receptor P2Y12	Homo sapiens	88-93
30911318-8	2019	Danshen inhibited carboxylesterase 1 and most enzyme of cytochrome P450, especially cytochrome P450 1A2, which may affect the metabolism of clopidogrel.	clopidogrel	140-151	carboxylesterase 1	Homo sapiens	18-36
30911318-8	2019	Danshen inhibited carboxylesterase 1 and most enzyme of cytochrome P450, especially cytochrome P450 1A2, which may affect the metabolism of clopidogrel.	clopidogrel	140-151	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	84-103
30911318-10	2019	Meanwhile, the inhibitory effect of Danshen on cytochrome P450 and carboxylesterase 1 could be partly responsible for the synergistic and attenuating effects of Danshen combined with clopidogrel.	clopidogrel	183-194	carboxylesterase 1	Homo sapiens	67-85
30527773-3	2019	After clopidogrel loading, ACS patients had higher P2Y12 reaction units and a greater prevalence of HPR based on VerifyNow P2Y12 assay.	clopidogrel	6-17	purinergic receptor P2Y12	Homo sapiens	51-56
30527773-3	2019	After clopidogrel loading, ACS patients had higher P2Y12 reaction units and a greater prevalence of HPR based on VerifyNow P2Y12 assay.	clopidogrel	6-17	purinergic receptor P2Y12	Homo sapiens	123-128
30729324-6	2019	Clopidogrel is the preferred P2Y12 agent in the dual antithrombotic regimens.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	29-34
30257062-2	2019	We reported that pharmacological blockade of P2Y12 receptor (R) with clopidogrel or prasugrel significantly ameliorated lithium-induced NDI in rodents.	clopidogrel	69-80	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	45-50
30506985-3	2019	AIM: To compare the risk of gastrointestinal bleeding (GIB) among users of third-generation P2Y12 inhibitors with clopidogrel.	clopidogrel	114-125	purinergic receptor P2Y12	Homo sapiens	92-97
29891858-4	2019	Six plasma miRNAs (miR-126, miR-130a, miR-27a, miR-106a, miR-21, and miR-142) were associated with clopidogrel-treated platelet aggregation.	clopidogrel	99-110	microRNA 126	Homo sapiens	19-26
29891858-4	2019	Six plasma miRNAs (miR-126, miR-130a, miR-27a, miR-106a, miR-21, and miR-142) were associated with clopidogrel-treated platelet aggregation.	clopidogrel	99-110	microRNA 130a	Homo sapiens	28-36
29891858-4	2019	Six plasma miRNAs (miR-126, miR-130a, miR-27a, miR-106a, miR-21, and miR-142) were associated with clopidogrel-treated platelet aggregation.	clopidogrel	99-110	microRNA 27a	Homo sapiens	38-45
29891858-4	2019	Six plasma miRNAs (miR-126, miR-130a, miR-27a, miR-106a, miR-21, and miR-142) were associated with clopidogrel-treated platelet aggregation.	clopidogrel	99-110	microRNA 106a	Homo sapiens	47-55
29891858-4	2019	Six plasma miRNAs (miR-126, miR-130a, miR-27a, miR-106a, miR-21, and miR-142) were associated with clopidogrel-treated platelet aggregation.	clopidogrel	99-110	microRNA 21	Homo sapiens	57-63
29891858-4	2019	Six plasma miRNAs (miR-126, miR-130a, miR-27a, miR-106a, miR-21, and miR-142) were associated with clopidogrel-treated platelet aggregation.	clopidogrel	99-110	microRNA 142	Homo sapiens	69-76
30406277-2	2019	However, the clinical use of P2Y12-R antagonists faces some limitations, such as a delayed onset of action (clopidogrel) or adverse effect profile (ticagrelor, cangrelor), justifying the development of a new generation of P2Y12-R antagonists with a better clinical benefit-risk balance.	clopidogrel	108-119	purinergic receptor P2Y12	Homo sapiens	29-36
29998574-1	2019	CYP3A enzymes participate in the elimination of ticagrelor and the bioactivation of clopidogrel and prasugrel.	clopidogrel	84-95	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-5
30656556-0	2019	The clinical effects of CYP2C19 *2 allele frequency on Palestinian patients receiving clopidogrel after percutaneous coronary intervention.	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
30656556-5	2019	Method The frequency of CYP2C19 *2 and *3 alleles was determined in 110 patients managed with percutaneous coronary intervention and clopidogrel.	clopidogrel	133-144	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
30656556-15	2019	Conclusion The CYP2C19 *2 allele is relatively common in our population, and its associated reduced metabolic activity deserves attention as it leads to an increased incidence of major adverse cardiac events in the follow-up of patients receiving clopidogrel.	clopidogrel	247-258	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
30661601-8	2019	Montelukast significantly diminished the up-regulation of CysLTR1, CysLTR2, and P2Y12R (P < 0.05 for each), while the effects of HAMI 3379 and clopidogrel were predominant on the expression of CysLTR2 and P2Y12R, respectively.	clopidogrel	143-154	cysteinyl leukotriene receptor 2	Mus musculus	193-200
30661601-9	2019	Montelukast predominantly diminished the cell count, while clopidogrel potently inhibited the release of interleukin (IL)-4, IL-5, and IL-13.	clopidogrel	59-70	interleukin 4	Mus musculus	105-123
30661601-9	2019	Montelukast predominantly diminished the cell count, while clopidogrel potently inhibited the release of interleukin (IL)-4, IL-5, and IL-13.	clopidogrel	59-70	interleukin 5	Mus musculus	125-129
30661601-9	2019	Montelukast predominantly diminished the cell count, while clopidogrel potently inhibited the release of interleukin (IL)-4, IL-5, and IL-13.	clopidogrel	59-70	interleukin 13	Mus musculus	135-140
30562722-2	2019	This study aims to analyze if there are differences in the incidence of cancer according to the type of P2Y12 inhibitor prescribed (clopidogrel, prasugrel, or ticagrelor), among a population of acute coronary syndrome (ACS) survivors treated with DAPT.	clopidogrel	132-143	purinergic receptor P2Y12	Homo sapiens	104-109
30609441-1	2019	Amlodipine has a potential to reduce clopidogrel bioactivation through the cytochrome P450 3A4 enzyme in vivo, but the clinical impact of this interaction remains controversial.	clopidogrel	37-48	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	75-94
29382249-4	2019	CES1 activities were determined by monitoring the depletion of known substrate, the clopidogrel.	clopidogrel	84-95	carboxylesterase 1	Homo sapiens	0-4
31512486-0	2019	The Effect of CYP2C19 and Nongenetic Factors on Clopidogrel Responsiveness in the MENA Region: A Systematic Review.	clopidogrel	48-59	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
31512486-2	2019	Some studies examined the effect of CYP2C19 polymorphism and nongenetic factors on clopidogrel response in the Middle East and North Africa (MENA) region.	clopidogrel	83-94	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	36-43
31512486-12	2019	Association between the CYP2C19*2 allele and clopidogrel resistance is common among MENA populations.	clopidogrel	45-56	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
30320560-4	2019	We blindly randomized them in two groups: pre-carotid angioplasty with stent (Pre-CAS group) receiving 300 mg of clopidogrel before stenting, and post-carotid angioplasty with stent (Post-CAS group) receiving 300 mg after stenting.	clopidogrel	113-124	BCAR1 scaffold protein, Cas family member	Homo sapiens	82-85
30772975-3	2019	Loss-of-function allele carriers of CYP2C19 were included and randomly divided into loading dose group (first dose of 300 mg clopidogrel) and standard dose group (first dose of 75 mg clopidogrel), 100 mg aspirin was gave at the same time, followed by aspirin 100 mg/d plus clopidogrel 75 mg/d maintaining for 20 days.	clopidogrel	125-136	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	36-43
30772975-3	2019	Loss-of-function allele carriers of CYP2C19 were included and randomly divided into loading dose group (first dose of 300 mg clopidogrel) and standard dose group (first dose of 75 mg clopidogrel), 100 mg aspirin was gave at the same time, followed by aspirin 100 mg/d plus clopidogrel 75 mg/d maintaining for 20 days.	clopidogrel	183-194	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	36-43
30772975-3	2019	Loss-of-function allele carriers of CYP2C19 were included and randomly divided into loading dose group (first dose of 300 mg clopidogrel) and standard dose group (first dose of 75 mg clopidogrel), 100 mg aspirin was gave at the same time, followed by aspirin 100 mg/d plus clopidogrel 75 mg/d maintaining for 20 days.	clopidogrel	183-194	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	36-43
30772975-14	2019	Loading dose clopidogrel may improve the prognosis of minor stroke/TIA by decreasing MAR of CYP2C19*2 carriers.	clopidogrel	13-24	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	92-99
30689068-2	2019	Treating ACS patients with dual antiplatelet therapy (DAPT) for a year by combining aspirin and a P2Y12 inhibitor (clopidogrel, ticagrelor, or prasugrel) has resulted in better outcomes and is currently the standard of therapy.	clopidogrel	115-126	purinergic receptor P2Y12	Homo sapiens	98-103
30614864-2	2019	In current clinical situation, availability of different oral P2Y12 inhibitors (clopidogrel, prasugrel, and ticagrelor) has enabled physicians to switch among therapies owing to specific clinical scenarios.	clopidogrel	80-91	purinergic receptor P2Y12	Homo sapiens	62-67
30215226-6	2019	RESULTS: In Col/EPI, 73.2% (365/499), 72.6% (390/537), and 55.3% (3,442/6,228) patients showed prolonged CTs for aspirin, clopidogrel, and NSAIDs, respectively.	clopidogrel	122-133	tissue factor pathway inhibitor	Homo sapiens	16-19
31834317-0	2019	Association of CYP2C19*2 polymorphism with clopidogrel resistance among patients with high cardiovascular risk in Northeastern Mexico.	clopidogrel	43-54	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
31834317-4	2019	The enzyme CYP2C19 has been reported to be the CYP isoform that activates CLO to its active metabolite.	clopidogrel	74-77	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	11-18
31834317-4	2019	The enzyme CYP2C19 has been reported to be the CYP isoform that activates CLO to its active metabolite.	clopidogrel	74-77	peptidylprolyl isomerase G	Homo sapiens	11-14
31834317-5	2019	Several single nucleotide polymorphisms in the CYP2C19 gene have been identified as strong predictors of CLO-impaired pharmacological response.	clopidogrel	105-108	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	47-54
31834317-12	2019	The prevalence of reduced CLO effectiveness was associated with the presence of CYP2C19*2 polymorphism among Mexican patients.	clopidogrel	26-29	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	80-87
31834317-13	2019	Conclusion: The presence of the CYP2C19*2 allele is related to resistance to the antiplatelet effect of CLO (p = 0.003).	clopidogrel	104-107	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
30098132-3	2019	Clopidogrel, a P2Y12 antagonist, plays an important role in the inhibition of platelet aggregation (IPA).	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	15-20
30302530-3	2019	In the last few decades, P2Y12 receptor inhibitors, such as clopidogrel, have been applied for the secondary prevention of non-cardioembolic ischemic stroke.	clopidogrel	60-71	purinergic receptor P2Y12	Homo sapiens	25-30
30506985-12	2019	CONCLUSION: Third-generation P2Y12 inhibitors were associated with increased risk of GIB and non-CABG major bleeding when compared with clopidogrel.	clopidogrel	136-147	purinergic receptor P2Y12	Homo sapiens	29-34
29791922-0	2019	P2Y12 Polymorphisms and the Risk of Adverse Clinical Events in Patients Treated with Clopidogrel: A Meta-Analysis.	clopidogrel	85-96	purinergic receptor P2Y12	Homo sapiens	0-5
29696643-2	2019	Ritonavir and clopidogrel are inhibitors of CYP3A4 and CYP2C8, respectively.	clopidogrel	14-25	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	44-50
29696643-2	2019	Ritonavir and clopidogrel are inhibitors of CYP3A4 and CYP2C8, respectively.	clopidogrel	14-25	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	55-61
29412111-2	2019	Of them, adenosine diphosphate receptor P2Y12 inhibitors clopidogrel, prasugrel and ticagrelor are currently used for post-ACS long-term treatment.	clopidogrel	57-68	purinergic receptor P2Y12	Homo sapiens	40-45
29412111-5	2019	This includes Pglycoprotein, carboxylesterase 1 and, most notably, CYP2C19 that is important in clopidogrel activation.	clopidogrel	96-107	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	67-74
29412111-6	2019	Common gain-of-function or loss-of-function alleles of CYP2C19 gene are associated with lower or higher platelet reactivity that may impact clinical outcomes of clopidogrel treatment.	clopidogrel	161-172	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	55-62
29791922-1	2019	BACKGROUND AND STUDY AIM: Some studies have reported an association between P2Y12 gene polymorphisms and clopidogrel adverse outcomes with inconsistent results.	clopidogrel	105-116	purinergic receptor P2Y12	Homo sapiens	76-81
29791922-2	2019	We aimed to explore the relationship between P2Y12 polymorphisms and the risk of adverse clinical events in patients treated with clopidogrel through a meta-analysis.	clopidogrel	130-141	purinergic receptor P2Y12	Homo sapiens	45-50
30662363-0	2019	Clopidogrel Reduces Fibronectin Accumulation and Improves Diabetes-Induced Renal Fibrosis.	clopidogrel	0-11	fibronectin 1	Homo sapiens	20-31
30745807-8	2019	CD42+/CD62P+ PMVs numbers correlated positively to the ADP-induced aggregation on clopidogrel (p&lt;0.01) or prasugrel (p&lt;0.05), which was absent in ticagrelor users (p=0.8).	clopidogrel	82-93	selectin P	Homo sapiens	6-11
30745807-10	2019	Conclusions: Higher antiplatelet potency of prasugrel and ticagrelor versus clopidogrel is associated with decreased plasma CD42+/CD62P+ PMVs numbers.	clopidogrel	76-87	selectin P	Homo sapiens	130-135
30251376-2	2019	In humans, evidence suggests that variable clopidogrel active metabolite (CAM) generation is the primary explanation for clopidogrel response variability with differences in body weight, sex, and variable metabolism of clopidogrel primarily due to polymorphisms of the gene encoding cytochrome P450 (CYP) 2C19 as some proposed mechanisms.	clopidogrel	43-54	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	283-309
30251376-2	2019	In humans, evidence suggests that variable clopidogrel active metabolite (CAM) generation is the primary explanation for clopidogrel response variability with differences in body weight, sex, and variable metabolism of clopidogrel primarily due to polymorphisms of the gene encoding cytochrome P450 (CYP) 2C19 as some proposed mechanisms.	clopidogrel	121-132	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	283-309
30251376-2	2019	In humans, evidence suggests that variable clopidogrel active metabolite (CAM) generation is the primary explanation for clopidogrel response variability with differences in body weight, sex, and variable metabolism of clopidogrel primarily due to polymorphisms of the gene encoding cytochrome P450 (CYP) 2C19 as some proposed mechanisms.	clopidogrel	121-132	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	283-309
30662363-6	2019	Clopidogrel, administered during the last three months, significantly decreased blood glucose, collagen and fibronectin expression compared to vehicle-treated diabetic mice.	clopidogrel	0-11	fibronectin 1	Mus musculus	108-119
30520344-2	2019	The purpose of this research is to describe the prevalence of pharmacogene variants associated with clopidogrel responsiveness (CYP2C19, B4GALT2, ABCB1, PON1, CES1 and P2RY12) in Hispanic/Latino patients of diverse backgrounds.	clopidogrel	100-111	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	128-135
30734681-4	2019	P2Y12 inhibitors, i.e. clopidogrel, prasugrel, ticagrelor, and cangrelor, are already used clinically to reduce coronary artery thrombosis risk and prevent acute coronary syndromes.	clopidogrel	23-34	purinergic receptor P2Y12	Homo sapiens	0-5
30520344-2	2019	The purpose of this research is to describe the prevalence of pharmacogene variants associated with clopidogrel responsiveness (CYP2C19, B4GALT2, ABCB1, PON1, CES1 and P2RY12) in Hispanic/Latino patients of diverse backgrounds.	clopidogrel	100-111	beta-1,4-galactosyltransferase 2	Homo sapiens	137-144
30520344-2	2019	The purpose of this research is to describe the prevalence of pharmacogene variants associated with clopidogrel responsiveness (CYP2C19, B4GALT2, ABCB1, PON1, CES1 and P2RY12) in Hispanic/Latino patients of diverse backgrounds.	clopidogrel	100-111	ATP binding cassette subfamily B member 1	Homo sapiens	146-151
30520344-2	2019	The purpose of this research is to describe the prevalence of pharmacogene variants associated with clopidogrel responsiveness (CYP2C19, B4GALT2, ABCB1, PON1, CES1 and P2RY12) in Hispanic/Latino patients of diverse backgrounds.	clopidogrel	100-111	paraoxonase 1	Homo sapiens	153-157
30520344-2	2019	The purpose of this research is to describe the prevalence of pharmacogene variants associated with clopidogrel responsiveness (CYP2C19, B4GALT2, ABCB1, PON1, CES1 and P2RY12) in Hispanic/Latino patients of diverse backgrounds.	clopidogrel	100-111	carboxylesterase 1	Homo sapiens	159-163
30520344-2	2019	The purpose of this research is to describe the prevalence of pharmacogene variants associated with clopidogrel responsiveness (CYP2C19, B4GALT2, ABCB1, PON1, CES1 and P2RY12) in Hispanic/Latino patients of diverse backgrounds.	clopidogrel	100-111	purinergic receptor P2Y12	Homo sapiens	168-174
29257922-0	2019	CYP2C19 genotype and adverse cardiovascular outcomes after stent implantation in clopidogrel-treated Asian populations: A systematic review and meta-analysis.	clopidogrel	81-92	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
29257922-1	2019	The effect of CYP2C19 gene polymorphism on clinical outcomes of patients with coronary artery disease (CAD) treated with clopidogrel remains controversial.	clopidogrel	121-132	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
29461906-5	2019	The P-selectin Aspirin Test revealed substantial inhibition of platelet function in all but three of 96 patients receiving aspirin with clopidogrel and in none of 51 patients receiving aspirin and prasugrel.	clopidogrel	136-147	selectin P	Homo sapiens	4-14
29257922-2	2019	Ethnicity has been proposed to influence clopidogrel response following stent implantation in CAD patients with different CYP2C19 genotypes.	clopidogrel	41-52	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	122-129
29461906-10	2019	The results obtained using the P-selectin P2Y12 Test in 102 patients taking aspirin and clopidogrel were similar to the more traditional approaches in that a wide scatter of results was obtained.	clopidogrel	88-99	selectin P	Homo sapiens	31-41
29257922-4	2019	We aimed to evaluate the impact of CYP2C19 gene polymorphism on clinical outcomes in Asian populations who underwent percutaneous coronary interventions (PCI) and received clopidogrel therapy.	clopidogrel	172-183	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	35-42
29777510-2	2018	Here we present genotype and phenotype study of Iranian patients undergoing PCI treated with clopidogrel during a 6-month period of follow-up; common variants of CYP2C19, CYP3A5, CYP3A4, and ABCB1 genes were determined as well as the patients" cardiovascular outcomes to find out the effect of these variants individually and in combination.	clopidogrel	93-104	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	162-169
29461906-10	2019	The results obtained using the P-selectin P2Y12 Test in 102 patients taking aspirin and clopidogrel were similar to the more traditional approaches in that a wide scatter of results was obtained.	clopidogrel	88-99	purinergic receptor P2Y12	Homo sapiens	42-47
29617185-3	2019	P2Y12 is a promising target for antiplatelet, but due to P2Y12 receptor constitutive activation, the clinical practical phenomena such as "clopidogrel resistance" are commonly occurring.	clopidogrel	139-150	purinergic receptor P2Y12	Homo sapiens	0-5
29617185-3	2019	P2Y12 is a promising target for antiplatelet, but due to P2Y12 receptor constitutive activation, the clinical practical phenomena such as "clopidogrel resistance" are commonly occurring.	clopidogrel	139-150	purinergic receptor P2Y12	Homo sapiens	57-62
29869937-7	2019	There was significant diurnal variability of clopidogrel effects as documented with VASP-P, Verify Now, and PAC-1 and P-sel (all p &lt; 0.05), whereas MEA did not differ over 24 h. Neither MPV nor RPF varied significantly over 24 h. In patients with high RPF, platelet function and activation was significantly higher in all assays, compared to patients with low RPF (all p &lt; 0.05).	clopidogrel	45-56	ADCYAP receptor type I	Homo sapiens	108-113
29869937-7	2019	There was significant diurnal variability of clopidogrel effects as documented with VASP-P, Verify Now, and PAC-1 and P-sel (all p &lt; 0.05), whereas MEA did not differ over 24 h. Neither MPV nor RPF varied significantly over 24 h. In patients with high RPF, platelet function and activation was significantly higher in all assays, compared to patients with low RPF (all p &lt; 0.05).	clopidogrel	45-56	selectin P	Homo sapiens	118-123
30500673-5	2019	Platelet reactivity was reduced by all P2Y12 inhibitors, demonstrated by OT prolongation (clopidogrel 378 +- 87 s vs. 491 +- 93 s, p &lt; 0.001; ticagrelor 416 +- 122 s vs. 549 +- 121 s, p &lt; 0.001; cangrelor 381 +- 146 s vs. 613 +- 210 s, p &lt; 0.001).	clopidogrel	90-101	purinergic receptor P2Y12	Homo sapiens	39-44
31184624-1	2019	To identify clinical and pharmacogenetic predictors of the efficacy of clopidogrel in patients with AI based on CYP2C19 and ABCB1 genotyping.	clopidogrel	71-82	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	112-119
31184624-1	2019	To identify clinical and pharmacogenetic predictors of the efficacy of clopidogrel in patients with AI based on CYP2C19 and ABCB1 genotyping.	clopidogrel	71-82	ATP binding cassette subfamily B member 1	Homo sapiens	124-129
30129678-7	2018	Similar to the FBLIM1 knockdown effect, clopidogrel-treated cells had attenuated functions of proliferation, migration, and invasiveness.	clopidogrel	40-51	filamin binding LIM protein 1	Homo sapiens	15-21
30129678-8	2018	Interestingly, clopidogrel treatment led to down-regulation of epidermal growth factor receptor (EGFR) and FBLIM1.	clopidogrel	15-26	epidermal growth factor receptor	Homo sapiens	63-95
30129678-8	2018	Interestingly, clopidogrel treatment led to down-regulation of epidermal growth factor receptor (EGFR) and FBLIM1.	clopidogrel	15-26	epidermal growth factor receptor	Homo sapiens	97-101
30129678-8	2018	Interestingly, clopidogrel treatment led to down-regulation of epidermal growth factor receptor (EGFR) and FBLIM1.	clopidogrel	15-26	filamin binding LIM protein 1	Homo sapiens	107-113
30129678-9	2018	These findings identify FBLIM1 as a putative therapeutic target by using clopidogrel for inhibiting over activation of EGFR signaling to prevent OSCC malignancy.	clopidogrel	73-84	filamin binding LIM protein 1	Homo sapiens	24-30
30129678-9	2018	These findings identify FBLIM1 as a putative therapeutic target by using clopidogrel for inhibiting over activation of EGFR signaling to prevent OSCC malignancy.	clopidogrel	73-84	epidermal growth factor receptor	Homo sapiens	119-123
30478067-1	2018	OBJECTIVE: After finding that the thienopyridines clopidogrel and prasugrel reduced migraine headache (MHA) symptoms in some patients with patent foramen ovale (PFO), this small pilot study was undertaken to determine whether ticagrelor, a nonthienopyridine P2Y12 inhibitor, would have similar MHA effects and might be better suited for a future randomized trial.	clopidogrel	50-61	purinergic receptor P2Y12	Homo sapiens	258-263
30608200-0	2018	Inhibition of Platelets by Clopidogrel Suppressed Ang II-Induced Vascular Inflammation, Oxidative Stress, and Remodeling.	clopidogrel	27-38	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	50-56
30608200-6	2018	We tested the efficacy of clopidogrel (15 mg/kg per day, followed by 5 mg/kg per day) on Ang II -induced platelet activation, P-M binding, vascular platelet accumulation, as well as vascular inflammation and remodeling at day 7 or 14.	clopidogrel	26-37	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	89-95
30608200-7	2018	Clopidogrel reduced platelet vascular deposition (28.7+-2.4% versus 18.3+-2.9%), suppressed inflammatory cell infiltration (3.6+-0.8x104/vessel versus 2.3+-1.2x104/vessel) and oxidative stress, and attenuated vascular remodeling and dysfunction (55.0+-5.5% versus 84.0+-6.0%) following Ang II stimulation at day 7 or 14.	clopidogrel	0-11	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	286-292
30608200-8	2018	Clopidogrel suppressed Ang II -induced P-M binding both at circulating (13.4+-3.3% versus 5.9+-2.7%) and regional (33.4+-4.3% versus 11.9+-2.7%) levels.	clopidogrel	0-11	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	23-29
30608200-10	2018	Clopidogrel prevented vascular inflammation in Ang II -infused mice.	clopidogrel	0-11	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	47-53
30074128-1	2018	This randomized double-blind crossover study aimed to investigate the influence of cytochrome P450 (CYP) 2C19 polymorphisms on the antiplatelet effects of prasugrel in patients with non-cardioembolic stroke treated with clopidogrel.	clopidogrel	220-231	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	83-109
30643395-10	2019	Proton-pump inhibitors in the Beers and STOPP criteria and clopidogrel in the PIM-Chinese accounted for most leading PIMs.	clopidogrel	59-70	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	78-81
30096456-0	2018	CRISPLD1 rs12115090 polymorphisms alters antiplatelet potency of clopidogrel in coronary artery disease patients in Chinese Han.	clopidogrel	65-76	cysteine rich secretory protein LCCL domain containing 1	Homo sapiens	0-8
30096456-13	2018	CONCLUSION: CYP2C19*2 reduced the antiplatelet potency of clopidogrel and increased the risk of HTPR, while CRISPLD1 rs12115090 A&gt;C polymorphism increased the antiplatelet potency of clopidogrel.	clopidogrel	58-69	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
30096456-13	2018	CONCLUSION: CYP2C19*2 reduced the antiplatelet potency of clopidogrel and increased the risk of HTPR, while CRISPLD1 rs12115090 A&gt;C polymorphism increased the antiplatelet potency of clopidogrel.	clopidogrel	186-197	cysteine rich secretory protein LCCL domain containing 1	Homo sapiens	108-116
30073432-0	2018	Clopidogrel utilization in patients with coronary artery disease and diabetes mellitus: should we determine CYP2C19*2 genotype?	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	108-115
30073432-2	2018	The goal of this study is to determine the effect of the cytochrome P450 CYP2C19*2 polymorphism on the platelet response to clopidogrel in patients with and without diabetes mellitus (DM).	clopidogrel	124-135	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	73-80
30073432-5	2018	Platelet reactivity was assessed by the VerifyNow P2Y12 assay and high on clopidogrel platelet reactivity (HPR) was defined as P2Y12 reaction units (PRU) &gt;= 208.	clopidogrel	74-85	purinergic receptor P2Y12	Homo sapiens	127-132
30073432-9	2018	Furthermore, 8.4% of the variability in percent inhibition by clopidogrel could be attributed to CYP2C19*2 carrier status.	clopidogrel	62-73	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	97-104
30422888-0	2018	Investigating the Effect of Demographics, Clinical Characteristics, and Polymorphism of MDR-1, CYP1A2, CYP3A4, and CYP3A5 on Clopidogrel Resistance.	clopidogrel	125-136	ATP binding cassette subfamily B member 1	Homo sapiens	88-93
30422888-0	2018	Investigating the Effect of Demographics, Clinical Characteristics, and Polymorphism of MDR-1, CYP1A2, CYP3A4, and CYP3A5 on Clopidogrel Resistance.	clopidogrel	125-136	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	95-101
30422888-0	2018	Investigating the Effect of Demographics, Clinical Characteristics, and Polymorphism of MDR-1, CYP1A2, CYP3A4, and CYP3A5 on Clopidogrel Resistance.	clopidogrel	125-136	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	103-109
30422888-0	2018	Investigating the Effect of Demographics, Clinical Characteristics, and Polymorphism of MDR-1, CYP1A2, CYP3A4, and CYP3A5 on Clopidogrel Resistance.	clopidogrel	125-136	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	115-121
29520080-13	2018	Among patients with minor stroke or TIA taking clopidogrel-aspirin treatment, CYP2C19 LOF carrier state was associated with higher risk of new stroke in those with eGFR &lt; 75 ml/min/1.73 m2.	clopidogrel	47-58	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	78-85
29520080-13	2018	Among patients with minor stroke or TIA taking clopidogrel-aspirin treatment, CYP2C19 LOF carrier state was associated with higher risk of new stroke in those with eGFR &lt; 75 ml/min/1.73 m2.	clopidogrel	47-58	CD59 molecule (CD59 blood group)	Homo sapiens	180-185
30452466-9	2018	Among loci which have extraordinary MAFs in Roma population two have strong proof of clinical importance: rs1799853 (CYP2C9) for warfarin dosage, and rs12248560 (CYP2C19) for clopidogrel dosage, efficacy and toxicity.	clopidogrel	175-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
30452466-9	2018	Among loci which have extraordinary MAFs in Roma population two have strong proof of clinical importance: rs1799853 (CYP2C9) for warfarin dosage, and rs12248560 (CYP2C19) for clopidogrel dosage, efficacy and toxicity.	clopidogrel	175-186	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	162-169
29574630-6	2018	Intravitreal injection of PSB 0739 or clopidogrel, both selective P2Y12 receptor antagonists, increased by 20 and 15%, respectively, the number of Ki-67-positive cells following 24 h of exposure.	clopidogrel	38-49	purinergic receptor P2Y12	Rattus norvegicus	66-71
29537938-5	2018	The use of platelet aggregation tests has also been advocated to monitor the treatment with antiplatelet agents (mostly the P2Y12 antagonist clopidogrel) of patients with thrombotic arterial occlusions, with the aim of improving their efficacy and safety.	clopidogrel	141-152	purinergic receptor P2Y12	Homo sapiens	124-129
30396378-8	2018	The CYP2C19 enzyme plays also a vital role in the two bioactivation steps of clopidogrel leading to lower (CYP2C19*17 carriers) or higher (CYP2C19*2 carriers) risk of major adverse cardiovascular events.	clopidogrel	77-88	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
30396378-8	2018	The CYP2C19 enzyme plays also a vital role in the two bioactivation steps of clopidogrel leading to lower (CYP2C19*17 carriers) or higher (CYP2C19*2 carriers) risk of major adverse cardiovascular events.	clopidogrel	77-88	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	107-114
30396378-8	2018	The CYP2C19 enzyme plays also a vital role in the two bioactivation steps of clopidogrel leading to lower (CYP2C19*17 carriers) or higher (CYP2C19*2 carriers) risk of major adverse cardiovascular events.	clopidogrel	77-88	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	107-114
30498334-5	2018	Results: Compared with treatment with aspirin + new P2Y12 inhibitor, treatment with aspirin + new P2Y12 inhibitor converted to clopidogrel clinically reduced the risk of major cardiovascular events or significant bleeding (OR: 0.30, 95% credibility interval: 0.12-0.75).	clopidogrel	127-138	purinergic receptor P2Y12	Homo sapiens	98-103
30498515-2	2018	The present study was to investigate the herb-drug interaction of Clopidogrel and XST by modulation of the pharmacodynamics and liver Carboxylesterase 1A(CES1A) metabolism.	clopidogrel	66-77	carboxylesterase 1A	Rattus norvegicus	154-159
30498515-12	2018	The animal study indicated that clopidogrel and XST coadministration produced significant herb-drug interactions at active CAMD pharmacokinetic and CES1A metabolic enzyme aspect.	clopidogrel	32-43	carboxylesterase 1A	Rattus norvegicus	148-153
29777510-2	2018	Here we present genotype and phenotype study of Iranian patients undergoing PCI treated with clopidogrel during a 6-month period of follow-up; common variants of CYP2C19, CYP3A5, CYP3A4, and ABCB1 genes were determined as well as the patients" cardiovascular outcomes to find out the effect of these variants individually and in combination.	clopidogrel	93-104	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	171-177
29777510-2	2018	Here we present genotype and phenotype study of Iranian patients undergoing PCI treated with clopidogrel during a 6-month period of follow-up; common variants of CYP2C19, CYP3A5, CYP3A4, and ABCB1 genes were determined as well as the patients" cardiovascular outcomes to find out the effect of these variants individually and in combination.	clopidogrel	93-104	ATP binding cassette subfamily B member 1	Homo sapiens	191-196
30498684-3	2018	For many years, dual antiplatelet therapy (DAPT) with aspirin and the P2Y12 inhibitor clopidogrel has represented the mainstay of treatment following an acute coronary syndrome (ACS) or in patients undergoing percutaneous coronary interventions (PCI).	clopidogrel	86-97	purinergic receptor P2Y12	Homo sapiens	70-75
29858511-3	2018	Clinical relevance of the cytochrome P450 (CYP) polymorphism related to dose, effectiveness and/or toxicity of key drugs are presented in this review, including that of warfarin, clopidogrel, tricyclic antidepressants, and proton pump inhibitors.	clopidogrel	179-190	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	26-41
29858511-3	2018	Clinical relevance of the cytochrome P450 (CYP) polymorphism related to dose, effectiveness and/or toxicity of key drugs are presented in this review, including that of warfarin, clopidogrel, tricyclic antidepressants, and proton pump inhibitors.	clopidogrel	179-190	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	43-46
30233700-0	2018	Effects of different CYP2C19 genotypes on prognosis of patients complicated with atrial fibrillation taking clopidogrel after PCI.	clopidogrel	108-119	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
30233700-1	2018	The effects of different cytochrome P450 2C19 (CYP2C19) genotypes on the prognosis of clopidogrel resistance in patients complicated with atrial fibrillation taking clopidogrel after percutaneous coronary intervention (PCI) were investigated.	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-45
30233700-1	2018	The effects of different cytochrome P450 2C19 (CYP2C19) genotypes on the prognosis of clopidogrel resistance in patients complicated with atrial fibrillation taking clopidogrel after percutaneous coronary intervention (PCI) were investigated.	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	47-54
30128710-0	2018	Aspirin plus clopidogrel may reduce the risk of early neurologic deterioration in ischemic stroke patients carrying CYP2C19*2 reduced-function alleles.	clopidogrel	13-24	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	116-123
30128710-11	2018	Stratified analyses revealed that clopidogrel plus aspirin could be more effective in reducing END than aspirin alone for carriers of CYP2C19*2 reduced-function alleles (18.8 vs. 34.9%, P = 0.006).	clopidogrel	34-45	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	134-141
30128710-13	2018	CONCLUSIONS: Dual therapy with clopidogrel and aspirin may be adequate for prevention of END in carriers of CYP2C19 reduced-function alleles, but not for noncarriers.	clopidogrel	31-42	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	108-115
30238704-2	2018	Potent P2Y12 inhibitors such as prasugrel and ticagrelor exhibit a strong and more consistent platelet inhibition when compared to clopidogrel.	clopidogrel	131-142	purinergic receptor P2Y12	Homo sapiens	7-12
30238704-5	2018	Our review focusses on P2Y12 receptor therapy de-escalation defined as a switch from a potent antiplatelet agent (ticagrelor or prasugrel) to clopidogrel.	clopidogrel	142-153	purinergic receptor P2Y12	Homo sapiens	23-28
29804887-4	2018	This relationship was first described in subjects after acute coronary syndrome due to the interference of proton pump inhibitors in the cytochrome P450 2C19 and the conversion of clopidogrel to its active metabolite.	clopidogrel	180-191	ATPase H+/K+ transporting non-gastric alpha2 subunit	Homo sapiens	107-118
29804887-4	2018	This relationship was first described in subjects after acute coronary syndrome due to the interference of proton pump inhibitors in the cytochrome P450 2C19 and the conversion of clopidogrel to its active metabolite.	clopidogrel	180-191	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	137-157
30193195-12	2018	CONCLUSIONS: CYP2C19 metabolizer status and GRACE score are readily available predictive approaches for MACEs, and their combination derives a more accurate long-term MACE prediction in clopidogrel-treated patients with ACS undergoing PCI.	clopidogrel	186-197	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
30199785-2	2018	As a thienopyridine antiplatelet agent which is approved by the US Food and Drug Administration for the treatment of cardiovascular diseases, currently, clopidogrel was once considered to be the most safe and effective antiplatelet drug in the P2Y12 receptor antagonists, however, it has become increasingly clear that clopidogrel does not satisfactorily inhibit the platelets of approximately one-third of patients.	clopidogrel	153-164	purinergic receptor P2Y12	Homo sapiens	244-249
30283338-0	2018	Association of N6AMT1 rs2254638 Polymorphism With Clopidogrel Response in Chinese Patients With Coronary Artery Disease.	clopidogrel	50-61	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	15-21
30283338-4	2018	Recently, the N-6-adenine-specific DNA methyltransferase 1 (N6AMT1) rs2254638 polymorphism is reported to be associated with clopidogrel response.	clopidogrel	125-136	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	14-58
30283338-4	2018	Recently, the N-6-adenine-specific DNA methyltransferase 1 (N6AMT1) rs2254638 polymorphism is reported to be associated with clopidogrel response.	clopidogrel	125-136	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	60-66
30283338-5	2018	To validate the association between N6AMT1 rs2254638 polymorphism and clopidogrel response, 435 Chinese CAD patients receiving aspirin and clopidogrel were recruited.	clopidogrel	70-81	N-6 adenine-specific DNA methyltransferase 1	Homo sapiens	36-42
30283338-13	2018	When the patients were grouped into clopidogrel resistance (CR) and non-clopidogrel resistance (non-CR) groups, CYP2C19 * 2 was associated with increased risk of CR in the entire cohort, the LD cohort and the MD cohort (p &lt; 0.001, p &lt; 0.001, and p = 0.019, respectively).	clopidogrel	36-47	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	112-119
30283338-13	2018	When the patients were grouped into clopidogrel resistance (CR) and non-clopidogrel resistance (non-CR) groups, CYP2C19 * 2 was associated with increased risk of CR in the entire cohort, the LD cohort and the MD cohort (p &lt; 0.001, p &lt; 0.001, and p = 0.019, respectively).	clopidogrel	72-83	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	112-119
30283338-16	2018	Our study confirmed the influence of CYP2C19 *2 and rs2254638 polymorphisms on clopidogrel resistance in Chinese CAD patients.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-44
29936693-2	2018	The aim of this pilot prospective study was to evaluate 12-month cardiovascular outcomes in elderly patients with acute coronary syndrome (ACS) receiving dual antiplatelet therapy (aspirin and clopidogrel) according to the clustering of CYP2C19 and ABCB1 genetic variants.	clopidogrel	193-204	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	237-244
30354213-1	2018	Objective- Dual-antiplatelet therapy with acetylsalicylic acid and a P2Y12 antagonist, such as clopidogrel, is the standard of care for acute coronary syndromes.	clopidogrel	95-106	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	69-74
30196683-3	2018	We investigated changes in the value of P2Y12 resistance unit (PRU) when prasugrel was administered to patients with clopidogrel resistance.	clopidogrel	117-128	purinergic receptor P2Y12	Homo sapiens	40-45
30103241-1	2018	BACKGROUND:  Phenotype-guided de-escalation (PGDE) of P2Y12-inhibitor treatment with an early switch from prasugrel to clopidogrel was identified as an effective alternative treatment strategy in acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI).	clopidogrel	119-130	purinergic receptor P2Y12	Homo sapiens	54-59
30103241-8	2018	CONCLUSION:  CYP2C19*2 and CYP2C19*17 carrier status correlates with PR in ACS patients treated with clopidogrel and thus might be useful for pre-selecting patients who will and who may not be suitable for PGDE of anti-platelet treatment.	clopidogrel	101-112	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
30103241-8	2018	CONCLUSION:  CYP2C19*2 and CYP2C19*17 carrier status correlates with PR in ACS patients treated with clopidogrel and thus might be useful for pre-selecting patients who will and who may not be suitable for PGDE of anti-platelet treatment.	clopidogrel	101-112	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	27-34
29052493-0	2018	Impaired liver cytochrome P450 2C11 activity after dual antiplatelet therapy with aspirin and clopidogrel in rats.	clopidogrel	94-105	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	15-35
29774574-0	2018	Nonsynonymous single nucleotide polymorphisms in candidate genes P2RY1, P2RY12 and CYP2C19 for clopidogrel efficacy in cats.	clopidogrel	95-106	purinergic receptor P2Y1	Felis catus	65-70
29774574-0	2018	Nonsynonymous single nucleotide polymorphisms in candidate genes P2RY1, P2RY12 and CYP2C19 for clopidogrel efficacy in cats.	clopidogrel	95-106	purinergic receptor P2Y12	Felis catus	72-78
30020015-0	2018	Beta-1,4-galactosyltransferase 2 c.909C&gt;T gene variant is predictive of on-clopidogrel platelet reactivity.	clopidogrel	78-89	beta-1,4-galactosyltransferase 2	Homo sapiens	0-32
30020015-1	2018	CYP2C19 genotype influences clopidogrel response but only accounts for a small part of the variability in platelet reactivity.	clopidogrel	28-39	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
30020015-3	2018	Carriers of the B4GALT2 c.909C&gt;T variant have lower platelet reactivity indicating that B4GALT2 could influence clopidogrel sensitivity and could expose to the risk of bleeding events.	clopidogrel	115-126	beta-1,4-galactosyltransferase 2	Homo sapiens	16-23
30020015-3	2018	Carriers of the B4GALT2 c.909C&gt;T variant have lower platelet reactivity indicating that B4GALT2 could influence clopidogrel sensitivity and could expose to the risk of bleeding events.	clopidogrel	115-126	beta-1,4-galactosyltransferase 2	Homo sapiens	91-98
30020015-4	2018	We undertook this observational retrospective study to determine if B4GALT2 c.909C&gt;T influences P2RY12-specific vasodilator-stimulated phosphoprotein phosphorylation and agonist-induced platelet aggregation in a nonselected cohort of 174 patients under clopidogrel-based antiplatelet therapy.	clopidogrel	256-267	beta-1,4-galactosyltransferase 2	Homo sapiens	68-75
30020015-4	2018	We undertook this observational retrospective study to determine if B4GALT2 c.909C&gt;T influences P2RY12-specific vasodilator-stimulated phosphoprotein phosphorylation and agonist-induced platelet aggregation in a nonselected cohort of 174 patients under clopidogrel-based antiplatelet therapy.	clopidogrel	256-267	purinergic receptor P2Y12	Homo sapiens	99-105
30028231-1	2018	It is well established that the CYP2C19 nonfunctional *2 and *3 polymorphisms impair the bioactivation and antiplatelet effects of clopidogrel, and increase the risk of adverse cardiovascular events following percutaneous coronary intervention.	clopidogrel	131-142	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
30049953-4	2018	CYP2C19 plays an integral part in the metabolism of clopidogrel to the active metabolite clopi-H4.	clopidogrel	52-63	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
29936693-0	2018	Clustering of ABCB1 and CYP2C19 Genetic Variants Predicts Risk of Major Bleeding and Thrombotic Events in Elderly Patients with Acute Coronary Syndrome Receiving Dual Antiplatelet Therapy with Aspirin and Clopidogrel.	clopidogrel	205-216	ATP binding cassette subfamily B member 1	Homo sapiens	14-19
29936693-0	2018	Clustering of ABCB1 and CYP2C19 Genetic Variants Predicts Risk of Major Bleeding and Thrombotic Events in Elderly Patients with Acute Coronary Syndrome Receiving Dual Antiplatelet Therapy with Aspirin and Clopidogrel.	clopidogrel	205-216	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
29807287-1	2018	BACKGROUND: Hepatitis B virus (HBV) infection has been reported to down-regulate the expression of CYP2C19 gene, which may decrease the bioactivation of clopidogrel into active metabolites.	clopidogrel	153-164	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	99-106
30381727-1	2018	We previously reported that the cytochrome P450 (CYP) 2C19 reduced-function polymorphism was associated with decreased responsiveness to clopidogrel and intra-stent thrombus formation, as well as subsequent ischemic events after drug-eluting stent (DES) implantation.	clopidogrel	137-148	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-58
29171020-0	2018	Clopidogrel but Not Prasugrel Significantly Inhibits the CYP2C8-Mediated Metabolism of Montelukast in Humans.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	57-63
29171020-5	2018	Our results imply that clopidogrel is at least a moderate inhibitor of CYP2C8, but prasugrel is not a clinically relevant CYP2C8 inhibitor.	clopidogrel	23-34	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	71-77
29171020-6	2018	The different interaction potentials of clopidogrel and prasugrel are important to consider when antiplatelet therapy is planned for patients at risk for polypharmacy with CYP2C8 substrates.	clopidogrel	40-51	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	172-178
29804161-0	2018	Dual therapy with clopidogrel and aspirin prevents early neurological deterioration in ischemic stroke patients carrying CYP2C19*2 reduced-function alleles.	clopidogrel	18-29	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	121-128
29804161-13	2018	Dual therapy with clopidogrel and aspirin may be adequate for patients carrying CYP2C19*2 reduced-function alleles.	clopidogrel	18-29	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	80-87
29496531-7	2018	The results suggested that multiple dose administration of Danshen capsules could induce cytochrome P450 (CYP) isoenzymes, thereby increasing the clearance of clopidogrel.	clopidogrel	159-170	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	89-104
29496531-7	2018	The results suggested that multiple dose administration of Danshen capsules could induce cytochrome P450 (CYP) isoenzymes, thereby increasing the clearance of clopidogrel.	clopidogrel	159-170	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	106-109
28963757-8	2018	Clopidogrel was the most common P2Y12 inhibitor used (79.6%).	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	32-37
29415954-0	2018	Antiplatelet Therapy in ACS Patients: Comparing Appropriate P2Y12 Inhibition by Clopidogrel to the Use of New P2Y12 Inhibitors.	clopidogrel	80-91	purinergic receptor P2Y12	Homo sapiens	60-65
29415954-3	2018	Whether new P2Y12 inhibitors reduce thrombotic events in a similar manner compared to the rate observed with appropriate P2Y12 inhibition by clopidogrel must still be determined.	clopidogrel	141-152	purinergic receptor P2Y12	Homo sapiens	121-126
28681220-0	2018	Comparison of platelet aggregation response in switching regimen from prasugrel to clopidogrel between CYP2C19 extensive versus non-extensive metabolizers.	clopidogrel	83-94	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	103-110
30017169-0	2018	Effects of CYP2C19 Genetic Polymorphisms on the Pharmacokinetic and Pharmacodynamic Properties of Clopidogrel and Its Active Metabolite in Healthy Chinese Subjects.	clopidogrel	98-109	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	11-18
30017169-1	2018	PURPOSE: Some studies in the white population have shown that carriers of at least 1 loss-of-function allele in the gene that encodes the cytochrome P-450 2C19 isozyme (CYP2C19) have lower levels of the clopidogrel active metabolite (CAM) and a reduced antiplatelet effect of clopidogrel.	clopidogrel	203-214	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	138-159
30017169-1	2018	PURPOSE: Some studies in the white population have shown that carriers of at least 1 loss-of-function allele in the gene that encodes the cytochrome P-450 2C19 isozyme (CYP2C19) have lower levels of the clopidogrel active metabolite (CAM) and a reduced antiplatelet effect of clopidogrel.	clopidogrel	203-214	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	169-176
30017169-1	2018	PURPOSE: Some studies in the white population have shown that carriers of at least 1 loss-of-function allele in the gene that encodes the cytochrome P-450 2C19 isozyme (CYP2C19) have lower levels of the clopidogrel active metabolite (CAM) and a reduced antiplatelet effect of clopidogrel.	clopidogrel	276-287	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	138-159
30017169-1	2018	PURPOSE: Some studies in the white population have shown that carriers of at least 1 loss-of-function allele in the gene that encodes the cytochrome P-450 2C19 isozyme (CYP2C19) have lower levels of the clopidogrel active metabolite (CAM) and a reduced antiplatelet effect of clopidogrel.	clopidogrel	276-287	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	169-176
30017169-4	2018	This study was aimed to investigate the influence of CYP2C19 genetic polymorphisms on the pharmacokinetic properties of CAM and the antiplatelet effect of clopidogrel in healthy Chinese volunteers, and to provide evidence for the role of a CYP2C19 genotyping test in predicting the antiplatelet effect of clopidogrel in the Chinese population.	clopidogrel	305-316	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-60
30017169-13	2018	IMPLICATION: In these healthy Chinese subjects, carriers of CYP2C19 loss-of-function allele(s) had significantly reduced exposure of CAM and decreased levels of inhibition of platelet aggregation with clopidogrel; these genotypes therefore might be a determinant for the formation of CAM and its antiplatelet effects.	clopidogrel	201-212	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	60-67
29667460-6	2018	Acute myocardial infarction and ischemic stroke are associated with high platelet reactivity on clopidogrel in 6-58% of patients when assessed with P-selectin expression, and high reactivity was associated with an increased risk of recurrence after myocardial infarction.	clopidogrel	96-107	selectin P	Homo sapiens	148-158
28737446-9	2018	The fm, CYP2B6 values for artemisinin, bupropion, clopidogrel, ketamine, selegiline, sertraline and ticlopidine were 0.24, 0.28, 0.15, 0.45, 0.46, 0.42 and 0.54, respectively, in HLM determined by chemical inhibition method.	clopidogrel	50-61	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	8-14
28737446-10	2018	The fm, CYP2B6 values for artemisinin, bupropion, clopidogrel, ketamine, selegiline, sertraline and ticlopidine were 0.46, 0.17, 0.15, 0.60, 0.51, 0.66 and 0.77, respectively, in HLM determined by chemical inhibition method in the presence of BSA (0.5% w/v).	clopidogrel	50-61	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	8-14
29738309-1	2018	BACKGROUND: The focus of the study is to determine the prevalence of CYP2C19 alleles, associated with the risk of changes in the pharmacological response to clopidogrel and proton pump inhibitors in patients with acute coronary syndrome (ACS) and gastric ulcer from Russian and Yakut ethnic groups.	clopidogrel	157-168	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	69-76
29936693-2	2018	The aim of this pilot prospective study was to evaluate 12-month cardiovascular outcomes in elderly patients with acute coronary syndrome (ACS) receiving dual antiplatelet therapy (aspirin and clopidogrel) according to the clustering of CYP2C19 and ABCB1 genetic variants.	clopidogrel	193-204	ATP binding cassette subfamily B member 1	Homo sapiens	249-254
29936693-3	2018	METHODS: Participants were 100 consecutive ACS patients who were genotyped for CYP2C19 (G681A and C-806T) and ABCB1 (C3435T) polymorphisms, which affect clopidogrel metabolism and bioavailability, using PCR-restriction fragment length polymorphism.	clopidogrel	153-164	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	79-86
29936693-3	2018	METHODS: Participants were 100 consecutive ACS patients who were genotyped for CYP2C19 (G681A and C-806T) and ABCB1 (C3435T) polymorphisms, which affect clopidogrel metabolism and bioavailability, using PCR-restriction fragment length polymorphism.	clopidogrel	153-164	ATP binding cassette subfamily B member 1	Homo sapiens	110-115
29526833-1	2018	BACKGROUND: Switching between different classes of P2Y12 inhibitors, including de-escalation from ticagrelor to clopidogrel, commonly occurs in clinical practice.	clopidogrel	112-123	purinergic receptor P2Y12	Homo sapiens	51-56
29411531-12	2018	Single nucleotide polymorphisms in serum paraoxonase/arylesterase 1 (PON1) gene was associated with aspirin HoTPR (P = 0.005) while SNP in phospholipase A2, group III (PLA2G3) gene was associated with clopidogrel HoTPR (P = 0.002).	clopidogrel	201-212	paraoxonase 1	Homo sapiens	35-67
29411531-12	2018	Single nucleotide polymorphisms in serum paraoxonase/arylesterase 1 (PON1) gene was associated with aspirin HoTPR (P = 0.005) while SNP in phospholipase A2, group III (PLA2G3) gene was associated with clopidogrel HoTPR (P = 0.002).	clopidogrel	201-212	paraoxonase 1	Homo sapiens	69-73
29309286-9	2018	CONCLUSION: In the present registry of a high-risk population, clopidogrel was the most used P2Y12 inhibitor at hospital discharge, confirming the "paradox" to treat sicker patients with the less effective drug.	clopidogrel	63-74	purinergic receptor P2Y12	Homo sapiens	93-98
29397568-0	2018	CYP2C19 and ABCB1 genetic polymorphisms correlate with the recurrence of ischemic cardiovascular adverse events after clopidogrel treatment.	clopidogrel	118-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
29914380-0	2018	Vasodilator-stimulated phosphoprotein-guided Clopidogrel maintenance therapy reduces cardiovascular events in atrial fibrillation patients requiring anticoagulation therapy and scheduled for percutaneous coronary intervention: a prospective cohort study.	clopidogrel	45-56	vasodilator stimulated phosphoprotein	Homo sapiens	0-37
29397568-0	2018	CYP2C19 and ABCB1 genetic polymorphisms correlate with the recurrence of ischemic cardiovascular adverse events after clopidogrel treatment.	clopidogrel	118-129	ATP binding cassette subfamily B member 1	Homo sapiens	12-17
29397568-1	2018	BACKGROUND: This study was aimed to investigate the correlation between CYP2C19 and ABCB1 polymorphisms and the recurrence of ischemic cardiovascular adverse events in patients with coronary artery disease treated with clopidogrel.	clopidogrel	219-230	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	72-79
29397568-1	2018	BACKGROUND: This study was aimed to investigate the correlation between CYP2C19 and ABCB1 polymorphisms and the recurrence of ischemic cardiovascular adverse events in patients with coronary artery disease treated with clopidogrel.	clopidogrel	219-230	ATP binding cassette subfamily B member 1	Homo sapiens	84-89
29914380-1	2018	BACKGROUND: In a previous study, we found that titrating clopidogrel maintenance doses (MDs) according to vasodilator-stimulated phosphoprotein (VASP) monitoring minimised the rate of major adverse cardiovascular and cerebral events (MACCE) after percutaneous coronary intervention (PCI) without increasing bleeding in patients with high on-treatment platelet reaction to clopidogrel.	clopidogrel	57-68	vasodilator stimulated phosphoprotein	Homo sapiens	106-143
29914380-1	2018	BACKGROUND: In a previous study, we found that titrating clopidogrel maintenance doses (MDs) according to vasodilator-stimulated phosphoprotein (VASP) monitoring minimised the rate of major adverse cardiovascular and cerebral events (MACCE) after percutaneous coronary intervention (PCI) without increasing bleeding in patients with high on-treatment platelet reaction to clopidogrel.	clopidogrel	57-68	vasodilator stimulated phosphoprotein	Homo sapiens	145-149
29397568-11	2018	CONCLUSION: CYP2C19*3 polymorphism could be an important predictive factor of HPR and ischemic cardiovascular adverse events after clopidogrel treatment.	clopidogrel	131-142	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
29914380-1	2018	BACKGROUND: In a previous study, we found that titrating clopidogrel maintenance doses (MDs) according to vasodilator-stimulated phosphoprotein (VASP) monitoring minimised the rate of major adverse cardiovascular and cerebral events (MACCE) after percutaneous coronary intervention (PCI) without increasing bleeding in patients with high on-treatment platelet reaction to clopidogrel.	clopidogrel	372-383	vasodilator stimulated phosphoprotein	Homo sapiens	106-143
29914380-1	2018	BACKGROUND: In a previous study, we found that titrating clopidogrel maintenance doses (MDs) according to vasodilator-stimulated phosphoprotein (VASP) monitoring minimised the rate of major adverse cardiovascular and cerebral events (MACCE) after percutaneous coronary intervention (PCI) without increasing bleeding in patients with high on-treatment platelet reaction to clopidogrel.	clopidogrel	372-383	vasodilator stimulated phosphoprotein	Homo sapiens	145-149
29449127-1	2018	BACKGROUND AND GOAL: Cytochrome P450 (CYP) enzymes are responsible for the conversion of clopidogrel into its active metabolite and the metabolism of proton pump inhibitors (PPIs), which may also inhibit CYP enzymes.	clopidogrel	89-100	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	21-36
29914380-2	2018	This study aimed to investigate whether VASP-guided clopidogrel MD could reduce thromboembolism and bleeding in atrial fibrillation (AF) patients requiring anticoagulation and scheduled for PCI.	clopidogrel	52-63	vasodilator stimulated phosphoprotein	Homo sapiens	40-44
29914380-5	2018	In the VASP-guided group, clopidogrel MD was titrated by the platelet reactivity index (PRI), whereas in the control group, clopidogrel MD was fixed at 75 mg per day.	clopidogrel	26-37	vasodilator stimulated phosphoprotein	Homo sapiens	7-11
29449127-1	2018	BACKGROUND AND GOAL: Cytochrome P450 (CYP) enzymes are responsible for the conversion of clopidogrel into its active metabolite and the metabolism of proton pump inhibitors (PPIs), which may also inhibit CYP enzymes.	clopidogrel	89-100	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	38-41
29449127-1	2018	BACKGROUND AND GOAL: Cytochrome P450 (CYP) enzymes are responsible for the conversion of clopidogrel into its active metabolite and the metabolism of proton pump inhibitors (PPIs), which may also inhibit CYP enzymes.	clopidogrel	89-100	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	204-207
29901608-0	2018	Efficacy and safety of CYP2C19 genotype in stroke or transient ischemic attack patients treated with clopidogrel monotherapy or clopidogrel plus aspirin: Protocol for a systemic review and meta-analysis.	clopidogrel	101-112	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	23-30
29896034-2	2018	This article compares the efficacy, safety, and other characteristics of the three available oral P2Y12 inhibitors-clopidogrel, prasugrel, and ticagrelor.	clopidogrel	115-126	purinergic receptor P2Y12	Homo sapiens	98-103
29510176-0	2018	Association between P2RY12 gene polymorphisms and adverse clinical events in coronary artery disease patients treated with clopidogrel: A systematic review and meta-analysis.	clopidogrel	123-134	purinergic receptor P2Y12	Homo sapiens	20-26
29510176-1	2018	OBJECTIVE: Investigate the association between P2Y12 Purinoceptor (P2RY12) polymorphisms and adverse clinical events in coronary artery disease (CAD) patients treated with clopidogrel.	clopidogrel	172-183	purinergic receptor P2Y12	Homo sapiens	67-73
29526765-11	2018	Furthermore, the identified biomarkers indicated that clopidogrel HTPR is multifactorial where the metabolic phenotypes of insulin resistance, type two diabetes mellitus, obesity, gut-microbiota and heart failure are associated with it.	clopidogrel	54-65	insulin	Homo sapiens	123-130
29743380-1	2018	BACKGROUND: Patients with reduced-function CYP2C19 genotypes on dual antiplatelet therapy (DAPT) with aspirin and clopidogrel show higher clinical risk for acute myocardial infarction (AMI).	clopidogrel	114-125	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	43-50
29703436-7	2018	Clopidogrel was the dominant P2Y12 inhibitor in both groups (unguided: 96% vs PFT guided: 85%, p &lt;0.001).	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	29-34
29432831-0	2018	PXR polymorphisms have impact on the clinical efficacy of clopidogrel in patients undergoing percutaneous coronary intervention.	clopidogrel	58-69	nuclear receptor subfamily 1 group I member 2	Homo sapiens	0-3
29432831-4	2018	The aim of this research is to investigate the association of pregnane X receptor (PXR, also called NR1I2) genetic polymorphisms with the clinical efficacy of clopidogrel in patients undergoing PCI.	clopidogrel	159-170	nuclear receptor subfamily 1 group I member 2	Homo sapiens	62-81
29432831-4	2018	The aim of this research is to investigate the association of pregnane X receptor (PXR, also called NR1I2) genetic polymorphisms with the clinical efficacy of clopidogrel in patients undergoing PCI.	clopidogrel	159-170	nuclear receptor subfamily 1 group I member 2	Homo sapiens	83-86
29432831-4	2018	The aim of this research is to investigate the association of pregnane X receptor (PXR, also called NR1I2) genetic polymorphisms with the clinical efficacy of clopidogrel in patients undergoing PCI.	clopidogrel	159-170	nuclear receptor subfamily 1 group I member 2	Homo sapiens	100-105
29432831-14	2018	CONCLUSIONS: The genotypes and haplotypes of PXR rs3814057, rs3814058 and rs6785049 have impact on the MACE in clopidogrel treated patients after PCI.	clopidogrel	111-122	nuclear receptor subfamily 1 group I member 2	Homo sapiens	45-48
29554005-0	2018	CYP2C19 Genotype is an Independent Predictor of Adverse Cardiovascular Outcome in Iraqi Patients on Clopidogrel After Percutaneous Coronary Intervention.	clopidogrel	100-111	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
29901608-0	2018	Efficacy and safety of CYP2C19 genotype in stroke or transient ischemic attack patients treated with clopidogrel monotherapy or clopidogrel plus aspirin: Protocol for a systemic review and meta-analysis.	clopidogrel	128-139	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	23-30
29901608-1	2018	BACKGROUND: The relationship of CYP2C19 genotype and clinical efficacy in stroke or transient ischemic attack (TIA) patients treated with clopidogrel monotherapy or clopidogrel plus aspirin remains unknown.	clopidogrel	138-149	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
29901608-1	2018	BACKGROUND: The relationship of CYP2C19 genotype and clinical efficacy in stroke or transient ischemic attack (TIA) patients treated with clopidogrel monotherapy or clopidogrel plus aspirin remains unknown.	clopidogrel	165-176	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
29901608-5	2018	RESULTS: This study will provide the evidence of the relationship between CYP2C19 genotype and clinical efficacy and safety in stroke/TIA patients taking clopidogrel by pooling the results of individual studies.	clopidogrel	154-165	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	74-81
29589775-0	2018	Role of CYP2C19 genotype testing in clinical use of clopidogrel: is it really useful?	clopidogrel	52-63	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	8-15
28875498-0	2018	Comparative Study of Effects of Vonoprazan and Esomeprazole on Antiplatelet Function of Clopidogrel or Prasugrel in Relation to CYP2C19 Genotype.	clopidogrel	88-99	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	128-135
28875498-3	2018	CYP2C19 and CYP3A4 are involved in the metabolism of clopidogrel, prasugrel, esomeprazole, and vonoprazan.	clopidogrel	53-64	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
28875498-3	2018	CYP2C19 and CYP3A4 are involved in the metabolism of clopidogrel, prasugrel, esomeprazole, and vonoprazan.	clopidogrel	53-64	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	12-18
29589775-2	2018	Areas covered: Clopidogrel efficacy can be significantly modified by polymorphism of CYP2C19 genotype (more than 25 allelic variants) involved in its metabolism that can adversely affect its anti-platelet activity.	clopidogrel	15-26	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	85-92
29589775-4	2018	Experts commentary: Currently, there is conflicting evidence in regards to the use of CYP2C19 genotyping to identify poor responders to clopidogrel in clinical practice.	clopidogrel	136-147	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	86-93
29618159-1	2018	BACKGROUND: Early escalation from clopidogrel to new generation P2Y12 inhibitors is common practice in patients with ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI).	clopidogrel	34-45	purinergic receptor P2Y12	Homo sapiens	64-69
29774880-1	2018	OBJECTIVE: To investigate the potential correlation between miR-223 level in leukocytes and platelet responses to clopidogrel in patients with coronary artery disease.	clopidogrel	114-125	microRNA 223	Homo sapiens	60-67
29774880-4	2018	Extreme cases of platelet responses to clopidogrel (ultra- vs. non-responder) were measured with miR-223-3p levels in leukocytes.	clopidogrel	39-50	microRNA 223	Homo sapiens	97-104
28520346-0	2012	Clopidogrel Therapy and CYP2C19 Genotype Clopidogrel is an antiplatelet agent used to reduce the risk of myocardial infarction (MI) and stroke among high-risk patients.	clopidogrel	41-52	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
28520346-2	2012	CYP2C19 is one of the principal enzymes involved in the hepatic bioactivation of clopidogrel.	clopidogrel	81-92	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
28520346-3	2012	Of note, the recommended doses of clopidogrel are less effective in patients with loss-of-function variant alleles in the CYP2C19 gene.	clopidogrel	34-45	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	122-129
28520346-5	2012	The FDA-approved drug label for clopidogrel contains a boxed warning, stating that clopidogrel has diminished effectiveness among CYP2C19 poor metabolizers.	clopidogrel	32-43	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	130-137
28520346-5	2012	The FDA-approved drug label for clopidogrel contains a boxed warning, stating that clopidogrel has diminished effectiveness among CYP2C19 poor metabolizers.	clopidogrel	83-94	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	130-137
29642909-1	2018	BACKGROUND: The CYP2C19 nonfunctional genotype reduces clopidogrel effectiveness after percutaneous coronary intervention (PCI).	clopidogrel	55-66	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
29127901-1	2018	The disposition dose of clopidogrel is different in CYP2C19*2 gene carriers and non-carriers.	clopidogrel	24-35	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	52-59
29127901-2	2018	High-dose clopidogrel has been recommended to overcome a low-responsiveness to clopidogrel in patients with the CYP2C19*2 gene.	clopidogrel	10-21	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	112-119
29127901-2	2018	High-dose clopidogrel has been recommended to overcome a low-responsiveness to clopidogrel in patients with the CYP2C19*2 gene.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	112-119
29127901-3	2018	To guide the choice of clopidogrel dosage and catalyse a development in the field of personalized therapy, we developed an ultrasensitive electrochemical biosensor to detect CYP2C19*2 gene.	clopidogrel	23-34	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	174-181
29707143-8	2018	However, in patients treated with clopidogrel, carriers of at least one CYP2C19 reduced-function allele had a 3-fold higher adjusted risk for primary outcome compared with noncarriers (95% confidence interval, 1.23 to 8.74).	clopidogrel	34-45	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	72-79
29707143-9	2018	Conclusions: Among IS patients treated with clopidogrel, carriers of a reduced-function CYP2C19 allele had a significantly higher rate of adverse vascular events than did noncarriers.	clopidogrel	44-55	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	88-95
29707143-10	2018	It should avoid prescribing clopidogrel to these patients with known CYP2C19 polymorphisms.	clopidogrel	28-39	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	69-76
29615454-1	2018	BACKGROUND: CYP2C19 loss-of-function (LOF) alleles impair clopidogrel effectiveness after percutaneous coronary intervention.	clopidogrel	58-69	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
29708956-3	2018	The choice of antiplatelet and anticoagulant drugs should be individualized with clopidogrel as a key P2Y12 inhibitor in this population.	clopidogrel	81-92	purinergic receptor P2Y12	Homo sapiens	102-107
29243114-1	2018	BACKGROUND AND OBJECTIVES: The objective of this study is to evaluate the effects of cytochrome P450 2C19 (CYP2C19) polymorphism on adverse cardiovascular events (MACE) in Hakka patients with acute coronary syndrome (ACS) receiving clopidogrel who had undergone coronary drug-eluting stent placement after percutaneous coronary intervention (PCI) in southern China.	clopidogrel	232-243	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	85-105
29243114-1	2018	BACKGROUND AND OBJECTIVES: The objective of this study is to evaluate the effects of cytochrome P450 2C19 (CYP2C19) polymorphism on adverse cardiovascular events (MACE) in Hakka patients with acute coronary syndrome (ACS) receiving clopidogrel who had undergone coronary drug-eluting stent placement after percutaneous coronary intervention (PCI) in southern China.	clopidogrel	232-243	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	107-114
29260275-0	2018	Analysis of the CYP2C19 genotype associated with bleeding in Serbian STEMI patients who have undergone primary PCI and treatment with clopidogrel.	clopidogrel	134-145	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
29260275-2	2018	The CYP2C19 gene is the most significant genetic factor which influences response to clopidogrel treatment.	clopidogrel	85-96	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
29260275-3	2018	We aimed to examine the contribution of the CYP2C19 gene to bleeding occurrence during clopidogrel therapy in Serbian patients with ST segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI).	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	44-51
29404632-0	2018	Correction to: Analysis of the CYP2C19 genotype associated with bleeding in Serbian STEMI patients who have undergone primary PCI and treatment with clopidogrel.	clopidogrel	149-160	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	31-38
29369476-15	2018	Clopidogrel prevented the early elevation of the plasma SAA protein level, decreased colitis severity, and delayed the formation of dysplastic lesions and adenocarcinoma.	clopidogrel	0-11	serum amyloid A cluster	Mus musculus	56-59
29615454-12	2018	The higher risk of major adverse cardiovascular or cerebrovascular associated with clopidogrel use in CYP2C19 LOF allele carriers suggests that use of genotype-guided DAPT in practice may improve clinical outcomes.	clopidogrel	83-94	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	102-109
29544699-13	2018	Clopidogrel was used as a P2Y12 inhibitor for DAPT in 1082 (79 7%) patients in the 6-month DAPT group and in 1109 (81 8%) patients in the 12-month or longer DAPT group.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	26-31
29336311-4	2018	During the early stages of the trial, the P2Y12 inhibitor of choice was prasugrel with some use of clopidogrel.	clopidogrel	99-110	purinergic receptor P2Y12	Homo sapiens	42-47
29588304-5	2018	As shown by a total thrombus-formation analysis approach, rivaroxaban treatment led to a significantly decreased coagulation-dependent (AR-chip) thrombus formation in patients treated with ASA plus P2Y12 inhibitor (clopidogrel/ticagrelor), whereas the pure platelet-dependent (PL-chip) thrombus formation was not affected at all.	clopidogrel	215-226	purinergic receptor P2Y12	Homo sapiens	198-203
29338536-4	2018	Therefore, we summarize data from relevant preclinical and clinical trials of currently approved P2Y12 receptor inhibitors (clopidogrel, prasugrel, ticagrelor, cangrelor) and provide strategies of drug switching and management of bleeding events.	clopidogrel	124-135	purinergic receptor P2Y12	Homo sapiens	97-102
29350995-4	2018	CLO is one such drug that specifically and irreversibly inhibits the P2Y12 subtype of ADP receptor.	clopidogrel	0-3	purinergic receptor P2Y12	Homo sapiens	69-74
29509167-0	2018	Impact of CYP2C19 Polymorphisms on Clinical Outcomes and Antiplatelet Potency of Clopidogrel in Caucasian Poststroke Survivors.	clopidogrel	81-92	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-17
29509167-2	2018	Impact of CYP2C19 genetic polymorphisms is an established marker linked to variable response after clopidogrel.	clopidogrel	99-110	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-17
29509167-4	2018	STUDY QUESTION: The primary aim was to evaluate the impact of CYP2C19 allele *2 in heterozygote form on major adverse clinical events in Caucasian poststroke survivors treated with clopidogrel.	clopidogrel	181-192	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	62-69
29509167-5	2018	The secondary aim was to analyze the potential link between CYP2C19 genetic polymorphism and variable response after clopidogrel.	clopidogrel	117-128	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	60-67
28990360-7	2018	Conversely, the CES1 c.428G&gt;A missense SNV (rs71647871) impaired the hydrolysis of clopidogrel, increased exposure to clopidogrel active metabolite and enhanced its antiplatelet effects.	clopidogrel	86-97	carboxylesterase 1	Homo sapiens	16-20
28990360-7	2018	Conversely, the CES1 c.428G&gt;A missense SNV (rs71647871) impaired the hydrolysis of clopidogrel, increased exposure to clopidogrel active metabolite and enhanced its antiplatelet effects.	clopidogrel	121-132	carboxylesterase 1	Homo sapiens	16-20
29138287-13	2018	These findings may have implications regarding the intracellular mechanisms leading to CYP2C8 inactivation by clopidogrel.	clopidogrel	110-121	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	87-93
29247634-1	2018	BACKGROUND: CYP2C19, a member of cytochrome P450 enzymes, is involved in various drug metabolisms, such as Clopidogrel.	clopidogrel	107-118	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
29247634-2	2018	Common Single Nucleotide Polymorphisms (SNPs) of CYP2C19 gene, CYP2C19*2 and CYP2C19*3, are liable for the poor metabolism of Clopidogrel.	clopidogrel	126-137	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	49-56
29247634-2	2018	Common Single Nucleotide Polymorphisms (SNPs) of CYP2C19 gene, CYP2C19*2 and CYP2C19*3, are liable for the poor metabolism of Clopidogrel.	clopidogrel	126-137	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	63-70
29247634-2	2018	Common Single Nucleotide Polymorphisms (SNPs) of CYP2C19 gene, CYP2C19*2 and CYP2C19*3, are liable for the poor metabolism of Clopidogrel.	clopidogrel	126-137	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	63-70
29407631-1	2018	OBJECTIVE: To investigate the association between PEAR1 (platelet endothelial aggregation receptor-1) polymorphisms and cardiovascular outcomes in acute coronary syndrome (ACS) in patients treated with aspirin and clopidogrel.	clopidogrel	214-225	platelet endothelial aggregation receptor 1	Homo sapiens	50-55
29407631-1	2018	OBJECTIVE: To investigate the association between PEAR1 (platelet endothelial aggregation receptor-1) polymorphisms and cardiovascular outcomes in acute coronary syndrome (ACS) in patients treated with aspirin and clopidogrel.	clopidogrel	214-225	platelet endothelial aggregation receptor 1	Homo sapiens	57-100
29407631-9	2018	CONCLUSIONS: For Chinese patients with ACS treated with aspirin and clopidogrel, genetic mutations in rs822441/rs822442 in PEAR1 correlated significantly with platelet activity after adjusting for CYP2C19 *2/*3 alleles.	clopidogrel	68-79	platelet endothelial aggregation receptor 1	Homo sapiens	123-128
30325490-1	2018	INTRODUCTION: Clopidogrel (clopi) is a prodrug widely prescribed in the management of coronary artery disease and requires the intervention of hepatic cytochrome P450 2C19 (CYP2C19) for its activation.	clopidogrel	14-25	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	151-171
30325490-1	2018	INTRODUCTION: Clopidogrel (clopi) is a prodrug widely prescribed in the management of coronary artery disease and requires the intervention of hepatic cytochrome P450 2C19 (CYP2C19) for its activation.	clopidogrel	14-25	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	173-180
30325490-1	2018	INTRODUCTION: Clopidogrel (clopi) is a prodrug widely prescribed in the management of coronary artery disease and requires the intervention of hepatic cytochrome P450 2C19 (CYP2C19) for its activation.	clopidogrel	27-32	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	151-171
30325490-1	2018	INTRODUCTION: Clopidogrel (clopi) is a prodrug widely prescribed in the management of coronary artery disease and requires the intervention of hepatic cytochrome P450 2C19 (CYP2C19) for its activation.	clopidogrel	27-32	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	173-180
30325490-4	2018	OBJECTIVE: To evaluate the effect of Cyp2C19 * 2 polymorphism on MACE occurrence and hemorrhagic complications in patients treated with clopi.	clopidogrel	136-141	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-44
29437596-7	2018	Of those with recurrent ischemic events, 101 of 1092 (9.3%) occurring in clopidogrel-treated patients led to P2Y12 inhibitor intensification.	clopidogrel	73-84	purinergic receptor P2Y12	Homo sapiens	109-114
29437596-10	2018	CONCLUSIONS: Few patients after MI with a recurrent ischemic event who were taking clopidogrel switched to a more potent P2Y12 inhibitor, even after stent thrombosis events.	clopidogrel	83-94	purinergic receptor P2Y12	Homo sapiens	121-126
29215418-1	2018	Ticagrelor and prasugrel are newer antiplatelet drugs which, like clopidogrel, block the P2Y12 platelet receptor to inhibit platelet aggregation.	clopidogrel	66-77	purinergic receptor P2Y12	Homo sapiens	89-94
29330312-1	2018	OBJECTIVE: To determine the relationship of high-sensitive C-reactive protein (hsCRP) and the efficacy and safety of dual antiplatelet therapy in patients with and without intracranial arterial stenosis (ICAS) in the Clopidogrel in High-Risk Patients with Acute Non-disabling Cerebrovascular Events (CHANCE) trial.	clopidogrel	217-228	C-reactive protein	Homo sapiens	59-77
29154109-1	2018	Vicagrel, an analog of clopidogrel, is a novel thienopyridine P2Y12 antagonist in clinical development in China for the treatment of acute coronary syndromes.	clopidogrel	23-34	purinergic receptor P2Y12	Homo sapiens	62-67
29456511-8	2018	Thus, P2Y12R antagonists, including clopidogrel, ticagrelor, and prasugrel, might represent potential anti-cancer agents, in addition to their role as effective antithrombotic drugs.	clopidogrel	36-47	purinergic receptor P2Y12	Homo sapiens	6-12
29350207-0	2018	Association between CYP2C19 and ABCB1 polymorphisms and clopidogrel resistance in clopidogrel-treated Chinese patients.	clopidogrel	56-67	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	20-27
29350207-0	2018	Association between CYP2C19 and ABCB1 polymorphisms and clopidogrel resistance in clopidogrel-treated Chinese patients.	clopidogrel	56-67	ATP binding cassette subfamily B member 1	Homo sapiens	32-37
29350207-0	2018	Association between CYP2C19 and ABCB1 polymorphisms and clopidogrel resistance in clopidogrel-treated Chinese patients.	clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	20-27
29350207-0	2018	Association between CYP2C19 and ABCB1 polymorphisms and clopidogrel resistance in clopidogrel-treated Chinese patients.	clopidogrel	82-93	ATP binding cassette subfamily B member 1	Homo sapiens	32-37
29350207-1	2018	OBJECTIVE: To investigate the association between CYP2C19 and ABCB1 polymorphisms and clopidogrel resistance (CR) in patients with cardiovascular disease in Beijing district.	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	50-57
29350207-1	2018	OBJECTIVE: To investigate the association between CYP2C19 and ABCB1 polymorphisms and clopidogrel resistance (CR) in patients with cardiovascular disease in Beijing district.	clopidogrel	86-97	ATP binding cassette subfamily B member 1	Homo sapiens	62-67
29350207-7	2018	CONCLUSION: The carriage of CYP2C19*2 or *3 mutant allele was significantly associated with attenuated platelet response to clopidogrel and increased CR risk.	clopidogrel	124-135	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
29424732-0	2018	Comment on "Association between CYP2C19 and ABCB1 polymorphisms and clopidogrel resistance in clopidogrel-treated Chinese patients".	clopidogrel	68-79	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
29424732-0	2018	Comment on "Association between CYP2C19 and ABCB1 polymorphisms and clopidogrel resistance in clopidogrel-treated Chinese patients".	clopidogrel	68-79	ATP binding cassette subfamily B member 1	Homo sapiens	44-49
29424732-0	2018	Comment on "Association between CYP2C19 and ABCB1 polymorphisms and clopidogrel resistance in clopidogrel-treated Chinese patients".	clopidogrel	94-105	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
29424732-0	2018	Comment on "Association between CYP2C19 and ABCB1 polymorphisms and clopidogrel resistance in clopidogrel-treated Chinese patients".	clopidogrel	94-105	ATP binding cassette subfamily B member 1	Homo sapiens	44-49
29240983-1	2018	Clopidogrel is predominantly hydrolyzed to clopidogrel carboxylic acid (CCA) by carboxylesterase 1, and subsequently CCA is glucuronidated to clopidogrel acyl glucuronide (CAG) by uridine diphosphate-glucuronosyltransferases (UGTs); however, the UGT isoenzymes glucuronidating CCA remain unidentified to date.	clopidogrel	0-11	carboxylesterase 1	Homo sapiens	80-98
29240983-1	2018	Clopidogrel is predominantly hydrolyzed to clopidogrel carboxylic acid (CCA) by carboxylesterase 1, and subsequently CCA is glucuronidated to clopidogrel acyl glucuronide (CAG) by uridine diphosphate-glucuronosyltransferases (UGTs); however, the UGT isoenzymes glucuronidating CCA remain unidentified to date.	clopidogrel	0-11	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	226-229
29240983-8	2018	These results reveal that UGT2B7 is the major enzyme catalyzing clopidogrel glucuronidation in the human liver, and that there is the potential for drug-drug interactions between clopidogrel and the other substrate drugs of UGT2B7.	clopidogrel	64-75	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	26-32
29240983-8	2018	These results reveal that UGT2B7 is the major enzyme catalyzing clopidogrel glucuronidation in the human liver, and that there is the potential for drug-drug interactions between clopidogrel and the other substrate drugs of UGT2B7.	clopidogrel	64-75	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	224-230
29240983-8	2018	These results reveal that UGT2B7 is the major enzyme catalyzing clopidogrel glucuronidation in the human liver, and that there is the potential for drug-drug interactions between clopidogrel and the other substrate drugs of UGT2B7.	clopidogrel	179-190	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	26-32
29240983-8	2018	These results reveal that UGT2B7 is the major enzyme catalyzing clopidogrel glucuronidation in the human liver, and that there is the potential for drug-drug interactions between clopidogrel and the other substrate drugs of UGT2B7.	clopidogrel	179-190	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	224-230
28653333-1	2018	Clopidogrel efficacy is influenced by genetic variation of cytochrome P450 (CYP)2C19, however, few studies have considered patients who have a stroke.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	76-84
28653333-7	2018	In conclusion, we have demonstrated the clinical impact of CYP2C19*2 on clopidogrel efficacy using a purely EMR approach.	clopidogrel	72-83	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	59-66
29138287-1	2018	The antiplatelet drug clopidogrel is metabolized to an acyl-beta-d-glucuronide, which causes time-dependent inactivation of CYP2C8.	clopidogrel	22-33	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	124-130
29138287-4	2018	The effects of relevant UGT polymorphisms on the pharmacokinetics of clopidogrel were evaluated in 106 healthy volunteers.	clopidogrel	69-80	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	24-27
29102571-2	2018	BACKGROUND: CYP2C19 loss-of-function alleles impair clopidogrel effectiveness after PCI.	clopidogrel	52-63	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
28689434-2	2018	Genetic variations of the cytochrome P450 (CYP) 2C19 enzyme, a key determinant in clopidogrel metabolism, have been associated with clopidogrel response profiles.	clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-52
28689434-2	2018	Genetic variations of the cytochrome P450 (CYP) 2C19 enzyme, a key determinant in clopidogrel metabolism, have been associated with clopidogrel response profiles.	clopidogrel	132-143	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-52
28689434-3	2018	Moreover, the presence of a CYP2C19 loss-of-function allele is associated with an increased risk of atherothrombotic events among clopidogrel-treated patients undergoing percutaneous coronary interventions (PCI), prompting studies evaluating the use of genetic tests to identify patients who may be potential candidates for alternative platelet P2Y12 receptor inhibiting therapies (prasugrel or ticagrelor).	clopidogrel	130-141	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
28689434-3	2018	Moreover, the presence of a CYP2C19 loss-of-function allele is associated with an increased risk of atherothrombotic events among clopidogrel-treated patients undergoing percutaneous coronary interventions (PCI), prompting studies evaluating the use of genetic tests to identify patients who may be potential candidates for alternative platelet P2Y12 receptor inhibiting therapies (prasugrel or ticagrelor).	clopidogrel	130-141	purinergic receptor P2Y12	Homo sapiens	345-350
29385765-0	2018	Pharmacogenomic Impact of CYP2C19 Variation on Clopidogrel Therapy in Precision Cardiovascular Medicine.	clopidogrel	47-58	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
29385765-4	2018	In the current pharmacogenomics era, genomic variation in CYP2C19 has led to the definition of pharmacokinetic phenotypes for response to antiplatelet therapy, in particular, clopidogrel.	clopidogrel	175-186	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	58-65
29102571-11	2018	CONCLUSIONS: These data from real-world observations demonstrate a higher risk for cardiovascular events in patients with a CYP2C19 loss-of-function allele if clopidogrel versus alternative therapy is prescribed.	clopidogrel	159-170	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	124-131
29347970-0	2018	A synergic effect between CYP2C19*2, CYP2C19*3 loss-of-function and CYP2C19*17 gain-of-function alleles is associated with Clopidogrel resistance among Moroccan Acute Coronary Syndromes patients.	clopidogrel	123-134	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
29347970-0	2018	A synergic effect between CYP2C19*2, CYP2C19*3 loss-of-function and CYP2C19*17 gain-of-function alleles is associated with Clopidogrel resistance among Moroccan Acute Coronary Syndromes patients.	clopidogrel	123-134	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-44
29347970-0	2018	A synergic effect between CYP2C19*2, CYP2C19*3 loss-of-function and CYP2C19*17 gain-of-function alleles is associated with Clopidogrel resistance among Moroccan Acute Coronary Syndromes patients.	clopidogrel	123-134	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-44
29347970-1	2018	OBJECTIVE: The main objective of our study was to investigate the association of CYP2C19*2 and CYP2C19*3 loss-of-function and CYP2C19*17 gain-of-function variants of CYP2C19 gene with Clopidogrel resistance in a sample of Moroccan Acute Coronary Syndromes patients.	clopidogrel	184-195	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	81-88
29347970-1	2018	OBJECTIVE: The main objective of our study was to investigate the association of CYP2C19*2 and CYP2C19*3 loss-of-function and CYP2C19*17 gain-of-function variants of CYP2C19 gene with Clopidogrel resistance in a sample of Moroccan Acute Coronary Syndromes patients.	clopidogrel	184-195	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	95-102
29347970-1	2018	OBJECTIVE: The main objective of our study was to investigate the association of CYP2C19*2 and CYP2C19*3 loss-of-function and CYP2C19*17 gain-of-function variants of CYP2C19 gene with Clopidogrel resistance in a sample of Moroccan Acute Coronary Syndromes patients.	clopidogrel	184-195	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	95-102
29347970-1	2018	OBJECTIVE: The main objective of our study was to investigate the association of CYP2C19*2 and CYP2C19*3 loss-of-function and CYP2C19*17 gain-of-function variants of CYP2C19 gene with Clopidogrel resistance in a sample of Moroccan Acute Coronary Syndromes patients.	clopidogrel	184-195	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	95-102
29347970-5	2018	Our results support a role of CYP2C19 gene variants as a potential marker of Clopidogrel response.	clopidogrel	77-88	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
29224649-1	2018	BACKGROUND: The use of the potent oral P2Y12 inhibitors prasugrel and ticagrelor in patients with acute coronary syndromes (ACS) has a favorable net clinical effect compared with clopidogrel and is recommended as first-line therapy.	clopidogrel	179-190	purinergic receptor P2Y12	Homo sapiens	39-44
29635252-10	2018	CONCLUSIONS: Our findings suggest that PEAR1, P2Y12, and UGT2A1 genetic variants may be potential biomarkers that can be used to guide clinical applications of clopidogrel and aspirin in Chinese patients.	clopidogrel	160-171	platelet endothelial aggregation receptor 1	Homo sapiens	39-44
29329963-13	2018	Six hours after daily dosing, VASP-PRI &gt;50% was found in 42% of clopidogrel and 2% of ticagrelor treated patients.	clopidogrel	67-78	vasodilator stimulated phosphoprotein	Homo sapiens	30-34
27637911-0	2018	Concomitant Use of Proton-Pump Inhibitors and Clopidogrel Increases the Risk of Adverse Outcomes in Patients With Ischemic Stroke Carrying Reduced-Function CYP2C19*2.	clopidogrel	46-57	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	156-163
27637911-2	2018	The aim of this study was to investigate the association between cytochrome P450 ( CYP) genetic variants and clinical adverse outcomes of concomitant use of PPIs and clopidogrel by patients.	clopidogrel	166-177	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	65-80
27637911-2	2018	The aim of this study was to investigate the association between cytochrome P450 ( CYP) genetic variants and clinical adverse outcomes of concomitant use of PPIs and clopidogrel by patients.	clopidogrel	166-177	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	83-86
27637911-13	2018	CONCLUSIONS: The concomitant use of PPIs and clopidogrel may be associated with an increased risk of RIS, MI, or vascular death in patients with IS carrying reduced-function CYP2C19*2.	clopidogrel	45-56	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	174-181
30621557-5	2018	Resistance to clopidogrel is largely a result of CYP2C19 enzyme loss of function alleles.	clopidogrel	14-25	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	49-56
29308737-5	2018	RESULTS: Pivotal large randomized clinical trials (RCT) in patients with ACS including STEMI, comparing clopidogrel, a first generation P2Y12 inhibitor against the newer prasugrel and ticagrelor showed major efficacy advantages of the latters although both drugs had more bleeding risk than clopidogrel.	clopidogrel	104-115	purinergic receptor P2Y12	Homo sapiens	136-141
29129512-2	2018	The thieno[3,2-c]pyridine class of therapeutic agents, of which clopidogrel is the most commonly used, target the P2Y12 receptor, and are often used in combination with acetylsalicylic acid (ASA).	clopidogrel	64-75	purinergic receptor P2Y12	Homo sapiens	114-119
29345984-12	2018	It will be a useful tool to screen for CYP2C19 loss-of-function alleles in patients before clopidogrel and proton pump inhibitor treatment.	clopidogrel	91-102	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	39-46
29894287-7	2018	RESULTS: Immunohistochemistry results showed that the average positive staining area percentage of IL-17 and MPO in the clopidogrel group was significantly higher than that in the ticagrelor group.	clopidogrel	120-131	interleukin 17A	Homo sapiens	99-104
29894287-7	2018	RESULTS: Immunohistochemistry results showed that the average positive staining area percentage of IL-17 and MPO in the clopidogrel group was significantly higher than that in the ticagrelor group.	clopidogrel	120-131	myeloperoxidase	Homo sapiens	109-112
28635374-3	2018	We aimed to assess P2Y12-mediated platelet reactivity (PR) during sepsis and recovery in patients under clopidogrel.	clopidogrel	104-115	purinergic receptor P2Y12	Homo sapiens	19-24
29178985-6	2018	TSSC6 KO mice treated with clopidogrel exhibited synergy in delayed kinetics of clot retraction, reduced collagen-mediated platelet aggregation, and platelet spreading on fibrinogen.	clopidogrel	27-38	tetraspanin 32	Mus musculus	0-5
29178985-8	2018	Clopidogrel treated TSSC6 KO arterioles showed smaller and less stable thrombi with increased tendency to embolise in vivo.	clopidogrel	0-11	tetraspanin 32	Mus musculus	20-25
29288619-2	2017	Variants in the CYP2C19 gene influence the pharmacokinetics and clinical response to antiplatelet drugs such as clopidogrel; however, there is no available data about the genetic variation of CYP2C19 in the Hakka population in China.	clopidogrel	112-123	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
28877606-0	2018	Discordance Between VASP Phosphorylation and Platelet Aggregation in Defining High On-Clopidogrel Platelet Reactivity After ST-Segment Elevation Myocardial Infarction.	clopidogrel	86-97	vasodilator stimulated phosphoprotein	Homo sapiens	20-24
29075924-6	2018	The dominant P2Y12 inhibitor was clopidogrel (69%) with a high rate of precathlab administration (51.3%).	clopidogrel	33-44	purinergic receptor P2Y12	Homo sapiens	13-18
28117433-0	2018	Cost-effectiveness of cytochrome P450 2C19 *2 genotype-guided selection of clopidogrel or ticagrelor in Chinese patients with acute coronary syndrome.	clopidogrel	75-86	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	22-42
28117433-1	2018	The choice of antiplatelet therapy among Asian populations for the treatment of acute coronary syndrome (ACS) is complicated owing to the high prevalence of cytochrome P450 2C19 (CYP2C19) genetic polymorphism that has been associated with reduced efficacy of clopidogrel.	clopidogrel	259-270	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	157-177
28117433-1	2018	The choice of antiplatelet therapy among Asian populations for the treatment of acute coronary syndrome (ACS) is complicated owing to the high prevalence of cytochrome P450 2C19 (CYP2C19) genetic polymorphism that has been associated with reduced efficacy of clopidogrel.	clopidogrel	259-270	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	179-186
28117433-7	2018	Genotype-guided treatment was cost-effective compared with universal clopidogrel use (ICER of USD2560/QALY).	clopidogrel	69-80	cAMP responsive element modulator	Homo sapiens	86-90
29311920-0	2017	Modulation of miR-26a-5p and miR-15b-5p Exosomal Expression Associated with Clopidogrel-Induced Hepatotoxicity in HepG2 Cells.	clopidogrel	76-87	microRNA 15b	Homo sapiens	29-36
29311920-6	2017	Exposure of HepG2 cells to high concentrations of clopidogrel (50 and 100 muM) for 24 h caused significant DNA fragmentation (17.6 and 44.4%, respectively; p &lt; 0.05) and 48 h (26.8 and 48.9%, respectively; p &lt; 0.05), indicating cellular toxicity.	clopidogrel	50-61	latexin	Homo sapiens	74-77
29311920-7	2017	Upregulation of miR-26a-5p and downregulation of miR-15b-5p was observed in cells exposed to 100 muM clopidogrel for 24 and 48 h. The miR-26a-5p target mRNAs HMGA2, EIF4G2, STRADB, and SENP5 were downregulated in HepG2 cells following exposure to cytotoxic concentrations of clopidogrel (50 and 100 muM) for 24 h, and HMGA2 levels remained low after 48 h of treatment.	clopidogrel	101-112	microRNA 15b	Homo sapiens	49-56
29311920-7	2017	Upregulation of miR-26a-5p and downregulation of miR-15b-5p was observed in cells exposed to 100 muM clopidogrel for 24 and 48 h. The miR-26a-5p target mRNAs HMGA2, EIF4G2, STRADB, and SENP5 were downregulated in HepG2 cells following exposure to cytotoxic concentrations of clopidogrel (50 and 100 muM) for 24 h, and HMGA2 levels remained low after 48 h of treatment.	clopidogrel	101-112	latexin	Homo sapiens	97-100
29311920-7	2017	Upregulation of miR-26a-5p and downregulation of miR-15b-5p was observed in cells exposed to 100 muM clopidogrel for 24 and 48 h. The miR-26a-5p target mRNAs HMGA2, EIF4G2, STRADB, and SENP5 were downregulated in HepG2 cells following exposure to cytotoxic concentrations of clopidogrel (50 and 100 muM) for 24 h, and HMGA2 levels remained low after 48 h of treatment.	clopidogrel	101-112	high mobility group AT-hook 2	Homo sapiens	158-163
29311920-7	2017	Upregulation of miR-26a-5p and downregulation of miR-15b-5p was observed in cells exposed to 100 muM clopidogrel for 24 and 48 h. The miR-26a-5p target mRNAs HMGA2, EIF4G2, STRADB, and SENP5 were downregulated in HepG2 cells following exposure to cytotoxic concentrations of clopidogrel (50 and 100 muM) for 24 h, and HMGA2 levels remained low after 48 h of treatment.	clopidogrel	101-112	eukaryotic translation initiation factor 4 gamma 2	Homo sapiens	165-171
29311920-7	2017	Upregulation of miR-26a-5p and downregulation of miR-15b-5p was observed in cells exposed to 100 muM clopidogrel for 24 and 48 h. The miR-26a-5p target mRNAs HMGA2, EIF4G2, STRADB, and SENP5 were downregulated in HepG2 cells following exposure to cytotoxic concentrations of clopidogrel (50 and 100 muM) for 24 h, and HMGA2 levels remained low after 48 h of treatment.	clopidogrel	101-112	STE20 related adaptor beta	Homo sapiens	173-179
29311920-7	2017	Upregulation of miR-26a-5p and downregulation of miR-15b-5p was observed in cells exposed to 100 muM clopidogrel for 24 and 48 h. The miR-26a-5p target mRNAs HMGA2, EIF4G2, STRADB, and SENP5 were downregulated in HepG2 cells following exposure to cytotoxic concentrations of clopidogrel (50 and 100 muM) for 24 h, and HMGA2 levels remained low after 48 h of treatment.	clopidogrel	101-112	SUMO specific peptidase 5	Homo sapiens	185-190
29311920-7	2017	Upregulation of miR-26a-5p and downregulation of miR-15b-5p was observed in cells exposed to 100 muM clopidogrel for 24 and 48 h. The miR-26a-5p target mRNAs HMGA2, EIF4G2, STRADB, and SENP5 were downregulated in HepG2 cells following exposure to cytotoxic concentrations of clopidogrel (50 and 100 muM) for 24 h, and HMGA2 levels remained low after 48 h of treatment.	clopidogrel	101-112	latexin	Homo sapiens	299-302
29311920-7	2017	Upregulation of miR-26a-5p and downregulation of miR-15b-5p was observed in cells exposed to 100 muM clopidogrel for 24 and 48 h. The miR-26a-5p target mRNAs HMGA2, EIF4G2, STRADB, and SENP5 were downregulated in HepG2 cells following exposure to cytotoxic concentrations of clopidogrel (50 and 100 muM) for 24 h, and HMGA2 levels remained low after 48 h of treatment.	clopidogrel	101-112	high mobility group AT-hook 2	Homo sapiens	318-323
29311920-7	2017	Upregulation of miR-26a-5p and downregulation of miR-15b-5p was observed in cells exposed to 100 muM clopidogrel for 24 and 48 h. The miR-26a-5p target mRNAs HMGA2, EIF4G2, STRADB, and SENP5 were downregulated in HepG2 cells following exposure to cytotoxic concentrations of clopidogrel (50 and 100 muM) for 24 h, and HMGA2 levels remained low after 48 h of treatment.	clopidogrel	275-286	microRNA 15b	Homo sapiens	49-56
29311920-7	2017	Upregulation of miR-26a-5p and downregulation of miR-15b-5p was observed in cells exposed to 100 muM clopidogrel for 24 and 48 h. The miR-26a-5p target mRNAs HMGA2, EIF4G2, STRADB, and SENP5 were downregulated in HepG2 cells following exposure to cytotoxic concentrations of clopidogrel (50 and 100 muM) for 24 h, and HMGA2 levels remained low after 48 h of treatment.	clopidogrel	275-286	latexin	Homo sapiens	97-100
29311920-7	2017	Upregulation of miR-26a-5p and downregulation of miR-15b-5p was observed in cells exposed to 100 muM clopidogrel for 24 and 48 h. The miR-26a-5p target mRNAs HMGA2, EIF4G2, STRADB, and SENP5 were downregulated in HepG2 cells following exposure to cytotoxic concentrations of clopidogrel (50 and 100 muM) for 24 h, and HMGA2 levels remained low after 48 h of treatment.	clopidogrel	275-286	high mobility group AT-hook 2	Homo sapiens	158-163
29311920-7	2017	Upregulation of miR-26a-5p and downregulation of miR-15b-5p was observed in cells exposed to 100 muM clopidogrel for 24 and 48 h. The miR-26a-5p target mRNAs HMGA2, EIF4G2, STRADB, and SENP5 were downregulated in HepG2 cells following exposure to cytotoxic concentrations of clopidogrel (50 and 100 muM) for 24 h, and HMGA2 levels remained low after 48 h of treatment.	clopidogrel	275-286	eukaryotic translation initiation factor 4 gamma 2	Homo sapiens	165-171
29311920-7	2017	Upregulation of miR-26a-5p and downregulation of miR-15b-5p was observed in cells exposed to 100 muM clopidogrel for 24 and 48 h. The miR-26a-5p target mRNAs HMGA2, EIF4G2, STRADB, and SENP5 were downregulated in HepG2 cells following exposure to cytotoxic concentrations of clopidogrel (50 and 100 muM) for 24 h, and HMGA2 levels remained low after 48 h of treatment.	clopidogrel	275-286	STE20 related adaptor beta	Homo sapiens	173-179
29311920-7	2017	Upregulation of miR-26a-5p and downregulation of miR-15b-5p was observed in cells exposed to 100 muM clopidogrel for 24 and 48 h. The miR-26a-5p target mRNAs HMGA2, EIF4G2, STRADB, and SENP5 were downregulated in HepG2 cells following exposure to cytotoxic concentrations of clopidogrel (50 and 100 muM) for 24 h, and HMGA2 levels remained low after 48 h of treatment.	clopidogrel	275-286	SUMO specific peptidase 5	Homo sapiens	185-190
29311920-7	2017	Upregulation of miR-26a-5p and downregulation of miR-15b-5p was observed in cells exposed to 100 muM clopidogrel for 24 and 48 h. The miR-26a-5p target mRNAs HMGA2, EIF4G2, STRADB, and SENP5 were downregulated in HepG2 cells following exposure to cytotoxic concentrations of clopidogrel (50 and 100 muM) for 24 h, and HMGA2 levels remained low after 48 h of treatment.	clopidogrel	275-286	latexin	Homo sapiens	299-302
29311920-7	2017	Upregulation of miR-26a-5p and downregulation of miR-15b-5p was observed in cells exposed to 100 muM clopidogrel for 24 and 48 h. The miR-26a-5p target mRNAs HMGA2, EIF4G2, STRADB, and SENP5 were downregulated in HepG2 cells following exposure to cytotoxic concentrations of clopidogrel (50 and 100 muM) for 24 h, and HMGA2 levels remained low after 48 h of treatment.	clopidogrel	275-286	high mobility group AT-hook 2	Homo sapiens	318-323
29311920-8	2017	TLK1, a target of miR-15b-5p, was downregulated by 50 and 100 muM clopidogrel at 24 h. In conclusion, our results suggest that exposure to high concentrations of clopidogrel modulates the expression of exosomal miR-26a-5p and miR-15b-5p and their target mRNAs in HepG2 cells.	clopidogrel	66-77	tousled like kinase 1	Homo sapiens	0-4
29311920-8	2017	TLK1, a target of miR-15b-5p, was downregulated by 50 and 100 muM clopidogrel at 24 h. In conclusion, our results suggest that exposure to high concentrations of clopidogrel modulates the expression of exosomal miR-26a-5p and miR-15b-5p and their target mRNAs in HepG2 cells.	clopidogrel	66-77	microRNA 15b	Homo sapiens	18-25
29311920-8	2017	TLK1, a target of miR-15b-5p, was downregulated by 50 and 100 muM clopidogrel at 24 h. In conclusion, our results suggest that exposure to high concentrations of clopidogrel modulates the expression of exosomal miR-26a-5p and miR-15b-5p and their target mRNAs in HepG2 cells.	clopidogrel	66-77	latexin	Homo sapiens	62-65
29311920-8	2017	TLK1, a target of miR-15b-5p, was downregulated by 50 and 100 muM clopidogrel at 24 h. In conclusion, our results suggest that exposure to high concentrations of clopidogrel modulates the expression of exosomal miR-26a-5p and miR-15b-5p and their target mRNAs in HepG2 cells.	clopidogrel	66-77	microRNA 15b	Homo sapiens	226-233
29311920-8	2017	TLK1, a target of miR-15b-5p, was downregulated by 50 and 100 muM clopidogrel at 24 h. In conclusion, our results suggest that exposure to high concentrations of clopidogrel modulates the expression of exosomal miR-26a-5p and miR-15b-5p and their target mRNAs in HepG2 cells.	clopidogrel	162-173	tousled like kinase 1	Homo sapiens	0-4
29311920-8	2017	TLK1, a target of miR-15b-5p, was downregulated by 50 and 100 muM clopidogrel at 24 h. In conclusion, our results suggest that exposure to high concentrations of clopidogrel modulates the expression of exosomal miR-26a-5p and miR-15b-5p and their target mRNAs in HepG2 cells.	clopidogrel	162-173	microRNA 15b	Homo sapiens	18-25
29311920-8	2017	TLK1, a target of miR-15b-5p, was downregulated by 50 and 100 muM clopidogrel at 24 h. In conclusion, our results suggest that exposure to high concentrations of clopidogrel modulates the expression of exosomal miR-26a-5p and miR-15b-5p and their target mRNAs in HepG2 cells.	clopidogrel	162-173	latexin	Homo sapiens	62-65
29311920-8	2017	TLK1, a target of miR-15b-5p, was downregulated by 50 and 100 muM clopidogrel at 24 h. In conclusion, our results suggest that exposure to high concentrations of clopidogrel modulates the expression of exosomal miR-26a-5p and miR-15b-5p and their target mRNAs in HepG2 cells.	clopidogrel	162-173	microRNA 15b	Homo sapiens	226-233
29188612-0	2017	[Influence of CYP2C19 gene polymorphisms on the efficacy of clopidogrel treatment for the prevention of ischemic stroke following coronary stent implantation].	clopidogrel	60-71	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
29188612-1	2017	OBJECTIVE: To assess the association of CYP2C19 gene polymorphisms with the incidence of ischemic stroke among patients receiving clopidogrel therapy following coronary stenting for coronary artery disease.	clopidogrel	130-141	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-47
29188612-12	2017	CONCLUSION: The efficacy of clopidogrel for the prevention of ischemic stroke in post-coronary stent patients may be reduced by the insufficiency of the CYP2C19 gene.	clopidogrel	28-39	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	153-160
29635252-10	2018	CONCLUSIONS: Our findings suggest that PEAR1, P2Y12, and UGT2A1 genetic variants may be potential biomarkers that can be used to guide clinical applications of clopidogrel and aspirin in Chinese patients.	clopidogrel	160-171	purinergic receptor P2Y12	Homo sapiens	46-51
29635252-10	2018	CONCLUSIONS: Our findings suggest that PEAR1, P2Y12, and UGT2A1 genetic variants may be potential biomarkers that can be used to guide clinical applications of clopidogrel and aspirin in Chinese patients.	clopidogrel	160-171	UDP glucuronosyltransferase family 2 member A1 complex locus	Homo sapiens	57-63
29300792-8	2017	Although clopidogrel may be the most widely used of the P2Y12 inhibitors recommended for dual antiplatelet therapy, there is evidence of an impaired response in patients with diabetes.	clopidogrel	9-20	purinergic receptor P2Y12	Homo sapiens	56-61
28806186-5	2017	Clopidogrel users with the CYP2C1912 variant had higher platelet aggregation values (median 43, range 30-54%) compared with 11 wild-type carriers (median 33, range 15-77%; P = 0.009).	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	27-32
28806186-10	2017	Plasma CYP4F2 concentrations were significantly lower in ticagrelor users than in clopidogrel users.	clopidogrel	82-93	cytochrome P450 family 4 subfamily F member 2	Homo sapiens	7-13
28914344-6	2017	RESULTS: It was found that the only significant covariate was the presence of CYP2C19*2 allele, which had an impact on lower conversion of clopidogrel to H4.	clopidogrel	139-150	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	78-85
29204116-3	2017	The P2Y12R antagonist and platelet inhibitor, clopidogrel, is widely used for secondary prevention after a stroke.	clopidogrel	46-57	purinergic receptor P2Y12	Homo sapiens	4-10
28817535-2	2017	There is limited evidence on the safety and efficacy of more potent P2Y12 antagonists in the reduction of the incidence of periprocedural myocardial injury among patients undergoing elective percutaneous coronary intervention (PCI) with inadequate response to clopidogrel.	clopidogrel	260-271	purinergic receptor P2Y12	Homo sapiens	68-73
29084738-2	2017	The availability of different oral P2Y12 inhibitors (clopidogrel, prasugrel, ticagrelor) has enabled physicians to contemplate switching among therapies because of specific clinical scenarios.	clopidogrel	53-64	purinergic receptor P2Y12	Homo sapiens	35-40
28267384-1	2017	Three oral platelet P2Y12 inhibitors, clopidogrel, prasugrel, and ticagrelor, are available for reducing the risk of cardiovascular death and stent thrombosis in patients with acute coronary syndromes (ACS).	clopidogrel	38-49	purinergic receptor P2Y12	Homo sapiens	20-25
28653847-5	2017	As interaction perpetrators with CYP2C8, glucuronides of gemfibrozil and clopidogrel showed marked clinical drug-drug interactions (e.g., with cerivastatin and repaglinide), which are more than expected from the parent drug.	clopidogrel	73-84	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	33-39
29263048-1	2017	BACKGROUND: CYP2C19 polymorphisms contribute about 12% of the variability in the antiplatelet effect of clopidogrel, which is commonly prescribed for patients undergoing percutaneous coronary intervention.	clopidogrel	104-115	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
28653184-0	2017	Reversal of the platelet inhibitory effect of the P2Y12 inhibitors clopidogrel, prasugrel, and ticagrelor in vitro: a new approach to an old issue.	clopidogrel	67-78	purinergic receptor P2Y12	Homo sapiens	50-55
28893489-15	2017	Loss-of-function carriers of enzyme CYP2C19, important in clopidogrel metabolism, have a 30% greater risk of ischemic events (P &lt; .001).	clopidogrel	58-69	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	36-43
27488859-0	2017	Changes in P2Y12 reaction units after switching treatments from prasugrel to clopidogrel in Japanese patients with acute coronary syndrome followed by elective coronary stenting.	clopidogrel	77-88	purinergic receptor P2Y12	Homo sapiens	11-16
29382029-3	2017	PATIENT CONCERNS: A 43-year-old Chinese male carrying two reduced-function CYP2C19 alleles was treated with a loading dose of clopidogrel 300 mg and aspirin 300 mg before SAC.	clopidogrel	126-137	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	75-82
29382029-8	2017	LESSONS: The present case demonstrates that CYP2C19 allele carriers may lead to a suppressed antiplatelet effect of clopidogrel and a high risk of ST in the meantime.	clopidogrel	116-127	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	44-51
27233747-0	2017	Interaction of CYP2C19, P2Y12, and GPIIIa Variants Associates With Efficacy of Clopidogrel and Adverse Events on Patients With Ischemic Stroke.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
28411400-1	2017	Dasabuvir, a nonnucleoside NS5B polymerase inhibitor, is a sensitive substrate of cytochrome P450 (CYP) 2C8 with a potential for drug-drug interaction (DDI) with clopidogrel.	clopidogrel	162-173	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	82-107
28411400-2	2017	A physiologically based pharmacokinetic (PBPK) model was developed for dasabuvir to evaluate the DDI potential with clopidogrel, the acyl-beta-D glucuronide metabolite of which has been reported as a strong mechanism-based inhibitor of CYP2C8 based on an interaction with repaglinide.	clopidogrel	116-127	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	236-242
28444890-3	2017	Clopidogrel may increase dasabuvir exposures primarily due to CYP2C8 inhibition by clopidogrel-acyl-beta-D-glucuronide.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	62-68
28623527-0	2017	Updating the Evidence of the Interaction Between Clopidogrel and CYP2C19-Inhibiting Selective Serotonin Reuptake Inhibitors: A Cohort Study and Meta-Analysis.	clopidogrel	49-60	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	65-72
28623527-3	2017	OBJECTIVE: The aim of this study was to assess clinical outcomes following initiation of a CYP2C19-inhibiting SSRI versus initiation of other SSRIs among patients treated with clopidogrel and to update existing evidence on the clinical impact of clopidogrel-SSRI interaction.	clopidogrel	176-187	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	91-98
28623527-3	2017	OBJECTIVE: The aim of this study was to assess clinical outcomes following initiation of a CYP2C19-inhibiting SSRI versus initiation of other SSRIs among patients treated with clopidogrel and to update existing evidence on the clinical impact of clopidogrel-SSRI interaction.	clopidogrel	246-257	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	91-98
28623527-12	2017	The updated evidence still indicates a small decrease in clopidogrel effectiveness associated with concomitant exposure to clopidogrel and CYP2C19-inhibiting SSRIs.	clopidogrel	57-68	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	139-146
28840395-1	2017	BACKGROUND: Clopidogrel is an irreversible antagonist of P2Y12 receptors (P2Y12Rs) used as an antiplatelet drug to reduce risk of thrombosis.	clopidogrel	12-23	purinergic receptor P2Y12	Homo sapiens	57-62
28840395-3	2017	AIM: To evaluate if blockade of P2Y12Rs by clopidogrel is associated with higher incidence of GI symptoms in patients with irritable bowel syndrome (IBS).	clopidogrel	43-54	purinergic receptor P2Y12	Homo sapiens	32-37
28840395-13	2017	CONCLUSIONS: Irreversible blockade of P2Y12R by clopidogrel is associated with higher incidence of GI symptoms in Female IBS patients, although Age or Sex alone contributes to symptomatology.	clopidogrel	48-59	purinergic receptor P2Y12	Homo sapiens	38-44
28204303-2	2017	With over 100 million prescriptions filled since its approval, clopidogrel is the most widely used P2Y12-receptor inhibitor.	clopidogrel	63-74	purinergic receptor P2Y12	Homo sapiens	99-104
29131238-4	2017	The limitations of clopidogrel with variable antiplatelet effects and delayed onset of action are well established and lead to the development of newer P2Y12 inhibitors.	clopidogrel	19-30	purinergic receptor P2Y12	Homo sapiens	152-157
29042978-1	2017	Adenosine diphosphate P2Y12 receptor antagonist clopidogrel is not sufficiently safe for the gastric mucosa in patients with high risk of peptic ulcer, since it may impair healing of gastric erosions.	clopidogrel	48-59	purinergic receptor P2Y12	Homo sapiens	22-27
28663045-9	2017	CONCLUSIONS: Clopidogrel remained the most common P2Y12 inhibitor employed for ACS.	clopidogrel	13-24	purinergic receptor P2Y12	Homo sapiens	50-55
28766499-10	2017	Being a carrier of the CYP2C19 LOF allele has a significant influence on clopidogrel response.	clopidogrel	73-84	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	23-30
27634953-7	2017	Carriers of CYP2C19 loss-of-function (LOF) alleles (*2 or *3, p=0.001), especially PMs (p=0.004), had an increased risk for clopidogrel resistance.	clopidogrel	124-135	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
27634953-12	2017	CONCLUSIONS: CYP2C19 genetic polymorphisms had significant influence on the antiplatelet effect of clopidogrel, and could be considered as risk factors of ischemic or bleeding events and even clinical outcomes of patients with intracranial aneurysms treated with stent-assisted coiling.	clopidogrel	99-110	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
27233747-0	2017	Interaction of CYP2C19, P2Y12, and GPIIIa Variants Associates With Efficacy of Clopidogrel and Adverse Events on Patients With Ischemic Stroke.	clopidogrel	79-90	purinergic receptor P2Y12	Homo sapiens	24-29
27233747-0	2017	Interaction of CYP2C19, P2Y12, and GPIIIa Variants Associates With Efficacy of Clopidogrel and Adverse Events on Patients With Ischemic Stroke.	clopidogrel	79-90	integrin subunit beta 3	Homo sapiens	35-41
28753533-7	2017	Furthermore, TRAF3 methylation has been associated with vascular recurrence after ischemic stroke in patients treated with clopidogrel.	clopidogrel	123-134	TNF receptor associated factor 3	Homo sapiens	13-18
28802144-0	2017	The effect of CYP2C19 genetic polymorphism and non-genetic factors on clopidogrel platelets inhibition in East Asian coronary artery disease patients.	clopidogrel	70-81	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
28993732-6	2017	Clopidogrel, a P2Y12 antagonist, is widely used for the treatment of thrombosis and stroke, blocking P2Y12 receptor-mediated platelet aggregation.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	15-20
29026425-0	2017	Effect of cytochrome P450 2C19*17 allelic variant on cardiovascular and cerebrovascular outcomes in clopidogrel-treated patients: A systematic review and meta-analysis.	clopidogrel	100-111	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-30
29026425-1	2017	BACKGROUND: We aimed to evaluate the associations of gain-of-function allele of CYP2C19*17 and risk of clinical events in clopidogrel-treated patients with cardiovascular and cerebrovascular diseases (CCVDs).	clopidogrel	122-133	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	80-87
28993732-6	2017	Clopidogrel, a P2Y12 antagonist, is widely used for the treatment of thrombosis and stroke, blocking P2Y12 receptor-mediated platelet aggregation.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	101-106
28975318-0	2017	In PCI-treated ACS, switching from aspirin + a newer P2Y12 blocker to aspirin + clopidogrel reduced adverse events.	clopidogrel	80-91	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	15-18
29156815-5	2017	Clopidogrel, which was used as a comparator due to its similar anti-platelet activity, also reduced endothelial activation but, unlike aspirin, enhanced netrin-1 levels (+20.96% from baseline; p=0.0033 vs untreated).	clopidogrel	0-11	netrin 1	Homo sapiens	153-161
28224612-2	2017	CYP2C8 is strongly inhibited by the clopidogrel metabolite acyl-beta-D-glucuronide.	clopidogrel	36-47	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	0-6
28754568-4	2017	Residual PR on clopidogrel, as measured by the VerifyNow P2Y12 point-of-care assay, was included as a continuous linear mediator variable in Cox proportional hazards regression.	clopidogrel	15-26	purinergic receptor P2Y12	Homo sapiens	57-62
29037010-7	2017	In patients with a poor CYP2C19 genotype for clopidogrel metabolism (n=484), the risk of recurrent stroke among those who received triflusal treatment was 2.9% per year, which was not significantly different from those who received clopidogrel treatment (2.2% per year; hazard ratio [HR], 1.23; 95% confidence interval [CI], 0.60-2.53).	clopidogrel	45-56	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
28885323-0	2017	PIK3CG single nucleotide polymorphisms are associated with poor responsiveness to clopidogrel and increased risk of ischemia in patients with coronary heart disease.	clopidogrel	82-93	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma	Homo sapiens	0-6
28885323-1	2017	BACKGROUND: This study explores the associations between PIK3CG single nucleotide polymorphisms (SNPs, rs1129293 and rs17398575) and patient responsiveness to clopidogrel to evaluate the risks of ischemia in patients with coronary heart disease (CHD).	clopidogrel	159-170	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma	Homo sapiens	57-63
28885323-14	2017	CONCLUSION: A positive correlation may exist between PIK3CG SNPs (rs1129293 and rs17398575) and patients with poor responsiveness to clopidogrel.	clopidogrel	133-144	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma	Homo sapiens	53-59
27808485-4	2017	PPIs can reduce the metabolism of clopidogrel by competing with CYP450 enzymes, mostly CYP2C19 isoform.	clopidogrel	34-45	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	87-94
27848264-7	2017	Platelets from patients treated with the ADP P2Y12 receptor antagonist clopidogrel showed a reduced response to lysates compared to platelets from healthy controls without antiplatelet treatment.	clopidogrel	71-82	purinergic receptor P2Y12	Homo sapiens	45-50
28734158-0	2017	Interaction between platelet-derived microRNAs and CYP2C19*2 genotype on clopidogrel antiplatelet responsiveness in patients with ACS.	clopidogrel	73-84	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	51-58
28734158-1	2017	BACKGROUND: Both platelet-derived microRNAs and the genotype of CYP2C19*2 were implicated for the variability of clopidogrel antiplatelet responsiveness.	clopidogrel	113-124	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	64-71
28734158-10	2017	ROC curve showed ideal discriminatory power of the platelet-derived miRNAs for the prediction of clopidogrel antiplatelet responsiveness (c-index=0.70 for miR-223; c-index=0.76 for miR-221; c-index=0.79 for miR-21).	clopidogrel	97-108	microRNA 223	Homo sapiens	155-162
28734158-10	2017	ROC curve showed ideal discriminatory power of the platelet-derived miRNAs for the prediction of clopidogrel antiplatelet responsiveness (c-index=0.70 for miR-223; c-index=0.76 for miR-221; c-index=0.79 for miR-21).	clopidogrel	97-108	microRNA 221	Homo sapiens	181-188
28734158-10	2017	ROC curve showed ideal discriminatory power of the platelet-derived miRNAs for the prediction of clopidogrel antiplatelet responsiveness (c-index=0.70 for miR-223; c-index=0.76 for miR-221; c-index=0.79 for miR-21).	clopidogrel	97-108	microRNA 21	Homo sapiens	207-213
28734158-11	2017	After stratified by the carrier status of CYP2C19*2, the association between platelet-derived miRNAs and clopidogrel antiplatelet responsiveness could be found only in CYP2C19*2 carriers, but not in non-carriers.	clopidogrel	105-116	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	42-49
28734158-11	2017	After stratified by the carrier status of CYP2C19*2, the association between platelet-derived miRNAs and clopidogrel antiplatelet responsiveness could be found only in CYP2C19*2 carriers, but not in non-carriers.	clopidogrel	105-116	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	168-175
28734158-12	2017	CONCLUSIONS: Platelet-derived miRNAs (miR-223, miR-221 and miR-21) are independently associated with clopidogrel antiplatelet responsiveness in ACS patients.	clopidogrel	101-112	microRNA 223	Homo sapiens	38-45
28734158-12	2017	CONCLUSIONS: Platelet-derived miRNAs (miR-223, miR-221 and miR-21) are independently associated with clopidogrel antiplatelet responsiveness in ACS patients.	clopidogrel	101-112	microRNA 221	Homo sapiens	47-54
28734158-12	2017	CONCLUSIONS: Platelet-derived miRNAs (miR-223, miR-221 and miR-21) are independently associated with clopidogrel antiplatelet responsiveness in ACS patients.	clopidogrel	101-112	microRNA 21	Homo sapiens	59-65
28661903-6	2017	Several clinical factors, including common genetic variants such as Cytochrome P450 2C19 loss-of-function alleles, have been shown to predispose to HPR among patients on clopidogrel.	clopidogrel	170-181	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	68-88
31249914-0	2017	Induction of Diabetes Abolishes the Antithrombotic Effect of Clopidogrel in Apolipoprotein E-Deficient Mice.	clopidogrel	61-72	apolipoprotein E	Mus musculus	76-92
31249914-5	2017	The antithrombotic effects of clopidogrel were similar in WT and apoE-deficient mice but were attenuated in diabetic apoE-deficient mice with the percent inhibition of thrombus area (microm 2 ) by clopidogrel being 85.5% (WT mice), 75.0% (apoE-deficient mice), and 1.9% (diabetic apoE-deficient mice).	clopidogrel	30-41	apolipoprotein E	Mus musculus	65-69
31249914-5	2017	The antithrombotic effects of clopidogrel were similar in WT and apoE-deficient mice but were attenuated in diabetic apoE-deficient mice with the percent inhibition of thrombus area (microm 2 ) by clopidogrel being 85.5% (WT mice), 75.0% (apoE-deficient mice), and 1.9% (diabetic apoE-deficient mice).	clopidogrel	30-41	apolipoprotein E	Mus musculus	117-121
31249914-5	2017	The antithrombotic effects of clopidogrel were similar in WT and apoE-deficient mice but were attenuated in diabetic apoE-deficient mice with the percent inhibition of thrombus area (microm 2 ) by clopidogrel being 85.5% (WT mice), 75.0% (apoE-deficient mice), and 1.9% (diabetic apoE-deficient mice).	clopidogrel	197-208	apolipoprotein E	Mus musculus	117-121
31249914-8	2017	In contrast, the effect of clopidogrel on the ex vivo expression of platelet P-selectin induced by protease-activated receptor 4-activating peptide was diminished in diabetic apoE-deficient mice compared with that in WT and apoE-deficient mice.	clopidogrel	27-38	selectin, platelet	Mus musculus	77-87
31249914-8	2017	In contrast, the effect of clopidogrel on the ex vivo expression of platelet P-selectin induced by protease-activated receptor 4-activating peptide was diminished in diabetic apoE-deficient mice compared with that in WT and apoE-deficient mice.	clopidogrel	27-38	apolipoprotein E	Mus musculus	175-179
31249914-9	2017	These data suggest that diabetic apoE-deficient mice may serve as a useful model to better understand the impaired responses to clopidogrel in patients with DM, which may partially reflect a reduction of the effect of clopidogrel on thrombin-induced platelet activation.	clopidogrel	218-229	coagulation factor II, thrombin	Homo sapiens	233-241
28783717-2	2017	This study aimed to investigate the influences of dual-dose clopidogrel, clopidogrel combined with tongxinluo, and ticagrelor on the platelet activity and MACE events of patients with CYP2C19*2 gene function deficiency and poor clopidogrel response after PCI.	clopidogrel	73-84	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	184-191
28783717-2	2017	This study aimed to investigate the influences of dual-dose clopidogrel, clopidogrel combined with tongxinluo, and ticagrelor on the platelet activity and MACE events of patients with CYP2C19*2 gene function deficiency and poor clopidogrel response after PCI.	clopidogrel	73-84	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	184-191
28371087-4	2017	METHODS: TNF-alpha-induced human umbilical vein endothelial cells (HUVEC) were exposed to clopidogrel.	clopidogrel	90-101	tumor necrosis factor	Homo sapiens	9-18
29050321-1	2017	PURPOSE: Genetic variants in cytochrome P450 (CYP), platelet membrane receptor (P2Y12, P2Y1), and glycoprotein IIIa (GPIIIa) genes are associated with the efficacy of clopidogrel and adverse clinical events on ischemic stroke (IS) patients.	clopidogrel	167-178	purinergic receptor P2Y12	Homo sapiens	80-85
29050321-1	2017	PURPOSE: Genetic variants in cytochrome P450 (CYP), platelet membrane receptor (P2Y12, P2Y1), and glycoprotein IIIa (GPIIIa) genes are associated with the efficacy of clopidogrel and adverse clinical events on ischemic stroke (IS) patients.	clopidogrel	167-178	purinergic receptor P2Y1	Homo sapiens	80-84
29050321-1	2017	PURPOSE: Genetic variants in cytochrome P450 (CYP), platelet membrane receptor (P2Y12, P2Y1), and glycoprotein IIIa (GPIIIa) genes are associated with the efficacy of clopidogrel and adverse clinical events on ischemic stroke (IS) patients.	clopidogrel	167-178	integrin subunit beta 3	Homo sapiens	117-123
28775293-0	2017	Effect of carboxylesterase 1 S75N on clopidogrel therapy among acute coronary syndrome patients.	clopidogrel	37-48	carboxylesterase 1	Homo sapiens	10-28
28775293-1	2017	Carboxylesterase 1 (CES1) hydrolyzes the prodrug clopidogrel to an inactive carboxylic acid metabolite.	clopidogrel	49-60	carboxylesterase 1	Homo sapiens	0-18
28775293-1	2017	Carboxylesterase 1 (CES1) hydrolyzes the prodrug clopidogrel to an inactive carboxylic acid metabolite.	clopidogrel	49-60	carboxylesterase 1	Homo sapiens	20-24
28775293-2	2017	The effects of CES1 S75N (rs2307240,C&gt;T) on clopidogrel response among 851 acute coronary syndrome patients who came from the north, central and south of China were studied.	clopidogrel	47-58	carboxylesterase 1	Homo sapiens	15-19
28775293-4	2017	The results showed that there was a significant association between CES1 S75N (rs2307240) and the outcome of clopidogrel therapy.	clopidogrel	109-120	carboxylesterase 1	Homo sapiens	68-72
28810280-1	2017	Background For secondary prevention of acute coronary syndrome, guidelines recommend dual antiplatelet therapy (DAPT) with acetylsalicylic acid and a P2Y12 receptor antagonist such as clopidogrel, prasugrel or ticagrelor for a period of 12 months.	clopidogrel	184-195	purinergic receptor P2Y12	Homo sapiens	150-155
28699807-3	2017	The CYP2C19 enzyme is involved in the biotransformation of clopidogrel to its pharmacologically active form, and variation in the CYP2C19 gene contributes to clopidogrel response variability.	clopidogrel	59-70	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
28699807-3	2017	The CYP2C19 enzyme is involved in the biotransformation of clopidogrel to its pharmacologically active form, and variation in the CYP2C19 gene contributes to clopidogrel response variability.	clopidogrel	59-70	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	130-137
28699807-3	2017	The CYP2C19 enzyme is involved in the biotransformation of clopidogrel to its pharmacologically active form, and variation in the CYP2C19 gene contributes to clopidogrel response variability.	clopidogrel	158-169	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
28699807-3	2017	The CYP2C19 enzyme is involved in the biotransformation of clopidogrel to its pharmacologically active form, and variation in the CYP2C19 gene contributes to clopidogrel response variability.	clopidogrel	158-169	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	130-137
28699807-5	2017	This article describes the impact of CYP2C19 genotype on clopidogrel pharmacokinetics, pharmacodynamics, and effectiveness.	clopidogrel	57-68	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-44
28699807-9	2017	In the meantime, data from pragmatic and observational studies and smaller trials support improved outcomes with genotyping after PCI and use of alternative antiplatelet therapy in patients with a CYP2C19 genotype associated with reduced clopidogrel effectiveness.	clopidogrel	238-249	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	197-204
28377187-6	2017	Switching from 75mg daily clopidogrel to 150mg daily fully overcomes low exposure to clopidogrel active metabolite in CYP2C19*2 carriers (means+-SD AUC, 32.35+-8.65 vs. 35.05+-12.34, P=0.314).	clopidogrel	26-37	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	118-125
28377187-6	2017	Switching from 75mg daily clopidogrel to 150mg daily fully overcomes low exposure to clopidogrel active metabolite in CYP2C19*2 carriers (means+-SD AUC, 32.35+-8.65 vs. 35.05+-12.34, P=0.314).	clopidogrel	85-96	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	118-125
28290236-9	2017	RESULTS: Clopidogrel resistance was identified in 43% of the patients in period 1, in 16% in period 2, and in 5% in period 3 (P &lt; 0.001).	clopidogrel	9-20	period circadian regulator 2	Homo sapiens	93-101
28745576-0	2017	Association of CYP2C19*2 polymorphism with clopidogrel response and 1-year major adverse cardiovascular events in a multiethnic population with drug-eluting stents.	clopidogrel	43-54	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
28745576-5	2017	Prevalences of aspirin and clopidogrel high on-treatment platelet reactivity (HPR; local cutoffs: 300 AU*min for aspirin and 600 AU*min for clopidogrel) were 11.5% and 19.8% respectively.	clopidogrel	27-38	haptoglobin-related protein	Homo sapiens	78-81
28745576-6	2017	In multivariate ana-lysis, clopidogrel HPR was found to be an independent predictor for 1-year MACE (adj HR: 3.48, p = 0.022 ).	clopidogrel	27-38	haptoglobin-related protein	Homo sapiens	39-42
28433569-0	2017	Vitamin D Binding Protein rs7041 polymorphism and high-residual platelet reactivity in patients receiving dual antiplatelet therapy with clopidogrel or ticagrelor.	clopidogrel	137-148	GC vitamin D binding protein	Homo sapiens	0-25
28371087-7	2017	Influence of clopidogrel was further evaluated in NOS3 downregulated HUVEC by RNAi.	clopidogrel	13-24	nitric oxide synthase 3	Homo sapiens	50-54
28371087-9	2017	Gene expressions of inflammatory markers IL-8 and MCP1 were reduced after clopidogrel treatment (P&lt;.05); however, only MCP-1 remained reduced at protein level.	clopidogrel	74-85	C-X-C motif chemokine ligand 8	Homo sapiens	41-45
28371087-9	2017	Gene expressions of inflammatory markers IL-8 and MCP1 were reduced after clopidogrel treatment (P&lt;.05); however, only MCP-1 remained reduced at protein level.	clopidogrel	74-85	C-C motif chemokine ligand 2	Homo sapiens	50-54
28371087-11	2017	Gene expression and protein expression of ICAM-1 were diminished by 24-hours clopidogrel exposure, whereas P-selectin was not modified.	clopidogrel	77-88	intercellular adhesion molecule 1	Homo sapiens	42-48
28371087-12	2017	NOS3 downregulated HUVEC model revealed that ICAM-1 modification by clopidogrel is dependent of this via, whereas MCP-1 is modulated in an NO-independent form.	clopidogrel	68-79	nitric oxide synthase 3	Homo sapiens	0-4
28371087-12	2017	NOS3 downregulated HUVEC model revealed that ICAM-1 modification by clopidogrel is dependent of this via, whereas MCP-1 is modulated in an NO-independent form.	clopidogrel	68-79	intercellular adhesion molecule 1	Homo sapiens	45-51
28378058-0	2017	Meta-analysis of effects of ABCB1 polymorphisms on clopidogrel response among patients with coronary artery disease.	clopidogrel	51-62	ATP binding cassette subfamily B member 1	Homo sapiens	28-33
28451807-2	2017	A recent case study showed that the antiplatelet agent clopidogrel inhibits paclitaxel metabolism via cytochrome P450 (CYP) 2C8, resulting in severe PIPN.	clopidogrel	55-66	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	102-127
28808507-11	2017	Conclusions: Given the varied effectiveness of clopidogrel due to its metabolism by CYP2C19 enzyme, and the relatively high frequency of both gain-of-function (18.8%) and loss-of-function (19.8%) alleles in our patient population, we believe that genotyping CYP2C19 is clinically important in order to improve patient outcomes and minimize patient risk.	clopidogrel	47-58	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	84-91
29060457-0	2017	A pharmacokinetic model of drug-drug interaction between clopidogrel and omeprazole at CYP2C19 in humans.	clopidogrel	57-68	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	87-94
29060457-2	2017	Clopidogrel is metabolized by hepatic CYP2C19 and CYP2B6, therefore, co-administration of clopidogrel and CYP2C19 inhibitors can alter pharmacokinetics of clopidogrel.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	38-45
29060457-2	2017	Clopidogrel is metabolized by hepatic CYP2C19 and CYP2B6, therefore, co-administration of clopidogrel and CYP2C19 inhibitors can alter pharmacokinetics of clopidogrel.	clopidogrel	0-11	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	50-56
29060457-2	2017	Clopidogrel is metabolized by hepatic CYP2C19 and CYP2B6, therefore, co-administration of clopidogrel and CYP2C19 inhibitors can alter pharmacokinetics of clopidogrel.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	106-113
29060457-2	2017	Clopidogrel is metabolized by hepatic CYP2C19 and CYP2B6, therefore, co-administration of clopidogrel and CYP2C19 inhibitors can alter pharmacokinetics of clopidogrel.	clopidogrel	90-101	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	38-45
29060457-2	2017	Clopidogrel is metabolized by hepatic CYP2C19 and CYP2B6, therefore, co-administration of clopidogrel and CYP2C19 inhibitors can alter pharmacokinetics of clopidogrel.	clopidogrel	90-101	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	50-56
29060457-2	2017	Clopidogrel is metabolized by hepatic CYP2C19 and CYP2B6, therefore, co-administration of clopidogrel and CYP2C19 inhibitors can alter pharmacokinetics of clopidogrel.	clopidogrel	155-166	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	38-45
29060457-2	2017	Clopidogrel is metabolized by hepatic CYP2C19 and CYP2B6, therefore, co-administration of clopidogrel and CYP2C19 inhibitors can alter pharmacokinetics of clopidogrel.	clopidogrel	155-166	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	50-56
29060457-2	2017	Clopidogrel is metabolized by hepatic CYP2C19 and CYP2B6, therefore, co-administration of clopidogrel and CYP2C19 inhibitors can alter pharmacokinetics of clopidogrel.	clopidogrel	155-166	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	106-113
28135763-0	2017	The CYP2C19*2 and CYP2C19*17 Polymorphisms play a Vital Role in Clopidogrel Responsiveness after Percutaneous Coronary Intervention: A Pharmacogenomics Study.	clopidogrel	64-75	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
28135763-0	2017	The CYP2C19*2 and CYP2C19*17 Polymorphisms play a Vital Role in Clopidogrel Responsiveness after Percutaneous Coronary Intervention: A Pharmacogenomics Study.	clopidogrel	64-75	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	18-25
28135763-1	2017	Clopidogrel inhibits platelet activation and aggregation by blocking the P2Y12 receptor.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	73-78
28135763-9	2017	A significant association was found between the CYP2C19*2 (G636A) polymorphism and non-responsiveness to clopidogrel therapy (p &lt; 0.001).	clopidogrel	105-116	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	48-55
28135763-13	2017	Our findings suggest that the CYP2C19*2 polymorphism is associated with non-responsiveness to clopidogrel therapy and the CYP2C19*17 polymorphism enhances antiplatelet activity of clopidogrel.	clopidogrel	94-105	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
28135763-13	2017	Our findings suggest that the CYP2C19*2 polymorphism is associated with non-responsiveness to clopidogrel therapy and the CYP2C19*17 polymorphism enhances antiplatelet activity of clopidogrel.	clopidogrel	180-191	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
28135763-13	2017	Our findings suggest that the CYP2C19*2 polymorphism is associated with non-responsiveness to clopidogrel therapy and the CYP2C19*17 polymorphism enhances antiplatelet activity of clopidogrel.	clopidogrel	180-191	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	122-129
28378058-2	2017	Molecular epidemiological research suggests that ABCB1 C3435T polymorphism may be associated with clopidogrel response, but results remain controversial.	clopidogrel	98-109	ATP binding cassette subfamily B member 1	Homo sapiens	49-54
28378058-3	2017	To derive a more precise evaluation of the associations between ABCB1 C3435T polymorphism and the clinical efficacy of clopidogrel, we have conducted a PRISMA-compliant meta-analysis.	clopidogrel	119-130	ATP binding cassette subfamily B member 1	Homo sapiens	64-69
28378058-10	2017	CONCLUSIONS: The results of the meta-analysis suggest that ABCB1 C3435T polymorphism may increase the risk of bleeding in Asian patients treated with clopidogrel.	clopidogrel	150-161	ATP binding cassette subfamily B member 1	Homo sapiens	59-64
28632784-14	2017	Parameters associated with a presumably higher risk of bleeding and side-effects against the more effective P2Y12 inhibitors were the most prominent factors for the prescription of clopidogrel.	clopidogrel	181-192	purinergic receptor P2Y12	Homo sapiens	108-113
28515278-7	2017	More interestingly, clopidogrel and ticagrelor, two P2Y12-specific antagonists, effectively alleviated the disease severity of EAE and inhibited Th17 differentiation both in vivo and in vitro.	clopidogrel	20-31	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	52-57
28618904-4	2017	The aim of this article is to provide an overview of the evidence from randomized clinical trials with a focus on the best association between aspirin and a P2Y12 inhibitor such as clopidogrel, prasugrel or ticagrelor, on the selection of the appropriate agent based on the revascularization strategy and on the optimal duration of such an intensive treatment.	clopidogrel	181-192	purinergic receptor P2Y12	Homo sapiens	157-162
28764183-1	2017	Acquired coagulation factor VIII inhibitor leads to a rare disease i.e., acquired haemophilia which is idiopathic in majority of cases and is seen with autoimmune diseases, haematologic and solid tumours, infections, in the post-partum period and also with certain long-term use of drugs like penicillin and its derivatives, phenytoin, sulfa antibiotics, chloramphenicol, methyldopa, chlorpromazine, levodopa, interferon-alpha, fludarabine, clopidogrel.	clopidogrel	441-452	coagulation factor VIII	Homo sapiens	9-32
27862978-0	2017	ABCC3 Polymorphisms and mRNA Expression Influence the Concentration of a Carboxylic Acid Metabolite in Patients on Clopidogrel and Aspirin Therapy.	clopidogrel	115-126	ATP binding cassette subfamily C member 3	Homo sapiens	0-5
27862978-4	2017	We investigated the relationship of ABC-type efflux subfamily C member 3 (ABCC3) polymorphisms and mRNA expression with plasma concentrations of clopidogrel, salicylic acid (SA) and a carboxylic acid metabolite (CAM).	clopidogrel	145-156	ATP binding cassette subfamily C member 3	Homo sapiens	74-79
27862978-13	2017	Therefore, ABCC3 may be a potential biomarker for the response to clopidogrel.	clopidogrel	66-77	ATP binding cassette subfamily C member 3	Homo sapiens	11-16
28279968-1	2017	OBJECTIVE: Aspirin together with thienopyridine P2Y12 inhibitors, commonly clopidogrel, is a cornerstone of antiplatelet therapy.	clopidogrel	75-86	purinergic receptor P2Y12	Homo sapiens	48-53
27909114-4	2017	Comorbidities in the form of coagulopathies secondary to chronic liver diseases, drugs (warfarin, ecosprin, clopidogrel), thrombocytopenia secondary to systemic illness are always a challenge to deal with in patients with CSDH.	clopidogrel	108-119	serine dehydratase like	Homo sapiens	222-226
28202132-10	2017	Blacks preloaded with clopidogrel (n = 17) had significantly lower results of VerifyNow (64 +- 65 vs 198 +- 86, p &lt;0.001) and vasodilator-stimulated phosphoprotein (12.8 +- 21.6 vs 58.9 +- 19.9, p &lt;0.001) at 1 hour compared with those with no clopidogrel preload.	clopidogrel	22-33	vasodilator stimulated phosphoprotein	Homo sapiens	129-166
27904973-0	2017	Platelet reactivity and clinical outcomes in patients using CYP3A4-metabolized statins with clopidogrel in percutaneous coronary intervention.	clopidogrel	92-103	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	60-66
27904973-1	2017	Statins are primarily metabolized by cytochrome P450 3A4 (CYP3A4), which reduces clopidogrel to its active metabolite.	clopidogrel	81-92	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	37-56
27904973-1	2017	Statins are primarily metabolized by cytochrome P450 3A4 (CYP3A4), which reduces clopidogrel to its active metabolite.	clopidogrel	81-92	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	58-64
27904973-2	2017	Recent studies suggest that CYP3A4-metabolized statins attenuate clopidogrel"s anti-aggregatory effect on platelets.	clopidogrel	65-76	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	28-34
27904973-10	2017	CYP3A4-metabolized statins slightly inhibit the antiplatelet activity of clopidogrel during dual antiplatelet therapy.	clopidogrel	73-84	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
28024166-9	2017	Recent studies in East Asian cohorts suggests that the potential of PPIs to attenuate the efficacy of clopidogrel could be minimized by the use of newer PPIs with weaker affinity for the CYP2C19 isoenzyme, namely, pantoprazole, dexlansoprazole, and rabeprazole.	clopidogrel	102-113	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	187-194
28336370-4	2017	Since clopidogrel, a selective inhibitor of G protein-coupled purinergic P2Y12 receptor (P2Y12R), achieved clinical success as an anti-platelet drug, P2YRs has been attracted more attention as new therapeutic targets of cardiovascular diseases.	clopidogrel	6-17	purinergic receptor P2Y12	Homo sapiens	73-87
28336370-4	2017	Since clopidogrel, a selective inhibitor of G protein-coupled purinergic P2Y12 receptor (P2Y12R), achieved clinical success as an anti-platelet drug, P2YRs has been attracted more attention as new therapeutic targets of cardiovascular diseases.	clopidogrel	6-17	purinergic receptor P2Y12	Homo sapiens	89-95
28511321-1	2017	Objective: To analyze association of CYP2C19 genotype and platelet function phenotype and their impact on clinical outcomes including bleeding events of coronary artery disease(CAD) patients received clopidogrel post percutaneous coronary intervention(PCI).	clopidogrel	200-211	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-44
28511321-10	2017	In multivariable Cox regression analysis, the adjusted risk of cardiovascular death, acute myocardial infarction, stent embolism, target lesion revascularization and angina onset was 2.305 times higher in clopidogrel poor metabolizers than in extensive and semi-metabolizers (95%CI=1.208-4.399, P=0.011).	clopidogrel	205-216	cytochrome c oxidase subunit 8A	Homo sapiens	17-20
28511321-12	2017	Conclusions: Among CAD patients underwent stenting and clopidogrel treatment, poor CYP2C19 metabolizers group carries a significantly higher risk for combined cardiovascular events than in extensive metabolizers group, while clopidogrel responders patients are at significantly higher risk for bleeding as compared to the semi-responders and non-responders.	clopidogrel	55-66	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	83-90
28511321-12	2017	Conclusions: Among CAD patients underwent stenting and clopidogrel treatment, poor CYP2C19 metabolizers group carries a significantly higher risk for combined cardiovascular events than in extensive metabolizers group, while clopidogrel responders patients are at significantly higher risk for bleeding as compared to the semi-responders and non-responders.	clopidogrel	225-236	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	83-90
28520385-2	2012	Prasugrel, along with other antiplatelet agents such as clopidogrel and ticagrelor, inhibits platelet activation by irreversibly binding to the platelet receptor, P2RY12.	clopidogrel	56-67	purinergic receptor P2Y12	Homo sapiens	163-169
28442925-1	2017	PURPOSE: The aim of this study is to investigate the frequency of CYP2C19*2, *3 allelic variants, associated with poor response to clopidogrel, and CYP2C19*17, associated with excessive response to clopidogrel, in patients with acute coronary syndrome (ACS) from Siberia and Moscow regions of Russia.	clopidogrel	131-142	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	66-73
28442925-1	2017	PURPOSE: The aim of this study is to investigate the frequency of CYP2C19*2, *3 allelic variants, associated with poor response to clopidogrel, and CYP2C19*17, associated with excessive response to clopidogrel, in patients with acute coronary syndrome (ACS) from Siberia and Moscow regions of Russia.	clopidogrel	198-209	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	66-73
28442925-1	2017	PURPOSE: The aim of this study is to investigate the frequency of CYP2C19*2, *3 allelic variants, associated with poor response to clopidogrel, and CYP2C19*17, associated with excessive response to clopidogrel, in patients with acute coronary syndrome (ACS) from Siberia and Moscow regions of Russia.	clopidogrel	198-209	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	148-155
28520385-6	2012	Consequently, clopidogrel is less effective among patients with decreased or no function variant alleles in the CYP2C19 gene.	clopidogrel	14-25	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	112-119
28321022-0	2017	Administration of Ticagrelor and Double-Dose Clopidogrel Based on Platelet Reactivity Determined by VerifyNow-P2Y12 for Chinese Subjects After Elective PCI.	clopidogrel	45-56	purinergic receptor P2Y12	Homo sapiens	110-115
28244953-11	2017	Thrombus size in clopidogrel blood was increased by combined PC and vWF treatment (by 50%, P &lt; .05), but this increase did not reach control levels (P &lt; .05).	clopidogrel	17-28	von Willebrand factor	Homo sapiens	68-71
26873108-0	2017	The Impact of CYP2C19 Loss-of-Function Polymorphisms, Clinical, and Demographic Variables on Platelet Response to Clopidogrel Evaluated Using Impedance Aggregometry.	clopidogrel	114-125	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
28045759-5	2017	Novel oral P2Y12 inhibitors significantly reduced the incidence of all-cause death (relative risk: 0.65, 95% confidence interval, 0.53-0.78), major adverse cardiac events [0.68 (0.56-0.83)], and stent thrombosis [0.56 (0.43-0.75)] without significant difference in bleeding (P = 0.11) compared with clopidogrel.	clopidogrel	299-310	purinergic receptor P2Y12	Homo sapiens	11-16
28289237-0	2017	Impact of Glycemic Control on Efficacy of Clopidogrel in Transient Ischemic Attack or Minor Stroke Patients With CYP2C19 Genetic Variants.	clopidogrel	42-53	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	113-120
28289237-8	2017	CONCLUSIONS: In patients with minor stroke or high-risk transient ischemic attack, clopidogrel-aspirin when compared with aspirin alone reduced stroke recurrence only in noncarriers of CYP2C19 loss-of-function allele and normal GA levels.	clopidogrel	83-94	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	185-192
30650510-0	2017	[Effect of Clopidogrel on Plasma Protein Binding Rates of Ginsenoside Rg1].	clopidogrel	11-22	protein phosphatase 1 regulatory subunit 3A	Homo sapiens	70-73
30650510-1	2017	Objective To observe the effect of clopidogrel on plasma protein binding rates of gin- senoside Rg1.	clopidogrel	35-46	protein phosphatase 1 regulatory subunit 3A	Homo sapiens	96-99
30650510-12	2017	The effect of clopidogrel on plasma protein binding rates of ginsenoside Rgl was observed u- sing equilibrium dialysis.	clopidogrel	14-25	ral guanine nucleotide dissociation stimulator like 1	Homo sapiens	73-76
30650510-26	2017	5% in the clopi- dogrel combined middle dose ginsenoside Rg1 group, 12.1% +- 1.	clopidogrel	10-23	protein phosphatase 1 regulatory subunit 3A	Homo sapiens	57-60
30650510-28	2017	They were lower in clopidogrel combined ginsenoside Rg1 groups than in ginsenoside Rg1 groups with statistical difference (P &lt;0.	clopidogrel	19-30	protein phosphatase 1 regulatory subunit 3A	Homo sapiens	52-55
30650510-31	2017	Conclusion Results of equilibrium dialysis and molecular docking comprehensively in- dicated clopidogrel had effect on plasma protein binding rate of ginsenoside Rg1.	clopidogrel	93-104	protein phosphatase 1 regulatory subunit 3A	Homo sapiens	162-165
28358842-0	2017	The risk of clopidogrel resistance is associated with ABCB1 polymorphisms but not promoter methylation in a Chinese Han population.	clopidogrel	12-23	ATP binding cassette subfamily B member 1	Homo sapiens	54-59
28358842-1	2017	The goal of our study was to investigate the contribution of ABCB1 expression to the risk of clopidogrel resistance (CR).	clopidogrel	93-104	ATP binding cassette subfamily B member 1	Homo sapiens	61-66
26873108-13	2017	Clopidogrel response was significantly influenced by the presence of CYP2C19 polymorphisms.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	69-76
28135786-9	2017	Material and methods The VerifyNow P2Y12 assay was performed in clopidogrel-treated patients undergoing non-urgent PCI included in a prospective cohort study.	clopidogrel	64-75	purinergic receptor P2Y12	Homo sapiens	35-40
28383427-0	2017	Associations between P2RY12 gene polymorphisms and risks of clopidogrel resistance and adverse cardiovascular events after PCI in patients with acute coronary syndrome.	clopidogrel	60-71	purinergic receptor P2Y12	Homo sapiens	21-27
28383427-2	2017	Clopidogrel targets the platelet membrane receptor P2RY12 to inhibit platelet aggregation via adenosine diphosphate (ADP).	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	51-57
28383427-3	2017	This study aimed to investigate the relationships between P2RY12 polymorphisms and the risk of clopidogrel resistance and adverse CVD events after PCI.	clopidogrel	95-106	purinergic receptor P2Y12	Homo sapiens	58-64
28383427-10	2017	Patients with T variations at C34T or G52T of P2RY12 had a significantly higher risk of clopidogrel resistance (C34T: P &lt; 0.001; G52T: P = 0.003) and total cardiovascular events (C34T: P = 0.013; G52T: P = 0.018) compared to those with the wild-type genotype.	clopidogrel	88-99	purinergic receptor P2Y12	Homo sapiens	46-52
28383427-13	2017	The P2RY12 gene polymorphisms C34T and G52T were significantly associated with a higher risk of clopidogrel resistance and sequential cardiovascular events in Chinese ACS patients after PCI.	clopidogrel	96-107	purinergic receptor P2Y12	Homo sapiens	4-10
28346068-1	2017	The University of Florida (UF) Health Personalized Medicine Program launched in 2012 with CYP2C19 genotyping for clopidogrel response at UF Health Shands Hospital.	clopidogrel	113-124	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	90-97
28690699-9	2017	CYP2C19 variant genotypes (i.e., *1/*2, *1/*17, and *2/*17) were found in the other three patients; alternative antiplatelet therapy was recommended for the patient with the *1/*2 genotype, while clopidogrel was recommended for those with *1/*17 and *2/*17 genotypes.	clopidogrel	196-207	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
26873108-4	2017	This study aimed to assess the impact of clinical and demographic variables and of cytochrome P450 2C19 (CYP2C19) loss-of-function polymorphisms on platelet response to clopidogrel evaluated using impedance aggregometry in an East European population.	clopidogrel	169-180	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	83-103
26873108-4	2017	This study aimed to assess the impact of clinical and demographic variables and of cytochrome P450 2C19 (CYP2C19) loss-of-function polymorphisms on platelet response to clopidogrel evaluated using impedance aggregometry in an East European population.	clopidogrel	169-180	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	105-112
26873108-11	2017	The highest level of association with clopidogrel response status was found for CYP2C19 polymorphisms, concomitant aspirin treatment, leukocyte and platelet count, history of myocardial infarction, arterial hypertension, and ward where patients were admitted.	clopidogrel	38-49	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	80-87
28267471-2	2017	Guidelines recommend at least 6- to 12 months of dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 receptor inhibitor such as clopidogrel.	clopidogrel	134-145	purinergic receptor P2Y12	Homo sapiens	101-106
28791856-0	2017	P2Y12 receptor gene polymorphism and the risk of resistance to clopidogrel: A meta-analysis and review of the literature.	clopidogrel	63-74	purinergic receptor P2Y12	Homo sapiens	0-5
28062501-7	2017	In addition, the number of P2Y12-positive VSMCs was decreased in the carotid artery plaque from patients receiving clopidogrel.	clopidogrel	115-126	purinergic receptor P2Y12	Homo sapiens	27-32
27512080-7	2017	Adding a PPI to clopidogrel treatment was associated with a higher rate of MACE occurrence in rapid metabolizers (RMs, *1/*1) of CYP2C19 (OR: 1.42; 95% CI: 1.12-1.81), but there was no obviously increased rate (OR: 1.43; 95% CI: 0.89-2.28) in decreased metabolizers (with 1 or 2 loss-of-function allele).	clopidogrel	16-27	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	129-136
27512080-10	2017	Only in the RMs of CYP2C19, PPIs were associated with significantly increased MACE in patients coadministered with clopidogrel.	clopidogrel	115-126	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	19-26
30650477-0	2017	[Correlation between CYP2C19 Gene Polymorphism with Clopidogrel Resistance and Distribution of Chinese Medicine Syndrome in 229 Acute Coronary Syndrome Patients].	clopidogrel	52-63	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
28791856-1	2017	A number of investigators have evaluated the association between T744C, G52T and C34T polymorphisms in the P2Y12 receptor gene and clopidogrel resistance (CR), but the results of their research are controversial.	clopidogrel	131-142	purinergic receptor P2Y12	Homo sapiens	107-112
28791856-8	2017	The evidence from the present metaanalysis indicates that P2Y12 receptor gene C34T and G52T polymorphism might be a risk factor for the poor response to the platelet in patients on clopidogrel therapy, whereas a lack of association was found for T744C polymorphism examined by various genetic models.	clopidogrel	181-192	purinergic receptor P2Y12	Homo sapiens	58-63
27922911-7	2017	However, newer P2Y12 inhibitors showed a significant increase in thrombosis in MI major or minor bleeding (OR = 1.21, 95% CI, 1.03-1.42, and I = 56%, P = 0.02) compared with clopidogrel.	clopidogrel	174-185	purinergic receptor P2Y12	Homo sapiens	15-20
27922911-8	2017	CONCLUSIONS: Based on this meta-analysis, newer P2Y12 inhibitors were significantly more effective than clopidogrel in the events of myocardial infarction and cardiovascular death in patients with ACS, although the incidence of thrombosis in MI-defined bleeding was higher compared with clopidogrel.	clopidogrel	287-298	purinergic receptor P2Y12	Homo sapiens	48-53
30650477-1	2017	Objective To observe correlation between CYP2C19 *2/CYP2C19 *3 gene polymorphism with clopidogrel resistance and distribution of Chinese medicine ( CM) syndrome in acute coronary syndrome (ACS) population.	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	41-48
30650477-1	2017	Objective To observe correlation between CYP2C19 *2/CYP2C19 *3 gene polymorphism with clopidogrel resistance and distribution of Chinese medicine ( CM) syndrome in acute coronary syndrome (ACS) population.	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	52-59
30650477-1	2017	Objective To observe correlation between CYP2C19 *2/CYP2C19 *3 gene polymorphism with clopidogrel resistance and distribution of Chinese medicine ( CM) syndrome in acute coronary syndrome (ACS) population.	clopidogrel	86-97	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	189-192
30650477-18	2017	(3) Correlation between CYP2C19 gene polymorphism and clopidogrel resistance: Clopidogrel resistance was more liable to occur in mutant homozygous than in mutant heterozygote and normal homozygous (R =0.	clopidogrel	54-65	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
30650477-18	2017	(3) Correlation between CYP2C19 gene polymorphism and clopidogrel resistance: Clopidogrel resistance was more liable to occur in mutant homozygous than in mutant heterozygote and normal homozygous (R =0.	clopidogrel	78-89	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
30650477-35	2017	Conclusions The polymorphism of CYP2C19 was closely correlated with clopidogrel resist- ance in 229 ACS patients.	clopidogrel	68-79	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
30650477-35	2017	Conclusions The polymorphism of CYP2C19 was closely correlated with clopidogrel resist- ance in 229 ACS patients.	clopidogrel	68-79	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	100-103
28260316-8	2017	Conclusion: The CYP2C19 gene mutation is high in the patients with AMI.The effect of antiplatelet of ticagrelor is stronger than clopidogrel, and this effect is not affected by CYP2C19 gene mutations.	clopidogrel	129-140	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
26891871-0	2017	Impact of CYP3A4*1G Allele on Clinical Pharmacokinetics and Pharmacodynamics of Clopidogrel.	clopidogrel	80-91	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	10-16
27939386-3	2017	SSRIs that inhibit the CYP2C19 enzyme have the potential to reduce the effectiveness of clopidogrel.	clopidogrel	88-99	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	23-30
27939386-10	2017	In conclusion, the findings from this large, population-based study suggest that being treated with a CYP2C19-inhibiting SSRI when initiating clopidogrel may be associated with slight decrease in effectiveness of clopidogrel.	clopidogrel	142-153	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	102-109
27939386-10	2017	In conclusion, the findings from this large, population-based study suggest that being treated with a CYP2C19-inhibiting SSRI when initiating clopidogrel may be associated with slight decrease in effectiveness of clopidogrel.	clopidogrel	213-224	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	102-109
28184261-1	2017	Dual antiplatelet therapy (DAPT) consisting of aspirin plus a P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor) is imperative for the treatment of acute coronary syndrome, particularly during the re-endothelialization period after percutaneous coronary intervention (PCI).	clopidogrel	79-90	purinergic receptor P2Y12	Homo sapiens	62-67
28184261-5	2017	After this period, it is generally recommended that the P2Y12 inhibitor be stopped for the amount of time necessary for platelet function recovery (clopidogrel 5-7 days, prasugrel 7-10 days, ticagrelor 3-5 days), and that aspirin be continued during the perioperative period.	clopidogrel	148-159	purinergic receptor P2Y12	Homo sapiens	56-61
27915083-0	2017	Pharmacodynamic and cytogenetic evaluation in CYP2C19*2 and CYP2C19*3 allelomorphism in South Indian population with clopidogrel therapy.	clopidogrel	117-128	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	46-53
27915083-0	2017	Pharmacodynamic and cytogenetic evaluation in CYP2C19*2 and CYP2C19*3 allelomorphism in South Indian population with clopidogrel therapy.	clopidogrel	117-128	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	60-67
27557470-5	2017	In addition, interindividual differences in the fraction absorbed and the CES1 activity were identified as sources of interindividual differences in clopidogrel"s active metabolite concentrations and, thus, platelet reactivity.	clopidogrel	149-160	carboxylesterase 1	Homo sapiens	74-78
27936524-7	2017	The antiplatelet aggregation effects of clopidogrel were determined by using two different ex-vivo platelet aggregation tests including the whole blood impedance assay (WBA) and the VerifyNow&lt;sup&gt; &lt;/sup&gt; P2Y12 assay.	clopidogrel	40-51	purinergic receptor P2Y12	Homo sapiens	216-221
28139897-4	2017	The P2Y12 inhibitor clopidogrel has established efficacy, but is associated with suboptimal and delayed platelet inhibition and variability in response.	clopidogrel	20-31	purinergic receptor P2Y12	Homo sapiens	4-9
26891871-3	2017	The aim of this study was to evaluate the influence of CYP3A4*1G (IVS10+12G&gt;A, rs2242480) on the pharmacokinetics and pharmacodynamics of clopidogrel.	clopidogrel	141-152	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	55-61
26891871-4	2017	METHODS: CYP3A4*1G polymorphism was determined in a group of 82 patients undergoing percutaneous coronary intervention and taking 75 mg of clopidogrel daily.	clopidogrel	139-150	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	9-15
27816182-0	2017	Response to the letter by Dr. Demetrios Moris "Reply to Effect of CYP2C19*2 and *3 on clinical outcome in ischemic stroke patients treated with clopidogrel".	clopidogrel	144-155	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	66-73
27823837-0	2017	Reply to effect of CYP2C19*2 and *3 on clinical outcome in ischemic stroke patients treated with Clopidogrel.	clopidogrel	97-108	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	19-26
28076455-0	2017	Decreased platelet responsiveness to clopidogrel correlates with CYP2C19 and PON1 polymorphisms in atherosclerotic patients.	clopidogrel	37-48	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	65-72
28076455-0	2017	Decreased platelet responsiveness to clopidogrel correlates with CYP2C19 and PON1 polymorphisms in atherosclerotic patients.	clopidogrel	37-48	paraoxonase 1	Homo sapiens	77-81
28076455-12	2017	In brief, PON1 and CYP2C19 polymorphisms were associated with lower clopidogrel responsiveness in this sample.	clopidogrel	68-79	paraoxonase 1	Homo sapiens	10-14
28076455-12	2017	In brief, PON1 and CYP2C19 polymorphisms were associated with lower clopidogrel responsiveness in this sample.	clopidogrel	68-79	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	19-26
27806998-2	2017	We performed a systematic review and meta-analysis to assess the association between genetic polymorphisms, especially CYP2C19 genotype, and clopidogrel efficacy for ischemic stroke or TIA.	clopidogrel	141-152	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	119-126
27806998-6	2017	RESULTS: Among 15 studies of 4762 patients with stroke or TIA treated with clopidogrel, carriers of CYP2C19 loss-of-function alleles (*2, *3, and *8) were at increased risk of stroke in comparison with noncarriers (12.0% versus 5.8%; risk ratio, 1.92, 95% confidence interval, 1.57-2.35; P&lt;0.001).	clopidogrel	75-86	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	100-107
27806998-10	2017	CONCLUSIONS: Carriers of CYP2C19 loss-of-function alleles are at greater risk of stroke and composite vascular events than noncarriers among patients with ischemic stroke or TIA treated with clopidogrel.	clopidogrel	191-202	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
29474768-1	2017	Binding of clopidogrel to serum albumin has been characterized in the presence and absence of linoleic acid by equilibrium dialysis method where ranitidine and diazepam were used as specific probes.	clopidogrel	11-22	albumin	Homo sapiens	26-39
29474768-5	2017	At higher concentrations, linoleic acid displaced clopidogrel from its binding sites on serum albumin.	clopidogrel	50-61	albumin	Homo sapiens	88-101
27628007-5	2017	A series of clinical antiplatelet drugs, such as clopidogrel and ticagrelor, are designed as indirect or direct antagonists of P2Y12 receptor to reduce incidence of thrombosis mainly for patients of acute coronary syndrome (ACS) who are at high risk of thrombotic events.	clopidogrel	49-60	purinergic receptor P2Y12	Homo sapiens	127-132
28785581-3	2017	Therefore, we aimed to evaluate the impact of the CYP2C19*2 variant (rs4244285) on in-stent restenosis occurrence in Chilean patients who underwent PCI and received clopidogrel.	clopidogrel	165-176	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	50-57
27380588-0	2017	CYP2C19 but not CYP2B6, CYP3A4, CYP3A5, ABCB1, PON1 or P2Y12 genetic polymorphism impacts antiplatelet response after clopidogrel in Koreans.	clopidogrel	118-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
27380588-3	2017	The extensive evidence indicates the importance of CYP2C19 variants in reducing efficacy of clopidogrel.	clopidogrel	92-103	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	51-58
27628007-7	2017	However, the clinical practical phenomena, such as "clopidogrel resistance" due to gene variations of cytochrome P450 or P2Y12 receptor constitutive activation, call for better antiplatelet agents.	clopidogrel	52-63	purinergic receptor P2Y12	Homo sapiens	121-126
28261502-0	2017	Does i-T744C P2Y12 Polymorphism Modulate Clopidogrel Response among Moroccan Acute Coronary Syndromes Patients?	clopidogrel	41-52	purinergic receptor P2Y12	Homo sapiens	13-18
28261502-4	2017	The objective of our study was to investigate the potential effect of i-T744C P2Y12 polymorphism on Clopidogrel response in a sample of Moroccan ACS patients.	clopidogrel	100-111	purinergic receptor P2Y12	Homo sapiens	78-83
27886818-1	2017	There is significant interpatient variability in clopidogrel effectiveness, which is due in part to cytochrome P450 (CYP) 2C19 genotype.	clopidogrel	49-60	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	100-126
29054193-2	2017	In addition, among patients who are not carriers of the CYP2C19 loss-of-function alleles, there is a reduced risk of stroke when clopidogrel is taken with aspirin compared to aspirin alone.	clopidogrel	129-140	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	56-63
27886818-2	2017	Approximately 30% of individuals carry CYP2C19 loss-of-function alleles, which have been consistently shown to reduce clopidogrel effectiveness after an acute coronary syndrome and percutaneous coronary intervention.	clopidogrel	118-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	39-46
28070995-0	2017	Haplotype of platelet receptor P2RY12 gene is associated with residual clopidogrel on-treatment platelet reactivity.	clopidogrel	71-82	purinergic receptor P2Y12	Homo sapiens	31-37
28070995-1	2017	OBJECTIVE: To investigate a possible association between common variations of the P2RY12 and the residual clopidogrel on-treatment platelet reactivity after adjusting for the influence of CYP2C19 tested by thromboelastography (TEG).	clopidogrel	106-117	purinergic receptor P2Y12	Homo sapiens	82-88
28070995-8	2017	CONCLUSIONS: The combination of common P2RY12 variations including regulatory regions rather than rs2046934 (T744C) that related to pharmacodynamics of clopidogrel in patients with ACS was independently associated with residual on-clopidogrel platelet reactivity.	clopidogrel	152-163	purinergic receptor P2Y12	Homo sapiens	39-45
28070995-8	2017	CONCLUSIONS: The combination of common P2RY12 variations including regulatory regions rather than rs2046934 (T744C) that related to pharmacodynamics of clopidogrel in patients with ACS was independently associated with residual on-clopidogrel platelet reactivity.	clopidogrel	231-242	purinergic receptor P2Y12	Homo sapiens	39-45
28362884-9	2017	For clopidogrel, the mean P2Y12 response unit was 191 +- 70 (range, 51-351); 77% showed therapeutic response.	clopidogrel	4-15	purinergic receptor P2Y12	Homo sapiens	26-31
28630782-9	2017	CONCLUSIONS: Aspirin and clopidogrel suppress stimulated platelet P-selectin, although one-quarter of patients on clopidogrel have high on-treatment platelet reactivity.	clopidogrel	25-36	selectin P	Homo sapiens	66-76
28064328-0	2017	Pharmacogenetics of CYP2C19 genetic polymorphism on clopidogrel response in patients with ischemic stroke from Saudi Arabia.	clopidogrel	52-63	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	20-27
28064328-1	2017	OBJECTIVE: To elucidate the degree of genetic polymorphisms CYP2C19 (CYP2C19*2, CYP2C19*3) of key drug metabolizing enzymes on the antiplatelet effect of clopidogrel response in patients with acute ischemic stroke from Saudi Arabia.	clopidogrel	154-165	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	60-67
28329746-13	2017	CONCLUSIONS: We documented a different effect of CYP2C19 and P2Y12 receptor polymorphisms on platelet reactivity and cardiovascular outcome in CAD patients after PCI on clopidogrel treatment.	clopidogrel	169-180	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	49-56
28329746-13	2017	CONCLUSIONS: We documented a different effect of CYP2C19 and P2Y12 receptor polymorphisms on platelet reactivity and cardiovascular outcome in CAD patients after PCI on clopidogrel treatment.	clopidogrel	169-180	purinergic receptor P2Y12	Homo sapiens	61-66
28421156-4	2017	Current methods for clopidogrel personalization include CYP2C19 genotyping, pharmacokinetics, and platelets function testing.	clopidogrel	20-31	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	56-63
28810096-0	2017	Point-Counterpoint: CYP2C19 Genotyping for Clopidogrel.	clopidogrel	43-54	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	20-27
28631703-7	2017	CONCLUSION: The carriage of the cytochrome P450 CYP2C19 681A allele rather than platelet receptor gene polymorphisms determines a risk for clopidogrel resistance in patients with CHD.	clopidogrel	139-150	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	48-55
27534996-9	2016	Clopidogrel is a P2Y12-R antagonist that potentiates the effect of vasopressin and increases AQP2 abundance.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	17-24
28058211-5	2016	Dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor such as clopidogrel, prasugrel and ticagrelor is instated post stenting to decrease the incident of ST. Cangrelor has recently been approved by Food and Drug Administration and can be used as a bridging antiplatelet drug.	clopidogrel	76-87	purinergic receptor P2Y12	Homo sapiens	52-57
27977637-1	2016	BACKGROUND The aim of this study was to observe the effects of genetic polymorphism of CYP2C19 on inhibitory effects of ticagrelor (Tic) and clopidogrel (Clo) towards post-percutaneous coronary intervention (PCI) platelet aggregation (IPA) and major cardiovascular events (MACE) in patients with acute coronary syndromes (ACS).	clopidogrel	141-152	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	87-94
27977637-1	2016	BACKGROUND The aim of this study was to observe the effects of genetic polymorphism of CYP2C19 on inhibitory effects of ticagrelor (Tic) and clopidogrel (Clo) towards post-percutaneous coronary intervention (PCI) platelet aggregation (IPA) and major cardiovascular events (MACE) in patients with acute coronary syndromes (ACS).	clopidogrel	154-157	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	87-94
28064328-1	2017	OBJECTIVE: To elucidate the degree of genetic polymorphisms CYP2C19 (CYP2C19*2, CYP2C19*3) of key drug metabolizing enzymes on the antiplatelet effect of clopidogrel response in patients with acute ischemic stroke from Saudi Arabia.	clopidogrel	154-165	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	69-76
28064328-1	2017	OBJECTIVE: To elucidate the degree of genetic polymorphisms CYP2C19 (CYP2C19*2, CYP2C19*3) of key drug metabolizing enzymes on the antiplatelet effect of clopidogrel response in patients with acute ischemic stroke from Saudi Arabia.	clopidogrel	154-165	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	69-76
28064328-6	2017	RESULTS: The CYP2C19*2 (681G&gt;A) and CYP2C19*3 (636 G&gt;A) polymorphism were seen to be in Hardy-Weinberg equilibrium and showed significant allelic and genotypic association between responders and non-responders to clopidogrel (p&lt;0.01).	clopidogrel	219-230	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
28064328-6	2017	RESULTS: The CYP2C19*2 (681G&gt;A) and CYP2C19*3 (636 G&gt;A) polymorphism were seen to be in Hardy-Weinberg equilibrium and showed significant allelic and genotypic association between responders and non-responders to clopidogrel (p&lt;0.01).	clopidogrel	219-230	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	39-46
28064328-10	2017	CONCLUSION: Our findings provide certain evidence on the genetic effect of CYP2C19 on clopidogrel responsiveness in stroke patients from Saudi Arabia.	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	75-82
27534996-9	2016	Clopidogrel is a P2Y12-R antagonist that potentiates the effect of vasopressin and increases AQP2 abundance.	clopidogrel	0-11	arginine vasopressin	Homo sapiens	67-78
27534996-9	2016	Clopidogrel is a P2Y12-R antagonist that potentiates the effect of vasopressin and increases AQP2 abundance.	clopidogrel	0-11	aquaporin 2	Homo sapiens	93-97
27447737-0	2016	Effect of long-term adherence to clopidogrel on the VASP-PRI after elective coronary stent implantation: a randomized controlled study.	clopidogrel	33-44	vasodilator stimulated phosphoprotein	Homo sapiens	52-56
28083610-1	2016	Distribution of cytochrome P450 2C19 enzyme gene (CYP2C19) variants affecting metabolism of clopidogrel was determined in 526 Czech patients after percutaneous coronary intervention using MassARRAY genotyping and compared to distribution in other populations of European descent.	clopidogrel	92-103	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	50-57
28083610-3	2016	Observed CYP2C19 genotypes were related to clopidogrel metabolism phenotypes and discussed in population context.	clopidogrel	43-54	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	9-16
27447737-6	2016	Clopidogrel response was assessed with the vasodilator-stimulated phosphoprotein-platelet reactivity index (VASP-PRI) at randomization, 3 months and 6 months.	clopidogrel	0-11	vasodilator stimulated phosphoprotein	Homo sapiens	108-112
27447737-15	2016	Poor adherence is associated with lower VASP-PRI only in initial good responders to clopidogrel.	clopidogrel	84-95	vasodilator stimulated phosphoprotein	Homo sapiens	40-44
27566695-0	2016	Associations of P2Y12R gene polymorphisms with susceptibility to coronary heart disease and clinical efficacy of antiplatelet treatment with clopidogrel.	clopidogrel	141-152	purinergic receptor P2Y12	Homo sapiens	16-22
27956673-7	2016	RESULTS: Based on VASP assay, 54% of patients showed high on-clopidogrel platelet activity inhibition.	clopidogrel	61-72	vasodilator stimulated phosphoprotein	Homo sapiens	18-22
27566695-10	2016	CONCLUSIONS: P2Y12R gene rs2046934 C&gt;T and rs3732759 A&gt;G polymorphisms might be associated with the risk of CHD and the efficacy of clopidogrel treatment for CHD.	clopidogrel	138-149	purinergic receptor P2Y12	Homo sapiens	13-19
27932982-0	2016	Impact of CYP2C19 Variants on Clinical Efficacy of Clopidogrel and 1-Year Clinical Outcomes in Coronary Heart Patients Undergoing Percutaneous Coronary Intervention.	clopidogrel	51-62	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-17
27539103-8	2016	Another two patients carried deletions in CYP2C19, which may predispose to clopidogrel-statin interactions.	clopidogrel	75-86	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	42-49
27525577-1	2016	Resistance of the patient to clopidogrel (an inactive prodrug) has been recently reported to be associated with increased messenger RNA expression of ABCC3 that encodes MRP3 (multidrug resistance-associated protein 3).	clopidogrel	29-40	ATP binding cassette subfamily C member 3	Homo sapiens	150-155
27525577-1	2016	Resistance of the patient to clopidogrel (an inactive prodrug) has been recently reported to be associated with increased messenger RNA expression of ABCC3 that encodes MRP3 (multidrug resistance-associated protein 3).	clopidogrel	29-40	ATP binding cassette subfamily C member 3	Homo sapiens	169-173
27525577-1	2016	Resistance of the patient to clopidogrel (an inactive prodrug) has been recently reported to be associated with increased messenger RNA expression of ABCC3 that encodes MRP3 (multidrug resistance-associated protein 3).	clopidogrel	29-40	ATP binding cassette subfamily C member 3	Homo sapiens	175-216
27525577-4	2016	Results indicated that Abcc3 KO mice exhibited increased formation of CAM and greater systemic exposure to clopidogrel and enhanced inhibition of adenosine diphosphate-induced platelet aggregation ex vivo by clopidogrel when compared with well-matched WT mice.	clopidogrel	107-118	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	23-28
27525577-4	2016	Results indicated that Abcc3 KO mice exhibited increased formation of CAM and greater systemic exposure to clopidogrel and enhanced inhibition of adenosine diphosphate-induced platelet aggregation ex vivo by clopidogrel when compared with well-matched WT mice.	clopidogrel	208-219	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	23-28
27525577-5	2016	We conclude that Abcc3 KO mice have enhanced platelet response to clopidogrel due to increased formation of CAM.	clopidogrel	66-77	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	17-22
27196064-0	2016	The Metabolism of Clopidogrel: CYP2C19 Is a Minor Pathway.	clopidogrel	18-29	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	31-38
27196064-1	2016	The major metabolic pathway of clopidogrel is conversion to carboxylic acid by an esterase (CES1), forming clopidogrelic acid (SR26334) that is inactive.	clopidogrel	31-42	carboxylesterase 1	Homo sapiens	92-96
27196064-5	2016	From a subsequent in vitro study by Sankyo of the metabolism of clopidogrel using recombinant DNA CYPs, it was concluded that CYP2C19 was the major oxidative pathway.	clopidogrel	64-75	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	126-133
27196064-8	2016	However, the view that clopidogrel is a CYP2C19 substrate was reinforced by a finding that omeprazole, a CYP2C19 inhibitor, reduced the ability of clopidogrel to inhibit platelet aggregation.	clopidogrel	23-34	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-47
27196064-8	2016	However, the view that clopidogrel is a CYP2C19 substrate was reinforced by a finding that omeprazole, a CYP2C19 inhibitor, reduced the ability of clopidogrel to inhibit platelet aggregation.	clopidogrel	147-158	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-47
27196064-8	2016	However, the view that clopidogrel is a CYP2C19 substrate was reinforced by a finding that omeprazole, a CYP2C19 inhibitor, reduced the ability of clopidogrel to inhibit platelet aggregation.	clopidogrel	147-158	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	105-112
27196064-11	2016	Clopidogrel is therefore now considered to be primarily a CYP3A4/5 substrate.	clopidogrel	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	58-64
27337147-5	2016	High on-treatment platelet reactivity (HTPR) to clopidogrel was estimated by vasodilator stimulated phosphoprotein (VASP) phosphorylation assay.	clopidogrel	48-59	vasodilator stimulated phosphoprotein	Homo sapiens	77-114
27337147-5	2016	High on-treatment platelet reactivity (HTPR) to clopidogrel was estimated by vasodilator stimulated phosphoprotein (VASP) phosphorylation assay.	clopidogrel	48-59	vasodilator stimulated phosphoprotein	Homo sapiens	116-120
27337147-10	2016	At 5 days post-treatment with either clopidogrel or ticagrelor, the TPR values were increased and the SC% values were reduced to a similar extent compared with baseline.	clopidogrel	37-48	translocated promoter region, nuclear basket protein	Homo sapiens	68-71
27488362-8	2016	P2Y12 reaction units (PRU) by VN significantly decreased over time with all P2Y12 inhibitors (clopidogrel p&lt;0.001; prasugrel p=0.016; ticagrelor p&lt;0.001).	clopidogrel	94-105	purinergic receptor P2Y12	Homo sapiens	0-5
27488362-8	2016	P2Y12 reaction units (PRU) by VN significantly decreased over time with all P2Y12 inhibitors (clopidogrel p&lt;0.001; prasugrel p=0.016; ticagrelor p&lt;0.001).	clopidogrel	94-105	purinergic receptor P2Y12	Homo sapiens	76-81
27789556-14	2016	At a molecular level, aquaporin-4 expression decreased and the expression and activation of AMP-activated protein kinase signaling and cyclooxygenase-2 increased in the ischemic myocardium of ticagrelor- versus clopidogrel-treated animals (P&lt;0.05).	clopidogrel	211-222	aquaporin 4	Sus scrofa	22-33
27932982-1	2016	The impact of pharmacogenetic variants of cytochrome P450 2C19 (CYP2C19) on clopidogrel-mediated effects on platelet inhibition, inflammatory response and endothelial function, as well as risk of major adverse cardiovascular events (MACE), in coronary heart patients undergoing percutaneous coronary intervention (PCI) was investigated.	clopidogrel	76-87	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	42-62
27932982-1	2016	The impact of pharmacogenetic variants of cytochrome P450 2C19 (CYP2C19) on clopidogrel-mediated effects on platelet inhibition, inflammatory response and endothelial function, as well as risk of major adverse cardiovascular events (MACE), in coronary heart patients undergoing percutaneous coronary intervention (PCI) was investigated.	clopidogrel	76-87	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	64-71
27932982-3	2016	CYP2C19*2 and *3 variants were identified using a clopidogrel-sensitive gene detection kit.	clopidogrel	50-61	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
27932982-7	2016	The data suggest that CYP2C19*2 and *3 variants modulate the drug efficacy of clopidogrel in coronary heart patients undergoing PCI and further enhance the risk of MACE.	clopidogrel	78-89	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	22-29
27932982-8	2016	Accordingly, CYP2C19 pharmacogenetic profiling may be beneficial for coronary heart patients undergoing PCI to predict the efficacy of treatment with clopidogrel.	clopidogrel	150-161	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
24942006-1	2016	Dual antiplatelet therapy comprising aspirin and a P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor) is essential to prevent thrombotic complications after percutaneous coronary intervention (PCI).	clopidogrel	68-79	purinergic receptor P2Y12	Homo sapiens	51-56
25738571-0	2016	Association of VEGFR-2 Gene Polymorphisms With Clopidogrel Resistance in Patients With Coronary Heart Disease.	clopidogrel	47-58	kinase insert domain receptor	Homo sapiens	15-22
25738571-2	2016	We investigated the correlation between VEGFR-2 polymorphisms and the risk of clopidogrel resistance (CR) in patients with coronary heart disease (CHD).	clopidogrel	78-89	kinase insert domain receptor	Homo sapiens	40-47
27514617-5	2016	The mean AUC and Cmax of the active metabolite of clopidogrel, but not those of prasugrel, were CYP2C19 genotype dependent.	clopidogrel	50-61	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	96-103
27511945-5	2016	Ticagrelor, dipyridamole and the active metabolite of clopidogrel (CAM), an alternative P2Y12 antagonist, inhibited osteoclast differentiation and promoted osteoblast differentiation in vitro.	clopidogrel	54-65	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	88-93
27767438-1	2016	INTRODUCTION: Clopidogrel, which is activated by the CYP2C19 enzyme, is among the drugs for which all major regulatory agencies recommend genetic testing to be performed to identify a patient"s CYP2C19 genotype in order to determine the optimal antiplatelet therapeutic scheme.	clopidogrel	14-25	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-60
27767438-1	2016	INTRODUCTION: Clopidogrel, which is activated by the CYP2C19 enzyme, is among the drugs for which all major regulatory agencies recommend genetic testing to be performed to identify a patient"s CYP2C19 genotype in order to determine the optimal antiplatelet therapeutic scheme.	clopidogrel	14-25	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	194-201
27767438-3	2016	AIMS: Here, we report our findings from a retrospective study to assess whether genotyping for the CYP2C19*2 allele was cost effective for myocardial infarction patients receiving clopidogrel treatment in the Serbian population compared with the nongenotype-guided treatment.	clopidogrel	180-191	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	99-106
27728892-12	2016	CYP2C19 genotyping combined with platelet reactivity is an independent and additive predictor of 1-year MACE in Chinese patients undergoing stenting with clopidogrel treatment, which is better than either test alone.	clopidogrel	154-165	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
27673643-0	2016	Allele Frequency Distribution of CYP2C19 Genotypes Associated with Clopidogrel Resistance in Russian Population.	clopidogrel	67-78	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-40
27459888-15	2016	In MDCKII-MDR1 cells, the P-gp-mediated efflux transport of clopidogrel was significantly inhibited by the DZSM extract.	clopidogrel	60-71	phosphoglycolate phosphatase	Rattus norvegicus	26-30
27459888-17	2016	CONCLUSIONS: DZSM significantly affects the pharmacokinetics of clopidogrel and its active metabolite by inhibiting the P-gp-mediated efflux transport and CYP450-mediated metabolism of clopidogrel.	clopidogrel	64-75	phosphoglycolate phosphatase	Rattus norvegicus	120-124
27653892-0	2016	Effect of CYP2C19*2 and *3 on clinical outcome in ischemic stroke patients treated with clopidogrel.	clopidogrel	88-99	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-17
27653892-1	2016	BACKGROUND: Despite clopidogrel has been widely applied to patients with ischemic stroke combined with aspirin, decreased metabolic activation of clopidogrel still occurs because of genetic variations in CYP2C19.	clopidogrel	146-157	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	204-211
27649539-0	2016	Association between CYP3A5 polymorphisms and the risk of adverse events in patients undergoing clopidogrel therapy: Meta-analysis.	clopidogrel	95-106	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	20-26
27649539-1	2016	INTRODUCTION: We wished to explore the relationship between CYP3A5 polymorphisms and adverse events in patients undergoing clopidogrel therapy.	clopidogrel	123-134	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	60-66
27647183-6	2016	Based on the previous reports, an inhibition of platelet aggregation (IPA) &lt;30% for TEG or a P2Y12 reaction unit (PRU) &gt;230 for VerifyNow was defined as high on-clopidogrel platelet reactivity (HPR).	clopidogrel	167-178	purinergic receptor P2Y12	Homo sapiens	96-101
25782570-1	2016	Clopidogrel is a second generation of thienopyridine, which has antiplatelet effect by inhibiting P2Y12 receptor.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	98-103
28164519-1	2016	BACKGROUND: Clopidogrel is a prodrug, the minority of which is converted to an active metabolite by hepatic cytochrome P450 (CYP2C19), however, most of it is metabolized to inactive substance by hepatic carboxylesterase1 (CES1).	clopidogrel	12-23	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	125-132
28164519-1	2016	BACKGROUND: Clopidogrel is a prodrug, the minority of which is converted to an active metabolite by hepatic cytochrome P450 (CYP2C19), however, most of it is metabolized to inactive substance by hepatic carboxylesterase1 (CES1).	clopidogrel	12-23	carboxylesterase 1	Homo sapiens	203-220
28164519-1	2016	BACKGROUND: Clopidogrel is a prodrug, the minority of which is converted to an active metabolite by hepatic cytochrome P450 (CYP2C19), however, most of it is metabolized to inactive substance by hepatic carboxylesterase1 (CES1).	clopidogrel	12-23	carboxylesterase 1	Homo sapiens	222-226
27457785-1	2016	Clopidogrel is reported to be associated with cerivastatin-induced rhabdomyolysis, and clopidogrel and its metabolites are capable of inhibiting CYP2C8 and OATP 1B1 in vitro.	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	145-151
27457785-1	2016	Clopidogrel is reported to be associated with cerivastatin-induced rhabdomyolysis, and clopidogrel and its metabolites are capable of inhibiting CYP2C8 and OATP 1B1 in vitro.	clopidogrel	87-98	solute carrier organic anion transporter family member 1B1	Homo sapiens	156-164
27457785-2	2016	The objective of the present study was to identify the mechanism of clopidogrel-mediated drug-drug interactions (DDIs) on the pharmacokinetics of OATP1B1 and/or CYP2C8 substrates in vivo.	clopidogrel	68-79	solute carrier organic anion transporter family member 1B1	Homo sapiens	146-153
27457785-2	2016	The objective of the present study was to identify the mechanism of clopidogrel-mediated drug-drug interactions (DDIs) on the pharmacokinetics of OATP1B1 and/or CYP2C8 substrates in vivo.	clopidogrel	68-79	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	161-167
27457785-5	2016	In addition, the AUC of pioglitazone M4, a CYP2C8-mediated metabolite of pioglitazone, was reduced to 70% of the control by coadministration of clopidogrel.	clopidogrel	144-155	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	43-49
27457785-7	2016	In conclusion, a single 300 mg of clopidogrel mainly inhibits CYP2C8-mediated metabolism by clopidogrel acyl-beta-glucuronide, but its effect on the pharmacokinetics of OATP1B1 substrates is negligible.	clopidogrel	34-45	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	62-68
27457785-7	2016	In conclusion, a single 300 mg of clopidogrel mainly inhibits CYP2C8-mediated metabolism by clopidogrel acyl-beta-glucuronide, but its effect on the pharmacokinetics of OATP1B1 substrates is negligible.	clopidogrel	34-45	solute carrier organic anion transporter family member 1B1	Homo sapiens	169-176
27457785-8	2016	Clopidogrel is expected to have an effect not only on CYP2C8 substrates, but also dual CYP2C8/OATP1B1 substrates as seen in the case of repaglinide.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	54-60
27457785-8	2016	Clopidogrel is expected to have an effect not only on CYP2C8 substrates, but also dual CYP2C8/OATP1B1 substrates as seen in the case of repaglinide.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	87-93
27457785-8	2016	Clopidogrel is expected to have an effect not only on CYP2C8 substrates, but also dual CYP2C8/OATP1B1 substrates as seen in the case of repaglinide.	clopidogrel	0-11	solute carrier organic anion transporter family member 1B1	Homo sapiens	94-101
27450232-12	2016	CONCLUSIONS: For Chinese patients with symptomatic extracranial or intracranial stenosis treated with clopidogrel, CYP2C19*3 mutation was associated with an increased risk of ischemic events, and the mutation of rs8192950 in CES1 is associated with a decreased risk of recurrent ischemic events.	clopidogrel	102-113	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	115-122
27450232-12	2016	CONCLUSIONS: For Chinese patients with symptomatic extracranial or intracranial stenosis treated with clopidogrel, CYP2C19*3 mutation was associated with an increased risk of ischemic events, and the mutation of rs8192950 in CES1 is associated with a decreased risk of recurrent ischemic events.	clopidogrel	102-113	carboxylesterase 1	Homo sapiens	225-229
26961113-0	2016	Association of Cytochrome P450 Genetic Variants with Clopidogrel Resistance and Outcomes in Acute Ischemic Stroke.	clopidogrel	53-64	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	15-30
26961113-10	2016	The frequency of CYP3A5 (rs776746) GG/AG and CYP2C19*2 (rs4244285) AA/AG genotypes was significantly higher in clopidogrel-resistant patients than in sensitive patients.	clopidogrel	111-122	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	17-23
26961113-10	2016	The frequency of CYP3A5 (rs776746) GG/AG and CYP2C19*2 (rs4244285) AA/AG genotypes was significantly higher in clopidogrel-resistant patients than in sensitive patients.	clopidogrel	111-122	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	45-52
26961113-12	2016	CYP2C19*2 AA and its interaction with CYP3A5 GG were independent predictors of clopidogrel resistance and affected the activity of platelet aggregation.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
26961113-12	2016	CYP2C19*2 AA and its interaction with CYP3A5 GG were independent predictors of clopidogrel resistance and affected the activity of platelet aggregation.	clopidogrel	79-90	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	38-44
26961113-13	2016	Diabetes mellitus, CYP2C19*2 (rs4244285), clopidogrel resistance, and the interaction of CYP2C19*2 with CYP3A5 were all independent risk factors for the primary outcomes of clopidogrel treatment.	clopidogrel	173-184	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	19-26
26961113-13	2016	Diabetes mellitus, CYP2C19*2 (rs4244285), clopidogrel resistance, and the interaction of CYP2C19*2 with CYP3A5 were all independent risk factors for the primary outcomes of clopidogrel treatment.	clopidogrel	173-184	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	89-96
26961113-13	2016	Diabetes mellitus, CYP2C19*2 (rs4244285), clopidogrel resistance, and the interaction of CYP2C19*2 with CYP3A5 were all independent risk factors for the primary outcomes of clopidogrel treatment.	clopidogrel	173-184	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	104-110
27573042-1	2016	AIM: This study explores clinical outcome in cytochrome P450 2C19 (CYP2C19)-related poor metaboliser patients treated with either clopidogrel or prasugrel after percutaneous coronary intervention (PCI) and investigates whether this could be cost-effective.	clopidogrel	130-141	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	45-65
27573042-1	2016	AIM: This study explores clinical outcome in cytochrome P450 2C19 (CYP2C19)-related poor metaboliser patients treated with either clopidogrel or prasugrel after percutaneous coronary intervention (PCI) and investigates whether this could be cost-effective.	clopidogrel	130-141	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	67-74
27573042-3	2016	Post PCI, CYP2C19 poor metaboliser patients were treated with clopidogrel or prasugrel, in addition to aspirin.	clopidogrel	62-73	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-17
27774962-0	2016	Effect of obesity and serum leptin level on clopidogrel resistance.	clopidogrel	44-55	leptin	Homo sapiens	28-34
27774962-5	2016	It has been proposed that clopidogrel effect could be diminished with high serum leptin levels.	clopidogrel	26-37	leptin	Homo sapiens	81-87
27774962-6	2016	The aim of the present trial was to further investigate the relationship between serum leptin level and clopidogrel resistance.	clopidogrel	104-115	leptin	Homo sapiens	87-93
27488401-0	2016	Genotype Frequencies of CYP2C19, P2Y12 and GPIIIa Polymorphisms in Coronary Heart Disease Patients of Han Ethnicity, and Their Impact on Clopidogrel Responsiveness.	clopidogrel	137-148	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
27488401-0	2016	Genotype Frequencies of CYP2C19, P2Y12 and GPIIIa Polymorphisms in Coronary Heart Disease Patients of Han Ethnicity, and Their Impact on Clopidogrel Responsiveness.	clopidogrel	137-148	purinergic receptor P2Y12	Homo sapiens	33-38
27488401-0	2016	Genotype Frequencies of CYP2C19, P2Y12 and GPIIIa Polymorphisms in Coronary Heart Disease Patients of Han Ethnicity, and Their Impact on Clopidogrel Responsiveness.	clopidogrel	137-148	integrin subunit beta 3	Homo sapiens	43-49
27488401-1	2016	To investigate the genotype frequencies of cytochrome P450, family2, subfamily C, polypeptide19 (CYP2C19); P2Y12 receptor; and glycoprotein IIIa polymorphisms in patients with coronary heart disease and their impact on clopidogrel responsiveness and major adverse cardiac events (MACEs).A total of 146 coronary heart disease patients of Han ethnicity, on a clopidogrel regimen, were enrolled.	clopidogrel	219-230	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	43-95
27542264-10	2016	TCF4 knockdown promoted HepG-2 cell differentiation and inhibited tumor formation, and TCF4 could be the potential downstream target for clopidogrel therapy.	clopidogrel	137-148	transcription factor 4	Homo sapiens	0-4
27542264-10	2016	TCF4 knockdown promoted HepG-2 cell differentiation and inhibited tumor formation, and TCF4 could be the potential downstream target for clopidogrel therapy.	clopidogrel	137-148	transcription factor 4	Homo sapiens	87-91
25782570-9	2016	Newer P2Y12 inhibitors, especially ticagrelor, could be effective and safe alternatives if patients had a history of clopidogrel-associated neutropenia.	clopidogrel	117-128	purinergic receptor P2Y12	Homo sapiens	6-11
27213804-0	2016	Exome sequencing of extreme clopidogrel response phenotypes identifies B4GALT2 as a determinant of on-treatment platelet reactivity.	clopidogrel	28-39	beta-1,4-galactosyltransferase 2	Homo sapiens	71-78
27650615-0	2016	The Diagnostic Utility of the Point-of-Care CYP2C19 Genotyping Assay in Patients with Acute Coronary Syndrome Dosing Clopidogrel: Comparison with Platelet Function Test and SNP Genotyping.	clopidogrel	117-128	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	44-51
27650615-1	2016	BACKGROUND: Clopidogrel is a widely used antiplatelet agent for dual antiplatelet therapy and metabolized by CYP2C19.	clopidogrel	12-23	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	109-116
27650615-2	2016	The polymorphism of CYP2C19 is associated with the therapeutic effect of clopidogrel.	clopidogrel	73-84	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	20-27
27650615-12	2016	Although the supplement of *17 allele detection should be accomplished, this novel point-of-care CYP2C19 genotyping instrument could determine the response to the clopidogrel and support the appropriate treatment of ACS patients.	clopidogrel	163-174	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	97-104
28164572-0	2016	Impact of the CYP2C19 Gene Polymorphism on Clopidogrel Personalized Drug Regimen and the Clinical Outcomes.	clopidogrel	43-54	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
27213804-2	2016	CYP2C19 influences clopidogrel response but only accounts for ~12% of the variability in platelet reactivity.	clopidogrel	19-30	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
28164572-1	2016	BACKGROUND: Although the relationship between CYP2C19 genotype and clopidogrel metabolism has been studied clearly, we have not seen the report that clopidogrel was administered at a dose adjusted based on genotyping.	clopidogrel	67-78	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	46-53
27213804-6	2016	B4GALT2 is a platelet-expressed galactosyltransferase, indicating that B4GALT2 c.909C&gt;T may influence clopidogrel sensitivity through atypical cell-surface glycoprotein processing and platelet adhesion.	clopidogrel	105-116	beta-1,4-galactosyltransferase 2	Homo sapiens	0-7
28164572-9	2016	The low responsiveness to clopidogrel in patients with diabetes is closely related to insulin resistance.	clopidogrel	26-37	insulin	Homo sapiens	86-93
27213804-6	2016	B4GALT2 is a platelet-expressed galactosyltransferase, indicating that B4GALT2 c.909C&gt;T may influence clopidogrel sensitivity through atypical cell-surface glycoprotein processing and platelet adhesion.	clopidogrel	105-116	beta-1,4-galactosyltransferase 2	Homo sapiens	71-78
28164572-11	2016	The occurrence of clopidogrel resistance is associated with the CYP2C19 polymorphism in the &lt; 65-year-old female patients.	clopidogrel	18-29	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	64-71
26315480-0	2016	Clopidogrel inhibits angiogenesis of gastric ulcer healing via downregulation of vascular endothelial growth factor receptor 2.	clopidogrel	0-11	kinase insert domain receptor	Homo sapiens	81-126
27309035-2	2016	Currently, three P2Y12 receptor inhibitors are approved for clinical use, including clopidogrel, prasugrel, and ticagrelor, with the latter two being preferred in patients presenting with an acute coronary syndrome.	clopidogrel	84-95	purinergic receptor P2Y12	Homo sapiens	17-22
26315480-8	2016	Clopidogrel treatment significantly decreased pERK, FGFR2, VEGF, VEGFR2, and PDGFRA expression at the ulcer margin when compared with those of the respective control group.	clopidogrel	0-11	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	46-50
26315480-8	2016	Clopidogrel treatment significantly decreased pERK, FGFR2, VEGF, VEGFR2, and PDGFRA expression at the ulcer margin when compared with those of the respective control group.	clopidogrel	0-11	fibroblast growth factor receptor 2	Homo sapiens	52-57
26315480-8	2016	Clopidogrel treatment significantly decreased pERK, FGFR2, VEGF, VEGFR2, and PDGFRA expression at the ulcer margin when compared with those of the respective control group.	clopidogrel	0-11	vascular endothelial growth factor A	Homo sapiens	59-63
26315480-8	2016	Clopidogrel treatment significantly decreased pERK, FGFR2, VEGF, VEGFR2, and PDGFRA expression at the ulcer margin when compared with those of the respective control group.	clopidogrel	0-11	kinase insert domain receptor	Homo sapiens	65-71
26315480-8	2016	Clopidogrel treatment significantly decreased pERK, FGFR2, VEGF, VEGFR2, and PDGFRA expression at the ulcer margin when compared with those of the respective control group.	clopidogrel	0-11	platelet derived growth factor receptor alpha	Homo sapiens	77-83
26315480-9	2016	In vitro, clopidogrel (10(-6)M) inhibited VEGF-stimulated (20 ng/mL) HUVEC proliferation, at least, via downregulation of VEGFR2 and pERK.	clopidogrel	10-21	vascular endothelial growth factor A	Homo sapiens	42-46
26315480-9	2016	In vitro, clopidogrel (10(-6)M) inhibited VEGF-stimulated (20 ng/mL) HUVEC proliferation, at least, via downregulation of VEGFR2 and pERK.	clopidogrel	10-21	kinase insert domain receptor	Homo sapiens	122-128
26315480-9	2016	In vitro, clopidogrel (10(-6)M) inhibited VEGF-stimulated (20 ng/mL) HUVEC proliferation, at least, via downregulation of VEGFR2 and pERK.	clopidogrel	10-21	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	133-137
26315480-10	2016	CONCLUSION: Clopidogrel inhibits the angiogenesis of gastric ulcer healing at least partially by the inhibition of the VEGF-VEGFR2-ERK signal transduction pathway.	clopidogrel	12-23	vascular endothelial growth factor A	Homo sapiens	119-123
26315480-10	2016	CONCLUSION: Clopidogrel inhibits the angiogenesis of gastric ulcer healing at least partially by the inhibition of the VEGF-VEGFR2-ERK signal transduction pathway.	clopidogrel	12-23	kinase insert domain receptor	Homo sapiens	124-130
29767595-2	2016	Our results draw attention to the impact of CYP3A4*1B on the clinical effect of clopidogrel during dual antiplatelet therapy after PCI.	clopidogrel	80-91	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	44-50
27556885-0	2016	Plasma miR-142 accounting for the missing heritability of CYP3A4/5 functionality is associated with pharmacokinetics of clopidogrel.	clopidogrel	120-131	microRNA 142	Homo sapiens	7-14
27061079-2	2016	Clopidogrel is the most commonly prescribed P2Y12 receptor inhibitor because it is effective in the general population and is not as costly as newer FDA-approved agents (prasugrel, ticagrelor).	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	44-49
27275527-2	2016	It is now well-established that approximately 30% of patients treated with the P2Y12 inhibitor clopidogrel display high residual platelet reactivity despite treatment.	clopidogrel	95-106	purinergic receptor P2Y12	Homo sapiens	79-84
26750665-6	2016	The results showed that pretreatment with GA potentiated clopidogrel-induced apoptosis by down-regulating CES1.	clopidogrel	57-68	carboxylesterase 1	Homo sapiens	106-110
27597810-2	2016	In the present study, we compared the effects of clopidogrel and prasugrel on high-sensitivity C-reactive protein (hs-CRP) in patients undergoing percutaneous coronary intervention (PCI).	clopidogrel	49-60	C-reactive protein	Homo sapiens	95-113
27597810-8	2016	Patients taking clopidogrel showed a significant reduction in hs-CRP level compared with the baseline values (P &lt; 0.001).	clopidogrel	16-27	C-reactive protein	Homo sapiens	65-68
27597810-10	2016	A significant 73% overall reduction in the hs-CRP level was seen with prasugrel compared with 39% overall reduction in hs-CRP level with clopidogrel (P = 0.002).	clopidogrel	137-148	C-reactive protein	Homo sapiens	122-125
27503012-0	2016	Efficacy of Leflunomide, Telmisartan, and Clopidogrel for Immunoglobulin A Nephropathy: A Randomized Controlled Trial.	clopidogrel	42-53	IGAN1	Homo sapiens	58-86
27534914-2	2016	OBJECTIVES The aim of the study was to investigate changes in the responder status to clopidogrel therapy over time with the use of 4 platelet function tests (light transmission aggregometry [LTA], multiple electrode aggregometry [MEA], vasodilator-stimulated phosphoprotein (VASP) phosphorylation, and INNOVANCE  PFA P2Y assays [PFA]) in patients after percutaneous coronary intervention (PCI).	clopidogrel	86-97	vasodilator stimulated phosphoprotein	Homo sapiens	237-274
27534914-2	2016	OBJECTIVES The aim of the study was to investigate changes in the responder status to clopidogrel therapy over time with the use of 4 platelet function tests (light transmission aggregometry [LTA], multiple electrode aggregometry [MEA], vasodilator-stimulated phosphoprotein (VASP) phosphorylation, and INNOVANCE  PFA P2Y assays [PFA]) in patients after percutaneous coronary intervention (PCI).	clopidogrel	86-97	vasodilator stimulated phosphoprotein	Homo sapiens	276-280
27534914-7	2016	RESULTS The responder status to clopidogrel changed in 5 patients (14%) as shown by MEA; in 7 patients (20%), by LTA and PFA; and in 13 patients (37%), by VASP.	clopidogrel	32-43	vasodilator stimulated phosphoprotein	Homo sapiens	155-159
27086085-0	2016	Parathyroid Hormone Levels and High-Residual Platelet Reactivity in Patients Receiving Dual Antiplatelet Therapy With Acetylsalicylic Acid and Clopidogrel or Ticagrelor.	clopidogrel	143-154	parathyroid hormone	Homo sapiens	0-19
27556885-0	2016	Plasma miR-142 accounting for the missing heritability of CYP3A4/5 functionality is associated with pharmacokinetics of clopidogrel.	clopidogrel	120-131	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	58-64
27556885-1	2016	AIM: To investigate whether plasma miRNAs targeting CYP3A4/5 have an impact on the variance of pharmacokinetics of clopidogrel.	clopidogrel	115-126	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	52-58
27556885-3	2016	The association between plasma miRNAs targeting CYP3A4/5 mRNA and clopidogrel pharmacokinetics was analyzed in 31 patients with coronary heart disease who received 300 mg loading dose of clopidogrel.	clopidogrel	66-77	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	48-54
27259818-1	2016	CYP2C8 is involved in the metabolic clearance of several important drugs and recent reports have shown that acyl glucuronides of gemfibrozil and clopidogrel are potent time-dependent inhibitors of CYP2C8 activity.	clopidogrel	145-156	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	0-6
27556885-5	2016	Plasma miR-142 was negatively associated with H4 Cmax (r = -0.5269; p = 0.0040) and associated with H4 AUC0-4h (r = -0.4986; p = 0.0069) after 300 mg loading dose of clopidogrel in coronary heart disease patients.	clopidogrel	166-177	microRNA 142	Homo sapiens	7-14
27556885-6	2016	CONCLUSION: miR-142 could account for a part of missing heritability of CYP3A4/5 functionality related to clopidogrel activation.	clopidogrel	106-117	microRNA 142	Homo sapiens	12-19
27556885-6	2016	CONCLUSION: miR-142 could account for a part of missing heritability of CYP3A4/5 functionality related to clopidogrel activation.	clopidogrel	106-117	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	72-78
26699760-8	2016	CONCLUSIONS: In a real-world East Asian PCI population taking clopidogrel, although the concurrent presence of CYP2C19 PM and ABCB1 TT is a strong independent predictor of adverse outcomes, the combined status of two at-risk variants does not have an incremental prognostic value beyond that of the conventional clinical risk factors.Genet Med 18 8, 833-841.	clopidogrel	62-73	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	111-118
26699760-8	2016	CONCLUSIONS: In a real-world East Asian PCI population taking clopidogrel, although the concurrent presence of CYP2C19 PM and ABCB1 TT is a strong independent predictor of adverse outcomes, the combined status of two at-risk variants does not have an incremental prognostic value beyond that of the conventional clinical risk factors.Genet Med 18 8, 833-841.	clopidogrel	62-73	ATP binding cassette subfamily B member 1	Homo sapiens	126-131
27260150-0	2016	Clopidogrel Markedly Increases Plasma Concentrations of CYP2C8 Substrate Pioglitazone.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	56-62
27260150-2	2016	The antiplatelet drug clopidogrel is metabolized to clopidogrel acyl-beta-d-glucuronide, which was recently found to be a strong time-dependent inhibitor of CYP2C8 in humans.	clopidogrel	22-33	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	157-163
27260150-9	2016	The M-IV-to-pioglitazone AUC0-  ratio was 49% (P &lt; 0.001, 90% CI 0.40-0.59) of that during the control phase, indicating that clopidogrel inhibited the CYP2C8-mediated biotransformation of pioglitazone.	clopidogrel	129-140	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	155-161
27260150-10	2016	Clopidogrel increases the exposure to pioglitazone by inhibiting its CYP2C8-mediated biotransformation.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	69-75
27259818-1	2016	CYP2C8 is involved in the metabolic clearance of several important drugs and recent reports have shown that acyl glucuronides of gemfibrozil and clopidogrel are potent time-dependent inhibitors of CYP2C8 activity.	clopidogrel	145-156	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	197-203
26660521-7	2016	Two phase-3 trials investigated the role of novel oral anticoagulant agents on top of aspirin and clopidogrel in patients with ACS.	clopidogrel	98-109	acyl-CoA synthetase long chain family member 5	Homo sapiens	127-130
26323597-6	2016	Further analysis indicated a strong effect of the CYP2C19*2A, but not the *17, allele on both metabolic steps in the conversion of clopidogrel to its active metabolite.	clopidogrel	131-142	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	50-57
27464309-1	2016	AIM: To study the association of ABCB1 and CYP2C19 polymorphisms and the clopidogrel response in Spanish peripheral artery disease patients following percutaneous transluminal angioplasty (PTA) and to perform a meta-analysis.	clopidogrel	73-84	ATP binding cassette subfamily B member 1	Homo sapiens	33-38
27464309-1	2016	AIM: To study the association of ABCB1 and CYP2C19 polymorphisms and the clopidogrel response in Spanish peripheral artery disease patients following percutaneous transluminal angioplasty (PTA) and to perform a meta-analysis.	clopidogrel	73-84	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	43-50
27464309-6	2016	CONCLUSION: The CYP2C19 and ABCB1 polymorphisms could be genetic markers of cardiovascular events in peripheral artery disease patients following PTA treated with clopidogrel.	clopidogrel	163-174	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
27464309-6	2016	CONCLUSION: The CYP2C19 and ABCB1 polymorphisms could be genetic markers of cardiovascular events in peripheral artery disease patients following PTA treated with clopidogrel.	clopidogrel	163-174	ATP binding cassette subfamily B member 1	Homo sapiens	28-33
29442035-0	2016	Assessment of the potential drug-drug interaction between carvedilol and clopidogrel mediated through intestinal P-glycoprotein.	clopidogrel	73-84	ATP binding cassette subfamily B member 1	Homo sapiens	113-127
29442035-2	2016	The purpose of this study was to investigate the role of the P-glycoprotein (P-gp) efflux pump in limiting the intestinal permeability of clopidogrel and the effect of a beta-blocker, namely, carvedilol, on its intestinal transport.	clopidogrel	138-149	ATP binding cassette subfamily B member 1	Homo sapiens	61-75
29442035-2	2016	The purpose of this study was to investigate the role of the P-glycoprotein (P-gp) efflux pump in limiting the intestinal permeability of clopidogrel and the effect of a beta-blocker, namely, carvedilol, on its intestinal transport.	clopidogrel	138-149	ATP binding cassette subfamily B member 1	Homo sapiens	77-81
29442035-6	2016	However, at the highest concentration tested (30 muM), clopidogrel exhibited 3 and 1.4 times higher Peff than those of metoprolol, an FDA high permeability reference standard, in the jejunum and ileum, respectively.	clopidogrel	55-66	latexin	Homo sapiens	49-52
27328699-0	2016	High-Sensitive C-Reactive Protein Predicts Recurrent Stroke and Poor Functional Outcome: Subanalysis of the Clopidogrel in High-Risk Patients With Acute Nondisabling Cerebrovascular Events Trial.	clopidogrel	108-119	C-reactive protein	Homo sapiens	15-33
27459657-0	2016	Clopidogrel-Proton Pump Inhibitor Drug-Drug Interaction and Risk of Adverse Clinical Outcomes Among PCI-Treated ACS Patients: A Meta-analysis.	clopidogrel	0-11	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	112-115
27475285-6	2016	Treatment of wild-type mice with the P2Y12 receptor antagonist clopidogrel increased biliary hyperplasia and cholangiofibrosis in wild-type mice exposed to the xenobiotic alpha-naphthylisothiocyanate (ANIT) for 4 weeks compared to vehicle-treated mice exposed to ANIT.	clopidogrel	63-74	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	37-42
27009617-2	2016	Both diabetes mellitus (DM) and carriage of the CYP2C19*2 allele are associated with a reduced response to clopidogrel.	clopidogrel	107-118	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	48-55
27348249-0	2016	Association Between CYP2C19 Loss-of-Function Allele Status and Efficacy of Clopidogrel for Risk Reduction Among Patients With Minor Stroke or Transient Ischemic Attack.	clopidogrel	75-86	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	20-27
27348249-1	2016	IMPORTANCE: Data are limited regarding the association between CYP2C19 genetic variants and clinical outcomes of patients with minor stroke or transient ischemic attack treated with clopidogrel.	clopidogrel	182-193	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	63-70
27348249-2	2016	OBJECTIVE: To estimate the association between CYP2C19 genetic variants and clinical outcomes of clopidogrel-treated patients with minor stroke or transient ischemic attack.	clopidogrel	97-108	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	47-54
27348249-13	2016	CONCLUSIONS AND RELEVANCE: Among patients with minor ischemic stroke or transient ischemic attack, the use of clopidogrel plus aspirin compared with aspirin alone reduced the risk of a new stroke only in the subgroup of patients who were not carriers of the CYP2C19 loss-of-function alleles.	clopidogrel	110-121	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	258-265
27009617-11	2016	Patients with both DM and CYP2C19*2 required a four-fold increase in clopidogrel maintenance dose as compared to patients without these factors to achieve a similar antiplatelet response.	clopidogrel	69-80	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
27133299-0	2016	Associations of CYP3A4, NR1I2, CYP2C19 and P2RY12 polymorphisms with clopidogrel resistance in Chinese patients with ischemic stroke.	clopidogrel	69-80	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	16-22
27133299-0	2016	Associations of CYP3A4, NR1I2, CYP2C19 and P2RY12 polymorphisms with clopidogrel resistance in Chinese patients with ischemic stroke.	clopidogrel	69-80	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	31-38
27133299-0	2016	Associations of CYP3A4, NR1I2, CYP2C19 and P2RY12 polymorphisms with clopidogrel resistance in Chinese patients with ischemic stroke.	clopidogrel	69-80	purinergic receptor P2Y12	Homo sapiens	43-49
27347418-2	2016	In recent years, the clopidogrel metabolite has been reported to potently inhibit CYP2C8.	clopidogrel	21-32	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	82-88
26693963-3	2016	Among 2,676 patients, 514 (19.2%) were found to have a CYP2C19 variant affecting clopidogrel metabolism.	clopidogrel	81-92	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	55-62
27464285-1	2016	For secondary prevention of acute coronary syndrome, guidelines recommend dual antiplatelet therapy with acetylsalicylic acid and a P2Y12 receptor antagonist such as clopidogrel, prasugrel or ticagrelor for a period of 12 months.	clopidogrel	166-177	purinergic receptor P2Y12	Homo sapiens	132-137
26953527-1	2016	Pretreatment with oral P2Y12 inhibitors occurs each time clopidogrel, prasugrel, ticagrelor are given to patients with suspected coronary artery disease before definition of the coronary anatomy.	clopidogrel	57-68	purinergic receptor P2Y12	Homo sapiens	23-28
27347088-9	2016	No differences in platelet VASP protein expression levels were detected between patients with high clopidogrel response and healthy subjects; whereas VASP protein expression was elevated in patients with low clopidogrel response.	clopidogrel	208-219	vasodilator stimulated phosphoprotein	Homo sapiens	150-154
27347088-10	2016	Furthermore VASP gene transcription was maintained at low levels in healthy subjects and patients with high clopidogrel response, whereas patients with low clopidogrel response exhibited increased VASP mRNA expression levels.	clopidogrel	108-119	vasodilator stimulated phosphoprotein	Homo sapiens	12-16
27347088-10	2016	Furthermore VASP gene transcription was maintained at low levels in healthy subjects and patients with high clopidogrel response, whereas patients with low clopidogrel response exhibited increased VASP mRNA expression levels.	clopidogrel	156-167	vasodilator stimulated phosphoprotein	Homo sapiens	197-201
27347088-14	2016	Combined miRNA and VASP PRI tests may aid the early diagnosis and prediction of clopidogrel resistance.	clopidogrel	80-91	vasodilator stimulated phosphoprotein	Homo sapiens	19-23
27756942-1	2016	INTRODUCTION: CYP2C19 and P2Y12 polymorphisms have been claimed to alter the pharmacodynamic response to clopidogrel.	clopidogrel	105-116	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
27756942-1	2016	INTRODUCTION: CYP2C19 and P2Y12 polymorphisms have been claimed to alter the pharmacodynamic response to clopidogrel.	clopidogrel	105-116	purinergic receptor P2Y12	Homo sapiens	26-31
27756942-2	2016	ABCB1 polymorphism has been associated with the efflux of clopidogrel resulting in decreased bioavailability.	clopidogrel	58-69	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
27756942-3	2016	Due to paucity of data from Indian population, the present study was undertaken to evaluate the association of genetic polymorphisms of CYP2C19, P2Y12, and ABCB1 with inhibition of platelet aggregation (IPA) by clopidogrel.	clopidogrel	211-222	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	136-143
27756942-3	2016	Due to paucity of data from Indian population, the present study was undertaken to evaluate the association of genetic polymorphisms of CYP2C19, P2Y12, and ABCB1 with inhibition of platelet aggregation (IPA) by clopidogrel.	clopidogrel	211-222	ATP binding cassette subfamily B member 1	Homo sapiens	156-161
27756942-17	2016	CONCLUSION: A trend of decrease in the IPA with CYP2C19 genotypes and an increase in the same with the H2 haplotype of P2Y12 following clopidogrel in Indian healthy adults were observed.	clopidogrel	135-146	purinergic receptor P2Y12	Homo sapiens	119-124
26847582-0	2016	Insulin autoimmune syndrome during the administration of clopidogrel.	clopidogrel	57-68	insulin	Homo sapiens	0-7
26109688-5	2016	Low response to clopidogrel was defined as P2Y12 reaction units &gt;=230 in this study.	clopidogrel	16-27	purinergic receptor P2Y12	Homo sapiens	43-48
27009617-4	2016	The objective of this study was to test the ability of clopidogrel doses up to 300 mg daily to decrease platelet reactivity in patients with DM and/or CYP2C19*2.	clopidogrel	55-66	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	151-158
27009617-7	2016	Both DM and CYP2C19*2 were independently associated with elevated on-treatment platelet reactivity with clopidogrel 75 mg daily (p&lt;0.0001 for each).	clopidogrel	104-115	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
27133596-3	2016	The first P2Y12R drug developed, clopidogrel, is a major success but there is still room for improvement with respect to bleeding profile and non-responders.	clopidogrel	33-44	purinergic receptor P2Y12	Homo sapiens	10-16
26934662-8	2016	New P2Y12 inhibitors (prasugrel and ticagrelor) have restricted clopidogrel use to situations where these potent agents are contraindicated.	clopidogrel	64-75	purinergic receptor P2Y12	Homo sapiens	4-9
26837379-1	2016	The current standard of antiplatelet therapy for patients with myocardial infarction (MI) includes the P2Y12-receptor antagonist clopidogrel, prasugrel or ticagrelor.	clopidogrel	129-140	purinergic receptor P2Y12	Homo sapiens	103-108
27139709-7	2016	Since the introduction of clopidogrel, there has been considerable development in this field with at least three novel P2Y12 antagonists approved by the Food and Drug Administration (FDA) over the past decade.	clopidogrel	26-37	purinergic receptor P2Y12	Homo sapiens	119-124
26763917-1	2016	RATIONALE AND AIM: The antiplatelet effect of clopidogrel is reportedly influenced by cytochrome P450 2C19 (CYP2C19) polymorphisms.	clopidogrel	46-57	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	86-106
26763917-1	2016	RATIONALE AND AIM: The antiplatelet effect of clopidogrel is reportedly influenced by cytochrome P450 2C19 (CYP2C19) polymorphisms.	clopidogrel	46-57	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	108-115
26299610-5	2016	Responsiveness to clopidogrel was assessed by measuring P2Y12 reaction unit (PRU) at 8 months.	clopidogrel	18-29	purinergic receptor P2Y12	Homo sapiens	56-61
27350664-1	2016	Polymorphisms of CYP2C19 are associated with platelet response to clopidogrel.	clopidogrel	66-77	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-24
27350664-6	2016	In this study, CYP2C19*2 and CYP2C19*17 were strongly associated with higher platelet aggregation and lower platelet aggregation to clopidogrel treatment, respectively (P &lt;0.001).	clopidogrel	132-143	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
27350664-6	2016	In this study, CYP2C19*2 and CYP2C19*17 were strongly associated with higher platelet aggregation and lower platelet aggregation to clopidogrel treatment, respectively (P &lt;0.001).	clopidogrel	132-143	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	29-36
27350664-10	2016	In conclusion, CYP2C19*2, CYP2C19*17 coexistence of CYP2B6*9 (rs8192719) and P2Y12 (rs2046934) and coexistence of CYP2B6*1B (rs7254579) and P2Y12 (rs2046934) were identified to be associated with response to clopidogrel treatment in Chinese Han patients.	clopidogrel	208-219	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
27368038-1	2016	CYP2C19 loss-of-function (LOF) alleles adversely affect clinical outcome of clopidogrel therapy.	clopidogrel	76-87	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
27368038-2	2016	Recent introduction of a newer-generation drug-eluting stent (DES) has significantly reduced the occurrence of stent thrombosis.The aim of this study was to evaluate the impact of CYP2C19 LOF alleles on clinical outcome in patients treated with the newer-generation DES.The effects of CYP2C19 genotypes were evaluated on clinical outcome of clopidogrel therapy in 2062 patients treated with percutaneous coronary intervention using either first-generation DES (sirolimus- and paclitaxel-eluting stent, n = 1349) or newer-generation DES (everolimus- and zotarolimus-eluting stent, n = 713).	clopidogrel	341-352	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	180-187
27278793-0	2016	Impaired P2Y12 inhibition by clopidogrel in kidney transplant recipients: results from a cohort study.	clopidogrel	29-40	purinergic receptor P2Y12	Homo sapiens	9-14
27350760-2	2016	There has been a concern that statins that are metabolized by cytochrome P450 3A4 may interfere with clopidogrel metabolism at high doses.	clopidogrel	101-112	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	62-81
26556101-7	2016	HTPR to clopidogrel was analyzed using the vasodilator-stimulated protein phosphorylation (VASP), HTPR to aspirin by light-transmission aggregometry (LTA).	clopidogrel	8-19	vasodilator stimulated phosphoprotein	Homo sapiens	91-95
26556524-0	2016	Switching from prasugrel to clopidogrel based on Cytochrome P450 2C19 genotyping in East Asian patients stabilized after acute myocardial infarction.	clopidogrel	28-39	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	49-69
26556524-1	2016	To evaluate the pharmacodynamic efficacy of de-escalating P2Y12 inhibition from prasugrel to clopidogrel based on cytochrome P450 (CYP) 2C19 genotyping, we genotyped 50 Korean patients with AMI who underwent percutaneous coronary intervention (PCI) for CYP2C19 *2,*3, or *17 using real-time PCR.	clopidogrel	93-104	purinergic receptor P2Y12	Homo sapiens	58-63
27247336-2	2016	Mechanisms translating their more potent antiplatelet activity into improved clinical outcomes versus the second-generation P2Y12 antagonist clopidogrel are unclear.	clopidogrel	141-152	purinergic receptor P2Y12	Homo sapiens	124-129
27323099-0	2016	CYP2C19 polymorphisms in acute coronary syndrome patients undergoing clopidogrel therapy in Zhengzhou population.	clopidogrel	69-80	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
27323099-1	2016	The goal of this study was to explore the polymorphisms of CYP2C19 (CYP2C19*2, CYP2C19*3) in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI) on clopidogrel therapy in Zhengzhou city for guidance on clinical medication and reduction in the incidence of thromboembolic events.	clopidogrel	192-203	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	59-66
27323099-4	2016	This study further explored the relationship between CYP2C19 polymorphisms and clopidogrel resistance in ACS patients.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-60
27323099-9	2016	In conclusion, CYP2C19*2/*3 polymorphisms may be associated with clopidogrel resistance.	clopidogrel	65-76	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
27323099-10	2016	Wild-type homozygote and single mutant heterozygote of CYP2C19*2/*3 can be given a normal dose of clopidogrel, while carriers with single mutant homozygote or double mutant heterozygote require ticagrelor antiplatelet therapy as an alternative.	clopidogrel	98-109	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	55-62
27221710-7	2016	The antiplatelet agent clopidogrel, which irreversibly inhibits P2Y12, inhibited Abeta aggregation in platelet cultures; in transgenic AD model mice, this drug reduced the amount of clusterin in the circulation and the incidence of CAA.	clopidogrel	23-34	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	64-69
27188755-9	2016	Clopidogrel treatment did not affect serotonin levels but led to a significant increase in s-VCAM1 (p = 0.03).	clopidogrel	0-11	vascular cell adhesion molecule 1	Homo sapiens	93-98
27035463-5	2016	It may be advisable to carry out a test specific for clopidogrel such as the P2Y12 to ensure that there is no residual action on platelet aggregation function, particularly in patients who may be slow metabolizers of clopidogrel.	clopidogrel	53-64	purinergic receptor P2Y12	Homo sapiens	77-82
26340851-0	2016	Antiplatelet efficacy of P2Y12 inhibitors (prasugrel, ticagrelor, clopidogrel) in patients treated with mild therapeutic hypothermia after cardiac arrest due to acute myocardial infarction.	clopidogrel	66-77	purinergic receptor P2Y12	Homo sapiens	25-30
26962983-0	2016	Association of PEAR1 genetic variants with platelet reactivity in response to dual antiplatelet therapy with aspirin and clopidogrel in the Chinese patient population after percutaneous coronary intervention.	clopidogrel	121-132	platelet endothelial aggregation receptor 1	Homo sapiens	15-20
26962983-2	2016	The aim of this study was to investigate whether PEAR1 genetic variations were associated with platelet reactivity as assessed by adenosine diphosphate(ADP)-induced platelet aggregation in Chinese patients treated with aspirin and clopidogrel.	clopidogrel	231-242	platelet endothelial aggregation receptor 1	Homo sapiens	49-54
26962983-12	2016	CONCLUSIONS: PEAR1 genetic variations were strongly associated with ADP-induced platelet aggregation in Chinese patients with CHD treated with aspirin and clopidogrel.	clopidogrel	155-166	platelet endothelial aggregation receptor 1	Homo sapiens	13-18
27137706-0	2016	Association of CYP2C19 Polymorphisms with the Clinical Efficacy of Clopidogrel Therapy in Patients Undergoing Carotid Artery Stenting in Asia.	clopidogrel	67-78	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
27137706-1	2016	The CYP2C19 gene plays a detrimental role in the metabolism of clopidogrel.	clopidogrel	63-74	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
27137706-2	2016	This study aimed to investigate the association between CYP2C19 polymorphisms and the clinical efficacy of clopidogrel therapy in patients who have undergone carotid artery stenting (CAS).	clopidogrel	107-118	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	56-63
27137706-10	2016	Our results suggest that CYP2C19 LOF alleles (*2 and *3) significantly impact the prognosis of patients on clopidogrel therapy after CAS and that the CYP2C19*2 and CYP2C19*3 alleles have the same effects on prognosis.	clopidogrel	107-118	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
27055904-9	2016	Interestingly, the number of circulating neutrophils was reduced in treated septic P2Y12 null mice, suggesting neutrophils as a target for clopidogrel pleiotropic effects.	clopidogrel	139-150	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	83-88
26751426-9	2016	CONCLUSION: Young platelets were more reactive and, consistent with the irreversible binding of clopidogrel to P2Y12, this effect was more pronounced after treatment with clopidogrel.	clopidogrel	96-107	purinergic receptor P2Y12	Homo sapiens	111-116
26751426-9	2016	CONCLUSION: Young platelets were more reactive and, consistent with the irreversible binding of clopidogrel to P2Y12, this effect was more pronounced after treatment with clopidogrel.	clopidogrel	171-182	purinergic receptor P2Y12	Homo sapiens	111-116
26062773-0	2016	Clopidogrel significantly lowers the development of atherosclerosis in ApoE-deficient mice in vivo.	clopidogrel	0-11	apolipoprotein E	Mus musculus	71-75
26062773-10	2016	After treatment with clopidogrel P-/E-selectin levels and cytokine levels of MCP-1 and PDGFbeta were significantly reduced as compared to controls.	clopidogrel	21-32	selectin, endothelial cell	Mus musculus	36-46
26062773-10	2016	After treatment with clopidogrel P-/E-selectin levels and cytokine levels of MCP-1 and PDGFbeta were significantly reduced as compared to controls.	clopidogrel	21-32	mast cell protease 1	Mus musculus	77-82
26062773-10	2016	After treatment with clopidogrel P-/E-selectin levels and cytokine levels of MCP-1 and PDGFbeta were significantly reduced as compared to controls.	clopidogrel	21-32	platelet derived growth factor, B polypeptide	Mus musculus	87-95
27035463-5	2016	It may be advisable to carry out a test specific for clopidogrel such as the P2Y12 to ensure that there is no residual action on platelet aggregation function, particularly in patients who may be slow metabolizers of clopidogrel.	clopidogrel	217-228	purinergic receptor P2Y12	Homo sapiens	77-82
27080842-4	2016	The best-known examples are AVK and VKORC1-CYP2C9 or clopidogrel and CYP2C19.	clopidogrel	53-64	vitamin K epoxide reductase complex subunit 1	Homo sapiens	36-42
27249437-5	2016	Thus, about 30% of patients CYP2C19*1/*2 acute coronary syndrome who live in Aktobe (Aktobe residents) are under the threat of a possible occurrence of new cardiovascular events due to low sensitivity to clopidogrel.	clopidogrel	204-215	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
27249437-6	2016	Our study confirms that CYP2C19 G (681A) genotype has impact on antiplatelet effect of clopidogrel.	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
27249437-7	2016	The peculiarity of our work lies in the fact that we were the first who conducted pharmacogenetic study in patients treated with clopidogrel with ACS/PCI in the region inhabited by persons of mixed Slavic and Kazakh nationality.	clopidogrel	129-140	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	146-149
27112608-0	2016	[Relationship between ATP-binding cassette subfamily B member 1 and cytochrome P450 2C19 polymorphisms and the effect of clopidogrel post percutaneous coronary intervention in patients with acute coronary syndrome].	clopidogrel	121-132	ATP binding cassette subfamily B member 1	Homo sapiens	22-63
27112608-0	2016	[Relationship between ATP-binding cassette subfamily B member 1 and cytochrome P450 2C19 polymorphisms and the effect of clopidogrel post percutaneous coronary intervention in patients with acute coronary syndrome].	clopidogrel	121-132	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	68-88
27112608-1	2016	OBJECTIVE: To observe the relationship between ATP-binding cassette subfamily B member 1 (ABCB1) and cytochrome P450 (CYP)2C19 polymorphisms and the effect of clopidogrel post percutaneous coronary intervention in patients with coronary artery disease.	clopidogrel	159-170	ATP binding cassette subfamily B member 1	Homo sapiens	47-88
27112608-17	2016	CONCLUSION: ABCB1 gene polymorphism is not but CYP2C19 gene polymorphisms is related with antiplatelet responsiveness of clopidogrel and clinical cardiovascular disease events in patients with acute coronary syndrome undergoing selected percutaneous coronary intervention.	clopidogrel	121-132	ATP binding cassette subfamily B member 1	Homo sapiens	12-17
27112608-17	2016	CONCLUSION: ABCB1 gene polymorphism is not but CYP2C19 gene polymorphisms is related with antiplatelet responsiveness of clopidogrel and clinical cardiovascular disease events in patients with acute coronary syndrome undergoing selected percutaneous coronary intervention.	clopidogrel	121-132	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	47-54
27433344-1	2016	The antiplatelet clopidogrel and the proton pump inhibitor esomeprazole demonstrate a pharmacokinetic interaction through CYP2C19 that could translate into clinical inefficacy of clopidogrel.	clopidogrel	17-28	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	122-129
27433344-1	2016	The antiplatelet clopidogrel and the proton pump inhibitor esomeprazole demonstrate a pharmacokinetic interaction through CYP2C19 that could translate into clinical inefficacy of clopidogrel.	clopidogrel	179-190	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	122-129
27157293-11	2016	RESULTS: Platelet activation markers (CD62p and CD63) and chemokine RANTES were significantly reduced in patients with PAD after 7 and 28days after treatment with clopidogrel.	clopidogrel	163-174	selectin P	Homo sapiens	38-43
27157293-11	2016	RESULTS: Platelet activation markers (CD62p and CD63) and chemokine RANTES were significantly reduced in patients with PAD after 7 and 28days after treatment with clopidogrel.	clopidogrel	163-174	CD63 molecule	Homo sapiens	48-52
27157293-11	2016	RESULTS: Platelet activation markers (CD62p and CD63) and chemokine RANTES were significantly reduced in patients with PAD after 7 and 28days after treatment with clopidogrel.	clopidogrel	163-174	C-C motif chemokine ligand 5	Homo sapiens	68-74
27157293-13	2016	CONCLUSION: The treatment with clopidogrel leads to a reduction of platelet reactivity and release of RANTES from the platelets of patients with PAD.	clopidogrel	31-42	C-C motif chemokine ligand 5	Homo sapiens	102-108
26749343-1	2016	BACKGROUND: There are increasing concerns about clinically significant interactions between proton pump inhibitors (PPIs) and clopidogrel, resulting in adverse cardiovascular outcomes in patients with acute coronary syndromes (ACS).	clopidogrel	126-137	ATPase H+/K+ transporting subunit alpha	Homo sapiens	92-103
26773298-6	2016	The on-clopidogrel platelet aggregation was measured by the use of P2Y12 reaction units (PRUs) with the VerifyNow system.	clopidogrel	7-18	purinergic receptor P2Y12	Homo sapiens	67-72
26773298-8	2016	In the aspirin/clopidogrel group, the PL24 -AUC10 was higher in poor metabolizers (PMs) with cytochrome P450 2C19(CYP2C19) polymorphisms (152 +- 112, 95% CI 103.4-200.6) than in the non-PM group (87 +- 74, 95% CI 73.8-100.2).	clopidogrel	15-26	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	93-113
26773298-8	2016	In the aspirin/clopidogrel group, the PL24 -AUC10 was higher in poor metabolizers (PMs) with cytochrome P450 2C19(CYP2C19) polymorphisms (152 +- 112, 95% CI 103.4-200.6) than in the non-PM group (87 +- 74, 95% CI 73.8-100.2).	clopidogrel	15-26	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	114-121
30132623-1	2016	Objective: The ginsenoside Rb1,which account for platelet aggregation of Xuesaitong dispersible tablet, was selected to investigate the synergistic effects of clopidogrel( CPG) and Xuesaitong dispersible tablet drug by modulating plasma protein binding rate aspect.	clopidogrel	159-170	RB transcriptional corepressor 1	Homo sapiens	27-30
27080842-4	2016	The best-known examples are AVK and VKORC1-CYP2C9 or clopidogrel and CYP2C19.	clopidogrel	53-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
27161676-10	2016	Importantly, BxPc-3 TF+ TMV-enhanced thrombosis was reduced in Par4-deficient mice and wild-type mice treated with the platelet inhibitor clopidogrel, suggesting that platelet activation was required for the enhanced thrombosis.	clopidogrel	138-149	coagulation factor II (thrombin) receptor-like 3	Mus musculus	63-67
27042080-0	2016	The use of oral suspension and rationally prescribing alternatives may be supplemental to the implementation of clopidogrel new algorithm comprising CYP2C19 pharmacogenetics and drug interactions.	clopidogrel	112-123	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	149-156
27005817-0	2016	Association between insulin receptor substrate-1 polymorphisms and high platelet reactivity with clopidogrel therapy in coronary artery disease patients with type 2 diabetes mellitus.	clopidogrel	97-108	insulin receptor substrate 1	Homo sapiens	20-48
27122952-0	2016	Non-Carriers of Reduced-Function CYP2C19 Alleles are Most Susceptible to Impairment of the Anti-Platelet Effect of Clopidogrel by Proton-Pump Inhibitors: A Pilot Study.	clopidogrel	115-126	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-40
27122952-1	2016	BACKGROUND: The phenomenon of CYP2C19 polymorphism affects the metabolism of both clopidogrel and proton-pump inhibitors (PPI).	clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
27122952-11	2016	CONCLUSIONS: Our study indicated that non-carriers of reduced-function CYP2C19 alleles are most susceptible to impairment of the anti-platelet effect of clopidogrel after concomitant PPI use.	clopidogrel	153-164	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
27122952-14	2016	KEY WORDS: Clopidogrel   CYP2C19 polymorphism   Platelet aggregation   Proton pump inhibitors   TEG   VASP.	clopidogrel	11-22	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
27122952-14	2016	KEY WORDS: Clopidogrel   CYP2C19 polymorphism   Platelet aggregation   Proton pump inhibitors   TEG   VASP.	clopidogrel	11-22	vasodilator stimulated phosphoprotein	Homo sapiens	102-106
27103915-1	2016	BACKGROUND: There is great debate on the possible adverse interaction between proton pump inhibitors (PPIs) and clopidogrel.	clopidogrel	112-123	ATPase H+/K+ transporting subunit alpha	Homo sapiens	78-89
26916483-0	2016	Impact of CYP2C19 Metabolizer Status on Patients With ACS Treated With Prasugrel Versus Clopidogrel.	clopidogrel	88-99	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-17
26916483-1	2016	BACKGROUND: Certain alleles of the CYP2C19 gene are associated with higher platelet reactivity and increased ischemic events among patients treated with clopidogrel.	clopidogrel	153-164	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	35-42
26712119-5	2016	SUMMARY:  BACKGROUND: Elevated plasma interleukin-10 (IL-10) levels were observed in patients who responded less to clopidogrel (a prodrug that is required for further metabolic bioactivation in the liver).	clopidogrel	116-127	interleukin 10	Homo sapiens	38-52
26802900-4	2016	Existing oral P2Y12 receptors inhibitors (clopidogrel, prasugrel, or ticagrelor) have several limitations such as delayed onset and offset of action, interindividual variation, and only oral availability.	clopidogrel	42-53	purinergic receptor P2Y12	Homo sapiens	14-19
26633836-4	2016	However, VKAs can interfere with clopidogrel metabolism via the cytochrome P450 (CYP) system which in turn may result in an increase in platelet reactivity.	clopidogrel	33-44	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	64-79
26633836-4	2016	However, VKAs can interfere with clopidogrel metabolism via the cytochrome P450 (CYP) system which in turn may result in an increase in platelet reactivity.	clopidogrel	33-44	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	81-84
26927051-3	2016	Thrombin also amplifies the response to the tissue injury, coagulation and platelet response, so the treatment of ACS is based on the combined use of both antiplatelet (such as aspirin, clopidogrel, prasugrel and ticagrelor) and antithrombotic drugs (unfractionated heparin, enoxaparin, fondaparinux and bivalirudin).	clopidogrel	186-197	coagulation factor II, thrombin	Homo sapiens	0-8
26446447-10	2016	CONCLUSION: This is the first report of a clopidogrel-paclitaxel interaction, suggesting that clinically used doses of clopidogrel can reduce the cytochrome P450 2C8 (CYP2C8)-mediated systemic clearance of paclitaxel, leading to an increased risk of paclitaxel toxicity.	clopidogrel	42-53	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	146-165
26446447-10	2016	CONCLUSION: This is the first report of a clopidogrel-paclitaxel interaction, suggesting that clinically used doses of clopidogrel can reduce the cytochrome P450 2C8 (CYP2C8)-mediated systemic clearance of paclitaxel, leading to an increased risk of paclitaxel toxicity.	clopidogrel	42-53	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	167-173
26446447-10	2016	CONCLUSION: This is the first report of a clopidogrel-paclitaxel interaction, suggesting that clinically used doses of clopidogrel can reduce the cytochrome P450 2C8 (CYP2C8)-mediated systemic clearance of paclitaxel, leading to an increased risk of paclitaxel toxicity.	clopidogrel	119-130	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	146-165
26446447-10	2016	CONCLUSION: This is the first report of a clopidogrel-paclitaxel interaction, suggesting that clinically used doses of clopidogrel can reduce the cytochrome P450 2C8 (CYP2C8)-mediated systemic clearance of paclitaxel, leading to an increased risk of paclitaxel toxicity.	clopidogrel	119-130	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	167-173
26526111-0	2016	Effect of CYP2C19 Polymorphisms on the Platelet Response to Clopidogrel and Influence on the Effect of High Versus Standard Dose Clopidogrel in Carotid Artery Stenting.	clopidogrel	60-71	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-17
26526111-3	2016	The influence of the most common allelic variants of CYP2C19 phenotypes and genotypes on response to baseline clopidogrel and on the pharmacodynamic effect of dose adjustment (high or standard dose of clopidogrel) in patients with high on-treatment reactivity after CAS was investigated.	clopidogrel	110-121	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-60
26526111-11	2016	CONCLUSIONS: In patients undergoing carotid stenting, those with the CYP2C19*2 allele had increased basal PRU values and in fact clopidogrel non-responders increased significantly among intermediate-poor metabolizers.	clopidogrel	129-140	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	69-76
26537850-12	2016	ADP% inhibition is a reliable method of testing clopidogrel response in neurovascular procedures and values of &lt;50% may predict thrombotic complications.	clopidogrel	48-59	WD and tetratricopeptide repeats 1	Homo sapiens	0-4
26612496-4	2016	On each challenge day, clopidogrel, a P2Y12 antagonist was administered 30 min.	clopidogrel	23-34	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	38-43
26576037-4	2016	Timely performed VASP-P, not an aggregation-based test, may be a surrogate for clopidogrel bioavailability.	clopidogrel	79-90	vasodilator stimulated phosphoprotein	Homo sapiens	17-23
26576037-15	2016	CONCLUSIONS: After 600 mg clopidogrel, VASP-P, but not whole-blood platelet aggregation measured by MEA, is almost entirely predicted by CAMCmax .	clopidogrel	26-37	vasodilator stimulated phosphoprotein	Homo sapiens	39-45
26520845-0	2016	Comparison of VerifyNow P2Y12 and thrombelastography for assessing clopidogrel response in stroke patients in China.	clopidogrel	67-78	purinergic receptor P2Y12	Homo sapiens	24-29
26520845-2	2016	The aim of the study was to compare the consistency of VerifyNow P2Y12 and thrombelastography (TEG) in acute ischemic stroke patients treated with clopidogrel.	clopidogrel	147-158	purinergic receptor P2Y12	Homo sapiens	65-70
25850030-1	2016	Treatment of carriers of the CYP2C19*2 allele and ABCB1 TT genotype with clopidogrel is associated with increased ischemic complications after percutaneous coronary intervention (PCI).	clopidogrel	73-84	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	29-36
25850030-1	2016	Treatment of carriers of the CYP2C19*2 allele and ABCB1 TT genotype with clopidogrel is associated with increased ischemic complications after percutaneous coronary intervention (PCI).	clopidogrel	73-84	ATP binding cassette subfamily B member 1	Homo sapiens	50-55
26837400-3	2016	Clopidogrel resistance was defined as &lt;=15% platelet inhibition or greater than 213 P2Y12 reaction units (PRU).	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	87-92
26815196-0	2016	Changes in CYP2C19 enzyme activity evaluated by the [(13)C]-pantoprazole breath test after co-administration of clopidogrel and proton pump inhibitors following percutaneous coronary intervention and correlation to platelet reactivity.	clopidogrel	112-123	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	11-18
26815196-4	2016	It has been reported that with the exception of pantoprazole and dexlanzoprazole, PPIs can impede conversion of clopidogrel by cytochrome P450 2C19 (CYP2C19) to its active metabolite, a critical step required for clopidogrel efficacy.	clopidogrel	112-123	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	127-147
26815196-4	2016	It has been reported that with the exception of pantoprazole and dexlanzoprazole, PPIs can impede conversion of clopidogrel by cytochrome P450 2C19 (CYP2C19) to its active metabolite, a critical step required for clopidogrel efficacy.	clopidogrel	112-123	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	149-156
26815196-4	2016	It has been reported that with the exception of pantoprazole and dexlanzoprazole, PPIs can impede conversion of clopidogrel by cytochrome P450 2C19 (CYP2C19) to its active metabolite, a critical step required for clopidogrel efficacy.	clopidogrel	213-224	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	127-147
26815196-4	2016	It has been reported that with the exception of pantoprazole and dexlanzoprazole, PPIs can impede conversion of clopidogrel by cytochrome P450 2C19 (CYP2C19) to its active metabolite, a critical step required for clopidogrel efficacy.	clopidogrel	213-224	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	149-156
26755608-3	2016	Mice treated with the P2RY12 inhibitor clopidogrel, as well as those in which P2RY12 was genetically ablated, exhibited significantly diminished movement of juxtavascular microglial processes and failed to close laser-induced openings of the BBB.	clopidogrel	39-50	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	22-28
26524713-5	2016	In particular, CYP2C19 intermediate and poor metabolizers converted 26.2% and 39.5% less clopidogrel to clop-AM, respectively, compared to extensive metabolizers.	clopidogrel	89-100	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
26828987-8	2016	Additionally, it was found that patients who have clopidogrel and/or aspirin resistance also have CYP2C19*1/*2 or CYPC19*2/*2 genotype.	clopidogrel	50-61	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	98-105
26828987-11	2016	In conclusion, it was suggested that there is a relation between CYP2C19*2 mutations and ST due to clopidogrel resistance, and CYP2C19*17 may have a protective role in this process.	clopidogrel	99-110	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	65-72
26828987-12	2016	The use of novel and more potent drug or high clopidogrel maintenance dosing before stent implantation may be beneficial treatment options for antiplatelet therapy in CYP2C19*2 carriers.	clopidogrel	46-57	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	167-174
26639039-4	2016	HPR on clopidogrel and aspirin was defined after PCI as P2Y12 reaction units (PRU) &gt;208 and aspirin reaction units &gt;550, respectively.	clopidogrel	7-18	purinergic receptor P2Y12	Homo sapiens	56-61
26338921-2	2016	CYP2C19 gene polymorphisms influence clopidogrel activity.	clopidogrel	37-48	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
26338921-6	2016	Clopidogrel response was tested by the VerifyNow P2Y12 assay.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	49-54
26338921-15	2016	CONCLUSIONS: Individuals with CYP2C19*17 may have increased risk of ischemic events following endovascular treatment, independent of clopidogrel responsiveness.	clopidogrel	133-144	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
26522758-1	2016	BACKGROUND: An association has been reported between CYP2C19 polymorphism and the altered antiplatelet activity of clopidogrel.	clopidogrel	115-126	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-60
26522758-8	2016	CONCLUSIONS: Approximately, 59.0% of Korean patients with cardiovascular disease receiving clopidogrel had CYP2C19 loss-of-function genotypes classified as IM or PM, and the frequency was similar to the data from Asian people.	clopidogrel	91-102	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	107-114
26522758-9	2016	The PFA-200, LTA, and VerifyNow platelet function tests revealed evidence of a significant association between the efficacy of clopidogrel and CYP2C19 genotypes.	clopidogrel	127-138	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	143-150
26573179-0	2016	PON1 Q192R genetic variant and response to clopidogrel and prasugrel: pharmacokinetics, pharmacodynamics, and a meta-analysis of clinical outcomes.	clopidogrel	43-54	paraoxonase 1	Homo sapiens	0-4
26573179-3	2016	It has been proposed that a genetic variant Q192R (rs662 A&gt;G) in PON1 significantly alters the biotransformation of clopidogrel and affects clinical outcomes; however, this assertion has limited support.	clopidogrel	119-130	paraoxonase 1	Homo sapiens	68-72
26573179-5	2016	We genotyped PON1 Q192R in 275 healthy subjects treated with clopidogrel or prasugrel and 2922 patients with an ACS undergoing PCI randomized to treatment with clopidogrel or prasugrel in the TRITON-TIMI 38 trial.	clopidogrel	61-72	paraoxonase 1	Homo sapiens	13-17
26386578-6	2016	The maximum effect of P2Y12 receptor inhibition assessed by flow cytometry using VASP was 70.42 (6.7), 69.45 (7.1), and 65.58 (12.6) for intravenous MDCO-157 at doses of 75, 150, and 300 mg, respectively, compared with 56.6 (17.5) with oral clopidogrel 300 mg administration (p &lt; 0.0001).	clopidogrel	241-252	purinergic receptor P2Y12	Homo sapiens	22-27
26426352-0	2016	The pharmacokinetic and pharmacodynamic interaction of clopidogrel and cilostazol in relation to CYP2C19 and CYP3A5 genotypes.	clopidogrel	55-66	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	97-104
26426352-0	2016	The pharmacokinetic and pharmacodynamic interaction of clopidogrel and cilostazol in relation to CYP2C19 and CYP3A5 genotypes.	clopidogrel	55-66	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	109-115
26426352-1	2016	AIM: The primary objective of the present study was to evaluate the pharmacokinetic and pharmacodynamic interactions between clopidogrel and cilostazol in relation to the CYP2C19 and CYP3A5 genotypes.	clopidogrel	125-136	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	171-178
26426352-1	2016	AIM: The primary objective of the present study was to evaluate the pharmacokinetic and pharmacodynamic interactions between clopidogrel and cilostazol in relation to the CYP2C19 and CYP3A5 genotypes.	clopidogrel	125-136	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	183-189
26426352-4	2016	RESULTS: The area under the plasma concentration-time curve (AUC) of the active thiol metabolite of clopidogrel was highest in the CYP2C19 extensive metabolizers (EM) and lowest in the poor metabolizers (PM).	clopidogrel	100-111	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	131-138
26426352-7	2016	The inhibition of platelet aggregation from 4 h to 24 h (IPA4-24 ) following the administration of clopidogrel alone was highest in the CYP2C19 EM genotype and lowest in the CYP2C19 PM genotype (59.05 +- 18.95 vs. 36.74 +- 13.26, P = 0.023).	clopidogrel	99-110	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	136-143
26426352-7	2016	The inhibition of platelet aggregation from 4 h to 24 h (IPA4-24 ) following the administration of clopidogrel alone was highest in the CYP2C19 EM genotype and lowest in the CYP2C19 PM genotype (59.05 +- 18.95 vs. 36.74 +- 13.26, P = 0.023).	clopidogrel	99-110	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	174-181
26426352-8	2016	However, the IPA of the CYP2C19 PM following co-administration of clopidogrel and cilostazol was comparable with that of the CYP2C19 EM and intermediate metabolizers (IM) only in CYP3A5*3/*3 subjects.	clopidogrel	66-77	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
26426352-9	2016	CONCLUSIONS: The additive antiplatelet effect of cilostazol plus clopidogrel is maximized in subjects with both the CYP2C19 PM and CYP3A5*3/*3 genotypes because of a lack of change of clopidogrel thiol metabolite exposure in CYP3A5*3/*3 as well as the highest cilostazol IPA in CYP2C19 PM and CYP3A5*3/*3 subjects.	clopidogrel	65-76	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	116-123
26426352-9	2016	CONCLUSIONS: The additive antiplatelet effect of cilostazol plus clopidogrel is maximized in subjects with both the CYP2C19 PM and CYP3A5*3/*3 genotypes because of a lack of change of clopidogrel thiol metabolite exposure in CYP3A5*3/*3 as well as the highest cilostazol IPA in CYP2C19 PM and CYP3A5*3/*3 subjects.	clopidogrel	65-76	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	131-137
26426352-9	2016	CONCLUSIONS: The additive antiplatelet effect of cilostazol plus clopidogrel is maximized in subjects with both the CYP2C19 PM and CYP3A5*3/*3 genotypes because of a lack of change of clopidogrel thiol metabolite exposure in CYP3A5*3/*3 as well as the highest cilostazol IPA in CYP2C19 PM and CYP3A5*3/*3 subjects.	clopidogrel	65-76	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	225-231
26426352-9	2016	CONCLUSIONS: The additive antiplatelet effect of cilostazol plus clopidogrel is maximized in subjects with both the CYP2C19 PM and CYP3A5*3/*3 genotypes because of a lack of change of clopidogrel thiol metabolite exposure in CYP3A5*3/*3 as well as the highest cilostazol IPA in CYP2C19 PM and CYP3A5*3/*3 subjects.	clopidogrel	65-76	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	278-285
26426352-9	2016	CONCLUSIONS: The additive antiplatelet effect of cilostazol plus clopidogrel is maximized in subjects with both the CYP2C19 PM and CYP3A5*3/*3 genotypes because of a lack of change of clopidogrel thiol metabolite exposure in CYP3A5*3/*3 as well as the highest cilostazol IPA in CYP2C19 PM and CYP3A5*3/*3 subjects.	clopidogrel	65-76	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	225-231
26757134-6	2016	In a logistic regression, CYP2C19 LOF variants (P = 0.011), age (P = 0.032), and body mass index (BMI, P = 0.039) were significantly associated with the incidence of MACE in patients taking clopidogrel.	clopidogrel	190-201	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
26757134-7	2016	CYP2C19 genetic variants, age, and BMI are potential predictors associated with variability to clopidogrel response in Egyptians.	clopidogrel	95-106	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
26663880-11	2016	RESULTS: Clopidogrel plus aspirin and clopidogrel plus placebo reduced beta-TG by a GMR of 0.51 (0.42-0.63) and 0.54 (0.46-0.64) at 2 h. Ticagrelor plus aspirin and ticagrelor plus placebo decreased beta-TG by a GMR of 0.38 (0.26-0.57) and 0.47 (0.31-0.72).	clopidogrel	9-20	pro-platelet basic protein	Homo sapiens	71-78
26663880-11	2016	RESULTS: Clopidogrel plus aspirin and clopidogrel plus placebo reduced beta-TG by a GMR of 0.51 (0.42-0.63) and 0.54 (0.46-0.64) at 2 h. Ticagrelor plus aspirin and ticagrelor plus placebo decreased beta-TG by a GMR of 0.38 (0.26-0.57) and 0.47 (0.31-0.72).	clopidogrel	9-20	colony stimulating factor 2 receptor subunit alpha	Homo sapiens	84-87
26663880-11	2016	RESULTS: Clopidogrel plus aspirin and clopidogrel plus placebo reduced beta-TG by a GMR of 0.51 (0.42-0.63) and 0.54 (0.46-0.64) at 2 h. Ticagrelor plus aspirin and ticagrelor plus placebo decreased beta-TG by a GMR of 0.38 (0.26-0.57) and 0.47 (0.31-0.72).	clopidogrel	9-20	pro-platelet basic protein	Homo sapiens	199-206
26663880-11	2016	RESULTS: Clopidogrel plus aspirin and clopidogrel plus placebo reduced beta-TG by a GMR of 0.51 (0.42-0.63) and 0.54 (0.46-0.64) at 2 h. Ticagrelor plus aspirin and ticagrelor plus placebo decreased beta-TG by a GMR of 0.38 (0.26-0.57) and 0.47 (0.31-0.72).	clopidogrel	9-20	colony stimulating factor 2 receptor subunit alpha	Homo sapiens	212-215
26663880-11	2016	RESULTS: Clopidogrel plus aspirin and clopidogrel plus placebo reduced beta-TG by a GMR of 0.51 (0.42-0.63) and 0.54 (0.46-0.64) at 2 h. Ticagrelor plus aspirin and ticagrelor plus placebo decreased beta-TG by a GMR of 0.38 (0.26-0.57) and 0.47 (0.31-0.72).	clopidogrel	38-49	pro-platelet basic protein	Homo sapiens	71-78
26663880-11	2016	RESULTS: Clopidogrel plus aspirin and clopidogrel plus placebo reduced beta-TG by a GMR of 0.51 (0.42-0.63) and 0.54 (0.46-0.64) at 2 h. Ticagrelor plus aspirin and ticagrelor plus placebo decreased beta-TG by a GMR of 0.38 (0.26-0.57) and 0.47 (0.31-0.72).	clopidogrel	38-49	colony stimulating factor 2 receptor subunit alpha	Homo sapiens	84-87
26663880-11	2016	RESULTS: Clopidogrel plus aspirin and clopidogrel plus placebo reduced beta-TG by a GMR of 0.51 (0.42-0.63) and 0.54 (0.46-0.64) at 2 h. Ticagrelor plus aspirin and ticagrelor plus placebo decreased beta-TG by a GMR of 0.38 (0.26-0.57) and 0.47 (0.31-0.72).	clopidogrel	38-49	pro-platelet basic protein	Homo sapiens	199-206
26663880-11	2016	RESULTS: Clopidogrel plus aspirin and clopidogrel plus placebo reduced beta-TG by a GMR of 0.51 (0.42-0.63) and 0.54 (0.46-0.64) at 2 h. Ticagrelor plus aspirin and ticagrelor plus placebo decreased beta-TG by a GMR of 0.38 (0.26-0.57) and 0.47 (0.31-0.72).	clopidogrel	38-49	colony stimulating factor 2 receptor subunit alpha	Homo sapiens	212-215
26712119-5	2016	SUMMARY:  BACKGROUND: Elevated plasma interleukin-10 (IL-10) levels were observed in patients who responded less to clopidogrel (a prodrug that is required for further metabolic bioactivation in the liver).	clopidogrel	116-127	interleukin 10	Homo sapiens	54-59
26712119-7	2016	OBJECTIVE: To systematically explore possible differences in the formation of and response to clopidogrel active metabolite (CAM) in mice with or without IL-10 gene expression.	clopidogrel	94-105	interleukin 10	Mus musculus	154-159
26712119-8	2016	METHODS: A single oral dose of clopidogrel (10 mg kg(-1)) was given to IL-10 knockout (KO) mice and wild-type (WT) control mice, respectively, and pharmacokinetic parameters of clopidogrel and CAM were calculated.	clopidogrel	31-42	interleukin 10	Mus musculus	71-76
27555873-0	2016	Simultaneous Two-Vessel Subacute Stent Thrombosis Caused by Clopidogrel Resistance from CYP2C19 Polymorphism.	clopidogrel	60-71	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	88-95
27413737-8	2016	SGD or clopidogrel after CI-RP reduced TNF-alpha and IL-1beta levels in brain tissue and serum levels of MCP-1, IL-1beta, and IL-10.	clopidogrel	7-18	tumor necrosis factor	Rattus norvegicus	39-48
27413737-8	2016	SGD or clopidogrel after CI-RP reduced TNF-alpha and IL-1beta levels in brain tissue and serum levels of MCP-1, IL-1beta, and IL-10.	clopidogrel	7-18	interleukin 1 beta	Rattus norvegicus	53-61
27413737-8	2016	SGD or clopidogrel after CI-RP reduced TNF-alpha and IL-1beta levels in brain tissue and serum levels of MCP-1, IL-1beta, and IL-10.	clopidogrel	7-18	mast cell protease 1-like 1	Rattus norvegicus	105-110
27413737-8	2016	SGD or clopidogrel after CI-RP reduced TNF-alpha and IL-1beta levels in brain tissue and serum levels of MCP-1, IL-1beta, and IL-10.	clopidogrel	7-18	interleukin 1 beta	Rattus norvegicus	112-120
27413737-8	2016	SGD or clopidogrel after CI-RP reduced TNF-alpha and IL-1beta levels in brain tissue and serum levels of MCP-1, IL-1beta, and IL-10.	clopidogrel	7-18	interleukin 10	Rattus norvegicus	126-131
27555873-1	2016	Clopidogrel resistance from CYP2C19 polymorphism has been associated with stent thrombosis in patients undergoing percutaneous coronary intervention with drug-eluting stents.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
27555873-5	2016	Although he was compliant with his dual antiplatelet therapy, he developed stent thrombosis, which was confirmed as clopidogrel resistance from homozygous CYP2C19 polymorphism.	clopidogrel	116-127	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	155-162
26984587-3	2016	Indeed, dual antiplatelet therapy (DAPT) with aspirin and the P2Y12inhibitor clopidogrel, which has represented the mainstay of treatment for many years, has significantly reduced the incidence of recurrent atherothrombotic events.	clopidogrel	77-88	purinergic receptor P2Y12	Homo sapiens	62-67
26444255-5	2016	Cangrelor blocks the binding to the platelet P2Y12 receptor of the active metabolite of the thienopyridines, clopidogrel and prasugrel.	clopidogrel	109-120	purinergic receptor P2Y12	Homo sapiens	45-50
26815196-14	2016	Co-administration of omeprazole or esomeprazole in patients treated with clopidogrel results in lower CYP2C19 enzyme activity and increased platelet reactivity as measured by VASP phosphorylation test while patients given pantoprazole or ranitidine did not show any significant changes in CYP2C19 enzyme activity and platelet reactivity.	clopidogrel	73-84	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	102-109
26815196-14	2016	Co-administration of omeprazole or esomeprazole in patients treated with clopidogrel results in lower CYP2C19 enzyme activity and increased platelet reactivity as measured by VASP phosphorylation test while patients given pantoprazole or ranitidine did not show any significant changes in CYP2C19 enzyme activity and platelet reactivity.	clopidogrel	73-84	vasodilator stimulated phosphoprotein	Homo sapiens	175-179
26815196-14	2016	Co-administration of omeprazole or esomeprazole in patients treated with clopidogrel results in lower CYP2C19 enzyme activity and increased platelet reactivity as measured by VASP phosphorylation test while patients given pantoprazole or ranitidine did not show any significant changes in CYP2C19 enzyme activity and platelet reactivity.	clopidogrel	73-84	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	289-296
26365936-1	2016	BACKGROUND AND AIM: High platelet reactivity (HPR) and presence of CYP2C19 loss-of-function alleles are associated with higher risk for periprocedural myocardial infarction in clopidogrel-treated patients undergoing percutaneous coronary intervention (PCI).	clopidogrel	176-187	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	67-74
27411384-6	2016	Further analysis showed that 53.3% of patients carrying the CYP2C19*2 gene variant had clopidogrel-HTPR, while in the wild type group there were 14.6% (p&lt;0.001).	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	60-67
27411384-7	2016	Multivariate logistic regression analysis identified the CYP2C19*2 variant allele (OR 4.384; 95% CI 1.296-14.833, p=0.017) and high total cholesterol level (OR 2.090; 95% CI 1.263-3.459, p=0.004) as the only independent risk factors for clopidogrel-HTPR.	clopidogrel	237-248	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	57-64
27411384-8	2016	CONCLUSION: The CYP2C19*2 gene variant and high total cholesterol level were major factors for clopidogrel- HTPR in patients with carotid artery stenosis undergoing CEA.	clopidogrel	95-106	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
26573281-0	2016	Impact of Cytochrome P450 2C19*2 and *3 on Clopidogrel Loading Dose in Saudi Patients with Acute Coronary Syndrome.	clopidogrel	43-54	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-30
26573281-1	2016	BACKGROUND: Emerging evidence shows that clopidogrel is greatly affected by nonfunctioning alleles measured by P2Y12 or platelet reactivity units (PRU).	clopidogrel	41-52	purinergic receptor P2Y12	Homo sapiens	111-116
26453463-6	2016	CONCLUSIONS: The current study suggests that switching to a novel P2Y12 agent in patients with ACS and/or patients undergoing coronary stenting is more efficacious than continuing clopidogrel.	clopidogrel	180-191	purinergic receptor P2Y12	Homo sapiens	66-71
26635063-7	2016	Concomitant use of PPIs with thienopyridines (e.g. clopidogrel) could be justified in patients without strong affinity to cytochrome CYP2C19 and with high risk of bleeding (e.g. patients with prior upper gastrointestinal bleeding, Helicobacter pylori infection, advanced age, steroid treatment, and nonsteroidal anti-inflammatory drug use).	clopidogrel	51-62	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	133-140
26824050-0	2016	Clopidogrel Protects Endothelium by Hindering TNFalpha-Induced VCAM-1 Expression through CaMKKbeta/AMPK/Nrf2 Pathway.	clopidogrel	0-11	tumor necrosis factor	Homo sapiens	46-54
26824050-0	2016	Clopidogrel Protects Endothelium by Hindering TNFalpha-Induced VCAM-1 Expression through CaMKKbeta/AMPK/Nrf2 Pathway.	clopidogrel	0-11	vascular cell adhesion molecule 1	Homo sapiens	63-69
26824050-0	2016	Clopidogrel Protects Endothelium by Hindering TNFalpha-Induced VCAM-1 Expression through CaMKKbeta/AMPK/Nrf2 Pathway.	clopidogrel	0-11	calcium/calmodulin dependent protein kinase kinase 2	Homo sapiens	89-98
26824050-0	2016	Clopidogrel Protects Endothelium by Hindering TNFalpha-Induced VCAM-1 Expression through CaMKKbeta/AMPK/Nrf2 Pathway.	clopidogrel	0-11	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	99-103
26824050-0	2016	Clopidogrel Protects Endothelium by Hindering TNFalpha-Induced VCAM-1 Expression through CaMKKbeta/AMPK/Nrf2 Pathway.	clopidogrel	0-11	NFE2 like bZIP transcription factor 2	Homo sapiens	104-108
26695516-0	2016	P-Glycoprotein Polymorphism C3435T Is Associated with Dose-Adjusted Clopidogrel and 2-Oxo-Clopidogrel Concentration.	clopidogrel	68-79	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
26695516-8	2016	CONCLUSION: The ABCB1 3435CC genotype is associated with increased clopidogrel and 2-oxo-clopidogrel dose-adjusted concentrations.	clopidogrel	67-78	ATP binding cassette subfamily B member 1	Homo sapiens	16-21
26695516-9	2016	Therefore, the ABCB1 C3435T genotyping should be one of the parameters taken into account when deciding about the dosing regimen of clopidogrel.	clopidogrel	132-143	ATP binding cassette subfamily B member 1	Homo sapiens	15-20
26721703-6	2016	Interestingly, recent findings indicate that the acyl-beta-glucuronides of gemfibrozil and clopidogrel cause metabolism-dependent inactivation of CYP2C8, leading to a strong potential for drug interactions.	clopidogrel	91-102	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	146-152
25927944-1	2016	High and low platelet reactivity, HPR and LPR respectively, to clopidogrel and aspirin have previously been associated with adverse events following percutaneous coronary intervention (PCI).	clopidogrel	63-74	haptoglobin-related protein	Homo sapiens	34-37
25927944-8	2016	We found an association between the cumulative number of PREDICT score variables and the incidence of HPR for clopidogrel (HPR (ADP)) (p &lt; 0.001) and aspirin (HPR (AA)) (p = 0.007).	clopidogrel	110-121	haptoglobin-related protein	Homo sapiens	102-105
25927944-8	2016	We found an association between the cumulative number of PREDICT score variables and the incidence of HPR for clopidogrel (HPR (ADP)) (p &lt; 0.001) and aspirin (HPR (AA)) (p = 0.007).	clopidogrel	110-121	haptoglobin-related protein	Homo sapiens	123-126
25927944-8	2016	We found an association between the cumulative number of PREDICT score variables and the incidence of HPR for clopidogrel (HPR (ADP)) (p &lt; 0.001) and aspirin (HPR (AA)) (p = 0.007).	clopidogrel	110-121	haptoglobin-related protein	Homo sapiens	123-126
26083485-9	2016	VASP phosphorylation and AA-induced platelet aggregation showed fair correlation in patients taking clopidogrel only.	clopidogrel	100-111	vasodilator stimulated phosphoprotein	Homo sapiens	0-4
26270719-5	2016	All P2Y12 antagonists studied resulted in strong P2Y12 receptor blockade (cangrelor: 93.6%; clopidogrel AM: 93.0%; prasugrel AM: 97.9%).	clopidogrel	92-103	purinergic receptor P2Y12	Homo sapiens	4-9
26270719-8	2016	In conclusion, in vitro cangrelor strongly inhibits the binding of clopidogrel and prasugrel AMs to the P2Y12 receptor, consistent with the previous observation of a negative pharmacodynamic interaction.	clopidogrel	67-78	purinergic receptor P2Y12	Homo sapiens	104-109
26367336-1	2016	Previously conducted studies revealed that smoking enhanced the efficacy of clopidogrel by increasing formation of the active metabolite (AM) from the prodrug through induction of the cytochrome CYP1A2.	clopidogrel	76-87	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	195-201
27980542-3	2016	The safety and efficacy of prasugrel and ticagrelor taken with oral anticoagulants also remain to be established in randomized trials; therefore the P2Y12 inhibitor clopidogrel on top of aspirin or without is now recommended to be used together with a VKA or NOAC.	clopidogrel	165-176	purinergic receptor P2Y12	Homo sapiens	149-154
26610376-11	2016	No specific predictors were found to be significantly associated with ST. New P2Y12 inhibitors were associated with more ST compared to clopidogrel (17.3% vs. 4.2%; respectively, p=0.05).	clopidogrel	136-147	purinergic receptor P2Y12	Homo sapiens	78-83
28356861-0	2016	Influence of Cyp2c19*2 Gene Variant on Therapeutic Response During Clopidogrel Treatment in Patients with Carotid Artery Stenosis.	clopidogrel	67-78	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
28356861-2	2016	The aim of our study was to determine the influence of CYP2C19*2 loss-of-function variant allele on clopidogrel responsiveness in patients with carotid artery stenosis.	clopidogrel	100-111	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	55-62
28356861-7	2016	The influence of CYP2C19*2 variant allele on clopidogrel platelet reactivity was determined using multiple-electrode aggregometry (MEA).	clopidogrel	45-56	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-24
28356861-13	2016	CONCLUSIONS: The CYP2C19*2 loss-of-function variant allele has significant influence on clopidogrel response in patients with carotid artery stenosis undergoing endarterectomy.	clopidogrel	88-99	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-24
27012029-12	2016	The mean VASP-PRI in the patient group treated with clopidogrel was significantly lower than that in the control group without antiplatelet therapy (54.88 +/- 16.81% vs. 79.86 +/- 10.24%, p &lt; 0.001).	clopidogrel	52-63	vasodilator stimulated phosphoprotein	Homo sapiens	9-13
27590033-1	2016	Dual antiplatelet therapy (DAPT) with acetylsalicylic acid and a P2Y12 inhibitor (clopidogrel, ticagrelor, or prasugrel) reduces thrombotic events in patients with acute coronary syndrome (ACS), but it is also associated with an increased risk of bleeding complications.	clopidogrel	82-93	purinergic receptor P2Y12	Homo sapiens	65-70
27239927-3	2016	They initially received dual antiplatelet therapy: clopidogrel 75 mg + acetylsalicylic acid (ASA) 300 mg. Genetic testing was performed in all the patients to reveal the carriage of allelic variants of the genes of cytochrome P-450 isoenzymes and the efficiency of antiplatelet therapy was evaluated.	clopidogrel	51-62	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	215-231
26423110-4	2016	Our objectives were (i) to demonstrate that the proportion of "rapid" metabolisers on 75 mg of clopidogrel within 30-208 (PRU) of P2Y12 inhibition is non-inferior to "slow" metabolisers on prasugrel 10 mg and (ii) to evaluate the same end-point after switching drugs.	clopidogrel	95-106	purinergic receptor P2Y12	Homo sapiens	130-135
26553698-0	2015	Efficacy of ex vivo autologous and in vivo platelet transfusion in the reversal of P2Y12 inhibition by clopidogrel, prasugrel, and ticagrelor: the APTITUDE study.	clopidogrel	103-114	purinergic receptor P2Y12	Homo sapiens	83-88
25855780-4	2015	Administration of clopidogrel bisulfate, an irreversible inhibitor of P2Y12-R, significantly increased urine concentration and AQP2 protein in the kidneys of Sprague-Dawley rats.	clopidogrel	18-39	purinergic receptor P2Y12	Rattus norvegicus	70-75
25855780-4	2015	Administration of clopidogrel bisulfate, an irreversible inhibitor of P2Y12-R, significantly increased urine concentration and AQP2 protein in the kidneys of Sprague-Dawley rats.	clopidogrel	18-39	aquaporin 2	Rattus norvegicus	127-131
25855780-6	2015	Clopidogrel administration also significantly ameliorated lithium-induced polyuria, improved urine concentrating ability and AQP2 protein abundance, and reversed the lithium-induced increase in free-water excretion, without decreasing blood or kidney tissue lithium levels.	clopidogrel	0-11	aquaporin 2	Rattus norvegicus	125-129
26527225-11	2015	Regarding safety, medium-dose aspirin (100-300 mg daily) and aspirin/clopidogrel combination showed an increased risk of MB compared with warfarin (RR 1.17 and 1.15, respectively), as per dabigatran 150 mg and rivaroxaban in older elderly (RR 1.17 and 1.12, respectively).	clopidogrel	69-80	ribonucleotide reductase catalytic subunit M1	Homo sapiens	148-152
26527225-11	2015	Regarding safety, medium-dose aspirin (100-300 mg daily) and aspirin/clopidogrel combination showed an increased risk of MB compared with warfarin (RR 1.17 and 1.15, respectively), as per dabigatran 150 mg and rivaroxaban in older elderly (RR 1.17 and 1.12, respectively).	clopidogrel	69-80	ribonucleotide reductase catalytic subunit M1	Homo sapiens	240-244
26398625-3	2015	Noncarriers of the CYP2C19 loss-of-function (LOF) allele received clopidogrel 75 mg daily.	clopidogrel	66-77	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	19-26
26398625-5	2015	CYP2C19 LOF allele(s) carriers who were intermediate metabolizers (IM) received high-dose clopidogrel (225 mg daily) and were tested for high on-treatment platelet reactivity (HTPR).	clopidogrel	90-101	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
26398625-9	2015	Sensitivity analyses found universal clopidogrel to be the preferred strategy if the prevalence of the CYP2C19 LOF allele was less than 2.6% or the incidence of HTPR in IM patients was greater than 82.8%.	clopidogrel	37-48	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	103-110
26663068-1	2015	OBJECTIVE: To assess the association of genetic polymorphisms of CYP2C19*2,*3,*17 with the recurrence risk of ischemic stroke during clopidogrel prevention in ethnic Han Chinese from Fujian Province.	clopidogrel	133-144	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	65-72
26663068-6	2015	During the antiplatelet therapy with clopidogrel, carriers of CYP2C19 poor metabolizer (CYP2C19*2/*2 or *2/*3) had a higher rate of recurrent stroke compared with extensive metabolizers (CYP2C19*1/*1) (OR=4.71, 95%CI: 1.18-18.80, P&lt;0.05).	clopidogrel	37-48	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	62-69
26663068-6	2015	During the antiplatelet therapy with clopidogrel, carriers of CYP2C19 poor metabolizer (CYP2C19*2/*2 or *2/*3) had a higher rate of recurrent stroke compared with extensive metabolizers (CYP2C19*1/*1) (OR=4.71, 95%CI: 1.18-18.80, P&lt;0.05).	clopidogrel	37-48	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	88-95
26663068-6	2015	During the antiplatelet therapy with clopidogrel, carriers of CYP2C19 poor metabolizer (CYP2C19*2/*2 or *2/*3) had a higher rate of recurrent stroke compared with extensive metabolizers (CYP2C19*1/*1) (OR=4.71, 95%CI: 1.18-18.80, P&lt;0.05).	clopidogrel	37-48	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	88-95
26663068-11	2015	CONCLUSION: For ethnic Han Chinese patients receiving clopidogrel treatment, carriers of poor metabolizer or homozygous mutant *2 allele (CYP2C19*2/*2) have a higher risk of recurrent stroke.	clopidogrel	54-65	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	138-145
26771969-0	2015	Prolonged CRP Increase After Percutaneous Coronary Intervention Is Associated with High Thrombin Concentrations and Low Platelet" Response to Clopidogrel in Patients with Stable Angina.	clopidogrel	142-153	C-reactive protein	Homo sapiens	10-13
26771969-11	2015	It may be advisable to assay post-procedural CRP in each patient with SCAD, who underwent PCI to predict those, with potentially low response to clopidogrel.	clopidogrel	145-156	C-reactive protein	Homo sapiens	45-48
26553698-5	2015	The percentage restoration of residual platelet aggregation achieved with 80% proportion PT (residual platelet aggregation 80% PT mix/residual platelet aggregation baselinex100) significantly decreased with increasing potency of P2Y12 RI (83.9+-11%, 73+-14%, 66.3+-15%, 40.9+-19% for clopidogrel 600 mg, clopidogrel 900 mg, prasugrel, and ticagrelor, respectively; P for trend &lt;0.0001).	clopidogrel	284-295	purinergic receptor P2Y12	Homo sapiens	229-234
26553698-5	2015	The percentage restoration of residual platelet aggregation achieved with 80% proportion PT (residual platelet aggregation 80% PT mix/residual platelet aggregation baselinex100) significantly decreased with increasing potency of P2Y12 RI (83.9+-11%, 73+-14%, 66.3+-15%, 40.9+-19% for clopidogrel 600 mg, clopidogrel 900 mg, prasugrel, and ticagrelor, respectively; P for trend &lt;0.0001).	clopidogrel	304-315	purinergic receptor P2Y12	Homo sapiens	229-234
26265231-3	2015	OBJECTIVE: The purpose of this study is to assess the relationships between CYP2C19 genotypes, clopidogrel pharmacodynamic response, and clinical outcome.	clopidogrel	95-106	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	76-83
26889454-0	2016	Changes of High Sensitivity C-Reactive Protein During Clopidogrel Therapy in Patients Undergoing Percutaneous Coronary Intervention.	clopidogrel	54-65	C-reactive protein	Homo sapiens	28-46
26889454-2	2016	However, there is insufficient data available to demonstrate the changes in high sensitivity C-reactive protein (hs-CRP) during clopidogrel therapy.	clopidogrel	128-139	C-reactive protein	Homo sapiens	93-111
26499518-4	2015	In addition, the lipophilicity of antiplatelet drug clopidogrel at the W/DCE interface is investigated and its ionic partition diagram has been constructed.	clopidogrel	52-63	24-dehydrocholesterol reductase	Homo sapiens	73-76
26402735-1	2015	OBJECTIVE: New P2Y12 inhibitors, classified as oral (prasugrel and ticagrelor) and intravenous (cangrelor and elinogrel) drugs, have shown improved antithrombotic effects compared with clopidogrel in patients with acute coronary syndrome (ACS) or patients undergoing percutaneous coronary intervention (PCI) in landmark trials.	clopidogrel	185-196	purinergic receptor P2Y12	Homo sapiens	15-20
26264906-0	2015	Association of CYP2C19, CYP3A5 and GPIIb/IIIa gene polymorphisms with Aspirin and Clopidogrel Resistance in a cohort of Indian patients with Coronary Artery Disease.	clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
26264906-0	2015	Association of CYP2C19, CYP3A5 and GPIIb/IIIa gene polymorphisms with Aspirin and Clopidogrel Resistance in a cohort of Indian patients with Coronary Artery Disease.	clopidogrel	82-93	integrin subunit alpha 2b	Homo sapiens	35-40
26264906-9	2015	The genotype and allele frequencies of CYP2C19*2 and PLA1/A2 gene polymorphisms were significantly different between clopidogrel semi-responders and responders.	clopidogrel	117-128	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	39-46
26264906-9	2015	The genotype and allele frequencies of CYP2C19*2 and PLA1/A2 gene polymorphisms were significantly different between clopidogrel semi-responders and responders.	clopidogrel	117-128	POU class 2 homeobox 3	Homo sapiens	53-57
26264906-13	2015	In an interim analysis on 72 Indian patients, a significant association was found between CYP2C19*2 and PLA1/A2 in clopidogrel semi-responders.	clopidogrel	115-126	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	90-97
26264906-13	2015	In an interim analysis on 72 Indian patients, a significant association was found between CYP2C19*2 and PLA1/A2 in clopidogrel semi-responders.	clopidogrel	115-126	POU class 2 homeobox 3	Homo sapiens	104-108
26063049-3	2015	The thienopyridine class of P2Y12 receptor antagonists, clopidogrel and prasugrel, have demonstrated efficacy.	clopidogrel	56-67	purinergic receptor P2Y12	Homo sapiens	28-33
26329790-3	2015	Clopidogrel and its metabolites inhibit OATP1B1 and CYP3A4 in vitro.	clopidogrel	0-11	solute carrier organic anion transporter family member 1B1	Homo sapiens	40-47
26329790-3	2015	Clopidogrel and its metabolites inhibit OATP1B1 and CYP3A4 in vitro.	clopidogrel	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	52-58
26298730-8	2015	The mean P2Y12 reaction units (PRU) on Day-0 was 186, and increased significantly to 283 PRU on Day-7 in a time-dependent manner after clopidogrel discontinuation (p = 0.001).	clopidogrel	135-146	purinergic receptor P2Y12	Homo sapiens	9-14
26553698-3	2015	METHODS AND RESULTS: In the Antagonize P2Y12 Treatment Inhibitors by Transfusion of Platelets in an Urgent or Delayed Timing After Acute Coronary Syndrome or Percutaneous Coronary Intervention Presentation-Acute Coronary Syndrome (APTITUDE-ACS) study, patients presenting with acute coronary syndrome or for elective percutaneous coronary intervention, receiving loading doses of clopidogrel (600 mg, n=13 or 900 mg, n=12), prasugrel 60 mg (n=10), or ticagrelor 180 mg (n=10) were included.	clopidogrel	380-391	purinergic receptor P2Y12	Homo sapiens	39-44
26245294-11	2015	CD151 KO mice treated with clopidogrel exhibited synergy in delayed kinetics of clot retraction, in PAR-4 and collagen-mediated platelet aggregation, platelet spreading on fibrinogen and without restricting cAMP inhibition.	clopidogrel	27-38	CD151 antigen	Mus musculus	0-5
26245294-11	2015	CD151 KO mice treated with clopidogrel exhibited synergy in delayed kinetics of clot retraction, in PAR-4 and collagen-mediated platelet aggregation, platelet spreading on fibrinogen and without restricting cAMP inhibition.	clopidogrel	27-38	coagulation factor II (thrombin) receptor-like 3	Mus musculus	100-105
26245294-12	2015	Clopidogrel treated CD151 KO arterioles showed smaller and less stable thrombi with increased tendency to embolise ex vivo and in vivo.	clopidogrel	0-11	CD151 antigen	Mus musculus	20-25
26305340-4	2015	By VerifyNow testing, median (interquartile range) P2Y12 reaction units (PRU) on clopidogrel were 166 (90-234), 195 (124-257), and 198 (141-252) on day 1, one month and six months after PCI, respectively (p=0.005 day 1 to 1 month, and p=0.86 1 month to 6 months).	clopidogrel	81-92	purinergic receptor P2Y12	Homo sapiens	51-56
26362473-0	2015	C3435T polymorphism of the ABCB1 gene is associated with poor clopidogrel responsiveness in a Mexican population undergoing percutaneous coronary intervention.	clopidogrel	62-73	ATP binding cassette subfamily B member 1	Homo sapiens	27-32
26362473-1	2015	BACKGROUND: Clopidogrel is a pro-drug and its intestinal absorption is limited by the P-glycoprotein encoded by the ABCB1 gene.	clopidogrel	12-23	ATP binding cassette subfamily B member 1	Homo sapiens	116-121
26362473-4	2015	The aim of this study was to determine the relationship between poor clopidogrel responsiveness and the ABCB1, CYP and P2RY12 gene polymorphisms among patients undergoing percutaneous coronary intervention (PCI).	clopidogrel	69-80	ATP binding cassette subfamily B member 1	Homo sapiens	104-109
26362473-4	2015	The aim of this study was to determine the relationship between poor clopidogrel responsiveness and the ABCB1, CYP and P2RY12 gene polymorphisms among patients undergoing percutaneous coronary intervention (PCI).	clopidogrel	69-80	peptidylprolyl isomerase G	Homo sapiens	111-114
26362473-4	2015	The aim of this study was to determine the relationship between poor clopidogrel responsiveness and the ABCB1, CYP and P2RY12 gene polymorphisms among patients undergoing percutaneous coronary intervention (PCI).	clopidogrel	69-80	purinergic receptor P2Y12	Homo sapiens	119-125
26362473-10	2015	The TT genotype of the C3435T polymorphism of the ABCB1 gene and omeprazole usage were each associated with poor clopidogrel responsiveness (Exp (beta) 2.73, p=0.009 and Exp (beta) 3.86, p=0.04, respectively).	clopidogrel	113-124	ATP binding cassette subfamily B member 1	Homo sapiens	50-55
26362473-10	2015	The TT genotype of the C3435T polymorphism of the ABCB1 gene and omeprazole usage were each associated with poor clopidogrel responsiveness (Exp (beta) 2.73, p=0.009 and Exp (beta) 3.86, p=0.04, respectively).	clopidogrel	113-124	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	146-153
26362473-10	2015	The TT genotype of the C3435T polymorphism of the ABCB1 gene and omeprazole usage were each associated with poor clopidogrel responsiveness (Exp (beta) 2.73, p=0.009 and Exp (beta) 3.86, p=0.04, respectively).	clopidogrel	113-124	eukaryotic translation elongation factor 1 beta 2 pseudogene 2	Homo sapiens	175-182
26362473-11	2015	CONCLUSION: Poor clopidogrel responsiveness is associated with the TT genotype of the C3435T polymorphism of the ABCB1 gene.	clopidogrel	17-28	ATP binding cassette subfamily B member 1	Homo sapiens	113-118
26164127-9	2015	In addition, AADAC did not hydrolyze several known CES1 substrates, including clopidogrel and oseltamivir, which have large acyl moieties and small alcohol moieties.	clopidogrel	78-89	arylacetamide deacetylase	Homo sapiens	13-18
26148794-3	2015	The aim of this study was to determine whether the astroglial-derived protein S100B that is released into blood can be used as a reliable negative predictive tool for intracranial bleeding in patients after MHI, when they are older than 65 years or being treated with antiplatelet drugs (low-dose aspirin, clopidogrel).	clopidogrel	306-317	S100 calcium binding protein B	Homo sapiens	78-83
26447442-3	2015	For example, genetic variability in the cytochrome P450 2D6 drug metabolizing enzyme can alter the clinical effects of some opioid analgesics (e.g., codeine, tramadol), whereas variability in the CYP2C19 enzyme affects the antiplatelet agent clopidogrel.	clopidogrel	242-253	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	40-59
26290157-8	2015	There was an elevated risk of delayed PPB on clopidogrel (OR = 9.7, 95% CI 3.1-30.8, P = 0.0, I(2)  = 0).	clopidogrel	45-56	histatin 1	Homo sapiens	38-41
26290157-9	2015	There was an increased risk of delayed PPB in patients on clopidogrel + aspirin and/or NSAIDs (OR = 3.4, 95% CI 1.3-8.8, P = 0.01, I(2)  = 0).	clopidogrel	58-69	histatin 1	Homo sapiens	39-42
26447442-3	2015	For example, genetic variability in the cytochrome P450 2D6 drug metabolizing enzyme can alter the clinical effects of some opioid analgesics (e.g., codeine, tramadol), whereas variability in the CYP2C19 enzyme affects the antiplatelet agent clopidogrel.	clopidogrel	242-253	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	196-203
26458411-1	2015	BACKGROUND: Certain proton pump inhibitors (PPIs) interfere with clopidogrel metabolism, potentially attenuating P2Y12 receptor inhibition.	clopidogrel	65-76	purinergic receptor P2Y12	Homo sapiens	113-118
25980448-0	2015	A population-based study of the drug interaction between clopidogrel and angiotensin converting enzyme inhibitors.	clopidogrel	57-68	angiotensin I converting enzyme	Homo sapiens	73-102
25980448-2	2015	Clopidogrel inhibits carboxylesterase 1 (CES1), the enzyme responsible for converting prodrug ACE inhibitors (such as ramipril and perindopril) to their active metabolites.	clopidogrel	0-11	carboxylesterase 1	Homo sapiens	21-39
25980448-2	2015	Clopidogrel inhibits carboxylesterase 1 (CES1), the enzyme responsible for converting prodrug ACE inhibitors (such as ramipril and perindopril) to their active metabolites.	clopidogrel	0-11	carboxylesterase 1	Homo sapiens	41-45
25980448-2	2015	Clopidogrel inhibits carboxylesterase 1 (CES1), the enzyme responsible for converting prodrug ACE inhibitors (such as ramipril and perindopril) to their active metabolites.	clopidogrel	0-11	angiotensin I converting enzyme	Homo sapiens	94-97
25980448-12	2015	CONCLUSIONS: Following myocardial infarction, use of clopidogrel with ACE inhibitors activated by CES1 is not associated with an increased risk of adverse cardiovascular outcomes relative to lisinopril.	clopidogrel	53-64	angiotensin I converting enzyme	Homo sapiens	70-73
25980448-12	2015	CONCLUSIONS: Following myocardial infarction, use of clopidogrel with ACE inhibitors activated by CES1 is not associated with an increased risk of adverse cardiovascular outcomes relative to lisinopril.	clopidogrel	53-64	carboxylesterase 1	Homo sapiens	98-102
25980448-13	2015	These findings suggest that the recently described drug interaction between clopidogrel and prodrug ACE inhibitors is of little clinical relevance.	clopidogrel	76-87	angiotensin I converting enzyme	Homo sapiens	100-103
26014752-8	2015	The associations of ADP-inducible activated GPIIb/IIIa and fold increase of activated GPIIb/IIIa after the addition of ADP with CCB therapy remained significant after adjustment for differences in patient characteristics and factors that were previously associated with clopidogrel response by multivariate regression analyses (both P &lt; 0.05).	clopidogrel	270-281	integrin subunit alpha 2b	Homo sapiens	44-49
26014752-8	2015	The associations of ADP-inducible activated GPIIb/IIIa and fold increase of activated GPIIb/IIIa after the addition of ADP with CCB therapy remained significant after adjustment for differences in patient characteristics and factors that were previously associated with clopidogrel response by multivariate regression analyses (both P &lt; 0.05).	clopidogrel	270-281	integrin subunit alpha 2b	Homo sapiens	86-91
26445541-0	2015	Optimizing clopidogrel dose response: a new clinical algorithm comprising CYP2C19 pharmacogenetics and drug interactions.	clopidogrel	11-22	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	74-81
25753965-6	2015	The antiplatelet effect of clopidogrel was significantly reduced following PCI as measured by VerifyNow P2Y12 and Multiplate ADP test.	clopidogrel	27-38	purinergic receptor P2Y12	Homo sapiens	104-109
26381736-2	2015	BACKGROUND: The active metabolite of clopidogrel cannot bind to P2Y12 when cangrelor occupies the receptor.	clopidogrel	37-48	purinergic receptor P2Y12	Homo sapiens	64-69
26445541-4	2015	The aim of the study is to investigate the cumulative effect of CYP2C19 gene polymorphisms and drug interactions that affects clopidogrel dosing, and apply it into a new clinical-pharmacogenetic algorithm that can be used by clinicians in optimizing clopidogrel-based treatment.	clopidogrel	126-137	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	64-71
26445541-4	2015	The aim of the study is to investigate the cumulative effect of CYP2C19 gene polymorphisms and drug interactions that affects clopidogrel dosing, and apply it into a new clinical-pharmacogenetic algorithm that can be used by clinicians in optimizing clopidogrel-based treatment.	clopidogrel	250-261	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	64-71
26445541-5	2015	METHOD: Clopidogrel dose optimization was analyzed based on two main parameters that affect clopidogrel metabolite area under the curve: different CYP2C19 genotypes and concomitant drug intake.	clopidogrel	8-19	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	147-154
26445541-6	2015	Clopidogrel adjusted dose was computed based on area under the curve ratios for different CYP2C19 genotypes when a drug interacting with CYP2C19 is added to clopidogrel treatment.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	90-97
26445541-6	2015	Clopidogrel adjusted dose was computed based on area under the curve ratios for different CYP2C19 genotypes when a drug interacting with CYP2C19 is added to clopidogrel treatment.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	137-144
26445541-8	2015	RESULTS: The study results show that all patients under clopidogrel treatment, whose genotypes are different from *1*1, and concomitantly taking other drugs metabolized by CYP2C19 require clopidogrel dose adjustment.	clopidogrel	56-67	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	172-179
26445541-8	2015	RESULTS: The study results show that all patients under clopidogrel treatment, whose genotypes are different from *1*1, and concomitantly taking other drugs metabolized by CYP2C19 require clopidogrel dose adjustment.	clopidogrel	188-199	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	172-179
26393490-5	2015	Postnatal studies revealed that SERT deficiency altered the cortical laminar distribution of subtypes of CGE-derived INs but not MGE-derived INs.	clopidogrel	105-108	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	32-36
26337986-7	2015	RESULTS: In patients with DM treated with insulin who received drug-eluting stents (DES), prolonged clopidogrel treatment was associated with a decreased risk of death (hazard ratio [HR]: 0.59; 95% confidence interval [CI]: 0.42 to 0.82) and death or MI (HR: 0.67; 95% CI: 0.49 to 0.92).	clopidogrel	100-111	insulin	Homo sapiens	42-49
26119655-1	2015	Newer oral P2Y12 inhibitors are more potent and have faster onset of action than clopidogrel.	clopidogrel	81-92	purinergic receptor P2Y12	Homo sapiens	11-16
26272900-4	2015	Groups were evaluated statistically as two separate comparisons; the first comparison being clopidogrel twice daily versus prasugrel and the second comparison being clopidogrel twice daily versus clopidogrel daily in those patients with a P2Y12 test result of less than 50%.	clopidogrel	165-176	purinergic receptor P2Y12	Homo sapiens	239-244
26272900-4	2015	Groups were evaluated statistically as two separate comparisons; the first comparison being clopidogrel twice daily versus prasugrel and the second comparison being clopidogrel twice daily versus clopidogrel daily in those patients with a P2Y12 test result of less than 50%.	clopidogrel	165-176	purinergic receptor P2Y12	Homo sapiens	239-244
26177117-0	2015	Influence of Genetic Polymorphisms on Clopidogrel Response and Clinical Outcomes in Patients with Acute Ischemic Stroke CYP2C19 Genotype on Clopidogrel Response.	clopidogrel	140-151	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	120-127
26177117-5	2015	Sixteen single nucleotide polymorphisms (SNPs) within 9 genes were selected and high on-clopidogrel platelet reactivity (HPR) was defined as P2Y12 reaction units (PRU) value &gt;=230.	clopidogrel	88-99	purinergic receptor P2Y12	Homo sapiens	141-146
26177117-12	2015	CONCLUSIONS: CYP2C19*2 and CYP2C19*3 had a significant impact on clopidogrel response, but was not associated with ischemic events during 1 year of follow-up in patients with acute ischemic stroke.	clopidogrel	65-76	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
26177117-12	2015	CONCLUSIONS: CYP2C19*2 and CYP2C19*3 had a significant impact on clopidogrel response, but was not associated with ischemic events during 1 year of follow-up in patients with acute ischemic stroke.	clopidogrel	65-76	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	27-34
26071277-0	2015	Omeprazole, pantoprazole, and CYP2C19 effects on clopidogrel pharmacokinetic-pharmacodynamic relationships in stable coronary artery disease patients.	clopidogrel	49-60	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
26071277-1	2015	PURPOSE: Proton-pump Inhibitors use and CYP2C19 loss-of-function alleles are associated with reduced responsiveness to standard clopidogrel doses and increased cardiovascular events.	clopidogrel	128-139	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-47
26413105-10	2015	CONCLUSION: Direct measurements of the reactivity of platelet GP IIb/IIIa were feasible using PAC1 and flow cytometry in patients taking clopidogrel.	clopidogrel	137-148	integrin subunit alpha 2b	Homo sapiens	62-68
25904241-6	2015	Antiplatelet therapy including the COX inhibitor aspirin and/or ADP receptor P2Y12 inhibitors such as clopidogrel, prasugrel and ticagrelor are the therapy of choice for various cardiovascular complications.	clopidogrel	102-113	purinergic receptor P2Y12	Homo sapiens	77-82
26156883-5	2015	Clinical evidence shows that P2Y12 inhibition by clopidogrel is associated with a reduction in platelet-related mediators of inflammation, such as soluble P-selectin and CD40L, following atherothrombosis.	clopidogrel	49-60	purinergic receptor P2Y12	Homo sapiens	29-34
26156883-5	2015	Clinical evidence shows that P2Y12 inhibition by clopidogrel is associated with a reduction in platelet-related mediators of inflammation, such as soluble P-selectin and CD40L, following atherothrombosis.	clopidogrel	49-60	selectin P	Homo sapiens	155-165
26156883-5	2015	Clinical evidence shows that P2Y12 inhibition by clopidogrel is associated with a reduction in platelet-related mediators of inflammation, such as soluble P-selectin and CD40L, following atherothrombosis.	clopidogrel	49-60	CD40 ligand	Homo sapiens	170-175
26156883-6	2015	Clopidogrel in addition to aspirin, compared to aspirin alone, also reduces markers of systemic inflammation such as tumour necrosis factor (TNF) alpha and C-reactive protein (CRP) following ACS.	clopidogrel	0-11	tumor necrosis factor	Homo sapiens	117-151
26156883-7	2015	The more potent thienopyridine P2Y12 inhibitor, prasugrel, has been shown to decrease platelet P-selectin expression and platelet-leukocyte aggregate formation compared to clopidogrel.	clopidogrel	172-183	purinergic receptor P2Y12	Homo sapiens	31-36
26317618-6	2015	44 patients were enrolled and the study was terminated early as clopidogrel use decreased sharply due to introduction of newer P2Y12 inhibitors.	clopidogrel	64-75	purinergic receptor P2Y12	Homo sapiens	127-132
26218263-0	2015	Implementation of Cell Samples as Controls in National Proficiency Testing for Clopidogrel Therapy-Related CYP2C19 Genotyping in China: A Novel Approach.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	107-114
26218263-1	2015	Laboratories are increasingly requested to perform CYP2C19 genetic testing when managing clopidogrel therapy, especially in patients with acute coronary syndrome undergoing percutaneous coronary intervention.	clopidogrel	89-100	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	51-58
25777663-3	2015	The landmark CURE trial showed that the addition of a P2Y12 antagonist, clopidogrel, to aspirin was beneficial in the treatment of acute coronary syndromes.	clopidogrel	72-83	purinergic receptor P2Y12	Homo sapiens	54-59
25777663-5	2015	Next-generation P2Y12 antagonists, prasugrel and ticagrelor, overcome these limitations and have been shown, in large-scale clinical trials for acute coronary syndromes, to reduce ischaemic events more than clopidogrel, at the expense of an increase in bleeding.	clopidogrel	207-218	purinergic receptor P2Y12	Homo sapiens	16-21
26151079-1	2015	Clopidogrel is a prodrug anticoagulant with active metabolites that irreversibly inhibit the platelet surface GPCR P2Y12 and thus inhibit platelet activation.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	115-120
26147597-2	2015	We investigated the correlation of CYP 2C19 681G &gt; A mutation with clopidogrel resistance (CR).	clopidogrel	70-81	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	35-43
26147597-9	2015	CONCLUSION: CYP 2C19*2 is associated with reduced clopidogrel antiplatelet activity and might be an important marker for poor prognosis of ACS.	clopidogrel	50-61	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-20
26220948-0	2015	Human Liver Cytochrome P450 Enzymes and Microsomal Thiol Methyltransferase Are Involved in the Stereoselective Formation and Methylation of the Pharmacologically Active Metabolite of Clopidogrel.	clopidogrel	183-194	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	12-27
25994355-1	2015	The newer oral P2Y12 inhibitors prasugrel and ticagrelor have been reported to be more potent and faster-acting antiplatelet agents than clopidogrel.	clopidogrel	137-148	purinergic receptor P2Y12	Homo sapiens	15-20
26265611-0	2015	CYP2C19*2 and Other Allelic Variants Affecting Platelet Response to Clopidogrel Tested by Thrombelastography in Patients with Acute Coronary Syndrome.	clopidogrel	68-79	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
26265611-1	2015	BACKGROUND: To investigate the contributions of CYP2C19 polymorphisms to the various clopidogrel responses tested by thrombelastography (TEG) in Chinese patients with the acute coronary syndrome (ACS).	clopidogrel	85-96	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	48-55
26265611-9	2015	CONCLUSIONS: Genetic CYP2C19 polymorphisms are relative to the inferior, the antiplatelet activity after clopidogrel admission and may increase the incidence of ischemic events in patients with ACS.	clopidogrel	105-116	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
26550258-0	2015	A randomized controlled trial to assess the efficacy and safety of doubling dose clopidogrel versus ticagrelor for the treatment of acute coronary syndrome in patients with CYP2C19*2 homozygotes.	clopidogrel	81-92	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	173-180
26550258-2	2015	The CYP2C19*2 allele is a common genetic variant in individuals that need given higher clopidogrel in acute coronary syndrome patients.	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
26550258-3	2015	OBJECTIVE: We aimed to assess a pharmacogenetic approach of doubling dose clopidogrel compare with standard dose of ticagrelor among carriers with the CYP2C19*2 homozygotes.	clopidogrel	74-85	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	151-158
26550258-8	2015	After the first 600 mg loading dose of clopidogrel, patients carrying two CYP2C19*2 allele had weaker PRU inhibition (39.8+-37.4 vs 27.9+-12.4; P = 0.001) and more bleeding adverse events (20.5% vs. 7.1%; hazard ratio = 2.88; 95% [CI], 1.34-6.15; P = 0.001) compared to those taking standard dose of ticagrelor.	clopidogrel	39-50	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	74-81
26237513-6	2015	Dual antiplatelet therapy with aspirin and clopidogrel was associated with significantly lower levels of sCD40L and lower platelet surface expressions of P-selectin and activated GPIIb/IIIa compared to aspirin monotherapy (all p&lt;=0.01).	clopidogrel	43-54	selectin P	Homo sapiens	154-164
26237513-6	2015	Dual antiplatelet therapy with aspirin and clopidogrel was associated with significantly lower levels of sCD40L and lower platelet surface expressions of P-selectin and activated GPIIb/IIIa compared to aspirin monotherapy (all p&lt;=0.01).	clopidogrel	43-54	integrin subunit alpha 2b	Homo sapiens	179-184
26099919-1	2015	Clopidogrel is an antiplatelet drug that requires biotransformation steps to its active metabolite via cytochromes P450 (CYP), particularly CYP2C19 and CYP3A5 as well as paraoxonase-1 (PON1).	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	140-147
26099919-1	2015	Clopidogrel is an antiplatelet drug that requires biotransformation steps to its active metabolite via cytochromes P450 (CYP), particularly CYP2C19 and CYP3A5 as well as paraoxonase-1 (PON1).	clopidogrel	0-11	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	152-158
26099919-1	2015	Clopidogrel is an antiplatelet drug that requires biotransformation steps to its active metabolite via cytochromes P450 (CYP), particularly CYP2C19 and CYP3A5 as well as paraoxonase-1 (PON1).	clopidogrel	0-11	paraoxonase 1	Homo sapiens	170-183
26099919-1	2015	Clopidogrel is an antiplatelet drug that requires biotransformation steps to its active metabolite via cytochromes P450 (CYP), particularly CYP2C19 and CYP3A5 as well as paraoxonase-1 (PON1).	clopidogrel	0-11	paraoxonase 1	Homo sapiens	185-189
26099919-5	2015	The areas under the antiplatelet effect-time curves, maximal and minimal antiplatelet effects of clopidogrel obtained from both methods were significantly different among subjects with different CYP2C19 genotypes.	clopidogrel	97-108	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	195-202
26099919-8	2015	Our data suggests that CYP2C19 genetic polymorphism play a major role in the clopidogrel response, however, the impact of CYP3A5 genetic polymorphism, may be pronounced in the subjects who carried the loss-functional allele of CYP2C19.	clopidogrel	77-88	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	23-30
26099919-8	2015	Our data suggests that CYP2C19 genetic polymorphism play a major role in the clopidogrel response, however, the impact of CYP3A5 genetic polymorphism, may be pronounced in the subjects who carried the loss-functional allele of CYP2C19.	clopidogrel	77-88	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	122-128
26099919-8	2015	Our data suggests that CYP2C19 genetic polymorphism play a major role in the clopidogrel response, however, the impact of CYP3A5 genetic polymorphism, may be pronounced in the subjects who carried the loss-functional allele of CYP2C19.	clopidogrel	77-88	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	227-234
25824964-8	2015	Administration of aspirin to ApoE(-/-) mice on HFD increased blood and arterial wall levels of netrin-1 independently of its effects on platelets, accompanied by reduced plaque size and content of monocytes/macrophages, compared with untreated or clopidogrel-treated mice.	clopidogrel	247-258	netrin 1	Mus musculus	95-103
26170954-0	2015	Allele frequency distribution of CYP2C19*2 allelic variants associated with clopidogrel resistance in cardiac patients.	clopidogrel	76-87	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-40
26049376-3	2015	RECENT FINDINGS: Dual therapy, with clopidogrel (a P2Y12 inhibitor) and OAC, may be an alternative to triple therapy, which usually consists of aspirin and clopidogrel in addition to OAC, in terms of improving clinical outcomes in patients on chronic OAC following PCI with stent implantation.	clopidogrel	36-47	purinergic receptor P2Y12	Homo sapiens	51-56
26108379-2	2015	Reduced CYP2C19 activity impairs clopidogrel bio-activation and increases risk of adverse clinical outcomes.	clopidogrel	33-44	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	8-15
26108379-3	2015	Patients with poor and intermediate CYP2C19 metabolizers treated with clopidogrel incur higher cardiovascular event rates, including myocardial infarction, stroke, and stent thrombosis, following ACS than patients with normal CYP2C19 function.	clopidogrel	70-81	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	36-43
26108379-3	2015	Patients with poor and intermediate CYP2C19 metabolizers treated with clopidogrel incur higher cardiovascular event rates, including myocardial infarction, stroke, and stent thrombosis, following ACS than patients with normal CYP2C19 function.	clopidogrel	70-81	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	226-233
26108379-11	2015	Initial market share for clopidogrel, prasugrel, and ticagrelor was 93%, 5%, and 2%, respectively; however, use of CYP2C19 genotyping is expected to shift market share from clopidogrel to either prasugrel or ticagrelor.	clopidogrel	173-184	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	115-122
26469115-10	2015	The most widely tested is gene CYP2C19, which produces the enzyme transforming clopidogrel into an active metabolite.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	31-38
25608085-7	2015	CGE also induced cell cycle arrest and had a fourfold increase in caspase activity (apoptosis) in PC-3 cells when treated at a dose of 0.5 or 1 mug/mL.	clopidogrel	0-3	chromobox 8	Homo sapiens	98-102
26170954-4	2015	There are many allelic variants of the CYP gene that are involved in clopidogrel resistance, of which CYP2C19*2 has been demonstrated to be one of the most significant loss-of-function alleles.	clopidogrel	69-80	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	102-109
26170954-10	2015	These results suggested that there are significant inter-ethnic variations in the allelic frequencies of CYP2C19*2, which may be responsible for the variable clopidogrel response in cardiac patients.	clopidogrel	158-169	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	105-112
26137210-2	2015	Three P2Y12 inhibitor options (clopidogrel, prasugrel and ticagrelor) are currently available, all having different efficacy and safety profiles along with contrasting contraindications, special warnings and precautions for use.	clopidogrel	31-42	purinergic receptor P2Y12	Homo sapiens	6-11
26196021-2	2015	The effects of proton pump inhibitors (PPIs) on clopidogrel metabolism have been described, but the clinical significance is not yet definitive.	clopidogrel	48-59	ATPase H+/K+ transporting subunit alpha	Homo sapiens	15-26
26309584-0	2015	Both PON1 Q192R and CYP2C19*2 influence platelet response to clopidogrel and ischemic events in Chinese patients undergoing percutaneous coronary intervention.	clopidogrel	61-72	paraoxonase 1	Homo sapiens	5-9
26309584-0	2015	Both PON1 Q192R and CYP2C19*2 influence platelet response to clopidogrel and ischemic events in Chinese patients undergoing percutaneous coronary intervention.	clopidogrel	61-72	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	20-27
26309584-2	2015	Previous studies found that genetic variants such as single nucleotide polymorphisms (SNPs) of CYP2C19 and PON1 may influence clopidogrel response, cause high platelet reactivity (HPR) and increase cardiovascular events.	clopidogrel	126-137	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	95-102
26309584-2	2015	Previous studies found that genetic variants such as single nucleotide polymorphisms (SNPs) of CYP2C19 and PON1 may influence clopidogrel response, cause high platelet reactivity (HPR) and increase cardiovascular events.	clopidogrel	126-137	paraoxonase 1	Homo sapiens	107-111
26294943-3	2015	Clopidogrel inhibits platelets via the P2Y12 receptor.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	39-44
26294943-4	2015	OFA may alter clopidogrel-associated platelet-inhibition via a possible combined effect on P2Y12 inhibition.	clopidogrel	14-25	purinergic receptor P2Y12	Homo sapiens	91-96
26294943-5	2015	To determine if OFA affects clopidogrel associated P2Y12 platelet receptor inhibition by comparing the percentage of responders in patients with cerebrovascular disease who were taking clopidogrel with or without OFA.	clopidogrel	28-39	purinergic receptor P2Y12	Homo sapiens	51-56
26294943-8	2015	For the 67 subjects who received loading doses of both clopidogrel and OFA, 71.6% had a P2Y12 inhibition response more than 20%, which is considered a positive response.	clopidogrel	55-66	purinergic receptor P2Y12	Homo sapiens	88-93
25877068-6	2015	Extension of these studies revealed that ADP-activated P2Y12 receptor is expressed in the kidney, and its irreversible blockade by the administration of clopidogrel bisulphate (Plavix( )) ameliorates Li-induced NDI in rodents.	clopidogrel	153-175	purinergic receptor P2Y12	Rattus norvegicus	55-60
25834071-8	2015	The P2Y12 receptor blocker clopidogrel demonstrated efficacy in limiting platelet activation and subsequent endothelial injury in this mouse model of renal microvascular injury.	clopidogrel	27-38	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	4-9
25800884-8	2015	Multivariate logistic regression analysis showed that the presence of CYP2C19 *2/*2 was the only independent predictor for intra-stent thrombi on OCT (OR: 3.488, 95 % CI: 1.992-9.046; p = 0.001), although both *1/*2 and *2/*2 were independent predictors for high on-clopidogrel platelet reactivity.	clopidogrel	266-277	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	70-77
25800884-9	2015	CYP2C19*2/*2 homozygous status is associated with subclinical intra-stent thrombi in clopidogrel-treated Chinese patients.	clopidogrel	85-96	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
25897998-2	2015	We aimed to assess the efficacy and safety of the P2Y12 inhibitors clopidogrel, ticlopidine, prasugrel, ticagrelor, and cangrelor according to diabetes status, age, gender, body mass index, and body weight.	clopidogrel	67-78	purinergic receptor P2Y12	Homo sapiens	50-55
25704243-0	2015	Carboxylesterase 1 c.428G&gt;A single nucleotide variation increases the antiplatelet effects of clopidogrel by reducing its hydrolysis in humans.	clopidogrel	97-108	carboxylesterase 1	Homo sapiens	0-18
25704243-1	2015	Carboxylesterase 1 (CES1) hydrolyzes the prodrug clopidogrel to an inactive carboxylic acid metabolite.	clopidogrel	49-60	carboxylesterase 1	Homo sapiens	0-18
25704243-1	2015	Carboxylesterase 1 (CES1) hydrolyzes the prodrug clopidogrel to an inactive carboxylic acid metabolite.	clopidogrel	49-60	carboxylesterase 1	Homo sapiens	20-24
25704243-3	2015	Clopidogrel carboxylic acid to clopidogrel area under the plasma concentration-time curve from 0 hours to infinity (AUC0-  ) ratio was 53% less in CES1 c.428G&gt;A carriers than in noncarriers (P = 0.009), indicating impaired hydrolysis of clopidogrel.	clopidogrel	31-42	carboxylesterase 1	Homo sapiens	147-151
25704243-3	2015	Clopidogrel carboxylic acid to clopidogrel area under the plasma concentration-time curve from 0 hours to infinity (AUC0-  ) ratio was 53% less in CES1 c.428G&gt;A carriers than in noncarriers (P = 0.009), indicating impaired hydrolysis of clopidogrel.	clopidogrel	240-251	carboxylesterase 1	Homo sapiens	147-151
25704243-5	2015	Consistent with these findings, the average inhibition of P2Y12 -mediated platelet aggregation 0-12 hours after clopidogrel intake was 19 percentage points higher in the c.428G&gt;A carriers than in noncarriers (P = 0.036).	clopidogrel	112-123	purinergic receptor P2Y12	Homo sapiens	58-63
25704243-6	2015	In conclusion, the CES1 c.428G&gt;A SNV increases clopidogrel active metabolite concentrations and antiplatelet effects by reducing clopidogrel hydrolysis to inactive metabolites.	clopidogrel	50-61	carboxylesterase 1	Homo sapiens	19-23
25704243-6	2015	In conclusion, the CES1 c.428G&gt;A SNV increases clopidogrel active metabolite concentrations and antiplatelet effects by reducing clopidogrel hydrolysis to inactive metabolites.	clopidogrel	132-143	carboxylesterase 1	Homo sapiens	19-23
25895737-1	2015	OPINION STATEMENT: Dual antiplatelet therapy with aspirin and a P2Y12 receptor blocker, particularly clopidogrel, has been the standard of therapy for secondary prevention in patients with acute coronary syndromes and patients treated with percutaneous coronary intervention.	clopidogrel	101-112	purinergic receptor P2Y12	Homo sapiens	64-69
25895737-2	2015	More potent P2Y12 inhibitors such as ticagrelor and prasugrel are associated with better pharmacodynamic effect and improved clinical outcomes but are associated with an increased risk of bleeding compared to clopidogrel.	clopidogrel	209-220	purinergic receptor P2Y12	Homo sapiens	12-17
25156215-2	2015	However, the impact of the CYP2C19 genotype on clopidogrel response and clinical outcome has not been fully understood to date.	clopidogrel	47-58	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	27-34
26056028-7	2015	Proposed strategies for management of clopidogrel hypersensitivity include treatment of the reaction with corticosteroids, clopidogrel desensitization, substituting an alternative P2Y12 inhibitor, or clopidogrel avoidance.	clopidogrel	38-49	purinergic receptor P2Y12	Homo sapiens	180-185
25809653-1	2015	BACKGROUND: Dual-antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor, mostly clopidogrel, is the default therapy in both acute coronary syndrome (ACS) and after intracoronary stents.	clopidogrel	88-99	purinergic receptor P2Y12	Homo sapiens	64-69
26149010-7	2015	Clopidogrel is the P2Y12R antagonist that is most widely used in the clinical setting.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	19-25
25761653-0	2015	Clopidogrel reduces apoptosis and promotes proliferation of human vascular endothelial cells induced by palmitic acid via suppression of the long non-coding RNA HIF1A-AS1 in vitro.	clopidogrel	0-11	HIF1A antisense RNA 1	Homo sapiens	161-170
25761653-7	2015	The expression of LncRNA HIF 1 alpha-antisense RNA 1 (HIF1A-AS1) was significantly altered in clopidogrel-treated cells.	clopidogrel	94-105	HIF1A antisense RNA 1	Homo sapiens	25-52
25761653-7	2015	The expression of LncRNA HIF 1 alpha-antisense RNA 1 (HIF1A-AS1) was significantly altered in clopidogrel-treated cells.	clopidogrel	94-105	HIF1A antisense RNA 1	Homo sapiens	54-63
25761653-10	2015	Hence, our results suggest that clopidogrel rescues apoptosis and promotes proliferation of PA-induced damage model of HUVECs through inhibiting the mediator LncRNA HIF1A-AS1.	clopidogrel	32-43	HIF1A antisense RNA 1	Homo sapiens	165-174
25761653-11	2015	These findings indicate that LncRNA HIF1A-AS1 may play an important role in the pathogenesis of CVD, and provide a novel molecular mechanism of clopidogrel for treatment of CVD.	clopidogrel	144-155	HIF1A antisense RNA 1	Homo sapiens	36-45
26061035-1	2015	BACKGROUND AND AIMS: Proton pump inhibitors (PPIs) have been associated with adverse clinical outcomes amongst clopidogrel users after an acute coronary syndrome.	clopidogrel	111-122	ATPase H+/K+ transporting subunit alpha	Homo sapiens	21-32
25585230-4	2015	Diabetic CAD patients are characterized by a pro-thrombotic milieu and by an impaired response to both aspirin and P2Y12 receptor inhibitors, especially to clopidogrel.	clopidogrel	156-167	purinergic receptor P2Y12	Homo sapiens	115-120
25746368-12	2015	Poor response to clopidogrel assessed by VerifyNow P2Y12 predicts myocardial necrosis.	clopidogrel	17-28	purinergic receptor P2Y12	Homo sapiens	51-56
25917561-3	2015	P2Y12 receptor antagonist efficacy was measured by VASP phosphorylation 24 +- 4 hours after a loading dose of clopidogrel (600 mg, N=407), prasugrel (60 mg, N=106), or ticagrelor (180 mg, N=76) and expressed by platelet reactivity index (PRI).	clopidogrel	110-121	purinergic receptor P2Y12	Homo sapiens	0-5
25810245-0	2015	Influence of CYP2C19 loss-of-function variants on the metabolism of clopidogrel in patients from north-western China.	clopidogrel	68-79	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
25810245-1	2015	WHAT IS KNOWN AND OBJECTIVE: Variation of the cytochrome P450 2C19 gene coding for the CYP2C19 enzyme has been reported to be associated with clopidogrel response variability.	clopidogrel	142-153	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	87-94
25810245-3	2015	METHODS: This study was conducted to assess the impact of CYP2C19 polymorphism on the clopidogrel metabolism, indirectly selecting the plasma concentration ratios of clopidogrel to its inactive metabolite SR26334 as an evaluation index.	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	58-65
25810245-10	2015	WHAT IS NEW AND CONCLUSION: Polymorphism of CYP2C19 was significantly associated with plasma concentration ratios of clopidogrel to its inactive metabolite SR26334.	clopidogrel	117-128	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	44-51
25810245-11	2015	Clopidogrel metabolism was regulated by CYP2C19.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-47
25800075-7	2015	CAM concentration as well as PRI by clopidogrel varied significantly (P &lt; 0.05) based on genotypic variation of CYP2C19*2 and CYP2C19*17 individually.	clopidogrel	36-47	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	115-122
26019129-1	2015	BACKGROUND: The role of the CYP2C19 genotype on clopidogrel efficacy has been studied widely, with data suggesting reduced clopidogrel efficacy in loss-of-function variant carriers taking clopidogrel after percutaneous coronary intervention; however, data are limited regarding the association between CYP2C19 genetic variants and outcomes in stroke patients.	clopidogrel	48-59	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
26019129-1	2015	BACKGROUND: The role of the CYP2C19 genotype on clopidogrel efficacy has been studied widely, with data suggesting reduced clopidogrel efficacy in loss-of-function variant carriers taking clopidogrel after percutaneous coronary intervention; however, data are limited regarding the association between CYP2C19 genetic variants and outcomes in stroke patients.	clopidogrel	48-59	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	302-309
26019129-1	2015	BACKGROUND: The role of the CYP2C19 genotype on clopidogrel efficacy has been studied widely, with data suggesting reduced clopidogrel efficacy in loss-of-function variant carriers taking clopidogrel after percutaneous coronary intervention; however, data are limited regarding the association between CYP2C19 genetic variants and outcomes in stroke patients.	clopidogrel	123-134	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
26019129-1	2015	BACKGROUND: The role of the CYP2C19 genotype on clopidogrel efficacy has been studied widely, with data suggesting reduced clopidogrel efficacy in loss-of-function variant carriers taking clopidogrel after percutaneous coronary intervention; however, data are limited regarding the association between CYP2C19 genetic variants and outcomes in stroke patients.	clopidogrel	123-134	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	302-309
26019129-1	2015	BACKGROUND: The role of the CYP2C19 genotype on clopidogrel efficacy has been studied widely, with data suggesting reduced clopidogrel efficacy in loss-of-function variant carriers taking clopidogrel after percutaneous coronary intervention; however, data are limited regarding the association between CYP2C19 genetic variants and outcomes in stroke patients.	clopidogrel	123-134	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
26019129-1	2015	BACKGROUND: The role of the CYP2C19 genotype on clopidogrel efficacy has been studied widely, with data suggesting reduced clopidogrel efficacy in loss-of-function variant carriers taking clopidogrel after percutaneous coronary intervention; however, data are limited regarding the association between CYP2C19 genetic variants and outcomes in stroke patients.	clopidogrel	123-134	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	302-309
26019129-7	2015	CONCLUSIONS: There were significant differences in recurrent stroke by CYP2C19 genotype-inferred metabolizer status in white subcortical stroke patients receiving dual antiplatelet therapy with aspirin and clopidogrel, consistent with cardiovascular studies on CYP2C19 and clopidogrel; however, the bleeding risk that led to early termination of the antiplatelet arm of the SPS3 trial does not appear to be explained by CYP2C19 genotype.	clopidogrel	206-217	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
26019129-7	2015	CONCLUSIONS: There were significant differences in recurrent stroke by CYP2C19 genotype-inferred metabolizer status in white subcortical stroke patients receiving dual antiplatelet therapy with aspirin and clopidogrel, consistent with cardiovascular studies on CYP2C19 and clopidogrel; however, the bleeding risk that led to early termination of the antiplatelet arm of the SPS3 trial does not appear to be explained by CYP2C19 genotype.	clopidogrel	273-284	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
25946232-12	2015	Platelet reactivity is higher in patients with heterozygous and homozygous carriers of CYP2C19*2 versus common genotype and may predict an increased risk of clopidogrel response variability and/or experiencing adverse cardiac events.	clopidogrel	157-168	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	87-94
25800075-7	2015	CAM concentration as well as PRI by clopidogrel varied significantly (P &lt; 0.05) based on genotypic variation of CYP2C19*2 and CYP2C19*17 individually.	clopidogrel	36-47	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	129-136
26008670-7	2015	CD63 and CD62p positivity was increased in normal and in diabetic patients" platelets after activation with ADP before clopidogrel.	clopidogrel	119-130	CD63 molecule	Homo sapiens	0-4
25583161-2	2015	Both the loss of function CYP2C19*2 allele and the gain of function CYP2C19*17 allele along with a range of clinical characteristics have been associated with variation in the response to clopidogrel.	clopidogrel	188-199	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
25583161-2	2015	Both the loss of function CYP2C19*2 allele and the gain of function CYP2C19*17 allele along with a range of clinical characteristics have been associated with variation in the response to clopidogrel.	clopidogrel	188-199	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	68-75
26008670-7	2015	CD63 and CD62p positivity was increased in normal and in diabetic patients" platelets after activation with ADP before clopidogrel.	clopidogrel	119-130	selectin P	Homo sapiens	9-14
26008670-9	2015	CD63 and CD62p positivity in resting and ADP stimulated patients" platelets was also decreased after clopidogrel treatment.	clopidogrel	101-112	CD63 molecule	Homo sapiens	0-4
25891840-1	2015	OBJECTIVES: The aim of this study was to investigate the effect of CYP2C19 polymorphism and co-therapy with esomeprazole on the antiplatelet efficacy of clopidogrel.	clopidogrel	153-164	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	67-74
25891840-2	2015	BACKGROUND: The antiplatelet efficacy of clopidogrel depends on CYP2C19 polymorphism or the co-administration of some kind of proton pump inhibitor (PPI).	clopidogrel	41-52	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	64-71
25976494-2	2015	Oral antiplatelet agents for secondary prevention include the cyclo-oxygenase-1 inhibitor aspirin, and the ADP dependent P2Y12 inhibitors clopidogrel, prasugrel and ticagrelor.	clopidogrel	138-149	purinergic receptor P2Y12	Homo sapiens	121-126
26008670-9	2015	CD63 and CD62p positivity in resting and ADP stimulated patients" platelets was also decreased after clopidogrel treatment.	clopidogrel	101-112	selectin P	Homo sapiens	9-14
25594796-1	2015	BACKGROUND: High on-clopidogrel platelet reactivity reflects a poor response to clopidogrel and is associated with ischemic events, which has been attributed to several factors such as demographic, clinical characteristics and a polymorphism of CYP2C19.	clopidogrel	20-31	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	245-252
26767297-2	2015	METHODS: The CES1, cytochrome P450 3A4, CYP450 2C19, CYP450 1A2 and CYP450 2B6 which involved in Clopidogrel metabolism were selected at first, the chemical ligand database were created then, and finally the interaction effects between the ligand database and Clopidogrel metabolism target were explored.	clopidogrel	97-108	carboxylesterase 1	Homo sapiens	13-17
25594796-1	2015	BACKGROUND: High on-clopidogrel platelet reactivity reflects a poor response to clopidogrel and is associated with ischemic events, which has been attributed to several factors such as demographic, clinical characteristics and a polymorphism of CYP2C19.	clopidogrel	80-91	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	245-252
26767297-2	2015	METHODS: The CES1, cytochrome P450 3A4, CYP450 2C19, CYP450 1A2 and CYP450 2B6 which involved in Clopidogrel metabolism were selected at first, the chemical ligand database were created then, and finally the interaction effects between the ligand database and Clopidogrel metabolism target were explored.	clopidogrel	97-108	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	19-38
26767297-2	2015	METHODS: The CES1, cytochrome P450 3A4, CYP450 2C19, CYP450 1A2 and CYP450 2B6 which involved in Clopidogrel metabolism were selected at first, the chemical ligand database were created then, and finally the interaction effects between the ligand database and Clopidogrel metabolism target were explored.	clopidogrel	260-271	carboxylesterase 1	Homo sapiens	13-17
26767297-2	2015	METHODS: The CES1, cytochrome P450 3A4, CYP450 2C19, CYP450 1A2 and CYP450 2B6 which involved in Clopidogrel metabolism were selected at first, the chemical ligand database were created then, and finally the interaction effects between the ligand database and Clopidogrel metabolism target were explored.	clopidogrel	260-271	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	19-38
26767297-6	2015	CONCLUSION: It is suggested that Fufang Danshen Dripping Pill has inhibitory effects on Clopidogrel metabolism enzymes target such as CES1, Cytochrome P450 3A4, CYP450 2C19, CYP450 1A2 and CYP450 2B6.	clopidogrel	88-99	carboxylesterase 1	Homo sapiens	134-138
26767297-6	2015	CONCLUSION: It is suggested that Fufang Danshen Dripping Pill has inhibitory effects on Clopidogrel metabolism enzymes target such as CES1, Cytochrome P450 3A4, CYP450 2C19, CYP450 1A2 and CYP450 2B6.	clopidogrel	88-99	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	140-159
25908081-0	2015	Elevated serum fibrinogen: an independent link between diabetes mellitus, impaired on-clopidogrel platelet inhibition, and major adverse cardiac events after percutaneous coronary intervention.	clopidogrel	86-97	fibrinogen beta chain	Homo sapiens	15-25
25908082-0	2015	Reply: elevated serum fibrinogen: an independent link between diabetes mellitus, impaired on-clopidogrel platelet inhibition, and major adverse cardiac events after percutaneous coronary intervention.	clopidogrel	93-104	fibrinogen beta chain	Homo sapiens	22-32
25476742-4	2015	In the general population, genetic polymorphisms in the CYP2C19 gene interfering with hepatic conversion and the ABCB1 gene interfering with gut absorption of clopidogrel, account for the large interindividual response to clopidogrel and clopidogrel resistance.	clopidogrel	159-170	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	56-63
25476742-4	2015	In the general population, genetic polymorphisms in the CYP2C19 gene interfering with hepatic conversion and the ABCB1 gene interfering with gut absorption of clopidogrel, account for the large interindividual response to clopidogrel and clopidogrel resistance.	clopidogrel	159-170	ATP binding cassette subfamily B member 1	Homo sapiens	113-118
25476742-4	2015	In the general population, genetic polymorphisms in the CYP2C19 gene interfering with hepatic conversion and the ABCB1 gene interfering with gut absorption of clopidogrel, account for the large interindividual response to clopidogrel and clopidogrel resistance.	clopidogrel	222-233	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	56-63
25476742-4	2015	In the general population, genetic polymorphisms in the CYP2C19 gene interfering with hepatic conversion and the ABCB1 gene interfering with gut absorption of clopidogrel, account for the large interindividual response to clopidogrel and clopidogrel resistance.	clopidogrel	222-233	ATP binding cassette subfamily B member 1	Homo sapiens	113-118
25476742-4	2015	In the general population, genetic polymorphisms in the CYP2C19 gene interfering with hepatic conversion and the ABCB1 gene interfering with gut absorption of clopidogrel, account for the large interindividual response to clopidogrel and clopidogrel resistance.	clopidogrel	222-233	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	56-63
25476742-4	2015	In the general population, genetic polymorphisms in the CYP2C19 gene interfering with hepatic conversion and the ABCB1 gene interfering with gut absorption of clopidogrel, account for the large interindividual response to clopidogrel and clopidogrel resistance.	clopidogrel	222-233	ATP binding cassette subfamily B member 1	Homo sapiens	113-118
25937796-0	2014	Effects of CYP2C19 and P2Y12 Gene Polymorphisms on Clinical Results of Patients Using Clopidogrel after Acute Ischemic Cerebrovascular Disease.	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	11-18
25937796-0	2014	Effects of CYP2C19 and P2Y12 Gene Polymorphisms on Clinical Results of Patients Using Clopidogrel after Acute Ischemic Cerebrovascular Disease.	clopidogrel	86-97	purinergic receptor P2Y12	Homo sapiens	23-28
25937796-1	2014	The CY2C19 and P2Y12 gene polymorphisms are responsible for resistance to clopidogrel, known as drug unresponsiveness.	clopidogrel	74-85	purinergic receptor P2Y12	Homo sapiens	15-20
25860557-9	2015	CONCLUSION: The current study suggests that common SNPs may predict OPR against clopidogrel as assessed by VerifyNow P2Y12, but are less likely to respond against aspirin as assessed by VerifyNow Aspirin.	clopidogrel	80-91	purinergic receptor P2Y12	Homo sapiens	117-122
25609219-0	2015	Physiologically based pharmacokinetic modeling for sequential metabolism: effect of CYP2C19 genetic polymorphism on clopidogrel and clopidogrel active metabolite pharmacokinetics.	clopidogrel	116-127	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	84-91
25660101-2	2015	CYP2C19 loss-of-function (LOF) allele(s) affect the responsiveness of clopidogrel, but not the new antiplatelet agents (prasugrel and ticagrelor).	clopidogrel	70-81	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
25896573-26	2015	Well-audited data are needed from a long-term UK clinical registry on defined ACS patient groups treated with PCI who receive prasugrel, ticagrelor and clopidogrel.	clopidogrel	152-163	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	78-81
25430046-0	2015	Impact of common ABCB1 polymorphism on pharmacokinetics and pharmacodynamics of clopidogrel and its metabolites.	clopidogrel	80-91	ATP binding cassette subfamily B member 1	Homo sapiens	17-22
25877345-0	2015	CYP2C19 polymorphism and clinical outcomes among patients of different races treated with clopidogrel: A systematic review and meta-analysis.	clopidogrel	90-101	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
25877345-1	2015	Several studies have investigated the association between CYP2C19 polymorphism and clinical outcomes of patients treated with clopidogrel, but few have noticed the difference in association between Westerners and Asians.	clopidogrel	126-137	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	58-65
25877345-8	2015	Secondly, the impact of CYP2C19 polymorphism on clinical outcomes of patients treated with clopidogrel varied with races.	clopidogrel	91-102	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
25877345-9	2015	Among Asians, only 2 reduced-function CYP2C19 mutant allele carriers had the reduced effect of clopidogrel.	clopidogrel	95-106	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	38-45
25877345-14	2015	It is suggested that CYP2C19 polymorphism affects the efficacy of clopidogrel differently among Westerners and Asians.	clopidogrel	66-77	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
25728969-6	2015	For example, the AHA/ACC recommends the P2Y12 inhibitor ticagrelor over clopidogrel in all patients with NSTE-ACS and clopidogrel, prasugrel, or ticagrelor for patients in whom percutaneous coronary intervention is planned, whereas the ESC guidelines specifically recommend individual P2Y12 inhibitors for particular patient subgroups.	clopidogrel	118-129	purinergic receptor P2Y12	Homo sapiens	40-45
25542807-0	2015	Genetic polymorphisms of CYP2C19 2 and ABCB1 C3435T affect the pharmacokinetic and pharmacodynamic responses to clopidogrel in 401 patients with acute coronary syndrome.	clopidogrel	112-123	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
25542807-0	2015	Genetic polymorphisms of CYP2C19 2 and ABCB1 C3435T affect the pharmacokinetic and pharmacodynamic responses to clopidogrel in 401 patients with acute coronary syndrome.	clopidogrel	112-123	ATP binding cassette subfamily B member 1	Homo sapiens	39-44
25542807-3	2015	Studies have shown that the genetic variation in CYP2C19*2 is associated with an impaired response to clopidogrel.	clopidogrel	102-113	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	49-56
25542807-10	2015	Notably, the carriers of ABCB1 C3435T were associated with lower levels of plasma clopidogrel and its active (clopi-H4) and inactive (CLPM) metabolites (all P&lt;0.05 vs. non-carriers) which also correlated with subsequently decreased platelet inhibition (P&lt;0.05 vs. non-carriers).	clopidogrel	82-93	ATP binding cassette subfamily B member 1	Homo sapiens	25-30
25542807-12	2015	CONCLUSIONS: CYP2C19*2 is a determinant for the formation of the active metabolite of clopidogrel and its antiplatelet effects.	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
25542807-13	2015	Meanwhile, ABCB1 C3435T plays an important role in intestinal absorption of clopidogrel which further affects the exposure to the active metabolite of clopidogrel and platelet aggregation.	clopidogrel	76-87	ATP binding cassette subfamily B member 1	Homo sapiens	11-16
25542807-13	2015	Meanwhile, ABCB1 C3435T plays an important role in intestinal absorption of clopidogrel which further affects the exposure to the active metabolite of clopidogrel and platelet aggregation.	clopidogrel	151-162	ATP binding cassette subfamily B member 1	Homo sapiens	11-16
25627210-10	2015	In separate studies, mice were treated with the platelet P2Y12 receptor inhibitor clopidogrel or placebo.	clopidogrel	82-93	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	57-62
25679803-8	2015	Similar differences were observed between the prasugrel and clopidogrel groups for patients with normal or reduced-function CYP2C19 alleles.	clopidogrel	60-71	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	124-131
25647335-1	2015	: The effects of CES1A2 A(-816)C and CYP2C19 loss-of-function polymorphisms on clopidogrel response variability among Chinese patients with coronary heart disease.	clopidogrel	79-90	carboxylesterase 1 pseudogene 1	Homo sapiens	17-23
25592204-3	2015	Dual antiplatelet therapy comprising aspirin plus a P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor) is recommended for patients with NSTE-ACS, and those with STEMI both during and after reperfusion.	clopidogrel	69-80	purinergic receptor P2Y12	Homo sapiens	52-57
25647335-1	2015	: The effects of CES1A2 A(-816)C and CYP2C19 loss-of-function polymorphisms on clopidogrel response variability among Chinese patients with coronary heart disease.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-44
25511576-0	2015	Effect of high-dose clopidogrel according to CYP2C19*2 genotype in patients undergoing percutaneous coronary intervention- a systematic review and meta-analysis.	clopidogrel	20-31	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	45-52
25511576-1	2015	INTRODUCTION: High-dose clopidogrel has been recommended to overcome clopidogrel non-responsiveness in patients undergoing percutaneous coronary intervention (PCI), especially those with CYP2C19 loss-of-function genotypes.	clopidogrel	24-35	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	187-194
25511576-3	2015	This meta-analysis was conducted to evaluate the antiplatelet effects of high-dose clopidogrel according to CYP2C19*2 alleles in patients undergoing PCI.	clopidogrel	83-94	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	108-115
25511576-8	2015	The incidence rate of HTPR was higher in CYP2C19*2 carriers after high-dose clopidogrel treatment (RR: 1.21, 95% CI:1.05-1.39, p = 0.008 for cutoff PRI &gt; 50% by VASP assay; RR: 1.69, 95% CI: 1.44-1.98, p &lt; 1 x 10(-4) for cutoff PRU &gt; 230 by VerifyNow P2Y12 assay).	clopidogrel	76-87	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	41-48
25511576-8	2015	The incidence rate of HTPR was higher in CYP2C19*2 carriers after high-dose clopidogrel treatment (RR: 1.21, 95% CI:1.05-1.39, p = 0.008 for cutoff PRI &gt; 50% by VASP assay; RR: 1.69, 95% CI: 1.44-1.98, p &lt; 1 x 10(-4) for cutoff PRU &gt; 230 by VerifyNow P2Y12 assay).	clopidogrel	76-87	vasodilator stimulated phosphoprotein	Homo sapiens	164-168
25511576-8	2015	The incidence rate of HTPR was higher in CYP2C19*2 carriers after high-dose clopidogrel treatment (RR: 1.21, 95% CI:1.05-1.39, p = 0.008 for cutoff PRI &gt; 50% by VASP assay; RR: 1.69, 95% CI: 1.44-1.98, p &lt; 1 x 10(-4) for cutoff PRU &gt; 230 by VerifyNow P2Y12 assay).	clopidogrel	76-87	purinergic receptor P2Y12	Homo sapiens	260-265
25511576-9	2015	As for clinical outcomes, CYP2C19*2 was associated with higher risk for MACE (RR: 1.68, 95% CI: 1.19- 2.37, p = 0.003), stent thrombosis (RR: 1.75, 95% CI: 1.31-2.34, p = 0.0001), as well as composite cardiovascular events (RR: 1.82, 95% CI: 1.42- 2.34, p &lt; 10(-5)) after treated by high-dose clopidogrel.	clopidogrel	296-307	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
25834652-3	2015	The aim of this study was to investigate the effectiveness of Ankaferd blood clotter (ABC) as a new topical herbal blood clotter to decrease mediastinal bleeding in emergent beating heart CABG patients who medicated with clopidogrel and acetyl salisilic acite (ASA) prior to CABG surgery.	clopidogrel	221-232	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	62-84
25834652-3	2015	The aim of this study was to investigate the effectiveness of Ankaferd blood clotter (ABC) as a new topical herbal blood clotter to decrease mediastinal bleeding in emergent beating heart CABG patients who medicated with clopidogrel and acetyl salisilic acite (ASA) prior to CABG surgery.	clopidogrel	221-232	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	86-89
25834652-18	2015	To provide cardiac tamponade because of excessive mediastinal bleeding and requirement of blood transfusion after emergent CABG patients who previously administered clopidogrel and ASA, we propose local use of ABC solution as a potent coagulant agent.	clopidogrel	165-176	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	210-213
25730082-7	2015	Thus, coexisting polymorphisms of CYP3A5*3 and 2C19*2, but not P2Y12*1, play an important role in the variability of clopidogrel"s curative effect.	clopidogrel	117-128	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	34-40
25730082-7	2015	Thus, coexisting polymorphisms of CYP3A5*3 and 2C19*2, but not P2Y12*1, play an important role in the variability of clopidogrel"s curative effect.	clopidogrel	117-128	purinergic receptor P2Y12	Homo sapiens	63-68
25489921-0	2015	Influence of CYP2C19 polymorphisms on platelet reactivity and clinical outcomes in ischemic stroke patients treated with clopidogrel.	clopidogrel	121-132	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
25758663-6	2015	In the presence of clopidogrel, the binding rates of Rg1 decreased to (22.13-+2.72)%, (21.42-+3.22)%, and (25.45-+3.52)%, and those of Rb1 to (40.13-+3.24)%, (41.25-+4.15)%, and (43.11-+3.31)%, receptively.	clopidogrel	19-30	protein phosphatase 1 regulatory subunit 3A	Homo sapiens	53-56
25758663-6	2015	In the presence of clopidogrel, the binding rates of Rg1 decreased to (22.13-+2.72)%, (21.42-+3.22)%, and (25.45-+3.52)%, and those of Rb1 to (40.13-+3.24)%, (41.25-+4.15)%, and (43.11-+3.31)%, receptively.	clopidogrel	19-30	RB transcriptional corepressor 1	Homo sapiens	135-138
25489921-15	2015	In conclusion, carriage of the CYP2C19 LOF allele has significant influence on clopidogrel response and prognosis in patients with ischemic stroke.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	31-38
25274959-1	2015	BACKGROUND: A number of studies have indicated that the conversion of clopidogrel to its active metabolite is reduced in patients who carry the CYP2C19 *2, *3, *4 or *5 loss-of-function allele, resulting in decreased response of platelet to clopidogrel treatment and worse cardiovascular outcome.	clopidogrel	70-81	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	144-151
25274959-1	2015	BACKGROUND: A number of studies have indicated that the conversion of clopidogrel to its active metabolite is reduced in patients who carry the CYP2C19 *2, *3, *4 or *5 loss-of-function allele, resulting in decreased response of platelet to clopidogrel treatment and worse cardiovascular outcome.	clopidogrel	241-252	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	144-151
25655085-3	2015	HYPOTHESIS: We hypothesized that perioperative measurement of platelet function with a point-of-care P2Y12 inhibitor assay could predict bleeding during CABG in patients exposed to clopidogrel.	clopidogrel	181-192	purinergic receptor P2Y12	Homo sapiens	101-106
25463363-0	2015	Joint effects of CYP2C19*2 and smoking status on clopidogrel responsiveness in patients with acute coronary syndrome.	clopidogrel	49-60	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-24
25435190-6	2015	The effects of CGE on the phosphatidylinositol 3-kinase (PI3K)/Akt pathway and mitogen-activated protein kinases (MAPKs) were assessed by immunoblotting.	clopidogrel	15-18	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	26-55
25435190-6	2015	The effects of CGE on the phosphatidylinositol 3-kinase (PI3K)/Akt pathway and mitogen-activated protein kinases (MAPKs) were assessed by immunoblotting.	clopidogrel	15-18	AKT serine/threonine kinase 1	Homo sapiens	63-66
25435190-11	2015	The induction of apoptosis was enhanced by the combined treatment of CGE with a PI3K inhibitor or an extracellular signal-regulated kinase (ERK) inhibitor, whereas the CGE-induced apoptosis was inhibited in the presence of caspase inhibitors, such as z-VAD-fmk and z-IETD-fmk.	clopidogrel	168-171	mitogen-activated protein kinase 1	Homo sapiens	101-138
25435190-11	2015	The induction of apoptosis was enhanced by the combined treatment of CGE with a PI3K inhibitor or an extracellular signal-regulated kinase (ERK) inhibitor, whereas the CGE-induced apoptosis was inhibited in the presence of caspase inhibitors, such as z-VAD-fmk and z-IETD-fmk.	clopidogrel	168-171	mitogen-activated protein kinase 1	Homo sapiens	140-143
25529343-0	2015	CYP2C19 genotype and early ischemic lesion recurrence in stroke patients treated with clopidogrel.	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
25529343-2	2015	We hypothesized that cytochrome P450 2C19 (CYP2C19) genotype influences the incidence of early recurrence on DWI in acute stroke patients treated with clopidogrel.	clopidogrel	151-162	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-41
25529343-2	2015	We hypothesized that cytochrome P450 2C19 (CYP2C19) genotype influences the incidence of early recurrence on DWI in acute stroke patients treated with clopidogrel.	clopidogrel	151-162	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	43-50
25529343-11	2015	CONCLUSIONS: CYP2C19 genotypes are significantly associated with early lesion recurrence in Korean acute stroke patients treated with clopidogrel.	clopidogrel	134-145	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
25001880-0	2015	Clinical outcomes associated with proton pump inhibitor use among clopidogrel-treated patients within CYP2C19 genotype groups following acute myocardial infarction.	clopidogrel	66-77	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	102-109
25001880-7	2015	These results indicate that the risks associated with PPI use among clopidogrel-treated Caucasian post-MI patients are impacted by CYP2C19 genotype, and suggest knowledge of genotype may be useful for personalizing PPI use among patients following AMI to reduce rehospitalization.	clopidogrel	68-79	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	131-138
25689244-16	2015	CONCLUSION: Fluvoxamine attenuated the laboratory response to clopidogrel, possibly through inhibition of CYP2C19, whereas citalopram did not affect this response.	clopidogrel	62-73	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	106-113
25997249-0	2015	ABCB1 hypomethylation is associated with decreased antiplatelet effects of clopidogrel in Chinese ischemic stroke patients.	clopidogrel	75-86	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
25997249-1	2015	Current predictive models including the CYP2C19 polymorphism and clinical factors still explain only about 12% of variability of clopidogrel responsiveness.	clopidogrel	129-140	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-47
25997249-3	2015	P-glycoprotein (P-gp) encoded by ABCB1, a transmembrane calcium-dependent efflux pump for clopidogrel, implicated a role in clopidogrel resistance.	clopidogrel	90-101	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
25997249-3	2015	P-glycoprotein (P-gp) encoded by ABCB1, a transmembrane calcium-dependent efflux pump for clopidogrel, implicated a role in clopidogrel resistance.	clopidogrel	90-101	ATP binding cassette subfamily B member 1	Homo sapiens	16-20
25997249-3	2015	P-glycoprotein (P-gp) encoded by ABCB1, a transmembrane calcium-dependent efflux pump for clopidogrel, implicated a role in clopidogrel resistance.	clopidogrel	90-101	ATP binding cassette subfamily B member 1	Homo sapiens	33-38
25997249-3	2015	P-glycoprotein (P-gp) encoded by ABCB1, a transmembrane calcium-dependent efflux pump for clopidogrel, implicated a role in clopidogrel resistance.	clopidogrel	124-135	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
25997249-3	2015	P-glycoprotein (P-gp) encoded by ABCB1, a transmembrane calcium-dependent efflux pump for clopidogrel, implicated a role in clopidogrel resistance.	clopidogrel	124-135	ATP binding cassette subfamily B member 1	Homo sapiens	16-20
25997249-3	2015	P-glycoprotein (P-gp) encoded by ABCB1, a transmembrane calcium-dependent efflux pump for clopidogrel, implicated a role in clopidogrel resistance.	clopidogrel	124-135	ATP binding cassette subfamily B member 1	Homo sapiens	33-38
25997249-4	2015	In this present study, we investigated the methylation status of ABCB1 gene promoter in relation to ABCB1 mRNA expressions and the antiplatelet effects of clopidogrel.	clopidogrel	155-166	ATP binding cassette subfamily B member 1	Homo sapiens	65-70
25997249-13	2015	In conclusions, hypomethylation of ABCB1 promoter is associated with a decreased response to clopidogrel in ischemic stroke patients via increased ABCB1 mRNA expression.	clopidogrel	93-104	ATP binding cassette subfamily B member 1	Homo sapiens	35-40
25997249-13	2015	In conclusions, hypomethylation of ABCB1 promoter is associated with a decreased response to clopidogrel in ischemic stroke patients via increased ABCB1 mRNA expression.	clopidogrel	93-104	ATP binding cassette subfamily B member 1	Homo sapiens	147-152
25460367-1	2015	BACKGROUND: Clopidogrel resistance is more common in patients with loss-of-function CYP2C19 genotypes.	clopidogrel	12-23	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	84-91
25489921-1	2015	CYP2C19 genetic polymorphisms influence clopidogrel response and clinical outcomes of cardiovascular disease.	clopidogrel	40-51	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
25489921-3	2015	We aimed to investigate the influence of CYP2C19 polymorphisms on platelet reactivity and clinical outcomes in ischemic stroke patients treated with clopidogrel.	clopidogrel	149-160	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	41-48
25489921-8	2015	After clopidogrel therapy for 7 days, the levels of ADP-PAg, PAC-1, CD62P and CD63 were higher in carriers than noncarriers.	clopidogrel	6-17	dual specificity phosphatase 2	Homo sapiens	61-66
25489921-8	2015	After clopidogrel therapy for 7 days, the levels of ADP-PAg, PAC-1, CD62P and CD63 were higher in carriers than noncarriers.	clopidogrel	6-17	selectin P	Homo sapiens	68-73
25489921-8	2015	After clopidogrel therapy for 7 days, the levels of ADP-PAg, PAC-1, CD62P and CD63 were higher in carriers than noncarriers.	clopidogrel	6-17	CD63 molecule	Homo sapiens	78-82
25489921-10	2015	CYP2C19 polymorphisms alone could explain 12.9%, 4.3%, 8.9% and 5.5% of the inter-individual variability of ADP-PAg, PAC-1, CD62P and CD63 after clopidogrel treatment, respectively.	clopidogrel	145-156	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
25311974-0	2015	Non-antiplatelet effect of clopidogrel: improving endothelial function in Chinese healthy subjects with different CYP2C19 genotype.	clopidogrel	27-38	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	114-121
25747989-0	2015	Carboxylesterase 1-mediated drug-drug interactions between clopidogrel and simvastatin.	clopidogrel	59-70	carboxylesterase 1	Homo sapiens	0-18
25747989-3	2015	Both CYP enzymes and carboxylesterase 1 (CES1) are involved in the metabolism of clopidogrel, while CES1 is believed to be the enzyme responsible for the activation of simvastatin.	clopidogrel	81-92	carboxylesterase 1	Homo sapiens	21-39
25747989-3	2015	Both CYP enzymes and carboxylesterase 1 (CES1) are involved in the metabolism of clopidogrel, while CES1 is believed to be the enzyme responsible for the activation of simvastatin.	clopidogrel	81-92	carboxylesterase 1	Homo sapiens	41-45
25747989-4	2015	Some in vitro studies have suggested that simvastatin could attenuate clopidogrel activation via inhibiting CYP3A activity.	clopidogrel	70-81	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	108-113
25747989-6	2015	The present study addresses these inconsistencies by exploring the potential role of CES1 in the metabolism of clopidogrel and simvastatin.	clopidogrel	111-122	carboxylesterase 1	Homo sapiens	85-89
25747989-11	2015	In summary, the inhibitory effect of simvastatin on the hydrolysis of clopidogrel and its principal metabolites may have offset the influence of simvastatin-mediated inhibition of CYP3A, and permitted the unaltered formation of the clopidogrel active metabolite.	clopidogrel	70-81	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	180-185
25744629-5	2015	A poor metabolizer (PM) of clopidogrel was defined as a homozygote of CYP2C19 loss-of-function alleles.	clopidogrel	27-38	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	70-77
25744739-3	2015	Clopidogrel is a second-generation thienopyridine that eliminates the serious side effects of ticlopidine, and new P2Y12 receptor blockers have emerged to overcome the limitations of clopidogrel.	clopidogrel	183-194	purinergic receptor P2Y12	Homo sapiens	115-120
25744739-6	2015	Treatment with aspirin and new P2Y12 receptor blockers has further reduced the rate of cardiovascular death, myocardial infarction or stroke after ACS compared with aspirin and clopidogrel.	clopidogrel	177-188	purinergic receptor P2Y12	Homo sapiens	31-36
25311974-2	2015	However, it remains unclear whether such an effect of clopidogrel is associated with CYP2C19 polymorphisms that determine the antiplatelet effect of clopidogrel.	clopidogrel	54-65	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	85-92
25311974-2	2015	However, it remains unclear whether such an effect of clopidogrel is associated with CYP2C19 polymorphisms that determine the antiplatelet effect of clopidogrel.	clopidogrel	149-160	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	85-92
25311974-7	2015	Flow-mediated dilation was significantly higher at 4 and 24 h after a loading-dose administration of clopidogrel in both the CYP2C19 EM and PM groups, but showed no significant difference between the two groups.	clopidogrel	101-112	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	125-132
25311974-8	2015	Adenosine diphosphate-induced platelet aggregation was significantly inhibited at 4 and 24 h after administration of clopidogrel in the CYP2C19 EM group.	clopidogrel	117-128	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	136-143
26173871-9	2015	Although limited prospective trial data are available to support the utility of routine CYP2C19 testing, the increased risks for reduced clopidogrel efficacy among ACS/PCI patients that carry CYP2C19 loss-of-function alleles should be considered when genotype results are available.	clopidogrel	137-148	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	192-199
25465810-1	2015	BACKGROUND: The contribution of clopidogrel response due to cytochrome P450 (CYP) 2C19 loss-of-function polymorphism after drug-eluting stent (DES) implantation is unclear.	clopidogrel	32-43	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	60-86
26311225-0	2015	Effects of CYP2C19 Polymorphism on Endothelial Function, Arterial Stiffness and Inflammation in Coronary Artery Disease Patients Under Clopidogrel Treatment.	clopidogrel	135-146	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	11-18
26369686-6	2015	The interaction between PPIs and consequent impaired effectiveness of clopidogrel has caused concern regarding the effect of genetic polymorphisms of the CYP2C19 which mediates conversion of clopidogrel to its active metabolite.	clopidogrel	191-202	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	154-161
26092217-0	2015	Review of clopidogrel dose escalation in the current era of potent P2Y12 inhibitors.	clopidogrel	10-21	purinergic receptor P2Y12	Homo sapiens	67-72
26224244-1	2015	INTRODUCTION: Clopidogrel, prasugrel, and ticagrelor are the currently available oral P2Y12 inhibitors for the treatment of ST-segment elevation myocardial infarction (STEMI), in association with aspirin.	clopidogrel	14-25	purinergic receptor P2Y12	Homo sapiens	86-91
24946154-0	2015	A systematic review and critical assessment of 11 discordant meta-analyses on reduced-function CYP2C19 genotype and risk of adverse clinical outcomes in clopidogrel users.	clopidogrel	153-164	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	95-102
25452814-1	2015	The aim of the present study was to examine clopidogrel resistance (CR) in patients with ischemic cerebral infarction and its potential association with a single nucleotide polymorphism (SNP; rs1045642) in the ABCB1 gene.	clopidogrel	44-55	ATP binding cassette subfamily B member 1	Homo sapiens	210-215
25628978-0	2015	Routine screening for CYP2C19 polymorphisms for patients being treated with clopidogrel is not recommended.	clopidogrel	76-87	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	22-29
25628978-3	2015	Cytochrome P-450 (CYP) 2C19 is an enzyme involved in the bioactivation of clopidogrel from a pro-drug to an active inhibitor of platelet action.	clopidogrel	74-85	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-27
24946154-1	2015	We systematically investigated how 11 overlapping meta-analyses on the association between CYP2C19 loss-of-function alleles and clinical efficacy of clopidogrel could yield contradictory outcomes.	clopidogrel	149-160	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	91-98
24946154-7	2015	In summary, meta-analyses on the association between CYP2C19 loss-of-function alleles and clinical efficacy of clopidogrel differed widely with regard to assessment and interpretation of heterogeneity and publication bias.	clopidogrel	111-122	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-60
25828136-0	2015	CYP2C19*2 genotype influence in acute coronary syndrome patients undergoing serial clopidogrel dose tailoring based on platelet function testing: Analysis from randomized controlled trial NCT02096419.	clopidogrel	83-94	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
25828314-4	2015	CYP2C19 is responsible for most of the clopidogrel bio-transformation and loss of function as well as, gain of function polymorphisms of this enzyme has been recognized.	clopidogrel	39-50	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
25897911-0	2015	CYP2C19 LOF alleles confer no risk for HTPR but higher risk for recurrent ischemic events in clopidogrel treated elderly ACS patients.	clopidogrel	93-104	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
25836953-0	2015	Efficacy of fibrinogen concentrate compared with cryoprecipitate for reversal of the antiplatelet effect of clopidogrel in an in vitro model, as assessed by multiple electrode platelet aggregometry, thromboelastometry, and modified thromboelastography.	clopidogrel	108-119	fibrinogen beta chain	Homo sapiens	12-22
26639695-3	2015	The non-responsiveness to clopidogrel in cardiac patients of different populations is due to genetic variations in the cytochrome P450 (CYP) gene [2].	clopidogrel	26-37	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	119-134
26639695-3	2015	The non-responsiveness to clopidogrel in cardiac patients of different populations is due to genetic variations in the cytochrome P450 (CYP) gene [2].	clopidogrel	26-37	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	136-139
26639695-4	2015	Carriers of at least one "poor metabolizer allele" of CYP2C19 (either *2 or *3) have lower levels of the active metabolite of clopidogrel and have reduced platelet inhibition [3].	clopidogrel	126-137	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	54-61
26639695-5	2015	Furthermore, the significant inter-ethnic variability in the allelic frequencies of CYP2C19*2 has been associated with differential clopidogrel resistance [4].	clopidogrel	132-143	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	84-91
26639695-6	2015	Such mutations in this variant allele are responsible for the inability of the CYP enzyme to convert clopidogrel into its active metabolite, which may result in the increased risk of death, heart attack or stroke among patients who have undergone percutaneous coronary intervention (PCI) [5].	clopidogrel	101-112	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	79-82
26639695-14	2015	Allele CYP2C19*3 is often found among alleles with reduced function and also associated with resistance to clopidogrel.	clopidogrel	107-118	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	7-14
25836953-3	2015	DESIGN: The study hypothesis was that fibrinogen concentrate would normalize in vitro hemostatic parameters after clopidogrel loading.	clopidogrel	114-125	fibrinogen beta chain	Homo sapiens	38-48
25393324-1	2015	Clopidogrel hydrogensulfate (HSCL) is an antiplatelet agent, one of top-selling drugs in the world.	clopidogrel	0-27	selenocysteine lyase	Homo sapiens	29-33
25297118-4	2015	PON1 (paraoxonase 1) plays an important role in the bioactivation of clopidogrel.	clopidogrel	69-80	paraoxonase 1	Homo sapiens	0-4
25297118-4	2015	PON1 (paraoxonase 1) plays an important role in the bioactivation of clopidogrel.	clopidogrel	69-80	paraoxonase 1	Homo sapiens	6-19
25674544-2	2015	Noteworthy, PCI patients require a dual antiplatelet therapy (DAPT), with aspirine and a thienopiridine (clopidogrel, prasugrel, ticagrelor), because of the high risk of stent thrombosis (ST), myocardial infarction (MI) and death, especially within the first month.	clopidogrel	105-116	serpin family A member 5	Homo sapiens	12-15
25273829-0	2015	Men with lower HDL cholesterol levels have significant increment of soluble CD40 ligand and high-sensitivity CRP levels following the cessation of long-term clopidogrel therapy.	clopidogrel	157-168	CD40 ligand	Homo sapiens	76-87
25663208-1	2015	Clopidogrel is an irreversible antiplatelet agent belonging to the thienopyridine group that acts to antagonize the adenosine diphosphate P2Y12 receptor on platelets.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	138-143
24617511-10	2015	Compared with non-carriers, carriers of reduced function CYP2C19 alleles tended to have higher platelet reactivity after clopidogrel treatment.	clopidogrel	121-132	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	57-64
24617511-13	2015	In conclusion, the PFA P2Y test showed a statistically significant association with CYP2C19 metabolizer phenotypes based on CYP2C19 genotyping and effectively determined the risk groups resistant to clopidogrel therapy, including PM.	clopidogrel	199-210	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	84-91
24617511-13	2015	In conclusion, the PFA P2Y test showed a statistically significant association with CYP2C19 metabolizer phenotypes based on CYP2C19 genotyping and effectively determined the risk groups resistant to clopidogrel therapy, including PM.	clopidogrel	199-210	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	124-131
24833046-0	2015	Platelet factor XIIIa release during platelet aggregation and plasma clot strength measured by thrombelastography in patients with coronary artery disease treated with clopidogrel.	clopidogrel	168-179	coagulation factor XIII A chain	Homo sapiens	9-21
25025694-12	2015	Furthermore, patients with LPR to clopidogrel had significantly fewer PMVs exposing CD62P than patients with HPR or those with NPR to clopidogrel.	clopidogrel	34-45	selectin P	Homo sapiens	84-89
25025694-12	2015	Furthermore, patients with LPR to clopidogrel had significantly fewer PMVs exposing CD62P than patients with HPR or those with NPR to clopidogrel.	clopidogrel	134-145	neuronal pentraxin receptor	Homo sapiens	127-130
25207801-1	2015	Polymorphisms of CYP2C19 have been associated with variant risk of subsequent cardiovascular events in survivors of myocardial infarction (MI) receiving clopidogrel.	clopidogrel	153-164	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-24
25207801-14	2015	In Chinese stroke survivors treated with clopidogrel, carriers of CYP2C19 LOF allele may have increased risk of recurrence.	clopidogrel	41-52	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	66-73
25350775-2	2015	However, higher on-treatment platelet reactivity was associated with lower plasma miR-223 in patients with coronary artery disease (CAD) on dual antiplatelet therapy (DAPT) including clopidogrel and aspirin.	clopidogrel	183-194	microRNA 223	Homo sapiens	82-89
25666703-8	2015	Dual antiplatelet therapy with ASA and clopidogrel increases the risk of gastrointestinal bleeding in patients with acute coronary syndrome in whom concomitant treatment with a proton-pump inhibitor (PPI) was less effective owing to the interaction of clopidogrel and PPI with the same hepatic cytochrome P-450.	clopidogrel	39-50	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	294-310
26677375-2	2015	Clopidogrel used to be the most broadly prescribed P2Y12 receptor inhibitor with undisputable benefits especially in combination with aspirin, but a considerable number of clopidogrel-treated patients experience adverse thrombotic events in whom insufficient P2Y12-inhibition and a consequential high on-treatment platelet reactivity is a common finding.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	51-56
26677375-2	2015	Clopidogrel used to be the most broadly prescribed P2Y12 receptor inhibitor with undisputable benefits especially in combination with aspirin, but a considerable number of clopidogrel-treated patients experience adverse thrombotic events in whom insufficient P2Y12-inhibition and a consequential high on-treatment platelet reactivity is a common finding.	clopidogrel	172-183	purinergic receptor P2Y12	Homo sapiens	259-264
26027242-5	2015	The impact of TBS1 gene polymorphism on the risk of clopidogrel resistance and cardiovascular events was analyzed during 18 months of follow-up.	clopidogrel	52-63	thromboxane A synthase 1	Homo sapiens	14-18
26027242-6	2015	RESULTS: The carriage of TBS1 gene polymorphism AA was shown to affect the risk of clopidogrel resistance.	clopidogrel	83-94	thromboxane A synthase 1	Homo sapiens	25-29
24971633-0	2014	Glucuronidation converts clopidogrel to a strong time-dependent inhibitor of CYP2C8: a phase II metabolite as a perpetrator of drug-drug interactions.	clopidogrel	25-36	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	77-83
25696877-1	2014	Clopidogrel, a platelet P2Y12 inhibitor, is one of the most widely prescribed drugs in cardiovascular medicine because it reduces ischemic and thrombotic complications.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	24-29
25696877-4	2014	Specifically, compared with noncarriers, carriers of at least one copy of a loss-of-function CYP2C19 allele have ~30% lower levels of active clopidogrel metabolite and ~25% relatively less platelet inhibition with clopidogrel.	clopidogrel	141-152	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	93-100
25222620-1	2014	Clopidogrel is an oral antiplatelet prodrug, the majority of which is hydrolyzed to an inactive metabolite by hepatic carboxylesterase 1 (CES1).	clopidogrel	0-11	carboxylesterase 1	Homo sapiens	118-136
25222620-1	2014	Clopidogrel is an oral antiplatelet prodrug, the majority of which is hydrolyzed to an inactive metabolite by hepatic carboxylesterase 1 (CES1).	clopidogrel	0-11	carboxylesterase 1	Homo sapiens	138-142
24372313-10	2014	Systemic administration of aspirin and clopidogrel induced a significant decrease ( p &lt; 0.05) in the expression of CXCL4.	clopidogrel	39-50	platelet factor 4	Rattus norvegicus	118-123
25457586-0	2014	VASP phosphorylation and genetic polymorphism for clopidogrel resistance in Chinese patients with non-cardioembolic ischemic stroke.	clopidogrel	50-61	vasodilator stimulated phosphoprotein	Homo sapiens	0-4
25457586-14	2014	CONCLUSION: In clinical practice,LCR and CYP2C19 gene polymorphism should be assessed in NCIS patients receiving clopidogrel treatment.	clopidogrel	113-124	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	41-48
25115434-0	2014	CYP2C19*17 increases clopidogrel-mediated platelet inhibition but does not alter the pharmacokinetics of the active metabolite of clopidogrel.	clopidogrel	21-32	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
25115434-1	2014	The aim of the present study was to determine the impact of CYP2C19*17 on the pharmacokinetics and pharmacodynamics of the active metabolite of clopidogrel and the pharmacokinetics of proguanil.	clopidogrel	144-155	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	60-67
25037531-2	2014	Oral antiplatelet agents for secondary prevention include the cyclo-oxygenase-1 inhibitor aspirin, and the ADP dependent P2Y12 inhibitors clopidogrel, prasugrel and ticagrelor.	clopidogrel	138-149	purinergic receptor P2Y12	Homo sapiens	121-126
25217066-0	2014	Relationship between ABCB1 polymorphisms, thromboelastography and risk of bleeding events in clopidogrel-treated patients with ST-elevation myocardial infarction.	clopidogrel	93-104	ATP binding cassette subfamily B member 1	Homo sapiens	21-26
25217066-1	2014	INTRODUCTION: This study sought to investigate the relationship of polymorphisms in ABCB1 and the predictive value of thromboelastography (TEG) on bleeding risk in clopidogrel-treated patients with ST-elevation myocardial infarction (STEMI).	clopidogrel	164-175	ATP binding cassette subfamily B member 1	Homo sapiens	84-89
25217066-10	2014	CONCLUSIONS: In STEMI patients treated with clopidogrel after PCI, the ABCB1 tag SNP rs1045642 is associated with higher risk of bleedings while rs7779562 is associated with lower bleeding risk, and ADP inhibition in TEG has a predictive value of bleedings.	clopidogrel	44-55	ATP binding cassette subfamily B member 1	Homo sapiens	71-76
25354550-4	2014	A poor metabolizer (PM) of clopidogrel was defined as a homozygote of CYP2C19 loss-of-function alleles.	clopidogrel	27-38	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	70-77
25696877-4	2014	Specifically, compared with noncarriers, carriers of at least one copy of a loss-of-function CYP2C19 allele have ~30% lower levels of active clopidogrel metabolite and ~25% relatively less platelet inhibition with clopidogrel.	clopidogrel	214-225	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	93-100
25696877-5	2014	Moreover, in patients treated with clopidogrel predominantly for percutaneous coronary intervention, carriers of 1 or 2 CYP2C19 loss-of-function alleles are at increased risk for major adverse cardiovascular outcomes, with an ~1.5-fold increase in the risk of cardiovascular death, myocardial infarction, or stroke as well as an ~3-fold increase in risk for stent thrombosis.	clopidogrel	35-46	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	120-127
25696877-6	2014	Tripling the dose of clopidogrel in carriers of a CYP2C19 loss-of-function allele can achieve on-treatment platelet reactivity comparable to that seen with the standard 75 mg dose in wild-type individuals, but the impact on clinical outcomes remains unknown.	clopidogrel	21-32	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	50-57
25258374-0	2014	CYP2C19 genotype has a greater effect on adverse cardiovascular outcomes following percutaneous coronary intervention and in Asian populations treated with clopidogrel: a meta-analysis.	clopidogrel	156-167	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
25258374-2	2014	Clopidogrel indication and ethnic population have been proposed to influence the effect of CYP2C19 genotype.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	91-98
25258374-4	2014	Meta-analysis of the CYP2C19 genotype effect was stratified by the predominant clopidogrel indication (percutaneous coronary intervention [PCI] versus non-PCI) and ethnic population (white versus Asian) of each primary study.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
25258374-9	2014	CONCLUSIONS: The reported association between CYP2C19 LoF allele carriage and major cardiovascular outcomes differs based on the ethnic population of the study and, to a lesser extent, the clopidogrel indication.	clopidogrel	189-200	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	46-53
25297833-3	2014	High on-treatment platelet reactivity to ADP (HPR) during clopidogrel therapy is an independent risk factor for ischemic event occurrences in post-percutaneous coronary intervention (post-PCI) patients.	clopidogrel	58-69	haptoglobin-related protein	Homo sapiens	46-49
25592800-2	2014	These recommendations are based primarily on large, phase III, randomized, controlled trials of the P2Y12 inhibitors clopidogrel, prasugrel, and ticagrelor.	clopidogrel	117-128	purinergic receptor P2Y12	Homo sapiens	100-105
24861855-4	2014	We identified an excess of ADRs related to clopidogrel in Singaporean Chinese, consistent with a higher frequency of a known risk variant in CYP2C19 in that population.	clopidogrel	43-54	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	141-148
25409778-2	2014	Here we show that the ionotropic serotonin receptor 3A (5-HT(3A)R) is specifically expressed in CGE-derived migrating interneurons and upregulated while they invade the developing cortex.	clopidogrel	96-99	5-hydroxytryptamine receptor 3A	Homo sapiens	33-54
25409778-2	2014	Here we show that the ionotropic serotonin receptor 3A (5-HT(3A)R) is specifically expressed in CGE-derived migrating interneurons and upregulated while they invade the developing cortex.	clopidogrel	96-99	5-hydroxytryptamine receptor 3A	Homo sapiens	56-63
24803100-1	2014	AIMS: Variability in responsiveness to clopidogrel is a clinical problem in secondary prevention after cerebral ischaemia which has been suggested to be linked to competitive metabolization of clopidogrel and cytochrome P450 (CYP) 3A4-oxidated statins such as simvastatin.	clopidogrel	39-50	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	209-224
24803100-1	2014	AIMS: Variability in responsiveness to clopidogrel is a clinical problem in secondary prevention after cerebral ischaemia which has been suggested to be linked to competitive metabolization of clopidogrel and cytochrome P450 (CYP) 3A4-oxidated statins such as simvastatin.	clopidogrel	39-50	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	226-229
25218311-15	2014	IMPLICATION: In patients with ACS, loading of generic clopidogrel bisulfate was associated with an antiplatelet effect comparable to that of branded clopidogrel bisulfate.	clopidogrel	54-75	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	30-33
25359405-4	2014	The third generation P2Y12 receptor antagonists prasugrel and ticagrelor provide stronger platelet inhibition than clopidogrel and improve the clinical outcome in patients with ACS; however, it is still under discussion which P2Y12 antagonist fits best to which subgroup of ACS patients.	clopidogrel	115-126	purinergic receptor P2Y12	Homo sapiens	21-26
25634391-1	2014	BACKGROUND: Clopidogrel has been the only available antiplatelet drug used along with aspirin in patients of ACS.	clopidogrel	12-23	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	109-112
24971633-5	2014	A physiologically based pharmacokinetic model indicated that inactivation of CYP2C8 by clopidogrel acyl-beta-D-glucuronide leads to uninterrupted 60-85% inhibition of CYP2C8 during daily clopidogrel treatment.	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	77-83
24971633-5	2014	A physiologically based pharmacokinetic model indicated that inactivation of CYP2C8 by clopidogrel acyl-beta-D-glucuronide leads to uninterrupted 60-85% inhibition of CYP2C8 during daily clopidogrel treatment.	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	167-173
24971633-7	2014	The results indicate that clopidogrel is a strong CYP2C8 inhibitor via its acyl-beta-D-glucuronide and imply that glucuronide metabolites should be considered potential inhibitors of CYP enzymes.	clopidogrel	26-37	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	50-56
25502126-0	2014	Point-of-care platelet reactivity determination with VerifyNow-P2Y12 following administration of clopidogrel or prasugrel: data from a real-world, clinical care inpatient setting.	clopidogrel	97-108	purinergic receptor P2Y12	Homo sapiens	63-68
25329996-0	2014	Effects of cytochrome P450 2C19 and paraoxonase 1 polymorphisms on antiplatelet response to clopidogrel therapy in patients with coronary artery disease.	clopidogrel	92-103	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	11-31
25329996-0	2014	Effects of cytochrome P450 2C19 and paraoxonase 1 polymorphisms on antiplatelet response to clopidogrel therapy in patients with coronary artery disease.	clopidogrel	92-103	paraoxonase 1	Homo sapiens	36-49
25329996-3	2014	Here, we sought to determine the associations of CYP2C19 and PON1 gene polymorphisms with clopidogrel response and their role in ADP-induced platelet aggregation.	clopidogrel	90-101	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	49-56
25329996-3	2014	Here, we sought to determine the associations of CYP2C19 and PON1 gene polymorphisms with clopidogrel response and their role in ADP-induced platelet aggregation.	clopidogrel	90-101	paraoxonase 1	Homo sapiens	61-65
25329996-5	2014	Polymorphisms in CYP2C19 and PON1 were genotyped and tested for association with clopidogrel resistance.	clopidogrel	81-92	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-24
25329996-5	2014	Polymorphisms in CYP2C19 and PON1 were genotyped and tested for association with clopidogrel resistance.	clopidogrel	81-92	paraoxonase 1	Homo sapiens	29-33
25329996-9	2014	After adjusting for established risk factors, CYP2C19*2 and *3 alleles independently increased the risk of clopidogrel resistance with adjusted ORs 2.94 (95%CI, 1.65-5.26; p&lt;0.001) and 11.26 (95%CI, 2.47-51.41; p = 0.002, respectively).	clopidogrel	107-118	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	46-53
25329996-15	2014	Our findings indicated that only CYP2C19*2 and *3 alleles had an influence on clopidogrel resistance.	clopidogrel	78-89	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-40
24589079-0	2014	Association between the microarray-based CYP2C19 genotyping assay and the platelet function test in cardiovascular patients receiving clopidogrel.	clopidogrel	134-145	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	41-48
25052834-1	2014	Although resistance to the P2Y12 antagonist clopidogrel is linked to altered drug metabolism, some studies suggest that these pharmacokinetic abnormalities only partially account for drug resistance.	clopidogrel	44-55	purinergic receptor P2Y12	Homo sapiens	27-32
24877854-0	2014	Patients carrying CYP2C19 loss of function alleles have a reduced response to clopidogrel therapy and a greater risk of in-stent restenosis after endovascular treatment of lower extremity peripheral arterial disease.	clopidogrel	78-89	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	18-25
24877854-9	2014	Carriers of at least one CYP2C19 loss-of-function (LOF) allele had a diminished pharmacodynamic response to clopidogrel (51.6 +- 20.1 vs. 39.8 +- 15.2 for patients without and with LOF alleles, respectively; P = .022).	clopidogrel	108-119	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
24877854-16	2014	CONCLUSIONS: CYP2C19 LOF alleles were associated with a diminished platelet response to clopidogrel treatment.	clopidogrel	88-99	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
24877854-17	2014	Patients carrying CYP2C19 LOF alleles who are treated with clopidogrel may trend toward a poor prognosis after ET.	clopidogrel	59-70	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	18-25
25154978-2	2014	These recommendations are based primarily on large, phase III, randomized, controlled trials of the P2Y12 inhibitors clopidogrel, prasugrel, and ticagrelor.	clopidogrel	117-128	purinergic receptor P2Y12	Homo sapiens	100-105
25220280-4	2014	Planning for University of Florida Health Personalized Medicine Program began in summer 2011 under leadership of a pharmacist, with clinical launch in June 2012 of a clopidogrel-CYP2C19 pilot project aimed at tailoring antiplatelet therapies for patients undergoing percutaneous coronary intervention and stent placement.	clopidogrel	166-177	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	178-185
25985567-0	2014	The association of ABCC3 promoter methylation with clopidogrel response in Chinese ischemic stroke patients.	clopidogrel	51-62	ATP binding cassette subfamily C member 3	Homo sapiens	19-24
25985567-1	2014	Multidrug resistance protein 3 (MRP3), encoded by ABCC3, is an ATP-dependent efflux pump mediating the transport of many drugs, implicated in clopidogrel resistance.	clopidogrel	142-153	ATP binding cassette subfamily B member 4	Homo sapiens	0-30
25985567-1	2014	Multidrug resistance protein 3 (MRP3), encoded by ABCC3, is an ATP-dependent efflux pump mediating the transport of many drugs, implicated in clopidogrel resistance.	clopidogrel	142-153	ATP binding cassette subfamily B member 4	Homo sapiens	32-36
25985567-1	2014	Multidrug resistance protein 3 (MRP3), encoded by ABCC3, is an ATP-dependent efflux pump mediating the transport of many drugs, implicated in clopidogrel resistance.	clopidogrel	142-153	ATP binding cassette subfamily C member 3	Homo sapiens	50-55
25175362-2	2014	So far, there has been little information about the response of clopidogrel in Asians, whose prevalence of a CYP2C19 loss-of-function (LOF) allele is high.	clopidogrel	64-75	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	109-116
25175362-4	2014	In univariate analysis, antiplatelet effects of clopidogrel in a steady state were associated with not only CYP2C19 genotypes but also several factors including dyslipidemia.	clopidogrel	48-59	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	108-115
25502126-1	2014	OBJECTIVES: To describe VerifyNow-P2Y12 (VN-P2Y12, Accumetrics, San Diego, CA) results from patients treated with either clopidogrel or prasugrel who were seeking care in a hospital setting.	clopidogrel	121-132	purinergic receptor P2Y12	Homo sapiens	34-39
25075638-1	2014	In the search of a potential backup for clopidogrel, we have initiated a HTS campaign designed to identify novel reversible P2Y12 antagonists.	clopidogrel	40-51	purinergic receptor P2Y12	Homo sapiens	124-129
25190236-0	2014	Impaired responsiveness to the platelet P2Y12 receptor antagonist clopidogrel in patients with type 2 diabetes and coronary artery disease.	clopidogrel	66-77	purinergic receptor P2Y12	Homo sapiens	40-45
25190236-12	2014	CONCLUSIONS: The present study suggests that among DM patients, impaired P2Y12 inhibition mediated by clopidogrel is largely attributable to attenuation of clopidogrel"s PK profile.	clopidogrel	102-113	purinergic receptor P2Y12	Homo sapiens	73-78
25190236-12	2014	CONCLUSIONS: The present study suggests that among DM patients, impaired P2Y12 inhibition mediated by clopidogrel is largely attributable to attenuation of clopidogrel"s PK profile.	clopidogrel	156-167	purinergic receptor P2Y12	Homo sapiens	73-78
25008027-1	2014	CYP2C19 genotype has been shown to impact response to clopidogrel 75-mg but not prasugrel 10-mg.	clopidogrel	54-65	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
24731293-3	2014	We hypothesized that HNP levels are associated with the formation of neutrophil-platelet aggregates, and that they influence the response to clopidogrel therapy.	clopidogrel	141-152	kallikrein related peptidase 8	Homo sapiens	21-24
25112801-0	2014	Single nucleotide polymorphism of CYP3A5*3 contributes to clopidogrel resistance in coronary artery disease patients among Tamilian population.	clopidogrel	58-69	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	34-40
25112801-4	2014	The aim of the present study was to evaluate the effect of CYP3A5*3 genetic polymorphism on clopidogrel resistance.	clopidogrel	92-103	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	59-65
25112801-11	2014	Homomutants of CYP3A5*3 gene had 2.78 (0.97-7.98; p &lt; 0.05) fold risk and heteromutants had 2.4 (0.93-6.46; p &lt; 0.05) fold risk of developing clopidogrel resistance.	clopidogrel	148-159	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	15-21
25112801-12	2014	Carriers of defective allele G of CYP3A5*3 had higher propensity to cause clopidogrel resistance with an odds ratio of 1.63.	clopidogrel	74-85	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	34-40
25112801-13	2014	Variant alleles and genotypes of CYP3A5*3 polymorphism contributed significantly to clopidogrel resistance with a higher odds ratio.	clopidogrel	84-95	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	33-39
24996381-1	2014	BACKGROUND: The relationship between CYP2C19*2 gene polymorphism and clopidogrel resistance reflected by platelet function assays has been studied extensively in the past several years, while no clear conclusion can be drawn from the previous studies.	clopidogrel	69-80	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-44
24996381-6	2014	The pooled analysis showed that CYP2C19*2 gene polymorphism was probably associated with clopidogrel resistance (OR (95% CI): GA vs. GG: 2.10 (1.74-2.53); AA vs. GG: 3.05 (2.10-4.45); dominant model: 2.22 (1.85-2.65); recessive model: 2.33 (1.62-3.36)).	clopidogrel	89-100	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
24996381-9	2014	CONCLUSION: The meta-analysis suggests that CYP2C19*2 gene polymorphism may be associated with clopidogrel resistance.	clopidogrel	95-106	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	44-51
24731293-11	2014	In conclusion, HNP levels are associated with ADP-inducible neutrophil-platelet aggregate formation and clopidogrel-mediated platelet inhibition.	clopidogrel	104-115	kallikrein related peptidase 8	Homo sapiens	15-18
24782221-0	2014	The influence of genetic polymorphism of Cyp2c19 isoenzyme on the pharmacokinetics of clopidogrel and its metabolites in patients with cardiovascular diseases.	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	41-48
24659260-11	2014	CONCLUSIONS: The reversible P2Y12 antagonists ticagrelor, cangrelor, and elinogrel have an increased incidence of dyspnea in increasing order when compared with irreversible P2Y12 inhibitors such as clopidogrel or prasugrel.	clopidogrel	199-210	purinergic receptor P2Y12	Homo sapiens	28-33
24608794-0	2014	CYP2C19 polymorphisms and coronary heart disease risk factors synergistically impact clopidogrel response variety after percutaneous coronary intervention.	clopidogrel	85-96	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
24608794-2	2014	CYP2C19 loss-of-function (LOF) alleles and risk factors of coronary heart disease (CAD) were reported to be associated with the low response of clopidogrel.	clopidogrel	144-155	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
24608794-3	2014	PURPOSE: This study was carried out to analyze the contributions of CYP2C19 polymorphisms and risk factors to the various clopidogrel responses in Chinese patients with stable CAD after PCI.	clopidogrel	122-133	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	68-75
24608794-11	2014	Carriers of two CYP2C19 LOF alleles, BMI, and the presence of type 2 diabetes were three independent risk factors for clopidogrel resistance.	clopidogrel	118-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
24608794-12	2014	CONCLUSION: Genetic CYP2C19 polymorphisms and CAD risk factors - type 2 diabetes mellitus and BMI - synergistically affect the antiplatelet activity of clopidogrel and the occurrence of major adverse cardiovascular events after PCI.	clopidogrel	152-163	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	20-27
24214141-0	2014	The effect of CYP2C19 genotype on the time course of platelet aggregation inhibition after clopidogrel administration.	clopidogrel	91-102	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
24214141-1	2014	We evaluated the effect of CYP2C19 genotype over time on the antiplatelet response of clopidogrel in healthy subjects.	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	27-34
24214141-3	2014	The subjects with CYP2C19 poor metabolizers (PM, N = 22) and intermediate metabolizers (IM, N = 37) had significantly delayed time to inhibition of platelet aggregation (IPA) compared with CYP2C19 extensive metabolizers (EM, N = 33) (12 vs. 9 vs. 2 hours as median Tmax , P &lt; .05) after a 300 mg of clopidogrel.	clopidogrel	302-313	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	18-25
24214141-4	2014	During maintenance doses of clopidogrel, IPA values of only CYP2C19 PM subjects were gradually decreased from 30.0 +- 21.9% on day 2 to 23.7 +- 16.6% on day 8 (P &gt; .05 for time effect; P &lt; .05 for time and genotype interaction effect).	clopidogrel	28-39	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	60-67
24504666-0	2014	Positive clinical response to clopidogrel is independent of paraoxonase 1 Q192R and CYP2C19 genetic variants.	clopidogrel	30-41	paraoxonase 1	Homo sapiens	60-73
24504666-0	2014	Positive clinical response to clopidogrel is independent of paraoxonase 1 Q192R and CYP2C19 genetic variants.	clopidogrel	30-41	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	84-91
24504666-1	2014	There is increasing controversy about the influence of serum paraoxonase type 1 and cytochrome CYP2C19 in the conversion of clopidogrel to its pharmaceutically active metabolite.	clopidogrel	124-135	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	95-102
24782221-8	2014	We concluded that the CYP2C19*2 genotype is the primary determinant of the antiplatelet response to clopidogrel therapy.	clopidogrel	100-111	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	22-29
24952863-8	2014	CONCLUSIONS: Among medically managed ACS patients &lt;75 years of age, the risk of ischemic outcomes was significantly reduced with prasugrel vs. clopidogrel among smokers vs. non-smokers.	clopidogrel	146-157	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	37-40
24710841-0	2014	Effectiveness of clopidogrel dose escalation to normalize active metabolite exposure and antiplatelet effects in CYP2C19 poor metabolizers.	clopidogrel	17-28	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	113-120
24710841-1	2014	Carriers of two copies of the loss-of-function CYP2C19*2 variant convert less clopidogrel into its active metabolite, resulting in diminished antiplatelet responses and higher cardiovascular event rates.	clopidogrel	78-89	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	47-54
24710841-7	2014	These results suggest that quadrupling the usual clopidogrel dose might be necessary to overcome the effect of poor CYP2C19 metabolism.	clopidogrel	49-60	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	116-123
24945780-0	2014	The influence of the CYP2C19*10 allele on clopidogrel activation and CYP2C19*2 genotyping.	clopidogrel	42-53	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
24945780-1	2014	BACKGROUND/OBJECTIVES: The polymorphic hepatic enzyme CYP2C19 catalyzes the metabolism of clinically important drugs such as clopidogrel, proton-pump inhibitors, and others and clinical pharmacogenetic testing for clopidogrel is increasingly common.	clopidogrel	125-136	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	54-61
24945780-1	2014	BACKGROUND/OBJECTIVES: The polymorphic hepatic enzyme CYP2C19 catalyzes the metabolism of clinically important drugs such as clopidogrel, proton-pump inhibitors, and others and clinical pharmacogenetic testing for clopidogrel is increasingly common.	clopidogrel	214-225	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	54-61
24945780-4	2014	However, the effect of the CYP2C19*10 allele on clopidogrel metabolism has not been explored to date.	clopidogrel	48-59	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	27-34
24945780-5	2014	METHODS: We measured the enzymatic activity of the CYP2C19.10 protein against clopidogrel.	clopidogrel	78-89	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	51-58
24945780-7	2014	RESULTS: The catalytic activity of CYP2C19.10 in the biotransformation of clopidogrel and 2-oxo-clopidogrel was significantly decreased relative to the wild-type CYP2C19.1B.	clopidogrel	74-85	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	35-42
24945780-7	2014	RESULTS: The catalytic activity of CYP2C19.10 in the biotransformation of clopidogrel and 2-oxo-clopidogrel was significantly decreased relative to the wild-type CYP2C19.1B.	clopidogrel	74-85	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	162-169
24945780-9	2014	CONCLUSIONS: Our data provide evidence that CYP2C19.10 variant partially metabolizes clopidogrel and 2-oxo-clopidogrel, and the presence of CYP2C19*10 allele affects the CY2C19*2 TaqMan genotyping assay and results in misclassification of CYP2C19*10/*2 as CYP2C19*2/*2.	clopidogrel	85-96	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	44-51
24945780-9	2014	CONCLUSIONS: Our data provide evidence that CYP2C19.10 variant partially metabolizes clopidogrel and 2-oxo-clopidogrel, and the presence of CYP2C19*10 allele affects the CY2C19*2 TaqMan genotyping assay and results in misclassification of CYP2C19*10/*2 as CYP2C19*2/*2.	clopidogrel	85-96	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	140-147
24945780-9	2014	CONCLUSIONS: Our data provide evidence that CYP2C19.10 variant partially metabolizes clopidogrel and 2-oxo-clopidogrel, and the presence of CYP2C19*10 allele affects the CY2C19*2 TaqMan genotyping assay and results in misclassification of CYP2C19*10/*2 as CYP2C19*2/*2.	clopidogrel	85-96	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	140-147
24945780-9	2014	CONCLUSIONS: Our data provide evidence that CYP2C19.10 variant partially metabolizes clopidogrel and 2-oxo-clopidogrel, and the presence of CYP2C19*10 allele affects the CY2C19*2 TaqMan genotyping assay and results in misclassification of CYP2C19*10/*2 as CYP2C19*2/*2.	clopidogrel	85-96	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	140-147
24718389-4	2014	The aim of the ISAR-HPR registry was to assess whether clopidogrel-treated HPR patients benefit from selective intensification of P2Y12 receptor inhibition.	clopidogrel	55-66	purinergic receptor P2Y12	Homo sapiens	130-135
24951432-1	2014	The P2Y12 inhibitors, clopidogrel, prasugrel, and ticagrelor, are administered in fixed doses without laboratory monitoring.	clopidogrel	22-33	purinergic receptor P2Y12	Homo sapiens	4-9
24951432-4	2014	Patients treated with standard-dose clopidogrel have substantial variability in platelet inhibition, which is partly explained by genetic polymorphisms encoding CYP2C19, the hepatic enzyme involved in biotransformation of clopidogrel to its active metabolite.	clopidogrel	36-47	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	161-168
24951432-4	2014	Patients treated with standard-dose clopidogrel have substantial variability in platelet inhibition, which is partly explained by genetic polymorphisms encoding CYP2C19, the hepatic enzyme involved in biotransformation of clopidogrel to its active metabolite.	clopidogrel	222-233	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	161-168
25117329-6	2014	We were able to correctly infer genotypes for the warfarin-related loci VKORC1 and CYP2C9 alleles 2, 3, 5, and 11 and also clopidogrel-related CYP2C19 alleles 2 and 17 for a small sample of Brazilian individuals, as well as for HapMap samples.	clopidogrel	123-134	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	143-150
25284925-4	2014	The purpose of the current investigation was to study the effect of selection of volunteers homozygous for the CYP2C19*1 haplotype on the bioavailability of clopidogrel.	clopidogrel	157-168	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	111-118
25284925-6	2014	It was found that selection of volunteers homozygous for the CYP2C19*1 haplotype, increased the stringency of bioequivalence statistics and resulted in bioinequivalence of a generic clopidogrel compound that otherwise proved equivalent when tested in an open unselected population.	clopidogrel	182-193	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	61-68
24202700-1	2014	To investigate the relationship between circulating microRNA 223 (miR-223) levels and clopidogrel responsiveness in patients with coronary heart disease.	clopidogrel	86-97	microRNA 223	Homo sapiens	66-73
24202700-8	2014	Our data suggest that circulating miR-223 may serve as a novel biomarker for assessment of clopidogrel responsiveness in troponin-negative NSTE-ACS patients.	clopidogrel	91-102	microRNA 223	Homo sapiens	34-41
25163307-3	2014	Clopidogrel is also commonly used antiplatelet agents, which is now known to block P2Y12 ADP receptor.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	83-88
25163321-4	2014	Polymorphism of CYP2C19 affecting clopidogrel activity might be one cause of such problems.	clopidogrel	34-45	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
25243032-7	2014	Relative risk of developing myocardial infarction and stroke between patients with and without variant CYP2C19 when receiving clopidogrel were estimated to be 1.34 and 3.66, respectively.	clopidogrel	126-137	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	103-110
24665827-7	2014	RESULTS: (1) PF4/H antibody-positive patients suffered a significantly higher incidence of thrombosis than those who were antibody-negative; (2) PF4/H antibody-positive patients who survived a thrombosis manifested a significantly longer bleeding time and decreased maximum percentage of platelet aggregation inhibition; (3) aspirin and clopidogrel decreased the incidence of thrombosis in PF4/H antibody-positive patients by inhibiting platelet activation.	clopidogrel	337-348	platelet factor 4	Homo sapiens	145-148
24665827-7	2014	RESULTS: (1) PF4/H antibody-positive patients suffered a significantly higher incidence of thrombosis than those who were antibody-negative; (2) PF4/H antibody-positive patients who survived a thrombosis manifested a significantly longer bleeding time and decreased maximum percentage of platelet aggregation inhibition; (3) aspirin and clopidogrel decreased the incidence of thrombosis in PF4/H antibody-positive patients by inhibiting platelet activation.	clopidogrel	337-348	platelet factor 4	Homo sapiens	13-18
24856643-8	2014	The benefits of prasugrel and ticagrelor compared to clopidogrel treated patients in terms of platelet inhibition were more pronounced in CYP2C19*2 carriers.	clopidogrel	53-64	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	138-145
24856643-11	2014	CONCLUSION: The results of this pilot study of treatment of patients in the early phase of ACS indicate that CYP2C19*2 POC genotyping might help to identify patients at risk with poor response to clopidogrel treatment, thereby benefiting from reloading and switching to alternative P2Y12 receptor inhibition.	clopidogrel	196-207	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	109-116
24856643-11	2014	CONCLUSION: The results of this pilot study of treatment of patients in the early phase of ACS indicate that CYP2C19*2 POC genotyping might help to identify patients at risk with poor response to clopidogrel treatment, thereby benefiting from reloading and switching to alternative P2Y12 receptor inhibition.	clopidogrel	196-207	purinergic receptor P2Y12	Homo sapiens	282-287
24203353-1	2014	We aimed to investigate the association of aspirin and/or clopidogrel low response with -455G/A polymorphism of beta-fibrinogen in patients with acute coronary syndrome (ACS).	clopidogrel	58-69	fibrinogen beta chain	Homo sapiens	112-127
23850044-0	2014	[Relevance of CYP2C19 2 regarding platelet reactivity in patients with acute coronary syndrome treated with clopidogrel].	clopidogrel	108-119	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
24418943-3	2014	To evaluate an impact of CYP2C19 G681A and CYP4F2 G1347A polymorphisms and clinical factors on dual antiplatelet effect of clopidogrel and aspirin.	clopidogrel	123-134	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
24418943-3	2014	To evaluate an impact of CYP2C19 G681A and CYP4F2 G1347A polymorphisms and clinical factors on dual antiplatelet effect of clopidogrel and aspirin.	clopidogrel	123-134	cytochrome P450 family 4 subfamily F member 2	Homo sapiens	43-49
24418943-12	2014	Our study confirms that CYP2C19 G681A genotype has an impact on antiplatelet effect of clopidogrel.	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
24762860-0	2014	Cytochrome p450 gene variants, race, and mortality among clopidogrel-treated patients after acute myocardial infarction.	clopidogrel	57-68	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	11-15
24762860-1	2014	BACKGROUND: Clopidogrel is recommended after acute myocardial infarction but has variable efficacy and safety, in part related to the effect of cytochrome P450 (CYP) polymorphisms on its metabolism.	clopidogrel	12-23	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	144-159
24762860-1	2014	BACKGROUND: Clopidogrel is recommended after acute myocardial infarction but has variable efficacy and safety, in part related to the effect of cytochrome P450 (CYP) polymorphisms on its metabolism.	clopidogrel	12-23	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	161-164
24762860-8	2014	CONCLUSIONS: Both loss-of-function and gain-of-function CYP polymorphisms affecting clopidogrel metabolism are associated with increased mortality among clopidogrel-treated patients after acute myocardial infarction; the specific polymorphism and the putative mechanism vary according to race.	clopidogrel	84-95	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	56-59
24762860-8	2014	CONCLUSIONS: Both loss-of-function and gain-of-function CYP polymorphisms affecting clopidogrel metabolism are associated with increased mortality among clopidogrel-treated patients after acute myocardial infarction; the specific polymorphism and the putative mechanism vary according to race.	clopidogrel	153-164	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	56-59
24566733-3	2014	A single 75-mg dose of clopidogrel was orally administered before and after 2 and 4 weeks of once-daily 100-mg aspirin administration in 18 healthy volunteers who were recruited based on CYP2C19 and PON1 genotypes.	clopidogrel	23-34	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	187-194
24566733-3	2014	A single 75-mg dose of clopidogrel was orally administered before and after 2 and 4 weeks of once-daily 100-mg aspirin administration in 18 healthy volunteers who were recruited based on CYP2C19 and PON1 genotypes.	clopidogrel	23-34	paraoxonase 1	Homo sapiens	199-203
24763934-10	2014	CONCLUSIONS: Our results suggest that antiplatelet response to clopidogrel in the late phase depends on the CYP3A5 polymorphism in PM with CYP2C19.	clopidogrel	63-74	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	108-114
24763934-10	2014	CONCLUSIONS: Our results suggest that antiplatelet response to clopidogrel in the late phase depends on the CYP3A5 polymorphism in PM with CYP2C19.	clopidogrel	63-74	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	139-146
24671606-3	2014	Based upon previous observations, we hypothesised that VN-P2Y12 overestimates the therapeutic effects of clopidogrel.	clopidogrel	105-116	purinergic receptor P2Y12	Homo sapiens	58-63
24671606-7	2014	In 59 patients loaded with clopidogrel 600 mg/900 mg, a greater proportion had a "therapeutic response" with VN-P2Y12 compared to s-TEG, regardless of the threshold for defining HPR with VN-PY12 (P2Y12 reaction units &gt;= 230 or 208).	clopidogrel	27-38	purinergic receptor P2Y12	Homo sapiens	112-117
24671606-10	2014	This could have implications for the ability of VN-P2Y12 to stratify patients as "responders" or "non-responders" to clopidogrel.	clopidogrel	117-128	purinergic receptor P2Y12	Homo sapiens	51-56
24402637-0	2014	Clopidogrel metaboliser status based on point-of-care CYP2C19 genetic testing in patients with coronary artery disease.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	54-61
24402637-3	2014	Pharmacokinetic exposure to clopidogrel"s active metabolite and pharmacodynamic measures with P2Y12 reaction units (PRU) (VerifyNow P2Y12 assay) and VASP PRI (PRI) were also assessed.	clopidogrel	28-39	purinergic receptor P2Y12	Homo sapiens	94-99
24402637-3	2014	Pharmacokinetic exposure to clopidogrel"s active metabolite and pharmacodynamic measures with P2Y12 reaction units (PRU) (VerifyNow P2Y12 assay) and VASP PRI (PRI) were also assessed.	clopidogrel	28-39	purinergic receptor P2Y12	Homo sapiens	132-137
24745727-2	2014	Dual anti-platelet therapy with acetylsalicylic acid (ASA) and a P2Y12 inhibitor (clopidogrel, prasugrel or ticagrelor) is the recommended strategy for patients undergoing a percutaneous coronary intervention (PCI), while patients that undergo coronary artery bypass grafting (CABG) are treated with ASA monotherapy.	clopidogrel	82-93	purinergic receptor P2Y12	Homo sapiens	65-70
24530383-0	2014	In vitro interaction of clopidogrel and its hydrolysate with OCT1, OCT2 and OAT1.	clopidogrel	24-35	solute carrier family 22 member 1	Rattus norvegicus	61-65
24530383-0	2014	In vitro interaction of clopidogrel and its hydrolysate with OCT1, OCT2 and OAT1.	clopidogrel	24-35	solute carrier family 22 member 2	Rattus norvegicus	67-71
24530383-0	2014	In vitro interaction of clopidogrel and its hydrolysate with OCT1, OCT2 and OAT1.	clopidogrel	24-35	solute carrier family 22 member 6	Rattus norvegicus	76-80
24758255-11	2014	Clopidogrel intake was independent predictor of lower CLU expression on carotid artery (p =0.045).	clopidogrel	0-11	clusterin	Homo sapiens	54-57
25606414-0	2014	ABCB1 C3435T and CYP2C19*2 polymorphisms in a Palestinian and Turkish population: A pharmacogenetic perspective to clopidogrel.	clopidogrel	115-126	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
25606414-0	2014	ABCB1 C3435T and CYP2C19*2 polymorphisms in a Palestinian and Turkish population: A pharmacogenetic perspective to clopidogrel.	clopidogrel	115-126	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-24
25606414-2	2014	Single nucleotide polymorphisms (SNPs) such as CYP2C19*2 and ABCB1 C3435T have been found to play a role in different individual responses to clopidogrel.	clopidogrel	142-153	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	47-54
25606414-2	2014	Single nucleotide polymorphisms (SNPs) such as CYP2C19*2 and ABCB1 C3435T have been found to play a role in different individual responses to clopidogrel.	clopidogrel	142-153	ATP binding cassette subfamily B member 1	Homo sapiens	61-66
24742198-5	2014	On the other hand, after clopidogrel and cilostazol combination therapy, galectin-3 level, lipoprotein-associated phospholipase A2 gene expression, and RhoA/ROCK-related protein expression in peripheral blood mononuclear cells were significantly suppressed (all p&lt;0.01).	clopidogrel	25-36	phospholipase A2 group VII	Homo sapiens	91-130
23981082-5	2014	Loss-of-function polymorphisms in CYP2C19 are the strongest individual variables affecting pharmacokinetics and antiplatelet response to clopidogrel, but explain no more than 5 to 12% of the variability in adenosine diphosphate-induced platelet aggregation on clopidogrel.	clopidogrel	137-148	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	34-41
23981082-5	2014	Loss-of-function polymorphisms in CYP2C19 are the strongest individual variables affecting pharmacokinetics and antiplatelet response to clopidogrel, but explain no more than 5 to 12% of the variability in adenosine diphosphate-induced platelet aggregation on clopidogrel.	clopidogrel	260-271	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	34-41
24636274-0	2014	Transient receptor potential ankyrin 1 (TRPA1) channel activation by the thienopyridine-type drugs ticlopidine, clopidogrel, and prasugrel.	clopidogrel	112-123	transient receptor potential cation channel subfamily A member 1	Homo sapiens	40-45
24636274-7	2014	These findings indicate that a robust TRPA1 activation by ticlopidine and clopidogrel correlates with the stimulatory effect on the secretion of 5-HT.	clopidogrel	74-85	transient receptor potential cation channel subfamily A member 1	Homo sapiens	38-43
24891841-0	2014	Thrombin based gelatin matrix and fibrin sealant mediated clot formation in the presence of clopidogrel.	clopidogrel	92-103	coagulation factor II, thrombin	Homo sapiens	0-8
24857912-2	2014	The variations in response to clopidogrel can be driven by genetic polymorphisms involved in the pathway of absorption, distribution, metabolism, excretion, and the target receptor P2Y12.	clopidogrel	30-41	purinergic receptor P2Y12	Homo sapiens	181-186
24857912-3	2014	A set of genetic variants known for causing variations in clopidogrel responses was selected, which included CYP2C19*2, *3, *17, CYP2B6*4, *6, *9, CYP3A4*18, CYP3A5*3, MDR1 2677G&gt;T/A, 3435C&gt;T, and P2Y12 H2 (742T&gt;C).	clopidogrel	58-69	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	109-116
24857912-3	2014	A set of genetic variants known for causing variations in clopidogrel responses was selected, which included CYP2C19*2, *3, *17, CYP2B6*4, *6, *9, CYP3A4*18, CYP3A5*3, MDR1 2677G&gt;T/A, 3435C&gt;T, and P2Y12 H2 (742T&gt;C).	clopidogrel	58-69	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	129-135
24857912-3	2014	A set of genetic variants known for causing variations in clopidogrel responses was selected, which included CYP2C19*2, *3, *17, CYP2B6*4, *6, *9, CYP3A4*18, CYP3A5*3, MDR1 2677G&gt;T/A, 3435C&gt;T, and P2Y12 H2 (742T&gt;C).	clopidogrel	58-69	ATP binding cassette subfamily B member 1	Homo sapiens	168-172
24857912-3	2014	A set of genetic variants known for causing variations in clopidogrel responses was selected, which included CYP2C19*2, *3, *17, CYP2B6*4, *6, *9, CYP3A4*18, CYP3A5*3, MDR1 2677G&gt;T/A, 3435C&gt;T, and P2Y12 H2 (742T&gt;C).	clopidogrel	58-69	purinergic receptor P2Y12	Homo sapiens	203-208
23771209-5	2014	METHODS: We reviewed our cerebrovascular database for all patients who were non-responders to clopidogrel, defined as P2Y12% inhibition &lt;30%, despite repeat clopidogrel loading dose of at least 600 mg, and who were then administered ticagrelor.	clopidogrel	94-105	purinergic receptor P2Y12	Homo sapiens	118-123
24670650-4	2014	P2Y12R regulates platelet activation and thrombus formation, and several antithrombotic drugs targeting P2Y12R--including the prodrugs clopidogrel (Plavix) and prasugrel (Effient) that are metabolized and bind covalently, and the nucleoside analogue ticagrelor (Brilinta) that acts directly on the receptor--have been approved for the prevention of stroke and myocardial infarction.	clopidogrel	135-146	purinergic receptor P2Y12	Homo sapiens	104-110
24670650-4	2014	P2Y12R regulates platelet activation and thrombus formation, and several antithrombotic drugs targeting P2Y12R--including the prodrugs clopidogrel (Plavix) and prasugrel (Effient) that are metabolized and bind covalently, and the nucleoside analogue ticagrelor (Brilinta) that acts directly on the receptor--have been approved for the prevention of stroke and myocardial infarction.	clopidogrel	148-154	purinergic receptor P2Y12	Homo sapiens	104-110
24670650-5	2014	However, limitations of these drugs (for example, a very long half-life of clopidogrel action and a characteristic adverse effect profile of ticagrelor) suggest that there is an unfulfilled medical need for developing a new generation of P2Y12R inhibitors.	clopidogrel	75-86	purinergic receptor P2Y12	Homo sapiens	238-244
24956245-0	2014	Clopidogrel dose adjustment after outpatient screening for CYP2C19 variant alleles: a pilot study.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	59-66
24956245-4	2014	In patients with CYP2C19*2, 150 mg daily of clopidogrel was associated with improved ADP-specific platelet inhibition (217 vs 258 P2Y12 reaction units, p = 0.01).	clopidogrel	44-55	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-24
24956245-4	2014	In patients with CYP2C19*2, 150 mg daily of clopidogrel was associated with improved ADP-specific platelet inhibition (217 vs 258 P2Y12 reaction units, p = 0.01).	clopidogrel	44-55	purinergic receptor P2Y12	Homo sapiens	130-135
24918808-7	2014	Because comparative studies indicate that omeprazole and esomeprazole have a greater effect on the CYP2C19-mediated conversion of clopidogrel to its active metabolite and, consequently, clopidogrel"s effect on platelet reactivity, FDA labeling recommends avoiding omeprazole and esomeprazole in patients taking clopidogrel.	clopidogrel	130-141	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	99-106
24918808-7	2014	Because comparative studies indicate that omeprazole and esomeprazole have a greater effect on the CYP2C19-mediated conversion of clopidogrel to its active metabolite and, consequently, clopidogrel"s effect on platelet reactivity, FDA labeling recommends avoiding omeprazole and esomeprazole in patients taking clopidogrel.	clopidogrel	186-197	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	99-106
24918808-7	2014	Because comparative studies indicate that omeprazole and esomeprazole have a greater effect on the CYP2C19-mediated conversion of clopidogrel to its active metabolite and, consequently, clopidogrel"s effect on platelet reactivity, FDA labeling recommends avoiding omeprazole and esomeprazole in patients taking clopidogrel.	clopidogrel	186-197	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	99-106
24719135-2	2014	CYP3A4 is involved in the metabolism of both clopidogrel and dihydropyridine calcium channel blockers (CCBs).	clopidogrel	45-56	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
24719135-4	2014	Accordingly, the aim of this study was to determine the effect of CCBs on the antiplatelet activity of clopidogrel by serial P2Y12 reaction unit (PRU) measurements.	clopidogrel	103-114	purinergic receptor P2Y12	Homo sapiens	125-130
24719135-6	2014	The antiplatelet activity of clopidogrel was measured by VerifyNow P2Y12 assay in the same patient while medicated with CCBs and at 8 weeks after discontinuation of CCBs.	clopidogrel	29-40	purinergic receptor P2Y12	Homo sapiens	67-72
24998658-1	2014	OBJECTIVE: To investigate the relation of clopidogrel resistance to polymorphism of adenosine diphosphate receptor (P2Y12).	clopidogrel	42-53	purinergic receptor P2Y12	Homo sapiens	116-121
24998658-10	2014	CONCLUSION: T-34, -52 mutations on P2Y12 receptor gene may be a risk factor for clopidogrel resistance and adverse cardiovascular events.	clopidogrel	80-91	purinergic receptor P2Y12	Homo sapiens	35-40
24636274-8	2014	As recipients of ticlopidine and clopidogrel frequently complain about gastrointestinal adverse events such as nausea, vomiting and diarrhoea, an activation of TRPA1 may contribute to adverse effects of such drugs in the digestive system.	clopidogrel	33-44	transient receptor potential cation channel subfamily A member 1	Homo sapiens	160-165
25400347-5	2014	Significantly, the tested sample population showed high prevalence (66%) of CYP2C19*2 variant, which determines response to clopidogrel therapy.	clopidogrel	124-135	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	76-83
24550106-8	2014	The CYP2C19-mediated interaction that seems to exist between clopidogrel and omeprazole or esomeprazole has been shown to be clinically important in research published since the 2006 review; this effect is not seen as a class effect of PPIs.	clopidogrel	61-72	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
24336012-5	2014	RESULTS: Clopidogrel therapy resulted in a significant reduction in soluble CD40 ligand (P = 0.03), a prothrombotic and proinflammatory molecule derived mainly from activated platelets.	clopidogrel	9-20	CD40 molecule	Homo sapiens	76-80
23849748-1	2014	BACKGROUND: Concern has recently been raised over the possibility of a reduced efficacy of clopidogrel because of genetic variations in cytochrome P450, family 2, subfamily C, polypeptide 19 (CYP2C19) metabolism.	clopidogrel	91-102	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	136-190
23849748-1	2014	BACKGROUND: Concern has recently been raised over the possibility of a reduced efficacy of clopidogrel because of genetic variations in cytochrome P450, family 2, subfamily C, polypeptide 19 (CYP2C19) metabolism.	clopidogrel	91-102	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	192-199
23849748-5	2014	METHODS: A retrospective review of all patients with stroke and transient ischemic attack (TIA) tested for the clopidogrel CYP2C19 genotype was performed, with a collection of data including race/ethnicity, CYP2C19 status, and the presence of recurrent vascular events.	clopidogrel	111-122	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	123-130
24535487-1	2014	OBJECTIVE: Carboxylesterase 1 hydrolyzes the majority of clopidogrel to the inactive metabolite.	clopidogrel	57-68	carboxylesterase 1	Homo sapiens	11-29
24535487-2	2014	The aim of this study was to assess the effects of the CES1A2 A(-816)C polymorphism and other genetic and clinical factors on clopidogrel response variability.	clopidogrel	126-137	carboxylesterase 1 pseudogene 1	Homo sapiens	55-61
24535487-13	2014	CONCLUSION: The CES1A2 -816C and the CYP2C19 LOF alleles were associated with attenuated platelet reactivity to clopidogrel.	clopidogrel	112-123	carboxylesterase 1 pseudogene 1	Homo sapiens	16-22
24535487-13	2014	CONCLUSION: The CES1A2 -816C and the CYP2C19 LOF alleles were associated with attenuated platelet reactivity to clopidogrel.	clopidogrel	112-123	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-44
24336891-8	2014	Platelet surface expression of CX3CR1 was increased in CHF rats, who displayed an impaired response to clopidogrel (platelet reactivity to ADP: CHF 30 +- 22%; Sham: 8 +- 5%, p&lt;0.05).	clopidogrel	103-114	C-X3-C motif chemokine receptor 1	Rattus norvegicus	31-37
24336891-9	2014	Similarly in humans with CHF, elevated fractalkine levels were accompanied by reduced clopidogrel responsiveness.	clopidogrel	86-97	C-X3-C motif chemokine ligand 1	Homo sapiens	39-50
24336891-10	2014	Patients with high on-clopidogrel treatment platelet P2Y12 reactivity displayed higher fractalkine levels (1525 +- 487 pg/ml) than those with sufficient clopidogrel response (684 +- 315 pg/ml, p&lt;0.01).	clopidogrel	22-33	purinergic receptor P2Y12	Homo sapiens	53-58
24336891-10	2014	Patients with high on-clopidogrel treatment platelet P2Y12 reactivity displayed higher fractalkine levels (1525 +- 487 pg/ml) than those with sufficient clopidogrel response (684 +- 315 pg/ml, p&lt;0.01).	clopidogrel	22-33	C-X3-C motif chemokine ligand 1	Homo sapiens	87-98
24336891-12	2014	Fractalkine diminished endothelial function beyond the impairment already observed in CHF and was associated with a reduced responsiveness to the platelet inhibitor clopidogrel.	clopidogrel	165-176	C-X3-C motif chemokine ligand 1	Homo sapiens	0-11
24336898-0	2014	Thrombin-induced platelet-fibrin clot strength: relation to high on-clopidogrel platelet reactivity, genotype, and post-percutaneous coronary intervention outcomes.	clopidogrel	68-79	coagulation factor II, thrombin	Homo sapiens	0-8
24440142-0	2014	Impact of CYP2C19 polymorphism and proton pump inhibitors on platelet reactivity to clopidogrel and clinical outcomes following stent implantation.	clopidogrel	84-95	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-17
24986003-9	2014	Previous antiplatelet agent - clopidogrel is ineffective due to genetic polymorphism in P450 (polymorphism of CYP2C19 and CYP3A4 allele - *1 isoforms in function, *2 and *3 non-functioning alleles) and due to failure of metabolic conversion to active molecule.	clopidogrel	30-41	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	110-117
24986003-9	2014	Previous antiplatelet agent - clopidogrel is ineffective due to genetic polymorphism in P450 (polymorphism of CYP2C19 and CYP3A4 allele - *1 isoforms in function, *2 and *3 non-functioning alleles) and due to failure of metabolic conversion to active molecule.	clopidogrel	30-41	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	122-128
24638017-12	2014	Clopidogrel also prevented vascular remodeling, evidenced by augmented media thickness in aortas from Ang II-hypertensive rats.	clopidogrel	0-11	angiogenin	Rattus norvegicus	102-105
24638017-13	2014	Clopidogrel has beneficial effects on the aortic endothelium of Ang II-hypertensive rats, but its effects do not seem to be directly related to the presence of P2Y12 receptors in this vessel.	clopidogrel	0-11	angiogenin	Rattus norvegicus	64-67
24477682-0	2014	Clopidogrel preserves whole kidney autoregulatory behavior in ANG II-induced hypertension.	clopidogrel	0-11	angiogenin	Rattus norvegicus	62-65
24477682-1	2014	This study tested the hypothesis that P2Y12 receptor blockade with clopidogrel preserves renal autoregulatory ability during ANG II-induced hypertension.	clopidogrel	67-78	purinergic receptor P2Y12	Rattus norvegicus	38-43
24477682-1	2014	This study tested the hypothesis that P2Y12 receptor blockade with clopidogrel preserves renal autoregulatory ability during ANG II-induced hypertension.	clopidogrel	67-78	angiotensinogen	Rattus norvegicus	125-131
24477682-2	2014	Clopidogrel was administered orally to male Sprague-Dawley rats chronically infused with ANG II.	clopidogrel	0-11	angiotensinogen	Rattus norvegicus	89-95
24477682-5	2014	However, clopidogrel treatment preserved autoregulatory behavior in ANG II-treated rats to levels indistinguishable from normotensive sham-operated (sham) rats (autoregulatory index: 0.04 +- 0.14).	clopidogrel	9-20	angiogenin	Rattus norvegicus	68-71
24477682-7	2014	Clopidogrel significantly reduced renal infiltration of T cells by 39 +- 9% and prevented interstitial artery thickening, ANG II-induced damage to the glomerular basement membrane, deposition of collagen type I, and tubulointerstitial fibrosis, despite the maintenance of hypertension.	clopidogrel	0-11	angiotensinogen	Rattus norvegicus	122-128
24477682-8	2014	These data demonstrate that systemic P2Y12 receptor blockade with clopidogrel protects against impairment of autoregulatory behavior and renal vascular injury in ANG II-induced hypertension, possibly by reducing renal T cell infiltration.	clopidogrel	66-77	purinergic receptor P2Y12	Rattus norvegicus	37-42
24477682-8	2014	These data demonstrate that systemic P2Y12 receptor blockade with clopidogrel protects against impairment of autoregulatory behavior and renal vascular injury in ANG II-induced hypertension, possibly by reducing renal T cell infiltration.	clopidogrel	66-77	angiotensinogen	Rattus norvegicus	162-168
24609741-2	2014	Thus, GP IIb-IIIa inhibitors could favour endogenous thrombolysis by reducing thrombus growth and preventing thrombus re-formation through competitive inhibition with fibrinogen and, due to their mechanism of action, are likely to have a more profound antiplatelet effect with more rapid onset than conventional antiplatelet agents, such as aspirin or clopidogrel.	clopidogrel	352-363	integrin subunit alpha 2b	Homo sapiens	6-12
24630752-3	2014	Until recently, clopidogrel was the key P2Y12 antagonist advocated, but due to several limitations as an antiplatelet agent, newer drugs with more predictable, rapid and potent effects have been developed.	clopidogrel	16-27	purinergic receptor P2Y12	Homo sapiens	40-45
23834376-6	2014	For carriers of the PlA2 allele, OR 0.924 (n = 2318; 95% CI 0.743, 1.151; P = 0.481) was observed for resistance to any antiplatelet drug, OR 0.862 (n = 2085; 95% CI 0.685, 1.086; P = 0.208) for resistance to aspirin and OR 1.429 (n = 233; 95% CI 0.791, 2.582; P = 0.237) for resistance to clopidogrel.	clopidogrel	290-301	phospholipase A2 group IB	Homo sapiens	20-24
24323317-10	2014	Furthermore, blocking EP3 reduced murine pulmonary embolism and intensified platelet inhibition by clopidogrel leaving tail bleeding times unchanged.	clopidogrel	99-110	prostaglandin E receptor 3 (subtype EP3)	Mus musculus	22-25
24322971-4	2014	Nevertheless, VKORC1, CYP2C9, and CYP4F2 variants have been associated with warfarin dose requirements, and CYP2C19 variants have been associated with perturbed antiplatelet response to clopidogrel.	clopidogrel	186-197	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	108-115
24632932-5	2014	PARTICIPANTS 18 patients taking clopidogrel, a drug metabolized by CYP2C19.	clopidogrel	32-43	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	67-74
24670466-0	2014	[Feasibility of monitoring clopidogrel resistance with flow cytometric analysis of platelet vasodilator stimulated phosphoprotein phosphorylation].	clopidogrel	27-38	vasodilator stimulated phosphoprotein	Homo sapiens	92-129
24670466-1	2014	OBJECTIVE: To evaluate the feasibility of monitoring clopidogrel resistance with flow cytometric analysis of platelet vasodilator stimulated phosphoprotein (VASP) phosphorylation.	clopidogrel	53-64	vasodilator stimulated phosphoprotein	Homo sapiens	118-155
24670466-1	2014	OBJECTIVE: To evaluate the feasibility of monitoring clopidogrel resistance with flow cytometric analysis of platelet vasodilator stimulated phosphoprotein (VASP) phosphorylation.	clopidogrel	53-64	vasodilator stimulated phosphoprotein	Homo sapiens	157-161
24670466-6	2014	CONCLUSION: Flow cytometric analysis of VASP phosphorylation is a more reliable test to specifically evaluate clopidogrel resistance.	clopidogrel	110-121	vasodilator stimulated phosphoprotein	Homo sapiens	40-44
24624918-4	2014	The most consistent results are on clopidogrel, where CYP2C19 loss-of-function alleles are associated with stent thrombosis events.	clopidogrel	35-46	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	54-61
24030523-0	2014	Proton pump inhibitors and clopidogrel: an association to avoid?	clopidogrel	27-38	ATPase H+/K+ transporting non-gastric alpha2 subunit	Homo sapiens	0-11
24357254-1	2014	Smoking enhances the P2Y12 receptor inhibitory effects of clopidogrel.	clopidogrel	58-69	purinergic receptor P2Y12	Homo sapiens	21-26
24357254-3	2014	However, the impact of cigarette smoking on platelet P2Y12 receptor binding in clopidogrel-treated patients with coronary artery disease (CAD) is unknown.	clopidogrel	79-90	purinergic receptor P2Y12	Homo sapiens	53-58
24357254-5	2014	P2Y12 receptor binding activity was determined by radioligand receptor binding prior and 24 h after a 600-mg loading dose of clopidogrel.	clopidogrel	125-136	purinergic receptor P2Y12	Homo sapiens	0-5
24357254-7	2014	After a 600-mg loading dose of clopidogrel, smokers showed a 6.4-fold reduction in P2Y12 receptor binding indicative of marked clopidogrel-mediated blockade, while there were minimal changes among nonsmokers.	clopidogrel	31-42	purinergic receptor P2Y12	Homo sapiens	83-88
24357254-7	2014	After a 600-mg loading dose of clopidogrel, smokers showed a 6.4-fold reduction in P2Y12 receptor binding indicative of marked clopidogrel-mediated blockade, while there were minimal changes among nonsmokers.	clopidogrel	127-138	purinergic receptor P2Y12	Homo sapiens	83-88
24395495-9	2014	Thrombin and fibrin activity assessed by clot generation parameters were all nonsignificantly different but showed trends towards enhanced antithrombotic activity with clopidogrel among heavy smokers.	clopidogrel	168-179	coagulation factor II, thrombin	Homo sapiens	0-8
24362676-7	2014	CLINICAL RELEVANCE: Mild therapeutic hypothermia is associated with impaired response to clopidogrel therapy, which might contribute to increase the risk of thrombotic events in ACS comatose patients undergoing PCI.	clopidogrel	89-100	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	178-181
24359966-5	2014	Aggregation &gt;50% induced by 5 muM ADP was indexed with high on-clopidogrel treatment platelet reactivity.	clopidogrel	66-77	latexin	Homo sapiens	33-36
24172891-1	2014	The current standard of antiplatelet therapy of patients after myocardial infarction includes the P2Y12 receptor antagonists clopidogrel, prasugrel or ticagrelor.	clopidogrel	125-136	purinergic receptor P2Y12	Homo sapiens	98-103
24211510-7	2014	RESULTS: The ADP-stimulated platelet fibrinogen binding, P-selectin expression, and platelet aggregation were lower on treatment with clopidogrel compared with baseline (p &lt; 0.0001), but returned to baseline levels by 7 days after discontinuation.	clopidogrel	134-145	fibrinogen beta chain	Homo sapiens	37-47
24211510-7	2014	RESULTS: The ADP-stimulated platelet fibrinogen binding, P-selectin expression, and platelet aggregation were lower on treatment with clopidogrel compared with baseline (p &lt; 0.0001), but returned to baseline levels by 7 days after discontinuation.	clopidogrel	134-145	selectin P	Homo sapiens	57-67
24170388-10	2014	Elevated hs-TnT predicts substantial benefit of ticagrelor over clopidogrel both in invasively and noninvasively managed patients, but no apparent benefit was seen at normal hs-TnT.	clopidogrel	64-75	troponin T1, slow skeletal type	Homo sapiens	12-15
24636047-7	2014	One of the main factors affecting the efficacy of Clopidogrel is the phenotype associated with polymorphisms in the gene CYP 2C9.	clopidogrel	50-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-128
25043069-7	2014	A quantitative interaction effect was observed between clopidogrel pretreatment strategy and CYP2C19 genotype (P = 0.001).	clopidogrel	55-66	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	93-100
24189502-1	2014	BACKGROUND: The prevalence of contraindications/special warnings and precautions (CON/SWP) for clopidogrel, prasugrel and ticagrelor use is not adequately studied and might affect P2Y12 inhibitor choice in acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI).	clopidogrel	95-106	purinergic receptor P2Y12	Homo sapiens	180-185
23782140-13	2014	In contrast, antisecretory drugs such as a proton pump inhibitor and histamine H2 receptor antagonists markedly suppressed the gastric bleeding and lesion responses to ASA plus clopidogrel under histamine-stimulated acid secretion, but had no effect on the responses to acidified ASA plus clopidogrel.	clopidogrel	177-188	histamine receptor H 2	Rattus norvegicus	69-90
23782140-13	2014	In contrast, antisecretory drugs such as a proton pump inhibitor and histamine H2 receptor antagonists markedly suppressed the gastric bleeding and lesion responses to ASA plus clopidogrel under histamine-stimulated acid secretion, but had no effect on the responses to acidified ASA plus clopidogrel.	clopidogrel	289-300	histamine receptor H 2	Rattus norvegicus	69-90
23885646-1	2014	Clopidogrel is a thienopyridine that selectively and irreversibly inhibits the ADP purinergic receptor P2Y12 and the subsequent ADP-mediated platelet activation.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	103-108
24988246-3	2014	Polymorphisms of the CES1 gene have been reported to affect the metabolism of dabigatran etexilate, methylphenidate, oseltamivir, imidapril, and clopidogrel, whereas variants of the CES2 gene have been found to affect aspirin and irinotecan.	clopidogrel	145-156	carboxylesterase 1	Homo sapiens	21-25
24096684-5	2014	RESULTS: More men were dispensed clopidogrel although the reported bleeding event risk after adjustment for number of patients exposed was higher in women (RR 1.40; 95 % CI, 1.00-1.96).	clopidogrel	33-44	ribonucleotide reductase catalytic subunit M1	Homo sapiens	156-160
24337310-2	2014	Dual antiplatelet therapy composed of aspirin plus a third generation P2Y12 inhibitor (prasugrel or ticagrelor) represents the gold standard, while aspirin plus second generation P2Y12 inhibitor (clopidogrel) may be used as an alternative in the presence of contraindications for third generation P2Y12 inhibitors and/or a high risk of bleeding.	clopidogrel	196-207	purinergic receptor P2Y12	Homo sapiens	179-184
24337310-2	2014	Dual antiplatelet therapy composed of aspirin plus a third generation P2Y12 inhibitor (prasugrel or ticagrelor) represents the gold standard, while aspirin plus second generation P2Y12 inhibitor (clopidogrel) may be used as an alternative in the presence of contraindications for third generation P2Y12 inhibitors and/or a high risk of bleeding.	clopidogrel	196-207	purinergic receptor P2Y12	Homo sapiens	179-184
24492689-6	2014	Clopidogrel resistance was defined as a P2Y12 Reaction Units (PRU) value of &gt;230 and/or % inhibition &lt;20%.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	40-45
24581091-2	2014	Genetic polymorphisms in CYP2C19 gene involved in hepatic activation of clopidogrel leads to clopidogrel non-responsiveness and may influence clinical outcomes.	clopidogrel	72-83	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
24581091-2	2014	Genetic polymorphisms in CYP2C19 gene involved in hepatic activation of clopidogrel leads to clopidogrel non-responsiveness and may influence clinical outcomes.	clopidogrel	93-104	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
24581091-4	2014	METHODS: We studied 110 consecutive patients (mean age 55.7 +- 10.7 years; 90% male) taking clopidogrel with angiographically proven CAD for various genetic polymorphisms in CYP2C19 gene.	clopidogrel	92-103	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	174-181
25400177-7	2014	Clopidogrel resistance was defined as a P2Y12 Reaction Units (PRU) value &gt;230 and/or % inhibition &lt;20%.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	40-45
24942407-1	2014	AIM: Proton pump inhibitor (PPI) therapy has been shown to attenuate the antiplatelet effects of clopidogrel.	clopidogrel	97-108	ATPase H+/K+ transporting non-gastric alpha2 subunit	Homo sapiens	5-16
24500235-1	2014	Clopidogrel is a prodrug that undergoes extensive enteric clearance and requires two-stage hepatic activation by cytochrome P450 (CYP) enzymes.	clopidogrel	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	113-128
24500235-1	2014	Clopidogrel is a prodrug that undergoes extensive enteric clearance and requires two-stage hepatic activation by cytochrome P450 (CYP) enzymes.	clopidogrel	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	130-133
25587544-8	2014	ACR was significantly correlated with the presence of cardiovascular disease, hypertension, and HbA1c levels and the administration of clopidogrel and ACEi or ARBs.	clopidogrel	135-146	acrosin	Homo sapiens	0-3
24406062-3	2014	Whereas the irreversible P2Y12 receptor inhibitors clopidogrel and prasugrel are prodrugs requiring cytochrome P450 (CYP) enzymes for metabolic activation, such activation is not necessary for the direct-acting reversible P2Y12 receptor inhibitor ticagrelor.	clopidogrel	51-62	purinergic receptor P2Y12	Homo sapiens	25-30
24406062-7	2014	In general, concomitant administration of P2Y12 receptor antagonists and strong inhibitors or inducers of CYP3A/CYP2C19 should be performed with caution in patients treated with clopidogrel/ticagrelor.	clopidogrel	178-189	purinergic receptor P2Y12	Homo sapiens	42-47
24406062-7	2014	In general, concomitant administration of P2Y12 receptor antagonists and strong inhibitors or inducers of CYP3A/CYP2C19 should be performed with caution in patients treated with clopidogrel/ticagrelor.	clopidogrel	178-189	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	112-119
24846362-12	2014	However, mean healthcare costs at a one year horizon (excluding drug costs and concomitant drugs) were 690 PLN higher for patients treated with clopidogrel.	clopidogrel	144-155	phospholamban	Homo sapiens	107-110
25060201-12	2014	CONCLUSIONS: In patients hyporesponsive to a routine clopidogrel doses the potency of additional LD and higher MD of clopidogrel is compromised by presence of CYP2C19*2 allele.	clopidogrel	53-64	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	159-166
25060201-12	2014	CONCLUSIONS: In patients hyporesponsive to a routine clopidogrel doses the potency of additional LD and higher MD of clopidogrel is compromised by presence of CYP2C19*2 allele.	clopidogrel	117-128	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	159-166
24518848-2	2014	Two recent meta-analyses concluded that the efficacy of the P2Y12 receptor antagonist clopidogrel in reducing cardiovascular events is more pronounced in smokers than in non-smokers.	clopidogrel	86-97	purinergic receptor P2Y12	Homo sapiens	60-65
24518848-3	2014	Most probably, this is due to induction of cytochrome p450 1A2 by smoking, which accelerates conversion of clopidogrel to its active metabolite.	clopidogrel	107-118	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	43-62
23527528-0	2014	Glucose intolerance and insulin resistance as predictors of low platelet response to clopidogrel in patients with minor ischemic stroke or TIA.	clopidogrel	85-96	insulin	Homo sapiens	24-31
23971745-1	2014	Published data suggests that the presence of CYP2C19*2 or *3 loss of function (LOF) alleles is indicative of increased platelet aggregation and a higher risk of adverse cardiovascular events after clopidogrel administration.	clopidogrel	197-208	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	45-52
24088578-1	2014	AIM: Carriers of the reduced-function CYP2C19 allele receiving dual antiplatelet therapy (DAPT) with aspirin and clopidogrel exhibit diminished platelet inhibition and an increased risk of events.	clopidogrel	113-124	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	38-45
26118162-0	2013	Comparison of P2Y12 receptor inhibition by clopidogrel and prasugrel in patients undergoing percutaneous coronary intervention.	clopidogrel	43-54	purinergic receptor P2Y12	Homo sapiens	14-19
26118162-2	2013	Clopidogrel and prasugrel act on P2Y12 platelet surface receptors.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	33-38
24745016-0	2014	Association of P2Y12 gene promoter DNA methylation with the risk of clopidogrel resistance in coronary artery disease patients.	clopidogrel	68-79	purinergic receptor P2Y12	Homo sapiens	15-20
24745016-1	2014	BACKGROUND: Clopidogrel inhibits the ADP receptor P2Y12 to keep down the platelet aggregation.	clopidogrel	12-23	purinergic receptor P2Y12	Homo sapiens	50-55
24745016-2	2014	The goal of our study is to investigate the contribution of P2Y12 promoter DNA methylation to the risk of clopidogrel resistance (CR).	clopidogrel	106-117	purinergic receptor P2Y12	Homo sapiens	60-65
24176022-7	2014	When clopidogrel response was analyzed as continuous variable, there was a good correlation between the different tests: LTA/VN (R(2 )= 0.642, p &lt; 0.001), LTA/VASP (R(2 )= 0.409, p &lt; 0.001) and VN/VASP (R(2 )= 0.616, p &lt; 0.001).	clopidogrel	5-16	vasodilator stimulated phosphoprotein	Homo sapiens	203-207
24433232-0	2014	A platelet P-selectin test predicts adverse cardiovascular events in patients with acute coronary syndromes treated with aspirin and clopidogrel.	clopidogrel	133-144	selectin P	Homo sapiens	11-21
24799926-5	2014	Currently, the most important role in the process of platelet inhibition is played by ADP P2Y12 blockers: clopidogrel, prasugrel and ticagrelor.	clopidogrel	106-117	purinergic receptor P2Y12	Homo sapiens	90-95
24751429-4	2014	Loss-of-function polymorphisms of CYP2C19, the gene encoding for the key enzyme in the metabolism of clopidogrel, are associated with reduced formation of the active metabolite of clopidogrel, a lower pharmacodynamic effect of the drug and a corresponding increase in adverse cardiovascular events.	clopidogrel	101-112	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	34-41
24751429-4	2014	Loss-of-function polymorphisms of CYP2C19, the gene encoding for the key enzyme in the metabolism of clopidogrel, are associated with reduced formation of the active metabolite of clopidogrel, a lower pharmacodynamic effect of the drug and a corresponding increase in adverse cardiovascular events.	clopidogrel	180-191	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	34-41
25518511-12	2014	Examining the effects of genetic variations in cytochrome P450 isoform CYP2C19 (a clopidogrel metabolizer) revealed the enhanced aggregation stimulated with 20 mumol of ADP in the carriers of slowly clopidogrel-metabolizing haplotype of CYP2C19 (differences were found on days 3-5 as compared to rapidly and routinely metabolizing haplotypes).	clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
25518511-12	2014	Examining the effects of genetic variations in cytochrome P450 isoform CYP2C19 (a clopidogrel metabolizer) revealed the enhanced aggregation stimulated with 20 mumol of ADP in the carriers of slowly clopidogrel-metabolizing haplotype of CYP2C19 (differences were found on days 3-5 as compared to rapidly and routinely metabolizing haplotypes).	clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	237-244
25518511-12	2014	Examining the effects of genetic variations in cytochrome P450 isoform CYP2C19 (a clopidogrel metabolizer) revealed the enhanced aggregation stimulated with 20 mumol of ADP in the carriers of slowly clopidogrel-metabolizing haplotype of CYP2C19 (differences were found on days 3-5 as compared to rapidly and routinely metabolizing haplotypes).	clopidogrel	199-210	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
25518511-12	2014	Examining the effects of genetic variations in cytochrome P450 isoform CYP2C19 (a clopidogrel metabolizer) revealed the enhanced aggregation stimulated with 20 mumol of ADP in the carriers of slowly clopidogrel-metabolizing haplotype of CYP2C19 (differences were found on days 3-5 as compared to rapidly and routinely metabolizing haplotypes).	clopidogrel	199-210	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	237-244
24453831-0	2013	Von Willebrand factor antigen predicts response to double dose of aspirin and clopidogrel by PFA-100 in patients undergoing primary angioplasty for ST elevation myocardial infarction.	clopidogrel	78-89	von Willebrand factor	Homo sapiens	0-21
24453831-3	2013	The objective of this study was to verify the effect of double dose (DD) of aspirin and clopidogrel on HPR detected by PFA-100 and its relation to VWF and to its regulatory metalloprotease ADAMTS-13.	clopidogrel	88-99	von Willebrand factor	Homo sapiens	147-150
24453831-3	2013	The objective of this study was to verify the effect of double dose (DD) of aspirin and clopidogrel on HPR detected by PFA-100 and its relation to VWF and to its regulatory metalloprotease ADAMTS-13.	clopidogrel	88-99	ADAM metallopeptidase with thrombospondin type 1 motif 13	Homo sapiens	189-198
23887740-6	2013	Clopidogrel treatment inhibited Ang II infusion-induced accumulation of alpha-SMA(+) myofibroblasts and cardiac fibrosis (4.17 +- 1.26 vs. 1.46 +- 0.81, p &lt; 0.05).	clopidogrel	0-11	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	32-38
23773422-0	2013	Epidemiology of CYP3A4-mediated clopidogrel drug-drug interactions and their clinical consequences.	clopidogrel	32-43	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	16-22
23887740-9	2013	Acute injection of Ang II or PE stimulated platelet activation and platelet-leukocyte conjugation, which were abolished by clopidogrel treatment.	clopidogrel	123-134	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	19-25
23773422-2	2013	The objective of this study was to evaluate the prevalence and clinical consequences of potential drug-drug interactions of clopidogrel with drugs affecting CYP3A4 activity.	clopidogrel	124-135	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	157-163
23773422-5	2013	RESULTS: In the nationwide analysis, 6.1%, 1.0%, and 20.8% of the clopidogrel-treated patients were exposed to concomitant use of CYP3A4 inhibitors, CYP3A4 inducers, and atorvastatin, respectively.	clopidogrel	66-77	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	130-136
23773422-5	2013	RESULTS: In the nationwide analysis, 6.1%, 1.0%, and 20.8% of the clopidogrel-treated patients were exposed to concomitant use of CYP3A4 inhibitors, CYP3A4 inducers, and atorvastatin, respectively.	clopidogrel	66-77	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	149-155
23773422-12	2013	CYP3A4 inhibitors and atorvastatin may reduce bleedings in clopidogrel users.	clopidogrel	59-70	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
23887740-10	2013	CONCLUSION: Thus, inhibition of platelet activation by clopidogrel prevents cardiac inflammation and fibrosis in response to Ang II.	clopidogrel	55-66	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	125-131
23770199-6	2013	Clopidogrel (10 and 100 muM) was also toxic for HepG2 cells expressing human CYP3A4 (HepG2/CYP3A4) and HepG2 cells co-incubated with CYP3A4 supersomes (HepG2/CYP3A4 supersome), but not for wild-type HepG2 cells (HepG2/wt).	clopidogrel	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	91-97
23770199-7	2013	Clopidogrel (100 muM) decreased the cellular glutathione content in HepG2/CYP3A4 supersome and triggered an oxidative stress reaction (10 and 100 microM) in HepG2/CYP3A4, but not in HepG2/wt.	clopidogrel	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	74-80
23413998-9	2013	The platelet reactivity index measured by the flow cytometric VASP method was 36.8% lower when clopidogrel was administered in conjunction with fluoxetine.	clopidogrel	95-106	vasodilator stimulated phosphoprotein	Homo sapiens	62-66
23770199-7	2013	Clopidogrel (100 muM) decreased the cellular glutathione content in HepG2/CYP3A4 supersome and triggered an oxidative stress reaction (10 and 100 microM) in HepG2/CYP3A4, but not in HepG2/wt.	clopidogrel	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	163-169
23770199-8	2013	Glutathione depletion significantly increased the cytotoxicity of clopidogrel (10 and 100 microM) in HepG2/CYP3A4 supersome.	clopidogrel	66-77	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	107-113
23770199-9	2013	Co-incubation with 1 muM ketoconazole or 10mM glutathione almost completely prevented the cytotoxic effect of clopidogrel in HepG2/CYP3A4 and HepG2/CYP3A4 supersome.	clopidogrel	110-121	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	131-137
23770199-5	2013	In primary human hepatocytes, clopidogrel (10 and 100 muM) was cytotoxic only after cytochrome P450 (CYP) induction by rifampicin.	clopidogrel	30-41	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	84-99
23770199-9	2013	Co-incubation with 1 muM ketoconazole or 10mM glutathione almost completely prevented the cytotoxic effect of clopidogrel in HepG2/CYP3A4 and HepG2/CYP3A4 supersome.	clopidogrel	110-121	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	148-154
23770199-5	2013	In primary human hepatocytes, clopidogrel (10 and 100 muM) was cytotoxic only after cytochrome P450 (CYP) induction by rifampicin.	clopidogrel	30-41	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	101-104
23770199-10	2013	HepG2/CYP3A4 incubated with 100 muM clopidogrel showed mitochondrial damage and cytochrome c release, eventually promoting apoptosis and/or necrosis.	clopidogrel	36-47	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	6-12
23770199-6	2013	Clopidogrel (10 and 100 muM) was also toxic for HepG2 cells expressing human CYP3A4 (HepG2/CYP3A4) and HepG2 cells co-incubated with CYP3A4 supersomes (HepG2/CYP3A4 supersome), but not for wild-type HepG2 cells (HepG2/wt).	clopidogrel	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	77-83
23770199-10	2013	HepG2/CYP3A4 incubated with 100 muM clopidogrel showed mitochondrial damage and cytochrome c release, eventually promoting apoptosis and/or necrosis.	clopidogrel	36-47	cytochrome c, somatic	Homo sapiens	80-92
23770199-6	2013	Clopidogrel (10 and 100 muM) was also toxic for HepG2 cells expressing human CYP3A4 (HepG2/CYP3A4) and HepG2 cells co-incubated with CYP3A4 supersomes (HepG2/CYP3A4 supersome), but not for wild-type HepG2 cells (HepG2/wt).	clopidogrel	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	91-97
23770199-6	2013	Clopidogrel (10 and 100 muM) was also toxic for HepG2 cells expressing human CYP3A4 (HepG2/CYP3A4) and HepG2 cells co-incubated with CYP3A4 supersomes (HepG2/CYP3A4 supersome), but not for wild-type HepG2 cells (HepG2/wt).	clopidogrel	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	91-97
23770199-12	2013	In conclusion, clopidogrel incubated with CYP3A4 is associated with the formation of metabolites that are toxic for hepatocytes and can be trapped by glutathione.	clopidogrel	15-26	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	42-48
23770199-13	2013	High CYP3A4 activity and low cellular glutathione stores may be risk factors for clopidogrel-associated hepatocellular toxicity.	clopidogrel	81-92	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	5-11
24009042-8	2013	For clopidogrel, genetic variants in CYP2C19, but not ABCB1 or PON1, affected PK and PD.	clopidogrel	4-15	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-44
24378836-3	2013	There are growing evidences that clopidogrel response variability is associated with cytochrome P450 (CYP) enzyme genetic polymorphisms, primarily CYP2C19 which is responsible for the conversion of clopidogrel into its active metabolite.	clopidogrel	33-44	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	85-100
24378836-3	2013	There are growing evidences that clopidogrel response variability is associated with cytochrome P450 (CYP) enzyme genetic polymorphisms, primarily CYP2C19 which is responsible for the conversion of clopidogrel into its active metabolite.	clopidogrel	33-44	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	102-105
24378836-3	2013	There are growing evidences that clopidogrel response variability is associated with cytochrome P450 (CYP) enzyme genetic polymorphisms, primarily CYP2C19 which is responsible for the conversion of clopidogrel into its active metabolite.	clopidogrel	33-44	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	147-154
24378836-3	2013	There are growing evidences that clopidogrel response variability is associated with cytochrome P450 (CYP) enzyme genetic polymorphisms, primarily CYP2C19 which is responsible for the conversion of clopidogrel into its active metabolite.	clopidogrel	198-209	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	85-100
24378836-3	2013	There are growing evidences that clopidogrel response variability is associated with cytochrome P450 (CYP) enzyme genetic polymorphisms, primarily CYP2C19 which is responsible for the conversion of clopidogrel into its active metabolite.	clopidogrel	198-209	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	102-105
24378836-3	2013	There are growing evidences that clopidogrel response variability is associated with cytochrome P450 (CYP) enzyme genetic polymorphisms, primarily CYP2C19 which is responsible for the conversion of clopidogrel into its active metabolite.	clopidogrel	198-209	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	147-154
24378836-5	2013	Yet, CYP2C19 status explains only 12% of clopidogrel response variability, indicating that genetic variants other than CYP2C19 might be important.	clopidogrel	41-52	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	5-12
24378836-6	2013	Clopidogrel undergoes intestinal efflux via P-glycoprotein, encoded by the ABCB1 gene.	clopidogrel	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	44-58
24378836-6	2013	Clopidogrel undergoes intestinal efflux via P-glycoprotein, encoded by the ABCB1 gene.	clopidogrel	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	75-80
24378836-8	2013	Similarly, a polymorphism in the gene encoding PON1, a rate-limiting enzyme for clopidogrel bioactivation, also affects the response to clopidogrel.	clopidogrel	80-91	paraoxonase 1	Homo sapiens	47-51
24378836-8	2013	Similarly, a polymorphism in the gene encoding PON1, a rate-limiting enzyme for clopidogrel bioactivation, also affects the response to clopidogrel.	clopidogrel	136-147	paraoxonase 1	Homo sapiens	47-51
24378837-2	2013	However, clopidogrel is associated with great variability in antiplatelet response, mostly caused by variable efficacy of cytochrome P450 (CYP) isoforms, which convert clopidogrel to its active metabolite in a two-step process.	clopidogrel	9-20	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	122-137
24378837-2	2013	However, clopidogrel is associated with great variability in antiplatelet response, mostly caused by variable efficacy of cytochrome P450 (CYP) isoforms, which convert clopidogrel to its active metabolite in a two-step process.	clopidogrel	9-20	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	139-142
24378837-2	2013	However, clopidogrel is associated with great variability in antiplatelet response, mostly caused by variable efficacy of cytochrome P450 (CYP) isoforms, which convert clopidogrel to its active metabolite in a two-step process.	clopidogrel	168-179	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	122-137
24378837-2	2013	However, clopidogrel is associated with great variability in antiplatelet response, mostly caused by variable efficacy of cytochrome P450 (CYP) isoforms, which convert clopidogrel to its active metabolite in a two-step process.	clopidogrel	168-179	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	139-142
24378838-7	2013	Importantly, both clopidogrel and prasugrel are prodrugs, i.e., they need to be converted in vivo into active metabolites that selectively and irreversibly bind the P2Y12 receptor.	clopidogrel	18-29	purinergic receptor P2Y12	Homo sapiens	165-170
24253460-4	2013	Genetic mutations in the CYP2C19 cytochrome (involved in the metabolism of clopidogrel and many other drugs) may lead to a lower concentration of active metabolites of the drug.	clopidogrel	75-86	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
24279856-0	2013	Cost-effectiveness of using CYP2C19 genotype to guide selection of clopidogrel or ticagrelor in Australia.	clopidogrel	67-78	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
24279856-1	2013	AIMS: This study aims to assess the cost-effectiveness in Australia of screening CYP2C19 loss-of-function (LoF) alleles to guide selection of clopidogrel or ticagrelor for individuals with acute coronary syndrome who are likely to undergo coronary stenting.	clopidogrel	142-153	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	81-88
24096929-5	2013	All of these options have demonstrated pharmacologic benefit in terms of greater antiplatelet effects compared with standard clopidogrel dosing in patients with high on-treatment platelet reactivity or a genetic loss-of-function variant of CYP2C19, the main enzyme responsible for clopidogrel activation.	clopidogrel	281-292	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	240-247
24070598-12	2013	There were significantly more clopidogrel low responders (PRU value&gt;230) in the ACS group (38% vs. 18%; p=0.04).	clopidogrel	30-41	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	83-86
24070598-13	2013	CONCLUSION: Our study confirms that initial clinical presentation, especially ACS, is a strong predictor of clopidogrel low response; this suggests that the evolution of coronary artery disease for one patient influences the clopidogrel response over time.	clopidogrel	108-119	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	78-81
24070598-13	2013	CONCLUSION: Our study confirms that initial clinical presentation, especially ACS, is a strong predictor of clopidogrel low response; this suggests that the evolution of coronary artery disease for one patient influences the clopidogrel response over time.	clopidogrel	225-236	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	78-81
24192573-1	2013	BACKGROUND: Patients treated with clopidogrel who have &gt;=1 loss of function alleles for CYP2C19 have an increased risk for adverse cardiovascular events.	clopidogrel	34-45	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	91-98
24192573-4	2013	METHODS AND RESULTS: Patients with recent acute coronary syndrome or percutaneous coronary intervention prescribed clopidogrel were offered CYP2C19 testing.	clopidogrel	115-126	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	140-147
23992465-2	2013	However, studies have observed a variable blockade of the P2Y12 adenosine diphosphate receptor between patients following clopidogrel intake.	clopidogrel	122-133	purinergic receptor P2Y12	Homo sapiens	58-63
24012947-0	2013	An allele-specific PCR system for rapid detection and discrimination of the CYP2C19*4A, *4B, and *17 alleles: implications for clopidogrel response testing.	clopidogrel	127-138	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	76-83
24012947-1	2013	CYP2C19 is involved in the metabolism of clinically relevant drugs, including the antiplatelet prodrug clopidogrel, which has prompted interest in clinical CYP2C19 genotyping.	clopidogrel	103-114	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
24012947-1	2013	CYP2C19 is involved in the metabolism of clinically relevant drugs, including the antiplatelet prodrug clopidogrel, which has prompted interest in clinical CYP2C19 genotyping.	clopidogrel	103-114	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	156-163
24012947-7	2013	In conclusion, this rapid and robust allele-specific PCR assay can refine CYP2C19 genotyping and metabolizer phenotype classification by determining the phase of the defining *17 and *4 variants, which may have utility when testing CYP2C19 for clopidogrel response.	clopidogrel	244-255	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	74-81
24012947-7	2013	In conclusion, this rapid and robust allele-specific PCR assay can refine CYP2C19 genotyping and metabolizer phenotype classification by determining the phase of the defining *17 and *4 variants, which may have utility when testing CYP2C19 for clopidogrel response.	clopidogrel	244-255	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	232-239
24262612-3	2013	High on-treatment platelet reactivity, which is common in clopidogrel-treated patients, and its clinical implications led to the development of the more effective platelet P2Y12 inhibitors prasugrel (a third-generation thienopyridine) and ticagrelor (a cyclopentyl-triazolo-pyrimidine).	clopidogrel	58-69	purinergic receptor P2Y12	Homo sapiens	172-177
23925438-1	2013	A new ELISA technique has been developed to measure the vasodilator-associated stimulated phosphoprotein (VASP) platelet reactivity index (PRI) in clopidogrel-treated patients.	clopidogrel	147-158	vasodilator stimulated phosphoprotein	Homo sapiens	56-104
23925438-1	2013	A new ELISA technique has been developed to measure the vasodilator-associated stimulated phosphoprotein (VASP) platelet reactivity index (PRI) in clopidogrel-treated patients.	clopidogrel	147-158	vasodilator stimulated phosphoprotein	Homo sapiens	106-110
24080149-0	2013	Paraoxonase-1 activity affects the clopidogrel response in CYP2C19 loss-of-function carriers.	clopidogrel	35-46	paraoxonase 1	Homo sapiens	0-13
24080149-0	2013	Paraoxonase-1 activity affects the clopidogrel response in CYP2C19 loss-of-function carriers.	clopidogrel	35-46	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	59-66
24080149-1	2013	BACKGROUND: The impact of paraoxonase-1 (PON1) activity on the response to clopidogrel may differ in patients treated with drug-eluting stents (DES) in association with CYP2C19 loss-of-function (LOF) polymorphisms.	clopidogrel	75-86	paraoxonase 1	Homo sapiens	26-39
24080149-1	2013	BACKGROUND: The impact of paraoxonase-1 (PON1) activity on the response to clopidogrel may differ in patients treated with drug-eluting stents (DES) in association with CYP2C19 loss-of-function (LOF) polymorphisms.	clopidogrel	75-86	paraoxonase 1	Homo sapiens	41-45
24080149-1	2013	BACKGROUND: The impact of paraoxonase-1 (PON1) activity on the response to clopidogrel may differ in patients treated with drug-eluting stents (DES) in association with CYP2C19 loss-of-function (LOF) polymorphisms.	clopidogrel	75-86	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	169-176
24080149-11	2013	CONCLUSION: Low PON1 activity is associated with a low response to clopidogrel and a high frequency of intra-stent thrombus only in LOF carriers.	clopidogrel	67-78	paraoxonase 1	Homo sapiens	16-20
23643422-0	2013	Newly identified synergy between clopidogrel and calcium-channel blockers for blood pressure regulation possibly involves CYP2C19 rs4244285.	clopidogrel	33-44	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	122-129
24439192-0	2013	[The effects of cytochrome P450 2C19 genetic polymorphism on clopidogrel resistance and recent prognosis of patients with acute coronary syndrome].	clopidogrel	61-72	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-36
23832067-11	2013	CONCLUSION: The variation in response to ASA may be related with an increased expression of IGF1 and IGF1R, as well as a response to clopidogrel can be affected by pharmacokinetic change related to the reverse transport pathway by increased expression of ABCC3.	clopidogrel	133-144	ATP binding cassette subfamily C member 3	Homo sapiens	255-260
23432706-5	2013	On the other hand, many factors are associated with clopidogrel resistance, and recent genetic studies showed that the CYP2C19*2 genotype (loss-of-function allele) is related to poor metabolism of clopidogrel, but larger studies are needed to definitively confirm or rule out the clinical significance of this genetic effect.	clopidogrel	52-63	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	119-126
23432706-5	2013	On the other hand, many factors are associated with clopidogrel resistance, and recent genetic studies showed that the CYP2C19*2 genotype (loss-of-function allele) is related to poor metabolism of clopidogrel, but larger studies are needed to definitively confirm or rule out the clinical significance of this genetic effect.	clopidogrel	197-208	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	119-126
24080325-0	2013	Cytochrome CYP2C19 polymorphism and risk of adverse clinical events in clopidogrel-treated patients: a meta-analysis based on 23,035 subjects.	clopidogrel	71-82	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	11-18
24080325-1	2013	BACKGROUND: Previous studies have investigated the relationship between CYP2C19 polymorphism and clinical prognosis in coronary artery disease patients treated with clopidogrel, but the results were inconsistent.	clopidogrel	165-176	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	72-79
24080325-8	2013	CONCLUSION: CYP2C19 polymorphism is significantly associated with risk of adverse clinical events in clopidogrel-treated patients.	clopidogrel	101-112	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
23311679-6	2013	After activation with ADP or TRAP-6, patients with clopidogrel therapy exhibited significantly higher platelet surface expressions of P-selectin and activated GPIIb/IIIa than prasugrel-treated patients (all P &lt;= 0.001).	clopidogrel	51-62	selectin P	Homo sapiens	134-144
23311679-6	2013	After activation with ADP or TRAP-6, patients with clopidogrel therapy exhibited significantly higher platelet surface expressions of P-selectin and activated GPIIb/IIIa than prasugrel-treated patients (all P &lt;= 0.001).	clopidogrel	51-62	integrin subunit alpha 2b	Homo sapiens	159-164
23311679-7	2013	Further, high P-selectin and high GPIIb/IIIa were significantly more frequent in clopidogrel-treated patients than in patients on prasugrel therapy (all P = 0.01).	clopidogrel	81-92	selectin P	Homo sapiens	14-24
23311679-7	2013	Further, high P-selectin and high GPIIb/IIIa were significantly more frequent in clopidogrel-treated patients than in patients on prasugrel therapy (all P = 0.01).	clopidogrel	81-92	integrin subunit alpha 2b	Homo sapiens	34-39
24246616-1	2013	BACKGROUND: Several studies have suggested that proton-pump inhibitors (PPIs), mostly omeprazole, interact with clopidogrel efficacy by inhibiting the formation of its active metabolite via CYP2C19 inhibition.	clopidogrel	112-123	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	190-197
22981273-5	2013	Eleven of 25 (44%) patients had HTPR on clopidogrel (&gt;= 194 P2Y12 reaction units on the P2Y12 cartridge).	clopidogrel	40-51	purinergic receptor P2Y12	Homo sapiens	63-68
24118870-1	2013	BACKGROUND: The VerifyNow P2Y12 assay assesses the adequacy of clopidogrel therapy by measuring ADP-induced platelet activation in whole blood.	clopidogrel	63-74	purinergic receptor P2Y12	Homo sapiens	26-31
23922007-0	2013	Impact of the CYP2C19*17 polymorphism on the clinical outcome of clopidogrel therapy in Asian patients undergoing percutaneous coronary intervention.	clopidogrel	65-76	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
23993903-0	2013	PON1 Q192R genotype influences clopidogrel responsiveness by relative platelet inhibition instead of on-treatment platelet reactivity.	clopidogrel	31-42	paraoxonase 1	Homo sapiens	0-4
24019397-0	2013	CYP2C19 poor metabolizer is associated with clinical outcome of clopidogrel therapy in acute myocardial infarction but not stable angina.	clopidogrel	64-75	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
24019397-2	2013	In this context, CYP2C19 genotype leading to reduced active metabolite formation may profoundly affect the clinical outcome of clopidogrel therapy in patients with AMI compared with those with stable angina.	clopidogrel	127-138	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-24
24019397-3	2013	METHODS AND RESULTS: Effects of CYP2C19 genotypes on the clinical outcome of clopidogrel therapy were evaluated in 2188 patients (532 patients with AMI and 1656 patients with stable angina) undergoing percutaneous coronary intervention.	clopidogrel	77-88	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
24019397-9	2013	CONCLUSIONS: CYP2C19 poor metabolizer is associated with poor clinical outcome of clopidogrel therapy in Asian patients with AMI but not in those with stable angina possibly because of differential requirement of platelet suppression in patients with AMI and stable angina.	clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
24183037-7	2013	PLAA of two groups one and two days after taking aspirin or plus clopidogrel were (24.2+-31.9)% vs. (49.6+-32.6)% and (13.8+-27.2)% vs. (37.6+-37.4)%, respectively (P&lt;0.05).	clopidogrel	65-76	phospholipase A2 activating protein	Homo sapiens	0-4
23402725-0	2013	The impact of CYP2C19 genotype on cardiovascular events and platelet reactivity in patients with coronary artery disease receiving clopidogrel.	clopidogrel	131-142	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
23735342-8	2013	CONCLUSIONS: Prorated over length of follow-up PLATO-NIS mortality rates after clopidogrel far exceeded those observed in a similar medically managed patients in a TRILOGY ACS trial.	clopidogrel	79-90	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	172-175
24003163-6	2013	Platelet P2Y12 receptors are the targets of very widely used antithrombotic drugs such as clopidogrel, prasugrel, and ticagrelor.	clopidogrel	90-101	purinergic receptor P2Y12	Homo sapiens	9-14
23993903-1	2013	BACKGROUND: paraoxonase-1 (PON1) was recently identified as the crucial enzyme for clopidogrel bioactivation, with PON1 Q192R (rs662) polymorphism determining the clopidogel antiplatelet efficacy.	clopidogrel	83-94	paraoxonase 1	Homo sapiens	12-25
23993903-1	2013	BACKGROUND: paraoxonase-1 (PON1) was recently identified as the crucial enzyme for clopidogrel bioactivation, with PON1 Q192R (rs662) polymorphism determining the clopidogel antiplatelet efficacy.	clopidogrel	83-94	paraoxonase 1	Homo sapiens	27-31
23993903-3	2013	This study aimed to evaluate the impact of PON1 Q192R in parallel to that of CYP2C19*2 (rs4244285) on clopidogrel responsiveness in a cohort of Chinese patients with unstable angina pectoris.	clopidogrel	102-113	paraoxonase 1	Homo sapiens	43-47
23993903-3	2013	This study aimed to evaluate the impact of PON1 Q192R in parallel to that of CYP2C19*2 (rs4244285) on clopidogrel responsiveness in a cohort of Chinese patients with unstable angina pectoris.	clopidogrel	102-113	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	77-84
23993903-5	2013	Clopidogrel responsiveness, measured by relative platelet inhibition {RI=[(pretreatment aggregation-posttreatment aggregation at 5days)/(pretreatment aggregation)] x100%}, was assessed in relation to PON1 Q192R and CYP2C19*2 genotypes.	clopidogrel	0-11	paraoxonase 1	Homo sapiens	200-204
23993903-5	2013	Clopidogrel responsiveness, measured by relative platelet inhibition {RI=[(pretreatment aggregation-posttreatment aggregation at 5days)/(pretreatment aggregation)] x100%}, was assessed in relation to PON1 Q192R and CYP2C19*2 genotypes.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	215-222
23993903-10	2013	PON1 192 QR and RR conferred increased risks for clopidogrel non-responsiveness [OR 3.64; 95% CI (1.21-10.92), p=0.02].	clopidogrel	49-60	paraoxonase 1	Homo sapiens	0-4
23993903-12	2013	An increased risk for clopidogrel non-responsiveness was found in patients with CYP2C19*2 genotype [OR 2.02; 95% CI (1.03-3.96), p=0.04].	clopidogrel	22-33	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	80-87
23993903-13	2013	CONCLUSIONS: Both PON1 Q192R and CYP2C19*2 genotypes influence clopidogrel responsiveness, with the impact of PON1 Q192R mainly on relative platelet inhibition instead of OTPR of clopidogrel.	clopidogrel	63-74	paraoxonase 1	Homo sapiens	18-22
23993903-13	2013	CONCLUSIONS: Both PON1 Q192R and CYP2C19*2 genotypes influence clopidogrel responsiveness, with the impact of PON1 Q192R mainly on relative platelet inhibition instead of OTPR of clopidogrel.	clopidogrel	63-74	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-40
23041015-3	2013	METHODS: The response to agonists specific for protease-activated receptors (PAR)-1 and -4 was tested by multiple electrode impedance aggregometry in 82 patients on stable doses of clopidogrel or prasugrel, and in 55 healthy controls.	clopidogrel	181-192	coagulation factor II thrombin receptor	Homo sapiens	47-90
23041015-8	2013	CONCLUSION: PAR responsiveness is preserved in the majority of patients with adequate clopidogrel-mediated inhibition of the platelet P2Y12 receptor, and still in about 20% of those with adequate inhibition by prasugrel.	clopidogrel	86-97	purinergic receptor P2Y12	Homo sapiens	134-139
23084816-11	2013	CONCLUSION: The present study confirmed that many diabetic patients treated with clopidogrel for ACS have inadequate platelet inhibition.	clopidogrel	81-92	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	97-100
24058556-6	2013	Gene ontology analysis revealed that response to stress and cell apoptosis dysfunction were ranked in the top 10 cellular events being affected, and that the major components of endoplasmic reticulum stress-mediated apoptosis pathway - CHOP and TRIB3- were up-regulated in a concentration- and time-dependent manner when cells were treated with clopidogrel.	clopidogrel	345-356	DNA damage inducible transcript 3	Homo sapiens	236-240
24058556-6	2013	Gene ontology analysis revealed that response to stress and cell apoptosis dysfunction were ranked in the top 10 cellular events being affected, and that the major components of endoplasmic reticulum stress-mediated apoptosis pathway - CHOP and TRIB3- were up-regulated in a concentration- and time-dependent manner when cells were treated with clopidogrel.	clopidogrel	345-356	tribbles pseudokinase 3	Homo sapiens	245-250
24058556-7	2013	Pathway analysis demonstrated that multiple MAPK kinases were phosphorylated in clopidogrel-treated GES-1 cells, but that only SB-203580 (a p38-specific MAPK inhibitor) attenuated cell apoptosis and CHOP over-expression, both of which were induced by clopidogrel.	clopidogrel	80-91	DNA damage inducible transcript 3	Homo sapiens	199-203
24058556-8	2013	CONCLUSIONS: Increased endoplasmic reticulum stress response is involved in clopidogrel-induced gastric mucosal injury, acting through p38 MAPK activation.	clopidogrel	76-87	mitogen-activated protein kinase 14	Homo sapiens	135-138
23670120-1	2013	From 2010 to 2012, nine systematic reviews reported highly variable conclusions regarding the association between carriage of a cytochrome P450 2C19 loss-of-function allele and the risk of adverse cardiovascular (CV) events in individuals using clopidogrel.	clopidogrel	245-256	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	128-148
23903277-2	2013	Clopidogrel is a pro-drug which requires hepatic cytochrome P450 (CYP) metabolic activation to produce the active metabolite that inhibits platelet aggregation.	clopidogrel	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	49-64
23698643-1	2013	Cytochrome P450 (CYP)2C19 catalyzes the bioactivation of the antiplatelet prodrug clopidogrel, and CYP2C19 loss-of-function alleles impair formation of active metabolites, resulting in reduced platelet inhibition.	clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-25
23698643-2	2013	In addition, CYP2C19 loss-of-function alleles confer increased risks for serious adverse cardiovascular (CV) events among clopidogrel-treated patients with acute coronary syndromes (ACSs) undergoing percutaneous coronary intervention (PCI).	clopidogrel	122-133	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
23903277-6	2013	Lipophilic statins, such as atorvastatin, are predominantly metabolized by CYP3A4 and may interfere with CYP activation of clopidogrel, contrary to what happens with hydrophilic statins, such as rosuvastin or pravastatin.	clopidogrel	123-134	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	75-78
22727972-1	2013	BACKGROUND: The CYP2C19*2 polymorphism is significantly associated with residual platelet reactivity (RPR) and maybe a major confounding factor in studies evaluating pharmacological interactions with clopidogrel.	clopidogrel	200-211	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
23810503-3	2013	Recently, five single nucleotide polymorphisms (SNPs) within CYP2C19 (rs4244285, rs4986893, rs12248560), ABCB1 (rs1045642), and ITGB3 (rs5918) were identified that contribute prominently to variability in response to clopidogrel.	clopidogrel	217-228	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	61-68
23809542-1	2013	BACKGROUND: Cytochrome P450 2C19 (CYP2C19) is the principal enzyme responsible for converting clopidogrel into its active metabolite, and common genetic variants have been identified, most notably CYP2C19*2 and CYP2C19*17, that are believed to alter its activity and expression, respectively.	clopidogrel	94-105	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-32
23809542-1	2013	BACKGROUND: Cytochrome P450 2C19 (CYP2C19) is the principal enzyme responsible for converting clopidogrel into its active metabolite, and common genetic variants have been identified, most notably CYP2C19*2 and CYP2C19*17, that are believed to alter its activity and expression, respectively.	clopidogrel	94-105	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	34-41
23809542-1	2013	BACKGROUND: Cytochrome P450 2C19 (CYP2C19) is the principal enzyme responsible for converting clopidogrel into its active metabolite, and common genetic variants have been identified, most notably CYP2C19*2 and CYP2C19*17, that are believed to alter its activity and expression, respectively.	clopidogrel	94-105	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	197-204
23809542-1	2013	BACKGROUND: Cytochrome P450 2C19 (CYP2C19) is the principal enzyme responsible for converting clopidogrel into its active metabolite, and common genetic variants have been identified, most notably CYP2C19*2 and CYP2C19*17, that are believed to alter its activity and expression, respectively.	clopidogrel	94-105	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	197-204
23809542-2	2013	OBJECTIVE: We evaluated whether the consequences of the CYP2C19*2 and CYP2C19*17 variants on clopidogrel response were independent of each other or genetically linked through linkage disequilibrium (LD).	clopidogrel	93-104	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	56-63
23809542-2	2013	OBJECTIVE: We evaluated whether the consequences of the CYP2C19*2 and CYP2C19*17 variants on clopidogrel response were independent of each other or genetically linked through linkage disequilibrium (LD).	clopidogrel	93-104	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	70-77
23809542-6	2013	In contrast, CYP2C19*17 was marginally associated with clopidogrel active metabolite levels and ADP-stimulated platelet aggregation before (beta = 1.57, P = 0.04 and beta = -1.98, P = 0.01, respectively) but not after (beta = 0.40, P = 0.59 and beta = -0.13, P = 0.69, respectively) adjustment for the CYP2C19*2 variant.	clopidogrel	55-66	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
23809542-7	2013	Stratified analyses of CYP2C19*2/CYP2C19*17 genotype combinations revealed that CYP2C19*2, and not CYP2C19*17, was the primary determinant in altering clopidogrel response.	clopidogrel	151-162	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	23-30
23809542-7	2013	Stratified analyses of CYP2C19*2/CYP2C19*17 genotype combinations revealed that CYP2C19*2, and not CYP2C19*17, was the primary determinant in altering clopidogrel response.	clopidogrel	151-162	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-40
23809542-7	2013	Stratified analyses of CYP2C19*2/CYP2C19*17 genotype combinations revealed that CYP2C19*2, and not CYP2C19*17, was the primary determinant in altering clopidogrel response.	clopidogrel	151-162	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-40
23809542-7	2013	Stratified analyses of CYP2C19*2/CYP2C19*17 genotype combinations revealed that CYP2C19*2, and not CYP2C19*17, was the primary determinant in altering clopidogrel response.	clopidogrel	151-162	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-40
23809542-8	2013	CONCLUSIONS: Our results suggest that CYP2C19*17 has a small (if any) effect on clopidogrel-related traits and that the observed effect of this variant is due to LD with the CYP2C19*2 loss-of-function variant.	clopidogrel	80-91	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	38-45
23809542-8	2013	CONCLUSIONS: Our results suggest that CYP2C19*17 has a small (if any) effect on clopidogrel-related traits and that the observed effect of this variant is due to LD with the CYP2C19*2 loss-of-function variant.	clopidogrel	80-91	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	174-181
23903277-2	2013	Clopidogrel is a pro-drug which requires hepatic cytochrome P450 (CYP) metabolic activation to produce the active metabolite that inhibits platelet aggregation.	clopidogrel	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	66-69
23903277-5	2013	Also drug-drug interactions that influence the function of CYP isoenzymes may affect the response to clopidogrel.	clopidogrel	101-112	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	59-62
23981380-1	2013	BACKGROUND: CYP2C19*2 polymorphism is related to metabolizer phenotypes resulting in reduced effectiveness in converting the antiplatelet drug clopidogrel to active drug.	clopidogrel	143-154	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
23943214-0	2013	Response to letter regarding article, "CYP2C19 polymorphisms and antiplatelet effects of clopidogrel in acute ischemic stroke in China".	clopidogrel	89-100	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	39-46
23943216-0	2013	Letter by Dong et al regarding article, "CYP2C19 polymorphisms and antiplatelet effects of clopidogrel in acute ischemic stroke in China".	clopidogrel	91-102	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	41-48
24019752-1	2013	Genetic variation in the cytochrome P450 2C19 (CYP2C19) gene has been documented gradually as the determinant conversion and variability in the antiplatelet effect of clopidogrel.	clopidogrel	167-178	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-45
24015225-8	2013	Indirect subgroup analysis provided insight into relationship between the clinical utility of genotyping CYP2C19 and the risk ratio of cardiovascular outcomes between CYP2C19 genotypes for individuals using clopidogrel.	clopidogrel	207-218	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	105-112
24015225-8	2013	Indirect subgroup analysis provided insight into relationship between the clinical utility of genotyping CYP2C19 and the risk ratio of cardiovascular outcomes between CYP2C19 genotypes for individuals using clopidogrel.	clopidogrel	207-218	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	167-174
24019752-1	2013	Genetic variation in the cytochrome P450 2C19 (CYP2C19) gene has been documented gradually as the determinant conversion and variability in the antiplatelet effect of clopidogrel.	clopidogrel	167-178	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	47-54
24019752-11	2013	As a result, CYP2C19 variants were associated with clopidogrel non-responders.	clopidogrel	51-62	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
23804278-1	2013	Platelet P2Y12-ADP and COX-1 receptor inhibition with oral clopidogrel (CLO) and low-dose aspirin (ASA), respectively, attenuates reflex-mediated cutaneous vasodilation, but little is known about how these medications affect local vasodilatory signaling.	clopidogrel	59-70	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	23-28
23804278-1	2013	Platelet P2Y12-ADP and COX-1 receptor inhibition with oral clopidogrel (CLO) and low-dose aspirin (ASA), respectively, attenuates reflex-mediated cutaneous vasodilation, but little is known about how these medications affect local vasodilatory signaling.	clopidogrel	72-75	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	23-28
23692149-0	2013	Efffect of the ABCC3 -211C/T polymorphism on clopidogrel responsiveness in patients with percutaneous coronary intervention.	clopidogrel	45-56	ATP binding cassette subfamily C member 3	Homo sapiens	15-20
23602770-9	2013	During clopidogrel therapy, calculated IPA was lower and P2Y12 reaction units and vasodilator-stimulated phosphoprotein phosphorylation and platelet reactivity index were higher in nonsmokers than in smokers (p = 0.043, p = 0.005, and p = 0.042, respectively).	clopidogrel	7-18	purinergic receptor P2Y12	Homo sapiens	57-62
23631863-1	2013	Assays monitoring P2Y12 platelet reactivity can accurately predict which patients will have a poor response to clopidogrel.	clopidogrel	111-122	purinergic receptor P2Y12	Homo sapiens	18-23
23895809-3	2013	The present study aims to evaluate on-treatment platelet reactivity to clopidogrel in AA patients and its interaction to race and CYP2C19*2 loss of function mutation.	clopidogrel	71-82	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	130-137
23692149-2	2013	The ABCC3 -211C/T polymorphism is associated with decreased MRP3 mRNA expression, and low MRP3 mRNA expression is associated with increased clopidogrel response in patients.	clopidogrel	140-151	ATP binding cassette subfamily C member 3	Homo sapiens	90-94
23608957-1	2013	PURPOSE: The aim of this study was to evaluate the association of PON1 genetic variants with the susceptibility to coronary artery disease (CAD) and with the clinical endpoints in aspirin and clopidogrel (dual antiplatelet therapy)-treated Han Chinese patients with CAD after percutaneous coronary intervention (PCI).	clopidogrel	192-203	paraoxonase 1	Homo sapiens	66-70
23661171-0	2013	CYP2C19 genotypes and their impact on clopidogrel responsiveness in percutaneous coronary intervention.	clopidogrel	38-49	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
23661171-1	2013	BACKGROUND: Cytochrome P450 2C19 (CYP2C19) loss-of-function polymorphisms are more common in Asian populations and have been associated with diminished antiplatelet response to clopidogrel.	clopidogrel	177-188	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-32
23661171-1	2013	BACKGROUND: Cytochrome P450 2C19 (CYP2C19) loss-of-function polymorphisms are more common in Asian populations and have been associated with diminished antiplatelet response to clopidogrel.	clopidogrel	177-188	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	34-41
23661171-3	2013	OBJECTIVE: This study aimed to investigate the prevalence and impact of CYP2C19*2, *3 and *17 genotypes on clopidogrel responsiveness in a multiethnic Malaysian population planned for percutaneous coronary intervention.	clopidogrel	107-118	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	72-79
23839753-7	2013	FINDINGS: Dual antiplatelet therapy with aspirin and a P2Y12 inhibitor (eg, ticlopidine, clopidogrel, prasugrel, ticagrelor) reduces the risk of stent thrombosis and subsequent cardiovascular events post-PCI (number needed to treat, 33-53) and is the current standard of care.	clopidogrel	89-100	purinergic receptor P2Y12	Homo sapiens	55-60
23830212-0	2013	Impact of the proton pump inhibitors and CYP2C19*2 polymorphism on platelet response to clopidogrel as assessed by four platelet function assays.	clopidogrel	88-99	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	41-48
23830212-1	2013	BACKGROUND: Previous studies suggested a possible negative interference of proton pump inhibitors (PPIs) on clopidogrel"s antiplatelet effect because of the competitive inhibition of the CYP 2C19 isoenzyme.	clopidogrel	108-119	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	187-195
23830212-2	2013	Moreover, carriers of the loss-of-function allele of CYP2C19 polymorphism (CYP2C19*2) display significantly lower responses to clopidogrel.	clopidogrel	127-138	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-60
23830212-2	2013	Moreover, carriers of the loss-of-function allele of CYP2C19 polymorphism (CYP2C19*2) display significantly lower responses to clopidogrel.	clopidogrel	127-138	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	75-82
23830212-3	2013	In this study, we investigated the association between CYP2C19*2 genotype, PPI intake and clopidogrel resistance in patients with coronary artery disease (CAD) and their effect on clinical outcome.	clopidogrel	90-101	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	55-62
23844259-0	2013	Comparison of a new P2Y12 receptor specific platelet aggregation test with other laboratory methods in stroke patients on clopidogrel monotherapy.	clopidogrel	122-133	purinergic receptor P2Y12	Homo sapiens	20-25
23844259-3	2013	OBJECTIVES: To develop a P2Y12-specific platelet aggregation test and to compare it with other methods used for monitoring clopidogrel therapy.	clopidogrel	123-134	purinergic receptor P2Y12	Homo sapiens	25-30
23844259-5	2013	The effect of clopidogrel was tested by a newly developed ADP(PGE1) aggregation test in which prostaglandin E1 treated platelets are used.	clopidogrel	14-25	WD and tetratricopeptide repeats 1	Homo sapiens	58-66
23905638-6	2013	Recently, P2Y12 receptor antagonists more potent than clopidogrel (e.g., prasugrel and ticagrelor) have been approved for patients with acute coronary syndromes and those undergoing percutaneous coronary interventions; these drugs provide greater platelet inhibition than clopidogrel.	clopidogrel	272-283	purinergic receptor P2Y12	Homo sapiens	10-15
23816027-0	2013	Relation between the vasodilator-stimulated phosphoprotein phosphorylation assay and light transmittance aggregometry in East Asian patients after high-dose clopidogrel loading.	clopidogrel	157-168	vasodilator stimulated phosphoprotein	Homo sapiens	21-58
23872648-11	2013	CONCLUSIONS: In patients with ACS, the CYP2C19 LOF allele was associated with post-procedure HTPR and a subsequently increased risk of adverse clinical events at one-year follow-up following DES implantation and clopidogrel administration.	clopidogrel	212-223	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	39-46
23474843-1	2013	The aim of this study is to investigate the effect of CYP2C19 polymorphism and cotherapy with rabeprazole or esomeprazole on the antiplatelet effect of clopidogrel.	clopidogrel	152-163	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	54-61
23652407-6	2013	Furthermore, clopidogrel and seven other drugs were shown to inhibit OATP1B1-mediated uptake of cerivastatin.	clopidogrel	13-24	solute carrier organic anion transporter family member 1B1	Homo sapiens	69-76
23623170-2	2013	Since activated platelets respond stronger to additional stimuli, the extent of endogenous thrombin generation may in part be responsible for the reported response variability to aspirin and clopidogrel therapy.	clopidogrel	191-202	coagulation factor II, thrombin	Homo sapiens	91-99
23726091-6	2013	RESULTS: Both CYP2C19*2 and *3 alleles were significantly associated with higher platelet aggregation after 5 days maintenance dose of clopidogrel administration (P&lt;0.00001 and P=0.042, respectively).	clopidogrel	135-146	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
23726091-12	2013	CONCLUSION: In clopidogrel treated Chinese patients with ACS, carriers of at least one CYP2C19 loss-of-function allele could predict greater risk of HPR, with the impact mainly attributing to CYP2C19*2.	clopidogrel	15-26	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	87-94
23726091-12	2013	CONCLUSION: In clopidogrel treated Chinese patients with ACS, carriers of at least one CYP2C19 loss-of-function allele could predict greater risk of HPR, with the impact mainly attributing to CYP2C19*2.	clopidogrel	15-26	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	192-199
23853364-2	2013	It has been suggested that clopidogrel may be less effective in inhibiting platelet aggregation among patients who are carriers of CYP2C19*2 and CYP2C19*3, two loss-of-function CYP2C19 alleles, which are associated with reduced conversion of clopidogrel to its active metabolite.	clopidogrel	27-38	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	131-138
23853364-2	2013	It has been suggested that clopidogrel may be less effective in inhibiting platelet aggregation among patients who are carriers of CYP2C19*2 and CYP2C19*3, two loss-of-function CYP2C19 alleles, which are associated with reduced conversion of clopidogrel to its active metabolite.	clopidogrel	27-38	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	145-152
23853364-2	2013	It has been suggested that clopidogrel may be less effective in inhibiting platelet aggregation among patients who are carriers of CYP2C19*2 and CYP2C19*3, two loss-of-function CYP2C19 alleles, which are associated with reduced conversion of clopidogrel to its active metabolite.	clopidogrel	27-38	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	145-152
23853364-2	2013	It has been suggested that clopidogrel may be less effective in inhibiting platelet aggregation among patients who are carriers of CYP2C19*2 and CYP2C19*3, two loss-of-function CYP2C19 alleles, which are associated with reduced conversion of clopidogrel to its active metabolite.	clopidogrel	242-253	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	131-138
23853364-2	2013	It has been suggested that clopidogrel may be less effective in inhibiting platelet aggregation among patients who are carriers of CYP2C19*2 and CYP2C19*3, two loss-of-function CYP2C19 alleles, which are associated with reduced conversion of clopidogrel to its active metabolite.	clopidogrel	242-253	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	145-152
23853364-2	2013	It has been suggested that clopidogrel may be less effective in inhibiting platelet aggregation among patients who are carriers of CYP2C19*2 and CYP2C19*3, two loss-of-function CYP2C19 alleles, which are associated with reduced conversion of clopidogrel to its active metabolite.	clopidogrel	242-253	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	145-152
22709725-10	2013	While several polymorphisms influence platelet activity, CYP2C19 variants are the most consistently linked to clopidogrel responsiveness.	clopidogrel	110-121	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	57-64
22075408-3	2013	It has been shown that besides CYP2C19, CYP2C9 is involved in the hepatic biotransformation of clopidogrel to its active metabolite.	clopidogrel	95-106	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	31-38
22075408-3	2013	It has been shown that besides CYP2C19, CYP2C9 is involved in the hepatic biotransformation of clopidogrel to its active metabolite.	clopidogrel	95-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
22075408-4	2013	Consequently, CYP2C9 polymorphisms may also affect the extent of clopidogrel-mediated platelet inhibition.	clopidogrel	65-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
22075408-5	2013	We therefore studied the influence of CYP2C9 allelic variants on clopidogrel-mediated platelet inhibition as assessed by 5 platelet function tests.	clopidogrel	65-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
22075408-10	2013	CONCLUSION: Results from the VerifyNow P2Y12 assay are significantly influenced by CYP2C9 LOF variants leading to decreased clopidogrel-mediated platelet inhibition and an increased rate of HRPR.	clopidogrel	124-135	purinergic receptor P2Y12	Homo sapiens	39-44
22075408-10	2013	CONCLUSION: Results from the VerifyNow P2Y12 assay are significantly influenced by CYP2C9 LOF variants leading to decreased clopidogrel-mediated platelet inhibition and an increased rate of HRPR.	clopidogrel	124-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
23579966-11	2013	Similarly, CYP2C19 polymorphisms have been associated with clopidogrel resistance in vitro, and have shown an association with stent thrombosis, but not with other cardiovascular outcomes in a consistent manner.	clopidogrel	59-70	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	11-18
23612493-2	2013	P2Y12 receptor is the major platelet receptor that mediates ADP-induced aggregation, P2Y12 receptor inhibitors such as clopidogrel and prasugrel inhibit platelet aggregation, and thus, they are used in the treatment and prevention of coronary artery disease.	clopidogrel	119-130	purinergic receptor P2Y12	Homo sapiens	0-5
23612493-2	2013	P2Y12 receptor is the major platelet receptor that mediates ADP-induced aggregation, P2Y12 receptor inhibitors such as clopidogrel and prasugrel inhibit platelet aggregation, and thus, they are used in the treatment and prevention of coronary artery disease.	clopidogrel	119-130	purinergic receptor P2Y12	Homo sapiens	85-90
23549239-5	2013	Doses greater than clopidogrel 150  mg daily are required to sufficiently overcome high reactivity in CYP2C19 loss-of-function (LOF) allele carriers.	clopidogrel	19-30	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	102-109
23940995-1	2013	Objective of this study was to assess platelet response to clopidogrel and its association with certain single nucleotide polymorphisms (SNPs) of the P2RY12 gene.	clopidogrel	59-70	purinergic receptor P2Y12	Homo sapiens	150-156
23474908-12	2013	Hence, 12 months of ACS treatment using ticagrelor/ASA instead of clopidogrel/ASA may offer a cost-effective therapeutic option, even when the generic price for clopidogrel is employed.	clopidogrel	161-172	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	20-23
23940995-3	2013	Pharmacological response to clopidogrel is mediated by the P2Y12 platelet receptor, therefore, SNPs of the P2RY12 gene may account for some of the observed variability in the cardiovascular risk.	clopidogrel	28-39	purinergic receptor P2Y12	Homo sapiens	107-113
23940995-11	2013	Our results suggest that 18C &gt; T SNP of the P2RY12 gene may be an independent predictor of pharmacological response to clopidogrel.	clopidogrel	122-133	purinergic receptor P2Y12	Homo sapiens	47-53
23149816-2	2013	Clopidogrel is a prodrug which requires a two-step hepatic biotransformation thanks to the cytochrome P450 (CYP450) enzyme system.	clopidogrel	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	91-106
23549485-14	2013	CYP2C19*2 allele carriers had a higher platelet reactivity after clopidogrel loading measured by adenosine diphosphate-induced aggregation in LTA (P=0.008) and vasodilator-stimulated phosphoprotein phosphorylation (P=0.035); however, there was no difference in the inflammatory markers.	clopidogrel	65-76	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
23462555-4	2013	Testing for mutations in CYP2C19, as recommended by the FDA, only correctly predicted if a patient would respond to clopidogrel 52.4% of the time.	clopidogrel	116-127	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
23397280-2	2013	The shortcomings of the most commonly used P2Y12 receptor inhibitor clopidogrel-that is its delayed onset of action, its interindividual response variability, and the phenomenon of high on-treatment platelet reactivity-led to the development of more potent P2Y12 receptor inhibitors (prasugrel and ticagrelor) that proved their superiority in terms of reducing thrombotic events compared to clopidogrel.	clopidogrel	68-79	purinergic receptor P2Y12	Homo sapiens	43-48
23149816-2	2013	Clopidogrel is a prodrug which requires a two-step hepatic biotransformation thanks to the cytochrome P450 (CYP450) enzyme system.	clopidogrel	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	108-114
23397280-2	2013	The shortcomings of the most commonly used P2Y12 receptor inhibitor clopidogrel-that is its delayed onset of action, its interindividual response variability, and the phenomenon of high on-treatment platelet reactivity-led to the development of more potent P2Y12 receptor inhibitors (prasugrel and ticagrelor) that proved their superiority in terms of reducing thrombotic events compared to clopidogrel.	clopidogrel	68-79	purinergic receptor P2Y12	Homo sapiens	257-262
23149816-3	2013	Genetic polymorphism of CYP450 system (e.g., CYP2C19*2) responsible for altered clopidogrel metabolism is a major cause of high on-treatment platelet reactivity (HTPR), which translates into thrombotic events in stented patients.	clopidogrel	80-91	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	24-30
23397280-2	2013	The shortcomings of the most commonly used P2Y12 receptor inhibitor clopidogrel-that is its delayed onset of action, its interindividual response variability, and the phenomenon of high on-treatment platelet reactivity-led to the development of more potent P2Y12 receptor inhibitors (prasugrel and ticagrelor) that proved their superiority in terms of reducing thrombotic events compared to clopidogrel.	clopidogrel	391-402	purinergic receptor P2Y12	Homo sapiens	43-48
23397280-2	2013	The shortcomings of the most commonly used P2Y12 receptor inhibitor clopidogrel-that is its delayed onset of action, its interindividual response variability, and the phenomenon of high on-treatment platelet reactivity-led to the development of more potent P2Y12 receptor inhibitors (prasugrel and ticagrelor) that proved their superiority in terms of reducing thrombotic events compared to clopidogrel.	clopidogrel	391-402	purinergic receptor P2Y12	Homo sapiens	257-262
23397280-4	2013	Thus, it still warrants further investigation if a tailored, platelet function guided, antiplatelet therapy in ACS patients with the available P2Y12 receptor inhibitors prasugrel, ticagrelor, and clopidogrel can lead to improved patients outcome.	clopidogrel	196-207	purinergic receptor P2Y12	Homo sapiens	143-148
23149816-3	2013	Genetic polymorphism of CYP450 system (e.g., CYP2C19*2) responsible for altered clopidogrel metabolism is a major cause of high on-treatment platelet reactivity (HTPR), which translates into thrombotic events in stented patients.	clopidogrel	80-91	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	45-52
23435863-2	2013	Current anti-platelet treatments are mainly based on inhibition of two important pathways of platelet activation: thromboxane A2 (TXA2) mediated (aspirin) and adenosine diphosphate (ADP)-P2Y12 receptor mediated (clopidogrel, prasugrel, and ticagrelor).	clopidogrel	212-223	purinergic receptor P2Y12	Homo sapiens	187-192
23543615-2	2013	However, the platelet inhibitory effect of clopidogrel, the most commonly used P2Y12 inhibitor, is variable between patients.	clopidogrel	43-54	purinergic receptor P2Y12	Homo sapiens	79-84
23618682-2	2013	An underlying cause for suboptimal platelet inhibition is varying response to clopidogrel, which is linked to polymorphisms in the CYP2C19 gene responsible for the metabolism and activation of clopidogrel.	clopidogrel	78-89	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	131-138
23672863-1	2013	The considerable progress in P2Y12-platelet blockers has important perioperative implications due to a family of novel agents beyond clopidogrel.	clopidogrel	133-144	purinergic receptor P2Y12	Homo sapiens	29-34
23697979-2	2013	Recent evidence supports a role of loss-of-function (LOF) variants in the cytochrome P450 enzyme CYP2C19 as a determinant of clopidogrel response.	clopidogrel	125-136	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	97-104
23517020-0	2013	Influence of CYP2C19*2 and *3 loss-of-function alleles on the pharmacodynamic effects of standard- and high-dose clopidogrel in East Asians undergoing percutaneous coronary intervention: the results of the ACCEL-DOUBLE-2N3 study.	clopidogrel	113-124	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
23694867-2	2013	This study sought to determine if trauma patients on preinjury clopidogrel with a higher degree of platelet inhibition (PI), as determined by the VerifyNow P2Y12 Test, experienced bleeding complications more frequently than did patients with a lower degree of PI.	clopidogrel	63-74	purinergic receptor P2Y12	Homo sapiens	156-161
23826440-0	2013	Clopidogrel Resistance by P2Y12 Platelet Function Testing in Patients Undergoing Neuroendovascular Procedures: Incidence of Ischemic and Hemorrhagic Complications.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	26-31
23588782-10	2013	CYP2C19 is responsible for metabolising clopidogrel, proton pump inhibitors (PPIs) and some antidepressants.	clopidogrel	40-51	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
23588782-11	2013	Carriers of CYP2C19 variant alleles exhibit a reduced capacity to produce the active metabolite of clopidogrel, and are at increased risk of adverse cardiovascular events.	clopidogrel	99-110	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
23640828-6	2013	RESULTS: The difference before and after clopidogrel treatment on adenosine diphosphate-induced platelet aggregation was significantly smaller in patients carrying 1 or 2 CYP2C19 loss-of-function alleles (*2, *3) compared with patients carrying none.	clopidogrel	41-52	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	171-178
23640828-8	2013	Regression analysis showed that CYP2C19 was an independent predictor of clopidogrel resistance.	clopidogrel	72-83	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
23640828-9	2013	CONCLUSIONS: CYP2C19 genotypes had significant impact on clopidogrel response and prognosis of patients with stroke.	clopidogrel	57-68	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
23498169-0	2013	Decreased platelet miR-223 expression is associated with high on-clopidogrel platelet reactivity.	clopidogrel	65-76	microRNA 223	Homo sapiens	19-26
23498169-1	2013	OBJECTIVES: We aimed to investigate the relationship between platelet microRNA (miR-223 and miR-96) expression and clopidogrel responsiveness in patients with coronary heart disease (CHD).	clopidogrel	115-126	microRNA 223	Homo sapiens	70-87
23498169-1	2013	OBJECTIVES: We aimed to investigate the relationship between platelet microRNA (miR-223 and miR-96) expression and clopidogrel responsiveness in patients with coronary heart disease (CHD).	clopidogrel	115-126	microRNA 96	Homo sapiens	92-98
23498169-10	2013	CONCLUSIONS: The present work identifies decreased platelet miR-223 expression as a novel mechanism involved in blunted platelet response to clopidogrel in a Chinese population.	clopidogrel	141-152	microRNA 223	Homo sapiens	60-67
23688069-6	2013	RESULTS: Among 7413 patients hospitalized with ACS and discharged taking clopidogrel, 34.5% had eGFR 30-60 and 11.6% had eGFR &lt; 30.	clopidogrel	73-84	epidermal growth factor receptor	Homo sapiens	96-100
23686351-4	2013	The body of literature that has led to the clinical implementation of CYP2C19 genotyping for clopidogrel, VKORC1, CYP2C9; and CYP4F2 for warfarin; and SLCO1B1 for statins is comprehensively described.	clopidogrel	93-104	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	70-77
23530880-4	2013	METHODS: A literature search was conducted for studies that investigated PPB in patients on continued clopidogrel therapy.	clopidogrel	102-113	histatin 1	Homo sapiens	73-76
23530880-5	2013	The primary outcome of interest was the pooled relative risk ratio (RR) of colonoscopic PPB in patients on continued clopidogrel therapy vs. controls.	clopidogrel	117-128	histatin 1	Homo sapiens	88-91
23530880-8	2013	The pooled RR for PPB on continued clopidogrel therapy was 2.54 (95% CI 1.68-3.84, P &lt; 0.00001).	clopidogrel	35-46	histatin 1	Homo sapiens	18-21
23618682-2	2013	An underlying cause for suboptimal platelet inhibition is varying response to clopidogrel, which is linked to polymorphisms in the CYP2C19 gene responsible for the metabolism and activation of clopidogrel.	clopidogrel	193-204	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	131-138
23618682-4	2013	Randomized controlled trials have shown that high doses of clopidogrel can overcome suboptimal platelet response in carriers of the CYP2C19(*)2 allele.	clopidogrel	59-70	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	132-139
23591705-5	2013	The mechanism of the interaction between smoking status and clopidogrel efficacy remains unclear but may be mediated by cytochrome P450 (CYP)1A2.	clopidogrel	60-71	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	120-144
23054787-4	2013	Lower detection limits were found to be 9.77 x 10(-6) M for PME-1 and 7.76 x 10(-7) M for CGE-1 with response time varying from 10 to 20 s. Also, these electrodes work within pH range of 2.0-6.0 for PME-1 and 1.5-6.5 for CGE-1.	clopidogrel	90-93	protein phosphatase methylesterase 1	Homo sapiens	199-210
23150151-0	2013	Effect of the CYP2C19 2 and 3 genotypes, ABCB1 C3435T and PON1 Q192R alleles on the pharmacodynamics and adverse clinical events of clopidogrel in Chinese people after percutaneous coronary intervention.	clopidogrel	132-143	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
23150151-0	2013	Effect of the CYP2C19 2 and 3 genotypes, ABCB1 C3435T and PON1 Q192R alleles on the pharmacodynamics and adverse clinical events of clopidogrel in Chinese people after percutaneous coronary intervention.	clopidogrel	132-143	ATP binding cassette subfamily B member 1	Homo sapiens	41-46
23150151-0	2013	Effect of the CYP2C19 2 and 3 genotypes, ABCB1 C3435T and PON1 Q192R alleles on the pharmacodynamics and adverse clinical events of clopidogrel in Chinese people after percutaneous coronary intervention.	clopidogrel	132-143	paraoxonase 1	Homo sapiens	58-62
23150151-2	2013	The effect of the ATP-binding cassette, sub-family B, member 1 (ABCB1), and paraoxonase 1 (PON1) variants on platelet reactivity and clinical outcomes of clopidogrel treatment has not yet been reported in Chinese patients after percutaneous coronary intervention.	clopidogrel	154-165	ATP binding cassette subfamily B member 1	Homo sapiens	18-62
23150151-2	2013	The effect of the ATP-binding cassette, sub-family B, member 1 (ABCB1), and paraoxonase 1 (PON1) variants on platelet reactivity and clinical outcomes of clopidogrel treatment has not yet been reported in Chinese patients after percutaneous coronary intervention.	clopidogrel	154-165	ATP binding cassette subfamily B member 1	Homo sapiens	64-69
23150151-2	2013	The effect of the ATP-binding cassette, sub-family B, member 1 (ABCB1), and paraoxonase 1 (PON1) variants on platelet reactivity and clinical outcomes of clopidogrel treatment has not yet been reported in Chinese patients after percutaneous coronary intervention.	clopidogrel	154-165	paraoxonase 1	Homo sapiens	76-89
23150151-2	2013	The effect of the ATP-binding cassette, sub-family B, member 1 (ABCB1), and paraoxonase 1 (PON1) variants on platelet reactivity and clinical outcomes of clopidogrel treatment has not yet been reported in Chinese patients after percutaneous coronary intervention.	clopidogrel	154-165	paraoxonase 1	Homo sapiens	91-95
23150151-3	2013	The aim of this study was to investigate the effect of the CYP2C19, ABCB1, and PON1 variants on clopidogrel pharmacodynamics and clinical outcomes in these patients.	clopidogrel	96-107	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	59-66
23150151-3	2013	The aim of this study was to investigate the effect of the CYP2C19, ABCB1, and PON1 variants on clopidogrel pharmacodynamics and clinical outcomes in these patients.	clopidogrel	96-107	ATP binding cassette subfamily B member 1	Homo sapiens	68-73
23150151-3	2013	The aim of this study was to investigate the effect of the CYP2C19, ABCB1, and PON1 variants on clopidogrel pharmacodynamics and clinical outcomes in these patients.	clopidogrel	96-107	paraoxonase 1	Homo sapiens	79-83
23150151-10	2013	The risk of a low response to clopidogrel and composite ischemic events increased with the number of CYP2C19 loss-of-function alleles.	clopidogrel	30-41	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	101-108
23150151-12	2013	CONCLUSIONS: The CYP2C19 loss-of-function alleles had a gene dose effect on the pharmacodynamics and composite ischemic events of clopidogrel in our study population.	clopidogrel	130-141	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-24
23467639-8	2013	Carriage of the *17 allele of cytochrome P450 2C19, which is associated with gain of function and enhanced response to clopidogrel, seems to be associated with increased bleeding risk, although studies showing lack of apparent effect of loss-of-function alleles provide contradictory evidence.	clopidogrel	119-130	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-50
23313628-4	2013	PAR-1 regulation was studied prospectively in 86 consecutive patients with stable coronary artery disease treated with aspirin and clopidogrel (67 patients) or prasugrel (19 patients) and correlated the data to ADP inducible platelet reactivity by impedance aggregometry.	clopidogrel	131-142	coagulation factor II thrombin receptor	Homo sapiens	0-5
22974728-0	2013	Besides CYP2C19, PON1 genetic variant influences post-clopidogrel platelet reactivity in Chinese patients.	clopidogrel	54-65	paraoxonase 1	Homo sapiens	17-21
24303458-0	2013	Low ADAMTS-13 in plavix induced thrombotic thrombocytopenic purpura.	clopidogrel	17-23	ADAM metallopeptidase with thrombospondin type 1 motif 13	Homo sapiens	4-13
23340030-1	2013	The present study was performed to compare the influence of cytochrome P459 2C19 (CYP2C19) *2 and *17 genetic variants on the platelet response to clopidogrel and prasugrel maintenance therapy and to assess the relation between platelet reactivity and bleeding complications.	clopidogrel	147-158	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	60-80
23340030-0	2013	Effect of CYP2C19*2 and *17 genetic variants on platelet response to clopidogrel and prasugrel maintenance dose and relation to bleeding complications.	clopidogrel	69-80	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-17
23340030-1	2013	The present study was performed to compare the influence of cytochrome P459 2C19 (CYP2C19) *2 and *17 genetic variants on the platelet response to clopidogrel and prasugrel maintenance therapy and to assess the relation between platelet reactivity and bleeding complications.	clopidogrel	147-158	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	82-89
23340030-9	2013	In conclusion, the present study showed that both clopidogrel and prasugrel have genetic modulation by CYP2C19 *2 and *17 alleles and that prasugrel provides greater platelet inhibition, regardless of the genotypes.	clopidogrel	50-61	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	103-110
23428385-4	2013	The mainstay of stent thrombosis prevention remains dual anti-platelet therapy with acetylsalicylic acid and a platelet ADP-receptor blocker, traditionally clopidogrel.	clopidogrel	156-167	purinergic receptor P2Y12	Homo sapiens	111-132
23001453-0	2013	Influence of CYP2C19 loss-of-function variants on the antiplatelet effects and cardiovascular events in clopidogrel-treated Chinese patients undergoing percutaneous coronary intervention.	clopidogrel	104-115	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
23001453-1	2013	BACKGROUND AND OBJECTIVES: A large number of clinical studies have well demonstrated that the loss-of-function variant allele CYP2C19 2 is associated with attenuated response to clopidogrel and increased risk of developing stent thrombosis (ST) in white or black patients with stenting.	clopidogrel	178-189	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	126-133
23001453-3	2013	This work was aimed at assessing the impact of the CYP2C19 2 and 3 variants on the antiplatelet effects and adverse cardiovascular events in clopidogrel-treated Chinese patients undergoing percutaneous coronary intervention (PCI).	clopidogrel	141-152	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	51-58
23001453-11	2013	CONCLUSIONS: Carriage of the loss-of-function genetic variants CYP2C19 2 and 3 is significantly associated with attenuated platelet response to clopidogrel and an increased risk of ST in Chinese patients treated with stenting.	clopidogrel	144-155	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	63-70
23570358-4	2013	Reduced pharmacodynamic effect and reduced clinical efficacy of clopidogrel have been well documented in high-risk coronary artery disease patients carrying a loss-of-function allele of the CYP2C19 gene.	clopidogrel	64-75	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	190-197
23364775-0	2013	Cardiovascular risk among patients on clopidogrel anti-platelet therapy after placement of drug-eluting stents is modified by genetic variants in both the CYP2C19 and ABCB1 genes.	clopidogrel	38-49	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	155-162
23364775-0	2013	Cardiovascular risk among patients on clopidogrel anti-platelet therapy after placement of drug-eluting stents is modified by genetic variants in both the CYP2C19 and ABCB1 genes.	clopidogrel	38-49	ATP binding cassette subfamily B member 1	Homo sapiens	167-172
23364775-2	2013	Genetic variants in both the ABCB1 and CYP2C19 genes have been associated with cardiovascular events among patients on clopidogrel.	clopidogrel	119-130	ATP binding cassette subfamily B member 1	Homo sapiens	29-34
23364775-2	2013	Genetic variants in both the ABCB1 and CYP2C19 genes have been associated with cardiovascular events among patients on clopidogrel.	clopidogrel	119-130	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	39-46
27323431-5	2013	The fact that the genetic and pharmacokinetic properties of clopidogrel, a P2Y(12) inhibitor, cause insufficient antiplatelet efficacy and inadequate offset of action has led to the introduction of new P2Y(12) inhibitors such as prasugrel, ticagrelor and cangrelor, which offer an improved antiplatelet efficacy with a bleeding risk within acceptable limits.	clopidogrel	60-71	purinergic receptor P2Y12	Homo sapiens	75-82
27323431-5	2013	The fact that the genetic and pharmacokinetic properties of clopidogrel, a P2Y(12) inhibitor, cause insufficient antiplatelet efficacy and inadequate offset of action has led to the introduction of new P2Y(12) inhibitors such as prasugrel, ticagrelor and cangrelor, which offer an improved antiplatelet efficacy with a bleeding risk within acceptable limits.	clopidogrel	60-71	purinergic receptor P2Y12	Homo sapiens	202-209
23537811-2	2013	Despite a minor influence of the CYP2C19*2 genetic variant on the pharmacodynamic response to clopidogrel (5% to 12%) and a limited or absent value for predicting stent thrombosis and MACE, this latter polymorphism is currently considered an important candidate to tailor anti-P2Y12 therapy during percutaneous coronary intervention.	clopidogrel	94-105	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-40
23275066-0	2013	Carboxylesterase 1 as a determinant of clopidogrel metabolism and activation.	clopidogrel	39-50	carboxylesterase 1	Homo sapiens	0-18
23392654-9	2013	CONCLUSION- Common genetic variation in PEAR1 may be a determinant of platelet response and cardiovascular events in patients on aspirin alone or in combination with clopidogrel.	clopidogrel	166-177	platelet endothelial aggregation receptor 1	Homo sapiens	40-45
23480885-1	2013	Hepatic cytochrome P450 (CYP) bioactivation of clopidogrel is reduced in subjects with the CYP2C19*2 loss-of-function allele.	clopidogrel	47-58	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	8-23
23480885-1	2013	Hepatic cytochrome P450 (CYP) bioactivation of clopidogrel is reduced in subjects with the CYP2C19*2 loss-of-function allele.	clopidogrel	47-58	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	25-28
23480885-1	2013	Hepatic cytochrome P450 (CYP) bioactivation of clopidogrel is reduced in subjects with the CYP2C19*2 loss-of-function allele.	clopidogrel	47-58	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	91-98
23480885-4	2013	This review briefly outlines the current evidence for the value of CYP2C19 genotyping to guide antiplatelet therapy with clopidogrel.	clopidogrel	121-132	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	67-74
23337798-1	2013	BACKGROUND: Cytochrome P450 (CYP) 2C19 plays a key role in clopidogrel activation and thus impacts the clinical outcome of patients with coronary artery disease (CAD).	clopidogrel	59-70	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-38
22782539-4	2013	RESULTS: Bioavailability was moderately increased when a loading dose of clopidogrel (300 mg in part 1 and 600 mg in part 3) was administered concomitantly with dabigatran etexilate 150 mg twice daily (bid).	clopidogrel	73-84	BH3 interacting domain death agonist	Homo sapiens	202-205
22955794-0	2013	Genetic polymorphisms of CYP2C19 influences the response to clopidogrel in ischemic heart disease patients in the South Indian Tamilian population.	clopidogrel	60-71	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
22955794-2	2013	Variation in the cytochrome P450 2C19 (CYP2C19) gene coding for the CYP2C19 enzyme is one of the major determinants of this variable response to clopidogrel.	clopidogrel	145-156	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-37
22955794-2	2013	Variation in the cytochrome P450 2C19 (CYP2C19) gene coding for the CYP2C19 enzyme is one of the major determinants of this variable response to clopidogrel.	clopidogrel	145-156	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	39-46
22955794-2	2013	Variation in the cytochrome P450 2C19 (CYP2C19) gene coding for the CYP2C19 enzyme is one of the major determinants of this variable response to clopidogrel.	clopidogrel	145-156	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	68-75
22955794-3	2013	The activity of the CYP2C19 enzyme, which plays a role in the conversion of the prodrug clopidogrel to its active metabolite, is genetically influenced by polymorphisms in its gene.	clopidogrel	88-99	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	20-27
22955794-4	2013	The aim of our study was to evaluate the association of CYP2C19 polymorphisms and the antiplatelet effect of clopidogrel in the South Indian Tamilian population.	clopidogrel	109-120	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	56-63
22955794-13	2013	CONCLUSION: Patients with CYP2C19 (*2 or *3) genetic polymorphisms had higher residual platelet activities and were associated with a reduced antiplatelet response to clopidogrel.	clopidogrel	167-178	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
23535745-1	2013	We report the development and demonstration of an assay that distinguishes the pharmacological effects of two widely used antiplatelet therapies, aspirin (COX-1 inhibitor) and clopidogrel (P2Y12 inhibitor).	clopidogrel	176-187	purinergic receptor P2Y12	Homo sapiens	189-194
23647895-0	2013	Polymorphisms of MDR1, CYP2C19 and P2Y12 genes in Indian population: effects on clopidogrel response.	clopidogrel	80-91	ATP binding cassette subfamily B member 1	Homo sapiens	17-21
23647895-0	2013	Polymorphisms of MDR1, CYP2C19 and P2Y12 genes in Indian population: effects on clopidogrel response.	clopidogrel	80-91	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	23-30
23647895-0	2013	Polymorphisms of MDR1, CYP2C19 and P2Y12 genes in Indian population: effects on clopidogrel response.	clopidogrel	80-91	purinergic receptor P2Y12	Homo sapiens	35-40
23647895-2	2013	In the present study, the prevalence of single nucleotide polymorphisms of MDR1 (C3435T), CYP2C19 [CYP2C19*2 CYP2C19*3, CYP2C19*17] and P2Y12 (i-T744C) in Indian population and their effects on clopidogrel response was analyzed.	clopidogrel	194-205	ATP binding cassette subfamily B member 1	Homo sapiens	75-79
23647895-7	2013	Variant allele of CYP2C19*3 was not observed while the prevalence of 3435T of MDR1 (0.524), CYP2C19*2 (681A, 0.352); i-744C of P2Y12 (0.088), as well as wild type allele CYP2C19*17 (C806, 0.897) associated with decrease clopidogrel response were observed.	clopidogrel	220-231	purinergic receptor P2Y12	Homo sapiens	127-132
23647895-8	2013	Trend toward poor response to clopidogrel was observed at 24 h with the variant genotypes of CYP2C19*2 and i-T744C of P2Y12 as compared to wild type.	clopidogrel	30-41	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	93-100
23647895-8	2013	Trend toward poor response to clopidogrel was observed at 24 h with the variant genotypes of CYP2C19*2 and i-T744C of P2Y12 as compared to wild type.	clopidogrel	30-41	purinergic receptor P2Y12	Homo sapiens	118-123
23647895-9	2013	CONCLUSION: The present study did show a trend toward impaired response of clopidogrel to inhibit platelet aggregation with variant genotypes of CYP2C19*2 and iT744C of P2Y12 compared to respective wild type genotype at 24 h.	clopidogrel	75-86	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	145-152
23647895-9	2013	CONCLUSION: The present study did show a trend toward impaired response of clopidogrel to inhibit platelet aggregation with variant genotypes of CYP2C19*2 and iT744C of P2Y12 compared to respective wild type genotype at 24 h.	clopidogrel	75-86	purinergic receptor P2Y12	Homo sapiens	169-174
23357840-8	2013	In addition, presence of CYP2C19*2 allele is strongly related to clopidogrel resistance (p &lt; 0.001).	clopidogrel	65-76	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
23357840-10	2013	CONCLUSION: Several factors might contribute to clopidogrel resistance including gender, concomitant use of calcium channel blockers, HDL and CYP2C19*2 polymorphism.	clopidogrel	48-59	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	142-149
23381692-1	2013	It has been presumed that CYP2C19 has a major role in the metabolism of clopidogrel.	clopidogrel	72-83	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
23381692-3	2013	If clopidogrel were primarily a CYP2C19 substrate, a drug/drug interaction with CYP2C19 inhibitors, such as proton pump inhibitors (PPIs), for example, omeprazole and lansoprazole would be anticipated.	clopidogrel	3-14	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
23381692-3	2013	If clopidogrel were primarily a CYP2C19 substrate, a drug/drug interaction with CYP2C19 inhibitors, such as proton pump inhibitors (PPIs), for example, omeprazole and lansoprazole would be anticipated.	clopidogrel	3-14	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	80-87
23275066-2	2013	Clopidogrel, a recognized substrate of hepatic carboxylesterase 1 (CES1), undergoes extensive hydrolytic metabolism in the liver.	clopidogrel	0-11	carboxylesterase 1	Homo sapiens	47-65
23275066-2	2013	Clopidogrel, a recognized substrate of hepatic carboxylesterase 1 (CES1), undergoes extensive hydrolytic metabolism in the liver.	clopidogrel	0-11	carboxylesterase 1	Homo sapiens	67-71
23275066-4	2013	We determined whether CES1 inhibition and CES1 genetic polymorphisms would significantly influence the biotransformation of clopidogrel and alter the formation of the active metabolite.	clopidogrel	124-135	carboxylesterase 1	Homo sapiens	22-26
23275066-4	2013	We determined whether CES1 inhibition and CES1 genetic polymorphisms would significantly influence the biotransformation of clopidogrel and alter the formation of the active metabolite.	clopidogrel	124-135	carboxylesterase 1	Homo sapiens	42-46
23275066-5	2013	Coincubation of clopidogrel with the CES1 inhibitor bis(4-nitrophenyl) phosphate in human liver s9 fractions significantly increased the concentrations of clopidogrel, 2-oxo-clopidogrel, and clopidogrel active metabolite, while the concentrations of all formed carboxylate metabolites were significantly decreased.	clopidogrel	16-27	carboxylesterase 1	Homo sapiens	37-41
23275066-5	2013	Coincubation of clopidogrel with the CES1 inhibitor bis(4-nitrophenyl) phosphate in human liver s9 fractions significantly increased the concentrations of clopidogrel, 2-oxo-clopidogrel, and clopidogrel active metabolite, while the concentrations of all formed carboxylate metabolites were significantly decreased.	clopidogrel	155-166	carboxylesterase 1	Homo sapiens	37-41
23275066-5	2013	Coincubation of clopidogrel with the CES1 inhibitor bis(4-nitrophenyl) phosphate in human liver s9 fractions significantly increased the concentrations of clopidogrel, 2-oxo-clopidogrel, and clopidogrel active metabolite, while the concentrations of all formed carboxylate metabolites were significantly decreased.	clopidogrel	155-166	carboxylesterase 1	Homo sapiens	37-41
23275066-6	2013	As anticipated, clopidogrel and 2-oxo-clopidogrel were efficiently hydrolyzed by the cell s9 fractions prepared from wild-type CES1 transfected cells.	clopidogrel	16-27	carboxylesterase 1	Homo sapiens	127-131
23275066-7	2013	The enzymatic activity of the CES1 variants G143E and D260fs were completely impaired in terms of catalyzing the hydrolysis of clopidogrel and 2-oxo-clopidogrel.	clopidogrel	127-138	carboxylesterase 1	Homo sapiens	30-34
23275066-9	2013	In summary, deficient CES1 catalytic activity resulting from CES1 inhibition or CES1 genetic variation may be associated with higher plasma concentrations of clopidogrel-active metabolite, and hence may enhance antiplatelet activity.	clopidogrel	158-169	carboxylesterase 1	Homo sapiens	22-26
23275066-9	2013	In summary, deficient CES1 catalytic activity resulting from CES1 inhibition or CES1 genetic variation may be associated with higher plasma concentrations of clopidogrel-active metabolite, and hence may enhance antiplatelet activity.	clopidogrel	158-169	carboxylesterase 1	Homo sapiens	61-65
23275066-9	2013	In summary, deficient CES1 catalytic activity resulting from CES1 inhibition or CES1 genetic variation may be associated with higher plasma concentrations of clopidogrel-active metabolite, and hence may enhance antiplatelet activity.	clopidogrel	158-169	carboxylesterase 1	Homo sapiens	61-65
23275066-10	2013	Additionally, CES1 genetic variants have the potential to serve as a biomarker to predict clopidogrel response and individualize clopidogrel dosing regimens in clinical practice.	clopidogrel	90-101	carboxylesterase 1	Homo sapiens	14-18
23275066-10	2013	Additionally, CES1 genetic variants have the potential to serve as a biomarker to predict clopidogrel response and individualize clopidogrel dosing regimens in clinical practice.	clopidogrel	129-140	carboxylesterase 1	Homo sapiens	14-18
23260377-1	2013	BACKGROUND: Variations of genes encoding cytochrome enzymes, drug transporters, and paraoxonase have recently been reported to be associated with clopidogrel response variability besides the well-known CYP2C19 loss-of-function (LOF) alleles.	clopidogrel	146-157	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	202-209
24023447-3	2013	One of them is clopidogrel drug-drug interaction with CYP2C19 and CYP3A4 enzyme inhibitors.	clopidogrel	15-26	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	54-61
24023447-3	2013	One of them is clopidogrel drug-drug interaction with CYP2C19 and CYP3A4 enzyme inhibitors.	clopidogrel	15-26	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	66-72
24023447-10	2013	The use of the potential CYP3A4 inhibitors - lipophilic statins and CCB - was increased after the prescription of clopidogrel too.	clopidogrel	114-125	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	25-31
24023447-12	2013	CONCLUSION: In the primary health care practices, it is revealed that there is co-medication of clopidogrel with weak CYP3A4 inhibitors, such as lipophilic statins and amlodipine, and with the moderate CYP2C19 inhibitor - omeprazole.	clopidogrel	96-107	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	118-124
24023447-12	2013	CONCLUSION: In the primary health care practices, it is revealed that there is co-medication of clopidogrel with weak CYP3A4 inhibitors, such as lipophilic statins and amlodipine, and with the moderate CYP2C19 inhibitor - omeprazole.	clopidogrel	96-107	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	202-209
23556336-1	2013	Recently published data indicate that CYP2C19*2 allele is the major determinant of metabolic bioactivation of clopidogrel and thereby variability of antiplatelet effect of clopidogrel in white or black patients undergoing elective coronary stent placement.	clopidogrel	110-121	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	38-45
23556336-1	2013	Recently published data indicate that CYP2C19*2 allele is the major determinant of metabolic bioactivation of clopidogrel and thereby variability of antiplatelet effect of clopidogrel in white or black patients undergoing elective coronary stent placement.	clopidogrel	172-183	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	38-45
23556336-3	2013	We sought to investigate whether the CYP2C19*2 or *3 alleles affects platelet reactivity of clopidogrel in Chinese stroke patients.	clopidogrel	92-103	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-44
23556336-9	2013	CYP2C19*2 or *3 allele does link to increased MPA and clopidogrel response.	clopidogrel	54-65	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
23333143-0	2013	Clopidogrel pharmacokinetics and pharmacodynamics vary widely despite exclusion or control of polymorphisms (CYP2C19, ABCB1, PON1), noncompliance, diet, smoking, co-medications (including proton pump inhibitors), and pre-existent variability in platelet function.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	109-116
23333143-0	2013	Clopidogrel pharmacokinetics and pharmacodynamics vary widely despite exclusion or control of polymorphisms (CYP2C19, ABCB1, PON1), noncompliance, diet, smoking, co-medications (including proton pump inhibitors), and pre-existent variability in platelet function.	clopidogrel	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	118-123
23333143-0	2013	Clopidogrel pharmacokinetics and pharmacodynamics vary widely despite exclusion or control of polymorphisms (CYP2C19, ABCB1, PON1), noncompliance, diet, smoking, co-medications (including proton pump inhibitors), and pre-existent variability in platelet function.	clopidogrel	0-11	paraoxonase 1	Homo sapiens	125-129
23333143-10	2013	CONCLUSIONS: Clopidogrel pharmacokinetics and pharmacodynamics vary widely despite rigorous exclusion or control of known disease, polymorphisms (CYP2C19, CYP3A5, ABCB1, PON1), noncompliance, co-medications, diet, smoking, alcohol, demographics, and pre-treatment platelet hyperreactivity.	clopidogrel	13-24	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	155-161
23333143-10	2013	CONCLUSIONS: Clopidogrel pharmacokinetics and pharmacodynamics vary widely despite rigorous exclusion or control of known disease, polymorphisms (CYP2C19, CYP3A5, ABCB1, PON1), noncompliance, co-medications, diet, smoking, alcohol, demographics, and pre-treatment platelet hyperreactivity.	clopidogrel	13-24	ATP binding cassette subfamily B member 1	Homo sapiens	163-168
23333143-10	2013	CONCLUSIONS: Clopidogrel pharmacokinetics and pharmacodynamics vary widely despite rigorous exclusion or control of known disease, polymorphisms (CYP2C19, CYP3A5, ABCB1, PON1), noncompliance, co-medications, diet, smoking, alcohol, demographics, and pre-treatment platelet hyperreactivity.	clopidogrel	13-24	paraoxonase 1	Homo sapiens	170-174
23260377-10	2013	CONCLUSIONS: Among genes postulated to be involved in clopidogrel metabolism, only the CYP2C19 genotype is associated with response variability and emerged as an independent predictor of high-OPR using two different cutoffs.	clopidogrel	54-65	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	87-94
23220562-8	2013	It is concluded that attenuated expression of the TJ proteins occludin and ZO-1 in human gastric epithelial cells could be involved in clopidogrel-induced gastric mucosal injury through activation of the p38 MAPK pathway.	clopidogrel	135-146	mitogen-activated protein kinase 1	Homo sapiens	208-212
23220562-0	2013	Attenuated expression of the tight junction proteins is involved in clopidogrel-induced gastric injury through p38 MAPK activation.	clopidogrel	68-79	mitogen-activated protein kinase 14	Homo sapiens	111-114
23220562-0	2013	Attenuated expression of the tight junction proteins is involved in clopidogrel-induced gastric injury through p38 MAPK activation.	clopidogrel	68-79	mitogen-activated protein kinase 1	Homo sapiens	115-119
23220562-6	2013	Results showed that clopidogrel significantly increased dextran permeability, induced apoptosis, suppressed GES-1 cell viability, and reduced the expression of the TJ proteins (occludin and ZO-1), acting through p38 MAPK phosphorylation.	clopidogrel	20-31	occludin	Homo sapiens	177-185
23220562-6	2013	Results showed that clopidogrel significantly increased dextran permeability, induced apoptosis, suppressed GES-1 cell viability, and reduced the expression of the TJ proteins (occludin and ZO-1), acting through p38 MAPK phosphorylation.	clopidogrel	20-31	tight junction protein 1	Homo sapiens	190-194
23220562-6	2013	Results showed that clopidogrel significantly increased dextran permeability, induced apoptosis, suppressed GES-1 cell viability, and reduced the expression of the TJ proteins (occludin and ZO-1), acting through p38 MAPK phosphorylation.	clopidogrel	20-31	mitogen-activated protein kinase 14	Homo sapiens	212-215
23355205-1	2013	Conversion of clopidogrel (Plavix) to its active metabolite is catalyzed largely by the P450 enzyme 2C19 (CYP2C19).	clopidogrel	14-25	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	106-113
23220562-6	2013	Results showed that clopidogrel significantly increased dextran permeability, induced apoptosis, suppressed GES-1 cell viability, and reduced the expression of the TJ proteins (occludin and ZO-1), acting through p38 MAPK phosphorylation.	clopidogrel	20-31	mitogen-activated protein kinase 1	Homo sapiens	216-220
23220562-7	2013	Furthermore, these observed effects were partially abolished by SB-203580 (a p38 MAPK inhibitor), rather than by either U-0126 (an ERK inhibitor) or SP-600125 (a JNK inhibitor), suggesting that clopidogrel-induced disruption in the gastric epithelial cells is mediated by the p38 MAPK pathway.	clopidogrel	194-205	mitogen-activated protein kinase 8	Homo sapiens	162-165
23220562-7	2013	Furthermore, these observed effects were partially abolished by SB-203580 (a p38 MAPK inhibitor), rather than by either U-0126 (an ERK inhibitor) or SP-600125 (a JNK inhibitor), suggesting that clopidogrel-induced disruption in the gastric epithelial cells is mediated by the p38 MAPK pathway.	clopidogrel	194-205	mitogen-activated protein kinase 14	Homo sapiens	276-279
23220562-7	2013	Furthermore, these observed effects were partially abolished by SB-203580 (a p38 MAPK inhibitor), rather than by either U-0126 (an ERK inhibitor) or SP-600125 (a JNK inhibitor), suggesting that clopidogrel-induced disruption in the gastric epithelial cells is mediated by the p38 MAPK pathway.	clopidogrel	194-205	mitogen-activated protein kinase 1	Homo sapiens	81-85
23220562-8	2013	It is concluded that attenuated expression of the TJ proteins occludin and ZO-1 in human gastric epithelial cells could be involved in clopidogrel-induced gastric mucosal injury through activation of the p38 MAPK pathway.	clopidogrel	135-146	occludin	Homo sapiens	62-70
23220562-8	2013	It is concluded that attenuated expression of the TJ proteins occludin and ZO-1 in human gastric epithelial cells could be involved in clopidogrel-induced gastric mucosal injury through activation of the p38 MAPK pathway.	clopidogrel	135-146	tight junction protein 1	Homo sapiens	75-79
23220562-8	2013	It is concluded that attenuated expression of the TJ proteins occludin and ZO-1 in human gastric epithelial cells could be involved in clopidogrel-induced gastric mucosal injury through activation of the p38 MAPK pathway.	clopidogrel	135-146	mitogen-activated protein kinase 14	Homo sapiens	204-207
24900671-1	2013	Clopidogrel (CPG) is an antithrombotic prodrug that needs hepatic cytochrome P450 (CYP) enzymes for its bioactivation.	clopidogrel	0-11	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	66-81
24900671-1	2013	Clopidogrel (CPG) is an antithrombotic prodrug that needs hepatic cytochrome P450 (CYP) enzymes for its bioactivation.	clopidogrel	0-11	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	83-86
23355205-1	2013	Conversion of clopidogrel (Plavix) to its active metabolite is catalyzed largely by the P450 enzyme 2C19 (CYP2C19).	clopidogrel	27-33	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	106-113
23355205-11	2013	This CYP2C19 genotyping assay is appropriate for clinical testing, demonstrating excellent interlaboratory concordance, enabling the selection of the most effective clopidogrel treatment regimen for patients undergoing percutaneous coronary intervention.	clopidogrel	165-176	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	5-12
23431496-2	2013	The CYP2C19*2 allele may be associated with a reduced antiplatelet effect for clopidogrel.	clopidogrel	78-89	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
23089672-6	2013	We conclude that recent studies have emphasized the importance of CYP2C19 polymorphism for the effects of clopidogrel, whereas the CYP2C9 polymorphism appears to have a role in anticoagulant treatment, although inferior to VKORC1.	clopidogrel	106-117	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	66-73
23200799-4	2013	Indeed, CYP2C19 is involved in the conversion of the clopidogrel pro-drug into its active metabolite and is involved in the metabolisation of PPI into inactive metabolites, acting as substrates/inhibitors of CYP2C19.	clopidogrel	53-64	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	208-215
23245937-1	2013	INTRODUCTION: Previous work suggests that the extent of platelet inhibition by P2Y(1) receptor antagonism may be underappreciated, particularly in the context of dual antiplatelet therapy with aspirin and clopidogrel.	clopidogrel	205-216	purinergic receptor P2Y1	Homo sapiens	79-94
22830954-5	2013	The CYP2B6*6/*6 subjects in the clopidogrel phase showed the highest molar AUC (M1 + M2) among three genotype groups throughout the three phases.	clopidogrel	32-43	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	4-10
23201489-1	2013	The objective of this study was to investigate the contribution of genetic polymorphism of cytochrome P450 2C19 gene (CYP2C19) and non-genetic factors to clopidogrel in Chinese patients by using the plasma concentrations of SR26334 as a surrogate.	clopidogrel	154-165	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	91-111
23201489-6	2013	Multiple linear regression models incorporating genetic polymorphism of CYP2C19 and non-genetic factors, such as blood collection time, smoking status and clopidogrel doses were developed, and explained up to 63.1% of the total variation (adjusted R(2) of 0.631) in the plasma concentrations of SR26334 in Chinese patients.	clopidogrel	155-166	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	72-79
22706585-10	2013	The CYP2C19 genetic polymorphism may impact the efficacy of clopidogrel.	clopidogrel	60-71	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
23200799-3	2013	The issue of the interaction between PPI and clopidogrel has been raised with the emergence of the concept of "high on-clopidogrel platelet reactivity" (or "clopidogrel resistance") together with the discovery of the role of CYP2C19 isoform in the pharmacokinetics of those two medications.	clopidogrel	45-56	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	225-232
23200799-4	2013	Indeed, CYP2C19 is involved in the conversion of the clopidogrel pro-drug into its active metabolite and is involved in the metabolisation of PPI into inactive metabolites, acting as substrates/inhibitors of CYP2C19.	clopidogrel	53-64	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	8-15
23525436-1	2013	BACKGROUND: Proton pump inhibitors (PPIs) may interfere with the metabolic activation of clopidogrel via inhibition of cytochrome P450 2C19, but the clinical implications remain unclear.	clopidogrel	89-100	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	119-139
23287370-3	2013	Elevated fibrinogen also contributes to high on-clopidogrel platelet reactivity.	clopidogrel	48-59	fibrinogen beta chain	Homo sapiens	9-19
23287370-14	2013	CONCLUSIONS: Elevated fibrinogen is independently associated with the risk of ischemic myocardial injury following elective PCI with clopidogrel pre-treatment regardless of platelet reactivity as measured by the VerifyNow assay.	clopidogrel	133-144	fibrinogen beta chain	Homo sapiens	22-32
23607088-0	2013	Feasibility of a microarray-based point-of-care CYP2C19 genotyping test for predicting clopidogrel on-treatment platelet reactivity.	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	48-55
23607088-1	2013	Clopidogrel is a prodrug which is converted into active metabolite by cytochrome P450 isoenzyme, CYP2C19.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	97-104
23607088-2	2013	Numerous polymorphisms of CYP2C19 are reported, and a strong link exists between loss-of-function (LOF) or gain-of-function polymorphisms, clopidogrel metabolism, and clinical outcome.	clopidogrel	139-150	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
23431496-3	2013	Here, we assessed whether CYP2C19*2 alleles correlate with clopidogrel responsiveness following the administration of clopidogrel in healthy Malaysian volunteers.	clopidogrel	59-70	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
23431496-3	2013	Here, we assessed whether CYP2C19*2 alleles correlate with clopidogrel responsiveness following the administration of clopidogrel in healthy Malaysian volunteers.	clopidogrel	118-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
23431496-10	2013	Following clopidogrel intake, CYP2C19*2/*2 carriers had a significantly higher mean PRU compared to the CYP2C19*1/*2 and CYP2C19*1/*1 (291.0 +- 62.1 versus 232.5 +- 81.4 versus 147.4 +- 87.2 PRU, P &lt; 0.001) carriers.	clopidogrel	10-21	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
23431496-13	2013	In healthy Malaysian volunteers, CYP2C19*2 allele was associated with a decrease in platelet responsiveness to clopidogrel.	clopidogrel	111-122	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-40
23431496-14	2013	However, clopidogrel nonresponders can be found not only in the carriers of CYP2C19*2/*2, but also in the carriers of CYP2C19*1/*2 and CYP2C19*1/*1.	clopidogrel	9-20	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	76-83
23431496-14	2013	However, clopidogrel nonresponders can be found not only in the carriers of CYP2C19*2/*2, but also in the carriers of CYP2C19*1/*2 and CYP2C19*1/*1.	clopidogrel	9-20	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	118-125
23431496-14	2013	However, clopidogrel nonresponders can be found not only in the carriers of CYP2C19*2/*2, but also in the carriers of CYP2C19*1/*2 and CYP2C19*1/*1.	clopidogrel	9-20	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	118-125
24107485-2	2013	Additionally, novel P2Y12 receptor antagonists such as prasugrel and ticagrelor are even recommended over clopidogrel in certain clinical guidelines.	clopidogrel	106-117	purinergic receptor P2Y12	Homo sapiens	20-25
24469880-8	2013	CONCLUSIONS: Increasing the dose of ASA from 75 mg to 150 mg daily or switching ASA 75 mg to clopidogrel 75 mg daily may reduce concentrations of some inflammatory markers (in particular hsCRP, IL-6 and CD40L) in T2DM patients with HPR treated previously with 75 mg of ASA.	clopidogrel	93-104	interleukin 6	Homo sapiens	194-198
24469880-8	2013	CONCLUSIONS: Increasing the dose of ASA from 75 mg to 150 mg daily or switching ASA 75 mg to clopidogrel 75 mg daily may reduce concentrations of some inflammatory markers (in particular hsCRP, IL-6 and CD40L) in T2DM patients with HPR treated previously with 75 mg of ASA.	clopidogrel	93-104	CD40 ligand	Homo sapiens	203-208
23400261-0	2013	CYP3A4 genetic status may be associated with increased vulnerability to the inhibitory effect of calcium-channel blockers on clopidogrel.	clopidogrel	125-136	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
23400261-1	2013	BACKGROUND: Calcium-channel blockers (CCBs) inhibit the CYP3A4 enzyme, which is involved in clopidogrel activation.	clopidogrel	92-103	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	56-62
23400261-3	2013	We investigated the relationship between CYP3A4 genotype and the inhibitory effect of CCBs on clopidogrel response.	clopidogrel	94-105	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	41-47
23400261-11	2013	The number of CYP3A4 (IVS10+12G&gt;A) A-alleles may be associated with an increased vulnerability to the effects of CCBs on clopidogrel response variation.	clopidogrel	124-135	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	14-20
23470885-0	2013	Relationship between CYP2C19 loss-of-function polymorphism and platelet reactivities with clopidogrel treatment in Japanese patients undergoing coronary stent implantation.	clopidogrel	90-101	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
23470885-1	2013	BACKGROUND:  CYP2C19 loss-of-function genotype (*2 and/or *3 alleles) is related to low responsiveness to clopidogrel, which is a risk factor for ischemic cardiac events.	clopidogrel	106-117	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
23360266-2	2013	CYP2C19 is one of the principal enzymes involved in the metabolism of clopidogrel.	clopidogrel	70-81	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
23360266-4	2013	A loss-of-function allele, CYP2C19*2, is associated with an increased risk of major adverse cardiovascular events, particularly stent thrombosis, in patients with acute coronary syndromes who are receiving clopidogrel, especially among those undergoing percutaneous coronary intervention.	clopidogrel	206-217	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	27-34
23412869-1	2013	BACKGROUND: Cytochrome P450 2C19 is responsible for the metabolism of many drugs, including the activation of clopidogrel.	clopidogrel	110-121	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-32
23676588-1	2013	OBJECTIVE: We previously reported that the antiplatelet action is intensified with combined use of clopidogrel and cilostazol in ischemic stroke patients using the VerifyNow P2Y12 Assay.	clopidogrel	99-110	purinergic receptor P2Y12	Homo sapiens	174-179
23676588-5	2013	Clopidogrel resistance was defined as P2Y12 Reaction Units (PRU) &gt;230 and/or % inhibition &lt;20%.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	38-43
23140172-9	2013	In platelets from mice dosed with ABT-263 in vivo, clopidogrel or deficiency of P2Y(12) receptor enhanced apoptosis along with increased Bak/Bax activation.	clopidogrel	51-62	BCL2-antagonist/killer 1	Mus musculus	137-140
23140172-9	2013	In platelets from mice dosed with ABT-263 in vivo, clopidogrel or deficiency of P2Y(12) receptor enhanced apoptosis along with increased Bak/Bax activation.	clopidogrel	51-62	BCL2-associated X protein	Mus musculus	141-144
24088005-1	2013	We studied occurrence of allele variants *1, *2, *3, and *17 of CYP2C19 gene and polymorphic variants of ABCB1 gene in clopidogrel treated patients from West Siberian and Far Eastern regions and determined contribution of these polymorphisms to laboratory efficacy of clopidogrel.	clopidogrel	119-130	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	64-71
24088005-1	2013	We studied occurrence of allele variants *1, *2, *3, and *17 of CYP2C19 gene and polymorphic variants of ABCB1 gene in clopidogrel treated patients from West Siberian and Far Eastern regions and determined contribution of these polymorphisms to laboratory efficacy of clopidogrel.	clopidogrel	119-130	ATP binding cassette subfamily B member 1	Homo sapiens	105-110
24088005-3	2013	We found association between polymorphic variant CYP2C19*2 with changes of platelet aggregation after administration of clopidogrel.	clopidogrel	120-131	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	49-56
23777967-3	2013	The recently observed benefit of an alternative P2Y12 receptor antagonist (ticragelor) on survival as compared with clopidogrel suggests that the toxicity of the clopidogrel/aspirin combination likely results from an "off-target" effect.	clopidogrel	162-173	purinergic receptor P2Y12	Homo sapiens	48-53
23111421-0	2013	The functional G143E variant of carboxylesterase 1 is associated with increased clopidogrel active metabolite levels and greater clopidogrel response.	clopidogrel	80-91	carboxylesterase 1	Homo sapiens	32-50
23111421-0	2013	The functional G143E variant of carboxylesterase 1 is associated with increased clopidogrel active metabolite levels and greater clopidogrel response.	clopidogrel	129-140	carboxylesterase 1	Homo sapiens	32-50
23111421-1	2013	INTRODUCTION: Carboxylesterase 1 (CES1) is the primary enzyme responsible for converting clopidogrel into biologically inactive carboxylic acid metabolites.	clopidogrel	89-100	carboxylesterase 1	Homo sapiens	14-32
23111421-1	2013	INTRODUCTION: Carboxylesterase 1 (CES1) is the primary enzyme responsible for converting clopidogrel into biologically inactive carboxylic acid metabolites.	clopidogrel	89-100	carboxylesterase 1	Homo sapiens	34-38
23111421-2	2013	METHODS: We genotyped a functional variant in CES1, G143E, in participants of the Pharmacogenomics of Anti-Platelet Intervention (PAPI) study (n=566) and in 350 patients with coronary heart disease treated with clopidogrel, and carried out an association analysis of bioactive metabolite levels, on-clopidogrel ADP-stimulated platelet aggregation, and cardiovascular outcomes.	clopidogrel	211-222	carboxylesterase 1	Homo sapiens	46-50
23111421-2	2013	METHODS: We genotyped a functional variant in CES1, G143E, in participants of the Pharmacogenomics of Anti-Platelet Intervention (PAPI) study (n=566) and in 350 patients with coronary heart disease treated with clopidogrel, and carried out an association analysis of bioactive metabolite levels, on-clopidogrel ADP-stimulated platelet aggregation, and cardiovascular outcomes.	clopidogrel	299-310	carboxylesterase 1	Homo sapiens	46-50
23111421-3	2013	RESULTS: The levels of clopidogrel active metabolite were significantly greater in CES1 143E-allele carriers (P=0.001).	clopidogrel	23-34	carboxylesterase 1	Homo sapiens	83-87
23111421-4	2013	Consistent with these findings, individuals who carried the CES1 143E-allele showed a better clopidogrel response as measured by ADP-stimulated platelet aggregation in both participants of the PAPI study (P=0.003) and clopidogrel-treated coronary heart disease patients (P=0.03).	clopidogrel	93-104	carboxylesterase 1	Homo sapiens	60-64
23111421-4	2013	Consistent with these findings, individuals who carried the CES1 143E-allele showed a better clopidogrel response as measured by ADP-stimulated platelet aggregation in both participants of the PAPI study (P=0.003) and clopidogrel-treated coronary heart disease patients (P=0.03).	clopidogrel	218-229	carboxylesterase 1	Homo sapiens	60-64
23111421-6	2013	CONCLUSION: Taken together, these findings suggest, for the first time, that genetic variation in CES1 may be an important determinant of the efficacy of clopidogrel.	clopidogrel	154-165	carboxylesterase 1	Homo sapiens	98-102
23429358-0	2013	Relationship of CYP2C19*2 and CYP2C19*3 gene polymorphism with clopidogrel response variability and recurrent cardiovascular events in Chinese patients undergoing percutaneous coronary intervention.	clopidogrel	63-74	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
23429358-0	2013	Relationship of CYP2C19*2 and CYP2C19*3 gene polymorphism with clopidogrel response variability and recurrent cardiovascular events in Chinese patients undergoing percutaneous coronary intervention.	clopidogrel	63-74	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
23429358-1	2013	BACKGROUND/AIMS: The study was conducted to assess the influence of CYP2C19 polymorphisms on clopidogrel response variability and recurrent cardiovascular (CV) events in Chinese patients undergoing percutaneous coronary intervention (PCI).	clopidogrel	93-104	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	68-75
23429358-6	2013	Multiple linear regression analysis demonstrated that CYP2C19*2 and CYP2C19*3 might be predictors of clopidogrel response variability.	clopidogrel	101-112	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	54-61
23429358-6	2013	Multiple linear regression analysis demonstrated that CYP2C19*2 and CYP2C19*3 might be predictors of clopidogrel response variability.	clopidogrel	101-112	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	68-75
23429358-9	2013	CONCLUSION: Polymorphisms in CYP2C19*2 and CYP2C19*3 contribute to variabilities in clopidogrel responsiveness.	clopidogrel	84-95	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	29-36
23429358-9	2013	CONCLUSION: Polymorphisms in CYP2C19*2 and CYP2C19*3 contribute to variabilities in clopidogrel responsiveness.	clopidogrel	84-95	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	43-50
22916844-0	2013	High frequency of CYP2C19*2 carriers in PCI-treated patients switched over from clopidogrel to prasugrel based on platelet function monitoring.	clopidogrel	80-91	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	18-25
23148794-2	2013	Anti-platelet response to clopidogrel was studied prospectively using the VerifyNow (VN) P2Y12 assay at the time of angiography and at 30 days post procedure in 151 patients admitted with ACS who underwent percutaneous coronary intervention (PCI).	clopidogrel	26-37	purinergic receptor P2Y12	Homo sapiens	89-94
24293976-8	2012	Although soluble P-selectin increased when clopidogrel was stopped (p = 0.006), there were no changes in plasma markers or vascular function.	clopidogrel	43-54	selectin P	Homo sapiens	17-27
22721490-2	2013	Clopidogrel resistance has been attributed to P2Y1 and P2Y12 adenosine diphosphate (ADP) receptor polymorphisms.	clopidogrel	0-11	purinergic receptor P2Y1	Homo sapiens	46-50
22721490-2	2013	Clopidogrel resistance has been attributed to P2Y1 and P2Y12 adenosine diphosphate (ADP) receptor polymorphisms.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	55-60
22721490-13	2013	On follow up, the two patients who developed myocardial infarction/acute coronary syndromes (MI/ACS) were clopidogrel semi- and non-responder, respectively.	clopidogrel	106-117	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	96-99
22721490-14	2013	Variability in clopidogrel response with 13% non-responders and 19% semi-responders was seen in this study with adverse outcome (MI/ACS) on follow up seen in two patients.	clopidogrel	15-26	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	132-135
22757746-11	2013	In conclusion, HPR assessed by VerifyNow P2Y12 test was associated with increased adverse clinical outcomes of clopidogrel-treated patients with CV disease.	clopidogrel	111-122	purinergic receptor P2Y12	Homo sapiens	41-46
23137413-1	2013	BACKGROUND: The CYP2C19 genotype is a predictor of adverse cardiovascular events in acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI) treated with clopidogrel.	clopidogrel	188-199	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
23142468-17	2013	Clopidogrel seems to be a feasible inhibitor for equine CYP2B6.	clopidogrel	0-11	cytochrome P450 family 2 subfamily B member 6	Equus caballus	56-62
23225796-3	2013	Clopidogrel hyporesponsiveness was defined as percent inhibition of P2Y12 reaction units (PRU) &lt;30% on VerifyNow P2Y12 assay.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	68-73
23225796-3	2013	Clopidogrel hyporesponsiveness was defined as percent inhibition of P2Y12 reaction units (PRU) &lt;30% on VerifyNow P2Y12 assay.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	116-121
22730179-2	2012	(R)-o-chloromandelic acid (R)-1, a key intermediate for the antithrombotic agent clopidogrel, was obtained in 65% yield and 98% ee by Dutch resolution of rac-1 with (S)-2-hydroxyl-3-(p-chlorophenoxy) propylamine (S)-5 as resolving agent and (S)-2-hydroxyl-3-(o-nitrophenoxy) propylamine (S)-4 as nucleation inhibitor.	clopidogrel	81-92	Rac family small GTPase 1	Homo sapiens	154-159
24293976-3	2012	We tested the hypothesis that some of the beneficial effect of clopidogrel may be due to the variable activity of this drug on the vascular system (assessed by plasma markers von Willebrand factor and soluble E-selectin, and functional arterial pulse wave velocity) and inflammation (C-reactive protein and interleukin-6) while 32 patients with coronary artery disease taking 75 mg clopidogrel daily, and again 2 weeks after cessation of clopidogrel therapy.	clopidogrel	63-74	selectin E	Homo sapiens	209-219
24293976-3	2012	We tested the hypothesis that some of the beneficial effect of clopidogrel may be due to the variable activity of this drug on the vascular system (assessed by plasma markers von Willebrand factor and soluble E-selectin, and functional arterial pulse wave velocity) and inflammation (C-reactive protein and interleukin-6) while 32 patients with coronary artery disease taking 75 mg clopidogrel daily, and again 2 weeks after cessation of clopidogrel therapy.	clopidogrel	63-74	C-reactive protein	Homo sapiens	284-302
24293976-3	2012	We tested the hypothesis that some of the beneficial effect of clopidogrel may be due to the variable activity of this drug on the vascular system (assessed by plasma markers von Willebrand factor and soluble E-selectin, and functional arterial pulse wave velocity) and inflammation (C-reactive protein and interleukin-6) while 32 patients with coronary artery disease taking 75 mg clopidogrel daily, and again 2 weeks after cessation of clopidogrel therapy.	clopidogrel	63-74	interleukin 6	Homo sapiens	307-320
23257377-2	2012	BACKGROUND: CYP2C19*2 loss-of-function allele and CYP2C19*17 gain-of-function allele have been linked with response to clopidogrel, but preliminary data did not show any significant influence of these alleles on prasugrel effect.	clopidogrel	119-130	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
23257377-2	2012	BACKGROUND: CYP2C19*2 loss-of-function allele and CYP2C19*17 gain-of-function allele have been linked with response to clopidogrel, but preliminary data did not show any significant influence of these alleles on prasugrel effect.	clopidogrel	119-130	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	50-57
22990067-2	2012	To address this issue, we assessed the relation of single nucleotide polymorphisms within genes modulating clopidogrel absorption (ABCB1), metabolic activation (CYP2B6, CYP2D6, CYP3A4, CYP2C9, and CYP2C19), and biologic activity (P2RY12) to the response of clopidogrel as measured by ex-vivo platelet reactivity and ischemic events during half a year of follow-up.	clopidogrel	107-118	ATP binding cassette subfamily B member 1	Homo sapiens	131-136
23346768-1	2012	It is well known that CYP2C19*2/*2 is associated with attenuated response to clopidogrel, but recent findings indicated that in white patients, paraoxonase-1 (PON1) 192Q/Q was a major determinant of clopidogrel efficacy.	clopidogrel	77-88	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	22-29
23346768-1	2012	It is well known that CYP2C19*2/*2 is associated with attenuated response to clopidogrel, but recent findings indicated that in white patients, paraoxonase-1 (PON1) 192Q/Q was a major determinant of clopidogrel efficacy.	clopidogrel	77-88	paraoxonase 1	Homo sapiens	144-157
23346768-1	2012	It is well known that CYP2C19*2/*2 is associated with attenuated response to clopidogrel, but recent findings indicated that in white patients, paraoxonase-1 (PON1) 192Q/Q was a major determinant of clopidogrel efficacy.	clopidogrel	77-88	paraoxonase 1	Homo sapiens	159-163
23346768-1	2012	It is well known that CYP2C19*2/*2 is associated with attenuated response to clopidogrel, but recent findings indicated that in white patients, paraoxonase-1 (PON1) 192Q/Q was a major determinant of clopidogrel efficacy.	clopidogrel	199-210	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	22-29
23346768-1	2012	It is well known that CYP2C19*2/*2 is associated with attenuated response to clopidogrel, but recent findings indicated that in white patients, paraoxonase-1 (PON1) 192Q/Q was a major determinant of clopidogrel efficacy.	clopidogrel	199-210	paraoxonase 1	Homo sapiens	144-157
23346768-1	2012	It is well known that CYP2C19*2/*2 is associated with attenuated response to clopidogrel, but recent findings indicated that in white patients, paraoxonase-1 (PON1) 192Q/Q was a major determinant of clopidogrel efficacy.	clopidogrel	199-210	paraoxonase 1	Homo sapiens	159-163
23346768-2	2012	The objective of this research was to assess the impact of PON1 Q192R polymorphism on the maximum platelet aggregation (MPA) and the anti-platelet effect of clopidogrel in clopidogrel-treated Chinese stroke patients.	clopidogrel	172-183	paraoxonase 1	Homo sapiens	59-63
23427948-1	2012	OBJECTIVE: Acetylsalicylic acid (ASA) and clopidogrel (KLP) therapy is associated with the high degree of variability in response to the drug and some patients are drug-resistant.	clopidogrel	42-53	kinesin family member 1B	Homo sapiens	55-58
22975710-7	2012	Clopidogrel (2mg and 10mg/kg/day) significantly decreased ulcer-induced gastric epithelial cell proliferation and ulcer-stimulated expressions of EGF receptor and phosphorylated extracellular signal-regulated kinase (PERK) at the ulcer margin (P&lt;0.05).	clopidogrel	0-11	epidermal growth factor like 1	Rattus norvegicus	146-149
22975710-8	2012	Clopidogrel (10(-6)M) also inhibited EGF-stimulated EGF receptor, PERK expression, and cell proliferation in RGM-1 cells (P&lt;0.05), and caused 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	0-11	epidermal growth factor like 1	Rattus norvegicus	37-40
22975710-8	2012	Clopidogrel (10(-6)M) also inhibited EGF-stimulated EGF receptor, PERK expression, and cell proliferation in RGM-1 cells (P&lt;0.05), and caused 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	0-11	epidermal growth factor like 1	Rattus norvegicus	52-55
22975710-8	2012	Clopidogrel (10(-6)M) also inhibited EGF-stimulated EGF receptor, PERK expression, and cell proliferation in RGM-1 cells (P&lt;0.05), and caused 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	0-11	epidermal growth factor like 1	Rattus norvegicus	52-55
22975710-8	2012	Clopidogrel (10(-6)M) also inhibited EGF-stimulated EGF receptor, PERK expression, and cell proliferation in RGM-1 cells (P&lt;0.05), and caused 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	0-11	epidermal growth factor like 1	Rattus norvegicus	52-55
22975710-9	2012	In conclusion, clopidogrel delays gastric ulcer healing in rats via inhibiting gastric epithelial cell proliferation, at least by inhibition of the EGF receptor-ERK signal transduction pathway.	clopidogrel	15-26	epidermal growth factor like 1	Rattus norvegicus	148-151
23075823-4	2012	PPIs can attenuate metabolism of clopidogrel to its active metabolite by inhibiting various hepatic CYP450 enzymes, mainly CYP2C19.	clopidogrel	33-44	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	123-130
22374717-0	2012	Clarifying the importance of CYP2C19 and PON1 in the mechanism of clopidogrel bioactivation and in vivo antiplatelet response.	clopidogrel	66-77	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	29-36
22374717-0	2012	Clarifying the importance of CYP2C19 and PON1 in the mechanism of clopidogrel bioactivation and in vivo antiplatelet response.	clopidogrel	66-77	paraoxonase 1	Homo sapiens	41-45
22374717-1	2012	AIMS: It is thought that clopidogrel bioactivation and antiplatelet response are related to cytochrome P450 2C19 (CYP2C19).	clopidogrel	25-36	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	92-112
22374717-1	2012	AIMS: It is thought that clopidogrel bioactivation and antiplatelet response are related to cytochrome P450 2C19 (CYP2C19).	clopidogrel	25-36	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	114-121
22374717-2	2012	However, a recent study challenged this notion by proposing CYP2C19 as wholly irrelevant, while identifying paraoxonase-1 (PON1) and its Q192R polymorphism as the major driver of clopidogrel bioactivation and efficacy.	clopidogrel	179-190	paraoxonase 1	Homo sapiens	108-121
22374717-2	2012	However, a recent study challenged this notion by proposing CYP2C19 as wholly irrelevant, while identifying paraoxonase-1 (PON1) and its Q192R polymorphism as the major driver of clopidogrel bioactivation and efficacy.	clopidogrel	179-190	paraoxonase 1	Homo sapiens	123-127
22374717-3	2012	The aim of this study was to systematically elucidate the mechanism and relative contribution of PON1 in comparison to CYP2C19 to clopidogrel bioactivation and antiplatelet response.	clopidogrel	130-141	paraoxonase 1	Homo sapiens	97-101
22374717-3	2012	The aim of this study was to systematically elucidate the mechanism and relative contribution of PON1 in comparison to CYP2C19 to clopidogrel bioactivation and antiplatelet response.	clopidogrel	130-141	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	119-126
22374717-8	2012	Secondly, metabolic profiling of clopidogrel in vitro confirmed the role of CYP2C19 in bioactivating clopidogrel to H4.	clopidogrel	101-112	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	76-83
22374717-11	2012	CONCLUSION: Our results demonstrate that PON1 does not mediate clopidogrel active metabolite formation or antiplatelet action, while CYP2C19 activity and genotype remains a predictor of clopidogrel pharmacokinetics and antiplatelet response.	clopidogrel	186-197	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	133-140
23046071-0	2012	The influence of omeprazole on platelet inhibition of clopidogrel in various CYP2C19 mutant alleles.	clopidogrel	54-65	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	77-84
23046071-1	2012	Currently, concerns of clopidogrel and proton pump inhibitors (especially omeprazole) interaction are raised, because they are both metabolized by CYP2C19.	clopidogrel	23-34	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	147-154
23046071-3	2012	The study was to compare the influence of omeprazole on platelet inhibition of clopidogrel in various CYP2C19 mutant alleles.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	102-109
23046071-11	2012	In conclusion, concomitant therapy with omeprazole appears to reduce the antiplatelet effect of clopidogrel most significantly in homEMs of CYP2C19.	clopidogrel	96-107	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	140-147
22965108-0	2012	Comparison of prasugrel and clopidogrel in the setting of ACS without revascularization.	clopidogrel	28-39	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	58-61
22797934-1	2012	Clopidogrel is a prodrug that undergoes bioconversion via cytochrome P450 system to form an active metabolite (AM) that binds to the platelet ADP receptor.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	133-154
22797934-2	2012	The antiplatelet effect of clopidogrel is commonly assessed by measuring the aggregatory response to 5 muM ADP by light transmission aggregation (LTA) or multiple electrode aggregometry (MEA) or by the vasodilator-stimulated phosphoprotein platelet reactivity index (VASP-PRI).	clopidogrel	27-38	vasodilator stimulated phosphoprotein	Homo sapiens	267-271
22855283-4	2012	The pre- and post-PCI corrected thrombolysis in myocardial infarction frame count (CTFC) and the 8-h post-treatment platelet vasodilator-stimulated phosphoprotein (VASP) index was compared with a matched historical Asian STEMI cohort (n = 65) receiving 600 mg of clopidogrel pretreatment.	clopidogrel	263-274	vasodilator stimulated phosphoprotein	Homo sapiens	164-168
23111862-6	2012	Severe deficiency of ADAMTS-13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) was present in 80% and antibodies to 100% of these TTP patients on ticlopidine, 0% of the patients with clopidogrel-associated TTP (p &lt; 0.05), and an unknown percentage of patients with prasugrel-associated TTP.	clopidogrel	219-230	ADAM metallopeptidase with thrombospondin type 1 motif 13	Homo sapiens	21-30
22782352-0	2012	Effects of pioglitazone on platelet P2Y12-mediated signalling in clopidogrel-treated patients with type 2 diabetes mellitus.	clopidogrel	65-76	purinergic receptor P2Y12	Homo sapiens	36-41
22974536-1	2012	BACKGROUND: A recent clinical trial has demonstrated that patients with acute coronary syndromes (ACS) and the reduced function allele CYP2C19*2 (*2 allele), who are treated with thienopyridines, have an increased risk of adverse cardiac events with clopidogrel, but not with prasugrel.	clopidogrel	250-261	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	135-142
23363669-10	2012	(3) Multivariate logistic regression analysis showed that history of renal failure (OR = 19.77, 95%CI 4.38 - 89.18, P &lt; 0.01) and clopidogrel (OR = 19.77, 95%CI 4.38 - 89.18, P &lt; 0.01) and GPIIb/IIIa receptor antagonist (OR = 343.57, 95%CI 40.39 - 999.99, P &lt; 0.01) use were the independent risk factors for bleeding.	clopidogrel	133-144	integrin subunit alpha 2b	Homo sapiens	195-200
23363670-1	2012	OBJECTIVE: To detect the single nucleotide polymorphisms of clopidogrel metabolism related genes (CYP2C19, ABCB1 and PON1) in Chinese patients with acute coronary syndrome (ACS) by genotype analysis.	clopidogrel	60-71	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	98-105
23363670-1	2012	OBJECTIVE: To detect the single nucleotide polymorphisms of clopidogrel metabolism related genes (CYP2C19, ABCB1 and PON1) in Chinese patients with acute coronary syndrome (ACS) by genotype analysis.	clopidogrel	60-71	ATP binding cassette subfamily B member 1	Homo sapiens	107-112
23363670-1	2012	OBJECTIVE: To detect the single nucleotide polymorphisms of clopidogrel metabolism related genes (CYP2C19, ABCB1 and PON1) in Chinese patients with acute coronary syndrome (ACS) by genotype analysis.	clopidogrel	60-71	paraoxonase 1	Homo sapiens	117-121
23139136-1	2012	In this study, we investigated pharmacokinetic drug interactions of clopidogrel with P-gp inhibitors in rats and dogs.	clopidogrel	68-79	phosphoglycolate phosphatase	Rattus norvegicus	85-89
22234956-3	2012	PPIs are reported to diminish the effect of clopidogrel because both are metabolized by CYP2C19.	clopidogrel	44-55	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	88-95
22782352-1	2012	Patients with type 2 diabetes mellitus (T2DM) have impaired clopidogrel-induced antiplatelet effects, which may be in part attributed to their reduced sensitivity to insulin and consequently, results in upregulation of the P2Y12 signalling pathway.	clopidogrel	60-71	purinergic receptor P2Y12	Homo sapiens	223-228
22782352-2	2012	It has been hypothesised that insulin sensitising strategies may enhance clopidogrel-mediated P2Y12 inhibitory effects.	clopidogrel	73-84	purinergic receptor P2Y12	Homo sapiens	94-99
22782352-3	2012	The aim of this pilot pharmacodynamics (PD) study was to assess the impact of pioglitazone on clopidogrel-mediated P2Y12 inhibitory effects in patients with T2DM.	clopidogrel	94-105	purinergic receptor P2Y12	Homo sapiens	115-120
22996695-10	2012	Finally, mice treated with the clinical inhibitor of P2RY12, clopidogrel, were protected from pathologic osteolysis.	clopidogrel	61-72	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	53-59
22372976-1	2012	OBJECTIVES: The P2Y(12) inhibitor clopidogrel inhibits platelet aggregation and is used in the treatment and prevention of coronary artery disease.	clopidogrel	34-45	purinergic receptor P2Y12	Homo sapiens	16-23
22372976-9	2012	CONCLUSIONS: Use of the P2Y(12) inhibitor clopidogrel is associated with risk of fractures.	clopidogrel	42-53	purinergic receptor P2Y12	Homo sapiens	24-31
23026663-2	2012	Treatment regimens using the newer CYP12 antagonists prasugrel and ticagrelor demonstrate improved ex-vivo platelet inhibition and superior clinical efficacy in large-scale clinical trials-even in patients demonstrating clopidogrel resistance.	clopidogrel	220-231	cytochrome P450 family 8 subfamily B member 1	Homo sapiens	35-40
23048056-11	2012	Genotyping showed the same efficacy between high-dose clopidogrel and prasugrel in the 18 (56.3%) CYP2C19*2 noncarriers (HTPR in 12.5% versus 0, P=0.274), whereas it was significantly worse in the 14 (43.7%) carriers (HTPR in 43.7% versus 0, P=0.003).	clopidogrel	54-65	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	98-105
23048056-13	2012	Conversely, high-dose clopidogrel can address HTPR only in CYP2C19*2 noncarriers.	clopidogrel	22-33	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	59-66
22989428-0	2012	Clinical significance of the clopidogrel-proton pump inhibitor interaction after peripheral endovascular intervention for claudication.	clopidogrel	29-40	ATPase H+/K+ transporting subunit alpha	Homo sapiens	41-52
22989428-1	2012	OBJECTIVE: Despite numerous studies in the cardiology literature, the clinical impact of proton pump inhibitor (PPI) administration on the antiplatelet effect of clopidogrel remains controversial.	clopidogrel	162-173	ATPase H+/K+ transporting subunit alpha	Homo sapiens	89-100
22651985-8	2012	Pre-incubation with recombinant human CYP3A4 not only caused degradation of clopidogrel and ticlopidine, but also increased cytotoxicity.	clopidogrel	76-87	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	38-44
22651985-10	2012	Pre-incubation with freshly isolated human granulocytes was not only associated with a myeloperoxidase-dependent degradation of clopidogrel, clopidogrel carboxylate and ticlopidine, but also with dose-dependent cytotoxicity of these compounds starting at 10 muM.	clopidogrel	128-139	myeloperoxidase	Homo sapiens	87-102
22651985-12	2012	Taking exposure data in humans into account, the myelotoxic element of clopidogrel therapy is likely to be secondary to the formation of metabolites from clopidogrel carboxylate by myeloperoxidase.	clopidogrel	71-82	myeloperoxidase	Homo sapiens	181-196
24175073-5	2012	HPR and CYP2C19 LoF carriage are associated with clinical outcomes in high-risk clopidogrel-treated patients who have undergone percutaneous coronary intervention (PCI).	clopidogrel	80-91	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	8-15
22450429-2	2012	Both loss- and gain-of-function single nucleotide variants of CYP2C19 genes have been identified that affect clopidogrel metabolism and anti-platelet response.	clopidogrel	109-120	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	62-69
24900388-0	2012	Identification of the Significant Involvement and Mechanistic Role of CYP3A4/5 in Clopidogrel Bioactivation.	clopidogrel	82-93	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	70-76
24900388-2	2012	Previous studies have suggested that genetic polymorphism of CYP2C19 might be one determinant of clopidogrel efficacy and led to the CYP2C19 genotype-tailored antithrombotic therapy.	clopidogrel	97-108	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	61-68
24900388-7	2012	Identifying the significant involvement of CYP3A4/5 and characterizing its mechanistic role in clopidogrel bioactivation might assist future pharmacogenomic studies in exploring the full mechanism underlying clopidogrel efficacy.	clopidogrel	208-219	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	43-49
22338575-3	2012	According to the present guidelines, a dual antiplatelet treatment regimen consisting of aspirin and a P2Y12 receptor inhibitor such as clopidogrel, prasugrel or ticagrelor is routinely administered to ACS patients and to patients undergoing PCI in order to prevent thrombotic vessel occlusions.	clopidogrel	136-147	purinergic receptor P2Y12	Homo sapiens	103-108
22338575-5	2012	Along with this development, more potent P2Y12 receptor inhibitors like prasugrel and ticagrelor are substitutes for clopidogrel in specific circumstances such as in ACS patients or in patients who do not adequately respond to standard clopidogrel treatment.	clopidogrel	236-247	purinergic receptor P2Y12	Homo sapiens	41-46
22450429-13	2012	Although several prior studies, including mainly stented patients, have emphasized the relationship between CYP2C19 loss-of-function alleles and efficacy of clopidogrel, this study of stable patients establishes a potential link with reduced bleeding complications.	clopidogrel	157-168	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	108-115
22507978-1	2012	AIMS: CYP3A4-metabolized statins can influence the pharmacodynamic effect of clopidogrel.	clopidogrel	77-88	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	6-12
22507978-12	2012	CONCLUSIONS: Among PCI-treated patients with HPR during co-administration of clopidogrel and atorvastatin, switching to a non-CYP3A4-metabolized statin can significantly decrease platelet reactivity and the prevalence of HPR.	clopidogrel	77-88	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	126-132
22569995-6	2012	The median peri-interventional concentration of beta-TG was 224.5 vs. 365.5 (P = 0.03) in the clopidogrel and placebo group.	clopidogrel	94-105	pro-platelet basic protein	Homo sapiens	48-55
22733806-0	2012	Glutaredoxin is involved in the formation of the pharmacologically active metabolite of clopidogrel from its GSH conjugate.	clopidogrel	88-99	glutaredoxin	Homo sapiens	0-12
22733806-12	2012	In conclusion, we found that human glutaredoxin is a main contributor to the formation of the pharmacologically active metabolite of clopidogrel from its GSH conjugate in human liver.	clopidogrel	133-144	glutaredoxin	Homo sapiens	35-47
22744772-10	2012	The Cox hazards regression model was used to estimate the risk of an adverse cardiovascular event in the clopidogrel plus PPI group versus the clopidogrel alone group.	clopidogrel	105-116	cytochrome c oxidase subunit 8A	Homo sapiens	4-7
23016454-0	2012	CYP2C19 681G &gt; A polymorphism and pharmacokinetics of clopidogrel in Chinese healthy volunteers.	clopidogrel	57-68	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
23016454-1	2012	The aim of this study was to investigate the contribution of the most frequent single nucleotide polymorphism of CYP2C19 681G&gt;A to the pharmacokinetics of clopidogrel in 20 healthy Chinese volunteers after administration of a single dose of clopidogrel 75mg.	clopidogrel	158-169	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	113-120
23016454-1	2012	The aim of this study was to investigate the contribution of the most frequent single nucleotide polymorphism of CYP2C19 681G&gt;A to the pharmacokinetics of clopidogrel in 20 healthy Chinese volunteers after administration of a single dose of clopidogrel 75mg.	clopidogrel	244-255	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	113-120
22704077-1	2012	INTRODUCTION: Thrombolysis, as reperfusion therapy for ST segment elevation myocardial infarction (STEMI), induces a pro-thrombotic status with enhanced platelet activity; this study aims to evaluate P2Y12 platelet reactivity and response to clopidogrel in the post-thrombolysis scenario.	clopidogrel	242-253	purinergic receptor P2Y12	Homo sapiens	200-205
22735685-1	2012	OBJECTIVE: To test the effect of a loss-of-function variation of the cytochrome P450 (CYP) 3A5 on drug-drug interaction between amlodipine and clopidogrel.	clopidogrel	143-154	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	69-94
22735685-2	2012	Amlodipine is a well-known inhibitor of CYP 3A4, an isoenzyme of CYP3A that activates clopidogrel.	clopidogrel	86-97	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	40-47
22534051-6	2012	Response to clopidogrel was determined by the VerifyNow P2Y12 assay (reported as P2Y12 response units) and multiple electrode aggregometry (MEA; reported as aggregation units).	clopidogrel	12-23	purinergic receptor P2Y12	Homo sapiens	56-61
22735685-4	2012	In the presence of CYP3A4 inhibitors such as amlodipine, the genetic variation of CYP3A5, the isoenzyme responsible for the backup CYP3A activity, may play an important role in clopidogrel activation.	clopidogrel	177-188	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	19-25
22735685-4	2012	In the presence of CYP3A4 inhibitors such as amlodipine, the genetic variation of CYP3A5, the isoenzyme responsible for the backup CYP3A activity, may play an important role in clopidogrel activation.	clopidogrel	177-188	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	82-88
22591668-0	2012	Meta-analysis of cytochrome P450 2C19 polymorphism and risk of adverse clinical outcomes among coronary artery disease patients of different ethnic groups treated with clopidogrel.	clopidogrel	168-179	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-37
22591668-1	2012	Loss-of-function (LOF) variants of cytochrome P450 2C19 (CYP2C19) have been hypothesized to be associated with lesser degrees of platelet inhibition and increased risk for recurrent ischemic events in patients with coronary artery disease on clopidogrel therapy; however, studies from Western countries have yielded mixed results.	clopidogrel	242-253	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	35-55
22591668-1	2012	Loss-of-function (LOF) variants of cytochrome P450 2C19 (CYP2C19) have been hypothesized to be associated with lesser degrees of platelet inhibition and increased risk for recurrent ischemic events in patients with coronary artery disease on clopidogrel therapy; however, studies from Western countries have yielded mixed results.	clopidogrel	242-253	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	57-64
22591668-7	2012	In conclusion, carrier status for LOF CYP2C19 is associated with an increased risk of adverse clinical events in patients with coronary artery disease on clopidogrel therapy despite differences in clinical significance according to ethnicity.	clopidogrel	154-165	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	38-45
22753481-6	2012	Treatment with aspirin and clopidogrel during the chronic phase of the disease diminished the number of intrahepatic HBV-specific CD8(+) T cells and HBV-nonspecific inflammatory cells, the severity of liver fibrosis, and the development of HCC.	clopidogrel	27-38	CD8a molecule	Homo sapiens	130-133
22883224-16	2012	Long-term antiplatelet treatment with aspirin alone seems to attenuate thrombin generation to a greater extent than with clopidogrel alone.	clopidogrel	121-132	coagulation factor II, thrombin	Homo sapiens	71-79
22534051-6	2012	Response to clopidogrel was determined by the VerifyNow P2Y12 assay (reported as P2Y12 response units) and multiple electrode aggregometry (MEA; reported as aggregation units).	clopidogrel	12-23	purinergic receptor P2Y12	Homo sapiens	81-86
22428615-2	2012	More recently, paraoxonase-1 (PON1) has been proposed as a major contributor to clopidogrel metabolism.	clopidogrel	80-91	paraoxonase 1	Homo sapiens	15-28
22428615-2	2012	More recently, paraoxonase-1 (PON1) has been proposed as a major contributor to clopidogrel metabolism.	clopidogrel	80-91	paraoxonase 1	Homo sapiens	30-34
22428615-3	2012	The purpose of this study was to assess the relative contribution of CYPs and PON1 to clopidogrel metabolism in vitro.	clopidogrel	86-97	paraoxonase 1	Homo sapiens	78-82
22428615-11	2012	Moreover, incubation with inhibitors of CYP3A, CYP2B6 and CYP2C19 significantly reduced clopidogrel bioactivation while a PON1 inhibitor, EDTA, had only a weak inhibitory effect.	clopidogrel	88-99	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	40-45
22428615-11	2012	Moreover, incubation with inhibitors of CYP3A, CYP2B6 and CYP2C19 significantly reduced clopidogrel bioactivation while a PON1 inhibitor, EDTA, had only a weak inhibitory effect.	clopidogrel	88-99	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	47-53
22428615-11	2012	Moreover, incubation with inhibitors of CYP3A, CYP2B6 and CYP2C19 significantly reduced clopidogrel bioactivation while a PON1 inhibitor, EDTA, had only a weak inhibitory effect.	clopidogrel	88-99	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	58-65
22428615-12	2012	CONCLUSION AND IMPLICATIONS: This in vitro study shows that the contribution of PON1 to clopidogrel metabolism is limited at clinically relevant concentrations.	clopidogrel	88-99	paraoxonase 1	Homo sapiens	80-84
22428615-13	2012	Moreover, CYP2C19, CYP2B6 and CYP3A play important roles in the bioactivation of clopidogrel.	clopidogrel	81-92	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-17
22428615-13	2012	Moreover, CYP2C19, CYP2B6 and CYP3A play important roles in the bioactivation of clopidogrel.	clopidogrel	81-92	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	19-25
22428615-13	2012	Moreover, CYP2C19, CYP2B6 and CYP3A play important roles in the bioactivation of clopidogrel.	clopidogrel	81-92	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	30-35
21883998-5	2012	A number of novel P2Y12 antagonists are approved or in advanced development and some have demonstrated superior platelet inhibition effect, clinical outcomes, and safety profile than clopidogrel in patients with acute coronary syndrome.	clopidogrel	183-194	purinergic receptor P2Y12	Homo sapiens	18-23
22992232-3	2012	Their data shows that the phenotyping of platelet response to clopidogrel by multiple electrode aggregometry was a better predictor of stent thrombosis than other platelet function assays used and even genotyping for the CYP2C19*2 allele.	clopidogrel	62-73	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	221-228
23030291-3	2012	Genotyping may have an emerging role in personalized antiplatelet therapy, particularly with the advent of new P2Y12 receptor blockers that have more rapid and potent pharmacodynamic properties than clopidogrel.	clopidogrel	199-210	purinergic receptor P2Y12	Homo sapiens	111-116
22674970-5	2012	On the other hand, polymorphisms in the CYP2C19 gene affect clopidogrel pharmacokinetics.	clopidogrel	60-71	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-47
22588534-5	2012	The P2Y12 antagonist, clopidogrel, was included as a reference agent.	clopidogrel	22-33	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	4-9
22584220-2	2012	In this work, we extended our studies of the metabolism of clopidogrel to human liver microsomes in the presence of four reductants, namely, GSH, l-Cys, N-acetyl-l-cysteine (NAC), and ascorbic acid.	clopidogrel	59-70	X-linked Kx blood group	Homo sapiens	174-177
21358751-0	2012	Identification of CYP2C19*4B: pharmacogenetic implications for drug metabolism including clopidogrel responsiveness.	clopidogrel	89-100	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	18-25
21358751-1	2012	CYP2C19 is a principal enzyme involved in the bioactivation of the antiplatelet prodrug clopidogrel and common CYP2C19 loss-of-function alleles are associated with adverse cardiovascular events.	clopidogrel	88-99	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
21358751-5	2012	Combining CYP2C19 and ABCB1 identified ~1 in 3 AJ and ~1 in 2 SJ individuals at increased risk for adverse responses to clopidogrel.	clopidogrel	120-131	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-17
21358751-5	2012	Combining CYP2C19 and ABCB1 identified ~1 in 3 AJ and ~1 in 2 SJ individuals at increased risk for adverse responses to clopidogrel.	clopidogrel	120-131	ATP binding cassette subfamily B member 1	Homo sapiens	22-27
22459907-0	2012	Protease activated receptor-1 (PAR-1) mediated platelet aggregation is dependent on clopidogrel response.	clopidogrel	84-95	coagulation factor II thrombin receptor	Homo sapiens	0-29
22459907-0	2012	Protease activated receptor-1 (PAR-1) mediated platelet aggregation is dependent on clopidogrel response.	clopidogrel	84-95	coagulation factor II thrombin receptor	Homo sapiens	31-36
22459907-1	2012	INTRODUCTION: Clopidogrel inhibits ADP mediated platelet aggregation through inhibition of the P2Y12 receptor by its active metabolite.	clopidogrel	14-25	purinergic receptor P2Y12	Homo sapiens	95-100
22459907-2	2012	Thrombin induces platelet aggregation by binding to protease activated receptor-1 (PAR-1), and inhibition of PAR-1 has been evaluated in patients treated with clopidogrel to reduce ischemic events after acute coronary syndromes.	clopidogrel	159-170	coagulation factor II thrombin receptor	Homo sapiens	109-114
22459907-3	2012	Residual PAR-1 mediated platelet aggregation may be dependent on extent of clopidogrel response.	clopidogrel	75-86	coagulation factor II thrombin receptor	Homo sapiens	9-14
22459907-6	2012	RESULTS: Increasing quartiles of 20 muM ADP induced platelet aggregation after clopidogrel loading were associated with increasing levels of TRAP mediated platelet aggregation.	clopidogrel	79-90	TRAP	Homo sapiens	141-145
22459907-7	2012	Patients in the highest quartile (clopidogrel non-responders) of post treatment ADP aggregation had significantly higher TRAP mediated aggregation than the patients in the lowest quartile (clopidogrel responders) [TRAP 15 muM: 79.6 +- 5% vs. 69.5 +- 8%, p&lt;0.001].	clopidogrel	34-45	TRAP	Homo sapiens	121-125
22459907-7	2012	Patients in the highest quartile (clopidogrel non-responders) of post treatment ADP aggregation had significantly higher TRAP mediated aggregation than the patients in the lowest quartile (clopidogrel responders) [TRAP 15 muM: 79.6 +- 5% vs. 69.5 +- 8%, p&lt;0.001].	clopidogrel	34-45	TRAP	Homo sapiens	214-218
22459907-7	2012	Patients in the highest quartile (clopidogrel non-responders) of post treatment ADP aggregation had significantly higher TRAP mediated aggregation than the patients in the lowest quartile (clopidogrel responders) [TRAP 15 muM: 79.6 +- 5% vs. 69.5 +- 8%, p&lt;0.001].	clopidogrel	189-200	TRAP	Homo sapiens	121-125
22459907-8	2012	CONCLUSIONS: Non-responders to clopidogrel show increased residual platelet aggregation induced by TRAP, whereas clopidogrel responders exhibit attenuated response to TRAP.	clopidogrel	31-42	TRAP	Homo sapiens	99-103
22459907-8	2012	CONCLUSIONS: Non-responders to clopidogrel show increased residual platelet aggregation induced by TRAP, whereas clopidogrel responders exhibit attenuated response to TRAP.	clopidogrel	113-124	TRAP	Homo sapiens	167-171
22459907-9	2012	Addition of PAR-1 antiplatelet drugs may be most effective in patients with reduced clopidogrel response and high residual TRAP mediated platelet aggregation.	clopidogrel	84-95	coagulation factor II thrombin receptor	Homo sapiens	12-17
22740070-0	2012	The extent of P2Y12 inhibition by clopidogrel in diabetes mellitus patients with acute coronary syndrome is not related to glycaemic control: roles of white blood cell count and body weight.	clopidogrel	34-45	purinergic receptor P2Y12	Homo sapiens	14-19
22740070-12	2012	In conclusion, in ACS DM patients undergoing PCI, the extent of P2Y12 inhibition by clopidogrel is not related to glycaemic control but is related to body weight and inflammatory status as assessed by the WBC.	clopidogrel	84-95	purinergic receptor P2Y12	Homo sapiens	64-69
22520065-0	2012	Influence of the paraoxonase-1 Q192R genetic variant on clopidogrel responsiveness and recurrent cardiovascular events: a systematic review and meta-analysis.	clopidogrel	56-67	paraoxonase 1	Homo sapiens	17-30
22652599-0	2012	Fractalkine activates a signal transduction pathway similar to P2Y12 and is associated with impaired clopidogrel responsiveness.	clopidogrel	101-112	C-X3-C motif chemokine ligand 1	Homo sapiens	0-11
22652599-1	2012	OBJECTIVE: Fractalkine (FKN) activates a G(alphai) protein-coupled signaling pathway similar to the one activated by ADP via P2Y(12), which is the drug target of clopidogrel.	clopidogrel	162-173	C-X3-C motif chemokine ligand 1	Homo sapiens	11-22
22652599-1	2012	OBJECTIVE: Fractalkine (FKN) activates a G(alphai) protein-coupled signaling pathway similar to the one activated by ADP via P2Y(12), which is the drug target of clopidogrel.	clopidogrel	162-173	C-X3-C motif chemokine ligand 1	Homo sapiens	24-27
22652599-2	2012	FKN levels are increased under several disease conditions associated with impaired clopidogrel responsiveness.	clopidogrel	83-94	C-X3-C motif chemokine ligand 1	Homo sapiens	0-3
22652599-5	2012	In vitro, FKN increased platelet reactivity index in clopidogrel-treated patients indicating potential activation of downstream targets of P2Y(12).	clopidogrel	53-64	C-X3-C motif chemokine ligand 1	Homo sapiens	10-13
22652599-6	2012	When stratifying patients by their FKN levels, patients within the highest quartile of FKN (2042 +- 25 pg/mL) had the weakest response to clopidogrel (platelet reactivity index, 68 +- 4%), and patients within the lowest quartile (479 +- 50 pg/mL) had the strongest response (platelet reactivity index, 48 +- 7%; P=0.0106).	clopidogrel	138-149	C-X3-C motif chemokine ligand 1	Homo sapiens	87-90
22652599-9	2012	FKN increased the platelet ADP response in clopidogrel-treated patients.	clopidogrel	43-54	C-X3-C motif chemokine ligand 1	Homo sapiens	0-3
23141010-0	2012	[Clinical application of VerifyNow-P2Y12 assay in evaluation of platelet inhibition efficacy of clopidogrel].	clopidogrel	96-107	purinergic receptor P2Y12	Homo sapiens	35-40
23141010-1	2012	OBJECTIVE: To evaluate the platelet inhibition efficacy in patients under regular maintenance dose of clopidogrel by VerifyNow-P2Y12 assay and explore the clinical characteristics of clopidogrel non-responders and related predicting factors.	clopidogrel	102-113	purinergic receptor P2Y12	Homo sapiens	127-132
23141010-12	2012	CONCLUSIONS: Clopidogrel responses could be reliably detected by VerifyNow-P2Y12 assay.	clopidogrel	13-24	purinergic receptor P2Y12	Homo sapiens	75-80
22682553-8	2012	Presence or absence of HPR following clopidogrel loading was determined by platelet function testing on a Multiplate analyzer (Verum Diagnostica, Munich, Germany).	clopidogrel	37-48	haptoglobin-related protein	Homo sapiens	23-26
22875498-0	2012	[Prevalence of CYP2C19 polymorphisms involved in clopidogrel metabolism in Fujian Han population].	clopidogrel	49-60	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
22875498-1	2012	OBJECTIVE: To investigate the frequency of CYP2C19 polymorphisms involved in clopidogrel metabolism in Fujian Han population.	clopidogrel	77-88	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	43-50
22875511-1	2012	OBJECTIVE: To investigate the impact of omeprazole on platelet response to clopidogrel and the effect of polymorphisms of CYP2C19 on the antiplatelet effect of clopidogrel.	clopidogrel	160-171	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	122-129
22875511-10	2012	The variant of CYP2C19*2 AA genotype is significantly associated with attenuated response to clopidogrel.	clopidogrel	93-104	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
22789884-2	2012	BACKGROUND: Newer P2Y12 inhibitors like prasugrel and ticagrelor provide stronger platelet inhibition compared with clopidogrel.	clopidogrel	116-127	purinergic receptor P2Y12	Homo sapiens	18-23
22795280-2	2012	BACKGROUND: The point-of-care VN-P2Y12 has been used to assess the antiplatelet effects in clopidogrel-treated patients but has not been evaluated in detail in patients treated with ticagrelor.	clopidogrel	91-102	purinergic receptor P2Y12	Homo sapiens	33-38
22795280-10	2012	CONCLUSIONS: The VerifyNow P2Y12 assay is effective in assessing the antiplatelet effects and in identifying HPR during clopidogrel or ticagrelor therapy.	clopidogrel	120-131	purinergic receptor P2Y12	Homo sapiens	27-32
22243420-1	2012	WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT:   The CYP3A4 inhibition by lipophilic statins may attenuate the effectiveness of clopidogrel.	clopidogrel	123-134	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	48-54
22568693-6	2012	Expression of the 3435T/T genetic variant encoding the MDR1 gene for the P-glycoprotein efflux transporter results in a significantly reduced maximum drug concentration and area under the plasma concentration-time curve as intestinal absorption of clopidogrel is reduced; and the expression of the mutant *2 allele of CYP2C19 results in similar pharmacokinetic effects as the two cytochrome P450 (CYP)-mediated steps required for the production of the active metabolite of clopidogrel are impaired.	clopidogrel	248-259	ATP binding cassette subfamily B member 1	Homo sapiens	55-59
22568693-6	2012	Expression of the 3435T/T genetic variant encoding the MDR1 gene for the P-glycoprotein efflux transporter results in a significantly reduced maximum drug concentration and area under the plasma concentration-time curve as intestinal absorption of clopidogrel is reduced; and the expression of the mutant *2 allele of CYP2C19 results in similar pharmacokinetic effects as the two cytochrome P450 (CYP)-mediated steps required for the production of the active metabolite of clopidogrel are impaired.	clopidogrel	248-259	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	318-325
22568693-6	2012	Expression of the 3435T/T genetic variant encoding the MDR1 gene for the P-glycoprotein efflux transporter results in a significantly reduced maximum drug concentration and area under the plasma concentration-time curve as intestinal absorption of clopidogrel is reduced; and the expression of the mutant *2 allele of CYP2C19 results in similar pharmacokinetic effects as the two cytochrome P450 (CYP)-mediated steps required for the production of the active metabolite of clopidogrel are impaired.	clopidogrel	248-259	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	380-395
22568693-6	2012	Expression of the 3435T/T genetic variant encoding the MDR1 gene for the P-glycoprotein efflux transporter results in a significantly reduced maximum drug concentration and area under the plasma concentration-time curve as intestinal absorption of clopidogrel is reduced; and the expression of the mutant *2 allele of CYP2C19 results in similar pharmacokinetic effects as the two cytochrome P450 (CYP)-mediated steps required for the production of the active metabolite of clopidogrel are impaired.	clopidogrel	248-259	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	318-321
22568693-6	2012	Expression of the 3435T/T genetic variant encoding the MDR1 gene for the P-glycoprotein efflux transporter results in a significantly reduced maximum drug concentration and area under the plasma concentration-time curve as intestinal absorption of clopidogrel is reduced; and the expression of the mutant *2 allele of CYP2C19 results in similar pharmacokinetic effects as the two cytochrome P450 (CYP)-mediated steps required for the production of the active metabolite of clopidogrel are impaired.	clopidogrel	473-484	ATP binding cassette subfamily B member 1	Homo sapiens	55-59
22568693-6	2012	Expression of the 3435T/T genetic variant encoding the MDR1 gene for the P-glycoprotein efflux transporter results in a significantly reduced maximum drug concentration and area under the plasma concentration-time curve as intestinal absorption of clopidogrel is reduced; and the expression of the mutant *2 allele of CYP2C19 results in similar pharmacokinetic effects as the two cytochrome P450 (CYP)-mediated steps required for the production of the active metabolite of clopidogrel are impaired.	clopidogrel	473-484	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	318-325
22568693-6	2012	Expression of the 3435T/T genetic variant encoding the MDR1 gene for the P-glycoprotein efflux transporter results in a significantly reduced maximum drug concentration and area under the plasma concentration-time curve as intestinal absorption of clopidogrel is reduced; and the expression of the mutant *2 allele of CYP2C19 results in similar pharmacokinetic effects as the two cytochrome P450 (CYP)-mediated steps required for the production of the active metabolite of clopidogrel are impaired.	clopidogrel	473-484	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	380-395
22568693-6	2012	Expression of the 3435T/T genetic variant encoding the MDR1 gene for the P-glycoprotein efflux transporter results in a significantly reduced maximum drug concentration and area under the plasma concentration-time curve as intestinal absorption of clopidogrel is reduced; and the expression of the mutant *2 allele of CYP2C19 results in similar pharmacokinetic effects as the two cytochrome P450 (CYP)-mediated steps required for the production of the active metabolite of clopidogrel are impaired.	clopidogrel	473-484	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	318-321
22588608-4	2012	In one year, approximately 3,000 patients, most of whom were scheduled for cardiac catheterization, were genotyped on a multiplexed platform that included genotyping for CYP2C19 variants that modulate response to the widely used antiplatelet drug clopidogrel.	clopidogrel	247-258	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	170-177
22565143-4	2012	The impact of CYP2C19 loss-of-function alleles on clopidogrel effect may be more modest than initially reported, though an impact on stent thrombosis is evident.	clopidogrel	50-61	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
22504157-7	2012	CES1 levels significantly correlated with hydrolysis of the CES1 substrates, clopidogrel (5 muM) and oxybutynin (10 muM), whereas CES2 levels correlated strongly with hydrolysis of the CES2 substrate, irinotecan (1 muM), indicating that quantified protein levels are highly reliable.	clopidogrel	77-88	carboxylesterase 1	Homo sapiens	0-4
22504157-7	2012	CES1 levels significantly correlated with hydrolysis of the CES1 substrates, clopidogrel (5 muM) and oxybutynin (10 muM), whereas CES2 levels correlated strongly with hydrolysis of the CES2 substrate, irinotecan (1 muM), indicating that quantified protein levels are highly reliable.	clopidogrel	77-88	latexin	Homo sapiens	92-95
22929815-0	2012	CYP2C19*2/ABCB1-C3435T polymorphism and risk of cardiovascular events in coronary artery disease patients on clopidogrel: is clinical testing helpful?	clopidogrel	109-120	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
22929815-0	2012	CYP2C19*2/ABCB1-C3435T polymorphism and risk of cardiovascular events in coronary artery disease patients on clopidogrel: is clinical testing helpful?	clopidogrel	109-120	ATP binding cassette subfamily B member 1	Homo sapiens	10-15
22929815-11	2012	CONCLUSION: In CAD patients on clopidogrel therapy, CYP2C19*2 polymorphism is associated with significantly increased adverse cardiovascular events.	clopidogrel	31-42	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	52-59
22520065-2	2012	Paraoxonase 1 (PON1) enzyme activity is modulated by the PON1-Q192R variant (rs662) and was recently suggested to be strongly involved in clopidogrel bioactivation, but the influence of the PON1-Q192R variant on the risk of MACE in clopidogrel-treated patients is controversial.	clopidogrel	138-149	paraoxonase 1	Homo sapiens	0-13
22520065-2	2012	Paraoxonase 1 (PON1) enzyme activity is modulated by the PON1-Q192R variant (rs662) and was recently suggested to be strongly involved in clopidogrel bioactivation, but the influence of the PON1-Q192R variant on the risk of MACE in clopidogrel-treated patients is controversial.	clopidogrel	138-149	paraoxonase 1	Homo sapiens	15-19
22520065-2	2012	Paraoxonase 1 (PON1) enzyme activity is modulated by the PON1-Q192R variant (rs662) and was recently suggested to be strongly involved in clopidogrel bioactivation, but the influence of the PON1-Q192R variant on the risk of MACE in clopidogrel-treated patients is controversial.	clopidogrel	232-243	paraoxonase 1	Homo sapiens	0-13
22520065-2	2012	Paraoxonase 1 (PON1) enzyme activity is modulated by the PON1-Q192R variant (rs662) and was recently suggested to be strongly involved in clopidogrel bioactivation, but the influence of the PON1-Q192R variant on the risk of MACE in clopidogrel-treated patients is controversial.	clopidogrel	232-243	paraoxonase 1	Homo sapiens	15-19
22520065-3	2012	OBJECTIVES: To determine whether the PON1-Q192R variant influences clopidogrel biological responsiveness and the risk of MACE in patients treated with clopidogrel.	clopidogrel	67-78	paraoxonase 1	Homo sapiens	37-41
22520065-3	2012	OBJECTIVES: To determine whether the PON1-Q192R variant influences clopidogrel biological responsiveness and the risk of MACE in patients treated with clopidogrel.	clopidogrel	151-162	paraoxonase 1	Homo sapiens	37-41
22520065-4	2012	METHODS: Systematic review and meta-analysis of studies of the association between the PON1-Q192R polymorphism and the biological response to clopidogrel and/or the risk of MACE during clopidogrel administration.	clopidogrel	142-153	paraoxonase 1	Homo sapiens	87-91
22520065-4	2012	METHODS: Systematic review and meta-analysis of studies of the association between the PON1-Q192R polymorphism and the biological response to clopidogrel and/or the risk of MACE during clopidogrel administration.	clopidogrel	185-196	paraoxonase 1	Homo sapiens	87-91
22285300-6	2012	Dose-adjustment was performed using up-to 3 additional loading doses (LD) of 600mg clopidogrel in order to obtain a VASP &lt;50% in patients with HTPR following the first LD.	clopidogrel	83-94	vasodilator stimulated phosphoprotein	Homo sapiens	116-120
22285300-12	2012	CONCLUSION: While CYP 2C19 2* is associated with HTPR after 600mg of clopidogrel, ABCB1 is responsible for the failure of a strategy of loading dose-adjustment according to PR monitoring.	clopidogrel	69-80	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	18-26
22535315-4	2012	The VASP index was used to assess PR inhibition after clopidogrel LD.	clopidogrel	54-65	vasodilator stimulated phosphoprotein	Homo sapiens	4-8
22627684-1	2012	Translational platelet function investigations performed in the percutaneous coronary intervention (PCI)-treated population receiving clopidogrel have identified high platelet reactivity to ADP (HPR) as a major risk factor for both acute as well as long-term ischaemic event occurrence, including stent thrombosis.	clopidogrel	134-145	haptoglobin-related protein	Homo sapiens	195-198
22313038-0	2012	Different effects of proton pump inhibitors and famotidine on the clopidogrel metabolic activation by recombinant CYP2B6, CYP2C19 and CYP3A4.	clopidogrel	66-77	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	114-120
22313038-0	2012	Different effects of proton pump inhibitors and famotidine on the clopidogrel metabolic activation by recombinant CYP2B6, CYP2C19 and CYP3A4.	clopidogrel	66-77	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	122-129
22313038-0	2012	Different effects of proton pump inhibitors and famotidine on the clopidogrel metabolic activation by recombinant CYP2B6, CYP2C19 and CYP3A4.	clopidogrel	66-77	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	134-140
22313038-1	2012	Inhibitory potential of proton pump inhibitors (PPIs) and famotidine, an H(2) receptor antagonist, on the metabolic activation of clopidogrel was evaluated using recombinant CYP2B6, CYP2C19 and CYP3A4.	clopidogrel	130-141	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	174-180
22313038-1	2012	Inhibitory potential of proton pump inhibitors (PPIs) and famotidine, an H(2) receptor antagonist, on the metabolic activation of clopidogrel was evaluated using recombinant CYP2B6, CYP2C19 and CYP3A4.	clopidogrel	130-141	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	194-200
22313038-3	2012	Omeprazole potently inhibited clopidogrel activation by CYP2C19 with an IC(50) of 12.8 mumol/L and more weakly inhibited that by CYP2B6 and CYP3A4.	clopidogrel	30-41	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	56-63
22313038-7	2012	These results provide direct evidence that PPIs inhibit clopidogrel metabolic activation and suggest that CYP2C19 inhibition is the main cause of drug-drug interaction between clopidogrel and omeprazole.	clopidogrel	176-187	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	106-113
22464343-2	2012	The CYP2C19*2 allele is a common genetic variant associated with increased rates of major adverse events in individuals given clopidogrel after percutaneous coronary intervention (PCI).	clopidogrel	126-137	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
22811359-1	2012	INTRODUCTION: VerifyNow P2Y12 is commonly used to measure responsiveness to clopidogrel.	clopidogrel	76-87	purinergic receptor P2Y12	Homo sapiens	24-29
22611308-3	2012	Clopidogrel needs metabolic activation predominantly by the hepatic cytochrome P450 isoenzyme Cytochrome 2C19 (CYP2C19) and proton pump inhibitors (PPIs) are extensively metabolized by the CYP2C19 isoenzyme as well.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	111-118
22611308-3	2012	Clopidogrel needs metabolic activation predominantly by the hepatic cytochrome P450 isoenzyme Cytochrome 2C19 (CYP2C19) and proton pump inhibitors (PPIs) are extensively metabolized by the CYP2C19 isoenzyme as well.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	189-196
21239075-0	2012	The EFFect of hIgh-dose ClopIdogrel treatmENT in patients with clopidogrel resistance (the EFFICIENT trial).	clopidogrel	24-35	immunoglobulin heavy locus	Homo sapiens	14-18
21239075-0	2012	The EFFect of hIgh-dose ClopIdogrel treatmENT in patients with clopidogrel resistance (the EFFICIENT trial).	clopidogrel	63-74	immunoglobulin heavy locus	Homo sapiens	14-18
21239075-1	2012	OBJECTIVES: The aim of this study was to evaluate the effect of high-dose clopidogrel continuation treatment on the development of MACCE after elective PCI in patients with clopidogrel resistance.	clopidogrel	74-85	immunoglobulin heavy locus	Homo sapiens	64-68
21239075-1	2012	OBJECTIVES: The aim of this study was to evaluate the effect of high-dose clopidogrel continuation treatment on the development of MACCE after elective PCI in patients with clopidogrel resistance.	clopidogrel	173-184	immunoglobulin heavy locus	Homo sapiens	64-68
21239075-5	2012	Clopidogrel resistance was evaluated with the VerifyNow P2Y12 test.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	56-61
21239075-10	2012	CONCLUSION: In patients who underwent elective PCI and had clopidogrel resistance, high-dose clopidogrel continuation therapy was more efficient in preventing MACCE than the standard dose.	clopidogrel	59-70	immunoglobulin heavy locus	Homo sapiens	83-87
21239075-10	2012	CONCLUSION: In patients who underwent elective PCI and had clopidogrel resistance, high-dose clopidogrel continuation therapy was more efficient in preventing MACCE than the standard dose.	clopidogrel	93-104	immunoglobulin heavy locus	Homo sapiens	83-87
22619259-4	2012	In the acute phase, an IV bolus of elinogrel achieved more rapid and potent antiplatelet effects compared with clopidogrel, which were sustained during the transition from the IV to the oral formulation in the first 24 hours of the peri-PCI period.	clopidogrel	111-122	serpin family A member 5	Homo sapiens	237-240
22239289-1	2012	AIMS: CYP2C19 variant alleles are independent predictors of clopidogrel response variability and occurrence of major adverse cardiovascular events in high-risk vascular patients on clopidogrel therapy.	clopidogrel	60-71	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	6-13
22239289-1	2012	AIMS: CYP2C19 variant alleles are independent predictors of clopidogrel response variability and occurrence of major adverse cardiovascular events in high-risk vascular patients on clopidogrel therapy.	clopidogrel	181-192	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	6-13
22674743-0	2012	Cost-effectiveness of cytochrome P450 2C19 genotype screening for selection of antiplatelet therapy with clopidogrel or prasugrel: a commentary.	clopidogrel	105-116	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	22-42
22209339-0	2012	ABCB1 C3435T polymorphism and risk of adverse clinical events in clopidogrel treated patients: a meta-analysis.	clopidogrel	65-76	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
22209339-1	2012	INTRODUCTION: The ABCB1 C3435T polymorphism limits oral bioavailability of clopidogrel and may influence prognosis of patients treated with clopidogrel.	clopidogrel	75-86	ATP binding cassette subfamily B member 1	Homo sapiens	18-23
22209339-1	2012	INTRODUCTION: The ABCB1 C3435T polymorphism limits oral bioavailability of clopidogrel and may influence prognosis of patients treated with clopidogrel.	clopidogrel	140-151	ATP binding cassette subfamily B member 1	Homo sapiens	18-23
22704413-10	2012	CONCLUSION: CYP2C19*17 allele is associated with enhanced response to clopidogrel and an increased risk of bleeding in patients with blood stasis syndrome of coronary artery disease treated by clopidogrel.	clopidogrel	70-81	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
22704413-10	2012	CONCLUSION: CYP2C19*17 allele is associated with enhanced response to clopidogrel and an increased risk of bleeding in patients with blood stasis syndrome of coronary artery disease treated by clopidogrel.	clopidogrel	193-204	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
22419147-8	2012	These epidemiological and in vitro findings suggest that clopidogrel may cause clinically important, dose-dependent drug-drug interactions with other medications metabolized by CYP2C8.	clopidogrel	57-68	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	177-183
22503564-2	2012	Measuring vasodilator-stimulated phosphoprotein (VASP) phosphorylation is currently the most specific method for assessing the clopidogrel effect.	clopidogrel	127-138	vasodilator stimulated phosphoprotein	Homo sapiens	10-47
22503564-2	2012	Measuring vasodilator-stimulated phosphoprotein (VASP) phosphorylation is currently the most specific method for assessing the clopidogrel effect.	clopidogrel	127-138	vasodilator stimulated phosphoprotein	Homo sapiens	49-53
22685981-0	2012	CYP2C19 genotype-guided antiplatelet therapy in a patient with clopidogrel resistance.	clopidogrel	63-74	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
22207144-11	2012	The CYP2C19*2 variant only explained 12% of the platelet response to clopidogrel.	clopidogrel	69-80	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
22513313-1	2012	The CYP2C19*2 loss-of-function allele is associated with reduced generation of active metabolites of clopidogrel.	clopidogrel	101-112	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
22189756-0	2012	High leukocyte count and interleukin-10 predict high on-treatment-platelet-reactivity in patients treated with clopidogrel.	clopidogrel	111-122	interleukin 10	Homo sapiens	25-39
25187763-10	2012	A number of genetic polymorphisms, in particular CYP 2C19*2, have been associated with clopidogrel hyporesponsiveness and clinical outcomes.	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	49-57
25187763-13	2012	While no prospective randomized trials currently exist to demonstrate improved clinical outcomes with genotype-based treatment for carriers of the CYP 2C19*2 polymorphism, a number of studies show that an increased dose of clopidogrel improves platelet inhibition in hyporesponders.	clopidogrel	223-234	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	147-155
22189756-14	2012	Higher concentrations of leukocytes and interleukin-10 were also an important factor associated with the risk of low clopidogrel responsiveness.	clopidogrel	117-128	interleukin 10	Homo sapiens	40-54
22154242-1	2012	BACKGROUND: The antiplatelet effect of clopidogrel has been linked to cytochrome P450 2C19 (CYP2C19) carrier status.	clopidogrel	39-50	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	70-90
22154242-1	2012	BACKGROUND: The antiplatelet effect of clopidogrel has been linked to cytochrome P450 2C19 (CYP2C19) carrier status.	clopidogrel	39-50	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	92-99
23077924-7	2012	Carriers of CYP2C19*2 or *3 alleles have been shown to respond poorly to standard doses of clopidogrel due to reduced metabolic activation of the drug.	clopidogrel	91-102	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
22464259-2	2012	BACKGROUND: Metabolism of clopidogrel requires cytochrome P450s (CYPs), including CYP2C19.	clopidogrel	26-37	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	82-89
22464259-3	2012	However, PPIs may inhibit CYP2C19, potentially reducing the effectiveness of clopidogrel.	clopidogrel	77-88	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
22265638-0	2012	The impact of genetic polymorphisms of P2Y12, CYP3A5 and CYP2C19 on clopidogrel response variability in Iranian patients.	clopidogrel	68-79	purinergic receptor P2Y12	Homo sapiens	39-44
22265638-0	2012	The impact of genetic polymorphisms of P2Y12, CYP3A5 and CYP2C19 on clopidogrel response variability in Iranian patients.	clopidogrel	68-79	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	46-52
22265638-0	2012	The impact of genetic polymorphisms of P2Y12, CYP3A5 and CYP2C19 on clopidogrel response variability in Iranian patients.	clopidogrel	68-79	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	57-64
22265638-1	2012	Clopidogrel is an inhibitor of platelet ADP P2Y12 receptors and currently used for prevention of stent thrombosis.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	44-49
22007612-2	2012	The pharmacokinetic and pharmacodynamic effects of clopidogrel have been significantly influenced by the enzyme activity of the ABCB1 C3435T and the CYP2C19 system.	clopidogrel	51-62	ATP binding cassette subfamily B member 1	Homo sapiens	128-133
22007612-2	2012	The pharmacokinetic and pharmacodynamic effects of clopidogrel have been significantly influenced by the enzyme activity of the ABCB1 C3435T and the CYP2C19 system.	clopidogrel	51-62	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	149-156
22368149-1	2012	BACKGROUND: A recent report suggested that carriers of the Q allele of the PON1 Q192R polymorphism had decreased biotransformation of clopidogrel into its active metabolite and decreased efficacy of clopidogrel in preventing cardiovascular events.	clopidogrel	134-145	paraoxonase 1	Homo sapiens	75-79
22368149-1	2012	BACKGROUND: A recent report suggested that carriers of the Q allele of the PON1 Q192R polymorphism had decreased biotransformation of clopidogrel into its active metabolite and decreased efficacy of clopidogrel in preventing cardiovascular events.	clopidogrel	199-210	paraoxonase 1	Homo sapiens	75-79
22186968-9	2012	CONCLUSIONS: Early inhibition of the platelet ADP-receptor with a high loading dose of 600 mg clopidogrel given in the prehospital phase in patients with STEMI scheduled for primary PCI is safe, did not increase pre-PCI patency of the infarct vessel, but was associated with a trend towards a reduction in clinical events.	clopidogrel	94-105	purinergic receptor P2Y12	Homo sapiens	37-58
22589111-0	2012	Rapid testing of clopidogrel resistance by genotyping of CYP2C19 and CYP2C9 polymorphisms using denaturing on-chip capillary electrophoresis.	clopidogrel	17-28	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	57-64
22589111-0	2012	Rapid testing of clopidogrel resistance by genotyping of CYP2C19 and CYP2C9 polymorphisms using denaturing on-chip capillary electrophoresis.	clopidogrel	17-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
22589111-3	2012	Kinetics of clopidogrel metabolism is driven by enzymatic activity of the Cytochrome P450 system.	clopidogrel	12-23	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	74-89
22589111-4	2012	Genotyping of CYP2C19 and CYP2C9 polymorphisms allows to identify slow metabolizers showing resistance to clopidogrel therapy.	clopidogrel	106-117	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
22589111-4	2012	Genotyping of CYP2C19 and CYP2C9 polymorphisms allows to identify slow metabolizers showing resistance to clopidogrel therapy.	clopidogrel	106-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
22589111-7	2012	Using an upgraded heater control, we present an optimization for allele separation of CYP2C19 I331V, CYP2C9 R144C, and CYP2C9 I359L polymorphisms employing run temperatures of up to 55 C. We demonstrate rapid and accessible approach to reproducible clopidogrel resistance with feasibility and low cost.	clopidogrel	249-260	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	86-93
22420660-3	2012	In this study, we have attempted to enhance the absorption of clopidogrel by improving its solubility and by inhibiting intestinal P-gp activity.	clopidogrel	62-73	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	131-135
22420660-1	2012	OBJECTIVES: Clopidogrel, a thienopyridine antiplatelet agent, is a poor aqueous soluble compound and a P-glycoprotein (P-gp) efflux pump substrate.	clopidogrel	12-23	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	103-117
22420660-1	2012	OBJECTIVES: Clopidogrel, a thienopyridine antiplatelet agent, is a poor aqueous soluble compound and a P-glycoprotein (P-gp) efflux pump substrate.	clopidogrel	12-23	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	119-123
22420660-8	2012	KEY FINDINGS: We noticed an enhancement of clopidogrel absorption by improving its solubility or by inhibiting the P-gp activity.	clopidogrel	43-54	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	115-119
22624833-8	2012	The portion of the risk of persistently high OTR at 30 days attributable to reduced-function CYP2C19 allele carriage was 5.2% in the patients randomly assigned to high-dose clopidogrel.	clopidogrel	173-184	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	93-100
22624833-9	2012	CONCLUSIONS: CYP2C19, but not PON1 or ABCB1, is a significant determinant of the pharmacodynamic effects of clopidogrel, both early and late after PCI.	clopidogrel	108-119	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
22461122-0	2012	Cost-effectiveness of cytochrome P450 2C19 genotype screening for selection of antiplatelet therapy with clopidogrel or prasugrel.	clopidogrel	105-116	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	22-42
22462746-0	2012	CYP2C19 and PON1 polymorphisms regulating clopidogrel bioactivation in Chinese, Malay and Indian subjects.	clopidogrel	42-53	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
22462746-0	2012	CYP2C19 and PON1 polymorphisms regulating clopidogrel bioactivation in Chinese, Malay and Indian subjects.	clopidogrel	42-53	paraoxonase 1	Homo sapiens	12-16
22462746-5	2012	CONCLUSION: Our data suggest that genotyping studies to investigate clopidogrel response should include CYP2C19*2 and *3 but not *17 polymorphisms in Chinese, and CYP2C19*2 and *17 polymorphisms but not *3 in Indians.	clopidogrel	68-79	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	104-111
22462746-5	2012	CONCLUSION: Our data suggest that genotyping studies to investigate clopidogrel response should include CYP2C19*2 and *3 but not *17 polymorphisms in Chinese, and CYP2C19*2 and *17 polymorphisms but not *3 in Indians.	clopidogrel	68-79	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	163-170
22377481-1	2012	BACKGROUND: Clopidogrel requires oxidation dependent on the cytochrome P450 enzyme 2C19 (CYP2C19) to form its active metabolite.	clopidogrel	12-23	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	60-87
22377481-1	2012	BACKGROUND: Clopidogrel requires oxidation dependent on the cytochrome P450 enzyme 2C19 (CYP2C19) to form its active metabolite.	clopidogrel	12-23	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	89-96
22377481-2	2012	The importance of loss-of-function alleles (particularly CYP2C19*2, 681G&gt;A) in poor platelet response to clopidogrel is well recognized.	clopidogrel	108-119	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	57-64
22260716-7	2012	The incidence of major bleedings (2.6%) was numerically higher in patients with an enhanced vs. poor response to clopidogrel assessed by MEA (4% vs. 0%) or in ultra-metabolizers vs. regular metabolizers (CYP2C19*17/*17 vs. CYP2C19*1/*1; 9.5% vs. 2%).	clopidogrel	113-124	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	204-211
22166712-6	2012	Activation of aortic PXR by classical agonists had several protective effects: increased xenobiotic metabolism demonstrated by bioactivation of the pro-drug clopidogrel, which reduced adenosine diphosphate-induced platelet aggregation; increased expression of multidrug resistance protein 1, mediating chemical efflux from the vasculature; and protection from reactive oxygen species-mediated cell death.	clopidogrel	157-168	nuclear receptor subfamily 1 group I member 2	Homo sapiens	21-24
22115701-2	2012	Recent findings suggest that paraoxonase-1 (PON1) is a major determinant for clopidogrel efficacy.	clopidogrel	77-88	paraoxonase 1	Homo sapiens	29-42
22115701-2	2012	Recent findings suggest that paraoxonase-1 (PON1) is a major determinant for clopidogrel efficacy.	clopidogrel	77-88	paraoxonase 1	Homo sapiens	44-48
22166712-6	2012	Activation of aortic PXR by classical agonists had several protective effects: increased xenobiotic metabolism demonstrated by bioactivation of the pro-drug clopidogrel, which reduced adenosine diphosphate-induced platelet aggregation; increased expression of multidrug resistance protein 1, mediating chemical efflux from the vasculature; and protection from reactive oxygen species-mediated cell death.	clopidogrel	157-168	ATP binding cassette subfamily B member 1	Homo sapiens	260-290
22425806-5	2012	Multiple drugs inhibit the CYP2C19 enzyme and their simultaneous use with clopidogrel is especially hazardous for patients with genetically decreased enzyme activity.	clopidogrel	74-85	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	27-34
22293861-3	2012	Research has implicated genetic variations in the CYP2C19 isozyme as at least partly responsible for the variable antiplatelet response seen with clopidogrel.	clopidogrel	146-157	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	50-57
22293861-4	2012	Studies have shown that patients possessing genetic variants of the CYP2C19 isozyme may be at increased risk of adverse cardiovascular events due to impaired clopidogrel efficacy, although this has not been definitively demonstrated.	clopidogrel	158-169	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	68-75
22440495-2	2012	BACKGROUND: Cigarette smoking is an inducer of cytochrome P450 1A2, a hepatic enzyme involved in clopidogrel metabolism.	clopidogrel	97-108	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	47-66
22448399-9	2012	Clopidogrel was discontinued a median of 6 days before surgery and 2 days prior to initiating GP IIb/IIIa inhibitor.	clopidogrel	0-11	integrin subunit alpha 2b	Homo sapiens	94-100
22448399-13	2012	CONCLUSIONS: In patients with DES, who require cessation of clopidogrel before surgery, bridging with GP IIb/IIIa inhibitors appears effective in preventing adverse cardiac outcomes but may be associated with bleeding in patients undergoing cardiac surgery.	clopidogrel	60-71	integrin subunit alpha 2b	Homo sapiens	102-108
21834799-1	2012	BACKGROUND: The CYP3A4 inhibition by calcium channel blockers (CCBs) may attenuate the effectiveness of clopidogrel.	clopidogrel	104-115	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	16-22
22116003-1	2012	INTRODUCTION AND OBJECTIVES: CYP2C19*2 and CYP2C19*17 alleles appear to contribute to heterogeneous clopidogrel metabolism.	clopidogrel	100-111	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	29-36
22116003-1	2012	INTRODUCTION AND OBJECTIVES: CYP2C19*2 and CYP2C19*17 alleles appear to contribute to heterogeneous clopidogrel metabolism.	clopidogrel	100-111	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	43-50
22116003-8	2012	CONCLUSIONS: Even though CYP2C19 genotype is associated with variable on-clopidogrel platelet reactivity, it has no significant clinical influence.	clopidogrel	73-84	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
22613391-3	2012	A total of 1021 patients were enrolled, with 178 of them prescribed clopidogrel and 843 patients were administrated clopidogrel combined with statins (CYP3A4-metabolized statins 636 and non CYP3A4-metabolized statins 207).	clopidogrel	116-127	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	151-157
22103858-6	2012	(Bouman et al., (2011) 17, 110) reported that the second step of clopidogrel bioactivation was not catalyzed by P450 enzymes but by paraoxonase-1(PON-1) and that PON-1 was a major determinant of clopidogrel efficacy.	clopidogrel	65-76	paraoxonase 1	Homo sapiens	132-145
22103858-6	2012	(Bouman et al., (2011) 17, 110) reported that the second step of clopidogrel bioactivation was not catalyzed by P450 enzymes but by paraoxonase-1(PON-1) and that PON-1 was a major determinant of clopidogrel efficacy.	clopidogrel	65-76	paraoxonase 1	Homo sapiens	146-151
22040781-0	2012	Increased clopidogrel response is associated with ABCC3 expression: a pilot study.	clopidogrel	10-21	ATP binding cassette subfamily C member 3	Homo sapiens	50-55
22040781-1	2012	BACKGROUND: The aim of this study was investigate the relationship between ABCB1 and ABCC3 gene expressions in peripheral blood cells (PBC) and the response to clopidogrel in patients with coronary arterial disease (CAD).	clopidogrel	160-171	ATP binding cassette subfamily B member 1	Homo sapiens	75-80
22040781-1	2012	BACKGROUND: The aim of this study was investigate the relationship between ABCB1 and ABCC3 gene expressions in peripheral blood cells (PBC) and the response to clopidogrel in patients with coronary arterial disease (CAD).	clopidogrel	160-171	ATP binding cassette subfamily C member 3	Homo sapiens	85-90
22040781-9	2012	Moreover, CAD patients with low ABCC3 expression (Qe1, &lt;2.5x10(-3)) had higher probability to have a good response to clopidogrel (OR: 18.00, 95%CI: 1.90-169.99, p=0.001).	clopidogrel	121-132	ATP binding cassette subfamily C member 3	Homo sapiens	32-37
22040781-12	2012	CONCLUSIONS: Low ABCC3 mRNA expression in peripheral blood cells is associated with increased clopidogrel response, but further studies are needed to describe the functional relationship of clopidogrel with the ABCC3.	clopidogrel	94-105	ATP binding cassette subfamily C member 3	Homo sapiens	17-22
22040781-12	2012	CONCLUSIONS: Low ABCC3 mRNA expression in peripheral blood cells is associated with increased clopidogrel response, but further studies are needed to describe the functional relationship of clopidogrel with the ABCC3.	clopidogrel	190-201	ATP binding cassette subfamily C member 3	Homo sapiens	17-22
22040781-12	2012	CONCLUSIONS: Low ABCC3 mRNA expression in peripheral blood cells is associated with increased clopidogrel response, but further studies are needed to describe the functional relationship of clopidogrel with the ABCC3.	clopidogrel	190-201	ATP binding cassette subfamily C member 3	Homo sapiens	211-216
21602258-3	2012	The plasma levels of CRP, P-selectin, sCD40L, IL-6 was higher in 65 (18.5%) patients with clopidogrel resistance than in those with normal responsiveness at 6 months after PCI.	clopidogrel	90-101	C-reactive protein	Homo sapiens	21-24
22103858-6	2012	(Bouman et al., (2011) 17, 110) reported that the second step of clopidogrel bioactivation was not catalyzed by P450 enzymes but by paraoxonase-1(PON-1) and that PON-1 was a major determinant of clopidogrel efficacy.	clopidogrel	65-76	paraoxonase 1	Homo sapiens	162-167
22103858-6	2012	(Bouman et al., (2011) 17, 110) reported that the second step of clopidogrel bioactivation was not catalyzed by P450 enzymes but by paraoxonase-1(PON-1) and that PON-1 was a major determinant of clopidogrel efficacy.	clopidogrel	195-206	paraoxonase 1	Homo sapiens	146-151
22103858-6	2012	(Bouman et al., (2011) 17, 110) reported that the second step of clopidogrel bioactivation was not catalyzed by P450 enzymes but by paraoxonase-1(PON-1) and that PON-1 was a major determinant of clopidogrel efficacy.	clopidogrel	195-206	paraoxonase 1	Homo sapiens	162-167
22186965-2	2012	The measurement of vasodilator-associated stimulated phosphoprotein (VASP) phosphorylation, expressed as platelet reactivity index (PRI), mirrors the degree of P2Y(12) receptor inhibition and can detect the well-known variable response to clopidogrel.	clopidogrel	239-250	vasodilator stimulated phosphoprotein	Homo sapiens	19-67
22186965-2	2012	The measurement of vasodilator-associated stimulated phosphoprotein (VASP) phosphorylation, expressed as platelet reactivity index (PRI), mirrors the degree of P2Y(12) receptor inhibition and can detect the well-known variable response to clopidogrel.	clopidogrel	239-250	vasodilator stimulated phosphoprotein	Homo sapiens	69-73
21831410-0	2012	CYP2C19*2 and other genetic variants affecting platelet response to clopidogrel in patients undergoing percutaneous coronary intervention.	clopidogrel	68-79	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
21831410-7	2012	CONCLUSIONS: Apart from the CYP2C19*2, other genetic variants involved in clopidogrel metabolism and action like CYP2B6*5 and P2RY12 seem to have an important association with HTPR.	clopidogrel	74-85	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	113-119
21831410-7	2012	CONCLUSIONS: Apart from the CYP2C19*2, other genetic variants involved in clopidogrel metabolism and action like CYP2B6*5 and P2RY12 seem to have an important association with HTPR.	clopidogrel	74-85	purinergic receptor P2Y12	Homo sapiens	126-132
22298798-1	2012	BACKGROUND: The prodrug clopidogrel requires intestinal absorption by the efflux pump P-glycoprotein MDR1 (multidrug resistant-1), encoded by the ABCB1 gene.	clopidogrel	24-35	ATP binding cassette subfamily B member 1	Homo sapiens	101-105
22298798-1	2012	BACKGROUND: The prodrug clopidogrel requires intestinal absorption by the efflux pump P-glycoprotein MDR1 (multidrug resistant-1), encoded by the ABCB1 gene.	clopidogrel	24-35	ATP binding cassette subfamily B member 1	Homo sapiens	107-128
22298798-1	2012	BACKGROUND: The prodrug clopidogrel requires intestinal absorption by the efflux pump P-glycoprotein MDR1 (multidrug resistant-1), encoded by the ABCB1 gene.	clopidogrel	24-35	ATP binding cassette subfamily B member 1	Homo sapiens	146-151
22298798-2	2012	Prior studies suggested that a common and functional genetic variant (C3435T, rs1045642) within ABCB1 influences clopidogrel treatment efficacy; however, existing data are highly inconsistent, because other studies failed to replicate this postulated association.	clopidogrel	113-124	ATP binding cassette subfamily B member 1	Homo sapiens	96-101
22298798-3	2012	Thus, the aim of this study was to assess the association of ABCB1 C3435T genotypes with the antiplatelet efficacy of clopidogrel and the risk of stent thrombosis (ST) in large cohorts of clopidogrel-treated patients undergoing percutaneous coronary intervention.	clopidogrel	118-129	ATP binding cassette subfamily B member 1	Homo sapiens	61-66
22319066-2	2012	BACKGROUND: Clopidogrel is an inactive prodrug; it is converted to its active metabolite through the cytochrome P450 (CYP3A4) pathway, which also metabolizes calcium channel blockers (CCBs).	clopidogrel	12-23	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	118-124
22190063-1	2012	Variants in ABCB1 and CYP2C19 have been identified as predictors of cardiac events during clopidogrel therapy initiated after myocardial infarction (MI) or percutaneous coronary intervention (PCI).	clopidogrel	90-101	ATP binding cassette subfamily B member 1	Homo sapiens	12-17
22190063-1	2012	Variants in ABCB1 and CYP2C19 have been identified as predictors of cardiac events during clopidogrel therapy initiated after myocardial infarction (MI) or percutaneous coronary intervention (PCI).	clopidogrel	90-101	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	22-29
22190063-6	2012	In this population, genetic signals for clopidogrel resistance in ABCB1 and CYP2C19 were replicated, supporting the use of EHRs for pharmacogenomic studies.	clopidogrel	40-51	ATP binding cassette subfamily B member 1	Homo sapiens	66-71
22190063-6	2012	In this population, genetic signals for clopidogrel resistance in ABCB1 and CYP2C19 were replicated, supporting the use of EHRs for pharmacogenomic studies.	clopidogrel	40-51	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	76-83
22261685-2	2012	As described in this issue, Delaney and co-workers validated the use of EHRs by demonstrating that loss-of-function CYP2C19*2 was associated with poorer cardiovascular outcomes in clopidogrel-treated patients with an effect size similar to that reported in more controlled clinical trials.	clopidogrel	180-191	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	116-123
22090195-4	2012	These warnings were largely based on in-vitro studies and observational analyses suggesting decreased efficacy of clopidogrel in the presence of proton pump inhibitors.	clopidogrel	114-125	ATPase H+/K+ transporting subunit alpha	Homo sapiens	145-156
22204719-0	2012	Effects of proton pump inhibitors on platelet function in patients receiving clopidogrel: a systematic review.	clopidogrel	77-88	ATPase H+/K+ transporting subunit alpha	Homo sapiens	11-22
22204719-1	2012	BACKGROUND: There is considerable debate regarding the negative impact of concomitant proton pump inhibitor (PPI) therapy on the antiplatelet efficacy of clopidogrel.	clopidogrel	154-165	ATPase H+/K+ transporting subunit alpha	Homo sapiens	86-97
21895760-2	2012	Newly developed P2Y12 inhibitors are more potent, more predictable, and have a faster onset of action than clopidogrel, characteristics that make them particularly attractive for high-risk percutaneous coronary intervention (PCI).	clopidogrel	107-118	purinergic receptor P2Y12	Homo sapiens	16-21
21895760-7	2012	Both prasugrel and ticagrelor, opposed to clopidogrel, have shown that stronger P2Y12 inhibition led respectively to significant 19 and 16% relative risk reduction of a similar primary end point combining cardiovascular death, non-fatal myocardial infarction, or non-fatal stroke.	clopidogrel	42-53	purinergic receptor P2Y12	Homo sapiens	80-85
21895760-10	2012	On the other hand, these newly developed P2Y12 inhibitors decrease mortality after PCI compared with clopidogrel.	clopidogrel	101-112	purinergic receptor P2Y12	Homo sapiens	41-46
21895761-8	2012	The enzymatic generation of the active metabolite of prasugrel is much more effective than that of clopidogrel where only about 5% of oral clopidogrel is transformed into the active compound by two-step CYP-dependent procedures.	clopidogrel	99-110	peptidylprolyl isomerase G	Homo sapiens	203-206
21895761-8	2012	The enzymatic generation of the active metabolite of prasugrel is much more effective than that of clopidogrel where only about 5% of oral clopidogrel is transformed into the active compound by two-step CYP-dependent procedures.	clopidogrel	139-150	peptidylprolyl isomerase G	Homo sapiens	203-206
22142030-9	2012	However, there is a subset of patients who have reduced conversion of clopidogrel to its active metabolites due to genetic polymorphism of hepatic P-450 (carriers of CYP2C19 loss-of-function alleles).	clopidogrel	70-81	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	166-173
22123356-0	2012	The gain-of-function variant allele CYP2C19*17: a double-edged sword between thrombosis and bleeding in clopidogrel-treated patients.	clopidogrel	104-115	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	36-43
22123356-1	2012	BACKGROUND: A large number of clinical studies have documented that a loss-of-function variant CYP2C19*2 affects clinical profiles of clopidogrel (efficacy and safety).	clopidogrel	134-145	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	95-102
22123356-3	2012	OBJECTIVES: To systematically summarize all available clinical data assessing the role of the CYP2C19*17 variant in patients taking clopidogrel.	clopidogrel	132-143	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	94-101
22123356-8	2012	Moreover, the presence of the CYP2C19*17 variant might lead to increased response to clopidogrel, as shown by a marked lower prevalence of HPR in carriers than in non-carriers (37.9% vs. 50.8%; OR, 0.60; 95% CI, 0.45-0.79; P = 0.0003; three studies).	clopidogrel	85-96	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
22123356-9	2012	CONCLUSIONS: Carriers of the CYP2C19*17 variant have greater therapeutic responsiveness to clopidogrel than non-carriers, but they have an increased risk of developing bleeding as well.	clopidogrel	91-102	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	29-36
21602258-3	2012	The plasma levels of CRP, P-selectin, sCD40L, IL-6 was higher in 65 (18.5%) patients with clopidogrel resistance than in those with normal responsiveness at 6 months after PCI.	clopidogrel	90-101	selectin P	Homo sapiens	26-36
21602258-3	2012	The plasma levels of CRP, P-selectin, sCD40L, IL-6 was higher in 65 (18.5%) patients with clopidogrel resistance than in those with normal responsiveness at 6 months after PCI.	clopidogrel	90-101	interleukin 6	Homo sapiens	46-50
21689142-0	2012	Pharmacokinetics and pharmacodynamics following maintenance doses of prasugrel and clopidogrel in Chinese carriers of CYP2C19 variants.	clopidogrel	83-94	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	118-125
21689142-8	2012	CONCLUSIONS: Prasugrel demonstrated higher active metabolite exposure and more consistent pharmacodynamic response across all three predicted phenotype groups compared with clopidogrel, confirming observations from previous research that CYP2C19 phenotype plays an important role in variability of response to clopidogrel, but has no impact on response to prasugrel.	clopidogrel	173-184	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	238-245
21689142-8	2012	CONCLUSIONS: Prasugrel demonstrated higher active metabolite exposure and more consistent pharmacodynamic response across all three predicted phenotype groups compared with clopidogrel, confirming observations from previous research that CYP2C19 phenotype plays an important role in variability of response to clopidogrel, but has no impact on response to prasugrel.	clopidogrel	310-321	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	238-245
22785462-1	2012	BACKGROUND:  Cytochrome P450 (CYP) 2C19 polymorphism is associated with reduced responsiveness to clopidogrel and poor clinical outcome after drug-eluting stent (DES) implantation, but its contribution to lesion outcome after DES implantation is unclear.	clopidogrel	98-109	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-39
22030270-0	2012	CYP2C19 gene variants cut-off levels for on-clopidogrel platelet aggregation.	clopidogrel	44-55	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
22906899-3	2012	P2Y(12) inhibitors include ticlopidine (now rarely used), clopidogrel, prasugrel, and ticagrelor.	clopidogrel	58-69	purinergic receptor P2Y12	Homo sapiens	0-7
22906906-2	2012	Candidate gene and genome-wide association studies have found that common genetic polymorphisms of the cytochrome P450 (CYP) 2C19 isoenzyme that result in a loss of functional activity are associated with less exposure of clopidogrel active metabolite and a diminished antiplatelet effect.	clopidogrel	222-233	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	103-129
22971905-0	2012	Association of CYP2C19 genotype with periprocedural myocardial infarction after uneventful stent implantation in Chinese patients receiving clopidogrel pretreatment.	clopidogrel	140-151	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
22427735-0	2012	Influence of paraoxonase-1 Q192R and cytochrome P450 2C19 polymorphisms on clopidogrel response.	clopidogrel	75-86	paraoxonase 1	Homo sapiens	13-26
22427735-0	2012	Influence of paraoxonase-1 Q192R and cytochrome P450 2C19 polymorphisms on clopidogrel response.	clopidogrel	75-86	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-57
22427735-3	2012	Conflicting results have been reported in regard to (1) the association of a common polymorphism of PON1 (Q192R) with reduced rates of coronary stent thrombosis in patients taking clopidogrel and (2) its effects on platelet inhibition in patient populations of European descent.	clopidogrel	180-191	paraoxonase 1	Homo sapiens	100-104
22427735-10	2012	CONCLUSION: CYP2C19*2 allele is associated with impaired platelet inhibition by clopidogrel and high on-treatment platelet aggregation.	clopidogrel	80-91	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
22724417-5	2012	Pharmacogenomic analyses have identified loss-of-function variant alleles of CYP 2C19 and specifically the 2C19*2 allele, to be the predominant genetic mediators of the antiplatelet effect of clopidogrel.	clopidogrel	192-203	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	77-85
22360514-2	2012	Ticlopidine, Clopidogrel, Prasugrel, Ticagrelor, Cangrelor and Elinogrel are the P2Y12 inhibitors that act as antiplatelet drugs.	clopidogrel	13-24	purinergic receptor P2Y12	Homo sapiens	81-86
22004687-0	2012	Effects of omeprazole and genetic polymorphism of CYP2C19 on the clopidogrel active metabolite.	clopidogrel	65-76	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	50-57
22004687-4	2012	In the current study, net CYP2C19 contribution to the active metabolite formation was determined from exposure of the active metabolite in two clinical studies (one phase I study with well balanced genetic polymorphic populations and a meta-analysis with a total of 396 healthy volunteers) at different clopidogrel doses.	clopidogrel	303-314	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
22153531-0	2012	Modified clopidogrel loading dose according to platelet reactivity monitoring in patients carrying ABCB1 variant alleles in patients with clopidogrel resistance.	clopidogrel	9-20	ATP binding cassette subfamily B member 1	Homo sapiens	99-104
22739809-8	2012	The new ESC guidelines on the management of ACS without ST segment elevation recommend the use of clopidogrel only when a new antiplatelet drug, e.g. ticagrelor or prasugrel is not available or contraindicated.	clopidogrel	98-109	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	44-47
22792485-1	2012	This study aimed to assess if proton pump inhibitors (PPIs) may reduce the effectiveness of clopidogrel, than H2 antagonist (anti-H2) in order to determine rehospitalization for acute coronary syndrome (re-ACS), target vessel revascularization (TVR) and cardiac death.	clopidogrel	92-103	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	206-209
22472213-2	2012	Clopidogrel is a prodrug and changed into active metabolite by cytochrome p450 enzymes (CYPs), especially CYP2C19.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	106-113
22169056-7	2012	It was further demonstrated that the derivatizing agent (MPB) does not affect clopidogrel levels, thus from one aliquot of blood drawn clinically, this method can simultaneously quantify both clopidogrel and CAMD with sensitivity in the picogram per mL range.	clopidogrel	192-203	AFA1	Homo sapiens	57-60
22623230-3	2012	AIM: To investigate whether omega-3 PUFA are able to modify platelet responsiveness to clopidogrel therapy in patients with CYP2C19 loss-of-function polymorphism undergoing percutaneous coronary intervention (PCI).	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	124-131
22623230-12	2012	CONCLUSIONS: The addition of omega-3 ethyl esters significantly potentiates platelet response to clopidogrel after PCI mostly in patients with CYP2C19 loss-of-function polymorphism.	clopidogrel	97-108	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	143-150
23098546-2	2012	Mechanism of action of clopidogrel and main trials which has proven its efficacy are presented as well as results of main large studies including authors own results demonstrating dependence of clinical efficacy of clopidogrel on carriage of polymorphisms of gene of CYP2C19 which accomplishes metabolism of the drug in the liver.	clopidogrel	23-34	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	267-274
23098546-2	2012	Mechanism of action of clopidogrel and main trials which has proven its efficacy are presented as well as results of main large studies including authors own results demonstrating dependence of clinical efficacy of clopidogrel on carriage of polymorphisms of gene of CYP2C19 which accomplishes metabolism of the drug in the liver.	clopidogrel	215-226	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	267-274
22839512-0	2012	[CYP2C19 gene polymorphism in patients with myocardial infarction who use clopidogrel].	clopidogrel	74-85	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	1-8
22839512-2	2012	Pharmacodynamic and clinical studies have demonstrated that the polymorphism CYP2C19 (CYP2C19*2 allele) is associated with a reduced antiplatelet effect of clopidogrel and an increase in the incidence of severe cardiovascular complications.	clopidogrel	156-167	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	77-84
22839512-2	2012	Pharmacodynamic and clinical studies have demonstrated that the polymorphism CYP2C19 (CYP2C19*2 allele) is associated with a reduced antiplatelet effect of clopidogrel and an increase in the incidence of severe cardiovascular complications.	clopidogrel	156-167	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	86-93
22075236-1	2012	BACKGROUND/OBJECTIVES: ACC/AHA/SCAI recommendations include dual anti-platelet therapy (aspirin and clopidogrel) for 12 months after drug-eluting stent percutaneous coronary intervention (DES PCI).	clopidogrel	100-111	suppressor of cancer cell invasion	Homo sapiens	31-35
22918731-2	2012	Among the P2Y12 receptor inhibitors, the group of thienopyridines include ticlopidine, clopidogrel and prasugrel, all of which are orally administered prodrugs leading to irreversible P2Y12 receptor inhibition.	clopidogrel	87-98	purinergic receptor P2Y12	Homo sapiens	10-15
22918731-2	2012	Among the P2Y12 receptor inhibitors, the group of thienopyridines include ticlopidine, clopidogrel and prasugrel, all of which are orally administered prodrugs leading to irreversible P2Y12 receptor inhibition.	clopidogrel	87-98	purinergic receptor P2Y12	Homo sapiens	184-189
21693476-0	2012	Meta-analyses of the association between cytochrome CYP2C19 loss- and gain-of-function polymorphisms and cardiovascular outcomes in patients with coronary artery disease treated with clopidogrel.	clopidogrel	183-194	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	52-59
21693476-1	2012	AIMS: To perform a meta-analysis of the association between CYP2C19 loss- and gain-of-function variants and cardiovascular outcomes and bleeding in patients with coronary artery disease treated with clopidogrel, and to explore the causes of heterogeneity between studies.	clopidogrel	199-210	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	60-67
21693476-9	2012	CONCLUSIONS: Not only CYP2C19 loss-of-function but also gain-of-function alleles should be considered to define the pharmacogenetic response to clopidogrel.	clopidogrel	144-155	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	22-29
21700758-1	2012	BACKGROUND: Although East Asians carry the cytochrome P450 (CYP) 2C19*2 allele more frequently than do Caucasians, the impact of the CYP2C19*2 allele on clopidogrel pharmacodynamics and clinical outcomes is unknown.	clopidogrel	153-164	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	133-140
21700758-2	2012	OBJECTIVE: To evaluate the effect of CYP2C19 variants on clopidogrel pharmacodynamics and long-term prognosis in East Asian patients with drug-eluting stents (DES).	clopidogrel	57-68	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-44
22166969-0	2012	Prediction of clopidogrel low responders by a rapid CYP2C19 activity test.	clopidogrel	14-25	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	52-59
22166969-1	2012	AIM: Clopidogrel, an essential drug for the prevention of stent thrombosis, is a prodrug activated by CYP enzyme family including CYP2C19.	clopidogrel	5-16	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	130-137
22166969-2	2012	It is known that activity-defective polymorphisms of CYP2C19 (CYP2C19*2 and*3) are associated with reduced clopidogrel efficacy and poor prognosis.	clopidogrel	107-118	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-60
22166969-2	2012	It is known that activity-defective polymorphisms of CYP2C19 (CYP2C19*2 and*3) are associated with reduced clopidogrel efficacy and poor prognosis.	clopidogrel	107-118	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	62-69
22166969-4	2012	The aim of this study is to evaluated the efficiency of the CYP2C19 activity test as a predictor of antiplatelet effect of clopidogrel.	clopidogrel	123-134	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	60-67
22390861-3	2012	The aim of our study was to evaluate if high on-clopidogrel platelet reactivity (HPR) by ADP is associated with an increased risk of major adverse coronary events (MACE) after ACS independent of CYP2C19*2 allele, i.e. whether genotyping patients for CYP2C19*2 polymorphism is sufficient to identify those to be switched to novel antiplatelets.	clopidogrel	48-59	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	250-257
22153531-0	2012	Modified clopidogrel loading dose according to platelet reactivity monitoring in patients carrying ABCB1 variant alleles in patients with clopidogrel resistance.	clopidogrel	138-149	ATP binding cassette subfamily B member 1	Homo sapiens	99-104
22153531-1	2012	OBJECTIVES: The aim of the present study was to investigate the impact of a adjusted clopidogrel loading dose (LD) according to platelet reactivity index in carriers of ABCB1 mutant allele undergoing percutaneous coronary intervention (PCI).	clopidogrel	85-96	ATP binding cassette subfamily B member 1	Homo sapiens	169-174
22153531-12	2012	After a second clopidogrel LD, the VASP index was significantly decreased in these patients (66.9+-12.8% vs.50.2+-18.3%; &lt;0.001).	clopidogrel	15-26	vasodilator stimulated phosphoprotein	Homo sapiens	35-39
23284748-6	2012	In a murine model of AAA, apolipoprotein E-knockout mice infused with 1,000 ng/kg/min angiotensin II, treatment with clopidogrel, an inhibitor of platelets, significantly suppressed aneurysm formation (47% decrease, P&lt;0.05).	clopidogrel	117-128	achalasia, adrenocortical insufficiency, alacrimia	Mus musculus	21-24
22153531-15	2012	CONCLUSIONS: Increased and adjusted clopidogrel loading dose according to platelet reactivity monitoring attenuated clopidogrel resistance in carriers of ABCB1 mutant allele.	clopidogrel	36-47	ATP binding cassette subfamily B member 1	Homo sapiens	154-159
23284748-6	2012	In a murine model of AAA, apolipoprotein E-knockout mice infused with 1,000 ng/kg/min angiotensin II, treatment with clopidogrel, an inhibitor of platelets, significantly suppressed aneurysm formation (47% decrease, P&lt;0.05).	clopidogrel	117-128	apolipoprotein E	Mus musculus	26-42
22153531-15	2012	CONCLUSIONS: Increased and adjusted clopidogrel loading dose according to platelet reactivity monitoring attenuated clopidogrel resistance in carriers of ABCB1 mutant allele.	clopidogrel	116-127	ATP binding cassette subfamily B member 1	Homo sapiens	154-159
22646492-7	2012	Clopidogrel resistance was simultaneously analysed by the INNOVANCE PFA P2Y test cartridge, ADP-induced LTA, the flow-cytometric vasodilator-stimulated phosphoprotein (VASP)-phosphorylation assay and the multiple electrode aggregometry (Multiplate).	clopidogrel	0-11	vasodilator stimulated phosphoprotein	Homo sapiens	129-166
22203539-2	2011	OBJECTIVE: To appraise evidence on the association of CYP2C19 genotype and clopidogrel response through systematic review and meta-analysis.	clopidogrel	75-86	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	54-61
22646492-9	2012	According to the cut-off points for clopidogrel resistance proposed by the literature, agreement was fair between INNOVANCE PFA-100 P2Y and LTA (74.4%) and Multiplate (75.6%), while poor agreement was noticed in VASP assay (63.3%).	clopidogrel	36-47	vasodilator stimulated phosphoprotein	Homo sapiens	212-216
22723959-2	2012	Recent studies have shown that cytochrome P450 (CYP), ATP-binding cassette transporters (ABCB1), and paraoxonase-1 (PON1) play crucial roles in clopidogrel bioactivation.	clopidogrel	144-155	ATP binding cassette subfamily B member 1	Homo sapiens	89-94
22723959-2	2012	Recent studies have shown that cytochrome P450 (CYP), ATP-binding cassette transporters (ABCB1), and paraoxonase-1 (PON1) play crucial roles in clopidogrel bioactivation.	clopidogrel	144-155	paraoxonase 1	Homo sapiens	101-114
22723959-2	2012	Recent studies have shown that cytochrome P450 (CYP), ATP-binding cassette transporters (ABCB1), and paraoxonase-1 (PON1) play crucial roles in clopidogrel bioactivation.	clopidogrel	144-155	paraoxonase 1	Homo sapiens	116-120
23056288-0	2012	ABCB1 C3435T polymorphism and response to clopidogrel treatment in coronary artery disease (CAD) patients: a meta-analysis.	clopidogrel	42-53	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
23056288-1	2012	BACKGROUND: A number of investigators have evaluated the association between the ABCB1 polymorphism and clopidogrel responding, but the results have been inconclusive.	clopidogrel	104-115	ATP binding cassette subfamily B member 1	Homo sapiens	81-86
23056288-2	2012	To examine the risk of high platelet activity and poor clinical outcomes associated with the ABCB1 C3435T polymorphism in CAD patients on clopidogrel, all available studies were included in the present meta-analysis.	clopidogrel	138-149	ATP binding cassette subfamily B member 1	Homo sapiens	93-98
23056288-5	2012	RESULTS: It was demonstrated that the ABCB1 C3435T variation was associated with the risk of early major adverse cardiovascular events (MACE) (T vs. C OR, 1.34; 95% CI, 1.10 to 1.62; P=0.003; TT vs. CC: OR, 1.77; 95% CI, 1.19 to 2.63; P=0.005; CT + TT vs.CC: OR, 1.48; 95% CI, 1.06 to 2.06; P=0.02) and the polymorphism was also associated with the risk of the long-term MACE in patients on clopidogrel LD 300 mg (T vs. C: OR, 1.28; 95% CI, 1.10 to 1.48; P=0.001; TT vs. CC: OR, 1.59; 95% CI, 1.19 to 2.13; P=0.002; CT + TT vs.CC: OR, 1.39; 95% CI, 1.08 to 1.79; P=0.01).	clopidogrel	391-402	ATP binding cassette subfamily B member 1	Homo sapiens	38-43
23056288-8	2012	CONCLUSIONS: The evidence from our meta-analysis indicated that the ABCB1 C3435T polymorphism might be a risk factor for the MACE in patients on clopidogrel LD 300 mg, and that TT homozygotes decreased the outcome of bleeding compared with CC homozygotes.	clopidogrel	145-156	ATP binding cassette subfamily B member 1	Homo sapiens	68-73
22203539-8	2011	In treatment-only analysis, individuals with 1 or more CYP2C19 alleles associated with lower enzyme activity had lower levels of active clopidogrel metabolites, less platelet inhibition, lower risk of bleeding (relative risk [RR], 0.84; 95% CI, 0.75-0.94; absolute risk reduction of 5-8 events per 1000 individuals), and higher risk of CVD events (RR, 1.18; 95% CI, 1.09-1.28; absolute risk increase of 8-12 events per 1000 individuals).	clopidogrel	136-147	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	55-62
22203539-13	2011	CONCLUSION: Although there was an association between the CYP2C19 genotype and clopidogrel responsiveness, overall there was no significant association of genotype with cardiovascular events.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	58-65
22184714-1	2011	Review: Reduced function CYP2C19 genotypes may increase risk for stent clots in patients receiving clopidogrel.	clopidogrel	99-110	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
20869129-9	2011	CONCLUSIONS: The use of longer-term ACE inhibitor/ARB, beta blocker or statin therapy was associated with a significantly lower risk; these risk reductions were of greater magnitude than those associated with clopidogrel.	clopidogrel	209-220	angiotensin I converting enzyme	Homo sapiens	36-39
21078615-0	2011	An anti-von Willebrand factor aptamer reduces platelet adhesion among patients receiving aspirin and clopidogrel in an ex vivo shear-induced arterial thrombosis.	clopidogrel	101-112	von Willebrand factor	Homo sapiens	8-29
21883990-1	2011	Clopidogrel is an inhibitor of the ADP receptor P2Y12 and platelet aggregation.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	48-53
22045970-2	2011	The influence of the CYP2C19 LOF alleles (*2 and *3) on clopidogrel response and clinical outcomes in East Asians with acute myocardial infarction (AMI) has not been reported.	clopidogrel	56-67	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
22045970-3	2011	We sought to evaluate the effect of the CYP2C19 variants on clopidogrel pharmacodynamics and long-term prognosis in these patients.	clopidogrel	60-71	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-47
22045970-14	2011	CONCLUSIONS: Among East Asian patients who survived an AMI, the CYP2C19 LOF allele carriage appears to affect clopidogrel pharmacodynamics and cardiovascular events according to the number of the CYP2C19 LOF allele; the influence of the CYP2C19*2 and *3 alleles on clopidogrel response and long-term outcomes does not differ.	clopidogrel	110-121	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	64-71
22045970-14	2011	CONCLUSIONS: Among East Asian patients who survived an AMI, the CYP2C19 LOF allele carriage appears to affect clopidogrel pharmacodynamics and cardiovascular events according to the number of the CYP2C19 LOF allele; the influence of the CYP2C19*2 and *3 alleles on clopidogrel response and long-term outcomes does not differ.	clopidogrel	110-121	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	196-203
22045970-14	2011	CONCLUSIONS: Among East Asian patients who survived an AMI, the CYP2C19 LOF allele carriage appears to affect clopidogrel pharmacodynamics and cardiovascular events according to the number of the CYP2C19 LOF allele; the influence of the CYP2C19*2 and *3 alleles on clopidogrel response and long-term outcomes does not differ.	clopidogrel	110-121	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	196-203
22045970-14	2011	CONCLUSIONS: Among East Asian patients who survived an AMI, the CYP2C19 LOF allele carriage appears to affect clopidogrel pharmacodynamics and cardiovascular events according to the number of the CYP2C19 LOF allele; the influence of the CYP2C19*2 and *3 alleles on clopidogrel response and long-term outcomes does not differ.	clopidogrel	265-276	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	64-71
22045970-14	2011	CONCLUSIONS: Among East Asian patients who survived an AMI, the CYP2C19 LOF allele carriage appears to affect clopidogrel pharmacodynamics and cardiovascular events according to the number of the CYP2C19 LOF allele; the influence of the CYP2C19*2 and *3 alleles on clopidogrel response and long-term outcomes does not differ.	clopidogrel	265-276	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	196-203
22045970-14	2011	CONCLUSIONS: Among East Asian patients who survived an AMI, the CYP2C19 LOF allele carriage appears to affect clopidogrel pharmacodynamics and cardiovascular events according to the number of the CYP2C19 LOF allele; the influence of the CYP2C19*2 and *3 alleles on clopidogrel response and long-term outcomes does not differ.	clopidogrel	265-276	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	196-203
22089343-4	2011	Paraoxonase 1 has been identified as the main determinant of the biological and clinical efficacy of clopidogrel.	clopidogrel	101-112	paraoxonase 1	Homo sapiens	0-13
22129581-4	2011	In particular, mutations of the gene encoding for cytochrome CYP2C19, responsible for clopidogrel metabolism, are associated with an increased risk of cardiovascular events.	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	61-68
21920970-9	2011	On multivariate analysis, clopidogrel pre-treatment remained an independent predictor of in-hospital mortality [odds ratio (OR) = 0.60, 95% confidence interval (CI) 0.35-0.99; P =0.048], especially in patients receiving additional GP IIb/IIIa antagonist therapy in the catheterization laboratory (OR = 0.40, 95% CI 0.19-0.83; P =0.01).	clopidogrel	26-37	integrin subunit alpha 2b	Homo sapiens	231-237
22090660-0	2011	Bleeding complications with the P2Y12 receptor antagonists clopidogrel and ticagrelor in the PLATelet inhibition and patient Outcomes (PLATO) trial.	clopidogrel	59-70	purinergic receptor P2Y12	Homo sapiens	32-37
21209232-2	2011	Clopidogrel is a mechanism-based inhibitor of CYP2B6 and CYP2C19.	clopidogrel	0-11	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	46-52
21209232-2	2011	Clopidogrel is a mechanism-based inhibitor of CYP2B6 and CYP2C19.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	57-64
21209232-10	2011	The CYP2B6 and CYP2C19 inhibitor clopidogrel significantly inhibited the formations of M1 from sibutramine and M2 from sibutramine by 37% and 64%, respectively.	clopidogrel	33-44	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	4-10
21209232-10	2011	The CYP2B6 and CYP2C19 inhibitor clopidogrel significantly inhibited the formations of M1 from sibutramine and M2 from sibutramine by 37% and 64%, respectively.	clopidogrel	33-44	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
22008470-1	2011	BACKGROUND: The paraoxonase activity of the enzyme paraoxonase-1 (PON-1) associated with high-density lipoprotein (HDL) may significantly influence clopidogrel"s antiplatelet and clinical efficacy as a result of its involvement in the clopidogrel biotransformation to the pharmacologically active thiol metabolite.	clopidogrel	148-159	paraoxonase 1	Homo sapiens	51-64
22008470-1	2011	BACKGROUND: The paraoxonase activity of the enzyme paraoxonase-1 (PON-1) associated with high-density lipoprotein (HDL) may significantly influence clopidogrel"s antiplatelet and clinical efficacy as a result of its involvement in the clopidogrel biotransformation to the pharmacologically active thiol metabolite.	clopidogrel	148-159	paraoxonase 1	Homo sapiens	66-71
22008470-1	2011	BACKGROUND: The paraoxonase activity of the enzyme paraoxonase-1 (PON-1) associated with high-density lipoprotein (HDL) may significantly influence clopidogrel"s antiplatelet and clinical efficacy as a result of its involvement in the clopidogrel biotransformation to the pharmacologically active thiol metabolite.	clopidogrel	235-246	paraoxonase 1	Homo sapiens	51-64
22008470-1	2011	BACKGROUND: The paraoxonase activity of the enzyme paraoxonase-1 (PON-1) associated with high-density lipoprotein (HDL) may significantly influence clopidogrel"s antiplatelet and clinical efficacy as a result of its involvement in the clopidogrel biotransformation to the pharmacologically active thiol metabolite.	clopidogrel	235-246	paraoxonase 1	Homo sapiens	66-71
22008470-8	2011	Similarly, the platelet activation markers were significantly higher in PON-1 Q192Q genotype carriers compared with those having one or two R alleles only in patients adequately responding to clopidogrel.	clopidogrel	192-203	paraoxonase 1	Homo sapiens	72-77
22008470-9	2011	CONCLUSIONS: PON-1 is an important determinant of clopidogrel antiplatelet efficacy only in patients adequately responding to clopidogrel.	clopidogrel	50-61	paraoxonase 1	Homo sapiens	13-18
22008470-9	2011	CONCLUSIONS: PON-1 is an important determinant of clopidogrel antiplatelet efficacy only in patients adequately responding to clopidogrel.	clopidogrel	126-137	paraoxonase 1	Homo sapiens	13-18
21841533-7	2011	An additional group of animals were pretreated with a platelet P2Y12 receptor antagonist (clopidogrel) before T/HS.	clopidogrel	90-101	purinergic receptor P2Y12	Rattus norvegicus	63-68
25083217-1	2011	The recent report that clopidogrel efficacy may be more dependent on paraoxonase-1 (PON1) than on cytochrome P450 2C19 (CYP2C19) activity raises questions about the roles of these and other enzymes in clopidogrel activation.	clopidogrel	23-34	paraoxonase 1	Homo sapiens	69-82
25083217-1	2011	The recent report that clopidogrel efficacy may be more dependent on paraoxonase-1 (PON1) than on cytochrome P450 2C19 (CYP2C19) activity raises questions about the roles of these and other enzymes in clopidogrel activation.	clopidogrel	23-34	paraoxonase 1	Homo sapiens	84-88
25083217-2	2011	To provide insight into the emerging PON1 versus CYP2C19 debate, this commentary summarizes the clinical evidence on the pharmacokinetic determinants of clopidogrel efficacy.	clopidogrel	153-164	paraoxonase 1	Homo sapiens	37-41
25083217-4	2011	There is agreement amongst in vitro studies regarding the involvement of CYP1A2 and CYP2B6 in the metabolism of clopidogrel to 2-oxo-clopidogrel.	clopidogrel	112-123	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	73-79
25083217-4	2011	There is agreement amongst in vitro studies regarding the involvement of CYP1A2 and CYP2B6 in the metabolism of clopidogrel to 2-oxo-clopidogrel.	clopidogrel	112-123	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	84-90
21794898-0	2011	Association of genetic variants in CYP2C19 and adverse clinical outcomes after treatment with clopidogrel: an updated meta-analysis.	clopidogrel	94-105	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	35-42
21862109-2	2011	The purpose of this study was to determine cut-off levels of VerifyNow P2Y12 system associated with effective inhibition of on-clopidogrel platelet aggregation to predict carriers of CYP2C19 reduced-function allele among patients undergoing percutaneous coronary intervention (PCI).	clopidogrel	127-138	purinergic receptor P2Y12	Homo sapiens	71-76
21862109-2	2011	The purpose of this study was to determine cut-off levels of VerifyNow P2Y12 system associated with effective inhibition of on-clopidogrel platelet aggregation to predict carriers of CYP2C19 reduced-function allele among patients undergoing percutaneous coronary intervention (PCI).	clopidogrel	127-138	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	183-190
21862109-10	2011	CONCLUSIONS: Our results suggested that the cut-off levels of PRU and %inhibition to discriminate carriers of CYP2C19 reduced-function allele from noncarriers are potentially useful clinically to provide optimal clopidogrel therapy in patients with stable CAD undergoing PCI.	clopidogrel	212-223	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	110-117
22011914-3	2011	This was a prospective observational PD study enrolling consecutive &gt;= 75-year-old patients on maintenance clopidogrel therapy (75 mg/day) who were tested for clopidogrel response by the VerifyNow P2Y12 assay and light transmittance aggregometry (LTA).	clopidogrel	162-173	purinergic receptor P2Y12	Homo sapiens	200-205
21946108-1	2011	Thienopyridines (ticlopidine, clopidogrel and prasugrel) are pro-drugs that require metabolism to exhibit a critical thiol group in the active form that binds to the P2Y12 receptor to inhibit platelet activation and prevent thrombus formation in vivo.	clopidogrel	30-41	purinergic receptor P2Y12	Homo sapiens	166-171
22088980-0	2011	Dosing clopidogrel based on CYP2C19 genotype and the effect on platelet reactivity in patients with stable cardiovascular disease.	clopidogrel	7-18	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
22088980-1	2011	CONTEXT: Variants in the CYP2C19 gene influence the pharmacologic and clinical response to the standard 75-mg daily maintenance dose of the antiplatelet drug clopidogrel.	clopidogrel	158-169	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
22088980-2	2011	OBJECTIVE: To test whether higher doses (up to 300 mg daily) improve the response to clopidogrel in the setting of loss-of-function CYP2C19 genotypes.	clopidogrel	85-96	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	132-139
22088980-9	2011	Whereas 52% of CYP2C19*2 heterozygotes were nonresponders (&gt;=230 PRU) with 75 mg of clopidogrel, only 10% were nonresponders with 225 or 300 mg (P &lt; .001 for both).	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
22088980-10	2011	Clopidogrel, 225 mg daily, reduced platelet reactivity in CYP2C19*2 heterozygotes to levels achieved with standard clopidogrel, 75 mg, in noncarriers (mean ratios of platelet reactivity, VASP PRI, 0.92; 90% CI, 0.85-0.99, and PRU, 0.94; 90% CI, 0.84-1.04).	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	58-65
21872198-5	2011	Post-treatment platelet reactivity was assessed by adenosine diphosphate 10 mumol/L-induced platelet aggregation and the specific pharmacologic response to clopidogrel by the platelet reactivity index vasoactive stimulated phosphoprotein.	clopidogrel	156-167	solute carrier family 35 member G1	Homo sapiens	0-4
21872198-9	2011	The post-treatment platelet reactivity in response to both the loading and the maintenance clopidogrel dose was greater in patients &gt; 75 years old than in the younger patients: 50 +- 17% versus 45 +- 17% (p = 0.002) and 57 +- 15% versus 53 +- 16% (p = 0.0005), respectively.	clopidogrel	91-102	solute carrier family 35 member G1	Homo sapiens	4-8
21872198-10	2011	The rate of high post-treatment platelet reactivity was significantly greater in patients aged &gt; 75 years after 600 mg and 150 mg clopidogrel: 14% versus 9% (p = 0.04) and 23% versus 15% (p = 0.02), respectively.	clopidogrel	133-144	solute carrier family 35 member G1	Homo sapiens	17-21
21706290-5	2011	Polymorphisms of genes encoding the cytochrome enzymes and P-glycoprotein involved in clopidogrel absorption are regarded as major determinants of the interindividual variability in the clopidogrel-induced platelet inhibition.	clopidogrel	86-97	ATP binding cassette subfamily B member 1	Homo sapiens	59-73
21718233-3	2011	Several studies have identified a link between CYP2C19*2 carriers and decreased clopidogrel responsiveness as assessed by platelet reactivity testing and clinical outcomes.	clopidogrel	80-91	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	47-54
21822146-2	2011	We hypothesized that formation of thienopyridine-derived nitrosothiols (ticlopidine-SNO, clopidogrel-SNO, and prasugrel-SNO) occurs directly from the respective parent drug.	clopidogrel	89-100	strawberry notch homolog 1	Homo sapiens	101-104
21822146-2	2011	We hypothesized that formation of thienopyridine-derived nitrosothiols (ticlopidine-SNO, clopidogrel-SNO, and prasugrel-SNO) occurs directly from the respective parent drug.	clopidogrel	89-100	strawberry notch homolog 1	Homo sapiens	101-104
21828263-6	2011	These studies show that, in vitro, CYP3A4/5, 2C19, and 2B6 are individually capable of converting clopidogrel and prasugrel to the AM and that the cytochrome P450 preference for these two thienopyridines is very similar.	clopidogrel	98-109	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	35-49
21153923-3	2011	In this regard, the present study focused on the genotype profile of Southern Iranians in order to compare allele frequencies of their CYP3A5 and P2Y12 (T744C) which have been shown to have roles in metabolizing clopidogrel, with those of other populations.	clopidogrel	212-223	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	135-141
21153923-3	2011	In this regard, the present study focused on the genotype profile of Southern Iranians in order to compare allele frequencies of their CYP3A5 and P2Y12 (T744C) which have been shown to have roles in metabolizing clopidogrel, with those of other populations.	clopidogrel	212-223	purinergic receptor P2Y12	Homo sapiens	146-151
21380557-2	2011	Numerous recent studies have shown that polymorphisms in the gene encoding the cytochrome P450 (CYP450) 2C19 enzyme (CYP2C19) contribute to variability in response to clopidogrel; patients with certain common genetic variants of CYP2C19 (2, 3) have a reduced metabolism of clopidogrel and have a higher rate of cardiovascular events or stent thrombosis compared to patients with the CYP2C19 (1) allele.	clopidogrel	167-178	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	117-124
21380557-2	2011	Numerous recent studies have shown that polymorphisms in the gene encoding the cytochrome P450 (CYP450) 2C19 enzyme (CYP2C19) contribute to variability in response to clopidogrel; patients with certain common genetic variants of CYP2C19 (2, 3) have a reduced metabolism of clopidogrel and have a higher rate of cardiovascular events or stent thrombosis compared to patients with the CYP2C19 (1) allele.	clopidogrel	167-178	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	229-236
21380557-2	2011	Numerous recent studies have shown that polymorphisms in the gene encoding the cytochrome P450 (CYP450) 2C19 enzyme (CYP2C19) contribute to variability in response to clopidogrel; patients with certain common genetic variants of CYP2C19 (2, 3) have a reduced metabolism of clopidogrel and have a higher rate of cardiovascular events or stent thrombosis compared to patients with the CYP2C19 (1) allele.	clopidogrel	167-178	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	229-236
21380557-2	2011	Numerous recent studies have shown that polymorphisms in the gene encoding the cytochrome P450 (CYP450) 2C19 enzyme (CYP2C19) contribute to variability in response to clopidogrel; patients with certain common genetic variants of CYP2C19 (2, 3) have a reduced metabolism of clopidogrel and have a higher rate of cardiovascular events or stent thrombosis compared to patients with the CYP2C19 (1) allele.	clopidogrel	273-284	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	117-124
21380557-2	2011	Numerous recent studies have shown that polymorphisms in the gene encoding the cytochrome P450 (CYP450) 2C19 enzyme (CYP2C19) contribute to variability in response to clopidogrel; patients with certain common genetic variants of CYP2C19 (2, 3) have a reduced metabolism of clopidogrel and have a higher rate of cardiovascular events or stent thrombosis compared to patients with the CYP2C19 (1) allele.	clopidogrel	273-284	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	229-236
21380557-2	2011	Numerous recent studies have shown that polymorphisms in the gene encoding the cytochrome P450 (CYP450) 2C19 enzyme (CYP2C19) contribute to variability in response to clopidogrel; patients with certain common genetic variants of CYP2C19 (2, 3) have a reduced metabolism of clopidogrel and have a higher rate of cardiovascular events or stent thrombosis compared to patients with the CYP2C19 (1) allele.	clopidogrel	273-284	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	229-236
21862689-0	2011	Mechanism-based inactivation of human cytochrome P450 2B6 by clopidogrel: involvement of both covalent modification of cysteinyl residue 475 and loss of heme.	clopidogrel	61-72	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	38-57
21862689-1	2011	We have investigated the mechanisms by which clopidogrel inactivates human cytochrome P450 2B6 (CYP2B6) in a reconstituted system.	clopidogrel	45-56	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	75-94
21862689-1	2011	We have investigated the mechanisms by which clopidogrel inactivates human cytochrome P450 2B6 (CYP2B6) in a reconstituted system.	clopidogrel	45-56	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	96-102
21862689-2	2011	It was found that clopidogrel and its thiolactone metabolite, 2-oxo-clopidogrel, both inactivate CYP2B6 in a time- and concentration-dependent manner.	clopidogrel	18-29	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	97-103
21862689-3	2011	On the basis of k(inact)/K(I) ratios, clopidogrel is approximately 5 times more efficient than 2-oxo-clopidogrel in inactivating CYP2B6.	clopidogrel	38-49	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	129-135
21862689-4	2011	Analysis of the molecular mass of the CYP2B6 wild-type (WT) protein that had been inactivated by either clopidogrel or 2-oxo-clopidogrel showed an increase in the mass of the protein by ~350 Da.	clopidogrel	104-115	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	38-44
21862689-5	2011	This increase in the protein mass corresponds to the addition of the active metabolite of clopidogrel to CYP2B6.	clopidogrel	90-101	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	105-111
21862689-10	2011	Furthermore, inactivation of both CYP2B6 WT and C475S by clopidogrel, but not by 2-oxo-clopidogrel, led to the loss of the heme, which accounts for most of the loss of the catalytic activity.	clopidogrel	57-68	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	34-40
21862689-11	2011	Collectively, these results suggest that clopidogrel inactivates CYP2B6 primarily through destruction of the heme, whereas 2-oxo-clopidogrel inactivates CYP2B6 through covalent modification of Cys475.	clopidogrel	41-52	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	65-71
22577456-1	2011	BACKGROUND: The polymorphisms of cytochrome P450 2C19 (CYP2C19) gene are major prognostic factors for the response to clopidogrel therapy in patients with coronary artery diseases (CAD).	clopidogrel	118-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-53
22577456-1	2011	BACKGROUND: The polymorphisms of cytochrome P450 2C19 (CYP2C19) gene are major prognostic factors for the response to clopidogrel therapy in patients with coronary artery diseases (CAD).	clopidogrel	118-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	55-62
22577456-2	2011	The CYP2C19*2 is the most important allele responsible for resistance to clopidogrel therapy.	clopidogrel	73-84	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
22088980-10	2011	Clopidogrel, 225 mg daily, reduced platelet reactivity in CYP2C19*2 heterozygotes to levels achieved with standard clopidogrel, 75 mg, in noncarriers (mean ratios of platelet reactivity, VASP PRI, 0.92; 90% CI, 0.85-0.99, and PRU, 0.94; 90% CI, 0.84-1.04).	clopidogrel	0-11	vasodilator stimulated phosphoprotein	Homo sapiens	187-191
22088980-11	2011	In CYP2C19*2 homozygotes, even with 300 mg daily of clopidogrel, mean VASP PRI was 68.3% (95% CI, 44.9%-91.6%) and mean PRU, 287.0 (95% CI, 170.2-403.8).	clopidogrel	52-63	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	3-10
22088980-11	2011	In CYP2C19*2 homozygotes, even with 300 mg daily of clopidogrel, mean VASP PRI was 68.3% (95% CI, 44.9%-91.6%) and mean PRU, 287.0 (95% CI, 170.2-403.8).	clopidogrel	52-63	vasodilator stimulated phosphoprotein	Homo sapiens	70-74
22088980-12	2011	CONCLUSION: Among patients with stable cardiovascular disease, tripling the maintenance dose of clopidogrel to 225 mg daily in CYP2C19*2 heterozygotes achieved levels of platelet reactivity similar to that seen with the standard 75-mg dose in noncarriers; in contrast, for CYP2C19*2 homozygotes, doses as high as 300 mg daily did not result in comparable degrees of platelet inhibition.	clopidogrel	96-107	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	127-134
22088980-12	2011	CONCLUSION: Among patients with stable cardiovascular disease, tripling the maintenance dose of clopidogrel to 225 mg daily in CYP2C19*2 heterozygotes achieved levels of platelet reactivity similar to that seen with the standard 75-mg dose in noncarriers; in contrast, for CYP2C19*2 homozygotes, doses as high as 300 mg daily did not result in comparable degrees of platelet inhibition.	clopidogrel	96-107	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	273-280
22190530-0	2011	[Effects of proton pump inhibitors on in-stent restenosis in patients receiving clopidogrel: a retrospective analysis].	clopidogrel	80-91	ATPase H+/K+ transporting subunit alpha	Homo sapiens	12-23
22190530-1	2011	OBJECTIVE: To determine the effect of proton pump inhibitor (PPI) on in-stent restenosis (ISR) in patients receiving clopidogrel therapy.	clopidogrel	117-128	ATPase H+/K+ transporting subunit alpha	Homo sapiens	38-49
21917683-3	2011	A recent black-box warning was included in the clopidogrel package insert indicating a significant clinical link between specific CYP2C19 genetic variants and poor metabolism of clopidogrel.	clopidogrel	47-58	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	130-137
21917683-3	2011	A recent black-box warning was included in the clopidogrel package insert indicating a significant clinical link between specific CYP2C19 genetic variants and poor metabolism of clopidogrel.	clopidogrel	178-189	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	130-137
21917683-5	2011	In patients who are carriers of a CYP2C19 *2 or *3 allele, the conversion of clopidogrel to its active metabolite may be reduced, which can lead to ischemic events and negative consequence for the patient.	clopidogrel	77-88	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	34-41
21799401-1	2011	We compared the ability of four test systems to detect platelet P2Y12 (ADP receptor) blockade by clopidogrel.	clopidogrel	97-108	purinergic receptor P2Y12	Homo sapiens	64-69
21352268-2	2011	The main enzyme responsible for activating clopidogrel is the cytochrome P450 (CYP) isoenzyme CYP2C19, which is polymorphic.	clopidogrel	43-54	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	62-77
21352268-2	2011	The main enzyme responsible for activating clopidogrel is the cytochrome P450 (CYP) isoenzyme CYP2C19, which is polymorphic.	clopidogrel	43-54	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	79-82
21352268-2	2011	The main enzyme responsible for activating clopidogrel is the cytochrome P450 (CYP) isoenzyme CYP2C19, which is polymorphic.	clopidogrel	43-54	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	94-101
21352268-3	2011	There is a growing body of literature showing that carriers of variant CYP2C19 alleles have impaired ability to metabolize clopidogrel (i.e. poor metabolizers), which is associated with decreased inhibition of platelet aggregation and increased cardiovascular risk.	clopidogrel	123-134	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
21352268-4	2011	Some proton pump inhibitors are also metabolized by the CYP2C19 enzyme and often given together with clopidogrel to reduce gastrointestinal side effects.	clopidogrel	101-112	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	56-63
21352268-5	2011	In particular, omeprazole has been shown to inhibit the CYP-mediated metabolism of clopidogrel, and some studies have shown that the combination was associated with a higher incidence of cardiovascular adverse reactions than clopidogrel given alone.	clopidogrel	83-94	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	56-59
21366666-4	2011	Furthermore, genetic testing has demonstrated a link between CYP2C19 genetic polymorphisms, altered clopidogrel metabolite concentrations and adverse clinical events.	clopidogrel	100-111	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	61-68
21972404-0	2011	CYP2C19 but not PON1 genetic variants influence clopidogrel pharmacokinetics, pharmacodynamics, and clinical efficacy in post-myocardial infarction patients.	clopidogrel	48-59	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
21972404-2	2011	Paraoxonase-1 (PON1) has recently been proposed as a key enzyme for clopidogrel metabolic activation.	clopidogrel	68-79	paraoxonase 1	Homo sapiens	0-13
21972404-2	2011	Paraoxonase-1 (PON1) has recently been proposed as a key enzyme for clopidogrel metabolic activation.	clopidogrel	68-79	paraoxonase 1	Homo sapiens	15-19
21972404-3	2011	We tested the effects of PON1 polymorphisms on clopidogrel pharmacokinetics and pharmacodynamics and the occurrence of cardiovascular outcomes in young post-myocardial infarction (MI) patients treated with clopidogrel.	clopidogrel	47-58	paraoxonase 1	Homo sapiens	25-29
22010185-0	2011	Unraveling the pharmacogenetics of clopidogrel: the paraoxonase-1 controversy.	clopidogrel	35-46	paraoxonase 1	Homo sapiens	52-65
21881565-1	2011	A common functional variant in paraoxonase 1 (PON1), Q192R, was recently reported to be a major determinant of clopidogrel response.	clopidogrel	111-122	paraoxonase 1	Homo sapiens	31-44
21881565-1	2011	A common functional variant in paraoxonase 1 (PON1), Q192R, was recently reported to be a major determinant of clopidogrel response.	clopidogrel	111-122	paraoxonase 1	Homo sapiens	46-50
21900887-2	2011	The absorption of clopidogrel is regulated by multidrug-resistance protein 1 (MDR1) in the intestinal epithelium.	clopidogrel	18-29	ATP binding cassette subfamily B member 1	Homo sapiens	46-76
21900887-2	2011	The absorption of clopidogrel is regulated by multidrug-resistance protein 1 (MDR1) in the intestinal epithelium.	clopidogrel	18-29	ATP binding cassette subfamily B member 1	Homo sapiens	78-82
21900887-3	2011	Given that aspirin induces MDR1 in cancer cells and peripheral blood cells, it may induce MDR1 in intestinal epithelial cells as well, thereby affecting the absorption of clopidogrel.	clopidogrel	171-182	ATP binding cassette subfamily B member 1	Homo sapiens	90-94
21900887-5	2011	Along with the upregulation of MDR1 proteins by aspirin, clopidogrel absorption was significantly decreased in the aspirin-treated Caco-2 cells and in rat intestine.	clopidogrel	57-68	ATP binding cassette subfamily B member 1	Homo sapiens	31-35
21918510-0	2011	Effect of paraoxonase-1 polymorphism on clinical outcomes in patients treated with clopidogrel after an acute myocardial infarction.	clopidogrel	83-94	paraoxonase 1	Homo sapiens	10-23
21918510-1	2011	Paraoxonase-1 (PON1) Q192R polymorphism was recently suggested to determine per se clopidogrel response on major cardiovascular events (MACEs).	clopidogrel	83-94	paraoxonase 1	Homo sapiens	0-13
21918510-1	2011	Paraoxonase-1 (PON1) Q192R polymorphism was recently suggested to determine per se clopidogrel response on major cardiovascular events (MACEs).	clopidogrel	83-94	paraoxonase 1	Homo sapiens	15-19
21826477-6	2011	Several other drugs (metabolized through CYP3A4 such as statins or antifungals) similarly impact the pharmacologic response to clopidogrel.	clopidogrel	127-138	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	41-47
21826477-7	2011	Conversely, agents that induce CYP activity increase clopidogrel responsiveness.	clopidogrel	53-64	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	31-34
21933840-4	2011	The exact mechanism of these observations is not yet fully understood, but appears to be related to reduced concentrations of circulating clopidogrel active metabolite, with less variability in pharmacodynamic and clinical response suggested by the evaluation of newer P2Y(12) antagonists, such as prasugrel and ticagrelor.	clopidogrel	138-149	purinergic receptor P2Y12	Homo sapiens	269-276
21819272-5	2011	In preclinical and Phase I - II studies, inhibition of thrombin-mediated platelet activation by a PAR-1 inhibitor, in general, has added to the antithrombotic efficacy of aspirin and clopidogrel without increasing bleeding.	clopidogrel	183-194	coagulation factor II, thrombin	Homo sapiens	55-63
21819272-5	2011	In preclinical and Phase I - II studies, inhibition of thrombin-mediated platelet activation by a PAR-1 inhibitor, in general, has added to the antithrombotic efficacy of aspirin and clopidogrel without increasing bleeding.	clopidogrel	183-194	coagulation factor II thrombin receptor	Homo sapiens	98-103
21795297-7	2011	Following clopidogrel withdrawal, there was (i) a predictable increase in ADP-induced platelet aggregation (ii) an unexpected significant increase in AA-induced platelet aggregation (iii) a decline in IL-6 and hsCRP at 1 week and 4 weeks respectively; and (iv) a non-significant increase in sCD40L at 4 weeks TXB(2) levels were consistently suppressed, indicating complete inhibition of cyclo-oxygenase-1 by aspirin.	clopidogrel	10-21	interleukin 6	Homo sapiens	201-205
21795297-7	2011	Following clopidogrel withdrawal, there was (i) a predictable increase in ADP-induced platelet aggregation (ii) an unexpected significant increase in AA-induced platelet aggregation (iii) a decline in IL-6 and hsCRP at 1 week and 4 weeks respectively; and (iv) a non-significant increase in sCD40L at 4 weeks TXB(2) levels were consistently suppressed, indicating complete inhibition of cyclo-oxygenase-1 by aspirin.	clopidogrel	10-21	prostaglandin-endoperoxide synthase 1	Homo sapiens	387-404
21215696-0	2011	Clopidogrel Resistance: case reports of CYP2C19 gene variants in suspected coronary stent thrombosis.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-47
21215696-2	2011	Clopidogrel is administered as a pro-drug and metabolised to its active metabolite by the hepatic cytochrome P450 2C19 (CYP2C19) enzyme.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	98-118
21215696-2	2011	Clopidogrel is administered as a pro-drug and metabolised to its active metabolite by the hepatic cytochrome P450 2C19 (CYP2C19) enzyme.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	120-127
21215696-4	2011	Recent studies demonstrate that single nucleotide polymorphisms, (SNP"s), in the gene for CYP2C19 result in significantly reduced production of the active metabolite of clopidogrel.	clopidogrel	169-180	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	90-97
21215696-5	2011	Additional studies demonstrate that patients with SNP"s in the CYP2C19 gene, including CYP2C19*2,*3,*4, and *5, have reduced production of the active metabolite of clopidogrel, reduced inhibition of platelet aggregation and increased incidence of coronary, cerebrovascular, and coronary stent thrombosis.	clopidogrel	164-175	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	63-70
21215696-5	2011	Additional studies demonstrate that patients with SNP"s in the CYP2C19 gene, including CYP2C19*2,*3,*4, and *5, have reduced production of the active metabolite of clopidogrel, reduced inhibition of platelet aggregation and increased incidence of coronary, cerebrovascular, and coronary stent thrombosis.	clopidogrel	164-175	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	87-94
21215696-6	2011	We have been interested in determining the CYP2C19 genotype in cases of coronary stent thrombosis whilst on clopidogrel treatment and provide two case reports of coronary stent thrombosis whilst taking clopidogrel with subsequent CYP2C19 genotyping.	clopidogrel	108-119	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	43-50
21215696-6	2011	We have been interested in determining the CYP2C19 genotype in cases of coronary stent thrombosis whilst on clopidogrel treatment and provide two case reports of coronary stent thrombosis whilst taking clopidogrel with subsequent CYP2C19 genotyping.	clopidogrel	202-213	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	230-237
21630270-10	2011	Renal cell apoptosis induced by IR was decreased in kidneys of mice pretreated by clopidogrel, with an increase in Bcl-2 and Bcl-xL expression and a decrease in caspase-3, caspase-8, and Bax expression.	clopidogrel	82-93	B cell leukemia/lymphoma 2	Mus musculus	115-120
21630270-10	2011	Renal cell apoptosis induced by IR was decreased in kidneys of mice pretreated by clopidogrel, with an increase in Bcl-2 and Bcl-xL expression and a decrease in caspase-3, caspase-8, and Bax expression.	clopidogrel	82-93	BCL2-like 1	Mus musculus	125-131
21630270-10	2011	Renal cell apoptosis induced by IR was decreased in kidneys of mice pretreated by clopidogrel, with an increase in Bcl-2 and Bcl-xL expression and a decrease in caspase-3, caspase-8, and Bax expression.	clopidogrel	82-93	caspase 3	Mus musculus	161-170
21630270-10	2011	Renal cell apoptosis induced by IR was decreased in kidneys of mice pretreated by clopidogrel, with an increase in Bcl-2 and Bcl-xL expression and a decrease in caspase-3, caspase-8, and Bax expression.	clopidogrel	82-93	caspase 8	Mus musculus	172-181
21630270-10	2011	Renal cell apoptosis induced by IR was decreased in kidneys of mice pretreated by clopidogrel, with an increase in Bcl-2 and Bcl-xL expression and a decrease in caspase-3, caspase-8, and Bax expression.	clopidogrel	82-93	BCL2-associated X protein	Mus musculus	187-190
21630270-13	2011	Furthermore, pretreatment by clopidogrel decreased the number of CD41-positive cells.	clopidogrel	29-40	integrin alpha 2b	Mus musculus	65-69
21730013-0	2011	A clopidogrel-insensitive inducible pool of P2Y12 receptors contributes to thrombus formation: inhibition by elinogrel, a direct-acting, reversible P2Y12 antagonist.	clopidogrel	2-13	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	44-49
21854540-1	2011	BACKGROUND: The carriage of CYP2C19*2 and the use of proton-pump inhibitors (PPIs) and calcium-channel blockers (CCBs) has been associated with the diminished efficacy of clopidogrel.	clopidogrel	171-182	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
21854540-3	2011	OBJECTIVES: The aim of the present study was to investigate the impact of the combined presence of three risk factors for clopidogrel poor response, that is, the use of CCBs, PPIs and the carriage of CYP2C19*2, on on-treatment platelet reactivity and the occurrence of atherothrombotic events in 725 patients on dual antiplatelet therapy undergoing elective coronary stenting.	clopidogrel	122-133	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	200-207
22001104-7	2011	RESULTS: Clopidogrel decreased MCP-1 expression in the carotid artery at 4 weeks after irradiation.	clopidogrel	9-20	mast cell protease 1	Mus musculus	31-36
21592545-3	2011	Pharmacogenomic analyses, including candidate-gene and genome-wide association studies, have confirmed that genetic polymorphisms in the hepatic cytochrome P450 (CYP) 2C19 dominantly affect the antiplatelet effects of clopidogrel.	clopidogrel	218-229	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	145-171
21592545-4	2011	CYP2C19 reduced-function alleles have been associated with a significant decrease in clopidogrel responsiveness and a higher risk of adverse cardiac events including stent thrombosis, myocardial infarction, and death in several prospective studies, although these effects were not reproduced in a recent large randomized study that included a randomized control group.	clopidogrel	85-96	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
21592545-6	2011	Although it is promising that CYP2C19 genotyping could be used to guide personalized antiplatelet clopidogrel therapy, currently there is insufficient evidence to recommend routine genetic testing.	clopidogrel	98-109	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
21592545-8	2011	In the most recent trial, paraoxonase-1 (PON1) was identified as a crucial new enzyme for clopidogrel bioactivation, with its common Q192R polymorphism determining the rate of active metabolite and the clinical activity of clopidogrel.	clopidogrel	90-101	paraoxonase 1	Homo sapiens	26-39
21592545-8	2011	In the most recent trial, paraoxonase-1 (PON1) was identified as a crucial new enzyme for clopidogrel bioactivation, with its common Q192R polymorphism determining the rate of active metabolite and the clinical activity of clopidogrel.	clopidogrel	90-101	paraoxonase 1	Homo sapiens	41-45
21592545-8	2011	In the most recent trial, paraoxonase-1 (PON1) was identified as a crucial new enzyme for clopidogrel bioactivation, with its common Q192R polymorphism determining the rate of active metabolite and the clinical activity of clopidogrel.	clopidogrel	223-234	paraoxonase 1	Homo sapiens	26-39
21592545-8	2011	In the most recent trial, paraoxonase-1 (PON1) was identified as a crucial new enzyme for clopidogrel bioactivation, with its common Q192R polymorphism determining the rate of active metabolite and the clinical activity of clopidogrel.	clopidogrel	223-234	paraoxonase 1	Homo sapiens	41-45
21592545-9	2011	Further studies are needed to investigate the comprehensive influence of a number of different polymorphisms of CYP2C19 and PON1 variant alleles or other genetic variants on clopidogrel in various ethnic populations.	clopidogrel	174-185	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	112-119
21592545-9	2011	Further studies are needed to investigate the comprehensive influence of a number of different polymorphisms of CYP2C19 and PON1 variant alleles or other genetic variants on clopidogrel in various ethnic populations.	clopidogrel	174-185	paraoxonase 1	Homo sapiens	124-128
21803320-0	2011	Usefulness of high clopidogrel maintenance dose according to CYP2C19 genotypes in clopidogrel low responders undergoing coronary stenting for non ST elevation acute coronary syndrome.	clopidogrel	19-30	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	61-68
21803320-0	2011	Usefulness of high clopidogrel maintenance dose according to CYP2C19 genotypes in clopidogrel low responders undergoing coronary stenting for non ST elevation acute coronary syndrome.	clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	61-68
21803320-5	2011	Clopidogrel response, assessed with platelet reactivity index vasoactive-stimulated phosphoprotein, was significantly affected by genotype, with lower clopidogrel response in CYP2C19*2 allele carriers (p = 0.01).	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	175-182
21803320-5	2011	Clopidogrel response, assessed with platelet reactivity index vasoactive-stimulated phosphoprotein, was significantly affected by genotype, with lower clopidogrel response in CYP2C19*2 allele carriers (p = 0.01).	clopidogrel	151-162	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	175-182
21803320-6	2011	Accordingly, the rate of clopidogrel nonresponse was higher in CYP2C19*2 allele carriers (53% vs 41%, p = 0.04).	clopidogrel	25-36	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	63-70
21803431-0	2011	Differential effect of clopidogrel and aspirin on the release of BDNF from platelets.	clopidogrel	23-34	brain derived neurotrophic factor	Homo sapiens	65-69
21803431-3	2011	Here, we show that a single oral dose of clopidogrel, but not aspirin, significantly reduced the release of BDNF from platelets in healthy volunteers.	clopidogrel	41-52	brain derived neurotrophic factor	Homo sapiens	108-112
21875913-1	2011	BACKGROUND: In the Gauging Responsiveness With A VerifyNow P2Y12 Assay: Impact on Thrombosis and Safety (GRAVITAS) trial, 6 months of high-dose clopidogrel did not reduce cardiovascular events compared with standard-dose clopidogrel in patients with high on-treatment platelet reactivity (OTR) after percutaneous coronary intervention, defined as OTR &gt;=230 P2Y12 reaction units according to the VerifyNow P2Y12 platelet function test.	clopidogrel	144-155	purinergic receptor P2Y12	Homo sapiens	59-64
21875913-1	2011	BACKGROUND: In the Gauging Responsiveness With A VerifyNow P2Y12 Assay: Impact on Thrombosis and Safety (GRAVITAS) trial, 6 months of high-dose clopidogrel did not reduce cardiovascular events compared with standard-dose clopidogrel in patients with high on-treatment platelet reactivity (OTR) after percutaneous coronary intervention, defined as OTR &gt;=230 P2Y12 reaction units according to the VerifyNow P2Y12 platelet function test.	clopidogrel	144-155	purinergic receptor P2Y12	Homo sapiens	360-365
21875913-1	2011	BACKGROUND: In the Gauging Responsiveness With A VerifyNow P2Y12 Assay: Impact on Thrombosis and Safety (GRAVITAS) trial, 6 months of high-dose clopidogrel did not reduce cardiovascular events compared with standard-dose clopidogrel in patients with high on-treatment platelet reactivity (OTR) after percutaneous coronary intervention, defined as OTR &gt;=230 P2Y12 reaction units according to the VerifyNow P2Y12 platelet function test.	clopidogrel	144-155	purinergic receptor P2Y12	Homo sapiens	360-365
21875913-1	2011	BACKGROUND: In the Gauging Responsiveness With A VerifyNow P2Y12 Assay: Impact on Thrombosis and Safety (GRAVITAS) trial, 6 months of high-dose clopidogrel did not reduce cardiovascular events compared with standard-dose clopidogrel in patients with high on-treatment platelet reactivity (OTR) after percutaneous coronary intervention, defined as OTR &gt;=230 P2Y12 reaction units according to the VerifyNow P2Y12 platelet function test.	clopidogrel	221-232	purinergic receptor P2Y12	Homo sapiens	59-64
21875913-8	2011	CONCLUSIONS: In the GRAVITAS trial, achievement of on-clopidogrel reactivity &lt;208 P2Y12 reaction units at 12 to 24 hours after percutaneous coronary intervention or during follow-up was associated with a lower risk for cardiovascular events.	clopidogrel	54-65	purinergic receptor P2Y12	Homo sapiens	85-90
21884870-1	2011	BACKGROUND: Pharmacodynamic studies reported an amplified on-clopidogrel platelet inhibition in smokers potentially caused by an increased metabolic drug activation via induction of cytochrome P450 1A2.	clopidogrel	61-72	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	182-201
21620406-6	2011	RESULTS: Several preventive treatments (statins and clopidogrel) were significantly associated with lower Lp-PLA(2) mass and activity.	clopidogrel	52-63	phospholipase A2 group VII	Homo sapiens	106-115
21706290-5	2011	Polymorphisms of genes encoding the cytochrome enzymes and P-glycoprotein involved in clopidogrel absorption are regarded as major determinants of the interindividual variability in the clopidogrel-induced platelet inhibition.	clopidogrel	186-197	ATP binding cassette subfamily B member 1	Homo sapiens	59-73
21479772-3	2011	METHODS: ADP- and TRAP-induced platelet aggregation was measured by impedance aggregometry in 28 patients with coronary stent implantation (observational group, OG) before and 1, 2, 6 and 17 weeks after clopidogrel cessation.	clopidogrel	203-214	TRAP	Homo sapiens	18-22
21455672-2	2011	AIMS: The aim of this study was to compare the rates of PPB for clopidogrel users and non-users.	clopidogrel	64-75	histatin 1	Homo sapiens	56-59
21455672-4	2011	We compared the frequency of delayed PPB (within 30 days) for patients on uninterrupted clopidogrel therapy with patients not taking clopidogrel.	clopidogrel	88-99	histatin 1	Homo sapiens	37-40
21455672-9	2011	CONCLUSIONS: The delayed PPB rate for our patients on clopidogrel was less than 1%, and PPB rates did not differ significantly between users and non-users.	clopidogrel	54-65	histatin 1	Homo sapiens	25-28
21684710-12	2011	Preoperative treatment with clopidogrel, particularly when it is continued to the day before surgery, and postoperative arterial hypertension seem to be associated with a higher risk of neck bleeding after CEA, requiring re-exploration in most cases.	clopidogrel	28-39	CEA cell adhesion molecule 3	Homo sapiens	206-209
21806387-10	2011	CONCLUSION: Genetic variants in CYP2C19 have a gene-dose effect on post-clopidogrel platelet reactivity, with homozygote LOF carriers having the highest risk for HTPR and for adverse ischemic events.	clopidogrel	72-83	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
21792575-5	2011	The latter receptor, the molecular target of the antithrombotic drugs clopidogrel, prasugrel and ticagrelor, is responsible for most of the potentiating effects of ADP when platelets are stimulated by agents such as thrombin, collagen or immune complexes.	clopidogrel	70-81	coagulation factor II, thrombin	Homo sapiens	216-224
21786436-0	2011	Cytochrome P450 2C19 polymorphism is associated with reduced clopidogrel response in cerebrovascular disease.	clopidogrel	61-72	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-20
21786436-1	2011	PURPOSE: Clopidogrel is a prodrug that requires transformation into an active metabolite by cytochrome P450 (CYP) in the liver in order to irreversibly inhibit the P2Y12 adenosine diphosphate platelet receptor.	clopidogrel	9-20	purinergic receptor P2Y12	Homo sapiens	164-169
21786436-2	2011	CYP2C19 polymorphism has been reported to correlate with reduced antiplatelet activity of clopidogrel in coronary artery disease.	clopidogrel	90-101	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
21786436-3	2011	We assessed the association between CYP2C19 polymorphism and clopidogrel resistance in patients with cerebrovascular disease.	clopidogrel	61-72	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	36-43
21786436-6	2011	Clopidogrel resistance was expressed in P2Y12 reaction units (PRU) and percent inhibition.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	40-45
21786436-9	2011	Clopidogrel resistance was assessed according to the subgroup of CYP2C19 polymorphism.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	65-72
21786436-13	2011	CONCLUSION: Intermediate and poor metabolizing CYP2C19 polymorphism is associated with reduced clopidogrel antiplatelet activity in patients with cerebrovascular disease.	clopidogrel	95-106	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	47-54
21719206-0	2011	Does CYP2C19 inhibition lead to clopidogrel thrombogenicity?	clopidogrel	32-43	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	5-12
21719206-4	2011	Thus a hypothesis is proposed, that the combination of proton-pump inhibitors and clopidogrel increases mortality as results of thrombogenic metabolites of clopidogrel, due to inhibition of CYP2C19 by proton-pump inhibitors.	clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	190-197
21646658-2	2011	The antiplatelet effects of clopidogrel originate through noncompetitive antagonism of the platelet ADP receptor, P2Y12, resulting in inhibition of platelet activation.	clopidogrel	28-39	purinergic receptor P2Y12	Homo sapiens	114-119
21826075-4	2011	The most robust data indicate an association between loss-of-function alleles of the CYP2C19 gene and adverse outcomes among high-risk patients treated with clopidogrel.	clopidogrel	157-168	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	85-92
21816733-0	2011	Impact of CYP2C19 variant genotypes on clinical efficacy of antiplatelet treatment with clopidogrel: systematic review and meta-analysis.	clopidogrel	88-99	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-17
21816733-1	2011	OBJECTIVE: To evaluate the accumulated information from genetic association studies investigating the impact of variants of the cytochrome P450 (CYP) 2C19 genotype on the clinical efficacy of clopidogrel.	clopidogrel	192-203	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	128-154
21835299-0	2011	Relationship between clopidogrel-induced platelet P2Y12 inhibition and stent thrombosis or myocardial infarction after percutaneous coronary intervention-a case-control study.	clopidogrel	21-32	purinergic receptor P2Y12	Homo sapiens	50-55
21835299-4	2011	On-clopidogrel platelet reactivity was measured with VerifyNow P2Y12 and vasodilator-stimulated phosphoprotein (VASP) phosphorylation assay.	clopidogrel	3-14	vasodilator stimulated phosphoprotein	Homo sapiens	53-110
21685174-1	2011	BACKGROUND: Recently published data indicate that the paraoxonase-1 (PON1) Q192R genotype-and not as previously shown activity of cytochrome P450 (CYP) 2C19-is the major determinant of metabolic bioactivation of clopidogrel and thereby variability of antiplatelet effect of clopidogrel.	clopidogrel	212-223	paraoxonase 1	Homo sapiens	54-67
21685174-1	2011	BACKGROUND: Recently published data indicate that the paraoxonase-1 (PON1) Q192R genotype-and not as previously shown activity of cytochrome P450 (CYP) 2C19-is the major determinant of metabolic bioactivation of clopidogrel and thereby variability of antiplatelet effect of clopidogrel.	clopidogrel	212-223	paraoxonase 1	Homo sapiens	69-73
21685174-1	2011	BACKGROUND: Recently published data indicate that the paraoxonase-1 (PON1) Q192R genotype-and not as previously shown activity of cytochrome P450 (CYP) 2C19-is the major determinant of metabolic bioactivation of clopidogrel and thereby variability of antiplatelet effect of clopidogrel.	clopidogrel	274-285	paraoxonase 1	Homo sapiens	54-67
21685174-1	2011	BACKGROUND: Recently published data indicate that the paraoxonase-1 (PON1) Q192R genotype-and not as previously shown activity of cytochrome P450 (CYP) 2C19-is the major determinant of metabolic bioactivation of clopidogrel and thereby variability of antiplatelet effect of clopidogrel.	clopidogrel	274-285	paraoxonase 1	Homo sapiens	69-73
21810378-4	2011	RESULTS: The inital hsCRP levels were similar and decreased significantly in all groups by one month of clopidogrel treatment (from 7.1+-1.9 to 3.8+-2.3 in BMS1 group, p=0,002, from 6.5+-2.8 to 4.3+-2.5 in BMS6 group, p= 0,01 and from 7.7+-2 to 3.6+-2.4 in DES group, p &lt; 0.001).	clopidogrel	104-115	BMS1 ribosome biogenesis factor	Homo sapiens	156-160
21810378-5	2011	In the BMS1 group, after termination of the clopidogrel therapy after the first month, hsCRP levels increased again at the third and sixth months.	clopidogrel	44-55	BMS1 ribosome biogenesis factor	Homo sapiens	7-11
21594586-3	2011	The large interindividual variability in clopidogrel responsiveness is related to several factors, including the genetic polymorphism of hepatic cytochrome P450 2C19 (CYP2C19*2), which recently has been highlighted by a warning from the U.S. Food and Drug Administration.	clopidogrel	41-52	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	145-165
21594586-3	2011	The large interindividual variability in clopidogrel responsiveness is related to several factors, including the genetic polymorphism of hepatic cytochrome P450 2C19 (CYP2C19*2), which recently has been highlighted by a warning from the U.S. Food and Drug Administration.	clopidogrel	41-52	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	167-174
21716274-7	2011	In healthy CYP2C19 PMs, a clopidogrel regimen of 600-mg LD/150 mg/day MD largely overcomes diminished clopi-H4 exposure and antiplatelet response, as assessed by MPA levels.	clopidogrel	26-37	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	11-18
21816478-15	2011	Patients treated with either type of clopidogrel showed significant inhibition (mean [SD]) of P2Y(12) (group A, -5.9% [15.1%]; group B, 23.4% [21.9%]; and group C, 19.5% [23.8%]; P &lt; 0.001).	clopidogrel	37-48	purinergic receptor P2Y12	Homo sapiens	94-101
21816478-16	2011	Differences between clopidogrel resinate and clopidogrel bisulfate in the inhibition of P2Y(12) did not exceed the predetermined value for inferiority (P for noninferiority, 0.02; 90% CI, -0.9 to 10.3).	clopidogrel	45-66	purinergic receptor P2Y12	Homo sapiens	88-95
21705400-0	2011	Carrying one or two reduced-function CYP2C19 alleles is associated with an increased risk of major adverse cardiovascular events in people undergoing percutaneous coronary intervention and treated with clopidogrel.	clopidogrel	202-213	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-44
21628721-0	2011	Variability in on-treatment platelet reactivity explained by CYP2C19*2 genotype is modest in clopidogrel pretreated patients undergoing coronary stenting.	clopidogrel	93-104	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	61-68
21692977-0	2011	Relationship between paraoxonase-1 activity, its Q192R genetic variant and clopidogrel responsiveness in the ADRIE study.	clopidogrel	75-86	paraoxonase 1	Homo sapiens	21-34
21505714-2	2011	Simultaneous inhibition of blood platelet cyclooxygenase-1 by aspirin and of the P2Y12 receptor by clopidogrel or prasugrel is currently recommended in this setting.	clopidogrel	99-110	purinergic receptor P2Y12	Homo sapiens	81-86
21497813-0	2011	The P-selectin gene Pro715 allele and low levels of soluble P-selectin are associated with reduced P2Y12 adenosine diphosphate receptor reactivity in clopidogrel-treated patients.	clopidogrel	150-161	selectin P	Homo sapiens	4-14
21497813-0	2011	The P-selectin gene Pro715 allele and low levels of soluble P-selectin are associated with reduced P2Y12 adenosine diphosphate receptor reactivity in clopidogrel-treated patients.	clopidogrel	150-161	selectin P	Homo sapiens	60-70
21497813-5	2011	CONCLUSION: The SELP Pro715 allele is linked to low levels of sP-selectin, and both are associated with decreased P2Y12 ADP receptor reactivity in patients on clopidogrel therapy.	clopidogrel	159-170	selectin P	Homo sapiens	16-20
21527445-3	2011	Recently published findings showed a highly significant impact of a common polymorphism (Q192R) within the paraoxonase-1 (PON1) gene on clopidogrel treatment efficacy but no influence of the CYP2C19*2 genetic variant as previously demonstrated.	clopidogrel	136-147	paraoxonase 1	Homo sapiens	107-120
21527445-3	2011	Recently published findings showed a highly significant impact of a common polymorphism (Q192R) within the paraoxonase-1 (PON1) gene on clopidogrel treatment efficacy but no influence of the CYP2C19*2 genetic variant as previously demonstrated.	clopidogrel	136-147	paraoxonase 1	Homo sapiens	122-126
21527445-4	2011	The aim of this study was to assess the impact of the PON1 Q192R genotype in parallel to that of CYP2C19*2 on the antiplatelet effect of clopidogrel and the risk of ST in clopidogrel-treated patients.	clopidogrel	137-148	paraoxonase 1	Homo sapiens	54-58
21527445-4	2011	The aim of this study was to assess the impact of the PON1 Q192R genotype in parallel to that of CYP2C19*2 on the antiplatelet effect of clopidogrel and the risk of ST in clopidogrel-treated patients.	clopidogrel	171-182	paraoxonase 1	Homo sapiens	54-58
21447613-1	2011	Clinical studies with clopidogrel or prasugrel show that although increased inhibition of P2Y(12) and platelet function improves efficacy, bleeding is also increased.	clopidogrel	22-33	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	90-97
21221715-5	2011	High platelet reactivity on clopidogrel (HPR(Clopidogrel)) was defined as a PRU value &gt;=240.	clopidogrel	28-39	haptoglobin-related protein	Homo sapiens	41-44
21221715-5	2011	High platelet reactivity on clopidogrel (HPR(Clopidogrel)) was defined as a PRU value &gt;=240.	clopidogrel	45-56	haptoglobin-related protein	Homo sapiens	41-44
21700086-1	2011	OBJECTIVES: The aim of this study was to assess the association between genetic variants of the insulin receptor substrate (IRS)-1 gene, platelet function, and long-term outcomes in patients with type 2 diabetes mellitus (DM) and stable coronary artery disease while on aspirin and clopidogrel therapy.	clopidogrel	282-293	insulin receptor substrate 1	Homo sapiens	96-130
22088240-0	2011	[Impact of cytochrome P450 2C19 polymorphisms on outcome of cardiovascular events in clopidogrel-treated Chinese patients after percutaneous coronary intervention].	clopidogrel	85-96	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	11-31
22088240-1	2011	OBJECTIVE: To investigate the impact of cytochrome P450 (CYP) 2C19 681G &gt; A polymorphism on long-term prognosis of clopidogrel-treated Chinese patients after percutaneous coronary intervention (PCI).	clopidogrel	118-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-66
22088240-10	2011	CONCLUSION: CYP2C19 681G &gt; A polymorphism is a determinant of prognosis in coronary heart disease patients receiving chronic clopidogrel treatment after PCI.	clopidogrel	128-139	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
21554368-10	2011	P2Y12 is the same receptor targeted by ticlopidine and clopidogrel, platelet inhibitors used in lieu of aspirin in people at risk for cardiovascular disease; thus, spontaneous bleeding is not expected unless there are other contributing factors.	clopidogrel	55-66	purinergic receptor P2Y12	Homo sapiens	0-5
20351750-0	2011	Cytochrome P450 2C19*2 polymorphism and cardiovascular recurrences in patients taking clopidogrel: a meta-analysis.	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-20
20351750-9	2011	The current meta-analysis, carried out on nearly 8000 patients with CAD undergoing clopidogrel treatment, shows that the CYP2C19(*)2 polymorphism is associated with an increased risk of major adverse cardiovascular events and stent thrombosis.	clopidogrel	83-94	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	121-128
21544314-2	2011	Clopidogrel is a pro drug and is metabolised by liver enzymes, particularly CYP2C19, into its active form.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	76-83
21544314-5	2011	Further, proton pump inhibitors (PPI) may interfere with clopidogrel"s actions by functionally reducing the ability of CYP2C19 to convert clopidogrel to its active metabolite.	clopidogrel	57-68	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	119-126
21544314-5	2011	Further, proton pump inhibitors (PPI) may interfere with clopidogrel"s actions by functionally reducing the ability of CYP2C19 to convert clopidogrel to its active metabolite.	clopidogrel	138-149	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	119-126
21385571-1	2011	BACKGROUND: CYP2C19 variants have been demonstrated to play an important role in determining response to clopidogrel and outcomes while on clopidogrel therapy.	clopidogrel	105-116	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
21385571-1	2011	BACKGROUND: CYP2C19 variants have been demonstrated to play an important role in determining response to clopidogrel and outcomes while on clopidogrel therapy.	clopidogrel	139-150	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
21287353-10	2011	Clopidogrel-treated CHF animals displayed enhanced phosphorylation of AKT and eNOS.	clopidogrel	0-11	AKT serine/threonine kinase 1	Rattus norvegicus	70-73
21464720-2	2011	Recent studies have raised concerns that PPIs could reduce clopidogrel"s efficacy by competitive inhibition of cytochrome P450 2C19 isoenzyme.	clopidogrel	59-70	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	111-131
21464720-8	2011	RESULTS: We observed a significant reduction in clopidogrel"s effect when patients were initiated with omeprazole; the mean P2Y12 reaction units (PRU) increased from 202+-52 to 235+-58 with omeprazole (P&lt;0.001).	clopidogrel	48-59	purinergic receptor P2Y12	Homo sapiens	124-129
21073332-8	2011	RESULTS: On periodontitis phase, Asp and Clo significantly reduced levels of TNF-alpha and Il-6 (P &lt;0.05), but only Asp decreased thromboxane A(2) (P &lt;0.05).	clopidogrel	41-44	tumor necrosis factor	Rattus norvegicus	77-86
21073332-8	2011	RESULTS: On periodontitis phase, Asp and Clo significantly reduced levels of TNF-alpha and Il-6 (P &lt;0.05), but only Asp decreased thromboxane A(2) (P &lt;0.05).	clopidogrel	41-44	interleukin 6	Rattus norvegicus	91-95
21538380-0	2011	Modifying clopidogrel maintenance doses according to vasodilator-stimulated phosphoprotein phosphorylation index improves clinical outcome in patients with clopidogrel resistance.	clopidogrel	10-21	vasodilator stimulated phosphoprotein	Homo sapiens	53-90
21538380-0	2011	Modifying clopidogrel maintenance doses according to vasodilator-stimulated phosphoprotein phosphorylation index improves clinical outcome in patients with clopidogrel resistance.	clopidogrel	156-167	vasodilator stimulated phosphoprotein	Homo sapiens	53-90
21538380-4	2011	HYPOTHESIS: We hypothesized that VASP-guided clopidogrel maintenance doses, compared to fixed doses, improved clinical outcome.	clopidogrel	45-56	vasodilator stimulated phosphoprotein	Homo sapiens	33-37
21538380-7	2011	In the VASP-guided group, patients received adjusted maintenance doses of clopidogrel to obtain platelet reactivity index (PRI) of &lt;50% during 1 year after PCI.	clopidogrel	74-85	vasodilator stimulated phosphoprotein	Homo sapiens	7-11
21287353-13	2011	Chronic P2Y(12)-blockade with clopidogrel improved adenylyl cyclase-mediated signaling including increased AKT- and eNOS-phosphorylation contributing to improved NO-mediated vasorelaxation.	clopidogrel	30-41	AKT serine/threonine kinase 1	Rattus norvegicus	107-110
21419895-0	2011	Does hemodialysis affect clopidogrel resistance as measured by VerifyNow P2Y12 test?	clopidogrel	25-36	purinergic receptor P2Y12	Homo sapiens	73-78
21479337-2	2011	According to these results, genotyping for the relevant gene polymorphisms, especially for the CYP2C19 loss-of-function alleles, has been discussed to be an effective method of individualising and optimising clopidogrel treatment.	clopidogrel	208-219	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	95-102
21479342-5	2011	Clopidogrel, the most widely used drug that inhibits P2Y12, is effective both in monotherapy and in combination with acetylsalicylic acid (ASA).	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	53-58
21436336-7	2011	Both patients presented with symptomatic acute occlusions of the PED constructs within 14 days of clopidogrel discontinuation.	clopidogrel	98-109	OCA2 melanosomal transmembrane protein	Homo sapiens	65-68
21393433-1	2011	AIMS: This study investigated the effect of clopidogrel treatment on inflammatory activity as evidenced by the change in high-sensitivity C-reactive protein (hsCRP) levels in a broad population of patients who are at high risk of atherothrombotic events.	clopidogrel	44-55	C-reactive protein	Homo sapiens	138-156
21572655-1	2011	Clopidogrel is a prodrug which requires cytochrome P450 2C19 (CYP 2C19) enzyme for its conversion to an active thiol metabolite.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-60
21474982-13	2011	The results of the present study confirmed that the genetic polymorphism of CYP2C19 could be important in clopidogrel response.	clopidogrel	106-117	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	76-83
21511218-2	2011	BACKGROUND: CYP2C19 loss-of-function alleles are associated with reduced responsiveness to standard clopidogrel doses.	clopidogrel	100-111	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
21511218-10	2011	CONCLUSIONS: Carriers of CYP2C19*2 display significantly lower responses to clopidogrel with a gene-dose effect.	clopidogrel	76-87	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
21511219-2	2011	BACKGROUND: High on-treatment platelet reactivity after clopidogrel administration after PCI is linked to the loss-of-function CYP2C19*2 allele and accompanied by an increased risk of adverse events.	clopidogrel	56-67	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	127-134
21572655-1	2011	Clopidogrel is a prodrug which requires cytochrome P450 2C19 (CYP 2C19) enzyme for its conversion to an active thiol metabolite.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	62-70
21572655-2	2011	Proton pump inhibitors (PPIs) inhibits enzyme CYP 2C19 interfering with the conversion of clopidogrel into its active metabolite.	clopidogrel	90-101	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	46-54
23960748-6	2011	However, clopidogrel produced significant elevation (P &lt; 0.05) in AST and ALT levels but placebo formula caused no significant alteration (P &gt; 0.05) in the serum levels of these two enzymes.	clopidogrel	9-20	solute carrier family 17 member 5	Homo sapiens	69-72
23960748-4	2011	Treatment with clopidogrel produced significant improvement (P &lt; 0.05) in fasting serum glucose (FSG), fasting serum insulin level, quantitative insulin sensitivity check index (QUICKI); and oxidative stress markers: serum malondialdehyde (MDA) and serum reduced glutathione (GSH) compared to their baseline levels.	clopidogrel	15-26	insulin	Homo sapiens	120-127
23960748-4	2011	Treatment with clopidogrel produced significant improvement (P &lt; 0.05) in fasting serum glucose (FSG), fasting serum insulin level, quantitative insulin sensitivity check index (QUICKI); and oxidative stress markers: serum malondialdehyde (MDA) and serum reduced glutathione (GSH) compared to their baseline levels.	clopidogrel	15-26	insulin	Homo sapiens	148-155
21237253-7	2011	In addition, being pretreated with LPS, HepG2 cells altered the cellular responsiveness to ester therapeutic agents, including clopidogrel (hydrolyzed by HCE1) and irinotecan (hydrolyzed by HCE2).	clopidogrel	127-138	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	154-158
21426546-2	2011	The presence of CYP 2C19*2 polymorphism can reduce the formation of the active metabolite of clopidogrel, resulting in less platelet inhibition.	clopidogrel	93-104	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-24
21426546-6	2011	RESULTS: The total frequency of clopidogrel resistance was 29.0% by VASP-PRI and 31.6% by VerifyNow-PRU.	clopidogrel	32-43	vasodilator stimulated phosphoprotein	Homo sapiens	68-72
21426546-11	2011	The frequency of clopidogrel resistance in patients with the polymorphism was 32% compared to 16% in wild-type patients when defined by VASP-PRI (p = 0.006).	clopidogrel	17-28	vasodilator stimulated phosphoprotein	Homo sapiens	136-140
21426546-13	2011	CONCLUSIONS: Clopidogrel treated patients with the CYP 2C19*2 polymorphism have significantly increased platelet reactivity compared to patients with the wild-type, evaluated with the VASP determination, and even more pronounced with the VerifyNow P2Y12 method.	clopidogrel	13-24	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	51-59
21426546-13	2011	CONCLUSIONS: Clopidogrel treated patients with the CYP 2C19*2 polymorphism have significantly increased platelet reactivity compared to patients with the wild-type, evaluated with the VASP determination, and even more pronounced with the VerifyNow P2Y12 method.	clopidogrel	13-24	vasodilator stimulated phosphoprotein	Homo sapiens	184-188
21426546-13	2011	CONCLUSIONS: Clopidogrel treated patients with the CYP 2C19*2 polymorphism have significantly increased platelet reactivity compared to patients with the wild-type, evaluated with the VASP determination, and even more pronounced with the VerifyNow P2Y12 method.	clopidogrel	13-24	purinergic receptor P2Y12	Homo sapiens	248-253
30524601-0	2011	Repeated intra-stent thrombus formation in a patient with acute coronary syndrome due to poor responsiveness to clopidogrel may be associated with cytochrome P-450 2C19*2 polymorphism.	clopidogrel	112-123	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	147-168
30524601-6	2011	This case suggests that the mechanism of stent thrombosis, while multi-factorial, is affected greatly by crossover of poor responsiveness to clopidogrel due to the CYP2C19*2 polymorphism.	clopidogrel	141-152	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	164-171
21392639-2	2011	Clopidogrel, a prodrug, requires hepatic cytochrome P450 (CYP) metabolic activation to produce the active metabolite that inhibits the platelet P2Y12 adenosine diphosphate (ADP) receptor, decreasing platelet activation and aggregation processes.	clopidogrel	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	41-56
21392639-2	2011	Clopidogrel, a prodrug, requires hepatic cytochrome P450 (CYP) metabolic activation to produce the active metabolite that inhibits the platelet P2Y12 adenosine diphosphate (ADP) receptor, decreasing platelet activation and aggregation processes.	clopidogrel	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	58-61
21392639-3	2011	Atorvastatin, omeprazole, and several other drugs have been shown in pharmacodynamic studies to competitively inhibit CYP activation of clopidogrel, reducing clopidogrel responsiveness.	clopidogrel	136-147	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	118-121
21392639-3	2011	Atorvastatin, omeprazole, and several other drugs have been shown in pharmacodynamic studies to competitively inhibit CYP activation of clopidogrel, reducing clopidogrel responsiveness.	clopidogrel	158-169	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	118-121
21392639-4	2011	Conversely, other agents increase clopidogrel responsiveness by inducing CYP activity.	clopidogrel	34-45	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	73-76
21392598-1	2011	Despite the proven efficacy of dual antiplatelet therapy with aspirin and one of the first-generation P2Y(12) antagonists (clopidogrel, prasugrel) in patients with atherothrombotic disease, residual ischemic risk remains substantial, and bleeding rates are increased.	clopidogrel	123-134	purinergic receptor P2Y12	Homo sapiens	102-109
21148426-0	2011	Enhanced clopidogrel responsiveness in smokers: smokers" paradox is dependent on cytochrome P450 CYP1A2 status.	clopidogrel	9-20	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	97-103
21148426-10	2011	CONCLUSIONS: Enhanced clopidogrel response in smokers, known as the smokers" paradox, is not universal but was observed only in cytochrome P450 CYP1A2 (-163C&gt;A) A-allele carriers, suggesting a genotype-dependent effect of smoking on clopidogrel responsiveness.	clopidogrel	22-33	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	144-150
21148426-10	2011	CONCLUSIONS: Enhanced clopidogrel response in smokers, known as the smokers" paradox, is not universal but was observed only in cytochrome P450 CYP1A2 (-163C&gt;A) A-allele carriers, suggesting a genotype-dependent effect of smoking on clopidogrel responsiveness.	clopidogrel	236-247	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	144-150
21266209-0	2011	Proton pump inhibitor co-therapy with clopidogrel: is there GI benefit or cardiovascular harm?	clopidogrel	38-49	ATPase H+/K+ transporting subunit alpha	Homo sapiens	0-11
21085001-0	2011	Pretreatment with different loading doses of clopidogrel influences P-selectin levels in patients undergoing percutaneous coronary intervention: results from the ARMYDA-2 (antiplatelet therapy for reduction of myocardial damage during angioplasty) SELECT substudy.	clopidogrel	45-56	selectin P	Homo sapiens	68-78
21085001-7	2011	CONCLUSION: Pretreatment with clopidogrel before PCI decreases peri-procedural P-selectin levels; moreover, a 600 mg clopidogrel loading dose, compared with the 300 mg regimen, is associated with reduction of peri-procedural myocardial damage and significant attenuation of P-selectin levels at the time of intervention.	clopidogrel	30-41	selectin P	Homo sapiens	79-89
21085001-7	2011	CONCLUSION: Pretreatment with clopidogrel before PCI decreases peri-procedural P-selectin levels; moreover, a 600 mg clopidogrel loading dose, compared with the 300 mg regimen, is associated with reduction of peri-procedural myocardial damage and significant attenuation of P-selectin levels at the time of intervention.	clopidogrel	30-41	selectin P	Homo sapiens	274-284
21085001-7	2011	CONCLUSION: Pretreatment with clopidogrel before PCI decreases peri-procedural P-selectin levels; moreover, a 600 mg clopidogrel loading dose, compared with the 300 mg regimen, is associated with reduction of peri-procedural myocardial damage and significant attenuation of P-selectin levels at the time of intervention.	clopidogrel	117-128	selectin P	Homo sapiens	274-284
21168310-1	2011	BACKGROUND AND PURPOSE: CYP2C19*2 loss-of-function allele in Caucasians may be associated with wide interindividual variability in platelet response to clopidogrel, and the incidence of gene mutation varies with racial differences, especially between Asians and Caucasians.	clopidogrel	152-163	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
29783409-5	2011	One needs only to look to the developing research associated with CYP2C19 genetic testing, a marker that indicates a poor response to the antiplatelet therapy clopidogrel for some 30% of patients that carry the specific alleles.	clopidogrel	159-170	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	66-73
20845077-0	2011	Cytochrome P450 2C19 polymorphism is associated with poor clinical outcomes in coronary artery disease patients treated with clopidogrel.	clopidogrel	125-136	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-20
20845077-2	2011	Cytochrome P450 (CYP) polymorphisms have been proposed as possible mechanisms for nonresponsiveness to clopidogrel.	clopidogrel	103-114	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-15
20845077-2	2011	Cytochrome P450 (CYP) polymorphisms have been proposed as possible mechanisms for nonresponsiveness to clopidogrel.	clopidogrel	103-114	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	17-20
20427204-9	2011	COL-MEA and ADP-MEA discriminated between preoperative ASA and clopidogrel intake (ASA: sensitivity = 86.3%, and specificity = 89.3%; clopidogrel: sensitivity = 87.5%, and specificity = 95.1%).	clopidogrel	63-74	WD and tetratricopeptide repeats 1	Homo sapiens	12-19
21509344-3	2011	Current consensus recommendations state that patients prescribed clopidogrel plus aspirin should receive a proton pump inhibitor (PPI) to reduce gastrointestinal bleeding.	clopidogrel	65-76	ATPase H+/K+ transporting subunit alpha	Homo sapiens	107-118
20966167-6	2011	Clopidogrel, the most widely used drug that inhibits P2Y12, is effective both in monotherapy and in combination with acetylsalicylic acid.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	53-58
20966167-7	2011	The most important drawback of clopidogrel is its inability to inhibit adequately P2Y12-dependent platelet function in approximately one-third of patients who are therefore not protected from major cardiovascular events.	clopidogrel	31-42	purinergic receptor P2Y12	Homo sapiens	82-87
21310311-6	2011	Higher clopidogrel dose was associated with decreased proportion of patients with P2Y(12) reaction units &gt;= 240 (12% vs. 32%; p = 0.001), flow-mediated vasodilation &lt;7% (16% vs. 58%; p = 0.0003), and high-sensitivity C-reactive protein levels &gt;3 mg/l (46% vs. 64%; p = 0.07).	clopidogrel	7-18	C-reactive protein	Homo sapiens	223-241
21285422-0	2011	Carriage of reduced-function CYP2C19 allele among patients treated with clopidogrel.	clopidogrel	72-83	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	29-36
21288101-0	2011	CYP2C19 genotype and outcomes of clopidogrel treatment.	clopidogrel	33-44	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
21288102-0	2011	CYP2C19 genotype and outcomes of clopidogrel treatment.	clopidogrel	33-44	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
21178986-0	2011	Differential impacts of CYP2C19 gene polymorphisms on the antiplatelet effects of clopidogrel and ticlopidine.	clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
21178986-1	2011	We examined the influence of CYP2C19 polymorphisms on the antiplatelet effects of clopidogrel and ticlopidine.	clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	29-36
21178986-3	2011	The degree of platelet aggregation in the clopidogrel group, although not in the ticlopidine group, depended on the CYP2C19 polymorphism, and the maximal platelet aggregation in poor metabolizers (PMs) taking clopidogrel was equivalent to that in the group taking aspirin alone.	clopidogrel	42-53	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	116-123
21178986-5	2011	These results suggest that CYP2C19 polymorphisms have a profound impact on the antiplatelet effect of clopidogrel but not on that of ticlopidine.	clopidogrel	102-113	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	27-34
20427204-10	2011	The postoperative transfusion risk was increased in patients diagnosed for clopidogrel treatment by ADP-MEA (odds ratio = 2.92; confidence interval: 1.44-5.92; p = 0.005).	clopidogrel	75-86	WD and tetratricopeptide repeats 1	Homo sapiens	100-107
21297211-4	2011	Laboratory evaluation of hypercoagulability yielded negative results, but low responsiveness for clopidogrel was revealed by the VerifyNow P2Y12 assay.	clopidogrel	97-108	purinergic receptor P2Y12	Homo sapiens	139-144
21262444-3	2011	In contrast, resistance to clopidogrel (a P2Y12 inhibitor), which is mostly due to inefficient metabolism of the pro-drug clopidogrel to its active metabolite, is a rather frequent condition, which is associated with lower clinical efficacy of the drug.	clopidogrel	27-38	purinergic receptor P2Y12	Homo sapiens	42-47
21262444-3	2011	In contrast, resistance to clopidogrel (a P2Y12 inhibitor), which is mostly due to inefficient metabolism of the pro-drug clopidogrel to its active metabolite, is a rather frequent condition, which is associated with lower clinical efficacy of the drug.	clopidogrel	122-133	purinergic receptor P2Y12	Homo sapiens	42-47
21262444-5	2011	The use of new P2Y12 inhibitors, such as prasugrel and ticagrelor, which adequately inhibit P2Y12-dependent platelet function in the vast majority of treated subjects, appears the best solution to the problem of clopidogrel resistance.	clopidogrel	212-223	purinergic receptor P2Y12	Homo sapiens	15-20
21251579-0	2011	Cardiovascular mortality in chronic kidney disease patients undergoing percutaneous coronary intervention is mainly related to impaired P2Y12 inhibition by clopidogrel.	clopidogrel	156-167	purinergic receptor P2Y12	Homo sapiens	136-141
21256376-0	2011	Double-dose clopidogrel in patients undergoing PCI for ACS.	clopidogrel	12-23	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	55-58
21256377-0	2011	Double-dose clopidogrel in patients undergoing PCI for ACS.	clopidogrel	12-23	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	55-58
20980920-0	2011	The effect of St John"s Wort on the pharmacodynamic response of clopidogrel in hyporesponsive volunteers and patients: increased platelet inhibition by enhancement of CYP3A4 metabolic activity.	clopidogrel	64-75	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	167-173
20980920-1	2011	Clopidogrel is metabolically activated by cytochrome P450 (CYP) isoenzymes.	clopidogrel	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	42-57
20980920-1	2011	Clopidogrel is metabolically activated by cytochrome P450 (CYP) isoenzymes.	clopidogrel	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	59-62
20980920-2	2011	We evaluated whether St. John"s wort (SJW), a CYP2C19 and CYP3A4 inducer, enhances the pharmacodynamic response of clopidogrel.	clopidogrel	115-126	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	46-53
21217483-3	2011	We report the use of a new P2Y12 point-of-care assay (VerifyNow; Accumetrics, San Diego, CA) to determine the magnitude of platelet inhibition in trauma patients using clopidogrel.	clopidogrel	168-179	purinergic receptor P2Y12	Homo sapiens	27-32
21217483-11	2011	CONCLUSIONS: The P2Y12 point-of-care assay determined that a large percentage of patients had undetectable or low platelet inhibition despite reportedly being on clopidogrel therapy.	clopidogrel	162-173	purinergic receptor P2Y12	Homo sapiens	17-22
21771376-1	2011	As both proton pump inhibitors (PPIs) and clopidogrel are metabolized by CYP2C19, an enzyme of the cytochrome P450 system, this could lead to drug competition.	clopidogrel	42-53	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	73-80
21771377-3	2011	Concomitant use of omeprazole and clopidogrel was found to decrease the exposure (AUC) to clopidogrel"s active metabolite by 50% and to sharply increase platelet reactivity, as a result of inhibition by omeprazole of CYP2C19, a cytochrome P450 (CYP) enzyme.	clopidogrel	34-45	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	217-224
21771377-3	2011	Concomitant use of omeprazole and clopidogrel was found to decrease the exposure (AUC) to clopidogrel"s active metabolite by 50% and to sharply increase platelet reactivity, as a result of inhibition by omeprazole of CYP2C19, a cytochrome P450 (CYP) enzyme.	clopidogrel	34-45	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	228-243
21771377-3	2011	Concomitant use of omeprazole and clopidogrel was found to decrease the exposure (AUC) to clopidogrel"s active metabolite by 50% and to sharply increase platelet reactivity, as a result of inhibition by omeprazole of CYP2C19, a cytochrome P450 (CYP) enzyme.	clopidogrel	34-45	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	217-220
20873965-4	2011	We tested this cartridge for its capacity to detect the inhibition of the P2Y12 receptor, which is the target for thienopyridine medication (e.g. clopidogrel).	clopidogrel	146-157	purinergic receptor P2Y12	Homo sapiens	74-79
20873965-7	2011	In volunteers, the intake of a 600 mg clopidogrel loading dose caused an increase of the CTs in all volunteers, although some of these volunteers were identified as "poor responders" by the VASP assay (no significant reduction of PRI levels).	clopidogrel	38-49	vasodilator stimulated phosphoprotein	Homo sapiens	190-194
21142408-1	2011	Clopidogrel is a prodrug that needs to be converted in?vivo by several cytochrome (CYP) P450 iso-enzymes to become active.	clopidogrel	0-11	peptidylprolyl isomerase G	Homo sapiens	83-86
21142408-2	2011	Both clopidogrel and the oral hypoglycemic drug class sulfonylureas are metabolized by the iso-enzyme CYP2C9.	clopidogrel	5-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
21262991-0	2011	CYP2C19 genotype and proton pump inhibitors in clopidogrel-treated patients: does it take two to tango?	clopidogrel	47-58	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
21262992-1	2011	BACKGROUND: Clopidogrel requires metabolic activation by cytochrome P450 2C19 (CYP2C19).	clopidogrel	12-23	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	57-77
21262992-1	2011	BACKGROUND: Clopidogrel requires metabolic activation by cytochrome P450 2C19 (CYP2C19).	clopidogrel	12-23	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	79-86
20971951-2	2011	Calcium and diacyglycerol-regulated guanine nucleotide exchange factor I (CalDAG-GEFI, RasGRP2) mediates the rapid but reversible activation of integrin alphaIIbbeta3, while the adenosine diphosphate receptor P2Y12, the target for antiplatelet drugs like clopidogrel, facilitates delayed but sustained integrin activation.	clopidogrel	255-266	RAS, guanyl releasing protein 2	Mus musculus	74-85
20971951-2	2011	Calcium and diacyglycerol-regulated guanine nucleotide exchange factor I (CalDAG-GEFI, RasGRP2) mediates the rapid but reversible activation of integrin alphaIIbbeta3, while the adenosine diphosphate receptor P2Y12, the target for antiplatelet drugs like clopidogrel, facilitates delayed but sustained integrin activation.	clopidogrel	255-266	RAS, guanyl releasing protein 2	Mus musculus	87-94
20971951-2	2011	Calcium and diacyglycerol-regulated guanine nucleotide exchange factor I (CalDAG-GEFI, RasGRP2) mediates the rapid but reversible activation of integrin alphaIIbbeta3, while the adenosine diphosphate receptor P2Y12, the target for antiplatelet drugs like clopidogrel, facilitates delayed but sustained integrin activation.	clopidogrel	255-266	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	209-214
21247447-1	2011	BACKGROUND: Recent studies have reported the clinical importance of CYP2C19 and ABCB1 polymorphisms in an individualized approach to clopidogrel treatment.	clopidogrel	133-144	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	68-75
21247447-1	2011	BACKGROUND: Recent studies have reported the clinical importance of CYP2C19 and ABCB1 polymorphisms in an individualized approach to clopidogrel treatment.	clopidogrel	133-144	ATP binding cassette subfamily B member 1	Homo sapiens	80-85
21226927-12	2011	The results for clopidogrel revealed that 69% of the CLR were treated effectively by increasing the clopidogrel dose to 150 mg daily.	clopidogrel	16-27	doublecortin like kinase 3	Homo sapiens	53-56
21226927-12	2011	The results for clopidogrel revealed that 69% of the CLR were treated effectively by increasing the clopidogrel dose to 150 mg daily.	clopidogrel	100-111	doublecortin like kinase 3	Homo sapiens	53-56
21586365-7	2011	The widely prescribed drug, clopidogrel, which results in irreversible blockade of the platelet P2Y(12) receptor, is the most important therapeutic agent that targets a P2Y receptor.	clopidogrel	28-39	purinergic receptor P2Y12	Homo sapiens	96-103
21811066-0	2011	Clopidogrel effectively suppresses endothelial microparticle generation induced by indoxyl sulfate via inhibition of the p38 mitogen-activated protein kinase pathway.	clopidogrel	0-11	mitogen-activated protein kinase 14	Homo sapiens	121-124
21811066-6	2011	RESULTS: (1) Indoxyl sulfate induced EMP release in HUVECs in a dose-dependent fashion; (2) all drugs (10-50 muM) inhibited EMP generation induced by indoxyl sulfate, with clopidogrel being the most effective; (3) the p38 MAPK inhibitor suppressed EMP generation induced by indoxyl sulfate, and (4) clopidogrel significantly suppressed MAPK signaling activated by indoxyl sulfate, with the most potency on p38.	clopidogrel	172-183	latexin	Homo sapiens	109-112
21811066-6	2011	RESULTS: (1) Indoxyl sulfate induced EMP release in HUVECs in a dose-dependent fashion; (2) all drugs (10-50 muM) inhibited EMP generation induced by indoxyl sulfate, with clopidogrel being the most effective; (3) the p38 MAPK inhibitor suppressed EMP generation induced by indoxyl sulfate, and (4) clopidogrel significantly suppressed MAPK signaling activated by indoxyl sulfate, with the most potency on p38.	clopidogrel	299-310	latexin	Homo sapiens	109-112
21811066-7	2011	CONCLUSION: The p38 signaling involves EMP generation induced by indoxyl sulfate and is effectively suppressed by clopidogrel.	clopidogrel	114-125	mitogen-activated protein kinase 14	Homo sapiens	16-19
21241972-0	2011	Prolonged clopidogrel application reduces tissue factor expression after percutaneous coronary intervention in the porcine model.	clopidogrel	10-21	coagulation factor III, tissue factor	Sus scrofa	42-55
21241972-3	2011	This study assessed the effect of prolonged clopidogrel treatment on tissue factor (TF) expression in coronary arteries and on the circulating TF level after percutaneous transluminal coronary angioplasty /ICBT in a porcine coronary model.	clopidogrel	44-55	coagulation factor III, tissue factor	Sus scrofa	69-82
21241972-3	2011	This study assessed the effect of prolonged clopidogrel treatment on tissue factor (TF) expression in coronary arteries and on the circulating TF level after percutaneous transluminal coronary angioplasty /ICBT in a porcine coronary model.	clopidogrel	44-55	coagulation factor III, tissue factor	Sus scrofa	84-86
21241972-11	2011	RESULTS: Prolonged clopidogrel application significantly reduced coronary TF at the protein (Group I vs. II, 8.975 +- 3.947% vs. 26.44 +- 5.375%, P = .007) and mRNA level [Group I vs. II, (0.3501 +- 0.0519) x 10(-3) vs. (0.7073 +- 0.0436) x 10(-3), P&lt;.0005].	clopidogrel	19-30	coagulation factor III, tissue factor	Sus scrofa	74-76
21241972-12	2011	Circulating TF protein tended to be lower after 3 months than after 1 month clopidogrel treatment post-PCI (Group I vs. Group II, 488.3 +- 35.37 pg/ml vs. 572.3 +- 39.9 pg/ml, P = .130).	clopidogrel	76-87	coagulation factor III, tissue factor	Sus scrofa	12-14
21241972-13	2011	CONCLUSIONS: Prolonged clopidogrel treatment reduced coronary TF expression and tended to reduce the blood TF level post-PCI, thus possibly modulating the risk of late thrombosis.	clopidogrel	23-34	coagulation factor III, tissue factor	Sus scrofa	62-64
21241972-13	2011	CONCLUSIONS: Prolonged clopidogrel treatment reduced coronary TF expression and tended to reduce the blood TF level post-PCI, thus possibly modulating the risk of late thrombosis.	clopidogrel	23-34	coagulation factor III, tissue factor	Sus scrofa	107-109
21099121-11	2011	CONCLUSIONS:  From these results it is suggested that CYP2C19*2 polymorphism is associated with subclinical thrombus formation among Japanese patients receiving clopidogrel.	clopidogrel	161-172	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	54-61
21498913-7	2011	In addition, the highest IL-6 quartile was an independent predictor of ST in those on clopidogrel (adjusted HR 7.70; 95%CI 1.97-30.13) but not in those who were off clopidogrel.	clopidogrel	86-97	interleukin 6	Homo sapiens	25-29
21498913-8	2011	CONCLUSIONS: Highest IL-6 quartile was associated with ST, especially in clopidogrel users regardless of the time of ST, suggesting the involvement of inflammatory cytokines in ST.	clopidogrel	73-84	interleukin 6	Homo sapiens	21-25
21568918-1	2011	Clopidogrel is a thienopyridine, which inhibits the platelet P2Y adenosine diphosphate (ADP) receptor termed P2Y(12).	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	109-116
21568918-4	2011	PPIs might diminish the antiplatelet effects and the clinical effectiveness of clopidogrel possibly through inhibition of CYP2C19 and CYP3A4 isoenzymes.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	122-129
21568918-4	2011	PPIs might diminish the antiplatelet effects and the clinical effectiveness of clopidogrel possibly through inhibition of CYP2C19 and CYP3A4 isoenzymes.	clopidogrel	79-90	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	134-140
21143117-4	2011	In addition, several factors such as poor absorption, drug-to-drug interactions, inadequate dosing, elevated body mass index, insulin resistance and the nature of acute coronary syndromes have been implicated in low clopidogrel response.	clopidogrel	216-227	insulin	Homo sapiens	126-133
21423686-4	2011	But percent inhibitions of Agg(max) and Agg(late) (IPAs) in CYP2C19*2/*2 genotype at 4 hours, 24 hours, 3 days, and 7 days after clopidogrel administration were all the lowest among three CYP2C19*2 genotypes (P &lt; .01), and IPAs in CYP2C19*1/*2 genotype were between CYP2C19*1/*1 and CYP2C19*2/*2.	clopidogrel	129-140	hypoxia inducible factor 3 subunit alpha	Homo sapiens	51-55
21423686-4	2011	But percent inhibitions of Agg(max) and Agg(late) (IPAs) in CYP2C19*2/*2 genotype at 4 hours, 24 hours, 3 days, and 7 days after clopidogrel administration were all the lowest among three CYP2C19*2 genotypes (P &lt; .01), and IPAs in CYP2C19*1/*2 genotype were between CYP2C19*1/*1 and CYP2C19*2/*2.	clopidogrel	129-140	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	60-67
21423686-4	2011	But percent inhibitions of Agg(max) and Agg(late) (IPAs) in CYP2C19*2/*2 genotype at 4 hours, 24 hours, 3 days, and 7 days after clopidogrel administration were all the lowest among three CYP2C19*2 genotypes (P &lt; .01), and IPAs in CYP2C19*1/*2 genotype were between CYP2C19*1/*1 and CYP2C19*2/*2.	clopidogrel	129-140	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	188-195
21423686-4	2011	But percent inhibitions of Agg(max) and Agg(late) (IPAs) in CYP2C19*2/*2 genotype at 4 hours, 24 hours, 3 days, and 7 days after clopidogrel administration were all the lowest among three CYP2C19*2 genotypes (P &lt; .01), and IPAs in CYP2C19*1/*2 genotype were between CYP2C19*1/*1 and CYP2C19*2/*2.	clopidogrel	129-140	hypoxia inducible factor 3 subunit alpha	Homo sapiens	226-230
21423686-4	2011	But percent inhibitions of Agg(max) and Agg(late) (IPAs) in CYP2C19*2/*2 genotype at 4 hours, 24 hours, 3 days, and 7 days after clopidogrel administration were all the lowest among three CYP2C19*2 genotypes (P &lt; .01), and IPAs in CYP2C19*1/*2 genotype were between CYP2C19*1/*1 and CYP2C19*2/*2.	clopidogrel	129-140	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	188-195
21423686-4	2011	But percent inhibitions of Agg(max) and Agg(late) (IPAs) in CYP2C19*2/*2 genotype at 4 hours, 24 hours, 3 days, and 7 days after clopidogrel administration were all the lowest among three CYP2C19*2 genotypes (P &lt; .01), and IPAs in CYP2C19*1/*2 genotype were between CYP2C19*1/*1 and CYP2C19*2/*2.	clopidogrel	129-140	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	188-195
21423686-4	2011	But percent inhibitions of Agg(max) and Agg(late) (IPAs) in CYP2C19*2/*2 genotype at 4 hours, 24 hours, 3 days, and 7 days after clopidogrel administration were all the lowest among three CYP2C19*2 genotypes (P &lt; .01), and IPAs in CYP2C19*1/*2 genotype were between CYP2C19*1/*1 and CYP2C19*2/*2.	clopidogrel	129-140	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	188-195
22118006-0	2011	Relationship between cytochrome P450 2C19*2 polymorphism and stent thrombosis following percutaneous coronary intervention in Chinese patients receiving clopidogrel.	clopidogrel	153-164	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-41
22118006-1	2011	This study investigated the relationship between the cytochrome P450 2C19 (CYP2C19) *2 polymorphism (681A) and definite stent thrombosis (ST) in patients undergoing percutaneous coronary intervention (PCI) and receiving clopidogrel (75 mg/day, orally).	clopidogrel	220-231	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-73
22118006-1	2011	This study investigated the relationship between the cytochrome P450 2C19 (CYP2C19) *2 polymorphism (681A) and definite stent thrombosis (ST) in patients undergoing percutaneous coronary intervention (PCI) and receiving clopidogrel (75 mg/day, orally).	clopidogrel	220-231	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	75-82
22118006-6	2011	The CYP2C19*2 genotype is associated with an increased risk of definite ST following coronary stent placement  among Chinese patients with coronary artery disease receiving clopidogrel.	clopidogrel	173-184	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
21170047-0	2011	Paraoxonase-1 is a major determinant of clopidogrel efficacy.	clopidogrel	40-51	paraoxonase 1	Homo sapiens	0-13
21170047-3	2011	Using in vitro metabolomic profiling techniques, we identified paraoxonase-1 (PON1) as the crucial enzyme for clopidogrel bioactivation, with its common Q192R polymorphism determining the rate of active metabolite formation.	clopidogrel	110-121	paraoxonase 1	Homo sapiens	63-76
21170047-3	2011	Using in vitro metabolomic profiling techniques, we identified paraoxonase-1 (PON1) as the crucial enzyme for clopidogrel bioactivation, with its common Q192R polymorphism determining the rate of active metabolite formation.	clopidogrel	110-121	paraoxonase 1	Homo sapiens	78-82
21170047-4	2011	We tested the clinical relevance of the PON1 Q192R genotype in a population of individuals with coronary artery disease who underwent stent implantation and received clopidogrel therapy.	clopidogrel	166-177	paraoxonase 1	Homo sapiens	40-44
21170047-6	2011	Thus, we identified PON1 as a key factor for the bioactivation and clinical activity of clopidogrel.	clopidogrel	88-99	paraoxonase 1	Homo sapiens	20-24
21251580-2	2011	BACKGROUND: CCBs inhibit a variety of cytochrome P-450 enzymes, some of which contribute to clopidogrel metabolic activation.	clopidogrel	92-103	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	38-54
21627411-8	2011	Only one gene polymorphism (CYP2C19*17) increases the clopidogrel metabolization and so the clopidogrel-induced platelet inhibition.	clopidogrel	92-103	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
23226058-6	2011	When a prodrug, such as clopidogrel or codeine, must undergo hepatic biotransformation to its active form, a loss-of-function P450 genotype leads to reduced concentrations of the active drug and decreased drug efficacy.	clopidogrel	24-35	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	126-130
22028806-0	2011	Clopidogrel, a P2Y12 receptor antagonist, potentiates the inflammatory response in a rat model of peptidoglycan polysaccharide-induced arthritis.	clopidogrel	0-11	purinergic receptor P2Y12	Rattus norvegicus	15-20
22028806-1	2011	The P2Y12 receptor plays a crucial role in the regulation of platelet activation by several agonists, which is irreversibly antagonized by the active metabolite of clopidogrel, a widely used anti-thrombotic drug.	clopidogrel	164-175	purinergic receptor P2Y12	Rattus norvegicus	4-9
22028806-4	2011	There were significant differences between the PG-PS+clopidogrel group when compared to the PG-PS group including: increased joint diameter and clinical manifestations of inflammation, elevated plasma levels of pro-inflammatory cytokines (IL-1 beta, interferon (IFN) gamma, and IL-6), an elevated neutrophil blood count and an increased circulating platelet count.	clopidogrel	53-64	interleukin 6	Rattus norvegicus	278-282
22028806-5	2011	Plasma levels of IL-10 were significantly lower in the PG-PS+clopidogrel group compared to the PG-PS group.	clopidogrel	61-72	interleukin 10	Rattus norvegicus	17-22
22028806-6	2011	Plasma levels of platelet factor 4 (PF4) were elevated in both the PG-PS and the PG-PS+clopidogrel groups, however PF4 levels showed no difference upon clopidogrel treatment, suggesting that the pro- inflammatory effect of clopidogrel may be due to its action on cells other than platelets.	clopidogrel	87-98	platelet factor 4	Rattus norvegicus	36-39
22028806-9	2011	Elucidation of the mechanism of clopidogrel-induced cell responses is important to understand the role of the P2Y12 receptor in inflammation.	clopidogrel	32-43	purinergic receptor P2Y12	Rattus norvegicus	110-115
21627411-3	2011	Clopidogrel pro-drug is absorbed in the intestine and this process is influenced by P-glycoprotein-1 (P-GP).	clopidogrel	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	84-100
21627411-3	2011	Clopidogrel pro-drug is absorbed in the intestine and this process is influenced by P-glycoprotein-1 (P-GP).	clopidogrel	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	102-106
21627411-8	2011	Only one gene polymorphism (CYP2C19*17) increases the clopidogrel metabolization and so the clopidogrel-induced platelet inhibition.	clopidogrel	54-65	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
21703110-4	2011	Prevalence of co-prescribing of clopidogrel, aspirin and PPI in diabetic patients and clopidogrel with various CYP2C19 inhibitors was also examined.	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	111-118
21703110-11	2011	Only one patient on clopidogrel was receiving a CYP2C19 inhibitor in addition to a PPI.	clopidogrel	20-31	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	48-55
21546883-2	2011	The thienopyridine clopidogrel is a prodrug that requires bioactivation by the cytochrome P450 (CYP) system in order to exert its antiplatelet effect.	clopidogrel	19-30	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	79-94
21546883-2	2011	The thienopyridine clopidogrel is a prodrug that requires bioactivation by the cytochrome P450 (CYP) system in order to exert its antiplatelet effect.	clopidogrel	19-30	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	96-99
21546883-3	2011	Common genetic polymorphisms that reduce the catalytic activity of the CYP2C19 isoenzyme decrease circulating levels of active metabolite, reduce levels of platelet inhibition, and increase the risk of ischemic events in clopidogrel-treated patients.	clopidogrel	221-232	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
21546883-4	2011	Herein, we review the impact of the CYP2C19 genotype on the pharmacokinetics and pharmacodynamics of clopidogrel, the association between CYP2C19 genotype and clinical outcome, and present the rationale for the implementation of CYP2C19 genotyping to individualize antiplatelet therapy in clinical practice.	clopidogrel	101-112	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	36-43
22080983-6	2011	This article reviews the impact of         poor clopidogrel responsiveness on clinical outcomes, the major clinical studies using         VerifyNow P2Y12 Assay  (Accumetrics, San Diego, CA) to assess on-clopidogrel         platelet reactivity, and efforts to determine a reliable cutoff.	clopidogrel	203-214	purinergic receptor P2Y12	Homo sapiens	148-153
21075428-1	2011	INTRODUCTION: Carriage of CYP2C19*2 allele is associated with diminished platelet response to clopidogrel.	clopidogrel	94-105	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
21901881-4	2011	The causes of clopidogrel resistance include inadequate doses of the drug, its low absorption, poor compliance with the treatment, polymorphism of ADP receptors, GP IIb/IIIa and cytochrome P450 genes, acute coronary syndrome and stroke, metabolic syndrome.	clopidogrel	14-25	integrin subunit alpha 2b	Homo sapiens	162-168
21075428-2	2011	However, the loss-of-function impact of CYP2C19*3 allele on antiplatelet effect of clopidogrel has not been definitely verified.	clopidogrel	83-94	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-47
21075428-3	2011	We conducted this study to compare decreased response to clopidogrel according to carriage of CYP2C19*2 vs. *3 allele.	clopidogrel	57-68	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	94-101
21075428-12	2011	CONCLUSION: Carriage of CYP2C19*3 allele is associated with diminished antiplatelet effect of clopidogrel, which may be as potent as the loss-of-function effect of CYP2C19*2 allele.	clopidogrel	94-105	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
21133697-0	2010	Backtracking on CYP2C19 genotyping in clopidogrel therapy?	clopidogrel	38-49	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
21079055-12	2010	Whereas CYP2C19 genotype influenced the antiplatelet effect of clopidogrel, there was no effect of CYP2C19 genotype during ticagrelor therapy.	clopidogrel	63-74	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	8-15
21111931-3	2010	Clopidogrel is a pro-drug that needs metabolic activation through a cytochrome P450-dependent pathway, with an extensive involvement of the CYP 2C19 isoenzyme.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	140-148
21111931-5	2010	In the past two years some scientific evidences have suggested a possible negative interference of PPIs on antiplatelet effect of clopidogrel because of the competitive inhibition of the CYP 2C19 isoenzyme.	clopidogrel	130-141	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	187-195
21084035-4	2010	The possible relative risk factors included advanced age, chronic and systemic diseases, and co-administration of cytochrome P450 3A (CYP3A) enzyme-dependent metabolic drugs or its inhibitors such as clopidogrel and diltiazem.	clopidogrel	200-211	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	114-132
21084035-4	2010	The possible relative risk factors included advanced age, chronic and systemic diseases, and co-administration of cytochrome P450 3A (CYP3A) enzyme-dependent metabolic drugs or its inhibitors such as clopidogrel and diltiazem.	clopidogrel	200-211	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	134-139
21073556-2	2010	Interactions described include those between aspirin and ibuprofen, aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), and the thienopyridine, clopidogrel, and drugs inhibiting CYP2C19, notably the proton pump inhibitors (PPI) omeprazole and esomeprazole.	clopidogrel	157-168	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	191-198
21073556-11	2010	For the clopidogrel CYP2C19 and CYP3A4/5 interactions, there is good evidence that these interactions occur.	clopidogrel	8-19	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	20-27
21073556-11	2010	For the clopidogrel CYP2C19 and CYP3A4/5 interactions, there is good evidence that these interactions occur.	clopidogrel	8-19	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	32-38
21073556-13	2010	Again, a reasonable strategy is to avoid the chronic use of drugs that inhibit CYP2C19, notably PPIs, in subjects taking clopidogrel and use high dose H2 antagonists instead.	clopidogrel	121-132	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	79-86
20838744-2	2010	Both high levels of C-reactive protein (CRP)and high on-clopidogrel treatment platelet reactivity (HPR) have been linked to an increased risk of ischaemic events after percutaneous coronary intervention (PCI).	clopidogrel	56-67	haptoglobin-related protein	Homo sapiens	99-102
20838744-9	2010	In conclusion, elevated levels of CRP, WBC count and fibrinogen were significantly associated with high platelet reactivity in patients under chronic clopidogrel treatment.	clopidogrel	150-161	C-reactive protein	Homo sapiens	34-37
21029814-8	2010	Propensity-adjusted Cox analysis showed significantly higher survival free of major adverse cardiac events in patients receiving 600-mg loading dose of clopidogrel compared to those receiving the lower dose (hazard ratio 0.57, 95% confidence interval 0.33 to 0.98, p = 0.04).	clopidogrel	152-163	cytochrome c oxidase subunit 8A	Homo sapiens	20-23
20967400-6	2010	Dabigatran etexilate 150 mg BID was estimated to significantly reduce the risk of any stroke compared with aspirin monotherapy by 63% (RR 0.37; 95% CI 0.20-0.69) and aspirin plus clopidogrel by 61% (RR 0.39; 95% CI 0.21-0.72).	clopidogrel	179-190	BH3 interacting domain death agonist	Homo sapiens	28-31
21139402-3	2010	Because both clopidogrel and PPIs are metabolized by cytochrome P450 (CYP) 2C19, there is a possibility that, through drug interaction, PPIs diminish the antiplatelet effect of clopidogrel.	clopidogrel	13-24	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-79
21139402-3	2010	Because both clopidogrel and PPIs are metabolized by cytochrome P450 (CYP) 2C19, there is a possibility that, through drug interaction, PPIs diminish the antiplatelet effect of clopidogrel.	clopidogrel	177-188	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-79
21302482-0	2010	[Relationships of blood stasis syndrome, CYP2C19 gene polymorphism with clopidogrel resistance and post-PCI prognosis].	clopidogrel	72-83	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	41-48
21302482-1	2010	OBJECTIVE: To study the relationships of blood stasis syndrome (BSS), CYP2C19 gene polymorphism with clopidogrel resistance (CR) and post-PCI prognosis.	clopidogrel	101-112	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	70-77
20708365-2	2010	BACKGROUND: CYP2C19*2 polymorphism is associated with reduced clopidogrel metabolism and a worse prognosis after percutaneous coronary intervention.	clopidogrel	62-73	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
20708365-10	2010	After a second clopidogrel LD, the VASP index was significantly decreased in these patients (69.7 +- 10.1% vs. 50.6 +- 17.6%; p &lt; 0.0001).	clopidogrel	15-26	vasodilator stimulated phosphoprotein	Homo sapiens	35-39
20708365-12	2010	CONCLUSIONS: Increased and tailored clopidogrel loading dose according to platelet reactivity monitoring overcome HTPR in carriers of the loss-of-function CYP2C19*2 polymorphism.	clopidogrel	36-47	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	155-162
19712984-7	2010	The mean VASP index was 53.7 +- 16.2% after the first LD of clopidogrel.	clopidogrel	60-71	vasodilator stimulated phosphoprotein	Homo sapiens	9-13
21048683-1	2010	Controversy currently surrounds the issue of proton pump inhibitor (PPI)-clopidogrel co-therapy.	clopidogrel	73-84	ATPase H+/K+ transporting subunit alpha	Homo sapiens	45-56
19712984-9	2010	Using up to 3 additional 600 mg LD of clopidogrel we were able to obtain a VASP &lt;50% in all these patients.	clopidogrel	38-49	vasodilator stimulated phosphoprotein	Homo sapiens	75-79
19712984-10	2010	The present study is the first to suggest that in homozygotes for CYP 2C19 2* loss of function polymorphism, increased loading dose of 55 clopidogrel is efficient to obtain an optimal level PR inhibition in patients undergoing PCI.	clopidogrel	138-149	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	66-74
21095272-1	2010	BACKGROUND: Smoking induces CYP1A2, thereby enhancing clopidogrel conversion to its active metabolite.	clopidogrel	54-65	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	28-34
21138823-7	2010	The advantages of ticagrelor over clopidogrel are a more rapid onset of action, offset, and reversibility at the platelet P2Y12 receptor site.	clopidogrel	34-45	purinergic receptor P2Y12	Homo sapiens	122-127
20977463-1	2010	BACKGROUND AND PURPOSE: After conversion to their active forms by the liver, ticlopidine and clopidogrel exert antiplatelet effects through irreversible inhibition of the P2Y12 receptor.	clopidogrel	93-104	purinergic receptor P2Y12	Homo sapiens	171-176
20977463-8	2010	Accordingly, these compounds showed a mixed-type inhibition of recombinant human NTPDase1 with an apparent K(i) (K(i,app) ) of 10 microM (clopidogrel) and 14 microM (ticlopidine).	clopidogrel	138-149	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	81-89
21163112-12	2010	CONCLUSION: Our study indicated that both CYP2C19 polymorphism and smoking independently affected response to clopidogrel.	clopidogrel	110-121	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	42-49
20839914-4	2010	AREAS COVERED IN THIS REVIEW: This review compares the metabolism of clopidogrel and prasugrel by carboxylesterases and the CYP system with emphasis on the formation of their respective active metabolites.	clopidogrel	69-80	peptidylprolyl isomerase G	Homo sapiens	124-127
21091895-1	2010	A proton pump inhibitor (PPI) is often co-prescribed with clopidogrel to reduce the gastrointestinal risk of bleeding ulcers in patients following acute coronary syndrome or a stent implant.	clopidogrel	58-69	ATPase H+/K+ transporting subunit alpha	Homo sapiens	2-13
21163112-0	2010	Impact of CYP2C19 polymorphism and smoking on response to clopidogrel in patients with stable coronary artery disease.	clopidogrel	58-69	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-17
21163112-2	2010	The present study was conducted to examine whether the CYP2C19 681G &gt; A polymorphism and cigarette smoking had independent or interactive effect on response to clopidogrel.	clopidogrel	163-174	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	55-62
20978260-0	2010	Reduced-function CYP2C19 genotype and risk of adverse clinical outcomes among patients treated with clopidogrel predominantly for PCI: a meta-analysis.	clopidogrel	100-111	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-24
21068524-4	2010	The current standard-of-care oral antiplatelet therapy for ACS is aspirin in combination with a P2Y12 adenosine diphosphate (ADP) receptor antagonist, most commonly clopidogrel.	clopidogrel	165-176	purinergic receptor P2Y12	Homo sapiens	96-101
21068525-7	2010	The present article reviews data on the clinical impact of enhanced P2Y12 inhibition with either higher clopidogrel dosing or new oral antiplatelet agents, including prasugrel and ticagrelor, in the setting of STEMI, focusing on results in the setting of primary PCI.	clopidogrel	104-115	purinergic receptor P2Y12	Homo sapiens	68-73
20978260-3	2010	OBJECTIVE: To define the risk of major adverse cardiovascular outcomes among carriers of 1 (  26% prevalence in whites) and carriers of 2 (  2% prevalence in whites) reduced-function CYP2C19 genetic variants in patients treated with clopidogrel.	clopidogrel	233-244	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	183-190
20978260-6	2010	DATA EXTRACTION: Investigators from 9 studies evaluating CYP2C19 genotype and clinical outcomes in patients treated with clopidogrel contributed the relevant hazard ratios (HRs) and 95% confidence intervals (CIs) for specific cardiovascular outcomes by genotype.	clopidogrel	121-132	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	57-64
20930120-3	2010	P2ry12(+/-) mouse platelets showed partially decreased responses to ADP, resembling those in clopidogrel-treated human platelets.	clopidogrel	93-104	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	0-6
20951320-3	2010	METHODS: Aspirin and clopidogrel response was measured with the VerifyNow system aspirin and P2Y12 assays.	clopidogrel	21-32	purinergic receptor P2Y12	Homo sapiens	93-98
20978260-11	2010	CONCLUSION: Among patients treated with clopidogrel for percutaneous coronary intervention, carriage of even 1 reduced-function CYP2C19 allele appears to be associated with a significantly increased risk of major adverse cardiovascular events, particularly stent thrombosis.	clopidogrel	40-51	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	128-135
20979470-0	2010	Effects of CYP2C19 genotype on outcomes of clopidogrel treatment.	clopidogrel	43-54	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	11-18
20979470-1	2010	BACKGROUND: It has been suggested that clopidogrel may be less effective in reducing the rate of cardiovascular events among persons who are carriers of loss-of-function CYP2C19 alleles that are associated with reduced conversion of clopidogrel to its active metabolite.	clopidogrel	39-50	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	170-177
20979470-1	2010	BACKGROUND: It has been suggested that clopidogrel may be less effective in reducing the rate of cardiovascular events among persons who are carriers of loss-of-function CYP2C19 alleles that are associated with reduced conversion of clopidogrel to its active metabolite.	clopidogrel	233-244	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	170-177
20801498-2	2010	CYP2C19 and ABCB1 genotypes are known to influence the effects of clopidogrel.	clopidogrel	66-77	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
21057581-7	2010	A delayed onset of action due to two-step conversion to the active metabolite, irreversible binding to P2Y12 receptors, and broad interindividual variability in levels of platelet response are the main limitations of clopidogrel.	clopidogrel	217-228	purinergic receptor P2Y12	Homo sapiens	103-108
20691446-7	2010	RESULTS: In patients undergoing elective CAG (without ad hoc percutaneous coronary intervention (PCI) and without clopidogrel pretreatment) a significant association was found between bleeding risk and variations in the gene coding for COX-1 (-842A&gt;G and 50C&gt;T) (both p=0.013).	clopidogrel	114-125	prostaglandin-endoperoxide synthase 1	Homo sapiens	236-241
20828266-4	2010	Clopidogrel resistance is multifactorial, but genetic polymorphisms in clopidogrel"s metabolic activation (e.g., cytochrome P450 2C19) and drug-drug interactions at this level (e.g., between proton pump inhibitors (PPIs) and clopidogrel) are both associated with decreased clopidogrel efficacy.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	113-133
20828266-4	2010	Clopidogrel resistance is multifactorial, but genetic polymorphisms in clopidogrel"s metabolic activation (e.g., cytochrome P450 2C19) and drug-drug interactions at this level (e.g., between proton pump inhibitors (PPIs) and clopidogrel) are both associated with decreased clopidogrel efficacy.	clopidogrel	71-82	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	113-133
20801494-0	2010	Genetic variants in ABCB1 and CYP2C19 and cardiovascular outcomes after treatment with clopidogrel and prasugrel in the TRITON-TIMI 38 trial: a pharmacogenetic analysis.	clopidogrel	87-98	ATP binding cassette subfamily B member 1	Homo sapiens	20-25
20801494-0	2010	Genetic variants in ABCB1 and CYP2C19 and cardiovascular outcomes after treatment with clopidogrel and prasugrel in the TRITON-TIMI 38 trial: a pharmacogenetic analysis.	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
20801494-1	2010	BACKGROUND: Clopidogrel and prasugrel are subject to efflux via P-glycoprotein (encoded by ABCB1, also known as MDR1).	clopidogrel	12-23	ATP binding cassette subfamily B member 1	Homo sapiens	64-78
20801494-1	2010	BACKGROUND: Clopidogrel and prasugrel are subject to efflux via P-glycoprotein (encoded by ABCB1, also known as MDR1).	clopidogrel	12-23	ATP binding cassette subfamily B member 1	Homo sapiens	91-96
20801494-1	2010	BACKGROUND: Clopidogrel and prasugrel are subject to efflux via P-glycoprotein (encoded by ABCB1, also known as MDR1).	clopidogrel	12-23	ATP binding cassette subfamily B member 1	Homo sapiens	112-116
20801494-5	2010	METHODS: We genotyped ABCB1 in 2932 patients with acute coronary syndromes undergoing percutaneous intervention who were treated with clopidogrel (n=1471) or prasugrel (n=1461) in the TRITON-TIMI 38 trial.	clopidogrel	134-145	ATP binding cassette subfamily B member 1	Homo sapiens	22-27
20801494-9	2010	FINDINGS: In patients treated with clopidogrel, ABCB1 3435C T genotype was significantly associated with the risk of cardiovascular death, myocardial infarction, or stroke (p=0 0064).	clopidogrel	35-46	ATP binding cassette subfamily B member 1	Homo sapiens	48-53
20801494-14	2010	INTERPRETATION: Individuals with the ABCB1 3435 TT genotype have reduced platelet inhibition and are at increased risk of recurrent ischaemic events during clopidogrel treatment.	clopidogrel	156-167	ATP binding cassette subfamily B member 1	Homo sapiens	37-42
20823393-1	2010	BACKGROUND: Among patients treated with clopidogrel, carriers of the cytochrome P450 (CYP) 2C19 loss-of-function allele have shown increased platelet reactivity and higher rates of ischemic events.	clopidogrel	40-51	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	69-95
20942779-8	2010	Numerous clinical studies have shown the influence of CYP2C19 polymorphism on clopidogrel antiplatelet activity.	clopidogrel	78-89	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	54-61
20942779-10	2010	Several studies have also demonstrated that CYP3A4/5 and CYP1A2 are important in clopidogrel bioactivation and should also be considered as potential targets for unwanted drug-drug interactions.	clopidogrel	81-92	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	44-50
20942779-10	2010	Several studies have also demonstrated that CYP3A4/5 and CYP1A2 are important in clopidogrel bioactivation and should also be considered as potential targets for unwanted drug-drug interactions.	clopidogrel	81-92	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	57-63
20965456-0	2010	Pilot study of the antiplatelet effect of increased clopidogrel maintenance dosing and its relationship to CYP2C19 genotype in patients with high on-treatment reactivity.	clopidogrel	52-63	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	107-114
20624109-0	2010	High-dose fibrinogen concentrate for haemostatic therapy of a major trauma patient with recent clopidogrel and aspirin intake.	clopidogrel	95-106	fibrinogen beta chain	Homo sapiens	10-20
20801498-2	2010	CYP2C19 and ABCB1 genotypes are known to influence the effects of clopidogrel.	clopidogrel	66-77	ATP binding cassette subfamily B member 1	Homo sapiens	12-17
20801498-8	2010	For the ABCB1 genotype, event rates for the primary outcome were also consistently lower in the ticagrelor than in the clopidogrel group for all genotype groups (interaction p=0 39; 8 8%vs 11 9%; 0 71, 0 55-0 92 for the high-expression genotype).	clopidogrel	119-130	ATP binding cassette subfamily B member 1	Homo sapiens	8-13
20801498-9	2010	In the clopidogrel group, the event rate at 30 days was higher in patients with than in those without any loss-of-function CYP2C19 alleles (5 7%vs 3 8%, p=0 028), leading to earlier separation of event rates between treatment groups in patients with loss-of-function alleles.	clopidogrel	7-18	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	123-130
20801498-10	2010	Patients on clopidogrel who had any gain-of-function CYP2C19 allele had a higher frequency of major bleeding (11 9%) than did those without any gain-of-function or loss-of-function alleles (9 5%; p=0 022), but interaction between treatment and genotype groups was not significant for any type of major bleeding.	clopidogrel	12-23	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-60
20451958-9	2010	These results may partially explain the recent observations that smokers derive greater clinical benefit from the P2Y12 antagonist clopidogrel than do non-smokers.	clopidogrel	131-142	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	114-119
20826260-0	2010	Protective effect of the CYP2C19 *17 polymorphism with increased activation of clopidogrel on cardiovascular events.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
21265493-0	2010	Proton pump inhibitors in patients treated with aspirin and clopidogrel after acute coronary syndrome.	clopidogrel	60-71	ATPase H+/K+ transporting non-gastric alpha2 subunit	Homo sapiens	0-11
21265493-2	2010	Numerous drugs are known to inhibit P-450 isoenzymes, including proton pump inhibitors (PPIs), which are often associated with aspirin and clopidogrel to prevent adverse gastrointestinal effects.	clopidogrel	139-150	ATPase H+/K+ transporting non-gastric alpha2 subunit	Homo sapiens	64-75
21268429-3	2010	Clopidogrel is a pro-drug which needs to be metabolized into its active metabolite, by cytochrome P450, especially by CYP2C19 isoenzyme.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	118-125
21268429-4	2010	Various PPIs can inhibit CYP2C19, which could possibly decrease clopidogrel bioactivation process and, therefore, its antiplatelet effect.	clopidogrel	64-75	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
20877456-7	2010	Testing for CYP2C19 polymorphisms may identify patients who will not respond adequately to the standard clopidogrel regimen and who should, consequently, be given an alternate treatment strategy.	clopidogrel	104-115	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
20716239-0	2010	Influences of different proton pump inhibitors on the anti-platelet function of clopidogrel in relation to CYP2C19 genotypes.	clopidogrel	80-91	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	107-114
20716239-1	2010	WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: Active metabolism of clopidogrel is mainly mediated by CYP2C19.	clopidogrel	63-74	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	97-104
20716239-3	2010	Therefore, active metabolism of clopidogrel is affected by CYP2C19 genotypes.	clopidogrel	32-43	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	59-66
20716239-8	2010	WHAT THIS STUDY ADDS: Whether a PPI attenuates the efficacy of clopidogrel depends on CYP2C19.	clopidogrel	63-74	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	86-93
20716239-9	2010	Individuals who are decreased metabolizers, i.e. carriers the allele of CYP2C19*2 and/or *3, are more likely to convert from "responder" to "non-responder" to clopidogrel when placed on a concomitant PPI.	clopidogrel	159-170	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	72-79
20716239-10	2010	We found that rabeprazole, whose affinity to CYP2C19 has been considered lower, attenuated the efficacy of clopidogrel.	clopidogrel	107-118	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	45-52
20716239-13	2010	AIMS: The efficacy of clopidogrel is influenced by CYP2C19 genotypes and substrates of CYP2C19, such as proton pump inhibitors (PPIs).	clopidogrel	22-33	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	51-58
20716239-13	2010	AIMS: The efficacy of clopidogrel is influenced by CYP2C19 genotypes and substrates of CYP2C19, such as proton pump inhibitors (PPIs).	clopidogrel	22-33	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	87-94
20735423-1	2010	BACKGROUND AND PURPOSE: The conversion of clopidogrel to its active metabolite, R-130964, is a two-step cytochrome P450 (CYP)-dependent process.	clopidogrel	42-53	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	104-119
20735423-1	2010	BACKGROUND AND PURPOSE: The conversion of clopidogrel to its active metabolite, R-130964, is a two-step cytochrome P450 (CYP)-dependent process.	clopidogrel	42-53	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	121-124
20735423-2	2010	The current investigations were performed to characterize in vitro the effects of different CYP inhibitors on the biotransformation and on the antiplatelet effect of clopidogrel.	clopidogrel	166-177	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	92-95
20735423-4	2010	KEY RESULTS: Experiments using HLM or specific CYPs (3A4, 2C19) revealed that at clopidogrel concentrations &gt;10 microM, CYP3A4 was primarily responsible for clopidogrel biotransformation.	clopidogrel	81-92	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	123-129
20735423-4	2010	KEY RESULTS: Experiments using HLM or specific CYPs (3A4, 2C19) revealed that at clopidogrel concentrations &gt;10 microM, CYP3A4 was primarily responsible for clopidogrel biotransformation.	clopidogrel	160-171	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	123-129
20735423-6	2010	Clarithromycin, another CYP3A4 inhibitor, impaired clopidogrel biotransformation and antiplatelet activity almost as effectively as ketoconazole.	clopidogrel	51-62	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	24-30
20735423-7	2010	The CYP3A4 substrates atorvastatin and simvastatin both inhibited clopidogrel biotransformation and antiplatelet activity, less potently than ketoconazole.	clopidogrel	66-77	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	4-10
20735423-9	2010	As clopidogrel itself inhibited CYP2C19 at concentrations &gt;10 microM, the CYP2C19 inhibitor lansozprazole affected clopidogrel biotransformation only at clopidogrel concentrations &lt; or =10 microM.	clopidogrel	3-14	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
20735423-9	2010	As clopidogrel itself inhibited CYP2C19 at concentrations &gt;10 microM, the CYP2C19 inhibitor lansozprazole affected clopidogrel biotransformation only at clopidogrel concentrations &lt; or =10 microM.	clopidogrel	118-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	77-84
20735423-9	2010	As clopidogrel itself inhibited CYP2C19 at concentrations &gt;10 microM, the CYP2C19 inhibitor lansozprazole affected clopidogrel biotransformation only at clopidogrel concentrations &lt; or =10 microM.	clopidogrel	118-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	77-84
20735423-11	2010	CONCLUSIONS AND IMPLICATIONS: At clopidogrel concentrations &gt;10 microM, CYP3A4 is mainly responsible for clopidogrel biotransformation, whereas CYP2C19 contributes only at clopidogrel concentrations &lt; or =10 microM.	clopidogrel	33-44	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	75-81
20735423-11	2010	CONCLUSIONS AND IMPLICATIONS: At clopidogrel concentrations &gt;10 microM, CYP3A4 is mainly responsible for clopidogrel biotransformation, whereas CYP2C19 contributes only at clopidogrel concentrations &lt; or =10 microM.	clopidogrel	108-119	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	75-81
20735423-11	2010	CONCLUSIONS AND IMPLICATIONS: At clopidogrel concentrations &gt;10 microM, CYP3A4 is mainly responsible for clopidogrel biotransformation, whereas CYP2C19 contributes only at clopidogrel concentrations &lt; or =10 microM.	clopidogrel	108-119	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	75-81
20735423-12	2010	CYP2C19 inhibition by clopidogrel at concentrations &gt;10 microM may explain the conflicting results between in vitro and in vivo investigations regarding drug interactions with clopidogrel.	clopidogrel	22-33	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
20735423-12	2010	CYP2C19 inhibition by clopidogrel at concentrations &gt;10 microM may explain the conflicting results between in vitro and in vivo investigations regarding drug interactions with clopidogrel.	clopidogrel	179-190	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
20716239-19	2010	RESULTS: In rapid metabolizers (RMs, *1/*1, n=15) of CYP2C19, omeprazole and rabeprazole significantly attenuated the anti-platelet function of clopidogrel.	clopidogrel	144-155	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-60
20826260-5	2010	RESULTS: Carriers of the CYP2C19*17 T-allele, with increased clopidogrel activation, had a 37% relative reduction in the TLR incidence, the primary end point (14.0% vs 22.3%, P = .002), and a 22% relative reduction of the secondary end point MACE (22.0% vs 28.1%, P = .04) compared with noncarriers, respectively.	clopidogrel	61-72	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
20826260-8	2010	CONCLUSIONS: Based on the genetic analysis in a high-risk population of acute MI patients with interventional treatment and continuous clopidogrel therapy, our study found a protective effect for carriers of an increased-function CYP2C19*17 T-allele with significantly lower rates of TLR and MACE.	clopidogrel	135-146	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	230-237
20664903-2	2010	Drug-drug interaction between statins metabolised by cytochrome P450 3A4 and clopidogrel have been claimed to attenuate the inhibitory effect of clopidogrel.	clopidogrel	145-156	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	53-72
20664906-1	2010	We previously showed that variability of response to clopidogrel is linked to occupancy of the P2Y12 receptor by clopidogrel active-metabolite, and that maximal platelet aggregation intensity (MAI) measured by light transmission aggregometry (LTA) correlates with occupancy.	clopidogrel	53-64	purinergic receptor P2Y12	Homo sapiens	95-100
20664906-1	2010	We previously showed that variability of response to clopidogrel is linked to occupancy of the P2Y12 receptor by clopidogrel active-metabolite, and that maximal platelet aggregation intensity (MAI) measured by light transmission aggregometry (LTA) correlates with occupancy.	clopidogrel	113-124	purinergic receptor P2Y12	Homo sapiens	95-100
20664906-9	2010	Sensitivity of the VerifyNow P2Y12 assay decreased at higher clopidogrel responses.	clopidogrel	61-72	purinergic receptor P2Y12	Homo sapiens	29-34
20664906-11	2010	In conclusion, LTA data correlate best with P2Y12 occupancy, the gold standard for detecting clopidogrel"s effect at the receptor level.	clopidogrel	93-104	purinergic receptor P2Y12	Homo sapiens	44-49
20492467-5	2010	Individuals with a CYP2C19 reduced-metabolizer genotype were estimated to have a substantial reduction in the risk of the composite primary outcome (cardiovascular death, myocardial infarction, or stroke) with prasugrel as compared with clopidogrel [relative risk (RR) 0.57; 95% confidence interval (CI) 0.39-0.83].	clopidogrel	237-248	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	19-26
20230539-1	2010	Our group has shown that platelet inhibition with clopidogrel, an antagonist of the P2Y12 adenosine diphosphate receptor on platelets, reduced the formation of transplant arteriosclerosis.	clopidogrel	50-61	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	84-89
20651323-8	2010	Several polymorphic CYP enzymes are involved in the activation of clopidogrel, and genetic polymorphisms may affect the activity of these enzymes.	clopidogrel	66-77	peptidylprolyl isomerase G	Homo sapiens	20-23
20651323-9	2010	Genetic variants, particularly the presence of the CYP2C19*2 allele, are associated with poor clinical outcomes after stent placement, along with increased ischemic events in clopidogrel-treated patients.	clopidogrel	175-186	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	51-58
20608754-12	2010	There is a possibility that PPIs may elicit detrimental effects by inhibiting CYP2C19-dominated metabolism of clopidogrel to its active metabolite.	clopidogrel	110-121	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	78-85
20659222-3	2010	Conflicting evidence exists as to the existence of an adverse interaction between clopidogrel and proton pump.	clopidogrel	82-93	ATPase H+/K+ transporting subunit alpha	Homo sapiens	98-109
20659222-4	2010	This review examines the original studies, which suggested the adverse interaction, the subsequent and most recent studies, the pharmaco-dynamics of the two drugs and suggests an algorithm for the use of clopidogrel with proton pump inhibitors.	clopidogrel	204-215	ATPase H+/K+ transporting subunit alpha	Homo sapiens	221-232
20492465-0	2010	Potentiation of clopidogrel active metabolite formation by rifampicin leads to greater P2Y12 receptor blockade and inhibition of platelet aggregation after clopidogrel.	clopidogrel	16-27	purinergic receptor P2Y12	Homo sapiens	87-92
20492467-2	2010	Analysis of a subset of the TRITON-TIMI 38 trial demonstrated that cytochrome P450 2C19 (CYP2C19) reduced-function genotypes are associated with differential clinical responses to clopidogrel, but not prasugrel.	clopidogrel	180-191	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	67-87
20471192-2	2010	Independently, in post hoc analyses, CYP2C19*2 has been associated with worse clinical outcomes during clopidogrel therapy.	clopidogrel	103-114	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-44
20620727-0	2010	Cardiovascular risk in clopidogrel-treated patients according to cytochrome P450 2C19*2 loss-of-function allele or proton pump inhibitor coadministration: a systematic meta-analysis.	clopidogrel	23-34	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	65-85
20620727-1	2010	OBJECTIVES: The aim of this study was to assess the association between the loss-of-function cytochrome P450 2C19 (CYP2C19)*2 variant (10 studies, 11,959 patients) or the use of proton pump inhibitors (PPIs) (13 studies, 48,674 patients) and ischemic outcomes (major adverse cardiovascular events [MACE]) in patients treated with clopidogrel.	clopidogrel	330-341	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	93-113
20620727-1	2010	OBJECTIVES: The aim of this study was to assess the association between the loss-of-function cytochrome P450 2C19 (CYP2C19)*2 variant (10 studies, 11,959 patients) or the use of proton pump inhibitors (PPIs) (13 studies, 48,674 patients) and ischemic outcomes (major adverse cardiovascular events [MACE]) in patients treated with clopidogrel.	clopidogrel	330-341	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	115-122
20620727-2	2010	BACKGROUND: In clopidogrel-treated patients, increased cardiovascular risk has been identified with the loss-of-function CYP2C19*2 allele or the use of PPIs, some of them CYP2C19 inhibitors.	clopidogrel	15-26	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	121-128
20620727-2	2010	BACKGROUND: In clopidogrel-treated patients, increased cardiovascular risk has been identified with the loss-of-function CYP2C19*2 allele or the use of PPIs, some of them CYP2C19 inhibitors.	clopidogrel	15-26	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	171-178
20620727-11	2010	CONCLUSIONS: In this global meta-analysis, reduced CYP2C19 function appears to expose clopidogrel-treated patients to excess cardiovascular risk and mortality.	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	51-58
20598967-1	2010	Practice guidelines recommend dual antiplatelet therapy with aspirin and clopidogrel for patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS) regardless of in-hospital management strategy.	clopidogrel	73-84	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	159-162
20598974-3	2010	Furthermore, the irreversible binding of clopidogrel to the P2Y(12) receptor for the life span of the platelet is associated with increased bleeding risk especially during urgent or emergency surgery.	clopidogrel	41-52	purinergic receptor P2Y12	Homo sapiens	60-67
20492467-2	2010	Analysis of a subset of the TRITON-TIMI 38 trial demonstrated that cytochrome P450 2C19 (CYP2C19) reduced-function genotypes are associated with differential clinical responses to clopidogrel, but not prasugrel.	clopidogrel	180-191	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	89-96
20492467-7	2010	CONCLUSIONS: Integration of the TRITON-TIMI 38 data suggests that the CYP2C19 genotype can discriminate between individuals who receive extensive benefit from using prasugrel instead of clopidogrel, and individuals with comparable clinical outcomes with prasugrel and clopidorel.	clopidogrel	186-197	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	70-77
20492469-0	2010	Isolated and interactive impact of common CYP2C19 genetic variants on the antiplatelet effect of chronic clopidogrel therapy.	clopidogrel	105-116	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	42-49
20597033-5	2010	Clopidogrel, an irreversible P2Y12 antagonist, has a delayed onset of action and high inter-individual variability.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	29-34
20597033-6	2010	Limitations of clopidogrel have necessitated the discovery of novel P2Y12 antagonists with superior pharmacological profiles.	clopidogrel	15-26	purinergic receptor P2Y12	Homo sapiens	68-73
20650435-15	2010	CONCLUSIONS: Among PCI-treated patients receiving high-MD clopidogrel, carriage of CYP2C19 variant relates to increased PR and predicts risk of HPPR.	clopidogrel	58-69	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	83-90
20377472-2	2010	Recently, there have been reports of a clinically significant drug interaction between clopidogrel and proton pump inhibitors (PPI), which are frequently co-prescribed to prevent DAT associated gastrointestinal (GI) bleeding.	clopidogrel	87-98	ATPase H+/K+ transporting subunit alpha	Homo sapiens	103-114
27263451-6	2010	In both groups, clopidogrel significantly reduced aggregation and expression of fibrinogen, but it elevated nitrite levels.	clopidogrel	16-27	fibrinogen beta chain	Homo sapiens	80-90
20979877-10	2010	Average CK, CK-MB, CTnI were significantly higher in duration of clopidogrel use &gt; or =1 years group than that in duration of clopidogrel use &lt;1 year group (P &lt; 0.0001).	clopidogrel	65-76	troponin I3, cardiac type	Homo sapiens	19-23
20538118-1	2010	Recent studies have suggested that proton pump inhibitors (PPIs) might reduce the inhibitory effect of clopidogrel on platelet aggregation, possibly through inhibition of the hepatic cytochrome P450 2C19 (CYP2C19) isoenzyme.	clopidogrel	103-114	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	183-203
20538118-1	2010	Recent studies have suggested that proton pump inhibitors (PPIs) might reduce the inhibitory effect of clopidogrel on platelet aggregation, possibly through inhibition of the hepatic cytochrome P450 2C19 (CYP2C19) isoenzyme.	clopidogrel	103-114	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	205-212
27263451-1	2010	OBJECTIVE: We aimed to detect novel in vitro effects of clopidogrel on platelets by assessment of the following parameters: malondialdehyde, glutathione, nitrite, aggregation response, and expressions of P-selectin, fibrinogen, apolipoprotein A1, apolipoprotein B, and phosphatidylserine.	clopidogrel	56-67	selectin P	Homo sapiens	204-214
27263451-1	2010	OBJECTIVE: We aimed to detect novel in vitro effects of clopidogrel on platelets by assessment of the following parameters: malondialdehyde, glutathione, nitrite, aggregation response, and expressions of P-selectin, fibrinogen, apolipoprotein A1, apolipoprotein B, and phosphatidylserine.	clopidogrel	56-67	fibrinogen beta chain	Homo sapiens	216-226
20597033-2	2010	Antiplatelet therapy includes the administration of aspirin and clopidogrel, either alone or in combination, which act through the inhibition of thromboxane A2 generation and blockade of the Gi-coupled P2Y12 purinergic receptor, respectively.	clopidogrel	64-75	purinergic receptor P2Y12	Homo sapiens	202-207
27263451-7	2010	Clopidogrel significantly decreased P-selectin and phosphatidylserine expression and malondialdehyde but increased expressions of apolipoproteins A1/B only in hyperlipidemics.	clopidogrel	0-11	selectin P	Homo sapiens	36-46
27263451-1	2010	OBJECTIVE: We aimed to detect novel in vitro effects of clopidogrel on platelets by assessment of the following parameters: malondialdehyde, glutathione, nitrite, aggregation response, and expressions of P-selectin, fibrinogen, apolipoprotein A1, apolipoprotein B, and phosphatidylserine.	clopidogrel	56-67	apolipoprotein A1	Homo sapiens	228-245
27263451-1	2010	OBJECTIVE: We aimed to detect novel in vitro effects of clopidogrel on platelets by assessment of the following parameters: malondialdehyde, glutathione, nitrite, aggregation response, and expressions of P-selectin, fibrinogen, apolipoprotein A1, apolipoprotein B, and phosphatidylserine.	clopidogrel	56-67	apolipoprotein B	Homo sapiens	247-263
27263451-7	2010	Clopidogrel significantly decreased P-selectin and phosphatidylserine expression and malondialdehyde but increased expressions of apolipoproteins A1/B only in hyperlipidemics.	clopidogrel	0-11	apolipoprotein A1	Homo sapiens	130-150
20200314-5	2010	A mimetic of active clopidogrel metabolite (AR-C69931 MX) reduced TF synthesis by 56 +/- 10%, an aspirin-like inhibitor (indomethacin) by 82 +/- 9%, and the combination by 96 +/- 2%, indicating that ADP release and thromboxane A(2) production followed by activation of P2Y12 and thromboxane receptors mediate surface-induced TF synthesis.	clopidogrel	20-31	purinergic receptor P2Y12	Homo sapiens	269-274
20200314-5	2010	A mimetic of active clopidogrel metabolite (AR-C69931 MX) reduced TF synthesis by 56 +/- 10%, an aspirin-like inhibitor (indomethacin) by 82 +/- 9%, and the combination by 96 +/- 2%, indicating that ADP release and thromboxane A(2) production followed by activation of P2Y12 and thromboxane receptors mediate surface-induced TF synthesis.	clopidogrel	20-31	coagulation factor III, tissue factor	Homo sapiens	325-327
20510210-1	2010	OBJECTIVES: The aim of this study was to evaluate the relative impact of demographic and clinical variables versus the cytochrome P450 2C19 (CYP2C19) polymorphism on antiplatelet effects of clopidogrel.	clopidogrel	190-201	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	119-139
20510210-1	2010	OBJECTIVES: The aim of this study was to evaluate the relative impact of demographic and clinical variables versus the cytochrome P450 2C19 (CYP2C19) polymorphism on antiplatelet effects of clopidogrel.	clopidogrel	190-201	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	141-148
20510210-3	2010	Several demographic and clinical characteristics as well as a polymorphism of CYP2C19 have been described as predictors for a low response to clopidogrel.	clopidogrel	142-153	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	78-85
20510210-8	2010	The classification and regression trees analysis demonstrated that CYP2C19*2 carrier status followed by diabetes mellitus was the best discriminator between a sufficient and an insufficient antiplatelet response to clopidogrel.	clopidogrel	215-226	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	67-74
20351565-8	2010	In contrast, clopidogrel- or atorvastatin-treated rabbits showed a significant reduction in progression of atherosclerosis, including a low expression of high sensitivity C-reactive protein and platelet-derived growth factor, a reduced intima thickness, and reduced ratio of bcl-2/bax in the vascular wall.	clopidogrel	13-24	C-reactive protein	Oryctolagus cuniculus	171-189
20345494-1	2010	Proton pump inhibitors are often prescribed for patients on clopidogrel to prevent gastrointestinal bleeding complications.	clopidogrel	60-71	ATPase H+/K+ transporting subunit alpha	Homo sapiens	0-11
20351565-8	2010	In contrast, clopidogrel- or atorvastatin-treated rabbits showed a significant reduction in progression of atherosclerosis, including a low expression of high sensitivity C-reactive protein and platelet-derived growth factor, a reduced intima thickness, and reduced ratio of bcl-2/bax in the vascular wall.	clopidogrel	13-24	BCL-2	Oryctolagus cuniculus	275-280
20351565-8	2010	In contrast, clopidogrel- or atorvastatin-treated rabbits showed a significant reduction in progression of atherosclerosis, including a low expression of high sensitivity C-reactive protein and platelet-derived growth factor, a reduced intima thickness, and reduced ratio of bcl-2/bax in the vascular wall.	clopidogrel	13-24	apoptosis regulator BAX	Oryctolagus cuniculus	281-284
19636246-5	2010	Polymorphisms in the hepatic enzymes involved in the metabolism of clopidogrel (e.g., CYP 1A2, CYP3A4, CYP2C19) or within the platelet membrane receptor (P2Y12) and/or polymorphism of platelet integrin alphaIIbbeta3 or integrin alpha2beta1 may affect platelet responses and could influence response to clopidogrel administration.	clopidogrel	67-78	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	86-93
20345494-3	2010	Both drugs are metabolized by similar pathways of the cytochrome P450 system, so proton pump inhibitors may inhibit the metabolism of clopidogrel to its active metabolite.	clopidogrel	134-145	ATPase H+/K+ transporting subunit alpha	Homo sapiens	81-92
20630458-0	2010	Impact of P2Y12 inhibition by clopidogrel on cardiovascular mortality in unselected patients treated by percutaneous coronary angioplasty: a prospective registry.	clopidogrel	30-41	purinergic receptor P2Y12	Homo sapiens	10-15
20630458-12	2010	CONCLUSIONS: In patients undergoing PCI, LR to clopidogrel assessed by VASP-FCT is an independent predictor of cardiovascular death at the PRI cutoff value of &gt; or =61%.	clopidogrel	47-58	vasodilator stimulated phosphoprotein	Homo sapiens	71-75
20200314-5	2010	A mimetic of active clopidogrel metabolite (AR-C69931 MX) reduced TF synthesis by 56 +/- 10%, an aspirin-like inhibitor (indomethacin) by 82 +/- 9%, and the combination by 96 +/- 2%, indicating that ADP release and thromboxane A(2) production followed by activation of P2Y12 and thromboxane receptors mediate surface-induced TF synthesis.	clopidogrel	20-31	coagulation factor III, tissue factor	Homo sapiens	66-68
20431852-1	2010	The thienopyridine P2Y12 receptor antagonists clopidogrel and prasugrel prevent arterial thrombosis and are routinely used following percutaneous coronary intervention.	clopidogrel	46-57	purinergic receptor P2Y12	Homo sapiens	19-24
20562062-3	2010	However, there are warnings against combining PPIs with clopidogrel because of their interactions with cytochrome P450 isoenzyme 2C19 (CYP2C19).	clopidogrel	56-67	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	103-133
20562062-3	2010	However, there are warnings against combining PPIs with clopidogrel because of their interactions with cytochrome P450 isoenzyme 2C19 (CYP2C19).	clopidogrel	56-67	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	135-142
19943165-0	2010	Clopidogrel affects leukocyte dependent platelet aggregation by P2Y12 expressing leukocytes.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	64-69
20349052-1	2010	BACKGROUNDS/AIMS: Clopidogrel, a platelet inhibitor, is metabolized by cytochrome P450 2C19 (CYP2C19) to its active metabolite and, consequently, its anti-platelet efficacy is influenced by CYP2C19 activity.	clopidogrel	18-29	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-91
20349052-1	2010	BACKGROUNDS/AIMS: Clopidogrel, a platelet inhibitor, is metabolized by cytochrome P450 2C19 (CYP2C19) to its active metabolite and, consequently, its anti-platelet efficacy is influenced by CYP2C19 activity.	clopidogrel	18-29	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	93-100
20349052-1	2010	BACKGROUNDS/AIMS: Clopidogrel, a platelet inhibitor, is metabolized by cytochrome P450 2C19 (CYP2C19) to its active metabolite and, consequently, its anti-platelet efficacy is influenced by CYP2C19 activity.	clopidogrel	18-29	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	190-197
20349052-2	2010	The aim of this study was to determine whether the [(13)C]pantoprazole breath test, a recently developed tool used to measure CYP2C19 activity, can predict the anti-platelet efficacy of clopidogrel.	clopidogrel	186-197	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	126-133
20462345-5	2010	The platelet inhibitor clopidogrel requires activation by the CYP2C19 enzyme.	clopidogrel	23-34	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	62-69
20435227-13	2010	The patient had a heterozygous null mutation in CYP2C19 suggesting probable clopidogrel resistance, several variants associated with a positive response to lipid-lowering therapy, and variants in CYP4F2 and VKORC1 that suggest he might have a low initial dosing requirement for warfarin.	clopidogrel	76-87	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	48-55
20560445-4	2010	A lymphocyte stimulation test (DLST) with clopidogrel was positive, and bronchoalveolar lavage fluid showed an increase in lymphocytes and a decrease in the CD4+/CD8+ ratio.	clopidogrel	42-53	dihydrolipoamide S-succinyltransferase	Homo sapiens	31-35
20352154-3	2010	However, some CCBs also have strong inhibitory effects on the drug transporter P-glycoprotein (Pgp), which mediates clopidogrel"s intestinal absorption.	clopidogrel	116-127	ATP binding cassette subfamily B member 1	Homo sapiens	79-93
20352154-3	2010	However, some CCBs also have strong inhibitory effects on the drug transporter P-glycoprotein (Pgp), which mediates clopidogrel"s intestinal absorption.	clopidogrel	116-127	ATP binding cassette subfamily B member 1	Homo sapiens	95-98
20352154-4	2010	It was the aim of this study to evaluate the effect of co-administration of Pgp-inhibiting and non-Pgp-inhibiting CCBs on on-clopidogrel platelet reactivity in patients on dual antiplatelet therapy undergoing elective percutaneous coronary intervention (PCI).	clopidogrel	125-136	ATP binding cassette subfamily B member 1	Homo sapiens	76-79
20352154-4	2010	It was the aim of this study to evaluate the effect of co-administration of Pgp-inhibiting and non-Pgp-inhibiting CCBs on on-clopidogrel platelet reactivity in patients on dual antiplatelet therapy undergoing elective percutaneous coronary intervention (PCI).	clopidogrel	125-136	ATP binding cassette subfamily B member 1	Homo sapiens	99-102
20352154-7	2010	Adjusted mean ADP-induced on-clopidogrel platelet reactivity was significantly higher in both users of Pgp-inhibiting CCBs and amlodipine as compared to CCB non-users (all p&lt;0.05).	clopidogrel	29-40	ATP binding cassette subfamily B member 1	Homo sapiens	103-106
20352154-9	2010	This study demonstrates that concomitant use of Pgp-inhibiting CCBs and amlodipine increases on-clopidogrel platelet reactivity.	clopidogrel	96-107	ATP binding cassette subfamily B member 1	Homo sapiens	48-51
19636246-5	2010	Polymorphisms in the hepatic enzymes involved in the metabolism of clopidogrel (e.g., CYP 1A2, CYP3A4, CYP2C19) or within the platelet membrane receptor (P2Y12) and/or polymorphism of platelet integrin alphaIIbbeta3 or integrin alpha2beta1 may affect platelet responses and could influence response to clopidogrel administration.	clopidogrel	67-78	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	95-101
19636246-5	2010	Polymorphisms in the hepatic enzymes involved in the metabolism of clopidogrel (e.g., CYP 1A2, CYP3A4, CYP2C19) or within the platelet membrane receptor (P2Y12) and/or polymorphism of platelet integrin alphaIIbbeta3 or integrin alpha2beta1 may affect platelet responses and could influence response to clopidogrel administration.	clopidogrel	67-78	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	103-110
20346323-10	2010	In conclusion, clopidogrel reduces endothelial cell sloughing and increases expression of endothelial progenitor cell phosphorylated Akt and phosphorylated adenosine monophosphate kinase in the peripheral blood of patients with type 2 diabetes mellitus.	clopidogrel	15-26	AKT serine/threonine kinase 1	Homo sapiens	133-136
19811450-1	2010	The P2Y12 receptor antagonist clopidogrel blocks platelet aggregation, improves systemic endothelial nitric oxide bioavailability, and has anti-inflammatory effects.	clopidogrel	30-41	purinergic receptor P2Y12	Rattus norvegicus	4-9
19811450-2	2010	Since P2Y12 receptors have been identified in the vasculature, we hypothesized that clopidogrel ameliorates angiotensin II (Ang II) -induced vascular functional changes by blockade of P2Y12 receptors in the vasculature.	clopidogrel	84-95	purinergic receptor P2Y12	Rattus norvegicus	6-11
19811450-2	2010	Since P2Y12 receptors have been identified in the vasculature, we hypothesized that clopidogrel ameliorates angiotensin II (Ang II) -induced vascular functional changes by blockade of P2Y12 receptors in the vasculature.	clopidogrel	84-95	angiotensinogen	Rattus norvegicus	108-122
19811450-2	2010	Since P2Y12 receptors have been identified in the vasculature, we hypothesized that clopidogrel ameliorates angiotensin II (Ang II) -induced vascular functional changes by blockade of P2Y12 receptors in the vasculature.	clopidogrel	84-95	angiotensinogen	Rattus norvegicus	124-130
19811450-2	2010	Since P2Y12 receptors have been identified in the vasculature, we hypothesized that clopidogrel ameliorates angiotensin II (Ang II) -induced vascular functional changes by blockade of P2Y12 receptors in the vasculature.	clopidogrel	84-95	purinergic receptor P2Y12	Rattus norvegicus	184-189
19888916-1	2010	Dual antiplatelet therapy with aspirin and clopidogrel, a P2Y12 antagonist, is a cornerstone for treatment of patients with stroke, peripheral arterial disease, and acute coronary artery disease followed with or without percutaneous coronary intervention.	clopidogrel	43-54	purinergic receptor P2Y12	Homo sapiens	58-63
20163283-4	2010	Clopidogrel requires conversion to active metabolite by CYP isoenzymes.	clopidogrel	0-11	peptidylprolyl isomerase G	Homo sapiens	56-59
20163283-5	2010	Recently, CYP2C19*2 polymorphism (G681A nucleotide substitution) has been shown to be associated with decreased metabolisation of clopidogrel, poor antiaggregant effect and increased adverse cardiovascular events.	clopidogrel	130-141	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-17
20163283-6	2010	AREAS COVERED IN THIS REVIEW: This review summarises the principal studies contributing to establish the relationship between CYP2C19*2 polymorphism and adverse outcomes in high risk patients on clopidogrel treatment.	clopidogrel	195-206	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	126-133
19888916-2	2010	Giachini and colleagues found that clopidogrel could normalize the increased phenylephrine-induced vascular contraction and impaired acetylcholine-induced vasodilatation in mesenteric arteries from angiotensin II-infused Sprague-Dawley rats.	clopidogrel	35-46	angiotensinogen	Rattus norvegicus	198-212
27713279-4	2010	The genetic variation in CYP2C19 activity seems to influence short- and long-term antithrombotic effects of clopidogrel to a substantial extent.	clopidogrel	108-119	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	25-32
20135061-4	2010	It was the objective of this study to assess the potential influence of alpha2A-AR and beta2-AR gene polymorphisms on platelet reactivity after dual antiplatelet therapy with aspirin and clopidogrel in ACS.	clopidogrel	187-198	adrenoceptor alpha 2A	Homo sapiens	72-82
20135061-4	2010	It was the objective of this study to assess the potential influence of alpha2A-AR and beta2-AR gene polymorphisms on platelet reactivity after dual antiplatelet therapy with aspirin and clopidogrel in ACS.	clopidogrel	187-198	adrenoceptor beta 2	Homo sapiens	87-95
27713279-5	2010	Prediction models for clopidogrel non-responsiveness that include CYP2C19 genotyping together with relevant non-genetic risk factors are needed to be verified for their potential benefit in individualization of antithrombotic therapy.	clopidogrel	22-33	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	66-73
19347265-3	2010	The study included clopidogrel, a selective inhibitor of CYP2C9 isozyme, to inhibit the metabolism of diclofenac.	clopidogrel	19-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
20235209-2	2010	Clopidogrel is a prodrug that requires metabolism in the liver by the cytochrome P450 system (CYP450), in particular cytochrome P450 2C19 (CYP2C19).	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	117-137
20235209-2	2010	Clopidogrel is a prodrug that requires metabolism in the liver by the cytochrome P450 system (CYP450), in particular cytochrome P450 2C19 (CYP2C19).	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	139-146
20210760-3	2010	As a result, this receptor has been a target for the development of clinically effective antiplatelet agents, such as the thienopyridines ticlopidine and, more recently, clopidogrel, the only two currently FDA-approved P2Y12 antagonists.	clopidogrel	170-181	purinergic receptor P2Y12	Homo sapiens	219-224
20230261-8	2010	Currently, the majority of data assessing clopidogrel nonresponsiveness focus on genetic variation in CYP2C19 and drug interactions with proton pump inhibitors.	clopidogrel	42-53	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	102-109
20040040-0	2010	Effect of an increased clopidogrel maintenance dose or lansoprazole co-administration on the antiplatelet response to clopidogrel in CYP2C19-genotyped healthy subjects.	clopidogrel	118-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	133-140
27713279-2	2010	Apart from CYP2C19 genetic polymorphisms, nongenetic factors, particularly drug-drug interactions, age and other clinical characteristics influence the interindividual variability in clopidogrel response to varying degrees.	clopidogrel	183-194	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	11-18
27713279-3	2010	The present article reviews the so far accumulated evidence on the role of pharmacogenetic traits influencing CYP-activity as determinants of the antiplatelet response to clopidogrel, and its clinical implications.	clopidogrel	171-182	peptidylprolyl isomerase G	Homo sapiens	110-113
20180610-2	2010	However, clopidogrel is a prodrug that needs to be metabolized to the active thiol metabolite by the cytochrome P450 (CYP) system.	clopidogrel	9-20	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	101-116
20180610-2	2010	However, clopidogrel is a prodrug that needs to be metabolized to the active thiol metabolite by the cytochrome P450 (CYP) system.	clopidogrel	9-20	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	118-121
20180610-5	2010	In addition, polymorphisms in the genes encoding P-glycoprotein (an efflux transporter) and purinergic receptor P2Y(12) (the active site for clopidogrel) have been studied for their role in clopidogrel responsiveness.	clopidogrel	141-152	purinergic receptor P2Y12	Homo sapiens	49-119
20180610-5	2010	In addition, polymorphisms in the genes encoding P-glycoprotein (an efflux transporter) and purinergic receptor P2Y(12) (the active site for clopidogrel) have been studied for their role in clopidogrel responsiveness.	clopidogrel	190-201	purinergic receptor P2Y12	Homo sapiens	49-119
20180610-9	2010	Polymorphisms in CYP2C19 and, to a lesser extent, the adenosine 5"-triphosphate-binding cassette gene, ABCB1, contribute to variability in clopidogrel responsiveness.	clopidogrel	139-150	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-24
20180610-9	2010	Polymorphisms in CYP2C19 and, to a lesser extent, the adenosine 5"-triphosphate-binding cassette gene, ABCB1, contribute to variability in clopidogrel responsiveness.	clopidogrel	139-150	ATP binding cassette subfamily B member 1	Homo sapiens	103-108
20180610-10	2010	Specifically, patients possessing at least one variant CYP2C19 allele (CYP2C19*2, *3) have impaired clopidogrel responsiveness due to decreased formation of the active metabolite.	clopidogrel	100-111	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	55-62
20180610-10	2010	Specifically, patients possessing at least one variant CYP2C19 allele (CYP2C19*2, *3) have impaired clopidogrel responsiveness due to decreased formation of the active metabolite.	clopidogrel	100-111	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
20180610-11	2010	In addition, one study found that considering ABCB1 genotype in addition to CYP2C19 allowed better prediction of clopidogrel nonresponsiveness.	clopidogrel	113-124	ATP binding cassette subfamily B member 1	Homo sapiens	46-51
20180610-11	2010	In addition, one study found that considering ABCB1 genotype in addition to CYP2C19 allowed better prediction of clopidogrel nonresponsiveness.	clopidogrel	113-124	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	76-83
20180610-12	2010	However, routine genotyping for CYP2C19 or ABCB1 polymorphisms in order to predict clopidogrel responsiveness cannot be recommended at this time because of logistic and cost considerations.	clopidogrel	83-94	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
20180610-12	2010	However, routine genotyping for CYP2C19 or ABCB1 polymorphisms in order to predict clopidogrel responsiveness cannot be recommended at this time because of logistic and cost considerations.	clopidogrel	83-94	ATP binding cassette subfamily B member 1	Homo sapiens	43-48
20304905-1	2010	BET 1: Adding clopidogrel to standard treatment for acute myocardial infarction.	clopidogrel	14-25	Bet1 golgi vesicular membrane trafficking protein	Homo sapiens	0-5
20653328-3	2010	Numerous clinical trials have shown the efficacy of clopidogrel, an inhibitor of the ADP P2Y12 receptor, in patients presenting with an acute coronary syndrome and undergoing percutaneous coronary intervention.	clopidogrel	52-63	purinergic receptor P2Y12	Homo sapiens	89-94
20218180-2	2010	Among the tests that are currently available, quantification of the phosphorylation status of the vasodilator phosphoprotein (VASP assay) is probably the most specific assay to evaluate the inhibition of the P2Y12 receptor by clopidogrel.	clopidogrel	226-237	vasodilator stimulated phosphoprotein	Homo sapiens	126-130
20218180-2	2010	Among the tests that are currently available, quantification of the phosphorylation status of the vasodilator phosphoprotein (VASP assay) is probably the most specific assay to evaluate the inhibition of the P2Y12 receptor by clopidogrel.	clopidogrel	226-237	purinergic receptor P2Y12	Homo sapiens	208-213
19919843-0	2010	Impact of genetic and acquired alteration in cytochrome P450 system on pharmacologic and clinical response to clopidogrel.	clopidogrel	110-121	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	45-60
19919843-2	2010	Clopidogrel, a thienopyridine, is a prodrug that is transformed in vivo to an active metabolite by the cytochrome P450 (CYP) enzyme system.	clopidogrel	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	103-118
19919843-2	2010	Clopidogrel, a thienopyridine, is a prodrug that is transformed in vivo to an active metabolite by the cytochrome P450 (CYP) enzyme system.	clopidogrel	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	120-123
19919843-4	2010	Recent data demonstrated patients carrying a genetic variant of CYP enzymes (e.g. CYP2C19) would have a higher rate of ischemic events than non-carriers due to an attenuation of the pharmacokinetic and pharmacodynamic responses to clopidogrel.	clopidogrel	231-242	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	64-67
19919843-4	2010	Recent data demonstrated patients carrying a genetic variant of CYP enzymes (e.g. CYP2C19) would have a higher rate of ischemic events than non-carriers due to an attenuation of the pharmacokinetic and pharmacodynamic responses to clopidogrel.	clopidogrel	231-242	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	82-89
19919843-6	2010	PPIs are extensively metabolized by the cytochrome P450 system and have been associated with decreased antiplatelet activity of clopidogrel.	clopidogrel	128-139	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	40-55
19904241-1	2010	Current consensus recommendations state that patients prescribed clopidogrel plus aspirin should receive a proton pump inhibitor (PPI) to reduce gastrointestinal bleeding.	clopidogrel	65-76	ATPase H+/K+ transporting non-gastric alpha2 subunit	Homo sapiens	107-118
19904241-2	2010	Clopidogrel is converted to its active metabolite by cytochrome P450 (CYP) enzymes.	clopidogrel	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	53-68
19904241-2	2010	Clopidogrel is converted to its active metabolite by cytochrome P450 (CYP) enzymes.	clopidogrel	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	70-73
19904241-3	2010	Clopidogrel users with decreased CYP2C19 function have less inhibition of platelet aggregation and increased cardiovascular (CV) events.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-40
19904241-4	2010	As PPI metabolism also involves CYP2C19, it was hypothesized that competition by PPIs might interfere with clopidogrel"s action.	clopidogrel	107-118	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
20083681-1	2010	BACKGROUND: The cytochrome P450 (CYP) 2C19 isoenzyme plays an important role in clopidogrel metabolization.	clopidogrel	80-91	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-42
20083681-2	2010	A recently explored CYP2C19*17 allelic variant has been linked to increased transcriptional activity, resulting in extensive metabolization of CYP2C19 substrates, which may lead to an enhanced platelet response to clopidogrel treatment.	clopidogrel	214-225	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	20-27
20083681-2	2010	A recently explored CYP2C19*17 allelic variant has been linked to increased transcriptional activity, resulting in extensive metabolization of CYP2C19 substrates, which may lead to an enhanced platelet response to clopidogrel treatment.	clopidogrel	214-225	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	143-150
20083681-3	2010	The aim of this study was to assess the impact of CYP2C19*17 on ADP-induced platelet aggregation, the risk of bleeding, and stent thrombosis in clopidogrel-treated patients undergoing percutaneous coronary intervention.	clopidogrel	144-155	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	50-57
20083681-12	2010	CONCLUSIONS: CYP2C19*17 carrier status is significantly associated with enhanced response to clopidogrel and an increased risk of bleeding.	clopidogrel	93-104	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
19902490-10	2010	Clopidogrel efficacy was assessed by measurement of vasodilator-stimulated phosphoprotein phosphorylation index.	clopidogrel	0-11	vasodilator stimulated phosphoprotein	Homo sapiens	52-89
19943879-9	2010	Interestingly, clopidogrel non-responders in the VASP phosphorylation assay without platelet hyperreactivity in MEA did not suffer from stent thrombosis.	clopidogrel	15-26	vasodilator stimulated phosphoprotein	Homo sapiens	49-53
20094648-2	2010	Aspirin and clopidogrel, the two most widely prescribed anti-platelet drugs, are metabolized to active compounds that covalently and irreversibly modify their respective therapeutic targets (COX1 and P2Y12).	clopidogrel	12-23	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	191-195
20094648-2	2010	Aspirin and clopidogrel, the two most widely prescribed anti-platelet drugs, are metabolized to active compounds that covalently and irreversibly modify their respective therapeutic targets (COX1 and P2Y12).	clopidogrel	12-23	purinergic receptor P2Y12	Homo sapiens	200-205
20094648-4	2010	As clopidogrel must be activated by cytochrome P450 metabolism, recent pharmacogenomic studies have revealed that patients lacking a functional allele of CYP2C19 derive no therapeutic benefit from the drug.	clopidogrel	3-14	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	154-161
20126830-1	2010	Novel P2Y12 inhibitors are in development to overcome the occurrence of atherothrombotic events associated with poor responsiveness to the widely used P2Y12 inhibitor clopidogrel.	clopidogrel	167-178	purinergic receptor P2Y12	Homo sapiens	6-11
20126830-1	2010	Novel P2Y12 inhibitors are in development to overcome the occurrence of atherothrombotic events associated with poor responsiveness to the widely used P2Y12 inhibitor clopidogrel.	clopidogrel	167-178	purinergic receptor P2Y12	Homo sapiens	151-156
20653328-4	2010	However, laboratory and clinical experience with clopidogrel have led to understanding some of the limitations of this drug, the most important of which is its broad range in interindividual response variability, resulting in the development of novel ADP P2Y12 receptor-inhibiting strategies.	clopidogrel	49-60	purinergic receptor P2Y12	Homo sapiens	255-260
20653328-5	2010	This article provides an overview of ADP P2Y12 receptor-inhibiting strategies, including high clopidogrel dosing regimens and novel agents under advanced clinical development.	clopidogrel	94-105	purinergic receptor P2Y12	Homo sapiens	41-46
19934793-0	2010	Besides CYP2C19*2, the variant allele CYP2C9*3 is associated with higher on-clopidogrel platelet reactivity in patients on dual antiplatelet therapy undergoing elective coronary stent implantation.	clopidogrel	76-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
20924183-1	2010	OBJECTIVES: To determine whether the 681 G&gt;A (*2) polymorphism of cytochrome P450 (CYP2C19) is related to suboptimal reperfusion and mortality in patients with acute myocardial infarction (AMI) pretreated with clopidogrel.	clopidogrel	213-224	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	86-93
20924183-11	2010	CONCLUSIONS: The CYP2C19*2 allele is an independent predictor of suboptimal reperfusion in patients with AMI undergoing PCI with stenting after pretreatment with clopidogrel and may increase the risk of all-cause mortality.	clopidogrel	162-173	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-24
20966600-8	2010	The rate of low responsiveness to clopidogrel, defined by VASP index &gt; 50%, was lower in the triple therapy group than in the dual therapy group (12.5% versus 55.9%; P = 0.047).	clopidogrel	34-45	vasodilator stimulated phosphoprotein	Homo sapiens	58-62
20966600-9	2010	Similarly, in DM patients the triple therapy group had a lower VASP index compared with the dual therapy group (23.1 +- 15.3% versus 47.0 +- 23.5%; P = 0.015).Clopidogrel plus cilostazol is more effective in inhibiting the platelet P2Y(12) ADP receptor pathway than clopidogrel alone.	clopidogrel	159-170	vasodilator stimulated phosphoprotein	Homo sapiens	63-67
19018951-6	2010	Patients taking clopidogrel 75 mg for &gt;or=7 days, 300 mg for 24 hours, and 600 mg same day load had a mean P2Y12/ADP inhibition of 45%, 35% (P-value = .09), and 16%, respectively (P-value = .005).	clopidogrel	16-27	purinergic receptor P2Y12	Homo sapiens	110-115
20659022-7	2010	It has been shown recently that loss of function alleles of some CYP450 genes especially CYP2C19*2 are responsible for reduced reaction of platelets to clopidogrel.	clopidogrel	152-163	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	89-96
20831051-2	2010	In a series of articles the authors consider clinical pharmacology and experience of clinical application of blockers of platelet P2Y12 receptors, most well known representatives of which ticlopidine and clopidogrel according to chemical structure belong to thienopyridine derivatives.	clopidogrel	204-215	purinergic receptor P2Y12	Homo sapiens	130-135
19904241-12	2010	As the presence of PPIs and clopidogrel in plasma is short lived, separation by 12-20 h should in theory prevent competitive inhibition of CYP metabolism and minimize any potential, though unproven, clinical interaction.	clopidogrel	28-39	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	139-142
19855266-7	2010	Levels of CD62P, CD63, and CD40L were more significantly reduced in the clopidogrel group than in the aspirin group in the first week after stroke.	clopidogrel	72-83	selectin P	Homo sapiens	10-15
19855266-7	2010	Levels of CD62P, CD63, and CD40L were more significantly reduced in the clopidogrel group than in the aspirin group in the first week after stroke.	clopidogrel	72-83	CD63 molecule	Homo sapiens	17-21
19855266-7	2010	Levels of CD62P, CD63, and CD40L were more significantly reduced in the clopidogrel group than in the aspirin group in the first week after stroke.	clopidogrel	72-83	CD40 ligand	Homo sapiens	27-32
22291500-3	2010	From pharmacologic and pharmacodynamic perspectives, there is a real interaction between clopidogrel and PPIs because of the competitive inhibition of CYP2C19 isoenzyme which is required for biotransformation of clopidogrel to its active metabolite.	clopidogrel	89-100	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	151-158
22291500-3	2010	From pharmacologic and pharmacodynamic perspectives, there is a real interaction between clopidogrel and PPIs because of the competitive inhibition of CYP2C19 isoenzyme which is required for biotransformation of clopidogrel to its active metabolite.	clopidogrel	212-223	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	151-158
19812348-0	2010	Identification of the human cytochrome P450 enzymes involved in the two oxidative steps in the bioactivation of clopidogrel to its pharmacologically active metabolite.	clopidogrel	112-123	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	39-43
19812348-1	2010	The aim of the current study is to identify the human cytochrome P450 (P450) isoforms involved in the two oxidative steps in the bioactivation of clopidogrel to its pharmacologically active metabolite.	clopidogrel	146-157	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	65-69
19812348-1	2010	The aim of the current study is to identify the human cytochrome P450 (P450) isoforms involved in the two oxidative steps in the bioactivation of clopidogrel to its pharmacologically active metabolite.	clopidogrel	146-157	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	71-75
19812348-2	2010	In the in vitro experiments using cDNA-expressed human P450 isoforms, clopidogrel was metabolized to 2-oxo-clopidogrel, the immediate precursor of its pharmacologically active metabolite.	clopidogrel	70-81	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	55-59
19812348-10	2010	These studies showed that CYP2C19 contributed substantially to both oxidative steps required in the formation of clopidogrel active metabolite and that CYP3A4 contributed substantially to the second oxidative step.	clopidogrel	113-124	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
19812348-10	2010	These studies showed that CYP2C19 contributed substantially to both oxidative steps required in the formation of clopidogrel active metabolite and that CYP3A4 contributed substantially to the second oxidative step.	clopidogrel	113-124	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	152-158
19812348-11	2010	These results help explain the role of genetic polymorphism of CYP2C19 and also the effect of potent CYP3A inhibitors on the pharmacokinetics and pharmacodynamics of clopidogrel in humans and on clinical outcomes.	clopidogrel	166-177	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	63-70
20035517-2	2010	We report a Janus kinase 2-homozygous patient with BCS who thrombosed a transjugular intrahepatic portosystemic shunt (TIPS) despite treatment with warfarin (international normalized ratio = 3.0), aspirin, and clopidogrel.	clopidogrel	210-221	Janus kinase 2	Homo sapiens	12-26
20217574-7	2010	Additionally, the assay has been used to demonstrate that CYP2C19 variants with decreased enzyme activity led to lower levels of the active clopidogrel metabolite, resulting in a decreased inhibition of platelets and a higher rate of cardiovascular events when compared to noncarriers of the DNA variant.	clopidogrel	140-151	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	58-65
19934793-3	2010	Several studies report that the genetic variation in CYP2C19 (*2) is associated with an impaired response to clopidogrel.	clopidogrel	109-120	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-60
19934793-10	2010	CONCLUSION: Besides CYP2C19*2, the variant allele CYP2C9*3 plays an important role in the response to clopidogrel in patients on dual antiplatelet therapy undergoing coronary stenting.	clopidogrel	102-113	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	20-27
19934793-10	2010	CONCLUSION: Besides CYP2C19*2, the variant allele CYP2C9*3 plays an important role in the response to clopidogrel in patients on dual antiplatelet therapy undergoing coronary stenting.	clopidogrel	102-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
20831298-9	2010	The other study is also set in community practice settings and compares cardiovascular outcomes of patients receiving clopidogrel who are extensive metabolizer phenotypes for the cytochrome P450 2C19 hepatic isoenzyme with all patients receiving prasugrel.	clopidogrel	118-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	179-199
23226041-7	2010	Recently, the loss-of-function CYP2C19*2 allele has been associated with decreased metabolization of clopidogrel, poor antiaggregant effect, and increased cardiovascular events.	clopidogrel	101-112	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	31-38
20148735-0	2010	VerifyNow and VASP phosphorylation assays give similar results for patients receiving clopidogrel, but they do not always correlate with platelet aggregation.	clopidogrel	86-97	vasodilator stimulated phosphoprotein	Homo sapiens	14-18
21067313-1	2010	Antiplatelet therapy for the management of patients with cardiovascular risks often includes a combination therapy of aspirin and clopidogrel, acting through inhibition of thromboxane generation and blockade of G(i)-coupled P2Y12 receptor, respectively.	clopidogrel	130-141	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	224-229
20089227-1	2010	Platelet P2Y12 receptor antagonism with clopidogrel has represented a major advancement in the pharmacological management of patients with atherothrombotic disease, in particular those with acute coronary syndromes and undergoing percutaneous coronary interventions.	clopidogrel	40-51	purinergic receptor P2Y12	Homo sapiens	9-14
19995331-0	2009	Interaction between clopidogrel and proton pump inhibitors: hypothesis to explain multifactorial CYP2C19 inhibition.	clopidogrel	20-31	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	97-104
19700402-6	2009	Platelets from mice dosed with clopidogrel also showed partial Akt phosphorylation, indicating that GPVI-mediated Akt phosphorylation is regulated by both secretion-dependent and -independent pathways.	clopidogrel	31-42	thymoma viral proto-oncogene 1	Mus musculus	63-66
19700402-6	2009	Platelets from mice dosed with clopidogrel also showed partial Akt phosphorylation, indicating that GPVI-mediated Akt phosphorylation is regulated by both secretion-dependent and -independent pathways.	clopidogrel	31-42	glycoprotein 6 (platelet)	Mus musculus	100-104
19700402-6	2009	Platelets from mice dosed with clopidogrel also showed partial Akt phosphorylation, indicating that GPVI-mediated Akt phosphorylation is regulated by both secretion-dependent and -independent pathways.	clopidogrel	31-42	thymoma viral proto-oncogene 1	Mus musculus	114-117
20031767-7	2009	Patients in the highest 2 tertiles of PAPP-A randomized to clopidogrel had fewer events (7.3% clopidogrel versus 13.1% placebo, P=0.01), but no benefit was seen in the lowest tertile.	clopidogrel	59-70	pappalysin 1	Homo sapiens	38-44
20031767-7	2009	Patients in the highest 2 tertiles of PAPP-A randomized to clopidogrel had fewer events (7.3% clopidogrel versus 13.1% placebo, P=0.01), but no benefit was seen in the lowest tertile.	clopidogrel	94-105	pappalysin 1	Homo sapiens	38-44
19925675-13	2009	In vitro clot strength and clot kinetics, as determined by TEG in heparin + clopidogrel samples, were positively associated with the amount of rThrombin activity added for clot initiation.	clopidogrel	76-87	coagulation factor II	Rattus norvegicus	143-152
19925675-14	2009	CONCLUSION: In an animal model designed to replicate the anti-coagulation regimens encountered in clinical settings, topical rThrombin at 1000 IU/mL more reliably controlled the pharmacological effects of heparin or heparin + clopidogrel on hemostasis than rThrombin at 125 IU/mL.	clopidogrel	226-237	coagulation factor II	Rattus norvegicus	125-134
19175636-1	2009	Mr C, a 68-year-old Chinese male with diabetes mellitus, previous stroke and ischaemic cardiomyopathy on clopidogrel, presented with haematochezia.	clopidogrel	105-116	CD200 molecule	Homo sapiens	0-4
19932784-4	2009	Cytochrome P450 (CYP) 2C19 polymorphism was a major determinant of the response to clopidogrel and could be responsible for a failure of dose adjustment.	clopidogrel	83-94	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-26
19932784-14	2009	In conclusion, high BMI, acute coronary syndrome, diabetes mellitus, and CYP2C19 2 are associated with HTPR after a 600-mg loading dose of clopidogrel.	clopidogrel	139-150	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	73-80
19726525-8	2009	It has most recently been demonstrated that resistance to clopidogrel is at least in part caused by polymorphism of CYP2C19.	clopidogrel	58-69	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	116-123
19995331-5	2009	A hypothesis is proposed to interpret the phenomenon of PPI inhibition based in part on the finding that clopidogrel is itself an inhibitor of CYP2C19.	clopidogrel	105-116	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	143-150
19704027-6	2009	Clopidogrel was largely hydrolyzed to an inactive acid metabolite (approximately 90% of total metabolites analyzed), and the clopidogrel concentrations consumed were correlated to human carboxylesterase 1 activity in each source of liver microsomes.	clopidogrel	0-11	carboxylesterase 1	Homo sapiens	186-204
19704027-6	2009	Clopidogrel was largely hydrolyzed to an inactive acid metabolite (approximately 90% of total metabolites analyzed), and the clopidogrel concentrations consumed were correlated to human carboxylesterase 1 activity in each source of liver microsomes.	clopidogrel	125-136	carboxylesterase 1	Homo sapiens	186-204
19704027-8	2009	The oxidation of clopidogrel to its thiolactone metabolite correlated with variable activities of CYP1A2, CYP2B6, and CYP2C19.	clopidogrel	17-28	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	98-104
19704027-8	2009	The oxidation of clopidogrel to its thiolactone metabolite correlated with variable activities of CYP1A2, CYP2B6, and CYP2C19.	clopidogrel	17-28	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	106-112
19704027-8	2009	The oxidation of clopidogrel to its thiolactone metabolite correlated with variable activities of CYP1A2, CYP2B6, and CYP2C19.	clopidogrel	17-28	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	118-125
19504052-3	2009	The effect of clopidogrel cessation after one year of therapy on markers of inflammation has been investigated in diabetics and showed an increase in platelet aggregation as well as hsCRP and surface P-selectin levels.	clopidogrel	14-25	selectin P	Homo sapiens	200-210
19925675-0	2009	Topical recombinant thrombin at a concentration of 1000 IU/mL reliably shortens in vivo TTH and delivers durable hemostasis in the presence of heparin anticoagulation and clopidogrel platelet inhibition in a rabbit model of vascular bleeding.	clopidogrel	171-182	prothrombin	Oryctolagus cuniculus	20-28
19925675-9	2009	TTH also decreased with increasing concentrations of rThrombin in heparin + clopidogrel treated animals; again it was significantly shorter after treatment with 1000 IU/mL rThrombin (71 seconds) than with 125 IU/mL rThrombin (177 seconds; p &lt; 0.001).	clopidogrel	76-87	coagulation factor II	Rattus norvegicus	53-62
19925675-9	2009	TTH also decreased with increasing concentrations of rThrombin in heparin + clopidogrel treated animals; again it was significantly shorter after treatment with 1000 IU/mL rThrombin (71 seconds) than with 125 IU/mL rThrombin (177 seconds; p &lt; 0.001).	clopidogrel	76-87	coagulation factor II	Rattus norvegicus	172-181
19925675-9	2009	TTH also decreased with increasing concentrations of rThrombin in heparin + clopidogrel treated animals; again it was significantly shorter after treatment with 1000 IU/mL rThrombin (71 seconds) than with 125 IU/mL rThrombin (177 seconds; p &lt; 0.001).	clopidogrel	76-87	coagulation factor II	Rattus norvegicus	172-181
19925675-10	2009	Variability in TTH was significantly smaller after treatment with 1000 IU/mL rThrombin than after 125 IU/mL rThrombin, indicating greater reliability of clot formation (p &lt; 0.001 for heparin or heparin + clopidogrel treatments).	clopidogrel	207-218	coagulation factor II	Rattus norvegicus	77-86
19926050-1	2009	OBJECTIVES: Our aim was to assess whether a higher clopidogrel maintenance dose has a greater antiplatelet effect in CYP2C19*2 allele carriers compared with noncarriers.	clopidogrel	51-62	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	117-124
19926050-2	2009	BACKGROUND: Clopidogrel is a prodrug that is biotransformed by the cytochrome P450 enzymes CYP2C19, 2C9, and 3A4, 2B6, 1A2.	clopidogrel	12-23	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	91-98
19926050-3	2009	The CYPC219*2 loss of function variant has been associated with a reduced antiplatelet response to clopidogrel and a 3-fold risk of stent thrombosis.	clopidogrel	99-110	peptidylprolyl isomerase C	Homo sapiens	4-8
19891556-3	2009	Clopidogrel is a prodrug that undergoes hepatic biotransformation by CYP2C19 into its active metabolite.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	69-76
19891556-4	2009	Several studies have reported that, compared with wild-type individuals, CYP2C19 variant allele carriers exhibit a significantly lower capacity to metabolize clopidogrel into its active metabolite and inhibit platelet activation, and are therefore at significantly higher risk of adverse cardiovascular events.	clopidogrel	158-169	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	73-80
19891556-5	2009	Consequently, the US FDA has recently changed clopidogrel"s prescribing information to highlight the impact of CYP2C19 genotype on clopidogrel pharmacokinetics, pharmacodynamics and clinical response.	clopidogrel	46-57	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	111-118
19891556-5	2009	Consequently, the US FDA has recently changed clopidogrel"s prescribing information to highlight the impact of CYP2C19 genotype on clopidogrel pharmacokinetics, pharmacodynamics and clinical response.	clopidogrel	131-142	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	111-118
19845434-0	2009	Comparison of mechanism-based inhibition of human cytochrome P450 2C19 by ticlopidine, clopidogrel, and prasugrel.	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	50-70
19845434-1	2009	Mechanism-based inhibition of CYP2C19 in human liver microsomes by the thienopyridine antiplatelet agents clopidogrel, prasugrel and their thiolactone metabolites was investigated by determining the time- and concentration-dependent inhibition of the activity of S-mephenytoin 4"-hydroxylase as typical CYP2C19 activity and compared with ticlopidine and its metabolite.	clopidogrel	106-117	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
19845434-2	2009	Clopidogrel was shown to be a mechanism-based inhibitor of CYP2C19 with the inactivation kinetic parameters, k(inact) and K(I), equal to 0.0557 min(-1) and 14.3 microM, respectively, as well as ticlopidine (0.0739 min(-1) and 3.32 microM, respectively).	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	59-66
19845434-3	2009	The thiolactone metabolite of ticlopidine and clopidogrel inhibited CYP2C19 only in a concentration-dependent manner.	clopidogrel	46-57	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	68-75
19845434-5	2009	The oxidation of the thiophene moiety of clopidogrel to form their respective thiolactones was found to be the critical reaction that produces the chemically reactive metabolites which cause the mechanism-based inhibition of CYP2C19.	clopidogrel	41-52	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	225-232
19845434-8	2009	In conclusion, clopidogrel is potent mechanism-based inhibitors of CYP2C19 as well as ticlopidine, whereas prasugrel did not inactivate CYP2C19.	clopidogrel	15-26	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	67-74
20031628-0	2009	Common variation in the platelet receptor P2RY12 gene is associated with residual on-clopidogrel platelet reactivity in patients undergoing elective percutaneous coronary interventions.	clopidogrel	85-96	purinergic receptor P2Y12	Homo sapiens	42-48
20031628-3	2009	The aim of this study was to comprehensively investigate the possible association between common variation in the entire P2RY12 locus and the magnitude of residual on-clopidogrel platelet reactivity measured by 2 commonly used platelet function assays in a large cohort of patients.	clopidogrel	167-178	purinergic receptor P2Y12	Homo sapiens	121-127
20031628-10	2009	CONCLUSIONS: Common variation in the P2RY12 gene is a significant determinant of the interindividual variability in residual on-clopidogrel platelet reactivity in patients with coronary artery disease.	clopidogrel	128-139	purinergic receptor P2Y12	Homo sapiens	37-43
19531897-0	2009	Impact of CYP2C19 polymorphisms on the antiplatelet effect of clopidogrel in an actual clinical setting in Japan.	clopidogrel	62-73	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-17
20015321-0	2009	Enhanced post-clopidogrel platelet reactivity in diabetic patients is independently related to plasma fibrinogen level but not to glycemic control.	clopidogrel	14-25	fibrinogen beta chain	Homo sapiens	102-112
19786240-10	2009	ERK 1/2 activation was significantly increased post-PTA in both the aspirin/clopidogrel and aspirin/placebo groups (P &lt; .001).	clopidogrel	76-87	mitogen-activated protein kinase 3	Homo sapiens	0-7
19786240-11	2009	There was a statistically significant decrease in PDGF (P = .004), and increase in vWF (P = .026), following loading with clopidogrel.	clopidogrel	122-133	von Willebrand factor	Homo sapiens	83-86
19550317-1	2009	PURPOSE OF REVIEW: The P2Y12 antagonist clopidogrel has a well established role as an antithrombotic agent in the settings of percutaneous coronary intervention and acute coronary syndromes.	clopidogrel	40-51	purinergic receptor P2Y12	Homo sapiens	23-28
19550317-2	2009	However, clopidogrel has a number of disadvantages that have led to the development of new P2Y12 antagonists.	clopidogrel	9-20	purinergic receptor P2Y12	Homo sapiens	91-96
19550317-5	2009	A patient"s response to clopidogrel is partly dependent on factors that decrease (reduced-function CYP2C19 allele; omeprazole) or increase (cigarette smoking) the metabolism of clopidogrel through cytochrome P450 in the liver.	clopidogrel	24-35	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	99-106
19706858-9	2009	Thirteen single-nucleotide polymorphisms on chromosome 10q24 within the CYP2C18-CYP2C19-CYP2C9-CYP2C8 cluster were associated with diminished clopidogrel response, with a high degree of statistical significance (P = 1.5 x 10(-13) for rs12777823, additive model).	clopidogrel	142-153	cytochrome P450 family 2 subfamily C member 18	Homo sapiens	72-79
19706858-9	2009	Thirteen single-nucleotide polymorphisms on chromosome 10q24 within the CYP2C18-CYP2C19-CYP2C9-CYP2C8 cluster were associated with diminished clopidogrel response, with a high degree of statistical significance (P = 1.5 x 10(-13) for rs12777823, additive model).	clopidogrel	142-153	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	80-87
19706858-9	2009	Thirteen single-nucleotide polymorphisms on chromosome 10q24 within the CYP2C18-CYP2C19-CYP2C9-CYP2C8 cluster were associated with diminished clopidogrel response, with a high degree of statistical significance (P = 1.5 x 10(-13) for rs12777823, additive model).	clopidogrel	142-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
19706858-9	2009	Thirteen single-nucleotide polymorphisms on chromosome 10q24 within the CYP2C18-CYP2C19-CYP2C9-CYP2C8 cluster were associated with diminished clopidogrel response, with a high degree of statistical significance (P = 1.5 x 10(-13) for rs12777823, additive model).	clopidogrel	142-153	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	95-101
19706858-10	2009	The rs12777823 polymorphism was in strong linkage disequilibrium with the CYP2C19*2 variant, and was associated with diminished clopidogrel response, accounting for 12% of the variation in platelet aggregation to ADP (P = 4.3 x 10(-11)).	clopidogrel	128-139	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	74-81
19706858-11	2009	The relation between CYP2C19*2 genotype and platelet aggregation was replicated in clopidogrel-treated patients undergoing coronary intervention (P = .02).	clopidogrel	83-94	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
19706858-13	2009	CONCLUSION: CYP2C19*2 genotype was associated with diminished platelet response to clopidogrel treatment and poorer cardiovascular outcomes.	clopidogrel	83-94	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
19576320-0	2009	Relation of genetic polymorphisms in the cytochrome P450 gene with clopidogrel resistance after drug-eluting stent implantation in Koreans.	clopidogrel	67-78	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	41-56
19576320-1	2009	Clopidogrel is a prodrug that has to be converted to an active metabolite by hepatic cytochrome P450 (CYP) isoenzymes to inhibit platelet aggregation.	clopidogrel	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	85-100
19576320-1	2009	Clopidogrel is a prodrug that has to be converted to an active metabolite by hepatic cytochrome P450 (CYP) isoenzymes to inhibit platelet aggregation.	clopidogrel	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	102-105
19576320-3	2009	In this study, we sought to determine the relation of genetic polymorphisms of CYP genes to clopidogrel resistance in Koreans.	clopidogrel	92-103	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	79-82
19576320-9	2009	In all subjects, the CYP2C19*3A allele was significantly more prevalent in the clopidogrel-resistant group compared with the clopidogrel-responsive group.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
19576320-9	2009	In all subjects, the CYP2C19*3A allele was significantly more prevalent in the clopidogrel-resistant group compared with the clopidogrel-responsive group.	clopidogrel	125-136	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
19576320-10	2009	Multiple logistic regression analysis demonstrated that CYP2C19*3 is an independent predictor of clopidogrel resistance.	clopidogrel	97-108	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	56-63
19576320-11	2009	In conclusion, CYP2C19*3 single-nucleotide polymorphisms is an independent risk factor of clopidogrel resistance in Korean subjects with coronary artery disease.	clopidogrel	90-101	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
19429918-0	2009	Genetic variation of CYP2C19 affects both pharmacokinetic and pharmacodynamic responses to clopidogrel but not prasugrel in aspirin-treated patients with coronary artery disease.	clopidogrel	91-102	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
19429918-2	2009	We hypothesized that decreased CYP2C19 activity affects the pharmacokinetic and pharmacodynamic response to clopidogrel but not prasugrel.	clopidogrel	108-119	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	31-38
20848331-9	2009	Certain polymorphisms (eg, CYP2C19) may prevent this conversion and lead to failure of clopidogrel to prevent major cardiovascular events.In patients with well-controlled or treated cardiovascular risk factors, aspirin plus extended-release dipyridamole and clopidogrel may provide similar results in preventing recurrent stroke, but aspirin plus extended-release dipyridamole may be associated with a slightly higher risk of major hemorrhage.	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	27-34
20848331-9	2009	Certain polymorphisms (eg, CYP2C19) may prevent this conversion and lead to failure of clopidogrel to prevent major cardiovascular events.In patients with well-controlled or treated cardiovascular risk factors, aspirin plus extended-release dipyridamole and clopidogrel may provide similar results in preventing recurrent stroke, but aspirin plus extended-release dipyridamole may be associated with a slightly higher risk of major hemorrhage.	clopidogrel	258-269	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	27-34
19504141-9	2009	RESULTS: Using flow cytometry, the mean inhibitory effect of clopidogrel on the CD62P expression was similar and no significant differences were noted in subjects treated with either of the clopidogrel formulas for hydrogensulfate or besylate salt (5 micromol/L ADP: 8.12 +/- 5.53 CHS vs. 6.48 +/- 5.01 CB; 15 micromol/L ADP: 9.33 +/- 6.44 CHS vs. 8.99 +/- 8.27 CB; 50 micromol/L ADP: 11.17 +/- 6.81 CHS vs. 9.52 +/- 6.17 CB).	clopidogrel	61-72	selectin P	Homo sapiens	80-85
19664380-8	2009	In recent years it has become apparent that approximately 20% to 25% of patients who would be expected to benefit from clopidogrel therapy are resistant to this drug, largely due to a polymorphism in the gene for cytochrome P450 2C19.	clopidogrel	119-130	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	213-233
19811222-8	2009	There were predictable and significant changes in the AUC15 of the ADP channel in response to clopidogrel and the corresponding %PIn and %CIn in both volunteers and patients.	clopidogrel	94-105	pyridoxal phosphatase	Homo sapiens	138-141
19575629-6	2009	Clopidogrel response variability is primarily a pharmacokinetic phenomenon associated with insufficient active metabolite generation that is secondary to i) limited intestinal absorption affected by an ABCB1 gene polymorphism; ii) functional variability in P450 isoenzyme activity; and iii) a genetic polymorphism of CYP450 isoenzymes.	clopidogrel	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	202-207
19496924-0	2009	The CYP2C19*17 allele is associated with better platelet response to clopidogrel in patients admitted for non-ST acute coronary syndrome.	clopidogrel	69-80	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
19784880-1	2009	BACKGROUND: Genetic C3435T polymorphism of the multidrug resistance gene-1 (MDR-1) limits oral bioavailability of clopidogrel and influences prognosis in patients with myocardial infarction.	clopidogrel	114-125	ATP binding cassette subfamily B member 1	Homo sapiens	47-74
19784880-1	2009	BACKGROUND: Genetic C3435T polymorphism of the multidrug resistance gene-1 (MDR-1) limits oral bioavailability of clopidogrel and influences prognosis in patients with myocardial infarction.	clopidogrel	114-125	ATP binding cassette subfamily B member 1	Homo sapiens	76-81
19652892-7	2009	For comparison, aspirin and clopidogrel induced only 2.0- to 2.6 -fold changes in other tests (VASP assay, Cone and Platelet Analyzer and PFA-100).	clopidogrel	28-39	vasodilator stimulated phosphoprotein	Homo sapiens	95-99
19531897-1	2009	BACKGROUND: The P2Y(12) adenosine diphosphate (ADP) receptor blocker, clopidogrel, an essential drug for the prevention of stent thrombosis after percutaneous coronary intervention (PCI), is a prodrug that requires CYP2C19- and CYP3A4-mediating activation.	clopidogrel	70-81	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	215-222
19531897-1	2009	BACKGROUND: The P2Y(12) adenosine diphosphate (ADP) receptor blocker, clopidogrel, an essential drug for the prevention of stent thrombosis after percutaneous coronary intervention (PCI), is a prodrug that requires CYP2C19- and CYP3A4-mediating activation.	clopidogrel	70-81	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	228-234
19531897-3	2009	CYP2C19 polymorphisms have been reported to exhibit weaker antiplatelet response to clopidogrel in healthy subjects.	clopidogrel	84-95	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
19531897-4	2009	The effect of polymorphisms of CYP2C19, CYP3A4 and P2Y(12) on the antiplatelet effect of clopidogrel in clinical patients was examined in the present study.	clopidogrel	89-100	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	31-38
19531897-4	2009	The effect of polymorphisms of CYP2C19, CYP3A4 and P2Y(12) on the antiplatelet effect of clopidogrel in clinical patients was examined in the present study.	clopidogrel	89-100	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	40-46
19531897-8	2009	CONCLUSIONS: CYP2C19 polymorphisms are frequent in Japanese, and the antiplatelet effect of clopidogrel is strongly affected by them in the real-world clinical setting.	clopidogrel	92-103	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
20166430-0	2009	Genetic CYP2C19 polymorphism dependent non-responders to clopidogrel therapy--does structural design, dosing and induction strategies have a role to play?	clopidogrel	57-68	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	8-15
20166430-1	2009	Recent evidences suggest that genetic CYP2C19 polymorphism plays a role in the development of treatment resistance for clopidogrel"s antiplatelet therapy.	clopidogrel	119-130	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	38-45
18606468-7	2009	Patients within the first quartile of ASE had significantly lower RPA after administration of clopidogrel than other patients (p &lt; 0.05).	clopidogrel	94-105	arylsulfatase L	Homo sapiens	38-41
18606468-8	2009	Establishing a threshold of 200 ASE responsiveness to clopidogrel could be predicted with a positive predictive value of 80% and a specificity of 91%.	clopidogrel	54-65	arylsulfatase L	Homo sapiens	32-35
19463513-5	2009	Prestenting adenosine diphosphate-induced platelet aggregation, P-selectin, and activated glycoprotein IIb/IIIa expression were lower in patients receiving long-term clopidogrel therapy compared with the clopidogrel-naive group (p &lt;0.001), accompanied by lower levels of selected inflammation markers (p &lt; or = 0.05).	clopidogrel	166-177	selectin P	Homo sapiens	64-74
19530321-10	2009	Inhibition of platelet reactivity, after 600 mg of clopidogrel, was significantly less in carriers of PlA2 (P=0.009) for mean decrease in platelet reactivity index.	clopidogrel	51-62	phospholipase A2 group IIA	Homo sapiens	102-106
19530321-11	2009	The proportion of clopidogrel nonresponders (platelet reactivity index &gt;50%) was apparently higher in PlA2 carriers in comparison with PlA1/PlA1 patients (54 vs. 24%, P=0.082).	clopidogrel	18-29	phospholipase A2 group IIA	Homo sapiens	105-109
19573471-15	2009	The ICER of 12 months" treatment with clopidogrel varied between 49,436 pounds and 58,691 pounds per QALY.	clopidogrel	38-49	cAMP responsive element modulator	Homo sapiens	4-8
19435740-4	2009	VASP platelet reactivity index (PRI) was lower in prasugrel-treated patients than in clopidogrel-treated patients at 1-2 h post-PCI (&gt;or=1 h after loading dose) (P &lt; 0.001) and at 30 days (P &lt; 0.001).	clopidogrel	85-96	vasodilator stimulated phosphoprotein	Homo sapiens	0-4
19435740-7	2009	Thienopyridine hyporesponsiveness, prespecified as VASP PRI &gt;50%, was more frequent in clopidogrel-treated patients than in prasugrel-treated patients at 1-2 h (P &lt; 0.001) and 30 days (P = 0.03).	clopidogrel	90-101	vasodilator stimulated phosphoprotein	Homo sapiens	51-55
19246723-5	2009	From other studies, it was appreciated that the patients who had clopidogrel resistance had a defective allele *2/ in the CYP2C19 gene.	clopidogrel	65-76	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	122-129
19246723-6	2009	Furthermore, there was a dose response evident in that the homozygotes CYP2C19*2/*2 had platelets that responded even less well to clopidogrel than the heterozygotes CYP2C19*2 that responded less well than the wild-type homozygote.	clopidogrel	131-142	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
19246723-8	2009	However, the major oxidative metabolic pathway for clopidogrel by which the reactive intermediate is formed is CYP3A4.	clopidogrel	51-62	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	111-117
19398604-0	2009	Clopidogrel inhibits CYP2C19-dependent hydroxylation of omeprazole related to CYP2C19 genetic polymorphisms.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
19398604-0	2009	Clopidogrel inhibits CYP2C19-dependent hydroxylation of omeprazole related to CYP2C19 genetic polymorphisms.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	78-85
19398604-1	2009	This study explores the impact of clopidogrel on the pharmacokinetics of omeprazole related to CYP2C19 genetic polymorphisms.	clopidogrel	34-45	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	95-102
19398604-5	2009	After clopidogrel treatment, the AUC(0-infinity) of omeprazole increases by 30.02% +/- 18.03% (P = .004) and that of 5-hydroxyomeprazole decreases by 24.30% +/- 11.66% (P = .032) in CYP2C19*1/*1.	clopidogrel	6-17	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	182-189
19398604-8	2009	Clopidogrel inhibits CYP2C19-dependent hydroxylation of omeprazole in CYP2C19*1/*1 and has no impact on CYP3A4-catalyzed sulfoxidation of omeprazole.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
19398604-8	2009	Clopidogrel inhibits CYP2C19-dependent hydroxylation of omeprazole in CYP2C19*1/*1 and has no impact on CYP3A4-catalyzed sulfoxidation of omeprazole.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	70-77
19323972-0	2009	Clopidogrel attenuates atheroma formation and induces a stable plaque phenotype in apolipoprotein E knockout mice.	clopidogrel	0-11	apolipoprotein E	Mus musculus	83-99
19323972-4	2009	Herein, we tested the hypothesis that clopidogrel will influence plaque size and composition in the atherosclerosis prone apolipoprotein E knockout (apoE KO) mouse model.	clopidogrel	38-49	apolipoprotein E	Mus musculus	122-138
19429918-9	2009	CONCLUSION: Variation in the gene encoding CYP2C19 in patients with stable CAD contributes to reduced exposure to clopidogrel"s active metabolite and a corresponding reduction in P2Y(12) inhibition, but has no significant influence on the response to prasugrel.	clopidogrel	114-125	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	43-50
19452618-4	2009	There are various subgroups of acquired TTP associated with HIV infection, pregnancy, pancreatitis, associated with bone marrow transplantation, various disseminated malignancies and certain drugs, particularly Clopidogrel.	clopidogrel	211-222	ZFP36 ring finger protein	Homo sapiens	40-43
19618315-0	2009	Thrombin formation and platelet activation at the site of vascular injury in patients with coronary artery disease treated with clopidogrel combined with aspirin.	clopidogrel	128-139	coagulation factor II, thrombin	Homo sapiens	0-8
19618315-2	2009	The platelet glycoprotein (GP) IIIa PlA2 allele has been suggested to modulate antithrombotic actions of clopidogrel.	clopidogrel	105-116	phospholipase A2 group IB	Homo sapiens	36-40
19618315-3	2009	AIM: We investigated whether clopidogrel combined with aspirin affects local thrombin formation and platelet activation triggered by vascular injury.	clopidogrel	29-40	coagulation factor II, thrombin	Homo sapiens	77-85
19618315-6	2009	RESULTS: Total amounts of thrombin markers produced at the site of injury were similar before and after addition of clopidogrel, whereas platelet release of sCD40L and P-selectin was lower during treatment with aspirin + clopidogrel by 33.8% and 27.8% (p &lt; 0.001), respectively.	clopidogrel	221-232	selectin P	Homo sapiens	168-178
19618315-9	2009	CONCLUSION: Our study shows that clopidogrel combined with aspirin does not reduce thrombin formation following vascular injury, but attenuates platelet sCD40L and P-selectin release.	clopidogrel	33-44	selectin P	Homo sapiens	164-174
19440925-0	2009	Measurement of platelet P-selectin for remote testing of platelet function during treatment with clopidogrel and/or aspirin.	clopidogrel	97-108	selectin P	Homo sapiens	24-34
19440925-2	2009	Here we have established methods to assess the effects of clopidogrel and aspirin on platelets based on measurements of platelet P-selectin.	clopidogrel	58-69	selectin P	Homo sapiens	129-139
19440925-8	2009	In healthy volunteers clopidogrel ex vivo and cangrelor in vitro markedly inhibited P-selectin expression induced by ADP/U4.	clopidogrel	22-33	selectin P	Homo sapiens	84-94
19440925-17	2009	It is concluded that measurements of P-selectin performed on fixed blood samples following platelet stimulation in whole blood in a remote setting can be used effectively to monitor the effects of clopidogrel and aspirin.	clopidogrel	197-208	selectin P	Homo sapiens	37-47
19232433-9	2009	Moreover, the P2Y(12)-receptor inhibition by in vivo clopidogrel correlated with the inhibition by in vitro ARMX measured prior to administration of clopidogrel.	clopidogrel	53-64	purinergic receptor P2Y12	Homo sapiens	14-21
19232433-9	2009	Moreover, the P2Y(12)-receptor inhibition by in vivo clopidogrel correlated with the inhibition by in vitro ARMX measured prior to administration of clopidogrel.	clopidogrel	149-160	purinergic receptor P2Y12	Homo sapiens	14-21
19232433-12	2009	Non-responders to clopidogrel had decreased responses also to another ADP receptor antagonist, which suggests that the impaired response occurs at the level of P2Y(12)-receptor.	clopidogrel	18-29	purinergic receptor P2Y12	Homo sapiens	160-167
19414633-1	2009	BACKGROUND: Both clopidogrel and prasugrel require biotransformation to active metabolites by cytochrome P450 (CYP) enzymes.	clopidogrel	17-28	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	94-109
19414633-1	2009	BACKGROUND: Both clopidogrel and prasugrel require biotransformation to active metabolites by cytochrome P450 (CYP) enzymes.	clopidogrel	17-28	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	111-114
19414633-2	2009	Among persons treated with clopidogrel, carriers of reduced-function CYP2C19 alleles have significantly lower levels of active metabolite, diminished platelet inhibition, and higher rates of adverse cardiovascular events.	clopidogrel	27-38	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	69-76
19419580-0	2009	Comparison of VerifyNow-P2Y12 test and Flow Cytometry for monitoring individual platelet response to clopidogrel.	clopidogrel	101-112	purinergic receptor P2Y12	Homo sapiens	24-29
19193675-1	2009	AIMS: Several studies have demonstrated that the mutant *2 allele of the CYP2C19 681G>A loss-of-function polymorphism is associated with diminished metabolization of clopidogrel into its active thiol metabolite and an attenuated platelet response to clopidogrel treatment.	clopidogrel	166-177	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	73-80
18485500-1	2009	BACKGROUND: Platelet hyperreactivity was reported in clopidogrel-naiotave carriers of the H2 haplotype of the P2Y(12) platelet ADP receptor.	clopidogrel	53-64	purinergic receptor P2Y12	Homo sapiens	110-139
19358940-2	2009	BACKGROUND: Cigarette smoking induces cytochrome P450 (CYP)1A2, which converts clopidogrel into its active metabolite, and prior studies suggest greater inhibition of platelet aggregation by clopidogrel in smokers of &gt; or =10 cigarettes/day.	clopidogrel	79-90	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	38-62
19358940-2	2009	BACKGROUND: Cigarette smoking induces cytochrome P450 (CYP)1A2, which converts clopidogrel into its active metabolite, and prior studies suggest greater inhibition of platelet aggregation by clopidogrel in smokers of &gt; or =10 cigarettes/day.	clopidogrel	191-202	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	38-62
19253920-2	2009	Previous studies have suggested that some statins may inhibit the antiplatelet effects of clopidogrel via competitive metabolism of its activating enzyme cytochrome P450 3A4 (CYP3A4).	clopidogrel	90-101	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	154-173
19253920-2	2009	Previous studies have suggested that some statins may inhibit the antiplatelet effects of clopidogrel via competitive metabolism of its activating enzyme cytochrome P450 3A4 (CYP3A4).	clopidogrel	90-101	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	175-181
19253920-11	2009	CONCLUSIONS: In this PCI cohort, the association of clopidogrel with CYP3A4-metabolized statins did not demonstrate an increased early risk of adverse cardiovascular events, although a small risk could not be completely excluded.	clopidogrel	52-63	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	69-75
19193675-1	2009	AIMS: Several studies have demonstrated that the mutant *2 allele of the CYP2C19 681G>A loss-of-function polymorphism is associated with diminished metabolization of clopidogrel into its active thiol metabolite and an attenuated platelet response to clopidogrel treatment.	clopidogrel	250-261	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	73-80
19193675-3	2009	The aim of this study was to assess the impact of the CYP2C19 681G>A loss-of-function polymorphism on ST following PCI performed after pre-treatment with clopidogrel.	clopidogrel	154-165	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	54-61
19074527-5	2009	Likewise, K262R showed 2-, 4-, and &gt;20-fold higher K(s) values than CYP2B6dH with clopidogrel, sertraline, and itraconazole, respectively.	clopidogrel	85-96	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	71-77
19260946-0	2009	Long-term clopidogrel administration following severe coronary injury reduces proliferation and inflammation via inhibition of nuclear factor-kappaB and activator protein 1 activation in pigs.	clopidogrel	10-21	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	153-172
19337788-0	2009	Frequency of CYP3A4, CYP3A5, CYP2C9, and CYP2C19 variant alleles in patients receiving clopidogrel that experience repeat acute coronary syndrome.	clopidogrel	87-98	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	13-19
19337788-0	2009	Frequency of CYP3A4, CYP3A5, CYP2C9, and CYP2C19 variant alleles in patients receiving clopidogrel that experience repeat acute coronary syndrome.	clopidogrel	87-98	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	21-27
19337788-0	2009	Frequency of CYP3A4, CYP3A5, CYP2C9, and CYP2C19 variant alleles in patients receiving clopidogrel that experience repeat acute coronary syndrome.	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
19337788-0	2009	Frequency of CYP3A4, CYP3A5, CYP2C9, and CYP2C19 variant alleles in patients receiving clopidogrel that experience repeat acute coronary syndrome.	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	41-48
19337788-1	2009	The presence of cytochrome P450 (CYP) variant alleles may reduce the activation of the prodrug clopidogrel to its active state.	clopidogrel	95-106	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	16-31
19337788-1	2009	The presence of cytochrome P450 (CYP) variant alleles may reduce the activation of the prodrug clopidogrel to its active state.	clopidogrel	95-106	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	33-36
19337788-2	2009	This research evaluated the frequency of variant alleles in the genes coding for CYP3A4, CYP3A5, CYP2C9, and CYP2C19 enzymes in patients on clopidogrel therapy and experiencing repeat acute coronary syndrome (ACS) compared to a control group with a matching ethnic composition.	clopidogrel	140-151	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	81-87
19337788-2	2009	This research evaluated the frequency of variant alleles in the genes coding for CYP3A4, CYP3A5, CYP2C9, and CYP2C19 enzymes in patients on clopidogrel therapy and experiencing repeat acute coronary syndrome (ACS) compared to a control group with a matching ethnic composition.	clopidogrel	140-151	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	89-95
19337788-2	2009	This research evaluated the frequency of variant alleles in the genes coding for CYP3A4, CYP3A5, CYP2C9, and CYP2C19 enzymes in patients on clopidogrel therapy and experiencing repeat acute coronary syndrome (ACS) compared to a control group with a matching ethnic composition.	clopidogrel	140-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
19337788-2	2009	This research evaluated the frequency of variant alleles in the genes coding for CYP3A4, CYP3A5, CYP2C9, and CYP2C19 enzymes in patients on clopidogrel therapy and experiencing repeat acute coronary syndrome (ACS) compared to a control group with a matching ethnic composition.	clopidogrel	140-151	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	109-116
19280520-2	2009	Prasugrel is rapidly hydrolysed by esterases to its thiolactone intermediate, while clopidogrel is oxidized by cytochrome P450 (CYP) isoforms to its thiolactone.	clopidogrel	84-95	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	111-126
19280520-2	2009	Prasugrel is rapidly hydrolysed by esterases to its thiolactone intermediate, while clopidogrel is oxidized by cytochrome P450 (CYP) isoforms to its thiolactone.	clopidogrel	84-95	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	128-131
19236702-5	2009	After clopidogrel, there was a significant increase in platelet aggregation for 5 and 20 muM ADP at 33  C compared to 37  C (46 +- 5 vs. 34 +- 5% and 58 +- 4 vs. 47 +- 4%, p &lt; 0.001, n = 8).	clopidogrel	6-17	latexin	Homo sapiens	89-92
19334620-1	2009	The key role in platelet aggregation is played by the platelet ADP receptor P2Y12, which is the target for antiaggregant drugs, clopidogrel and ticlopidine.	clopidogrel	128-139	purinergic receptor P2Y12	Homo sapiens	76-81
18801777-1	2009	OBJECTIVE: To assess the prognostic value of the baseline C-reactive protein (CRP) level in patients undergoing percutaneous coronary intervention (PCI) after pre-treatment with 600 mg of clopidogrel and whether there is an interaction between CRP level and abciximab in terms of outcome.	clopidogrel	188-199	C-reactive protein	Homo sapiens	58-76
19047469-0	2009	Mechanism-based inhibition of human cytochrome P450 2B6 by ticlopidine, clopidogrel, and the thiolactone metabolite of prasugrel.	clopidogrel	72-83	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	36-55
19047469-1	2009	Mechanism-based inhibition of CYP2B6 in human liver microsomes by thienopyridine antiplatelet agents ticlopidine and clopidogrel and the thiolactone metabolites of those two agents plus that of prasugrel were investigated by determining the time- and concentration-dependent inhibition of the activity of bupropion hydroxylase as the typical CYP2B6 activity.	clopidogrel	117-128	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	30-36
19047469-4	2009	In conclusion, ticlopidine, its thiolactone metabolite, and clopidogrel were more potent mechanism-based inhibitors of CYP2B6 than the thiolactone metabolite of prasugrel.	clopidogrel	60-71	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	119-125
19249429-0	2009	Assessment of P2Y(12) inhibition with the point-of-care device VerifyNow P2Y12 in patients treated with prasugrel or clopidogrel coadministered with aspirin.	clopidogrel	117-128	purinergic receptor P2Y12	Homo sapiens	73-78
19249429-9	2009	Correlation was also observed between exposure to clopidogrel"s active metabolite and VN-P2Y12 during MD and LD, whereas it was observed only with prasugrel MD.	clopidogrel	50-61	purinergic receptor P2Y12	Homo sapiens	89-94
19249429-11	2009	VN-P2Y12 also correlated to exposure to the active metabolite of prasugrel and clopidogrel up to levels associated with assumed saturation of the P2Y(12) receptor.	clopidogrel	79-90	purinergic receptor P2Y12	Homo sapiens	3-8
18801777-11	2009	CONCLUSION: In patients with CAD undergoing PCI after pretreatment with 600 mg of clopidogrel, baseline CRP level predicts one-year mortality and MACE.	clopidogrel	82-93	C-reactive protein	Homo sapiens	104-107
19118249-10	2009	CONCLUSIONS: RPR to ADP with clopidogrel therapy, measured by the point-of-care assay VerifyNow P2Y12, is able to detect acute coronary syndrome patients at risk of 12-month cardiovascular death and nonfatal MI.	clopidogrel	29-40	purinergic receptor P2Y12	Homo sapiens	96-101
19172522-11	2009	Using DNA microarray technology, we could show that clopidogrel suppressed endotoxin-induced up-regulation of inflammation-relevant genes, including arachidonate-5-lipoxygenase activating protein and leukotriene B4 receptor 1.	clopidogrel	52-63	leukotriene B4 receptor	Homo sapiens	200-225
19180126-3	2009	Ironically, use of anti-platelet agents, the thienopyridine derivates clopidogrel and ticlopidine, is associated with drug induced TTP.	clopidogrel	70-81	ZFP36 ring finger protein	Homo sapiens	131-134
19180126-5	2009	Ticlopidine and clopidogrel are the two most common drugs associated with TTP in FDA safety databases.	clopidogrel	16-27	ZFP36 ring finger protein	Homo sapiens	74-77
19108880-0	2009	Cytochrome P450 2C19 polymorphism in young patients treated with clopidogrel after myocardial infarction: a cohort study.	clopidogrel	65-76	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-20
19108880-2	2009	The frequent genetic functional variant 681 G&gt;A (*2) of cytochrome P450 2C19 (CYP2C19) is an important contributor to the wide variability between individuals of the antiplatelet effect of clopidogrel.	clopidogrel	192-203	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	59-79
19108880-2	2009	The frequent genetic functional variant 681 G&gt;A (*2) of cytochrome P450 2C19 (CYP2C19) is an important contributor to the wide variability between individuals of the antiplatelet effect of clopidogrel.	clopidogrel	192-203	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	81-88
19108880-3	2009	We assessed whether the CYP2C19*2 polymorphism affected long-term prognosis of patients who were chronically treated with clopidogrel.	clopidogrel	122-133	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
19108880-11	2009	The detrimental effect of the CYP2C19*2 genetic variant persisted from 6 months after clopidogrel initiation up to the end of follow-up (HR 3.00 [1.27-7.10], p=0.009).	clopidogrel	86-97	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
19108880-13	2009	INTERPRETATION: The CYP2C19*2 genetic variant is a major determinant of prognosis in young patients who are receiving clopidogrel treatment after myocardial infarction.	clopidogrel	118-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	20-27
19081411-3	2009	METHODS: Responsiveness to clopidogrel was assessed by the vasodilator-stimulated phosphoprotein phosphorylation (VASP) assay and aggregometry (Multiplate Analyzer) in 300 patients with coronary artery disease (CAD) undergoing percutaneous coronary intervention (PCI).	clopidogrel	27-38	vasodilator stimulated phosphoprotein	Homo sapiens	59-112
19106083-10	2009	CONCLUSIONS: Among patients with an acute myocardial infarction who were receiving clopidogrel, those carrying CYP2C19 loss-of-function alleles had a higher rate of subsequent cardiovascular events than those who were not.	clopidogrel	83-94	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	111-118
19106084-1	2009	BACKGROUND: Clopidogrel requires transformation into an active metabolite by cytochrome P-450 (CYP) enzymes for its antiplatelet effect.	clopidogrel	12-23	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	77-93
19106084-1	2009	BACKGROUND: Clopidogrel requires transformation into an active metabolite by cytochrome P-450 (CYP) enzymes for its antiplatelet effect.	clopidogrel	12-23	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	95-98
19106084-3	2009	METHODS: We tested the association between functional genetic variants in CYP genes, plasma concentrations of active drug metabolite, and platelet inhibition in response to clopidogrel in 162 healthy subjects.	clopidogrel	173-184	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	74-77
19106084-5	2009	RESULTS: In healthy subjects who were treated with clopidogrel, carriers of at least one CYP2C19 reduced-function allele (approximately 30% of the study population) had a relative reduction of 32.4% in plasma exposure to the active metabolite of clopidogrel, as compared with noncarriers (P&lt;0.001).	clopidogrel	51-62	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	89-96
19106084-5	2009	RESULTS: In healthy subjects who were treated with clopidogrel, carriers of at least one CYP2C19 reduced-function allele (approximately 30% of the study population) had a relative reduction of 32.4% in plasma exposure to the active metabolite of clopidogrel, as compared with noncarriers (P&lt;0.001).	clopidogrel	246-257	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	89-96
19106084-8	2009	CONCLUSIONS: Among persons treated with clopidogrel, carriers of a reduced-function CYP2C19 allele had significantly lower levels of the active metabolite of clopidogrel, diminished platelet inhibition, and a higher rate of major adverse cardiovascular events, including stent thrombosis, than did noncarriers.	clopidogrel	40-51	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	84-91
19106084-8	2009	CONCLUSIONS: Among persons treated with clopidogrel, carriers of a reduced-function CYP2C19 allele had significantly lower levels of the active metabolite of clopidogrel, diminished platelet inhibition, and a higher rate of major adverse cardiovascular events, including stent thrombosis, than did noncarriers.	clopidogrel	158-169	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	84-91
19081411-1	2009	BACKGROUND: Clopidogrel is activated by CYP2C19, which also metabolizes proton pump inhibitors (PPI).	clopidogrel	12-23	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-47
19537521-2	2009	This debate has been invigorated by reports suggesting the ability of inhibitors of the cytochrome P450 isoenzyme, CYP 2C19, to interfere with clopidogrel efficacy.	clopidogrel	143-154	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	115-123
19537521-5	2009	In a two-step sequence, both crucially dependent on the function of CYP 2C19, about 15% of a given dose of clopidogrel are converted into an active metabolite.	clopidogrel	107-118	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	68-76
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	clopidogrel	57-68	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	102-124
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	clopidogrel	57-68	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	126-131
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	clopidogrel	57-68	glycoprotein Ib platelet subunit alpha	Homo sapiens	133-159
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	clopidogrel	57-68	multimerin 1	Homo sapiens	161-166
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	clopidogrel	57-68	integrin subunit alpha 2b	Homo sapiens	172-178
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	clopidogrel	57-68	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	185-191
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	clopidogrel	57-68	purinergic receptor P2Y1	Homo sapiens	195-201
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	clopidogrel	57-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-218
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	clopidogrel	57-68	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	220-226
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	clopidogrel	57-68	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	231-237
19155974-7	2009	RESULTS: Treatment with clopidogrel resulted in significantly decreased blood concentrations of sCD40L and P-selectin after transplantation.	clopidogrel	24-35	selectin, platelet	Mus musculus	107-117
19155974-10	2009	Intragraft mRNA expression confirmed these results and showed significant lower production of P-/E-selectin, ICAM-1, and PDGF-beta after treatment with clopidogrel.	clopidogrel	152-163	intercellular adhesion molecule 1	Mus musculus	109-115
19155974-10	2009	Intragraft mRNA expression confirmed these results and showed significant lower production of P-/E-selectin, ICAM-1, and PDGF-beta after treatment with clopidogrel.	clopidogrel	152-163	platelet derived growth factor, B polypeptide	Mus musculus	121-130
19729693-9	2009	Response to aspirin and clopidogrel was assessed by interaction with collagen (2microg/ml) and Adenosine diphosphate (ADP) (10micro/ml) respectively.	clopidogrel	24-35	WD and tetratricopeptide repeats 1	Homo sapiens	95-122
18049795-3	2009	Treatment with clopidogrel 600 mg significantly reduced P-selectin expression in comparison with tirofiban alone at all time points (group B vs. A: P &lt; 0.0001).	clopidogrel	15-26	selectin P	Homo sapiens	56-66
18049795-7	2009	The addition of clopidogrel to tirofiban does not add any anti-aggregatory effect, but reduces P-selectin expression, thus likely adding a significant biological and clinical protective effect and providing a rationale for the combined use of the two drugs.	clopidogrel	16-27	selectin P	Homo sapiens	95-105
19463124-3	2009	In a series of articles the authors consider clinical pharmacology and experience of clinical application of blockers of platelet P2Y12 receptors, most well known representatives of which ticlopidine and clopidogrel according to chemical structure belong to thienopyridine derivatives.	clopidogrel	204-215	purinergic receptor P2Y12	Homo sapiens	130-135
19845526-3	2009	In a series of articles the authors consider clinical pharmacology and experience of clinical application of blockers of platelet P2Y12 receptors, most well known representatives of which ticlopidine and clopidogrel according to chemical structure belong to thienopyridine derivatives.	clopidogrel	204-215	purinergic receptor P2Y12	Homo sapiens	130-135
19845526-5	2009	We discuss results of randomized studies and clinical observations which have shown that pharmacokinetics of clopidogrel might vary substantially in dependence of polymorphisms of genes responsible for synthesis of P2Y12 receptors of platelets or cytochromic isoenzymes P-450 CYP of liver with participation of which formation of active metabolite of clopidogrel occurs.	clopidogrel	109-120	purinergic receptor P2Y12	Homo sapiens	215-220
19845526-5	2009	We discuss results of randomized studies and clinical observations which have shown that pharmacokinetics of clopidogrel might vary substantially in dependence of polymorphisms of genes responsible for synthesis of P2Y12 receptors of platelets or cytochromic isoenzymes P-450 CYP of liver with participation of which formation of active metabolite of clopidogrel occurs.	clopidogrel	351-362	purinergic receptor P2Y12	Homo sapiens	215-220
20038285-3	2009	In a series of articles the authors consider clinical pharmacology and experience of clinical application of blockers of platelet P2Y12 receptors, most well known representatives of which ticlopidine and clopidogrel according to chemical structure belong to thienopyridine derivatives.	clopidogrel	204-215	purinergic receptor P2Y12	Homo sapiens	130-135
20038286-3	2009	In a series of articles the authors consider clinical pharmacology and experience of clinical application of blockers of platelet P2Y12 receptors, most well known representatives of which ticlopidine and clopidogrel according to chemical structure belong to thienopyridine derivatives.	clopidogrel	204-215	purinergic receptor P2Y12	Homo sapiens	130-135
19081411-3	2009	METHODS: Responsiveness to clopidogrel was assessed by the vasodilator-stimulated phosphoprotein phosphorylation (VASP) assay and aggregometry (Multiplate Analyzer) in 300 patients with coronary artery disease (CAD) undergoing percutaneous coronary intervention (PCI).	clopidogrel	27-38	vasodilator stimulated phosphoprotein	Homo sapiens	114-118
19101221-6	2009	In the VASP-guided group, patients received up to 3 additional 600-mg LDs of clopidogrel to obtain a VASP index &lt;50% before PCI.	clopidogrel	77-88	vasodilator stimulated phosphoprotein	Homo sapiens	7-11
19101221-6	2009	In the VASP-guided group, patients received up to 3 additional 600-mg LDs of clopidogrel to obtain a VASP index &lt;50% before PCI.	clopidogrel	77-88	vasodilator stimulated phosphoprotein	Homo sapiens	101-105
19101221-11	2009	Despite a 2,400-mg LD of clopidogrel, 8% of patients in the VASP-guided group remained low responders.	clopidogrel	25-36	vasodilator stimulated phosphoprotein	Homo sapiens	60-64
19475783-4	2009	To overcome these shortcomings of clopidogrel, new more potent inhibitors of P2Y12 receptors, which have a more rapid onset of action have been introduced for clinical evaluation.	clopidogrel	34-45	purinergic receptor P2Y12	Homo sapiens	77-82
19034031-10	2008	Clopidogrel significantly lowered the convulxin, thrombin plus ADP coated-platelet production (11.0% AR; 20.1% RR for 1.5 microM and 11.2% AR; 19.1% RR for 6 microM).	clopidogrel	0-11	coagulation factor II, thrombin	Homo sapiens	49-57
19463375-2	2008	BACKGROUND: Variability in clopidogrel response might be influenced by polymorphisms in genes coding for drug metabolism enzymes (cytochrome P450 [CYP] family), transport proteins (P-glycoprotein) and/or target proteins for the drug (adenosine diphosphate-receptor P2Y12).	clopidogrel	27-38	purinergic receptor P2Y12	Homo sapiens	265-270
19463379-8	2008	CONCLUSIONS: The present study suggested benefit of tailored antiplatelet therapy during elective PCI with GP IIb/IIIa antagonist for clopidogrel nonresponders without increased bleeding risk.	clopidogrel	134-145	integrin subunit alpha 2b	Homo sapiens	107-113
18781853-0	2008	CYP2C19 and nongenetic factors predict poor responsiveness to clopidogrel loading dose after coronary stent implantation.	clopidogrel	62-73	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
20069077-8	2009	Data from this study suggest that clopidogrel can decrease the expression of the CD40-ligand biomarker.	clopidogrel	34-45	CD40 ligand	Homo sapiens	81-92
18848137-0	2008	Elevated plasma fibrinogen and diabetes mellitus are associated with lower inhibition of platelet reactivity with clopidogrel.	clopidogrel	114-125	fibrinogen beta chain	Homo sapiens	16-26
18848137-9	2008	CONCLUSIONS: Elevated plasma fibrinogen (&gt; or =375 mg/dl) in the presence of diabetes mellitus and increased BMI (&gt; or =25 kg/m(2)) are associated with lower PI with clopidogrel in patients with CVD.	clopidogrel	172-183	fibrinogen beta chain	Homo sapiens	29-39
20069077-5	2009	There was a significant difference at Week 6 in model-adjusted CD40-ligand levels in favor of clopidogrel plus aspirin compared with placebo plus aspirin in both the intent-to-treat population (difference between least-squares means = -186.5; 95% confidence interval, -342.3 to -30.8; P = 0.02) and the per-protocol population (P = 0.05).	clopidogrel	94-105	CD40 ligand	Homo sapiens	63-74
19007592-1	2008	OBJECTIVES: Because of the known CYP3A4 inhibition by calcium-channel blockers (CCBs), we hypothesized that there might be a drug-drug interaction between clopidogrel and dihydropyridines in patients with coronary artery disease.	clopidogrel	155-166	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	33-39
19007592-2	2008	BACKGROUND: Clopidogrel is activated by CYP3A4, which also metabolizes CCBs of the dihydropyridine class.	clopidogrel	12-23	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	40-46
19007592-3	2008	METHODS: Responsiveness to clopidogrel was assessed by the vasodilator-stimulated phosphoprotein (VASP) phosphorylation assay and aggregometry in 200 patients with coronary artery disease undergoing percutaneous coronary intervention.	clopidogrel	27-38	vasodilator stimulated phosphoprotein	Homo sapiens	59-96
19007592-3	2008	METHODS: Responsiveness to clopidogrel was assessed by the vasodilator-stimulated phosphoprotein (VASP) phosphorylation assay and aggregometry in 200 patients with coronary artery disease undergoing percutaneous coronary intervention.	clopidogrel	27-38	vasodilator stimulated phosphoprotein	Homo sapiens	98-102
19007592-4	2008	RESULTS: The platelet reactivity index (PRI) (in the VASP assay, normal range 69% to 100%) was higher in patients receiving both clopidogrel and CCBs (61%) as compared with patients receiving clopidogrel without CCBs (48%).	clopidogrel	129-140	vasodilator stimulated phosphoprotein	Homo sapiens	53-57
19059569-2	2008	Assessing the phosphorylation of intraplatelet vasodilator-stimulated phosphoprotein (VASP) is an easy and reliable method of evaluating biological response to clopidogrel.	clopidogrel	160-171	vasodilator stimulated phosphoprotein	Homo sapiens	47-84
19059569-2	2008	Assessing the phosphorylation of intraplatelet vasodilator-stimulated phosphoprotein (VASP) is an easy and reliable method of evaluating biological response to clopidogrel.	clopidogrel	160-171	vasodilator stimulated phosphoprotein	Homo sapiens	86-90
19059569-5	2008	VASP index was calculated from the median fluorescence intensity (MFI) of samples incubated with prostaglandin E1 (PGE1) and adenosine diphosphate according to the formula [(MFI(PGE1)-MFI(PGE1-ADP))/MFI(PGE1)]x100, and was determined at baseline and at days 1 and 4 after starting clopidogrel.	clopidogrel	281-292	vasodilator stimulated phosphoprotein	Homo sapiens	0-4
19059569-11	2008	CONCLUSION: Assessment of VASP index in ACS patients identifies low responders to clopidogrel who are at increased risk of recurrent cardiovascular events.	clopidogrel	82-93	vasodilator stimulated phosphoprotein	Homo sapiens	26-30
18979368-1	2008	The platelet vasodilator-stimulated phosphoprotein (VASP) phosphorylation test is a new platelet function assay used to determine responsiveness to clopidogrel.	clopidogrel	148-159	vasodilator stimulated phosphoprotein	Homo sapiens	13-50
18979368-1	2008	The platelet vasodilator-stimulated phosphoprotein (VASP) phosphorylation test is a new platelet function assay used to determine responsiveness to clopidogrel.	clopidogrel	148-159	vasodilator stimulated phosphoprotein	Homo sapiens	52-56
18979368-4	2008	The VASP assay was performed in 280 patients on clopidogrel therapy and 35 volunteers without clopidogrel therapy.	clopidogrel	48-59	vasodilator stimulated phosphoprotein	Homo sapiens	4-8
18781853-1	2008	AIMS: To investigate an association of responsiveness to clopidogrel loading dose with genotypes of cytochrome P450 (CYP) 2C19, other CYP isozymes and nongenetic factors in patients with coronary artery disease.	clopidogrel	57-68	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	100-126
18781853-8	2008	CONCLUSIONS: Prediction of responsiveness after clopidogrel loading dose may substantially be improved by adding CYP2C19*2 genotype to nongenetic risk factors.	clopidogrel	48-59	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	113-120
18489507-10	2008	CONCLUSIONS: The use of GPIIb/IIIa inhibitors upstream in high-risk NSTE-ACS patients (TIMI score &gt; or = 3) pretreated with aspirin and clopidogrel is cost-effective, particularly in the younger age groups.	clopidogrel	139-150	integrin subunit alpha 2b	Homo sapiens	24-29
18577829-0	2008	Coexisting polymorphisms of P2Y12 and CYP2C19 genes as a risk factor for persistent platelet activation with clopidogrel.	clopidogrel	109-120	purinergic receptor P2Y12	Homo sapiens	28-33
18687246-3	2008	Clopidogrel is metabolically activated by several hepatic cytochrome P450 (CYP) isoenzymes, including CYP1A2.	clopidogrel	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	58-73
18687246-3	2008	Clopidogrel is metabolically activated by several hepatic cytochrome P450 (CYP) isoenzymes, including CYP1A2.	clopidogrel	0-11	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	75-78
18687246-3	2008	Clopidogrel is metabolically activated by several hepatic cytochrome P450 (CYP) isoenzymes, including CYP1A2.	clopidogrel	0-11	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	102-108
18687246-4	2008	Cigarette smoking induces CYP1A2 and may, therefore, enhance the conversion of clopidogrel to its active metabolite.	clopidogrel	79-90	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	26-32
18687246-10	2008	RESULTS: Current smokers on chronic clopidogrel therapy displayed significantly lower PA and ADP-stimulated active GP IIb/IIIa expression compared with NS (p &lt; or = 0.0008 for both).	clopidogrel	36-47	integrin subunit alpha 2b	Homo sapiens	115-121
18687246-11	2008	Similarly, CS treated with 600 mg of clopidogrel displayed greater platelet inhibition and lower active GP IIb/IIIa expression compared with NS (p &lt; or = 0.05).	clopidogrel	37-48	integrin subunit alpha 2b	Homo sapiens	104-110
18346178-0	2008	Inhibition of ADP-induced platelet aggregation by clopidogrel is related to CYP2C19 genetic polymorphisms.	clopidogrel	50-61	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	76-83
18346178-3	2008	The aim of the present study was to evaluate the contribution of CYP2C19 genetic polymorphisms to the inhibition of ADP-induced platelet aggregation by clopidogrel in healthy Chinese volunteers.	clopidogrel	152-163	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	65-72
18346178-9	2008	There were significant decrease in 2 and 5 micromol/L ADP-induced platelet aggregation at 4, 24 and 72 h after clopidogrel among the three CYP2C19 genotypes compared with baseline (P &lt; 0.001).	clopidogrel	111-122	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	139-146
18346178-10	2008	The change in 5 micromol/L ADP-induced platelet aggregation in subjects with the CYP2C19*1/CYP2C19*1 genotype was greater than that in subjects with the CYP2C19*2/CYP2C19*2and*3 genotype at 4 h (49.0 +/- 15.5 vs 29.7 +/- 17.4%, respectively; P = 0.029), 24 h (48.7 +/- 20.5 vs 25.0 +/- 17.6%, respectively; P = 0.035) and 72 h (45.5 +/- 15.2 vs 26.5 +/- 15.8%, respectively; P = 0.030) after clopidogrel administration.	clopidogrel	392-403	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	81-88
18346178-10	2008	The change in 5 micromol/L ADP-induced platelet aggregation in subjects with the CYP2C19*1/CYP2C19*1 genotype was greater than that in subjects with the CYP2C19*2/CYP2C19*2and*3 genotype at 4 h (49.0 +/- 15.5 vs 29.7 +/- 17.4%, respectively; P = 0.029), 24 h (48.7 +/- 20.5 vs 25.0 +/- 17.6%, respectively; P = 0.035) and 72 h (45.5 +/- 15.2 vs 26.5 +/- 15.8%, respectively; P = 0.030) after clopidogrel administration.	clopidogrel	392-403	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	91-98
18346178-10	2008	The change in 5 micromol/L ADP-induced platelet aggregation in subjects with the CYP2C19*1/CYP2C19*1 genotype was greater than that in subjects with the CYP2C19*2/CYP2C19*2and*3 genotype at 4 h (49.0 +/- 15.5 vs 29.7 +/- 17.4%, respectively; P = 0.029), 24 h (48.7 +/- 20.5 vs 25.0 +/- 17.6%, respectively; P = 0.035) and 72 h (45.5 +/- 15.2 vs 26.5 +/- 15.8%, respectively; P = 0.030) after clopidogrel administration.	clopidogrel	392-403	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	91-98
18346178-10	2008	The change in 5 micromol/L ADP-induced platelet aggregation in subjects with the CYP2C19*1/CYP2C19*1 genotype was greater than that in subjects with the CYP2C19*2/CYP2C19*2and*3 genotype at 4 h (49.0 +/- 15.5 vs 29.7 +/- 17.4%, respectively; P = 0.029), 24 h (48.7 +/- 20.5 vs 25.0 +/- 17.6%, respectively; P = 0.035) and 72 h (45.5 +/- 15.2 vs 26.5 +/- 15.8%, respectively; P = 0.030) after clopidogrel administration.	clopidogrel	392-403	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	91-98
18346178-12	2008	In conclusion, CYP2C19*2 and CYP2C19*3 genetic polymorphisms reduced clopidogrel inhibition of ADP-induced platelet aggregation, with the degree of inhition dependent on the genetic polymorphism present.	clopidogrel	69-80	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22
18346178-12	2008	In conclusion, CYP2C19*2 and CYP2C19*3 genetic polymorphisms reduced clopidogrel inhibition of ADP-induced platelet aggregation, with the degree of inhition dependent on the genetic polymorphism present.	clopidogrel	69-80	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	29-36
18690336-3	2008	As compared to unfractionated heparin (UFH), among patients treated with thrombolysis, low-molecular-weight heparins (LMWHs), mainly enoxaparin, fondaparinux and clopidogrel have been shown to improve outcome in terms of death and reinfarction, whereas GP IIb-IIIa inhibitors, mainly abciximab, and direct thrombin inhibitors have reduced reinfarction, but not mortality.	clopidogrel	162-173	coagulation factor II, thrombin	Homo sapiens	306-314
18474675-2	2008	Mechanism-based CYP2B6 inhibitors (i.e., clopidogrel, ticlopidine, and triethylenethiophoramide) significantly inhibited the formation of M1 from sibutramine and M2 from M1, respectively; in contrast, no effect was observed when using potent inhibitors of eight P450 isozymes (CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A).	clopidogrel	41-52	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	16-22
18474675-2	2008	Mechanism-based CYP2B6 inhibitors (i.e., clopidogrel, ticlopidine, and triethylenethiophoramide) significantly inhibited the formation of M1 from sibutramine and M2 from M1, respectively; in contrast, no effect was observed when using potent inhibitors of eight P450 isozymes (CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A).	clopidogrel	41-52	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	277-283
18474675-2	2008	Mechanism-based CYP2B6 inhibitors (i.e., clopidogrel, ticlopidine, and triethylenethiophoramide) significantly inhibited the formation of M1 from sibutramine and M2 from M1, respectively; in contrast, no effect was observed when using potent inhibitors of eight P450 isozymes (CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A).	clopidogrel	41-52	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	285-291
18474675-2	2008	Mechanism-based CYP2B6 inhibitors (i.e., clopidogrel, ticlopidine, and triethylenethiophoramide) significantly inhibited the formation of M1 from sibutramine and M2 from M1, respectively; in contrast, no effect was observed when using potent inhibitors of eight P450 isozymes (CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A).	clopidogrel	41-52	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	293-299
18474675-2	2008	Mechanism-based CYP2B6 inhibitors (i.e., clopidogrel, ticlopidine, and triethylenethiophoramide) significantly inhibited the formation of M1 from sibutramine and M2 from M1, respectively; in contrast, no effect was observed when using potent inhibitors of eight P450 isozymes (CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A).	clopidogrel	41-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	301-307
18474675-2	2008	Mechanism-based CYP2B6 inhibitors (i.e., clopidogrel, ticlopidine, and triethylenethiophoramide) significantly inhibited the formation of M1 from sibutramine and M2 from M1, respectively; in contrast, no effect was observed when using potent inhibitors of eight P450 isozymes (CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A).	clopidogrel	41-52	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	309-316
18474675-2	2008	Mechanism-based CYP2B6 inhibitors (i.e., clopidogrel, ticlopidine, and triethylenethiophoramide) significantly inhibited the formation of M1 from sibutramine and M2 from M1, respectively; in contrast, no effect was observed when using potent inhibitors of eight P450 isozymes (CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A).	clopidogrel	41-52	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	318-324
18474675-2	2008	Mechanism-based CYP2B6 inhibitors (i.e., clopidogrel, ticlopidine, and triethylenethiophoramide) significantly inhibited the formation of M1 from sibutramine and M2 from M1, respectively; in contrast, no effect was observed when using potent inhibitors of eight P450 isozymes (CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A).	clopidogrel	41-52	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	326-332
18474675-2	2008	Mechanism-based CYP2B6 inhibitors (i.e., clopidogrel, ticlopidine, and triethylenethiophoramide) significantly inhibited the formation of M1 from sibutramine and M2 from M1, respectively; in contrast, no effect was observed when using potent inhibitors of eight P450 isozymes (CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A).	clopidogrel	41-52	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	338-343
19110786-4	2008	In patients with RPA &lt; or = 14%, who continued on 75 mg clopidogrel, RPA increased during the first 14 days by 4.5% (0-14%; P&lt;0.001).	clopidogrel	59-70	replication protein A1	Homo sapiens	17-20
19110786-4	2008	In patients with RPA &lt; or = 14%, who continued on 75 mg clopidogrel, RPA increased during the first 14 days by 4.5% (0-14%; P&lt;0.001).	clopidogrel	59-70	replication protein A1	Homo sapiens	72-75
18577829-0	2008	Coexisting polymorphisms of P2Y12 and CYP2C19 genes as a risk factor for persistent platelet activation with clopidogrel.	clopidogrel	109-120	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	38-45
18611364-0	2008	Should Prasugrel or Clopidogrel Be Used in Patients with ACS?	clopidogrel	20-31	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	57-60
18485086-5	2008	METHODS: The effects of cangrelor and the active metabolites of clopidogrel (C-AM) and prasugrel (P-AM) on platelet function were assessed by ADP-induced platelet P-selectin expression in whole blood.	clopidogrel	64-75	selectin P	Homo sapiens	163-173
18520610-0	2008	Assessment of VerifyNow P2Y12 assay accuracy in evaluating clopidogrel-induced platelet inhibition.	clopidogrel	59-70	purinergic receptor P2Y12	Homo sapiens	24-29
18532997-0	2008	The common gene variants of CYP2C19 affect pharmacokinetics and pharmacodynamics in an active metabolite of clopidogrel in healthy subjects.	clopidogrel	108-119	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
18385991-0	2008	Effect of CYP3A5*3 genotype on the pharmacokinetics and antiplatelet effect of clopidogrel in healthy subjects.	clopidogrel	79-90	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	10-16
18385991-1	2008	OBJECTIVE: Clopidogrel is activated by cytochrome P450 3A (CYP3A) to generate an active metabolite that inhibits adenosine diphosphate (ADP)-induced platelet aggregation through irreversible binding to the platelet P2Y12 receptor.	clopidogrel	11-22	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	39-57
18385991-1	2008	OBJECTIVE: Clopidogrel is activated by cytochrome P450 3A (CYP3A) to generate an active metabolite that inhibits adenosine diphosphate (ADP)-induced platelet aggregation through irreversible binding to the platelet P2Y12 receptor.	clopidogrel	11-22	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	59-64
18385991-2	2008	The objective of this study was to assess the effect of the CYP3A5 genotype on the pharmacokinetics and antiplatelet effect of clopidogrel in healthy subjects.	clopidogrel	127-138	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	60-66
18385991-8	2008	CONCLUSION: The CYP3A5*3 genotype plays a minor role in causing interindividual variability of the disposition of clopidogrel and its antiplatelet effect in humans.	clopidogrel	114-125	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	16-22
18581073-18	2008	For clopidogrel, an increased platelet inhibition has been described with double dose (75 mg bid), but the clinical relevance is unknown.	clopidogrel	4-15	BH3 interacting domain death agonist	Homo sapiens	93-96
18581077-5	2008	Actual ACC/AHA/SCAI guidelines recommend the use of 75 mg clopidogrel once daily after stent implantation.	clopidogrel	58-69	suppressor of cancer cell invasion	Homo sapiens	15-19
18506123-21	2008	The favorable clinical outcomes with aspirin and clopidogrel have validated COX-1 and P2Y12 receptors as targets for new drug development.	clopidogrel	49-60	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	76-81
18506123-21	2008	The favorable clinical outcomes with aspirin and clopidogrel have validated COX-1 and P2Y12 receptors as targets for new drug development.	clopidogrel	49-60	purinergic receptor P2Y12	Homo sapiens	86-91
18549843-4	2008	Clopidogrel response was measured with P2Y12 reaction units (PRUs) and percent inhibition P2Y12 from baseline (percent inhibition P2Y12) and aspirin response with aspirin reaction units (ARUs).	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	39-44
18549843-4	2008	Clopidogrel response was measured with P2Y12 reaction units (PRUs) and percent inhibition P2Y12 from baseline (percent inhibition P2Y12) and aspirin response with aspirin reaction units (ARUs).	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	90-95
18549843-4	2008	Clopidogrel response was measured with P2Y12 reaction units (PRUs) and percent inhibition P2Y12 from baseline (percent inhibition P2Y12) and aspirin response with aspirin reaction units (ARUs).	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	90-95
18549843-9	2008	Stratification of percent inhibition P2Y12 isolated a quartile of clopidogrel nonresponders (inhibition P2Y12 &lt;15%) with significantly higher incidence of PMI (44% vs 15%, odds ratio 4.6, 95% confidence interval 1.9 to 11.5, p=0.001).	clopidogrel	66-77	purinergic receptor P2Y12	Homo sapiens	37-42
18549843-9	2008	Stratification of percent inhibition P2Y12 isolated a quartile of clopidogrel nonresponders (inhibition P2Y12 &lt;15%) with significantly higher incidence of PMI (44% vs 15%, odds ratio 4.6, 95% confidence interval 1.9 to 11.5, p=0.001).	clopidogrel	66-77	purinergic receptor P2Y12	Homo sapiens	104-109
18520610-2	2008	The aim of this study was to evaluate the ability of the VerifyNow P2Y12 assay to estimate the inhibition of platelet aggregation provided by clopidogrel in the absence of baseline off-drug aggregation data.	clopidogrel	142-153	purinergic receptor P2Y12	Homo sapiens	67-72
18520610-8	2008	Further studies are required to establish the clinical usefulness of the VerifyNow P2Y12 assay to accurately predict the occurrence of major adverse cardiovascular events in patients with reduced clopidogrel efficacy before it can be implemented in clinical practice.	clopidogrel	196-207	purinergic receptor P2Y12	Homo sapiens	83-88
18482659-1	2008	OBJECTIVES: We investigated whether the loss of function CYP2C19 681G&gt;A *2 polymorphism is associated with high (&gt;14%) residual platelet aggregation (RPA) on clopidogrel and whether high on-clopidogrel RPA impacts clinical outcome after elective coronary stent placement.	clopidogrel	164-175	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	57-64
18296509-7	2008	Microinjecting eggs with mutant-unphosphorylatable MARCKS reduced the intensity of 12-O-tetradecanoylphorbol 13-acetate or ionomycin-induced CGE by 50%, indicating that phosphorylation of MARCKS by novel and/or conventional PKCs (n/cPKCs) is a pivotal event associated with CGE.	clopidogrel	141-144	myristoylated alanine rich protein kinase C substrate	Homo sapiens	51-57
18296509-7	2008	Microinjecting eggs with mutant-unphosphorylatable MARCKS reduced the intensity of 12-O-tetradecanoylphorbol 13-acetate or ionomycin-induced CGE by 50%, indicating that phosphorylation of MARCKS by novel and/or conventional PKCs (n/cPKCs) is a pivotal event associated with CGE.	clopidogrel	141-144	myristoylated alanine rich protein kinase C substrate	Homo sapiens	188-194
18296509-7	2008	Microinjecting eggs with mutant-unphosphorylatable MARCKS reduced the intensity of 12-O-tetradecanoylphorbol 13-acetate or ionomycin-induced CGE by 50%, indicating that phosphorylation of MARCKS by novel and/or conventional PKCs (n/cPKCs) is a pivotal event associated with CGE.	clopidogrel	274-277	myristoylated alanine rich protein kinase C substrate	Homo sapiens	51-57
18296509-7	2008	Microinjecting eggs with mutant-unphosphorylatable MARCKS reduced the intensity of 12-O-tetradecanoylphorbol 13-acetate or ionomycin-induced CGE by 50%, indicating that phosphorylation of MARCKS by novel and/or conventional PKCs (n/cPKCs) is a pivotal event associated with CGE.	clopidogrel	274-277	myristoylated alanine rich protein kinase C substrate	Homo sapiens	188-194
18440347-1	2008	BACKGROUND: Clopidogrel is inactive in vitro and is metabolized by hepatic cytochrome P-450-3A4 to produce active metabolites.	clopidogrel	12-23	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	75-95
18482659-2	2008	BACKGROUND: The cytochrome P450 (CYP)-dependent conversion of clopidogrel to its active metabolite may contribute to the variability in antiplatelet effect of clopidogrel.	clopidogrel	62-73	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	16-31
18482659-2	2008	BACKGROUND: The cytochrome P450 (CYP)-dependent conversion of clopidogrel to its active metabolite may contribute to the variability in antiplatelet effect of clopidogrel.	clopidogrel	62-73	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	33-36
18482659-2	2008	BACKGROUND: The cytochrome P450 (CYP)-dependent conversion of clopidogrel to its active metabolite may contribute to the variability in antiplatelet effect of clopidogrel.	clopidogrel	159-170	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	16-31
18482659-2	2008	BACKGROUND: The cytochrome P450 (CYP)-dependent conversion of clopidogrel to its active metabolite may contribute to the variability in antiplatelet effect of clopidogrel.	clopidogrel	159-170	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	33-36
18482659-11	2008	CONCLUSIONS: Patients carrying at least one CYP2C19*2 allele are more prone to high-on clopidogrel platelet reactivity, which is associated with poor clinical outcome after coronary stent placement (Effect of Clopidogrel Loading and Risk of PCI [EXCELSIOR]; NCT00457236).	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	44-51
18482659-11	2008	CONCLUSIONS: Patients carrying at least one CYP2C19*2 allele are more prone to high-on clopidogrel platelet reactivity, which is associated with poor clinical outcome after coronary stent placement (Effect of Clopidogrel Loading and Risk of PCI [EXCELSIOR]; NCT00457236).	clopidogrel	209-220	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	44-51
18387444-0	2008	Adjusted clopidogrel loading doses according to vasodilator-stimulated phosphoprotein phosphorylation index decrease rate of major adverse cardiovascular events in patients with clopidogrel resistance: a multicenter randomized prospective study.	clopidogrel	9-20	vasodilator stimulated phosphoprotein	Homo sapiens	48-85
18387444-0	2008	Adjusted clopidogrel loading doses according to vasodilator-stimulated phosphoprotein phosphorylation index decrease rate of major adverse cardiovascular events in patients with clopidogrel resistance: a multicenter randomized prospective study.	clopidogrel	178-189	vasodilator stimulated phosphoprotein	Homo sapiens	48-85
18387444-1	2008	OBJECTIVES: This study evaluates the clinical impact of adjusting the loading dose of clopidogrel according to vasodilator-stimulated phosphoprotein (VASP) index in patients with clopidogrel resistance undergoing percutaneous coronary intervention (PCI).	clopidogrel	86-97	vasodilator stimulated phosphoprotein	Homo sapiens	111-148
18387444-1	2008	OBJECTIVES: This study evaluates the clinical impact of adjusting the loading dose of clopidogrel according to vasodilator-stimulated phosphoprotein (VASP) index in patients with clopidogrel resistance undergoing percutaneous coronary intervention (PCI).	clopidogrel	179-190	vasodilator stimulated phosphoprotein	Homo sapiens	111-148
18387444-1	2008	OBJECTIVES: This study evaluates the clinical impact of adjusting the loading dose of clopidogrel according to vasodilator-stimulated phosphoprotein (VASP) index in patients with clopidogrel resistance undergoing percutaneous coronary intervention (PCI).	clopidogrel	179-190	vasodilator stimulated phosphoprotein	Homo sapiens	150-154
18387444-4	2008	METHODS: In this prospective, randomized, multicenter study, clopidogrel resistance was defined as a VASP index of more than 50% after a 600-mg loading dose.	clopidogrel	61-72	vasodilator stimulated phosphoprotein	Homo sapiens	101-105
18387444-11	2008	CONCLUSIONS: This is the first study to suggest that adjusting the clopidogrel loading dose according to platelet monitoring using the VASP index is safe and may significantly improve the clinical outcome after PCI in patients with clopidogrel resistance despite a first 600-mg loading dose.	clopidogrel	67-78	vasodilator stimulated phosphoprotein	Homo sapiens	135-139
18387444-11	2008	CONCLUSIONS: This is the first study to suggest that adjusting the clopidogrel loading dose according to platelet monitoring using the VASP index is safe and may significantly improve the clinical outcome after PCI in patients with clopidogrel resistance despite a first 600-mg loading dose.	clopidogrel	232-243	vasodilator stimulated phosphoprotein	Homo sapiens	135-139
17995973-6	2008	* However, the observed variability of the platelet response to the cyclooxygenase inhibitor acetylsalicylic acid (in our study) and to the P2Y(12) ADP receptor blocker clopidogrel (in a study by Angiolillo et al) in patients with coronary artery disease is clearly not determined by common P2Y(12) ADP receptor polymorphisms.	clopidogrel	169-180	purinergic receptor P2Y12	Homo sapiens	140-147
17995973-6	2008	* However, the observed variability of the platelet response to the cyclooxygenase inhibitor acetylsalicylic acid (in our study) and to the P2Y(12) ADP receptor blocker clopidogrel (in a study by Angiolillo et al) in patients with coronary artery disease is clearly not determined by common P2Y(12) ADP receptor polymorphisms.	clopidogrel	169-180	purinergic receptor P2Y12	Homo sapiens	291-298
18458661-2	2008	However, the benefits of Gp IIb/IIIa inhibition in patients pretreated with clopidogrel are less clear.	clopidogrel	76-87	integrin subunit alpha 2b	Homo sapiens	25-31
18394438-5	2008	After covariate adjustment, the CYP2C19*2 allele was more frequent in clopidogrel nonresponders, defined by persistent high post-treatment platelet reactivity (ADP-induced platelet aggregation &gt;70%; p = 0.03).	clopidogrel	70-81	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
18174449-1	2008	The P2Y12 antagonist clopidogrel has a well-established role as an antithrombotic agent in the settings of percutaneous coronary intervention and acute coronary syndromes.	clopidogrel	21-32	purinergic receptor P2Y12	Homo sapiens	4-9
18481820-4	2008	There appears to be a relationship between the use of GP IIb/IIIa antagonists with clopidogrel loading and attenuation of early inflammatory and cardiac marker release.	clopidogrel	83-94	integrin subunit alpha 2b	Homo sapiens	54-60
17957565-5	2007	Large differences were demonstrated in both aspirin and clopidogrel groups in response to therapy as assessed by both the area under the curve at 15 minutes and %CIn.	clopidogrel	56-67	pyridoxal phosphatase	Homo sapiens	162-165
18232657-1	2008	Platelet P2Y12 receptors play a central role in the regulation of platelet function and inhibition of this receptor by treatment with drugs such as clopidogrel results in a reduction of atherothrombotic events.	clopidogrel	148-159	purinergic receptor P2Y12	Homo sapiens	9-14
17214996-6	2008	Inhibition of the platelet ADP P2Y12 receptor by clopidogrel was monitored by the ex vivo analysis of ADP effects on prostaglandin-induced platelet VASP phosphorylation.	clopidogrel	49-60	vasodilator stimulated phosphoprotein	Homo sapiens	148-152
18343263-15	2008	Expression of PECAM-1 (P = 0.03) and GP IIb/IIIa activity (P = 0.01) was reduced at day 15 in clopidogrel-treated patients.	clopidogrel	94-105	platelet and endothelial cell adhesion molecule 1	Homo sapiens	14-21
18343263-15	2008	Expression of PECAM-1 (P = 0.03) and GP IIb/IIIa activity (P = 0.01) was reduced at day 15 in clopidogrel-treated patients.	clopidogrel	94-105	integrin subunit alpha 2b	Homo sapiens	37-43
18278193-0	2008	The use of the VerifyNow P2Y12 point-of-care device to monitor platelet function across a range of P2Y12 inhibition levels following prasugrel and clopidogrel administration.	clopidogrel	147-158	purinergic receptor P2Y12	Homo sapiens	25-30
18278200-0	2008	Residual prothrombotic status in low responder patients to clopidogrel identified by Vasodilator-Stimulated Phosphoprotein Phosphorylation (VASP) analysis?	clopidogrel	59-70	vasodilator stimulated phosphoprotein	Homo sapiens	85-138
18278200-0	2008	Residual prothrombotic status in low responder patients to clopidogrel identified by Vasodilator-Stimulated Phosphoprotein Phosphorylation (VASP) analysis?	clopidogrel	59-70	vasodilator stimulated phosphoprotein	Homo sapiens	140-144
18206732-9	2008	RESULTS: Omeprazole significantly decreased clopidogrel inhibitory effect on platelet P2Y12 as assessed by VASP phosphorylation test.	clopidogrel	44-55	purinergic receptor P2Y12	Homo sapiens	86-91
18206732-9	2008	RESULTS: Omeprazole significantly decreased clopidogrel inhibitory effect on platelet P2Y12 as assessed by VASP phosphorylation test.	clopidogrel	44-55	vasodilator stimulated phosphoprotein	Homo sapiens	107-111
17630652-15	2008	CONCLUSIONS: Tight relationships between aggregation and cytometric quantification of platelet markers in whole blood, in particular CD62P, allow to predict aggregation response to ADP from flow data in patients treated with aspirin alone or with aspirin plus clopidogrel.	clopidogrel	260-271	selectin P	Homo sapiens	133-138
19122335-2	2008	Ticlopidine and clopidogrel inhibited CYP2B6 with IC(50) values of 0.0517+/-0.0323 microM and 0.0182+/-0.0069 microM, respectively, and inhibited CYP2C19 with IC(50) values of 0.203+/-0.124 microM and 0.524+/-0.160 microM, respectively.	clopidogrel	16-27	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	38-44
19122335-2	2008	Ticlopidine and clopidogrel inhibited CYP2B6 with IC(50) values of 0.0517+/-0.0323 microM and 0.0182+/-0.0069 microM, respectively, and inhibited CYP2C19 with IC(50) values of 0.203+/-0.124 microM and 0.524+/-0.160 microM, respectively.	clopidogrel	16-27	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	146-153
17334935-10	2007	CONCLUSION: Routine upstream GP IIb/IIIa is mainly effective in patients with elevated troponin on admission and those not pretreated with clopidogrel.	clopidogrel	139-150	integrin subunit alpha 2b	Homo sapiens	29-35
17900275-0	2007	Common polymorphisms of CYP2C19 and CYP2C9 affect the pharmacokinetic and pharmacodynamic response to clopidogrel but not prasugrel.	clopidogrel	102-113	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
17900275-0	2007	Common polymorphisms of CYP2C19 and CYP2C9 affect the pharmacokinetic and pharmacodynamic response to clopidogrel but not prasugrel.	clopidogrel	102-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
17900275-3	2007	OBJECTIVE: To determine the relationship between genetic variation in cytochrome P450 (CYP) isoenzymes and the pharmacokinetic/pharmacodynamic response to prasugrel and clopidogrel.	clopidogrel	169-180	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	70-85
17900275-3	2007	OBJECTIVE: To determine the relationship between genetic variation in cytochrome P450 (CYP) isoenzymes and the pharmacokinetic/pharmacodynamic response to prasugrel and clopidogrel.	clopidogrel	169-180	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	87-90
17900275-5	2007	RESULTS: In subjects receiving clopidogrel, the presence of the CYP2C19*2 loss of function variant was significantly associated with lower exposure to clopidogrel active metabolite, as measured by the area under the concentration curve (AUC(0-24); P = 0.004) and maximal plasma concentration (C(max); P = 0.020), lower inhibition of platelet aggregation at 4 h (P = 0.003) and poor-responder status (P = 0.030).	clopidogrel	31-42	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	64-71
17900275-5	2007	RESULTS: In subjects receiving clopidogrel, the presence of the CYP2C19*2 loss of function variant was significantly associated with lower exposure to clopidogrel active metabolite, as measured by the area under the concentration curve (AUC(0-24); P = 0.004) and maximal plasma concentration (C(max); P = 0.020), lower inhibition of platelet aggregation at 4 h (P = 0.003) and poor-responder status (P = 0.030).	clopidogrel	151-162	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	64-71
17900275-8	2007	CONCLUSIONS: The common loss of function polymorphisms of CYP2C19 and CYP2C9 are associated with decreased exposure to the active metabolite of clopidogrel but not prasugrel.	clopidogrel	144-155	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	58-65
17900275-8	2007	CONCLUSIONS: The common loss of function polymorphisms of CYP2C19 and CYP2C9 are associated with decreased exposure to the active metabolite of clopidogrel but not prasugrel.	clopidogrel	144-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
18004210-1	2007	OBJECTIVES: The aim of this study was to evaluate the effect of polymorphisms affecting the clopidogrel metabolism (CYP3A4 IVS10+12G/A and CYP2C19*2) and the P2Y12 receptor (P2Y12 T744C) on modulating platelet function in acute coronary syndrome patients on dual antiplatelet treatment.	clopidogrel	92-103	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	116-122
18004210-1	2007	OBJECTIVES: The aim of this study was to evaluate the effect of polymorphisms affecting the clopidogrel metabolism (CYP3A4 IVS10+12G/A and CYP2C19*2) and the P2Y12 receptor (P2Y12 T744C) on modulating platelet function in acute coronary syndrome patients on dual antiplatelet treatment.	clopidogrel	92-103	purinergic receptor P2Y12	Homo sapiens	174-179
18064330-7	2007	Clopidogrel treatment inhibited ADP-induced platelet P-selectin expression by 64% (22-87%), and attenuated the P-selectin response to thrombin (p &lt; 0.001), and platelet aggregation induced by low-dose collagen (p &lt; 0.01).	clopidogrel	0-11	selectin P	Homo sapiens	53-63
18064330-7	2007	Clopidogrel treatment inhibited ADP-induced platelet P-selectin expression by 64% (22-87%), and attenuated the P-selectin response to thrombin (p &lt; 0.001), and platelet aggregation induced by low-dose collagen (p &lt; 0.01).	clopidogrel	0-11	selectin P	Homo sapiens	111-121
18064330-7	2007	Clopidogrel treatment inhibited ADP-induced platelet P-selectin expression by 64% (22-87%), and attenuated the P-selectin response to thrombin (p &lt; 0.001), and platelet aggregation induced by low-dose collagen (p &lt; 0.01).	clopidogrel	0-11	coagulation factor II, thrombin	Homo sapiens	134-142
18064330-12	2007	In conclusion, adding clopidogrel to aspirin treatment inhibited platelet activation by both ADP, thrombin and collagen in vitro, but did not influence the prothrombotic responses to exercise.	clopidogrel	22-33	coagulation factor II, thrombin	Homo sapiens	98-106
17682072-3	2007	In this report, we describe the selectivity of 2-phenyl-2-(1-piperidinyl)propane (PPP) as an inactivator of CYP2B6 and compare this selectivity versus other CYP2B6 inactivators: 1,1",1""-phosphinothioylidynetrisaziridine (thioTEPA), clopidogrel, and ticlopidine.	clopidogrel	233-244	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	108-114
18378613-3	2008	METHODS AND RESULTS: We measured ST2 at baseline in 1239 patients with ST-elevation myocardial infarction from the CLopidogrel as Adjunctive ReperfusIon TherapY-Thrombolysis in Myocardial Infarction 28 (CLARITY-TIMI 28) trial.	clopidogrel	115-126	ST2	Homo sapiens	33-36
18398394-5	2008	Resistance to clopidogrel was determined by flow cytometry of intraplatelet vasodilator-stimulated phosphoprotein (VASP) phosphorylation.	clopidogrel	14-25	vasodilator stimulated phosphoprotein	Homo sapiens	76-113
18398394-5	2008	Resistance to clopidogrel was determined by flow cytometry of intraplatelet vasodilator-stimulated phosphoprotein (VASP) phosphorylation.	clopidogrel	14-25	vasodilator stimulated phosphoprotein	Homo sapiens	115-119
18393143-18	2008	The favorable clinical outcomes with aspirin and clopidogrel have validated cyclooxygenase (COX)-1 and P2Y (12) receptors as targets for new drug development.	clopidogrel	49-60	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	76-98
18206732-3	2008	In a previous observational study, we found clopidogrel activity on platelets, tested by vasodilator-stimulated phosphoprotein (VASP) phosphorylation, to be diminished in patients receiving proton pump inhibitor (PPI) treatment.	clopidogrel	44-55	vasodilator stimulated phosphoprotein	Homo sapiens	89-126
18206732-3	2008	In a previous observational study, we found clopidogrel activity on platelets, tested by vasodilator-stimulated phosphoprotein (VASP) phosphorylation, to be diminished in patients receiving proton pump inhibitor (PPI) treatment.	clopidogrel	44-55	vasodilator stimulated phosphoprotein	Homo sapiens	128-132
18206732-5	2008	Clopidogrel effect was tested on days 1 and 7 in both groups by measuring platelet phosphorylated-VASP expressed as a platelet reactivity index (PRI).	clopidogrel	0-11	vasodilator stimulated phosphoprotein	Homo sapiens	98-102
17989111-6	2008	alpha-Actin expression increased from control of 0.6 +/- 0.4% of mesangial area to 6.3 +/- 1.9% in ANG II-infused rats and this response was prevented by clopidogrel (0.4 +/- 0.2%) and PPADS.	clopidogrel	154-165	angiogenin	Rattus norvegicus	99-102
17989111-7	2008	The increase in AAWT from 4.7 +/- 0.1 to 6.0 +/- 0.1 mm in ANG II rats was also prevented by clopidogrel (4.8 +/- 0.1 mm) and PPADS.	clopidogrel	93-104	angiogenin	Rattus norvegicus	59-62
17989111-8	2008	ANG II infusion led to interstitial macrophage infiltration (105 +/- 16 vs. 62 +/- 4 cell/mm(2)) and tubular proliferation (71 +/- 15 vs. 20 +/- 4 cell/mm(2)) and these effects were prevented by clopidogrel (52 +/- 4 and 36 +/- 3 cell/mm(2)) and PPADS.	clopidogrel	195-206	angiogenin	Rattus norvegicus	0-3
18045851-6	2008	Rats that underwent five-sixths nephrectomy had higher markers of platelet activation (plasma GMP-140 and renal cortical fibrin deposition) than sham-operated rats, and clopidogrel attenuated these effects.	clopidogrel	169-180	selectin P	Rattus norvegicus	94-101
19544679-3	2008	Recent studies suggest that statins metabolized by CYP3A4 attenuate the anti-aggregatory effect of clopidogrel.	clopidogrel	99-110	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	51-57
17631948-9	2008	CONCLUSION: To achieve sustained platelet P2Y12 inhibition in patients treated with cangrelor, clopidogrel administration should be started when the cangrelor infusion is terminated.	clopidogrel	95-106	purinergic receptor P2Y12	Homo sapiens	42-47
17681590-2	2008	The second aim is to test the influence of the CYP 2C19*2 allele on clopidogrel responsiveness.	clopidogrel	68-79	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	47-55
17681590-9	2008	CONCLUSIONS: Increasing the maintenance dose of clopidogrel from 75 to 150 mg/day for 15 days in "low responders" is associated with a relative 20%-increase in its biological effect, independently of the CYP2C19 genotype, but without reaching the levels observed in "responders".	clopidogrel	48-59	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	204-211
18217157-1	2008	Platelet inhibition as measured by vasodilator-stimulated phosphoprotein (VASP) and light transmission aggregometry (LTA) have shown concordance following dosing of clopidogrel.	clopidogrel	165-176	vasodilator stimulated phosphoprotein	Homo sapiens	74-78
18217157-8	2008	Twenty-four hours after prasgurel 60 mg or clopidogrel 300 mg and 600 mg, respectively, VASP-PRI decreased from approximately 80% to 8.9%, 54.7%, and 39.0%, and maximal platelet aggregation (MPA) decreased from approximately 79% to 10.8%, 42.7%, and 31.2%, with an overall VASP:MPA correlation of 0.88 (p &lt; 0.01).	clopidogrel	43-54	vasodilator stimulated phosphoprotein	Homo sapiens	88-92
18217157-9	2008	VASP assay responses after the clopidogrel LDs showed a wider range of values (300 mg: 0-93%; 600 mg: 0-80%) than prasugrel (0-13%); MPA responses followed a similar trend.	clopidogrel	31-42	vasodilator stimulated phosphoprotein	Homo sapiens	0-4
18558425-0	2008	Clopidogrel pretreatment abolishes increase of PAI-1 after coronary stent implantation.	clopidogrel	0-11	serpin family E member 1	Homo sapiens	47-52
18558425-12	2008	CONCLUSION: Clopidogrel pretreatment completely abolishes the increase of PAI-1 active antigen after coronary stent implantation.	clopidogrel	12-23	serpin family E member 1	Homo sapiens	74-79
18941611-6	2008	Although 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors were initially suspected to decrease response to clopidogrel, later studies refuted this possibility.	clopidogrel	127-138	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	9-66
17957565-7	2007	CONCLUSION: Modified TEG, employing AUC15 and %CIn, is a promising tool for assessing responses to aspirin and clopidogrel.	clopidogrel	111-122	pyridoxal phosphatase	Homo sapiens	47-50
17156785-8	2007	In contrast, clopidogrel, aspirin or atorvastatin treated rabbits showed a significant reduction in progression of atherosclerosis and decreased the levels of P-selection, intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1) and monocyte chemotactic protein-1 (MCP-1) in serum and vascular wall.	clopidogrel	13-24	ICAM-1	Oryctolagus cuniculus	207-213
17156785-8	2007	In contrast, clopidogrel, aspirin or atorvastatin treated rabbits showed a significant reduction in progression of atherosclerosis and decreased the levels of P-selection, intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1) and monocyte chemotactic protein-1 (MCP-1) in serum and vascular wall.	clopidogrel	13-24	vascular cell adhesion protein 1	Oryctolagus cuniculus	216-244
17156785-8	2007	In contrast, clopidogrel, aspirin or atorvastatin treated rabbits showed a significant reduction in progression of atherosclerosis and decreased the levels of P-selection, intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1) and monocyte chemotactic protein-1 (MCP-1) in serum and vascular wall.	clopidogrel	13-24	vascular cell adhesion protein 1	Oryctolagus cuniculus	246-252
17156785-8	2007	In contrast, clopidogrel, aspirin or atorvastatin treated rabbits showed a significant reduction in progression of atherosclerosis and decreased the levels of P-selection, intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1) and monocyte chemotactic protein-1 (MCP-1) in serum and vascular wall.	clopidogrel	13-24	C-C motif chemokine 2	Oryctolagus cuniculus	258-288
17156785-8	2007	In contrast, clopidogrel, aspirin or atorvastatin treated rabbits showed a significant reduction in progression of atherosclerosis and decreased the levels of P-selection, intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1) and monocyte chemotactic protein-1 (MCP-1) in serum and vascular wall.	clopidogrel	13-24	C-C motif chemokine 2	Oryctolagus cuniculus	290-295
17938809-1	2007	Clopidogrel responsiveness has been proposed to be involved in recurrent ischemic events after stenting for non-ST elevation acute coronary syndromes (NSTE ACS).	clopidogrel	0-11	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	156-159
17697139-0	2007	Influence of CYP2C19 and CYP3A4 gene polymorphisms on clopidogrel responsiveness in healthy subjects.	clopidogrel	54-65	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
17697139-0	2007	Influence of CYP2C19 and CYP3A4 gene polymorphisms on clopidogrel responsiveness in healthy subjects.	clopidogrel	54-65	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	25-31
17938809-4	2007	We studied 195 consecutive NSTE ACS patients undergoing PCI after a 600 mg loading dose of clopidogrel.	clopidogrel	91-102	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	32-35
17938809-10	2007	In patients with NSTE ACS undergoing PCI, ADP-Ag and PRI VASP identify low responders to clopidogrel with an increased risk of recurrent ischemic events with respective cut-off values of 70% and 53%.	clopidogrel	89-100	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	22-25
17938809-10	2007	In patients with NSTE ACS undergoing PCI, ADP-Ag and PRI VASP identify low responders to clopidogrel with an increased risk of recurrent ischemic events with respective cut-off values of 70% and 53%.	clopidogrel	89-100	vasodilator stimulated phosphoprotein	Homo sapiens	57-61
17938817-0	2007	Impaired platelet responsiveness to clopidogrel identified by flow cytometric vasodilator-stimulated phosphoprotein (VASP) phosphorylation in patients with subacute stent thrombosis.	clopidogrel	36-47	vasodilator stimulated phosphoprotein	Homo sapiens	78-115
17938817-0	2007	Impaired platelet responsiveness to clopidogrel identified by flow cytometric vasodilator-stimulated phosphoprotein (VASP) phosphorylation in patients with subacute stent thrombosis.	clopidogrel	36-47	vasodilator stimulated phosphoprotein	Homo sapiens	117-121
17719296-0	2007	Effects of recombinant human erythropoietin on antiplatelet action of aspirin and clopidogrel in healthy subjects: results of a double-blind, placebo-controlled randomized trial.	clopidogrel	82-93	erythropoietin	Homo sapiens	29-43
17537833-0	2007	Interleukin-6 alters the cellular responsiveness to clopidogrel, irinotecan, and oseltamivir by suppressing the expression of carboxylesterases HCE1 and HCE2.	clopidogrel	52-63	interleukin 6	Homo sapiens	0-13
17537833-0	2007	Interleukin-6 alters the cellular responsiveness to clopidogrel, irinotecan, and oseltamivir by suppressing the expression of carboxylesterases HCE1 and HCE2.	clopidogrel	52-63	carboxylesterase 2	Homo sapiens	126-143
17537833-0	2007	Interleukin-6 alters the cellular responsiveness to clopidogrel, irinotecan, and oseltamivir by suppressing the expression of carboxylesterases HCE1 and HCE2.	clopidogrel	52-63	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	144-148
17537833-0	2007	Interleukin-6 alters the cellular responsiveness to clopidogrel, irinotecan, and oseltamivir by suppressing the expression of carboxylesterases HCE1 and HCE2.	clopidogrel	52-63	carboxylesterase 2	Homo sapiens	153-157
17537833-7	2007	In addition, pretreatment with IL-6 altered the cellular responsiveness in an opposite manner of overexpression of HCE1 and HCE2 toward various ester therapeutic agents (e.g., clopidogrel).	clopidogrel	176-187	interleukin 6	Homo sapiens	31-35
17537833-7	2007	In addition, pretreatment with IL-6 altered the cellular responsiveness in an opposite manner of overexpression of HCE1 and HCE2 toward various ester therapeutic agents (e.g., clopidogrel).	clopidogrel	176-187	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	115-119
17537833-7	2007	In addition, pretreatment with IL-6 altered the cellular responsiveness in an opposite manner of overexpression of HCE1 and HCE2 toward various ester therapeutic agents (e.g., clopidogrel).	clopidogrel	176-187	carboxylesterase 2	Homo sapiens	124-128
17537833-8	2007	Transfection of HCE1, for example, decreased the cytotoxicity induced by antithrombogenic agent clopidogrel, whereas pretreatment with IL-6 increased the cytotoxicity.	clopidogrel	96-107	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	16-20
18404440-4	2007	Most recently, several members of the P2Y(12)-like receptor group, which includes the clopidogrel-sensitive ADP receptor P2Y(12), have been deorphanized.	clopidogrel	86-97	purinergic receptor P2Y12	Homo sapiens	38-45
18404440-4	2007	Most recently, several members of the P2Y(12)-like receptor group, which includes the clopidogrel-sensitive ADP receptor P2Y(12), have been deorphanized.	clopidogrel	86-97	purinergic receptor P2Y12	Homo sapiens	121-128
18088036-15	2007	Dual antiaggregational therapy was administered relatively late on the way to the catheterization lab (the first-aid station missed the opportunity to administer clopidogrel in 84% of patients, aspirin in 86%, other hospitals did not administer clopidogrel in 40% and aspirin in 41% of patients).	clopidogrel	162-173	activation induced cytidine deaminase	Homo sapiens	113-116
17656657-6	2007	Before surgery, clopidogrel produced a significant reduction in the platelet response to ADP; for example, with 10(-6)M ADP, 77.32+/-2.3% bound fibrinogen in placebo group compared with 67.16+/-3.1% after clopidogrel (P=0.01).	clopidogrel	16-27	fibrinogen beta chain	Homo sapiens	144-154
17656657-7	2007	This was accentuated after surgery when the percentage of platelets binding fibrinogen in response to ADP was 76.53+/-2.2% in patients given placebo and 62.84+/-3.3% in the clopidogrel group (P=0.002).	clopidogrel	173-184	fibrinogen beta chain	Homo sapiens	76-86
17765648-1	2007	OBJECTIVE: We determined the effect of prolonged treatment with clopidogrel on C-reactive protein (CRP) concentrations and blood thrombogenicity after percutaneous transluminal coronary angioplasty followed by intracoronary brachytherapy in the porcine model.	clopidogrel	64-75	C-reactive protein	Sus scrofa	79-97
17696811-4	2007	The use of clopidogrel in combination with other antithrombotics in the acute setting is considered, including glycoprotein IIb/IIIa receptor antagonists and direct thrombin inhibitors.	clopidogrel	11-22	coagulation factor II, thrombin	Homo sapiens	165-173
17488353-15	2007	CONCLUSIONS: VASP phosphorylation analysis can evaluate the individual response to clopidogrel loading dose prior to PCI and predict postprocedural MACE.	clopidogrel	83-94	vasodilator stimulated phosphoprotein	Homo sapiens	13-17
17659194-2	2007	BACKGROUND: There are conflicting data regarding whether statins predominantly metabolized by CYP3A4 reduce the metabolism of clopidogrel to its active metabolite and diminish its clinical efficacy.	clopidogrel	126-137	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	94-100
17765648-1	2007	OBJECTIVE: We determined the effect of prolonged treatment with clopidogrel on C-reactive protein (CRP) concentrations and blood thrombogenicity after percutaneous transluminal coronary angioplasty followed by intracoronary brachytherapy in the porcine model.	clopidogrel	64-75	C-reactive protein	Sus scrofa	99-102
17765648-10	2007	RESULTS: Clopidogrel treatment for 3 months reduced CRP levels more than did clopidogrel therapy for 1 month only at 3 months post-PCI (27.9+/-3.9 vs. 56.6+/-11.3 microg/ml; P=.019).	clopidogrel	9-20	C-reactive protein	Sus scrofa	52-55
17765648-13	2007	CONCLUSIONS: Prolonged treatment with clopidogrel reduced CRP levels post-PCI.	clopidogrel	38-49	C-reactive protein	Sus scrofa	58-61
18404433-0	2007	Residual platelet ADP reactivity after clopidogrel treatment is dependent on activation of both the unblocked P2Y(1) and the P2Y (12) receptor and is correlated with protein expression of P2Y (12).	clopidogrel	39-50	purinergic receptor P2Y1	Homo sapiens	110-116
17331131-9	2007	TF concentration in blood drawn pre and 96 h post clopidogrel administration was measured by enzyme-linked immunosorbent assay.	clopidogrel	50-61	coagulation factor III, tissue factor	Homo sapiens	0-2
17331131-0	2007	Clopidogrel-mediated reduction of circulating tissue factor in patients with stable coronary artery disease.	clopidogrel	0-11	coagulation factor III, tissue factor	Homo sapiens	46-59
17361128-3	2007	Clopidogrel"s activation involves two sequential steps by CYP3A, CYP1A2, CYP2C9, CYP2C19, and/or CYP2B6.	clopidogrel	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	58-63
17361128-3	2007	Clopidogrel"s activation involves two sequential steps by CYP3A, CYP1A2, CYP2C9, CYP2C19, and/or CYP2B6.	clopidogrel	0-11	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	65-71
17361128-3	2007	Clopidogrel"s activation involves two sequential steps by CYP3A, CYP1A2, CYP2C9, CYP2C19, and/or CYP2B6.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
17361128-3	2007	Clopidogrel"s activation involves two sequential steps by CYP3A, CYP1A2, CYP2C9, CYP2C19, and/or CYP2B6.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	81-88
17361128-3	2007	Clopidogrel"s activation involves two sequential steps by CYP3A, CYP1A2, CYP2C9, CYP2C19, and/or CYP2B6.	clopidogrel	0-11	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	97-103
17361128-9	2007	We conclude that CYP3A4 and CYP3A5 inhibition by ketoconazole affects formation of clopidogrel"s but not prasugrel"s active metabolite.	clopidogrel	83-94	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	17-23
17361128-9	2007	We conclude that CYP3A4 and CYP3A5 inhibition by ketoconazole affects formation of clopidogrel"s but not prasugrel"s active metabolite.	clopidogrel	83-94	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	28-34
17442686-1	2007	This study assessed the effects of clopidogrel, a CYP 2C9 inhibitor, on fluvastatin pharmacokinetics in healthy volunteers.	clopidogrel	35-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-57
17303701-8	2007	Given the efficacy of clopidogrel, which blocks the G(i/o)-coupled P2Y purinoceptor 12, as an antiplatelet/antithrombotic drug, our data suggest that specifically blocking only PAR1-mediated G(i/o) signaling could also be an effective therapeutic approach with the possibility of less unwanted bleeding.	clopidogrel	22-33	purinergic receptor P2Y12	Homo sapiens	67-86
17303701-8	2007	Given the efficacy of clopidogrel, which blocks the G(i/o)-coupled P2Y purinoceptor 12, as an antiplatelet/antithrombotic drug, our data suggest that specifically blocking only PAR1-mediated G(i/o) signaling could also be an effective therapeutic approach with the possibility of less unwanted bleeding.	clopidogrel	22-33	coagulation factor II thrombin receptor	Homo sapiens	177-181
17615799-5	2007	There is also substantial evidence that therapy with clopidogrel, a specific antagonist of the platelet P2Y12 ADP-receptor, also leads to reductions in serum levels of CD40 ligand, C-reactive protein, P-selectin, and platelet-leukocyte aggregate formation.	clopidogrel	53-64	CD40 molecule	Homo sapiens	168-172
17615799-5	2007	There is also substantial evidence that therapy with clopidogrel, a specific antagonist of the platelet P2Y12 ADP-receptor, also leads to reductions in serum levels of CD40 ligand, C-reactive protein, P-selectin, and platelet-leukocyte aggregate formation.	clopidogrel	53-64	C-reactive protein	Homo sapiens	181-199
17615799-5	2007	There is also substantial evidence that therapy with clopidogrel, a specific antagonist of the platelet P2Y12 ADP-receptor, also leads to reductions in serum levels of CD40 ligand, C-reactive protein, P-selectin, and platelet-leukocyte aggregate formation.	clopidogrel	53-64	selectin P	Homo sapiens	201-211
17263784-0	2007	The flow cytometric VASP assay can be used to determine the effectiveness of clopidogrel in patients treated with abciximab.	clopidogrel	77-88	vasodilator stimulated phosphoprotein	Homo sapiens	20-24
17287623-7	2007	Therapy with clopidogrel resulted in a significant inhibition of platelet activity assessed by ADP-induced and epinephrine-induced aggregation, closure time, expression of PECAM-1, glycoprotein Ib, glycoprotein IIb/IIIa antigen, glycoprotein IIb/IIIa activity with PAC-1, CD151, and reduced formation of platelet-leukocyte conjugates when compared with baseline.	clopidogrel	13-24	platelet and endothelial cell adhesion molecule 1	Homo sapiens	172-179
17287623-7	2007	Therapy with clopidogrel resulted in a significant inhibition of platelet activity assessed by ADP-induced and epinephrine-induced aggregation, closure time, expression of PECAM-1, glycoprotein Ib, glycoprotein IIb/IIIa antigen, glycoprotein IIb/IIIa activity with PAC-1, CD151, and reduced formation of platelet-leukocyte conjugates when compared with baseline.	clopidogrel	13-24	dual specificity phosphatase 2	Homo sapiens	265-270
17287623-7	2007	Therapy with clopidogrel resulted in a significant inhibition of platelet activity assessed by ADP-induced and epinephrine-induced aggregation, closure time, expression of PECAM-1, glycoprotein Ib, glycoprotein IIb/IIIa antigen, glycoprotein IIb/IIIa activity with PAC-1, CD151, and reduced formation of platelet-leukocyte conjugates when compared with baseline.	clopidogrel	13-24	CD151 molecule (Raph blood group)	Homo sapiens	272-277
17331131-5	2007	This study examined the effect of clopidogrel on TF level in the blood of patients with stable CAD and ST-elevation myocardial infarction (STEMI) as well as healthy controls.	clopidogrel	34-45	coagulation factor III, tissue factor	Homo sapiens	49-51
17331131-11	2007	Clopidogrel reduced TF in stable CAD patients to levels seen in healthy controls.	clopidogrel	0-11	coagulation factor III, tissue factor	Homo sapiens	20-22
17331131-15	2007	CONCLUSION: Clopidogrel leads to a reduction of not only sCD40L but also TF in stable CAD.	clopidogrel	12-23	coagulation factor III, tissue factor	Homo sapiens	73-75
17331131-16	2007	The reduction of TF may lead to a reduced thrombogenicity, contributing to the benefits of clopidogrel therapy.	clopidogrel	91-102	coagulation factor III, tissue factor	Homo sapiens	17-19
17261397-2	2007	Previous laboratory studies have shown a possible drug-drug interaction of statins metabolized by cytochrome P450 3A4 and clopidogrel (prodrug metabolized by cytochrome P450 3A4), resulting in an impaired inhibitory effect of clopidogrel on platelet aggregation.	clopidogrel	122-133	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	158-177
17261397-2	2007	Previous laboratory studies have shown a possible drug-drug interaction of statins metabolized by cytochrome P450 3A4 and clopidogrel (prodrug metabolized by cytochrome P450 3A4), resulting in an impaired inhibitory effect of clopidogrel on platelet aggregation.	clopidogrel	226-237	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	98-117
17261397-2	2007	Previous laboratory studies have shown a possible drug-drug interaction of statins metabolized by cytochrome P450 3A4 and clopidogrel (prodrug metabolized by cytochrome P450 3A4), resulting in an impaired inhibitory effect of clopidogrel on platelet aggregation.	clopidogrel	226-237	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	158-177
16914369-0	2007	Effects of aspirin and clopidogrel on plasma brain natriuretic peptide in patients with heart failure receiving ACE inhibitors.	clopidogrel	23-34	natriuretic peptide B	Homo sapiens	45-70
16914369-3	2007	AIM: To investigate the effect of aspirin and clopidogrel on brain natriuretic peptide (BNP) levels in HF patients treated with ACE inhibitors.	clopidogrel	46-57	natriuretic peptide B	Homo sapiens	61-86
16914369-3	2007	AIM: To investigate the effect of aspirin and clopidogrel on brain natriuretic peptide (BNP) levels in HF patients treated with ACE inhibitors.	clopidogrel	46-57	natriuretic peptide B	Homo sapiens	88-91
17343035-5	2007	OBJECTIVES: (i) to determine the proportion of "low-responders" or "resistants" patients during coronary syndrome (ii) to identify determinants of interindividual variability response to clopidogrel (iii) to compare aggregometry and VASP phosphorylation measured by flow cytometry.	clopidogrel	187-198	vasodilator stimulated phosphoprotein	Homo sapiens	233-237
17264949-3	2007	It was the aim of the present study to assess whether the response to aspirin and clopidogrel may be influenced by the 807 C/T polymorphism of the glycoprotein Ia (GpIa) gene in patients with non-ST elevation acute coronary syndrome (NSTE ACS).	clopidogrel	82-93	multimerin 1	Homo sapiens	147-162
17264949-3	2007	It was the aim of the present study to assess whether the response to aspirin and clopidogrel may be influenced by the 807 C/T polymorphism of the glycoprotein Ia (GpIa) gene in patients with non-ST elevation acute coronary syndrome (NSTE ACS).	clopidogrel	82-93	multimerin 1	Homo sapiens	164-168
17343035-21	2007	Possible mechanisms linking clopidogrel "resistance" measured by VASP assay and enhanced thrombogenicity remain to be characterized.	clopidogrel	28-39	vasodilator stimulated phosphoprotein	Homo sapiens	65-69
17343035-22	2007	Indeed, clopidogrel "resistance" defined by VASP analysis was not associated with higher platelet aggregation.	clopidogrel	8-19	vasodilator stimulated phosphoprotein	Homo sapiens	44-48
17432927-5	2007	An increased degree of platelet reactivity was also reported in Pl(A2) carriers compared with Pl(A1/A1) patients after administration of a clopidogrel 300mg loading dose.	clopidogrel	139-150	phospholipase A2 group IIA	Homo sapiens	64-69
17432927-6	2007	OBJECTIVES: The aim of this study was to assess the modulatory effect of the Pl(A2) allele on platelet aggregation in patients taking long-term clopidogrel.	clopidogrel	144-155	phospholipase A2 group IIA	Homo sapiens	77-82
17432927-7	2007	M ETHODS: The prevalence of the Pl(A2) allele was assessed in 38 (21 males, 17 females; mean age 63 +/- 13 years) clopidogrel-resistant and 59 (26 males, 33 females; mean age 63 +/- 11 years) clopidogrel-responsive patients.	clopidogrel	114-125	phospholipase A2 group IIA	Homo sapiens	32-37
17432927-13	2007	These findings and data from our previous studies suggest that patients with a Pl(A2) allele homozygosity may benefit from antiplatelet therapy based on clopidogrel rather than aspirin.	clopidogrel	153-164	phospholipase A2 group IIA	Homo sapiens	79-84
17180146-0	2007	Is clopidogrel associated with poor outcome in patients with non-ST-segment elevation ACS after early CABG surgery?	clopidogrel	3-14	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	86-89
17073575-5	2006	Thiotepa is the most selective of the inhibitors, but is not useful as an in vivo inhibitor, whereas ticlopidine and clopidogrel can be used as CYP2B6-selective probes in human clinical studies.	clopidogrel	117-128	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	144-150
17112805-0	2006	Impact of P-glycoprotein on clopidogrel absorption.	clopidogrel	28-39	ATP binding cassette subfamily B member 1	Homo sapiens	10-24
17112805-3	2006	We tested the hypothesis that the intestinal efflux transporter P-glycoprotein (P-gp) limits the oral bioavailability of clopidogrel and that variance in the MDR1 gene encoding P-gp predicts absorption variability.	clopidogrel	121-132	ATP binding cassette subfamily B member 1	Homo sapiens	64-78
17112805-3	2006	We tested the hypothesis that the intestinal efflux transporter P-glycoprotein (P-gp) limits the oral bioavailability of clopidogrel and that variance in the MDR1 gene encoding P-gp predicts absorption variability.	clopidogrel	121-132	ATP binding cassette subfamily B member 1	Homo sapiens	80-84
17112805-4	2006	METHODS AND RESULTS: P-gp-mediated transport of clopidogrel was assessed by transflux, influx, and efflux experiments by use of Caco-2 cells.	clopidogrel	48-59	ATP binding cassette subfamily B member 1	Homo sapiens	21-25
17112805-9	2006	CONCLUSIONS: Clopidogrel absorption and thereby active metabolite formation are diminished by P-gp-mediated efflux and are influenced by the MDR1 C3435T genotype.	clopidogrel	13-24	ATP binding cassette subfamily B member 1	Homo sapiens	94-98
17112805-9	2006	CONCLUSIONS: Clopidogrel absorption and thereby active metabolite formation are diminished by P-gp-mediated efflux and are influenced by the MDR1 C3435T genotype.	clopidogrel	13-24	ATP binding cassette subfamily B member 1	Homo sapiens	141-145
17080224-8	2006	Likewise, in the clopidogrel group the level of TNFa was significantly reduced after one year; 0.99 versus 1.19 pg/ml (p &lt; 0.001).	clopidogrel	17-28	tumor necrosis factor	Homo sapiens	48-52
17043144-9	2006	Their localization within tumor vessels prompted the idea of treating BALB/NeuT and CD40-KO/NeuT mice chronically with the anti-platelet drug clopidogrel, known to inhibit platelet CD40L expression.	clopidogrel	142-153	CD40 antigen	Mus musculus	84-88
17043144-9	2006	Their localization within tumor vessels prompted the idea of treating BALB/NeuT and CD40-KO/NeuT mice chronically with the anti-platelet drug clopidogrel, known to inhibit platelet CD40L expression.	clopidogrel	142-153	CD40 ligand	Mus musculus	181-186
16563469-1	2007	INTRODUCTION: Clopidogrel inhibits platelet P2Y12 ADP receptors, while ADP, as an inductor of aggregation, stimulates both P2Y12 and P2Y1 platelet receptors.	clopidogrel	14-25	purinergic receptor P2Y12	Homo sapiens	44-49
16563469-1	2007	INTRODUCTION: Clopidogrel inhibits platelet P2Y12 ADP receptors, while ADP, as an inductor of aggregation, stimulates both P2Y12 and P2Y1 platelet receptors.	clopidogrel	14-25	purinergic receptor P2Y1	Homo sapiens	44-48
16563469-3	2007	The VerifyNow-P2Y12 is a rapid assay that test platelet activity over 3 min and uses of the combination of ADP and prostaglandin E1 (PGE1) to directly measure the effects of clopidogrel on the P2Y12 receptor.	clopidogrel	174-185	purinergic receptor P2Y12	Homo sapiens	14-19
16563469-3	2007	The VerifyNow-P2Y12 is a rapid assay that test platelet activity over 3 min and uses of the combination of ADP and prostaglandin E1 (PGE1) to directly measure the effects of clopidogrel on the P2Y12 receptor.	clopidogrel	174-185	purinergic receptor P2Y12	Homo sapiens	193-198
16563469-13	2007	Distribution of PRU values for the VerifyNow-P2Y12 assay shows a separation from baseline to post-clopidogrel assay values with some overlap due to high inter-individual variations in response.	clopidogrel	98-109	purinergic receptor P2Y12	Homo sapiens	45-50
16563469-14	2007	CONCLUSIONS: VerifyNow-P2Y12 is a reliable, fast and sensitive device suitable for monitoring of platelet inhibition during clopidogrel therapy.	clopidogrel	124-135	purinergic receptor P2Y12	Homo sapiens	23-28
16581111-11	2007	The only trend observed was lower reduction in PAC-1 binding following clopidogrel in PlA(2) carriers (P=0.065).	clopidogrel	71-82	dual specificity phosphatase 2	Homo sapiens	47-52
16806409-0	2007	Delayed thrombin-induced platelet-fibrin clot generation by clopidogrel: a new dose-related effect demonstrated by thrombelastography in patients undergoing coronary artery stenting.	clopidogrel	60-71	coagulation factor II, thrombin	Homo sapiens	8-16
16806409-2	2007	However, the effect of the clopidogrel loading dose on the rate of thrombin-induced platelet-fibrin clot formation is unknown in this patient population.	clopidogrel	27-38	coagulation factor II, thrombin	Homo sapiens	67-75
16806409-8	2007	CONCLUSIONS: Delayed thrombin-induced platelet-fibrin clot formation as measured by TEG is a newly reported dose-related effect of clopidogrel that may contribute to the overall antithrombotic properties of the drug in patients undergoing stenting.	clopidogrel	131-142	coagulation factor II, thrombin	Homo sapiens	21-29
17137616-10	2007	RESULTS: With flow cytometry, the percentage of platelets expressing P-selectin (p=0.03) on their surface decreased significantly after the bolus dose of clopidogrel.	clopidogrel	154-165	selectin P	Homo sapiens	69-79
17337040-0	2007	Role of the T744C polymorphism of the P2Y12 gene on platelet response to a 600-mg loading dose of clopidogrel in 597 patients with non-ST-segment elevation acute coronary syndrome.	clopidogrel	98-109	purinergic receptor P2Y12	Homo sapiens	38-43
17337040-3	2007	Recently, the T744C polymorphism of the P2Y12 receptor gene has been associated with enhanced platelet aggregation in healthy volunteers, suggesting a possible mechanism for modulation of clopidogrel response.	clopidogrel	188-199	purinergic receptor P2Y12	Homo sapiens	40-45
17337040-4	2007	AIM OF THIS STUDY: To assess whether the clopidogrel response may be influenced by the T744C P2Y12 gene polymorphism in patients with non ST elevation acute coronary syndrome (NSTE ACS).	clopidogrel	41-52	purinergic receptor P2Y12	Homo sapiens	93-98
17337040-4	2007	AIM OF THIS STUDY: To assess whether the clopidogrel response may be influenced by the T744C P2Y12 gene polymorphism in patients with non ST elevation acute coronary syndrome (NSTE ACS).	clopidogrel	41-52	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	181-184
17337040-7	2007	Clopidogrel response was assessed by post-treatment ADP 10 micromol/L-induced platelet aggregation (ADP-Ag), VASP phosphorylation (PRI VASP) and P-selectin expression (PS).	clopidogrel	0-11	vasodilator stimulated phosphoprotein	Homo sapiens	109-113
17337040-7	2007	Clopidogrel response was assessed by post-treatment ADP 10 micromol/L-induced platelet aggregation (ADP-Ag), VASP phosphorylation (PRI VASP) and P-selectin expression (PS).	clopidogrel	0-11	vasodilator stimulated phosphoprotein	Homo sapiens	135-139
17337040-7	2007	Clopidogrel response was assessed by post-treatment ADP 10 micromol/L-induced platelet aggregation (ADP-Ag), VASP phosphorylation (PRI VASP) and P-selectin expression (PS).	clopidogrel	0-11	selectin P	Homo sapiens	145-155
17482663-10	2007	CONCLUSIONS: The VASP phosphorylation assay appeared to be advantageous for the assessment of clopidogrel action compared to the Multiplate ADP+PG test, the P-selectin assay, and the Multiplate ADP test (listed in descending order).	clopidogrel	94-105	vasodilator stimulated phosphoprotein	Homo sapiens	17-21
17161243-6	2006	A marked reduction in platelet aggregation and active GP IIb/IIIa expression (p &lt; or = 0.001) with clopidogrel + eptifibatide was associated with a decrease in CRP and TNF-alpha release (p &lt; or = 0.001).	clopidogrel	102-113	integrin subunit alpha 2b	Homo sapiens	54-60
17161243-6	2006	A marked reduction in platelet aggregation and active GP IIb/IIIa expression (p &lt; or = 0.001) with clopidogrel + eptifibatide was associated with a decrease in CRP and TNF-alpha release (p &lt; or = 0.001).	clopidogrel	102-113	C-reactive protein	Homo sapiens	163-166
17161243-6	2006	A marked reduction in platelet aggregation and active GP IIb/IIIa expression (p &lt; or = 0.001) with clopidogrel + eptifibatide was associated with a decrease in CRP and TNF-alpha release (p &lt; or = 0.001).	clopidogrel	102-113	tumor necrosis factor	Homo sapiens	171-180
17161243-7	2006	CONCLUSIONS: A strategy of clopidogrel with GP IIb/IIIa blockade resulted in superior inhibition of inflammation and cardiac marker release, which was accompanied by superior platelet inhibition immediately after percutaneous coronary intervention compared with a strategy of clopidogrel alone.	clopidogrel	27-38	integrin subunit alpha 2b	Homo sapiens	44-50
16943252-0	2006	Antiplatelet agents aspirin and clopidogrel are hydrolyzed by distinct carboxylesterases, and clopidogrel is transesterificated in the presence of ethyl alcohol.	clopidogrel	32-43	carboxylesterase 1	Homo sapiens	71-88
16943252-8	2006	Consistent with the tissue distribution of two carboxylesterases human carboxylesterase (HCE) 1 and HCE2, recombinant HCE1 hydrolyzed clopidogrel, whereas recombinant HCE2 hydrolyzed aspirin.	clopidogrel	134-145	carboxylesterase 2	Homo sapiens	100-104
16943252-8	2006	Consistent with the tissue distribution of two carboxylesterases human carboxylesterase (HCE) 1 and HCE2, recombinant HCE1 hydrolyzed clopidogrel, whereas recombinant HCE2 hydrolyzed aspirin.	clopidogrel	134-145	carboxylesterase 1	Homo sapiens	118-122
16943252-9	2006	In addition, hydrolysis of clopidogrel among liver samples was correlated well with the level of HCE1, and hydrolysis of aspirin with HCE2.	clopidogrel	27-38	carboxylesterase 1	Homo sapiens	97-101
17139367-8	2006	TF-PCA levels declined following treatment with clopidogrel alone, and with combinations of clopidogrel with aspirin or cilostazol, with the lowest levels being with the triple-drug combination.	clopidogrel	48-59	coagulation factor III, tissue factor	Homo sapiens	0-2
17139367-8	2006	TF-PCA levels declined following treatment with clopidogrel alone, and with combinations of clopidogrel with aspirin or cilostazol, with the lowest levels being with the triple-drug combination.	clopidogrel	92-103	coagulation factor III, tissue factor	Homo sapiens	0-2
17010792-9	2006	CONCLUSIONS: In NSTE ACS patients undergoing coronary stenting, a 600-mg loading dose of clopidogrel shows its benefit on platelet reactivity and clinical prognosis.	clopidogrel	89-100	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	21-24
16772608-0	2006	Cytochrome P450 2C19 loss-of-function polymorphism is a major determinant of clopidogrel responsiveness in healthy subjects.	clopidogrel	77-88	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-20
16772608-2	2006	To determine whether frequent functional variants of genes coding for candidate cytochrome P450 (CYP) isoenzymes involved in clopidogrel metabolic activation (CYP2C19*2, CYP2B6*5, CYP1A2*1F, and CYP3A5*3 variants) influence the platelet responsiveness to clopidogrel, we conducted a prospective pharmacogenetic study in 28 healthy white male volunteers treated for 7 days with clopidogrel 75 mg/d.	clopidogrel	125-136	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	80-95
16772608-2	2006	To determine whether frequent functional variants of genes coding for candidate cytochrome P450 (CYP) isoenzymes involved in clopidogrel metabolic activation (CYP2C19*2, CYP2B6*5, CYP1A2*1F, and CYP3A5*3 variants) influence the platelet responsiveness to clopidogrel, we conducted a prospective pharmacogenetic study in 28 healthy white male volunteers treated for 7 days with clopidogrel 75 mg/d.	clopidogrel	125-136	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	97-100
16772608-2	2006	To determine whether frequent functional variants of genes coding for candidate cytochrome P450 (CYP) isoenzymes involved in clopidogrel metabolic activation (CYP2C19*2, CYP2B6*5, CYP1A2*1F, and CYP3A5*3 variants) influence the platelet responsiveness to clopidogrel, we conducted a prospective pharmacogenetic study in 28 healthy white male volunteers treated for 7 days with clopidogrel 75 mg/d.	clopidogrel	125-136	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	159-166
16772608-2	2006	To determine whether frequent functional variants of genes coding for candidate cytochrome P450 (CYP) isoenzymes involved in clopidogrel metabolic activation (CYP2C19*2, CYP2B6*5, CYP1A2*1F, and CYP3A5*3 variants) influence the platelet responsiveness to clopidogrel, we conducted a prospective pharmacogenetic study in 28 healthy white male volunteers treated for 7 days with clopidogrel 75 mg/d.	clopidogrel	125-136	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	180-186
16772608-2	2006	To determine whether frequent functional variants of genes coding for candidate cytochrome P450 (CYP) isoenzymes involved in clopidogrel metabolic activation (CYP2C19*2, CYP2B6*5, CYP1A2*1F, and CYP3A5*3 variants) influence the platelet responsiveness to clopidogrel, we conducted a prospective pharmacogenetic study in 28 healthy white male volunteers treated for 7 days with clopidogrel 75 mg/d.	clopidogrel	255-266	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	80-95
16772608-2	2006	To determine whether frequent functional variants of genes coding for candidate cytochrome P450 (CYP) isoenzymes involved in clopidogrel metabolic activation (CYP2C19*2, CYP2B6*5, CYP1A2*1F, and CYP3A5*3 variants) influence the platelet responsiveness to clopidogrel, we conducted a prospective pharmacogenetic study in 28 healthy white male volunteers treated for 7 days with clopidogrel 75 mg/d.	clopidogrel	255-266	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	97-100
16772608-2	2006	To determine whether frequent functional variants of genes coding for candidate cytochrome P450 (CYP) isoenzymes involved in clopidogrel metabolic activation (CYP2C19*2, CYP2B6*5, CYP1A2*1F, and CYP3A5*3 variants) influence the platelet responsiveness to clopidogrel, we conducted a prospective pharmacogenetic study in 28 healthy white male volunteers treated for 7 days with clopidogrel 75 mg/d.	clopidogrel	255-266	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	80-95
16772608-2	2006	To determine whether frequent functional variants of genes coding for candidate cytochrome P450 (CYP) isoenzymes involved in clopidogrel metabolic activation (CYP2C19*2, CYP2B6*5, CYP1A2*1F, and CYP3A5*3 variants) influence the platelet responsiveness to clopidogrel, we conducted a prospective pharmacogenetic study in 28 healthy white male volunteers treated for 7 days with clopidogrel 75 mg/d.	clopidogrel	255-266	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	97-100
16772608-3	2006	We observed that pharmacodynamic response to clopidogrel was significantly associated with the CYP2C19 genotype.	clopidogrel	45-56	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	95-102
16772608-8	2006	The CYP2C19*2 loss-of-function allele is associated with a marked decrease in platelet responsiveness to clopidogrel in young healthy male volunteers and may therefore be an important genetic contributor to clopidogrel resistance in the clinical setting.	clopidogrel	105-116	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
16772608-8	2006	The CYP2C19*2 loss-of-function allele is associated with a marked decrease in platelet responsiveness to clopidogrel in young healthy male volunteers and may therefore be an important genetic contributor to clopidogrel resistance in the clinical setting.	clopidogrel	207-218	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-11
17174877-6	2006	CASE REPORT: We present a case of recurrent acute in-stent thrombosis in a patient with mild antithrombin III (AT) deficiency despite the combined administration of clopidogrel and aspirin.	clopidogrel	165-176	serpin family C member 1	Homo sapiens	93-109
17020571-6	2006	It would thus be anticipated that clopidogrel-resistant patients would benefit from GP IIb/IIIa blockade, particularly during the period immediately after intervention.	clopidogrel	34-45	integrin subunit alpha 2b	Homo sapiens	84-90
17008981-6	2006	Clopidogrel is metabolized to an active thiol metabolite by the CYP 3A4 enzyme.	clopidogrel	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	64-71
17008981-7	2006	Some HMG CoA reductase inhibitors have the ability to inhibit the CYP 3A4 enzyme, which can result in a possible interaction if administered concomitantly with clopidogrel.	clopidogrel	160-171	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	5-22
17008981-7	2006	Some HMG CoA reductase inhibitors have the ability to inhibit the CYP 3A4 enzyme, which can result in a possible interaction if administered concomitantly with clopidogrel.	clopidogrel	160-171	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	66-73
17224865-2	2006	Limitations of clopidogrel therapy include the relatively long time course required to achieve maximal inhibition of platelet aggregation, individual variability in response to its effect, the risk of bleeding during its administration, and the irreversible nature of P2Y12 receptor binding, which leads to a prolonged time course for recovery of platelet function following discontinuation of clopidogrel.	clopidogrel	15-26	purinergic receptor P2Y12	Homo sapiens	268-273
17026894-10	2006	Compared with the patients treated with clopidogrel and ASA in the CURE study, we also found a three times greater risk of major bleeding in period 2.	clopidogrel	40-51	period circadian regulator 2	Homo sapiens	141-149
16837456-8	2006	P2Y12 receptor inhibitors clinically in use such as clopidogrel are postulated to decrease platelet aggregation through partial inhibition of PAR1 signaling.	clopidogrel	52-63	purinergic receptor P2Y12	Homo sapiens	0-5
16837456-8	2006	P2Y12 receptor inhibitors clinically in use such as clopidogrel are postulated to decrease platelet aggregation through partial inhibition of PAR1 signaling.	clopidogrel	52-63	coagulation factor II thrombin receptor	Homo sapiens	142-146
16908717-0	2006	Clopidogrel reduces platelet-leucocyte aggregation, monocyte activation and RANTES secretion in type 2 diabetes mellitus.	clopidogrel	0-11	C-C motif chemokine ligand 5	Homo sapiens	76-82
16645157-7	2006	During the steady phase of clopidogrel treatment, IVS10+12A allele carriers had reduced GP IIb/IIIa activation (P=0.025) and better responsiveness (P=0.02); similarly, clopidogrel-naive patients carriers of the IVS10+12A allele had reduced GP IIb/IIIa activation during the first 24 hours after a loading dose (P=0.025), increased platelet inhibition (P=0.006), and a more optimal drug response (P=0.003).	clopidogrel	27-38	integrin subunit alpha 2b	Homo sapiens	88-94
16961610-0	2006	Recombinant factor VIIa reverses the inhibitory effect of aspirin or aspirin plus clopidogrel on in vitro thrombin generation.	clopidogrel	82-93	coagulation factor II, thrombin	Homo sapiens	106-114
17243268-5	2006	It also allows the measure of the function of the ADP receptor P2Y12 by the phosphorylation level of the VASP protein, method currently under evaluation to monitor the platelet response to clopidogrel treatment.	clopidogrel	189-200	purinergic receptor P2Y12	Homo sapiens	63-68
17243268-5	2006	It also allows the measure of the function of the ADP receptor P2Y12 by the phosphorylation level of the VASP protein, method currently under evaluation to monitor the platelet response to clopidogrel treatment.	clopidogrel	189-200	vasodilator stimulated phosphoprotein	Homo sapiens	105-109
16904555-12	2006	Clopidogrel might therefore allow COX-2 inhibitors to be used without raising risk of thrombotic occlusion.	clopidogrel	0-11	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	34-39
16377010-4	2006	Because the phenomenon of clopidogrel resistance is associated with an increased risk of recurrent cardiovascular events, genetic variants of a platelet receptor P2Y(12) might be the risk factor.	clopidogrel	26-37	purinergic receptor P2Y12	Homo sapiens	162-169
16875906-2	2006	A concern has been raised that atorvastatin may competitively inhibit the metabolism of the prodrug clopidogrel to its active metabolites by the cytochrome P450 3A4 (CYP3A4) enzyme, thereby potentially negating its antiplatelet effect.	clopidogrel	100-111	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	145-164
16875906-2	2006	A concern has been raised that atorvastatin may competitively inhibit the metabolism of the prodrug clopidogrel to its active metabolites by the cytochrome P450 3A4 (CYP3A4) enzyme, thereby potentially negating its antiplatelet effect.	clopidogrel	100-111	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	166-172
16645157-0	2006	Contribution of gene sequence variations of the hepatic cytochrome P450 3A4 enzyme to variability in individual responsiveness to clopidogrel.	clopidogrel	130-141	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	56-75
16645157-1	2006	OBJECTIVE: Metabolic activity of cytochrome P450 (CYP) 3A4 has been associated with clopidogrel response variability.	clopidogrel	84-95	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	33-58
16645157-2	2006	Because metabolic activity of CYP3A4 is genetically regulated, we hypothesized that genetic variations of this enzyme may contribute to clopidogrel response variability.	clopidogrel	136-147	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	30-36
16645157-10	2006	CONCLUSIONS: The IVS10+12G&gt;A polymorphism of the CYP3A4 gene modulates platelet activation in patients treated with clopidogrel and may therefore contribute to clopidogrel response variability.	clopidogrel	119-130	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	52-58
16645157-10	2006	CONCLUSIONS: The IVS10+12G&gt;A polymorphism of the CYP3A4 gene modulates platelet activation in patients treated with clopidogrel and may therefore contribute to clopidogrel response variability.	clopidogrel	163-174	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	52-58
16928609-0	2006	Effects of ad hoc clopidogrel loading versus pre-treatment on P-selectin expression after coronary stent implantation.	clopidogrel	18-29	selectin P	Homo sapiens	62-72
16928609-3	2006	In this study, we investigated the effects of ad hoc clopidogrel treatment compared to a clopidogrel pretreated group on platelet P-selectin expression.	clopidogrel	53-64	selectin P	Homo sapiens	130-140
16928609-3	2006	In this study, we investigated the effects of ad hoc clopidogrel treatment compared to a clopidogrel pretreated group on platelet P-selectin expression.	clopidogrel	89-100	selectin P	Homo sapiens	130-140
16835302-0	2006	The active metabolite of Clopidogrel disrupts P2Y12 receptor oligomers and partitions them out of lipid rafts.	clopidogrel	25-36	purinergic receptor P2Y12	Homo sapiens	46-51
16835302-1	2006	P2Y12, a G protein-coupled receptor that plays a central role in platelet activation has been recently identified as the receptor targeted by the antithrombotic drug, clopidogrel.	clopidogrel	167-178	purinergic receptor P2Y12	Homo sapiens	0-5
16835302-2	2006	In this study, we further deciphered the mechanism of action of clopidogrel and of its active metabolite (Act-Met) on P2Y12 receptors.	clopidogrel	64-75	purinergic receptor P2Y12	Homo sapiens	118-123
16835302-4	2006	In vitro treatment with Act-Met or in vivo oral administration to rats with clopidogrel induced the breakdown of these oligomers into dimeric and monomeric entities in P2Y12 expressing HEK293 and platelets respectively.	clopidogrel	76-87	purinergic receptor P2Y12	Rattus norvegicus	168-173
16835302-5	2006	In addition, we showed the predominant association of P2Y12 oligomers to cell membrane lipid rafts and the partitioning of P2Y12 out of rafts in response to clopidogrel and Act-Met.	clopidogrel	157-168	purinergic receptor P2Y12	Homo sapiens	123-128
16843176-2	2006	BACKGROUND: Adherence in community practice to American College of Cardiology/American Heart Association guidelines for clopidogrel use among NSTE ACS patients has not been previously characterized.	clopidogrel	120-131	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	147-150
16843176-9	2006	CONCLUSIONS: Despite guideline recommendations, the overwhelming majority of NSTE ACS patients treated with acute clopidogrel needing CABG have their surgery within &lt; or =5 days of treatment.	clopidogrel	114-125	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	82-85
16549375-12	2006	Amongst the remaining 55 patients, the mean reduction in fibrinogen binding after clopidogrel administration was 51.5% (95% CI: 43.8-59.2).	clopidogrel	82-93	fibrinogen beta chain	Homo sapiens	57-67
16675725-10	2006	Urinary excretion of 8-iso-prostaglandin F2alpha and plasma levels of hsCRP, sCD40L, and RANTES were reduced in patients on additional treatment with clopidogrel, but not in patients on placebo.	clopidogrel	150-161	C-C motif chemokine ligand 5	Homo sapiens	89-95
16549375-13	2006	Amongst responders there was a wide variability in reduction of fibrinogen binding in response to clopidogrel (range 8.11-97.7%).	clopidogrel	98-109	fibrinogen beta chain	Homo sapiens	64-74
17088858-6	2006	Clopidogrel nonresponsiveness has been a consistently observed phenomenon in studies utilizing various P2Y12 receptor-specific assays.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	103-108
16807649-9	2006	Furthermore, the influence of aspirin or clopidogrel on prolactin stimulated P-selectin expression in vitro was tested, showing that aspirin was without effect, whereas clopidogrel significantly inhibited platelet P-selectin expression.	clopidogrel	169-180	selectin P	Homo sapiens	214-224
16466948-3	2006	Due to its central role in the formation and stabilization of a thrombus, the P2Y12 receptor is a well established target of antithrombotic drugs like clopidogrel which has proved efficacious in many clinical trials and experimental models of thrombosis.	clopidogrel	151-162	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	78-83
16368572-8	2006	Advances in understanding the importance of the P2Y12 receptor has resulted in the development of drugs like clopidogrel and ticlopidine that is being successfully used clinically in the treatment of thrombotic disorders.	clopidogrel	109-120	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	48-53
19804082-4	2006	The VerifyNow P2Y12 assay (Accumetrics, Inc., CA, USA) is a point-of-care device that can accurately and rapidly measure the degree of platelet inhibition in patients taking clopidogrel.	clopidogrel	174-185	purinergic receptor P2Y12	Homo sapiens	14-19
16961610-3	2006	This study investigated: (a) whether a regimen of aspirin or clopidogrel plus aspirin significantly inhibited platelet thrombin generation (TG); and (b) the reversal of this inhibition by recombinant activated factor VII (rFVIIa).	clopidogrel	61-72	coagulation factor II, thrombin	Homo sapiens	119-127
16961627-0	2006	Role of the P2Y12 gene polymorphism in platelet responsiveness to clopidogrel in healthy subjects.	clopidogrel	66-77	purinergic receptor P2Y12	Homo sapiens	12-17
16754899-1	2006	BACKGROUND: Clopidogrel is a prodrug requiring metabolism by cytochrome P450 3A (CYP3A) isoenzymes, including CYP3A5, in order to be active.	clopidogrel	12-23	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	61-79
16754899-1	2006	BACKGROUND: Clopidogrel is a prodrug requiring metabolism by cytochrome P450 3A (CYP3A) isoenzymes, including CYP3A5, in order to be active.	clopidogrel	12-23	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	81-86
16754899-1	2006	BACKGROUND: Clopidogrel is a prodrug requiring metabolism by cytochrome P450 3A (CYP3A) isoenzymes, including CYP3A5, in order to be active.	clopidogrel	12-23	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	110-116
16754899-3	2006	We investigated the influence of CYP3A5 polymorphism on the drug interaction of clopidogrel.	clopidogrel	80-91	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	33-39
16754899-9	2006	Multivariable analysis showed that the CYP3A5 polymorphism was a predictor of atherothrombotic events in clopidogrel users.	clopidogrel	105-116	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	39-45
16754899-10	2006	INTERPRETATION: People with the CYP3A5 non-expressor genotype are vulnerable to drug interactions between clopidogrel and CYP3A inhibitors.	clopidogrel	106-117	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	32-38
16754899-10	2006	INTERPRETATION: People with the CYP3A5 non-expressor genotype are vulnerable to drug interactions between clopidogrel and CYP3A inhibitors.	clopidogrel	106-117	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	32-37
16845449-0	2006	Validation of a VerifyNow-P2Y12 cartridge for monitoring platelet inhibition with clopidogrel.	clopidogrel	82-93	purinergic receptor P2Y12	Homo sapiens	26-31
16845449-3	2006	We validated a new VerifyNow-P2Y12 assay to measure inhibition of the P2Y12 platelet receptors by clopidogrel by evaluating its receptor specificity, precision, and potential interference with platelet count, hematocrit, age, cholesterol, triglycerides, and other antiplatelet agents.	clopidogrel	98-109	purinergic receptor P2Y12	Homo sapiens	29-34
16845449-3	2006	We validated a new VerifyNow-P2Y12 assay to measure inhibition of the P2Y12 platelet receptors by clopidogrel by evaluating its receptor specificity, precision, and potential interference with platelet count, hematocrit, age, cholesterol, triglycerides, and other antiplatelet agents.	clopidogrel	98-109	purinergic receptor P2Y12	Homo sapiens	70-75
16769602-1	2006	The efficacy of the platelet P2Y12 receptor antagonist clopidogrel, which undergoes cytochrome-mediated metabolism to its active form, shows marked inter-individual variability.	clopidogrel	55-66	purinergic receptor P2Y12	Homo sapiens	29-34
16679086-7	2006	The increase in C-reactive protein and troponin was lower among patients undergoing DES implantation (median 2.1 vs 3.5 mg/L for C-reactive protein, median 0.11 vs 0.41 ng/ml for troponin), even after adjustment for randomized treatment, clopidogrel before treatment, diabetes mellitus status, epicardial patency, left anterior descending artery location, and myocardial perfusion (p = 0.036 and p = 0.039, respectively).	clopidogrel	238-249	C-reactive protein	Homo sapiens	16-34
16505243-1	2006	Inhibition of the P2Y12 pathway by the platelet antagonist clopidogrel is associated with a marked reduction in platelet reactivity.	clopidogrel	59-70	purinergic receptor P2Y12	Homo sapiens	18-23
19804078-7	2006	Future research for the evaluation of clopidogrel resistance should be based on the assessment of selective P2Y12 receptor inhibition (e.g., the vasodilator-stimulated phosphoprotein-assay or the measurement of stabilization of platelet aggregates) with quick and simple tests.	clopidogrel	38-49	purinergic receptor P2Y12	Homo sapiens	108-113
16460446-6	2006	In addition, AYPGKF- and thrombin-induced TXA2 generation was significantly reduced in platelets from mice dosed with clopidogrel, confirming the results obtained with the human platelets.	clopidogrel	118-129	coagulation factor II	Mus musculus	25-33
16503718-3	2006	Investigators have proposed that the use of statins that are metabolized by the cytochrome P450 (CYP) system may diminish the conversion of clopidogrel to its active form by inhibiting the CYP3A4 isoenzyme.	clopidogrel	140-151	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	189-195
16421011-6	2006	Clopidogrel reduced PAI-1 (ng/ml) in volunteers, -5.30 (2.20) (p &lt; 0.05), and patients, -3.61 (2.75) (non-significant trend).	clopidogrel	0-11	serpin family E member 1	Homo sapiens	20-25
16421012-0	2006	Effect of combined administration of clopidogrel and lysine acetylsalicylate versus clopidogrel and aspirin on platelet aggregation and activated GPIIb/IIIa expression in healthy volunteers.	clopidogrel	37-48	integrin subunit alpha 2b	Homo sapiens	146-151
16505243-10	2006	In conclusion, clopidogrel withdrawal is associated with an increase in platelet and inflammatory biomarkers in diabetic patients, supporting pleiotropic effects coupled with P2Y12 receptor antagonism.	clopidogrel	15-26	purinergic receptor P2Y12	Homo sapiens	175-180
16442924-2	2006	Our study was designed to test the effects of clopidogrel on soluble CD40 ligand (sCD40l) and on high-sensitivity C-reactive protein (hs-CRP) in patients with stable coronary artery disease (CAD).	clopidogrel	46-57	CD40 molecule	Homo sapiens	69-73
16456606-16	2006	Pravastatin plus clopidogrel significantly decreased CRP, platelet activity, total serum cholesterol, and IH while pravastatin alone decreased only CRP and platelet activity.	clopidogrel	17-28	C-reactive protein	Rattus norvegicus	53-56
16308186-4	2006	A loading dose of 225 mg clopidogrel leads to a significant reduction (p &lt; 0.01) in the ADP-stimulated retention index (RI) from 69 +/- 15 to 48 +/- 21%, in the aggregation response to 5 microM ADP (from 50 +/- 20 to 29 +/- 21%) and the expression of CD62P (from 64 +/- 11 to 41 +/- 17%).	clopidogrel	25-36	selectin P	Homo sapiens	254-259
16442361-0	2006	Impact of clopidogrel on suppression of circulating levels of soluble CD40 ligand in patients with unstable angina undergoing coronary stenting.	clopidogrel	10-21	CD40 molecule	Homo sapiens	70-74
16442361-1	2006	This study investigated whether a regimen that comprised a loading dose of 300 mg of clopidogrel followed by 75 mg/day could significantly suppress circulating levels of soluble CD40 ligand (sCD40L) in patients who had unstable angina and underwent coronary stenting.	clopidogrel	85-96	CD40 molecule	Homo sapiens	178-182
16454979-13	2006	CONCLUSIONS: Aspirin plus clopidogrel treatment reduced levels of serum hs-CRP and TNF-alpha in patients with NSTEACS significantly more than aspirin alone.	clopidogrel	26-37	tumor necrosis factor	Homo sapiens	83-92
16386660-18	2006	They also had lower response to clopidogrel, assessed by platelet aggregation and activation markers (flow cytometry-determined PAC-1 binding and P-selectin expression).	clopidogrel	32-43	dual specificity phosphatase 2	Homo sapiens	128-133
16386660-18	2006	They also had lower response to clopidogrel, assessed by platelet aggregation and activation markers (flow cytometry-determined PAC-1 binding and P-selectin expression).	clopidogrel	32-43	selectin P	Homo sapiens	146-156
16611111-3	2006	The assumption exists that the effect of clopidogrel in inhibiting platelet aggregation is attenuated by co-administration of lipophilic statins such as atorvastatin or simvastatin which are metabolised by the CYP3A4 system to inactive substrates.	clopidogrel	41-52	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	210-216
16611111-8	2006	However, these clinical studies showed a trend towards a diminishing effect of clopidogrel on those treated with cytochrome CYP3A4 metabolised statins.	clopidogrel	79-90	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	124-130
16611111-11	2006	This effect of clopidogrel resistance seems to be more important as the potential interference between CYP3A4 metabolized statins and clopidogrel.	clopidogrel	15-26	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	103-109
16194864-0	2005	PAR-1 genotype influences platelet aggregation and procoagulant responses in patients with coronary artery disease prior to and during clopidogrel therapy.	clopidogrel	135-146	coagulation factor II thrombin receptor	Homo sapiens	0-5
16456606-9	2006	Pravastatin alone and pravastatin plus clopidogrel significantly decreased CRP compared to controls (120.2 +/-11.2 and 134.1 +/- 9.9 vs 191.1 +/- 9.2 microg/mL, respectively p = 0.003 and p =0.0024).	clopidogrel	39-50	C-reactive protein	Rattus norvegicus	75-78
16264203-1	2005	BACKGROUND: A recent ex vivo study suggests that the metabolic activation of clopidogrel is catalyzed by cytochrom P450 (CYP) 3A4 and is competitively inhibited by atorvastatin, but not pravastatin.	clopidogrel	77-88	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	115-129
16264203-2	2005	OBJECTIVE: To determine whether the incidence of procedure-related myocardial injury, assessed by cardiac troponin T (cTnT) release, is altered when clopidogrel is coadministered with a statin that is predominantly CYP3A4-metabolized.	clopidogrel	149-160	troponin T2, cardiac type	Homo sapiens	98-116
16264203-2	2005	OBJECTIVE: To determine whether the incidence of procedure-related myocardial injury, assessed by cardiac troponin T (cTnT) release, is altered when clopidogrel is coadministered with a statin that is predominantly CYP3A4-metabolized.	clopidogrel	149-160	troponin T2, cardiac type	Homo sapiens	118-122
15955565-5	2005	Due to its central role in the formation and stabilization of a thrombus, the P2Y12 receptor is a well-established target of antithrombotic drugs like ticlopidine or clopidogrel, which have proved efficacy in many clinical trials and experimental models of thrombosis.	clopidogrel	166-177	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	78-83
16041401-12	2005	Clopidogrel administration reduced P-selectin expression with respect to untreated infarcted rabbits.	clopidogrel	0-11	P-selectin	Oryctolagus cuniculus	35-45
16041401-13	2005	CD40 ligand and tissue factor expression was increased in the ischemic coronary artery and reduced after clopidogrel administration.	clopidogrel	105-116	tumor necrosis factor receptor superfamily member 5	Oryctolagus cuniculus	0-4
16041401-13	2005	CD40 ligand and tissue factor expression was increased in the ischemic coronary artery and reduced after clopidogrel administration.	clopidogrel	105-116	tissue factor	Oryctolagus cuniculus	16-29
16195618-9	2005	CONCLUSION: Less than one-third of CD62p expression was suppressed at 24 h by the conventional loading dose (300 mg) of clopidogrel in patients with UA following coronary stenting.	clopidogrel	120-131	selectin P	Homo sapiens	35-40
16270649-0	2005	High stability of blood samples for flow cytometric analysis of VASP phosphorylation to measure the clopidogrel responsiveness in patients with coronary artery disease.	clopidogrel	100-111	vasodilator stimulated phosphoprotein	Homo sapiens	64-68
16323337-1	2005	Vasodilator-stimulated phosphoprotein (VASP) 239 phosphorylation flow cytometric assessment has been reported as a tool to evaluate the responsiveness to clopidogrel in coronary heart disease (CHD) patients.	clopidogrel	154-165	vasodilator stimulated phosphoprotein	Homo sapiens	0-37
16323337-1	2005	Vasodilator-stimulated phosphoprotein (VASP) 239 phosphorylation flow cytometric assessment has been reported as a tool to evaluate the responsiveness to clopidogrel in coronary heart disease (CHD) patients.	clopidogrel	154-165	vasodilator stimulated phosphoprotein	Homo sapiens	39-43
16388413-4	2005	Autoantibodies against ADAMTS13 were present in majority of patients with idiopathic TTP and ticlopidine- and clopidogrel-associated TTP.	clopidogrel	110-121	ADAM metallopeptidase with thrombospondin type 1 motif 13	Homo sapiens	23-31
16411409-9	2005	Furthermore, clopidogrel only depressed thrombin generation at the site of microvascular injury (p &lt; 0.01) in P1(A2) patients and prolonged closure time measured in vitro by PFA-100 (p &lt; 0.05).	clopidogrel	13-24	coagulation factor II, thrombin	Homo sapiens	40-48
16411409-11	2005	Clopidogrel lowered the expression of both markers affecting more P1(A2) carriers, so that the difference in binding PAC-1 antibody between platelets from P1(A1) and P1(A2) carriers disappeared, while the difference in P-selectin expression slightly diminished.	clopidogrel	0-11	dual specificity phosphatase 2	Homo sapiens	117-122
16411409-11	2005	Clopidogrel lowered the expression of both markers affecting more P1(A2) carriers, so that the difference in binding PAC-1 antibody between platelets from P1(A1) and P1(A2) carriers disappeared, while the difference in P-selectin expression slightly diminished.	clopidogrel	0-11	selectin P	Homo sapiens	219-229
19758929-4	2005	However, their routine use has been questioned in recent studies.Clopidogrel 600 mg given at least 2 hours preprocedure negates the need for additional routine GP IIb/IIIa blockade in elective, even diabetic patients.	clopidogrel	65-76	integrin subunit alpha 2b	Homo sapiens	160-166
16154027-5	2005	The GPIIIa PLA1/PLA2 polymorphism has been associated with clopidogrel and orbofiban platelet response.	clopidogrel	59-70	integrin subunit beta 3	Homo sapiens	4-10
16154027-5	2005	The GPIIIa PLA1/PLA2 polymorphism has been associated with clopidogrel and orbofiban platelet response.	clopidogrel	59-70	POU class 2 homeobox 3	Homo sapiens	11-15
16154027-5	2005	The GPIIIa PLA1/PLA2 polymorphism has been associated with clopidogrel and orbofiban platelet response.	clopidogrel	59-70	phospholipase A2 group IB	Homo sapiens	16-20
16154027-9	2005	This polymorphism may modulate the effect of P2Y12 antagonists like clopidogrel and its clinical implication is currently under study.	clopidogrel	68-79	purinergic receptor P2Y12	Homo sapiens	45-50
16268474-5	2005	Clopidogrel inhibited platelet aggregation, expression of P-selectin, platelet-PMN adhesion and platelet-dependent ROS production in mouse PMN.	clopidogrel	0-11	selectin, platelet	Mus musculus	58-68
16268474-6	2005	Similarly pretreatment of human platelets with the active metabolite of clopidogrel in vitro resulted in a profound inhibition of platelet P-selectin expression, platelet-PMN adhesion and production of ROS by PMN.	clopidogrel	72-83	selectin P	Homo sapiens	139-149
16098428-2	2005	BACKGROUND: Clopidogrel selectively inhibits the P2Y12 receptor, the major role of which is stabilization of aggregation, whereas initiation of aggregation depends on activity of both P2Y1 and P2Y12 receptors.	clopidogrel	12-23	purinergic receptor P2Y12	Homo sapiens	49-54
16098428-2	2005	BACKGROUND: Clopidogrel selectively inhibits the P2Y12 receptor, the major role of which is stabilization of aggregation, whereas initiation of aggregation depends on activity of both P2Y1 and P2Y12 receptors.	clopidogrel	12-23	purinergic receptor P2Y1	Homo sapiens	49-53
16098428-2	2005	BACKGROUND: Clopidogrel selectively inhibits the P2Y12 receptor, the major role of which is stabilization of aggregation, whereas initiation of aggregation depends on activity of both P2Y1 and P2Y12 receptors.	clopidogrel	12-23	purinergic receptor P2Y12	Homo sapiens	193-198
16098428-5	2005	RESULTS: Clopidogrel similarly inhibited adenosine 5"-diphosphate (ADP)-induced Agg(max) with either anticoagulant, but significantly more Agg(6min) (75% vs. 31%), P-selectin (72% vs. 53%), and PAC-1 (62% vs. 24%) in hirudin/PPACK.	clopidogrel	9-20	selectin P	Homo sapiens	164-174
16098428-5	2005	RESULTS: Clopidogrel similarly inhibited adenosine 5"-diphosphate (ADP)-induced Agg(max) with either anticoagulant, but significantly more Agg(6min) (75% vs. 31%), P-selectin (72% vs. 53%), and PAC-1 (62% vs. 24%) in hirudin/PPACK.	clopidogrel	9-20	dual specificity phosphatase 2	Homo sapiens	194-199
16194864-3	2005	We also determined whether the P2Y12 antagonist clopidogrel could offset any observed functional polymorphism of the PAR-1 receptor by inhibiting P2Y12-mediated amplification of TRAP-induced responses.	clopidogrel	48-59	purinergic receptor P2Y12	Homo sapiens	31-36
16194864-3	2005	We also determined whether the P2Y12 antagonist clopidogrel could offset any observed functional polymorphism of the PAR-1 receptor by inhibiting P2Y12-mediated amplification of TRAP-induced responses.	clopidogrel	48-59	coagulation factor II thrombin receptor	Homo sapiens	117-122
16194864-3	2005	We also determined whether the P2Y12 antagonist clopidogrel could offset any observed functional polymorphism of the PAR-1 receptor by inhibiting P2Y12-mediated amplification of TRAP-induced responses.	clopidogrel	48-59	purinergic receptor P2Y12	Homo sapiens	146-151
16194864-3	2005	We also determined whether the P2Y12 antagonist clopidogrel could offset any observed functional polymorphism of the PAR-1 receptor by inhibiting P2Y12-mediated amplification of TRAP-induced responses.	clopidogrel	48-59	TRAP	Homo sapiens	178-182
16194864-10	2005	Higher platelet reactivity associated with PAR-1 IVSn-14 A allele homozygotes persists despite clopidogrel therapy.	clopidogrel	95-106	coagulation factor II thrombin receptor	Homo sapiens	43-48
16011979-1	2005	The antiplatelet potency of clopidogrel may be attenuated by short-term co-administration of lipophilic statins metabolized through the cytochrome P-450, isoform 3A4.	clopidogrel	28-39	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	136-152
16113837-1	2005	Recent studies suggest that cytochrome P450 (CYP) 3A4 metabolized statins attenuate the antiaggregatory effect of clopidogrel.	clopidogrel	114-125	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	28-53
15968399-9	2005	In PRP from stroke patients of older age, the P2Y(12)-mediated contribution to thrombin generation was variably reduced by two weeks of clopidogrel medication.	clopidogrel	136-147	prion protein	Homo sapiens	3-6
15933261-2	2005	We tested for an association of gene sequence variations in P2Y12 and occurrence of neurological adverse events in patients with symptomatic peripheral artery disease (PAD) during clopidogrel treatment.	clopidogrel	180-191	purinergic receptor P2Y12	Homo sapiens	60-65
15968882-0	2005	P-selectin (CD62p) and P-selectin glycoprotein ligand-1 (PSGL-1) polymorphisms: minor phenotypic differences in the formation of platelet-leukocyte aggregates and response to clopidogrel.	clopidogrel	175-186	selectin P	Homo sapiens	0-10
15968882-0	2005	P-selectin (CD62p) and P-selectin glycoprotein ligand-1 (PSGL-1) polymorphisms: minor phenotypic differences in the formation of platelet-leukocyte aggregates and response to clopidogrel.	clopidogrel	175-186	selectin P ligand	Homo sapiens	23-55
15968882-0	2005	P-selectin (CD62p) and P-selectin glycoprotein ligand-1 (PSGL-1) polymorphisms: minor phenotypic differences in the formation of platelet-leukocyte aggregates and response to clopidogrel.	clopidogrel	175-186	selectin P ligand	Homo sapiens	57-63
15968882-2	2005	Deficient variants (namely the Thr715Pro-SNP for CD62p and a VNTR-polymorphism for PSGL-1) might affect PLA formation and probably the response to clopidogrel (which is known to reduce PLA-formation).	clopidogrel	147-158	selectin P	Homo sapiens	49-54
15968882-2	2005	Deficient variants (namely the Thr715Pro-SNP for CD62p and a VNTR-polymorphism for PSGL-1) might affect PLA formation and probably the response to clopidogrel (which is known to reduce PLA-formation).	clopidogrel	147-158	selectin P ligand	Homo sapiens	83-89
15817818-9	2005	CONCLUSIONS: VASP phosphorylation assays are reliable for quantifying clopidogrel effects.	clopidogrel	70-81	vasodilator stimulated phosphoprotein	Homo sapiens	13-17
15817818-10	2005	Because the VASP assay directly measures the function of the clopidogrel target, the P2Y12 receptor, the assay is selective for clopidogrel effects rather than effects of other platelet inhibitors commonly in use.	clopidogrel	61-72	vasodilator stimulated phosphoprotein	Homo sapiens	12-16
15817818-10	2005	Because the VASP assay directly measures the function of the clopidogrel target, the P2Y12 receptor, the assay is selective for clopidogrel effects rather than effects of other platelet inhibitors commonly in use.	clopidogrel	128-139	vasodilator stimulated phosphoprotein	Homo sapiens	12-16
15961986-0	2005	Effect of clopidogrel and ticlopidine on cytochrome P450 2B6 activity as measured by bupropion hydroxylation.	clopidogrel	10-21	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	41-60
15961986-1	2005	OBJECTIVE: Our objective was to study the effect of the antiplatelet agents clopidogrel and ticlopidine on bupropion (INN, amfebutamone) hydroxylation, a probe reaction for cytochrome P450 (CYP) 2B6 activity.	clopidogrel	76-87	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	173-198
15961986-8	2005	CONCLUSIONS: Both clopidogrel and ticlopidine significantly inhibited the CYP2B6-catalyzed bupropion hydroxylation.	clopidogrel	18-29	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	74-80
15961986-9	2005	Patients receiving either clopidogrel or ticlopidine are likely to require dose adjustments when treated with drugs primarily metabolized by CYP2B6.	clopidogrel	26-37	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	141-147
15968399-9	2005	In PRP from stroke patients of older age, the P2Y(12)-mediated contribution to thrombin generation was variably reduced by two weeks of clopidogrel medication.	clopidogrel	136-147	coagulation factor II, thrombin	Homo sapiens	79-87
15795539-3	2005	The aim of this study was to test in patients (n = 416) scheduled for coronary artery stenting whether P2Y12 haplotype H2 carriage is associated with increased ADP-induced platelet aggregation after administration of a 600 mg loading dose of clopidogrel.	clopidogrel	242-253	purinergic receptor P2Y12	Homo sapiens	103-108
15885609-2	2005	There is a significant variability of responsiveness among individuals towards clopidogrel, which is a specific inhibitor of the low-affinity human purinergic receptor (P2Y12).	clopidogrel	79-90	purinergic receptor P2Y12	Homo sapiens	169-174
15609386-7	2005	RESULTS: Within 12 h of the loading dose, platelet activation in the clopidogrel group had decreased (P-selectin by 27.3 per cent, P = 0.017; fibrinogen binding by 34.7 per cent, P = 0.024; stimulated fibrinogen binding by 49.2 per cent, P &lt; 0.001).	clopidogrel	69-80	selectin P	Homo sapiens	102-112
15816504-3	2005	However, the agents currently on the market (ticlopidine and clopidogrel), or known to be in development (cangrelor, AZD-6140 and prasugrel), all target the P2Y12 receptor.	clopidogrel	61-72	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	157-162
15816504-4	2005	The thienopyridines (ticlopidine, clopidogrel and prasugrel) irreversibly inactivate the P2Y12 receptor via the covalent binding of an active metabolite generated in the liver, while the other compounds are competitive antagonists.	clopidogrel	34-45	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	89-94
15823862-3	2005	We aimed to investigate the effects of clopidogrel ex vivo and another ADP-antagonist, AR-C69931MX in vitro on thrombin receptor activating peptide (TRAP)-induced platelet aggregation, procoagulant activity, microparticle formation and [Ca(2+)]i responses in patients with ACS.	clopidogrel	39-50	TRAP	Homo sapiens	149-153
15823862-5	2005	Clopidogrel (300 mg loading dose plus 75 mg daily) significantly inhibited TRAP-induced aggregation, procoagulant activity (annexin V binding) and microparticle production (all P &lt; 0.05) but not as extensively as AR-C69931MX (400 nmol/l).	clopidogrel	0-11	TRAP	Homo sapiens	75-79
15823862-6	2005	[Ca(2+)]i responses induced by a combination of TRAP and ADP designed to mimic the physiological effects of released ADP showed that clopidogrel partially and AR-C69931MX completely removed the ADP component of the [Ca(2+)]i responses (n = 6).	clopidogrel	133-144	TRAP	Homo sapiens	48-52
15679472-2	2005	Clopidogrel is an inactive prodrug, which requires activation by the cytochrome P450 3A4 system in order to exert its antiplatelet action.	clopidogrel	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	69-88
15679472-4	2005	From a theoretical point of view, a clinical relevant interaction may exist between clopidogrel and cytochrome P450 3A4 metabolized statins.	clopidogrel	84-95	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	100-119
15852218-5	2005	This receptor, the molecular target of the antithrombotic drug clopidogrel, is responsible for most of the potentiating effects of ADP when platelets are stimulated by agents such as thrombin, collagen, or immune complexes.	clopidogrel	63-74	coagulation factor II, thrombin	Homo sapiens	183-191
15738352-10	2005	CONCLUSIONS: In elective stenting without clopidogrel pretreatment, use of a GPIIb/IIIa inhibitor produces superior platelet inhibition and lower myocardial necrosis compared with high-dose (600 mg) or standard-dose (300 mg) clopidogrel loading alone.	clopidogrel	225-236	integrin subunit alpha 2b	Homo sapiens	77-82
15726594-3	2005	Despite these in vitro and ex vivo findings, we observed two patients develop acute HIT while receiving both clopidogrel and aspirin: both patients" sera tested strongly positive in a heparin-dependent washed platelet activation assay (100% serotonin release) and PF4/heparin-enzyme-immunoassay (2.594 and 2.190 absorbance units).	clopidogrel	109-120	platelet factor 4	Homo sapiens	264-267
15609386-7	2005	RESULTS: Within 12 h of the loading dose, platelet activation in the clopidogrel group had decreased (P-selectin by 27.3 per cent, P = 0.017; fibrinogen binding by 34.7 per cent, P = 0.024; stimulated fibrinogen binding by 49.2 per cent, P &lt; 0.001).	clopidogrel	69-80	fibrinogen beta chain	Homo sapiens	142-152
15609386-7	2005	RESULTS: Within 12 h of the loading dose, platelet activation in the clopidogrel group had decreased (P-selectin by 27.3 per cent, P = 0.017; fibrinogen binding by 34.7 per cent, P = 0.024; stimulated fibrinogen binding by 49.2 per cent, P &lt; 0.001).	clopidogrel	69-80	fibrinogen beta chain	Homo sapiens	201-211
15609386-9	2005	Platelet function in the clopidogrel group was significantly suppressed compared with baseline at 1 h, 24 h and 30 days after endovascular intervention (stimulated fibrinogen binding by 53.9, 51.7 and 57.2 per cent respectively; all P &lt; 0.001).	clopidogrel	25-36	fibrinogen beta chain	Homo sapiens	164-174
15657204-6	2005	During hospital stay the typical course of clopidogrel associated TTP was observed with thrombocytopenia and petechial purpura occurring 14 days after drug initiation and prompt response to therapeutic plasma exchanges.	clopidogrel	43-54	ZFP36 ring finger protein	Homo sapiens	66-69
15816325-4	2005	VASP analysis is the most selective method for clopidogrel"s effect.	clopidogrel	47-58	vasodilator stimulated phosphoprotein	Homo sapiens	0-4
15604326-1	2005	OBJECTIVE: To assess a clinically significant interaction between cytochrome P450 3A4 (CYP3A4) metabolised statin and clopidogrel.	clopidogrel	118-129	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	66-85
15782500-11	2005	Meanwhile, aspirin, clopidogrel, and their combination also decreased serum CRP (P &lt; 0.05-0.01), without affecting lipid levels.	clopidogrel	20-31	C-reactive protein	Oryctolagus cuniculus	76-79
15813672-8	2005	In a mechanism possibly unrelated to its effect on platelet reactivity to aggregating stimuli, the presence of the PL(A2) allele might influence the antiaggregatory effect of platelet inhibitory drugs such as aspirin (acetylsalicylic acid), clopidogrel, and GPIIb/IIIa antagonists.	clopidogrel	241-252	phospholipase A2 group IIA	Homo sapiens	115-120
15604326-1	2005	OBJECTIVE: To assess a clinically significant interaction between cytochrome P450 3A4 (CYP3A4) metabolised statin and clopidogrel.	clopidogrel	118-129	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	87-93
15604326-6	2005	MAIN OUTCOME MEASURE: Association of CYP3A4 metabolised statin and clopidogrel use with in-hospital and six month mortality.	clopidogrel	67-78	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	37-43
15604326-9	2005	CONCLUSIONS: Use of a combination of a CYP3A4 statin plus clopidogrel was associated with lower six month mortality and morbidity in patients with acute coronary syndromes.	clopidogrel	58-69	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	39-45
15634270-0	2005	Flow cytometric analysis of intraplatelet VASP phosphorylation for the detection of clopidogrel resistance in patients with ischemic cardiovascular diseases.	clopidogrel	84-95	vasodilator stimulated phosphoprotein	Homo sapiens	42-46
15634270-3	2005	The phosphorylation of vasodilator-stimulated phosphoprotein (VASP), an intraplatelet actin regulatory protein, is dependent on the level of activation of the platelet P2Y12 receptor, which is targeted by clopidogrel.	clopidogrel	205-216	vasodilator stimulated phosphoprotein	Homo sapiens	23-60
15634270-3	2005	The phosphorylation of vasodilator-stimulated phosphoprotein (VASP), an intraplatelet actin regulatory protein, is dependent on the level of activation of the platelet P2Y12 receptor, which is targeted by clopidogrel.	clopidogrel	205-216	vasodilator stimulated phosphoprotein	Homo sapiens	62-66
15634270-3	2005	The phosphorylation of vasodilator-stimulated phosphoprotein (VASP), an intraplatelet actin regulatory protein, is dependent on the level of activation of the platelet P2Y12 receptor, which is targeted by clopidogrel.	clopidogrel	205-216	purinergic receptor P2Y12	Homo sapiens	168-173
15634270-4	2005	The aim of this study was to use a flow cytometric VASP phosphorylation assay to evaluate the efficacy of clopidogrel therapy.	clopidogrel	106-117	vasodilator stimulated phosphoprotein	Homo sapiens	51-55
15634270-9	2005	The flow cytometric analysis of VASP phosphorylation seems to be a suitable test to evaluate the efficacy of clopidogrel treatment.	clopidogrel	109-120	vasodilator stimulated phosphoprotein	Homo sapiens	32-36
16149027-7	2005	Via intracellular signaling, the adenosine diphosphate (ADP) receptor mechanism is closely involved in the activation of GPIIb/IIIa receptors so that also ADP receptor antagonists of the thienopyridine type, especially clopidogrel, can be quantitatively determined by the PADA.	clopidogrel	219-230	integrin subunit alpha 2b	Homo sapiens	121-126
15763887-6	2004	Clopidogrel significantly inhibited both ADP and TRAP-induced platelet responses over time, with steady state inhibition achieved by day 10.	clopidogrel	0-11	TRAP	Homo sapiens	49-53
15280513-9	2004	Statins, glitazones, glycoprotein IIb/IIIa inhibitors, and clopidogrel have been demonstrated to effectively reduce CD40L levels both in vitro and in vivo.	clopidogrel	59-70	CD40 ligand	Homo sapiens	116-121
15583724-2	2004	After metabolic activation, the active clopidogrel metabolite irreversibly impairs the human platelet P2Y12 ADP receptor.	clopidogrel	39-50	purinergic receptor P2Y12	Homo sapiens	102-107
15583724-3	2004	Gialpha-protein activation and inhibition of vasodilator-stimulated phosphoprotein (VASP) phosphorylation are two key elements of the P2Y12 receptor pathway suitable for quantitation of clopidogrel effects.	clopidogrel	186-197	vasodilator stimulated phosphoprotein	Homo sapiens	45-82
15583724-3	2004	Gialpha-protein activation and inhibition of vasodilator-stimulated phosphoprotein (VASP) phosphorylation are two key elements of the P2Y12 receptor pathway suitable for quantitation of clopidogrel effects.	clopidogrel	186-197	vasodilator stimulated phosphoprotein	Homo sapiens	84-88
15583724-3	2004	Gialpha-protein activation and inhibition of vasodilator-stimulated phosphoprotein (VASP) phosphorylation are two key elements of the P2Y12 receptor pathway suitable for quantitation of clopidogrel effects.	clopidogrel	186-197	purinergic receptor P2Y12	Homo sapiens	134-139
15583724-5	2004	We investigated clopidogrel effects in 57 patients after percutaneous coronary intervention and stent implantation by flow cytometry for the analysis of intracellular VASP phosphorylation.	clopidogrel	16-27	vasodilator stimulated phosphoprotein	Homo sapiens	167-171
15583724-9	2004	Comparable amounts of Gialpha and VASP were found in two clopidogrel low-responding patients as well as in two responding patients.	clopidogrel	57-68	vasodilator stimulated phosphoprotein	Homo sapiens	34-38
15583725-6	2004	Individual platelet activation determinations in patients receiving either clopidogrel or abciximab showed a variation in platelet activation as assayed by MPC and CD62P expression.	clopidogrel	75-86	selectin P	Homo sapiens	164-169
15550024-7	2004	Aspirin and clopidogrel were thus found to have similar effects on thrombotic variables and CRP in this patient population.	clopidogrel	12-23	C-reactive protein	Homo sapiens	92-95
15262828-9	2004	In both groups, 600 mg clopidogrel loading significantly inhibited ADP-induced expression of glycoprotein IIb/IIIa and P-selectin receptors.	clopidogrel	23-34	selectin P	Homo sapiens	119-129
15351859-5	2004	Whole blood platelet agglutination was tested by a platelet function assay.TRAP and - in trend - ADP induced p-selectin exposure was reduced by the atorvastatin pretreatment before clopidogrel was added.	clopidogrel	181-192	TRAP	Homo sapiens	75-79
15351859-5	2004	Whole blood platelet agglutination was tested by a platelet function assay.TRAP and - in trend - ADP induced p-selectin exposure was reduced by the atorvastatin pretreatment before clopidogrel was added.	clopidogrel	181-192	selectin P	Homo sapiens	109-119
15351859-6	2004	Combining clopidogrel with atorvastatin in the healthy individuals led to a further reduction in ADP-induced platelet p-selectin exposure.	clopidogrel	10-21	selectin P	Homo sapiens	118-128
15487851-6	2004	Clopidogrel has additional effects on the ADP-induced expression of adhesion molecules (P-selectin, GPIIb/IIIa) and inflammatory mediators (CD40L).	clopidogrel	0-11	selectin P	Homo sapiens	88-98
15487851-6	2004	Clopidogrel has additional effects on the ADP-induced expression of adhesion molecules (P-selectin, GPIIb/IIIa) and inflammatory mediators (CD40L).	clopidogrel	0-11	integrin subunit alpha 2b	Homo sapiens	100-105
15487851-6	2004	Clopidogrel has additional effects on the ADP-induced expression of adhesion molecules (P-selectin, GPIIb/IIIa) and inflammatory mediators (CD40L).	clopidogrel	0-11	CD40 ligand	Homo sapiens	140-145
15291969-10	2004	CONCLUSIONS: The most interesting findings were the high mRNA expression of P2Y12 receptors in lymphocytes potentially explaining the anti-inflammatory effects of clopidogrel, P2Y13 receptors in monocytes and a previously unrecognised expression of P2X4 in lymphocytes and monocytes.	clopidogrel	163-174	purinergic receptor P2Y12	Homo sapiens	76-81
15276105-0	2004	Effect of clopidogrel pretreatment on periprocedural rise in C-reactive protein after percutaneous coronary intervention.	clopidogrel	10-21	C-reactive protein	Homo sapiens	61-79
15276105-1	2004	This study sought to determine the effect of clopidogrel pretreatment on the increase in C-reactive protein (CRP) after percutaneous coronary intervention.	clopidogrel	45-56	C-reactive protein	Homo sapiens	89-107
15276105-1	2004	This study sought to determine the effect of clopidogrel pretreatment on the increase in C-reactive protein (CRP) after percutaneous coronary intervention.	clopidogrel	45-56	C-reactive protein	Homo sapiens	109-112
15276105-2	2004	Clopidogrel pretreatment attenuated the periprocedural increase in CRP by 65% and was independently associated with an attenuation in the CRP increase in a multivariate model.	clopidogrel	0-11	C-reactive protein	Homo sapiens	67-70
15276105-2	2004	Clopidogrel pretreatment attenuated the periprocedural increase in CRP by 65% and was independently associated with an attenuation in the CRP increase in a multivariate model.	clopidogrel	0-11	C-reactive protein	Homo sapiens	138-141
15269827-1	2004	The adenosine diphosphate (ADP) receptor P2Y12 blocking agent clopidogrel is clinically proven to be efficient in preventing thrombotic events.	clopidogrel	62-73	purinergic receptor P2Y12	Homo sapiens	41-46
15205592-8	2004	In conclusion, the T allele of the GP Ia gene modulates platelet aggregation and clopidogrel antiplatelet effects, suggesting an enhanced reactivity to fibrillar collagens (exposed during coronary stenting) in T allele carriers and might contribute to an increased thrombotic risk in these patients.	clopidogrel	81-92	multimerin 1	Homo sapiens	35-40
15156004-7	2004	Platelet aggregation, as well as P-selectin and PAC-1 expression were significantly lower in clopidogrel pre-treated patients at baseline (p&lt;0.001) and at 4 hours (p&lt;0.01), while they were similarly inhibited 24 hours after intervention.	clopidogrel	93-104	selectin P	Homo sapiens	33-43
15316304-1	2004	There has been recent concern regarding the potential for certain HMG CoA reductase inhibitors (statins) to interfere with the activation of clopidogrel, thereby leaving patients susceptible to thrombotic events.	clopidogrel	141-152	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	66-83
15155956-8	2004	However, CD62p expression was significantly suppressed by aspirin treatment (P=0.024) and more substantially suppressed by clopidogrel (P&lt;0.0001) on day 90.	clopidogrel	123-134	selectin P	Homo sapiens	9-14
15155956-9	2004	Furthermore, only clopidogrel treatment (P=0.0016) was significantly independently associated with decreased CD62p expression on day 90.	clopidogrel	18-29	selectin P	Homo sapiens	109-114
15172401-6	2004	RESULTS: Clopidogrel attenuated platelet aggregation to both ADP (10 micromol/l) and TRAP (10 micromol/l) by 22% and P-selectin expression by 16% and 25%, respectively.	clopidogrel	9-20	TRAP	Homo sapiens	85-89
15172401-6	2004	RESULTS: Clopidogrel attenuated platelet aggregation to both ADP (10 micromol/l) and TRAP (10 micromol/l) by 22% and P-selectin expression by 16% and 25%, respectively.	clopidogrel	9-20	selectin P	Homo sapiens	117-127
15172401-9	2004	CONCLUSIONS: Clopidogrel attenuates the agonist effects of ADP and TRAP on platelet secretion, aggregation, and formation of platelet-monocyte and platelet-neutrophil conjugates in patients with ACS.	clopidogrel	13-24	TRAP	Homo sapiens	67-71
15156004-7	2004	Platelet aggregation, as well as P-selectin and PAC-1 expression were significantly lower in clopidogrel pre-treated patients at baseline (p&lt;0.001) and at 4 hours (p&lt;0.01), while they were similarly inhibited 24 hours after intervention.	clopidogrel	93-104	dual specificity phosphatase 2	Homo sapiens	48-53
15149337-2	2004	The present study analyzes the effect of the platelet inhibitor clopidogrel on the early injury and subsequent repair phase of experimental anti-thy1 glomerulonephritis.	clopidogrel	64-75	Thy-1 cell surface antigen	Rattus norvegicus	145-149
15706927-0	2004	[The influence of CGE on expression of IL-1beta and c-fos protein in the hippocampus region in rats following cerebral ischemia-reperfusion].	clopidogrel	18-21	interleukin 1 beta	Rattus norvegicus	39-47
15706927-0	2004	[The influence of CGE on expression of IL-1beta and c-fos protein in the hippocampus region in rats following cerebral ischemia-reperfusion].	clopidogrel	18-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
15706927-1	2004	OBJECTIVE: To observe inhibiting effect of CGE (compound ginseng extract) on increased expression of IL-1beta and c-fos protein following cerebral ischemia-reperfusion.	clopidogrel	43-46	interleukin 1 beta	Rattus norvegicus	101-109
15706927-1	2004	OBJECTIVE: To observe inhibiting effect of CGE (compound ginseng extract) on increased expression of IL-1beta and c-fos protein following cerebral ischemia-reperfusion.	clopidogrel	43-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
15706927-8	2004	CGE inhibited the expression of hippocampus IL-1beta protein, taking effect from the 2 h after reperfusion.	clopidogrel	0-3	interleukin 1 beta	Rattus norvegicus	44-52
15706927-13	2004	The effect of CGE is associated with its dosage, i.e. a larger dosage has a better effect on expression of c-fos protein in post-stroke dementia.	clopidogrel	14-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
15019868-9	2004	Clopidogrel pretreatment was associated with lower ADP-activated platelet CD40L expression in baseline and postprocedural samples.	clopidogrel	0-11	CD40 ligand	Homo sapiens	74-79
15019868-10	2004	Similarly, platelet CD62P expression at all time points in ADP-activated and in baseline and postprocedural TRAP-activated samples was lower in patients pretreated with clopidogrel.	clopidogrel	169-180	selectin P	Homo sapiens	20-25
15019868-10	2004	Similarly, platelet CD62P expression at all time points in ADP-activated and in baseline and postprocedural TRAP-activated samples was lower in patients pretreated with clopidogrel.	clopidogrel	169-180	TRAP	Homo sapiens	108-112
14736431-5	2004	RESULTS: After platelet activation with adenosine diphosphate, thrombin receptor-activating peptide, or U46-619, relative reductions in conformationally activated GP IIb/IIIa receptor expression (evaluated with PAC-1) of 48%, 43%, and 33%, respectively (all p &lt; 0.0001), were seen with clopidogrel, but further 80%, 78%, and 72% (all p &lt; 0.0001) reductions were seen with eptifibatide.	clopidogrel	289-300	integrin subunit alpha 2b	Homo sapiens	163-169
15085057-4	2004	Especially the additional value of GP IIb/IIIa inhibition on top of an aggressive antithrombotic therapy (including aspirin, heparins, and clopidogrel) requires further clarification.	clopidogrel	139-150	integrin subunit alpha 2b	Homo sapiens	35-41
15039127-8	2004	The patients with modest response to clopidogrel had higher levels of c-peptide (1.5 nmol/L) than the ones responding well (0.9 nmol/L, P&lt;0.05).	clopidogrel	37-48	insulin	Homo sapiens	70-79
15154604-3	2004	Aspirin inhibits thromboxane A2 synthesis and clopidogrel acts on the P2Y12 platelet ADP receptor.	clopidogrel	46-57	purinergic receptor P2Y12	Homo sapiens	70-97
14707025-0	2004	Contribution of hepatic cytochrome P450 3A4 metabolic activity to the phenomenon of clopidogrel resistance.	clopidogrel	84-95	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	24-43
14707025-3	2004	Because the prodrug clopidogrel is activated by hepatic cytochrome P450 (CYP) 3A4, we hypothesized that interindividual variability in clopidogrel efficacy might be related to interindividual differences in CYP3A4 metabolic activity.	clopidogrel	20-31	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	56-81
14707025-3	2004	Because the prodrug clopidogrel is activated by hepatic cytochrome P450 (CYP) 3A4, we hypothesized that interindividual variability in clopidogrel efficacy might be related to interindividual differences in CYP3A4 metabolic activity.	clopidogrel	20-31	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	207-213
14707025-3	2004	Because the prodrug clopidogrel is activated by hepatic cytochrome P450 (CYP) 3A4, we hypothesized that interindividual variability in clopidogrel efficacy might be related to interindividual differences in CYP3A4 metabolic activity.	clopidogrel	135-146	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	56-81
14707025-3	2004	Because the prodrug clopidogrel is activated by hepatic cytochrome P450 (CYP) 3A4, we hypothesized that interindividual variability in clopidogrel efficacy might be related to interindividual differences in CYP3A4 metabolic activity.	clopidogrel	135-146	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	207-213
14707025-10	2004	Percent platelet aggregation after clopidogrel inversely correlated with CYP3A4 activity (r=-0.6, P=0.003).	clopidogrel	35-46	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	73-79
14707025-12	2004	CONCLUSIONS: Clopidogrel administration results in interindividual variability in platelet inhibition, which correlates with CYP3A4 metabolic activity.	clopidogrel	13-24	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	125-131
14736431-6	2004	With the same agonists, fibrinogen binding was significantly reduced after clopidogrel by 70%, 64%, and 81% (all p &lt; 0.0001) and again further reduced with eptifibatide by 90%, 95%, and 69% (all p &lt; 0.0001).	clopidogrel	75-86	fibrinogen beta chain	Homo sapiens	24-34
12969982-2	2004	Ex vivo inhibition of the P2Y12 ADP receptor by clopidogrel administration diminished the rapid exposure of tissue factor (TF), the major initiator of coagulation, in conjugates of platelets with leukocytes established by the contact of whole blood with fibrillar collagen.	clopidogrel	48-59	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	26-31
12969982-2	2004	Ex vivo inhibition of the P2Y12 ADP receptor by clopidogrel administration diminished the rapid exposure of tissue factor (TF), the major initiator of coagulation, in conjugates of platelets with leukocytes established by the contact of whole blood with fibrillar collagen.	clopidogrel	48-59	coagulation factor III	Mus musculus	108-121
12969982-2	2004	Ex vivo inhibition of the P2Y12 ADP receptor by clopidogrel administration diminished the rapid exposure of tissue factor (TF), the major initiator of coagulation, in conjugates of platelets with leukocytes established by the contact of whole blood with fibrillar collagen.	clopidogrel	48-59	coagulation factor III	Mus musculus	123-125
14563790-0	2004	Potent mechanism-based inhibition of human CYP2B6 by clopidogrel and ticlopidine.	clopidogrel	53-64	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	43-49
15166949-6	2004	PlA2 carriers had a higher degree of GPIIb/IIIa activation (P = 0.05) and P-selectin expression (P = 0.02) during the overall study time course and a lower antiplatelet effect to a 300 mg clopidogrel loading-dose up to 24 h following intervention (P &lt; 0.05).	clopidogrel	188-199	phospholipase A2 group IB	Homo sapiens	0-4
15166949-7	2004	In conclusion, the Pl polymorphism of the GPIIIa gene modulates platelet reactivity towards clopidogrel front loading in patients undergoing coronary stenting.	clopidogrel	92-103	integrin subunit beta 3	Homo sapiens	42-48
14670370-0	2004	Inhibition of ADP-induced intracellular Ca2+ responses and platelet aggregation by the P2Y12 receptor antagonists AR-C69931MX and clopidogrel is enhanced by prostaglandin E1.	clopidogrel	130-141	purinergic receptor P2Y12	Homo sapiens	87-92
14730251-7	2004	In healthy volunteers, CD40L expression in platelets is not significantly inhibited by acetylsalicylic acid (ASA) alone, but is inhibited after treatment with the ADP-receptor antagonist clopidogrel or with clopidogrel plus ASA.	clopidogrel	187-198	CD40 ligand	Homo sapiens	23-28
14730251-7	2004	In healthy volunteers, CD40L expression in platelets is not significantly inhibited by acetylsalicylic acid (ASA) alone, but is inhibited after treatment with the ADP-receptor antagonist clopidogrel or with clopidogrel plus ASA.	clopidogrel	207-218	CD40 ligand	Homo sapiens	23-28
14979400-7	2004	Flow cytometry demonstrated a significant reduction in ADP-induced platelet P-selectin expression and GPIIb/IIIa activation following treatment with clopidogrel but not with placebo.	clopidogrel	149-160	selectin P	Homo sapiens	76-86
14979400-7	2004	Flow cytometry demonstrated a significant reduction in ADP-induced platelet P-selectin expression and GPIIb/IIIa activation following treatment with clopidogrel but not with placebo.	clopidogrel	149-160	integrin subunit alpha 2b	Homo sapiens	102-107
14563790-4	2004	Both clopidogrel and ticlopidine inhibited CYP2B6 with highest potency and CYP2C19 with lower potency.	clopidogrel	5-16	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	43-49
14563790-4	2004	Both clopidogrel and ticlopidine inhibited CYP2B6 with highest potency and CYP2C19 with lower potency.	clopidogrel	5-16	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	75-82
14563790-5	2004	Clopidogrel also inhibited CYP2C9, and ticlopidine also inhibited CYP1A2, with lower potency.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
14563790-9	2004	A chemical mechanism is discussed based on the known metabolic activation of clopidogrel and on the finding that hemoprotein integrity of recombinant CYP2B6 was not affected by irreversible inhibition.	clopidogrel	77-88	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	150-156
14717977-1	2004	The P2Y12 ADP receptor is one of the major regulators of platelet activation and the target of antithrombotic thienopyridines (ticlopidine and clopidogrel).	clopidogrel	143-154	purinergic receptor P2Y12	Homo sapiens	4-9
14717977-4	2004	Both effects were blocked by the active metabolite of clopidogrel, a specific antagonist of P2Y12.	clopidogrel	54-65	purinergic receptor P2Y12	Homo sapiens	92-97
15381386-6	2004	Clopidogrel treatment inhibited ADP-induced platelet P-selectin expression by 72% (54-85%).	clopidogrel	0-11	selectin P	Homo sapiens	53-63
15381386-8	2004	Clopidogrel prolonged filtragometry readings and attenuated agonist stimulated P-selectin expression at rest, but did not influence TxM in plasma or urine or attenuate platelet or leukocyte responses to exercise.	clopidogrel	0-11	selectin P	Homo sapiens	79-89
14522569-1	2003	AIMS: Clopidogrel is a pro-drug which is converted to an active, unstable drug by cytochrome P450 (CYP).	clopidogrel	6-17	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	82-97
14597948-4	2003	Results and conclusions The therapy with aspirin plus clopidogrel attenuated agonist-induced platelet aggregation and P-selectin surface exposure (P &lt;.05 vs aspirin monotherapy).	clopidogrel	54-65	selectin P	Homo sapiens	118-128
14597979-3	2003	Clopidogrel is a potent antithrombotic compound, metabolised by the liver which generates an active metabolite containing a thiol reactive group, responsible for an irreversible interaction with the platelet P2Y(12) ADP receptor.	clopidogrel	0-11	purinergic receptor P2Y12	Rattus norvegicus	208-215
14522569-1	2003	AIMS: Clopidogrel is a pro-drug which is converted to an active, unstable drug by cytochrome P450 (CYP).	clopidogrel	6-17	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	99-102
14522569-3	2003	It has been recently suggested that the most abundant human CYP isoform, 3A4, activates clopidogrel.	clopidogrel	88-99	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	60-63
14522569-6	2003	ADP-stimulated (1, 10, 100 micromol/l) expression of P-selectin (CD62P) on platelets was measured by flow cytometry, and used as a marker for the antiplatelet effect of clopidogrel.	clopidogrel	169-180	selectin P	Homo sapiens	53-63
14522569-9	2003	CONCLUSION: Certain statins which are substrates of the CYP3A4 isoform competitively inhibit the metabolic activation of clopidogrel.	clopidogrel	121-132	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	56-62
14522569-10	2003	As a result the relative clopidogrel induced platelet inhibition (P-selectin-expression) is diminished--but still there is a relative clopidogrel effect of more than 80% in the maintenance phase.	clopidogrel	25-36	selectin P	Homo sapiens	66-76
14522478-10	2003	CONCLUSIONS: Among patients undergoing coronary stent placement with aspirin and a GP IIb/IIIa inhibitor, clopidogrel pretreatment is associated with a reduction of death and MI irrespective of the type of GP IIb/IIIa inhibitor used.	clopidogrel	106-117	integrin subunit alpha 2b	Homo sapiens	83-89
14610915-4	2003	P2Y12 inhibits adenylyl cyclase through a glycoprotein i (Gi)-dependent pathway, and is the target of the clinically used thienopyridines, ticlopidine (Ticlid, F. Hoffman-La Roche) and clopidogrel (Plavix, Bristol-Myers Squibb/Sanofi-Synthelabo).	clopidogrel	185-196	purinergic receptor P2Y12	Homo sapiens	0-5
12925453-1	2003	BACKGROUND: Statins primarily metabolized by cytochrome P450 3A4 (CYP3A4) reportedly reduce clopidogrel"s metabolism to active metabolite, thus attenuating its inhibition of platelet aggregation ex vivo.	clopidogrel	92-103	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	45-64
12925453-1	2003	BACKGROUND: Statins primarily metabolized by cytochrome P450 3A4 (CYP3A4) reportedly reduce clopidogrel"s metabolism to active metabolite, thus attenuating its inhibition of platelet aggregation ex vivo.	clopidogrel	92-103	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	66-72
12925453-9	2003	This clopidogrel benefit was similar with statin use, irrespective of treatment with a CYP3A4-MET (7.6% clopidogrel, 11.8% control, RRR 36.4%, 95% CI 3.9 to 57.9; P=0.03) or non-CYP3A4-MET statin (5.4% clopidogrel, 13.6% control, RRR 60.6%, 95% CI -23.9 to 87.4; P=0.11).	clopidogrel	5-16	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	178-184
12925453-12	2003	CONCLUSIONS: Although ex vivo testing has suggested a potential negative interaction when coadministering a CYP3A4-metabolized statin with clopidogrel, this was not clinically observed statistically in a post hoc analysis of a placebo-controlled study.	clopidogrel	139-150	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	108-114
12913786-4	2003	P2Y(12) is the target of antithrombotic drugs (ticlopidine, clopidogrel), whereas the role of P2Y(1) in thrombosis remains to be fully established.	clopidogrel	60-71	purinergic receptor P2Y12	Homo sapiens	0-7
12883841-23	2003	CONCLUSION: In patients with FA taking aspirin and clopidogrel, selective thrombin injection is more effective than manual compression.	clopidogrel	51-62	coagulation factor II, thrombin	Homo sapiens	74-82
12560222-3	2003	The thiol agent p-chloromercuribenzene sulfonic acid (pCMBS) and the active metabolites from antiplatelet drugs, clopidogrel and CS-747, inactivate the P2Y(12) receptor and are predicted to interact with the extracellular cysteine residues on the P2Y(12) receptor.	clopidogrel	113-124	purinergic receptor P2Y12	Homo sapiens	152-159
12560222-3	2003	The thiol agent p-chloromercuribenzene sulfonic acid (pCMBS) and the active metabolites from antiplatelet drugs, clopidogrel and CS-747, inactivate the P2Y(12) receptor and are predicted to interact with the extracellular cysteine residues on the P2Y(12) receptor.	clopidogrel	113-124	purinergic receptor P2Y12	Homo sapiens	247-254
12560222-11	2003	We speculate that the active metabolites of clopidogrel and CS-747 form disulfide bridges with both Cys17 and Cys270 in the P2Y(12) receptor, and thereby inactivate the receptor.	clopidogrel	44-55	purinergic receptor P2Y12	Homo sapiens	124-131
14610915-4	2003	P2Y12 inhibits adenylyl cyclase through a glycoprotein i (Gi)-dependent pathway, and is the target of the clinically used thienopyridines, ticlopidine (Ticlid, F. Hoffman-La Roche) and clopidogrel (Plavix, Bristol-Myers Squibb/Sanofi-Synthelabo).	clopidogrel	198-204	purinergic receptor P2Y12	Homo sapiens	0-5
12652502-12	2003	In patients with false aneurysms and failed compression therapy under full-dose aspirin, clopidogrel, and heparin, selective thrombin injection is highly effective and safe.	clopidogrel	89-100	coagulation factor II, thrombin	Homo sapiens	125-133
14618072-1	2003	GP IIb/IIIa antagonists are qualitatively different from classical antiplatelet agents, such as aspirin or clopidogrel.	clopidogrel	107-118	integrin subunit alpha 2b	Homo sapiens	0-6
12812377-16	2003	When administered with such GP IIb/IIIa inhibitors as the Abciximab, Aggrastat or Eptifibratide, these drugs may require dosage adjustment However, since the introduction of the front loading of Clopidogrel, the unqualified use of GP IIb/IIIa is debated.	clopidogrel	195-206	integrin subunit alpha 2b	Homo sapiens	28-34
12812377-16	2003	When administered with such GP IIb/IIIa inhibitors as the Abciximab, Aggrastat or Eptifibratide, these drugs may require dosage adjustment However, since the introduction of the front loading of Clopidogrel, the unqualified use of GP IIb/IIIa is debated.	clopidogrel	195-206	integrin subunit alpha 2b	Homo sapiens	231-237
12812379-1	2003	Clopidogrel acts on the P2Y12 adenosine diphosphate (ADP) purinergic receptors on human platelets.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	24-29
12637702-9	2003	CONCLUSIONS: CD63 expression reflecting the release of platelet lysosomes is consistently increased after stroke and incompletely suppressed by treatment with aspirin, clopidogrel, or both.	clopidogrel	168-179	CD63 molecule	Homo sapiens	13-17
12621388-0	2003	Clopidogrel but not aspirin reduces P-selectin expression and formation of platelet-leukocyte aggregates in patients with atherosclerotic vascular disease.	clopidogrel	0-11	selectin P	Homo sapiens	36-46
12621388-5	2003	Up-regulation of MAC-1 on monocytes after stimulation with thrombin receptor-activating peptide and adenosine diphosphate was significantly lower in patients treated with clopidogrel and aspirin.	clopidogrel	171-182	integrin subunit alpha M	Homo sapiens	17-22
12419297-12	2002	The persistence of thrombin generation despite long-term clopidogrel and aspirin therapy suggests that even more intensive antithrombotic therapy may be required in these patients.	clopidogrel	57-68	coagulation factor II, thrombin	Homo sapiens	19-27
12595840-9	2003	Clopidogrel inhibited GP Ib, platelet/endothelial cell adhesion molecule-1, CD 107a, CD 151, and GP IIb/IIIa expression at day 5 poststenting.	clopidogrel	0-11	lysosomal associated membrane protein 1	Homo sapiens	76-83
12595840-9	2003	Clopidogrel inhibited GP Ib, platelet/endothelial cell adhesion molecule-1, CD 107a, CD 151, and GP IIb/IIIa expression at day 5 poststenting.	clopidogrel	0-11	CD151 molecule (Raph blood group)	Homo sapiens	85-91
12595840-9	2003	Clopidogrel inhibited GP Ib, platelet/endothelial cell adhesion molecule-1, CD 107a, CD 151, and GP IIb/IIIa expression at day 5 poststenting.	clopidogrel	0-11	integrin subunit alpha 2b	Homo sapiens	97-103
12588350-11	2003	Clopidogrel and SR121566 inhibited the increase in tyrosine phosphorylation induced by 2MesADP and concomitantly inhibited platelet aggregation, indicating that most of the phosphorylations are GPIIb/IIIa dependent.	clopidogrel	0-11	integrin subunit alpha 2b	Homo sapiens	194-199
14529392-6	2003	Ticlopidine and clopidogrel are irreversible P2Y12 antagonists and have been repeatedly proven as clinical antithrombotic agents.	clopidogrel	16-27	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	45-50
14529392-9	2003	Clinical studies show that AR-C69931MX is as effective as clopidogrel; furthermore, the combination of AR-C69931MX (cangrelor) and clopidogrel confers greater antagonism of P2Y12 than either antagonist alone.	clopidogrel	131-142	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	173-178
12485953-0	2003	The metabolism of clopidogrel is catalyzed by human cytochrome P450 3A and is inhibited by atorvastatin.	clopidogrel	18-29	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	63-67
12485953-1	2003	The prodrug clopidogrel (Plavix) is activated by cytochrome p450 (p450) to a metabolite that inhibits ADP-induced platelet aggregation.	clopidogrel	12-23	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	60-64
12485953-1	2003	The prodrug clopidogrel (Plavix) is activated by cytochrome p450 (p450) to a metabolite that inhibits ADP-induced platelet aggregation.	clopidogrel	12-23	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	66-70
12485953-1	2003	The prodrug clopidogrel (Plavix) is activated by cytochrome p450 (p450) to a metabolite that inhibits ADP-induced platelet aggregation.	clopidogrel	25-31	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	60-64
12891293-3	2003	AIM: To study changes of parameters of fibrinolysis during short term use of ticlopidine and clopidogrel in NSTEACS patients treated with aspirin and antithrombin.	clopidogrel	93-104	serpin family C member 1	Homo sapiens	150-162
12891293-10	2003	Clopidogrel treated patients on days 3, 7 and 14 had higher levels of TPA both compared with controls (25.7 and 20.2, p&lt;0.05; 26.5 and 12.9, p&lt;0.01; 24.6 and 15.7 ng/ml, p&lt;0.01; respectively) and baseline.	clopidogrel	0-11	plasminogen activator, tissue type	Homo sapiens	70-73
12891293-14	2003	The use of clopidogrel in similar patients treated with aspirin and enoxaparin was associated with elevated levels of TPA and D-dimer what presumably reflected augmentation of fibrinolytic activity.	clopidogrel	11-22	plasminogen activator, tissue type	Homo sapiens	118-121
12515739-2	2003	Because atorvastatin is metabolized by cytochrome P450 (CYP) 3A4, we hypothesized that clopidogrel might be activated by CYP3A4.	clopidogrel	87-98	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	121-127
12515739-7	2003	CONCLUSIONS: CYP3A4 activates clopidogrel.	clopidogrel	30-41	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	13-19
12698015-2	2003	Clopidogrel and ticlopidine are adenosine diphosphate (ADP)-receptor antagonists that inhibit ADP-induced fibrinogen binding to platelets, a necessary step in the platelet aggregation process.	clopidogrel	0-11	fibrinogen beta chain	Homo sapiens	106-116
12485953-1	2003	The prodrug clopidogrel (Plavix) is activated by cytochrome p450 (p450) to a metabolite that inhibits ADP-induced platelet aggregation.	clopidogrel	25-31	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	66-70
12485953-2	2003	Clopidogrel is frequently administered to patients in conjunction with the CYP3A4 substrate atorvastatin (Lipitor).	clopidogrel	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	75-81
12485953-3	2003	Since clinical studies indicate that atorvastatin inhibits the antiplatelet activity of clopidogrel, we investigated whether CYP3A4 metabolized clopidogrel in vitro.	clopidogrel	144-155	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	125-131
12485953-4	2003	Microsomes prepared from dexamethasone-pretreated rats metabolized clopidogrel at a rate of 3.8 nmol min(-1) nmol of p450(-1), which is 65 and 1270% faster than the rate of metabolism by microsomes from control and beta-napthoflavone-treated rats, respectively.	clopidogrel	67-78	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	117-121
12485953-5	2003	To identify the human p450s responsible for clopidogrel oxidation, genetically engineered microsomes containing a single human p450 isozyme were tested for their ability to oxidize clopidogrel.	clopidogrel	44-55	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	22-26
12485953-6	2003	CYP3A4 and 3A5 metabolized clopidogrel at a significantly higher rate than eight other p450 isozymes, suggesting that CYP3A4 and 3A5 are primarily responsible for in vivo clopidogrel metabolism.	clopidogrel	27-38	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
12485953-6	2003	CYP3A4 and 3A5 metabolized clopidogrel at a significantly higher rate than eight other p450 isozymes, suggesting that CYP3A4 and 3A5 are primarily responsible for in vivo clopidogrel metabolism.	clopidogrel	27-38	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	118-124
12485953-6	2003	CYP3A4 and 3A5 metabolized clopidogrel at a significantly higher rate than eight other p450 isozymes, suggesting that CYP3A4 and 3A5 are primarily responsible for in vivo clopidogrel metabolism.	clopidogrel	171-182	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
12485953-6	2003	CYP3A4 and 3A5 metabolized clopidogrel at a significantly higher rate than eight other p450 isozymes, suggesting that CYP3A4 and 3A5 are primarily responsible for in vivo clopidogrel metabolism.	clopidogrel	171-182	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	87-91
12485953-6	2003	CYP3A4 and 3A5 metabolized clopidogrel at a significantly higher rate than eight other p450 isozymes, suggesting that CYP3A4 and 3A5 are primarily responsible for in vivo clopidogrel metabolism.	clopidogrel	171-182	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	118-124
12485953-7	2003	Clopidogrel interacts with human CYP3A4 with a spectral dissociation constant (K(s)), K(m), and V(max) of 12 microM, 14 +/- 1 microM and 6.7 +/- 1 nmol min(-1) nmol p450(-1), respectively.	clopidogrel	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	33-39
12485953-7	2003	Clopidogrel interacts with human CYP3A4 with a spectral dissociation constant (K(s)), K(m), and V(max) of 12 microM, 14 +/- 1 microM and 6.7 +/- 1 nmol min(-1) nmol p450(-1), respectively.	clopidogrel	0-11	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	165-169
12485953-10	2003	Since CYP3A4 and 3A5 metabolize clopidogrel faster than other human p450 isozymes and are the most abundant p450s in human liver, they are predicted to be predominantly responsible for the activation of clopidogrel in vivo.	clopidogrel	32-43	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	6-12
12485953-10	2003	Since CYP3A4 and 3A5 metabolize clopidogrel faster than other human p450 isozymes and are the most abundant p450s in human liver, they are predicted to be predominantly responsible for the activation of clopidogrel in vivo.	clopidogrel	203-214	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	6-12
12485953-10	2003	Since CYP3A4 and 3A5 metabolize clopidogrel faster than other human p450 isozymes and are the most abundant p450s in human liver, they are predicted to be predominantly responsible for the activation of clopidogrel in vivo.	clopidogrel	203-214	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	68-72
14593356-1	2003	Some characteristics of coagulation and von Willebrand factor during short term use of ticlopidine or clopidogrel].	clopidogrel	102-113	von Willebrand factor	Homo sapiens	40-61
14593356-4	2003	AIM: To study changes of markers of coagulation and platelet activation during short term use of ticlopidine and clopidogrel in NSTEACS patients treated with aspirin and antithrombin.	clopidogrel	113-124	serpin family C member 1	Homo sapiens	170-182
14593356-11	2003	In substudy with clopidogrel differences between groups existed only in vWF levels.	clopidogrel	17-28	von Willebrand factor	Homo sapiens	72-75
14593356-12	2003	In clopidogrel treated patients the level vWF was lower relative to controls on days 3 (152 and 185%, r&lt;0.05) and 7 (141 and 166%, r&lt;0.05).	clopidogrel	3-14	von Willebrand factor	Homo sapiens	42-45
14593356-15	2003	Both ticlopidine and clopidogrel used in regimes with loading doses in NSTEACS patients treated with aspirin and antithrombin prevented acute phase elevation of vWF.	clopidogrel	21-32	serpin family C member 1	Homo sapiens	113-125
14593356-15	2003	Both ticlopidine and clopidogrel used in regimes with loading doses in NSTEACS patients treated with aspirin and antithrombin prevented acute phase elevation of vWF.	clopidogrel	21-32	von Willebrand factor	Homo sapiens	161-164
15013268-5	2003	RESULTS: Pretreatment with clopidogrel before PCI exhibited a slight reduction of beta-TG (from 178 to 139 ng/ml, p=0.085) and of f1.2 (from 0.81 to 0.75 nmol/l, p=0.045) in venous blood.	clopidogrel	27-38	pro-platelet basic protein	Homo sapiens	82-89
15013268-5	2003	RESULTS: Pretreatment with clopidogrel before PCI exhibited a slight reduction of beta-TG (from 178 to 139 ng/ml, p=0.085) and of f1.2 (from 0.81 to 0.75 nmol/l, p=0.045) in venous blood.	clopidogrel	27-38	coagulation factor XII	Homo sapiens	130-134
12421153-9	2002	An immunoglobulin (Ig) G autoantibody to the vWF-cleaving metalloprotease is found transiently in many adult patients with acquired acute idiopathic, recurrent, and ticlopidine/clopidogrel-associated TTP.	clopidogrel	177-188	von Willebrand factor	Homo sapiens	45-48
12464982-4	2002	Recently, clopidogrel has been shown to reduce recurrent ischemic events, both early and during the first year after the index ACS.	clopidogrel	10-21	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	127-130
13679651-4	2002	In PRP it is diminished in thrombopathies, in von Willebrand disease, by antibodies blocking GPIIb-IIIa or GPIb, or by antiplatelet drugs like aspirin and clopidogrel.	clopidogrel	155-166	prion protein	Homo sapiens	3-6
12714834-0	2002	Changes in platelet P-selectin and in plasma C-reactive protein in acute atherosclerotic ischemic stroke treated with a loading dose of clopidogrel.	clopidogrel	136-147	selectin P	Homo sapiens	20-30
12714834-0	2002	Changes in platelet P-selectin and in plasma C-reactive protein in acute atherosclerotic ischemic stroke treated with a loading dose of clopidogrel.	clopidogrel	136-147	C-reactive protein	Homo sapiens	45-63
12714834-2	2002	In this study, we showed that the combination regimen of clopidogrel with aspirin could downregulate the P-selectin expression on platelets and the plasma concentration of C-reactive protein (CRP) in acute stage of atherosclerotic ischemic stroke.	clopidogrel	57-68	selectin P	Homo sapiens	105-115
12714834-2	2002	In this study, we showed that the combination regimen of clopidogrel with aspirin could downregulate the P-selectin expression on platelets and the plasma concentration of C-reactive protein (CRP) in acute stage of atherosclerotic ischemic stroke.	clopidogrel	57-68	C-reactive protein	Homo sapiens	172-190
12714834-2	2002	In this study, we showed that the combination regimen of clopidogrel with aspirin could downregulate the P-selectin expression on platelets and the plasma concentration of C-reactive protein (CRP) in acute stage of atherosclerotic ischemic stroke.	clopidogrel	57-68	C-reactive protein	Homo sapiens	192-195
12714834-5	2002	RESULTS: The combined regimen of clopidogrel and aspirin significantly reduced platelet P-selectin expression (93.6 +/- 16.6, p &lt; 0.01) and plasma concentration of CRP (1.2 +/- 1.5 mg/dl, p &lt; 0.01) after 7 days of stroke onset compared with the values (P-selectin; 115.5 +/- 20.7, CRP; 2.5 +/- 2.8 mg/dl) of initial 24 hr.	clopidogrel	33-44	selectin P	Homo sapiens	88-98
12714834-5	2002	RESULTS: The combined regimen of clopidogrel and aspirin significantly reduced platelet P-selectin expression (93.6 +/- 16.6, p &lt; 0.01) and plasma concentration of CRP (1.2 +/- 1.5 mg/dl, p &lt; 0.01) after 7 days of stroke onset compared with the values (P-selectin; 115.5 +/- 20.7, CRP; 2.5 +/- 2.8 mg/dl) of initial 24 hr.	clopidogrel	33-44	C-reactive protein	Homo sapiens	167-170
12714834-5	2002	RESULTS: The combined regimen of clopidogrel and aspirin significantly reduced platelet P-selectin expression (93.6 +/- 16.6, p &lt; 0.01) and plasma concentration of CRP (1.2 +/- 1.5 mg/dl, p &lt; 0.01) after 7 days of stroke onset compared with the values (P-selectin; 115.5 +/- 20.7, CRP; 2.5 +/- 2.8 mg/dl) of initial 24 hr.	clopidogrel	33-44	selectin P	Homo sapiens	259-269
12714834-5	2002	RESULTS: The combined regimen of clopidogrel and aspirin significantly reduced platelet P-selectin expression (93.6 +/- 16.6, p &lt; 0.01) and plasma concentration of CRP (1.2 +/- 1.5 mg/dl, p &lt; 0.01) after 7 days of stroke onset compared with the values (P-selectin; 115.5 +/- 20.7, CRP; 2.5 +/- 2.8 mg/dl) of initial 24 hr.	clopidogrel	33-44	C-reactive protein	Homo sapiens	287-290
12353080-2	2002	Clopidogrel and the novel intravenous antithrombotic agent AR-C69931MX act at the level of the platelet P2Y12 receptor, which is known to amplify platelet activation, aggregation and other responses induced by numerous platelet agonists.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	104-109
12353080-6	2002	Clopidogrel and AR-C69931MX suppressed ADP-induced platelet aggregation, P-selectin expression and platelet-leukocyte conjugate formation whereas aspirin had no inhibitory effect.	clopidogrel	0-11	selectin P	Homo sapiens	73-83
12121059-3	2002	Clopidogrel is a ticlopidin-related antiplatelet drug, with the same mechanism of action; it reduces the expression of the glycoprotein IIb/IIIa, the fibrinogen receptor on the platelet surface.	clopidogrel	0-11	fibrinogen beta chain	Homo sapiens	150-160
12204495-2	2002	BACKGROUND: No data are available yet as to whether additional administration of a GP IIb/IIIa receptor antagonist might be beneficial in patients undergoing elective PCI already pretreated with aspirin and clopidogrel.	clopidogrel	207-218	integrin subunit alpha 2b	Homo sapiens	83-89
12204495-7	2002	CONCLUSIONS: Troponin T release occurs after successful intervention in 74% of the patients undergoing elective PCI after 48 h even after pretreatment with aspirin and clopidogrel.	clopidogrel	168-179	troponin T1, slow skeletal type	Homo sapiens	13-23
11904526-3	2002	Adenosine diphosphate (ADP)-induced expression of P-selectin and of PAC-1 was significantly reduced after 2 wk of clopidogrel but not of ASA treatment.	clopidogrel	114-125	selectin P	Homo sapiens	50-60
11904526-3	2002	Adenosine diphosphate (ADP)-induced expression of P-selectin and of PAC-1 was significantly reduced after 2 wk of clopidogrel but not of ASA treatment.	clopidogrel	114-125	dual specificity phosphatase 2	Homo sapiens	68-73
11904526-7	2002	ADP-induced platelet degranulation, activation of GPIIb/IIIa receptor, and aggregation in vivo are effectively inhibited by clopidogrel.	clopidogrel	124-135	integrin subunit alpha 2b	Homo sapiens	50-55
11875746-2	2002	We have recently demonstrated that the thienopyridine SR 25989 an enantiomer of the anti-aggregant clopidogrel (Plavix) lacking anti-aggregant activity, inhibits endothelial cell proliferation in vitro by increasing the expression of endogenous thrombospondin-1, a natural potent inhibitor of angiogenesis.	clopidogrel	99-110	thrombospondin 1	Mus musculus	245-261
11907492-0	2002	Clopidogrel, but not abciximab, reduces platelet leukocyte conjugates and P-selectin expression in a human ex vivo in vitro model.	clopidogrel	0-11	selectin P	Homo sapiens	74-84
11907492-3	2002	Expression of CD62 was significantly reduced 30% to 50% with clopidogrel, depending on the type and concentration of the inducer, but addition of abciximab led to a significant approximately 30% increase in CD62 expression when platelets were stimulated by ADP.	clopidogrel	61-72	selectin P	Homo sapiens	14-18
11861803-3	2002	The principal findings were 1) expression of CD62 as a constituent of platelet alpha-granule membrane and secretion of PDGF, an important ingredient of alpha-granules, can be stimulated by TRAP-induced activation in a dose-dependent fashion; 2) the activation marker and secretion product are closely correlated with each other; and 3) changes in the CD62 expression induced by a drug, namely clopidogrel, or by a disease, namely diabetes, are paralleled by changes in PDGF secretion.	clopidogrel	393-404	selectin P	Homo sapiens	45-49
11861803-3	2002	The principal findings were 1) expression of CD62 as a constituent of platelet alpha-granule membrane and secretion of PDGF, an important ingredient of alpha-granules, can be stimulated by TRAP-induced activation in a dose-dependent fashion; 2) the activation marker and secretion product are closely correlated with each other; and 3) changes in the CD62 expression induced by a drug, namely clopidogrel, or by a disease, namely diabetes, are paralleled by changes in PDGF secretion.	clopidogrel	393-404	TRAP	Homo sapiens	189-193
12168564-9	2002	Administration of clopidogrel but not aspirin significantly decreased serum levels of soluble intercellular adhesion molecule-1, whereas no changes in levels of soluble vascular cell adhesion molecule-1, P-selectin, L-selectin, von Willebrand factor, platelet-derived growth factor, vascular-endothelial growth factor, and transforming growth factor-beta were observed.	clopidogrel	18-29	vascular endothelial growth factor A	Homo sapiens	283-317
11773921-0	2002	Effect of 300- and 450-mg clopidogrel loading doses on membrane and soluble P-selectin in patients undergoing coronary stent implantation.	clopidogrel	26-37	selectin P	Homo sapiens	76-86
11818464-5	2002	An IgG autoantibody to the vWf-cleaving metalloprotease is found transiently in many adult patients with acute idiopathic, recurrent, and ticlopidine/clopidogrel-associated TTP.	clopidogrel	150-161	von Willebrand factor	Homo sapiens	27-30
12214159-4	2002	Aspirin plus clopidogrel significantly inhibited platelet aggregation, fibrinogen receptor activation and release of P-selectin and prolonged in vitro bleeding time (p &lt; 0.01).	clopidogrel	13-24	selectin P	Homo sapiens	117-127
11520515-0	2001	Clopidogrel in invasive management of non-ST-elevation ACS.	clopidogrel	0-11	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	55-58
11816721-4	2001	MAP4-RPPGF administration had a sustained antiplatelet effect, preventing gamma-thrombin-induced (12.5 nM) platelet activation for 4 h. Its antiplatelet effect summated with that of aspirin and/or clopidogrel.	clopidogrel	197-208	microtubule associated protein 4	Canis lupus familiaris	0-4
11454254-3	2001	The thienopyridines, ticlopidine and clopidogrel, act, via metabolites, on the platelet ADP receptor subtype now designated P2Y(12 )(formerly P(2T), P2T (AC), P2Y (ADP) or P2Y(cyc)) and these agents have proven clinical efficacy.	clopidogrel	37-48	purinergic receptor P2Y12	Homo sapiens	159-168
11413167-4	2001	P2Y12 has been shown to be the target of the thienopyridine drugs, ticlopidine and clopidogrel.	clopidogrel	83-94	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	0-5
11454254-3	2001	The thienopyridines, ticlopidine and clopidogrel, act, via metabolites, on the platelet ADP receptor subtype now designated P2Y(12 )(formerly P(2T), P2T (AC), P2Y (ADP) or P2Y(cyc)) and these agents have proven clinical efficacy.	clopidogrel	37-48	purinergic receptor P2Y12	Homo sapiens	172-180
11209975-7	2000	Studies with P2Y1 knock-out mice as well as the use of selective P2Y1 antagonists have shown that, in addition to the P2Y receptor, which is the target of clopidogrel, the P2Y1 receptor is an important potential target for new antithrombotic drugs.	clopidogrel	155-166	purinergic receptor P2Y, G-protein coupled 1	Mus musculus	65-69
11416985-6	2001	Recently it is found that vWF protease is deficient in hereditary TTP, intermittent relapsing TTP, idiopathic acute TTP and ticlopidine- and clopidogrel-induced TTP, but normal in hemolytic uremic syndrome and organ transplantation-related thrombotic microangiopathy.	clopidogrel	141-152	von Willebrand factor	Homo sapiens	26-29
11297035-0	2001	Platelet CD40 ligand (CD40L)--subcellular localization, regulation of expression, and inhibition by clopidogrel.	clopidogrel	100-111	CD40 ligand	Homo sapiens	9-20
11297035-0	2001	Platelet CD40 ligand (CD40L)--subcellular localization, regulation of expression, and inhibition by clopidogrel.	clopidogrel	100-111	CD40 ligand	Homo sapiens	22-27
11297035-10	2001	In contrast, clopidogrel treatment completely abolished ADP-induced expression of CD40L.	clopidogrel	13-24	CD40 ligand	Homo sapiens	82-87
11316916-4	2001	A potential clinically useful advantage of clopidogrel is its low propensity for adverse interaction with angiotensin-converting enzyme (ACE) inhibitors, contrary to what may be seen with aspirin, as observed in a post-hoc CAPRIE analysis.	clopidogrel	43-54	angiotensin I converting enzyme	Homo sapiens	106-135
11316916-4	2001	A potential clinically useful advantage of clopidogrel is its low propensity for adverse interaction with angiotensin-converting enzyme (ACE) inhibitors, contrary to what may be seen with aspirin, as observed in a post-hoc CAPRIE analysis.	clopidogrel	43-54	angiotensin I converting enzyme	Homo sapiens	137-140
11316916-5	2001	The putative aspirin-ACE inhibitor interaction is being tested prospectively in the Warfarin and Antiplatelet Therapy in Chronic Heart Failure (WATCH) trial - a randomized comparison of warfarin, clopidogrel and aspirin in patients with chronic heart failure.	clopidogrel	196-207	angiotensin I converting enzyme	Homo sapiens	21-24
11192941-1	2000	We propose that anti-platelet thienopyridines, such as ticlopidine or clopidogrel, are thrombolytic owing to endothelial release of prostacyclin (PGI2) and tissue plasminogen activator (t-PA).	clopidogrel	70-81	plasminogen activator, tissue type	Rattus norvegicus	156-190
10446085-0	1999	Specific impairment of human platelet P2Y(AC) ADP receptor-mediated signaling by the antiplatelet drug clopidogrel.	clopidogrel	103-114	purinergic receptor P2Y12	Homo sapiens	38-45
10987587-6	2000	Clopidogrel with or without aspirin significantly suppressed expression of platelet activation markers CD 62p, CD 63 and PAC-1 after stimulation with ADP or thrombin (p &lt; 0.001).	clopidogrel	0-11	selectin P	Homo sapiens	103-109
10987587-6	2000	Clopidogrel with or without aspirin significantly suppressed expression of platelet activation markers CD 62p, CD 63 and PAC-1 after stimulation with ADP or thrombin (p &lt; 0.001).	clopidogrel	0-11	CD63 molecule	Homo sapiens	111-116
10987587-6	2000	Clopidogrel with or without aspirin significantly suppressed expression of platelet activation markers CD 62p, CD 63 and PAC-1 after stimulation with ADP or thrombin (p &lt; 0.001).	clopidogrel	0-11	ADCYAP receptor type I	Homo sapiens	121-126
10987587-6	2000	Clopidogrel with or without aspirin significantly suppressed expression of platelet activation markers CD 62p, CD 63 and PAC-1 after stimulation with ADP or thrombin (p &lt; 0.001).	clopidogrel	0-11	coagulation factor II, thrombin	Homo sapiens	157-165
10987587-10	2000	Clopidogrel in combination with aspirin showed synergistic inhibitory effects after stimulation with collagen and thrombin compared with monotherapies.	clopidogrel	0-11	coagulation factor II, thrombin	Homo sapiens	114-122
11317178-3	2000	The clinical significance of this event as well as a possible interaction between clopidogrel and other drugs metabolized by the cytochrome P450 2C9 pathways coadministered to this patient are discussed.	clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-148
10741635-7	2000	Fibrinogen binding to the platelet GPIIb/IIIa receptor was reduced for aspirin to 69% (difference not significant), to 63% for clopidogrel (difference not significant), and to 63% for the clopidogrel plus aspirin combination (P &lt; .01).	clopidogrel	127-138	integrin subunit alpha 2b	Homo sapiens	35-40
10741635-7	2000	Fibrinogen binding to the platelet GPIIb/IIIa receptor was reduced for aspirin to 69% (difference not significant), to 63% for clopidogrel (difference not significant), and to 63% for the clopidogrel plus aspirin combination (P &lt; .01).	clopidogrel	188-199	integrin subunit alpha 2b	Homo sapiens	35-40
10741635-8	2000	CD62 expression as a marker of platelet granular secretion was reduced to 66% by clopidogrel (P &lt; .01) and to 41% by the combination of clopidogrel and aspirin; aspirin alone had no effect.	clopidogrel	81-92	selectin P	Homo sapiens	0-4
10741635-8	2000	CD62 expression as a marker of platelet granular secretion was reduced to 66% by clopidogrel (P &lt; .01) and to 41% by the combination of clopidogrel and aspirin; aspirin alone had no effect.	clopidogrel	139-150	selectin P	Homo sapiens	0-4
10741635-9	2000	In vitro, with pretreatment with aspirin and clopidogrel, inhibitory effects of the GPIIb/IIIa inhibitors on fibrinogen binding were additive to changes observed with aspirin or clopidogrel alone.	clopidogrel	45-56	integrin subunit alpha 2b	Homo sapiens	84-89
10741635-11	2000	Aspirin and clopidogrel reinforced effects of the GPIIb/IIIa inhibitors on adenosine diphosphate (5 micromol/L)-induced aggregation in an additive manner, a supra-additive effect was observed with collagen (2 microg x mL(-1))-induced aggregation.	clopidogrel	12-23	integrin subunit alpha 2b	Homo sapiens	50-55
10741635-12	2000	CONCLUSION: The augmentation of the antiaggregatory effects of GPIIb/IIIa inhibitors by aspirin and clopidogrel and the lack of antisecretory effects of GPIIb/IIIa inhibitors may favor their combination with clopidogrel.	clopidogrel	100-111	integrin subunit alpha 2b	Homo sapiens	63-68
10446085-7	1999	In contrast, clopidogrel treatment specifically impairs the ADP receptor coupled to G(i)/adenylyl cyclase (P2Y(AC) ADP receptors).	clopidogrel	13-24	purinergic receptor P2Y12	Homo sapiens	107-114
10446085-8	1999	Clopidogrel abolishes the inhibitory P2Y(AC) receptor-mediated ADP effects on prostaglandin E(1)-stimulated, cAMP-dependent phosphorylation of VASP without affecting epinephrine, thrombin, and thromboxane signaling.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	37-44
10446085-8	1999	Clopidogrel abolishes the inhibitory P2Y(AC) receptor-mediated ADP effects on prostaglandin E(1)-stimulated, cAMP-dependent phosphorylation of VASP without affecting epinephrine, thrombin, and thromboxane signaling.	clopidogrel	0-11	vasodilator stimulated phosphoprotein	Homo sapiens	143-147
10446085-10	1999	Therefore, inhibition of the platelet P2Y(AC) ADP receptor and its intracellular signaling, including decreased VASP phosphorylation, is suggested as a molecular mechanism of clopidogrel action.	clopidogrel	175-186	purinergic receptor P2Y12	Homo sapiens	38-45
10446085-10	1999	Therefore, inhibition of the platelet P2Y(AC) ADP receptor and its intracellular signaling, including decreased VASP phosphorylation, is suggested as a molecular mechanism of clopidogrel action.	clopidogrel	175-186	vasodilator stimulated phosphoprotein	Homo sapiens	112-116
9792116-7	1998	The intravenous injection of clopidogrel and ticlopidine caused significant vasomodulatory actions in both femoral and pulmonary ring preparations showing a marked desensitization to serotonin, endothelin-1, serum, and platelet rich plasma/arachidonic acid mixtures.	clopidogrel	29-40	endothelin 1	Canis lupus familiaris	194-206
10581998-6	1999	Among antiplatelet agents, the logic combination of aspirin and ticlopidine or clopidogrel is already challenging the anti-GP IIb/IIIa orally active compounds.	clopidogrel	79-90	integrin subunit alpha 2b	Homo sapiens	123-129
10404775-0	1999	Effect of clopidogrel on thrombin generation in platelet-rich plasma in the rat.	clopidogrel	10-21	coagulation factor II	Rattus norvegicus	25-33
10404775-3	1999	Clopidogrel reduced the area under the curve (23%, p &lt;0.05) and the thrombin peak concentration (35%, p &lt;0.05) but did not affect the lag phase of thrombin generation.	clopidogrel	0-11	coagulation factor II	Rattus norvegicus	71-79
10440415-1	1999	The inhibition of platelet aggregation by clopidogrel, a novel platelet ADP-receptor antagonist, was evaluated in healthy male volunteers in two single-dose studies.	clopidogrel	42-53	purinergic receptor P2Y12	Homo sapiens	63-84
10440416-1	1999	The effect of repeated doses of clopidogrel, a novel platelet ADP-receptor antagonist, on platelet aggregation and its tolerance were assessed in two randomized, double-blind studies in healthy male adults.	clopidogrel	32-43	purinergic receptor P2Y12	Homo sapiens	53-74
9447704-0	1997	Angiogenesis inhibitor SR 25989 upregulates thrombospondin-1 expression in human vascular endothelial cells and foreskin fibroblasts.	clopidogrel	23-31	thrombospondin 1	Homo sapiens	44-60
9447464-10	1997	As determined by the use of inhibitor, CaMKII activity is associated with 2PBE and PF but not with CGE.	clopidogrel	99-102	calcium/calmodulin-dependent protein kinase II, beta	Mus musculus	39-45
9447704-2	1997	Human endothelial cells grown in the presence of SR 25989 showed moderate increases in the production of activators (tissue plasminogen activator and urokinase) and one inhibitor (plasminogen activator inhibitor type 1) of fibrinolysis, together with a significant rise in intracellular thrombospondin-1.	clopidogrel	49-57	thrombospondin 1	Homo sapiens	287-303
9447704-3	1997	SR 25989 induced a similar increase in thrombospondin-1 in human foreskin fibroblasts.	clopidogrel	0-8	thrombospondin 1	Homo sapiens	39-55
9136964-6	1997	Clopidogrel treatment inhibited the increase in phosphorylation of P140, P100, P80/85, P66 and P55 concomitantly with the inhibition of platelet aggregation.	clopidogrel	0-11	TATA-box binding protein associated factor 6	Rattus norvegicus	73-85
9219328-6	1997	The aortas harvested from both the rabbits and rats treated with clopidogrel or ticlopidine exhibited marked desensitization to the serotonin, endothelin-1, serum and platelet rich plasma/arachidonic acid mixtures.	clopidogrel	65-76	endothelin 1	Rattus norvegicus	143-155
9136964-6	1997	Clopidogrel treatment inhibited the increase in phosphorylation of P140, P100, P80/85, P66 and P55 concomitantly with the inhibition of platelet aggregation.	clopidogrel	0-11	MAGUK p55 scaffold protein 1	Rattus norvegicus	95-98
8977459-9	1996	Flow cytometry confirmed that the number of ligand-occupied GP IIb/IIIa complexes was much lower on platelets stimulated with ADP or 2-MeS-ADP after clopidogrel treatment.	clopidogrel	149-160	integrin subunit alpha 2b	Homo sapiens	60-66
8171410-0	1994	Effect of aspirin and clopidogrel on platelet-dependent tissue factor expression in endothelial cells.	clopidogrel	22-33	coagulation factor III, tissue factor	Rattus norvegicus	56-69
8578547-3	1995	Oral clopidogrel (3-10mg/kg) inhibited ex-vivo platelet aggregation induced by ADP, thrombin or the thromboxane A2 mimetic, and U46619, when platelets had been primed with low concentration of phorbol myristate acetate.	clopidogrel	5-16	coagulation factor II	Rattus norvegicus	84-92
7630043-3	1995	Vapiprost, a specific TXA2-receptor antagonist; clopidogrel, which has the thienopyridine structure of ticlopidine and is a more potent inhibitor of ADP-induced platelet aggregation than ticlopidine; argatroban, a specific thrombin inhibitor; or heparin was administered intravenously before rose bengal injection.	clopidogrel	48-59	coagulation factor II	Rattus norvegicus	223-231
8171410-6	1994	When administered orally at the dose of 25 mg/kg, clopidogrel, a potent and selective analogue of ticlopidine, was able to inhibit platelet-induced tissue factor expression whereas aspirin (100 mg/kg, p.o.)	clopidogrel	50-61	coagulation factor III, tissue factor	Rattus norvegicus	148-161
24140755-1	2013	The clinical efficacy of the P2Y12 receptor antagonist clopidogrel as an agent to prevent thrombotic events predominantly reflects its anti-aggregatory effects.	clopidogrel	55-66	purinergic receptor P2Y12	Homo sapiens	29-34
2053105-7	1991	Under these conditions, it was not surprising to find that clopidogrel also potently inhibited that effect of thrombin on platelet adenylate cyclase.	clopidogrel	59-70	coagulation factor II	Rattus norvegicus	110-118
33795788-2	2021	However, the efficacy of clopidogrel has been shown to be affected by cytochrome P450 2C19 (CYP2C19) polymorphisms.	clopidogrel	25-36	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	92-99
33795788-4	2021	In order to optimize antiplatelet therapy for these patients and avoid the waste of medical resources, it is important to identify the subgroups that genuinely benefit from DAPT with clopidogrel plus aspirin through CYP2C19 genotyping.	clopidogrel	183-194	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	216-223
33774763-0	2021	Risk of major adverse cardiovascular events for concomitant use of clopidogrel and proton pump inhibitors in patients inheriting CYP2C19 loss-of-function alleles: meta-analysis.	clopidogrel	67-78	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	129-136
33774763-1	2021	Background Efficacy of clopidogrel may be diminished due to either co-administration of proton pump inhibitors or carrying CYP2C19 loss-of-function alleles.	clopidogrel	23-34	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	123-130
33774763-2	2021	However, patients may be at greater risk of major adverse cardiovascular events if taking clopidogrel together with proton pump inhibitors and also inherited the CYP2C19 loss-of-function alleles which may cause further reduction of clopidogrel efficacy.	clopidogrel	232-243	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	162-169
33774763-12	2021	Conclusion Patients inheriting CYP2C19 loss-of-function alleles have significantly increased risk of major adverse cardiovascular events when taking clopidogrel and proton pump inhibitors concurrently.	clopidogrel	149-160	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	31-38
33817306-0	2021	ABCB1 polymorphism in clopidogrel-treated Montenegrin patients.	clopidogrel	22-33	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
33819246-2	2021	The potent P2Y12 blocker, Ticagrelor has greater anti-platelet effects than Clopidogrel.	clopidogrel	76-87	purinergic receptor P2Y12	Homo sapiens	11-16
33232268-0	2020	A SNP involved in alternative splicing of ABCB1 is associated with clopidogrel resistance in coronary heart disease in Chinese population.	clopidogrel	67-78	ATP binding cassette subfamily B member 1	Homo sapiens	42-47
26159874-5	2015	The incidence of PM status by phenotype following administration of omeprazole/esomeprazole (known inhibitors of CYP2C19) was 10-fold higher than those who are genetically PMs in the general population, which could have critical clinical implications for personalizing medications primarily metabolized by CYP2C19, such as clopidogrel, PPI, cyclophosphamide, thalidomide, citalopram, clonazepam, diazepam, phenytoin, etc.	clopidogrel	323-334	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	113-120
24140755-5	2013	Considerable attention has been so far directed to the finding that stent thrombosis occurs more frequently in patients with loss-of-function mutations of CYP2C19, thus limiting clopidogrel bioactivation.	clopidogrel	178-189	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	155-162
24140755-8	2013	Here we critically review available literature and speculate on the possibility that non-genetic causes of clopidogrel "resistance" may arise from impairments of the intracellular signaling cascade initiated by P2Y12 receptor inhibition.	clopidogrel	107-118	purinergic receptor P2Y12	Homo sapiens	211-216
24140755-9	2013	In such cases, "resistance" to clopidogrel may also theoretically occur with other P2Y12 receptor antagonists, irrespective of the need for bioactivation.	clopidogrel	31-42	purinergic receptor P2Y12	Homo sapiens	83-88
21806493-6	2012	A maximum reduction of ADP- or TRAP-induced platelet aggregation in 28 clopidogrel responding patients was observed at 5 days postclopidogrel loading, whereas in nonresponders, it was achieved at 30-days along with a significant decrease in the PRI values.	clopidogrel	71-82	TRAP	Homo sapiens	31-35
23506580-0	2013	Effects of coexisting polymorphisms of CYP2C19 and P2Y12 on clopidogrel responsiveness and clinical outcome in patients with acute coronary syndromes undergoing stent-based coronary intervention.	clopidogrel	60-71	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	39-46
23506580-0	2013	Effects of coexisting polymorphisms of CYP2C19 and P2Y12 on clopidogrel responsiveness and clinical outcome in patients with acute coronary syndromes undergoing stent-based coronary intervention.	clopidogrel	60-71	purinergic receptor P2Y12	Homo sapiens	51-56
23506580-1	2013	BACKGROUND: The CYP2C19 G681A single polymorphism has been proven to affect clopidogrel responsiveness.	clopidogrel	76-87	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
23506580-3	2013	This study investigated the effect of coexisting polymorphisms of CYP2C19 and P2Y12 on clopidogrel responsiveness and adverse clinical events in Chinese patients.	clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	66-73
23506580-3	2013	This study investigated the effect of coexisting polymorphisms of CYP2C19 and P2Y12 on clopidogrel responsiveness and adverse clinical events in Chinese patients.	clopidogrel	87-98	purinergic receptor P2Y12	Homo sapiens	78-83
34474410-0	2022	Platelet miR-107 Participates in Clopidogrel Resistance after PCI Treatment by Regulating P2Y12.	clopidogrel	33-44	microRNA 107	Homo sapiens	9-16
22751292-6	2012	The new, more potent P2Y12 receptor blockers overcome the limitations of clopidogrel therapy and are associated with better clinical efficacy, but are more costly and associated with more bleeding.	clopidogrel	73-84	purinergic receptor P2Y12	Homo sapiens	21-26
34213715-0	2022	Association of lipoprotein(a) with intrinsic and on-clopidogrel platelet reactivity.	clopidogrel	52-63	lipoprotein(a)	Homo sapiens	15-29
34357557-2	2022	The cornerstone of treatment of patients with ACS is dual antiplatelet therapy (DAPT) consisting of low-dose aspirin and a P2Y12 inhibitor (clopidogrel, prasugrel or ticagrelor) for 12 months, or less in those patients at higher risk for bleeding.	clopidogrel	140-151	purinergic receptor P2Y12	Homo sapiens	123-128
34866404-2	2022	This review aimed to investigate the effect of polymorphisms of G6PD, GCLC, GCLM, GSS, GST, GSR, HK and GLRX genes on clopidogrel during phase II metabolism through exploring previous studies.	clopidogrel	118-129	glucose-6-phosphate dehydrogenase	Homo sapiens	64-68
34866404-2	2022	This review aimed to investigate the effect of polymorphisms of G6PD, GCLC, GCLM, GSS, GST, GSR, HK and GLRX genes on clopidogrel during phase II metabolism through exploring previous studies.	clopidogrel	118-129	glutamate-cysteine ligase catalytic subunit	Homo sapiens	70-74
34866404-2	2022	This review aimed to investigate the effect of polymorphisms of G6PD, GCLC, GCLM, GSS, GST, GSR, HK and GLRX genes on clopidogrel during phase II metabolism through exploring previous studies.	clopidogrel	118-129	glutamate-cysteine ligase modifier subunit	Homo sapiens	76-80
34866404-2	2022	This review aimed to investigate the effect of polymorphisms of G6PD, GCLC, GCLM, GSS, GST, GSR, HK and GLRX genes on clopidogrel during phase II metabolism through exploring previous studies.	clopidogrel	118-129	glutathione synthetase	Homo sapiens	82-85
34866404-2	2022	This review aimed to investigate the effect of polymorphisms of G6PD, GCLC, GCLM, GSS, GST, GSR, HK and GLRX genes on clopidogrel during phase II metabolism through exploring previous studies.	clopidogrel	118-129	glutaredoxin	Homo sapiens	104-108
34958683-7	2022	A retrospective multivariate analysis indicated that patients belonging to the non-responder phenotype to treatment with aspirin and clopidogrel were older, presented with diffuse coronary disease, a group largely overlapping with type 2 insulin-dependent diabetes mellitus, and were taking dihidropyrimidinic calcium channel blockers.	clopidogrel	133-144	insulin	Homo sapiens	238-245
33033370-1	2021	Patients bearing polymorphisms termed CYP2C19 loss of function (LoF) alleles and ABCB1-C3435T may do not properly respond to standard dosage of clopidogrel and have an increased risk of thrombosis.	clopidogrel	144-155	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	38-45
33033370-1	2021	Patients bearing polymorphisms termed CYP2C19 loss of function (LoF) alleles and ABCB1-C3435T may do not properly respond to standard dosage of clopidogrel and have an increased risk of thrombosis.	clopidogrel	144-155	ATP binding cassette subfamily B member 1	Homo sapiens	81-86
33033370-5	2021	In addition, we have made a comparison of the literature data with our findings concerning patients eligible for vascular surgery and treated with clopidogrel, in whom we used a combined management based on the CYP2C19 and ABCB1 pharmacogenetic testing with monitoring of therapeutic adherence and PPIs-clopidogrel interaction.	clopidogrel	147-158	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	211-218
33033370-5	2021	In addition, we have made a comparison of the literature data with our findings concerning patients eligible for vascular surgery and treated with clopidogrel, in whom we used a combined management based on the CYP2C19 and ABCB1 pharmacogenetic testing with monitoring of therapeutic adherence and PPIs-clopidogrel interaction.	clopidogrel	147-158	ATP binding cassette subfamily B member 1	Homo sapiens	223-228
34666508-1	2022	BACKGROUND AND PURPOSE: The age, body mass index, chronic kidney disease, diabetes, and genotyping (ABCD-GENE) score is a validated risk score integrating CYP2C19 genotypes with clinical risk factors influencing clopidogrel response that would allow the more precise identification of subjects at risk for high platelet reactivity and adverse clinical outcomes.	clopidogrel	212-223	renin binding protein	Homo sapiens	28-31
34666508-1	2022	BACKGROUND AND PURPOSE: The age, body mass index, chronic kidney disease, diabetes, and genotyping (ABCD-GENE) score is a validated risk score integrating CYP2C19 genotypes with clinical risk factors influencing clopidogrel response that would allow the more precise identification of subjects at risk for high platelet reactivity and adverse clinical outcomes.	clopidogrel	212-223	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	155-162
34666508-11	2022	Our study suggests that CYP2C19 genotypes and clinical risk factors can be integrated by ABCD-GENE score to estimate the efficacy of clopidogrel-aspirin therapy.	clopidogrel	133-144	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	24-31
34474410-0	2022	Platelet miR-107 Participates in Clopidogrel Resistance after PCI Treatment by Regulating P2Y12.	clopidogrel	33-44	purinergic receptor P2Y12	Homo sapiens	90-95
34474410-15	2022	CONCLUSION: Platelet miR-107 participated in clopidogrel resistance in ACS/PCI patients by regulating P2Y12 expression.	clopidogrel	45-56	microRNA 107	Homo sapiens	21-28
34474410-15	2022	CONCLUSION: Platelet miR-107 participated in clopidogrel resistance in ACS/PCI patients by regulating P2Y12 expression.	clopidogrel	45-56	purinergic receptor P2Y12	Homo sapiens	102-107
34410044-0	2022	Translational aspects of cytochrome P450-mediated drug-drug interactions: a case study with clopidogrel.	clopidogrel	92-103	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	25-40
34410044-10	2022	This MiniReview provides an overview of translational approaches to study CYP-mediated DDIs, going beyond regulatory DDI guidelines, and an illustrative case study of how the DDI potential of clopidogrel was unveiled by combining these different methods.	clopidogrel	192-203	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	74-77
34415054-8	2022	In diet-induced obese mice, systemic exposure of clopidogrel active metabolite H4 was significantly reduced but that of its hydrolytic metabolite was increased due to down-regulation of certain P450s but up-regulation of Ces1 in the liver.	clopidogrel	49-60	carboxylesterase 1G	Mus musculus	221-225
34954768-0	2022	Associations of CYP2C19 and F2R genetic polymorphisms with platelet reactivity in Chinese ischemic stroke patients receiving clopidogrel therapy.	clopidogrel	125-136	coagulation factor II thrombin receptor	Homo sapiens	28-31
34954768-8	2022	The newly identified rs168753 in F2R gene may influence the efficacy to clopidogrel-aspirin therapy for ischemic stroke patients.	clopidogrel	72-83	coagulation factor II thrombin receptor	Homo sapiens	33-36
34903548-0	2021	Analysis of CYP2C19 genetic variants with ischaemic events in UK patients prescribed clopidogrel in primary care: a retrospective cohort study.	clopidogrel	85-96	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
34903548-1	2021	OBJECTIVE: To determine whether CYP2C19 loss-of-function (LoF) alleles increase risk of ischaemic stroke and myocardial infarction (MI) in UK primary care patients prescribed clopidogrel.	clopidogrel	175-186	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
34903548-12	2021	In lifetables using observed incidence rates, 22.5% (95% CI 14.4% to 34.0%) of CYP2C19 LoF carriers on clopidogrel were projected to develop an ischaemic stroke by age 79 (oldest age in the study), compared with 15.4% (95% CI 11.4% to 20.5%) in non-carriers, that is, 7.1% excess stroke incidence in LoF carriers by age 79.	clopidogrel	103-114	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	79-86
34851561-0	2021	CYP2C19*2 genetic polymorphism and incidence of in-stent restenosis in patients on clopidogrel: a matched case-control study.	clopidogrel	83-94	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
34870596-0	2021	Is clopidogrel as the P2Y12 inhibitor a wise choice for long-term monotherapy in patients undergoing stenting?	clopidogrel	3-14	purinergic receptor P2Y12	Homo sapiens	22-27
34840926-7	2021	The ADP-induced TRAP could be inhibited by clopidogrel a P2Y12 inhibitor.	clopidogrel	43-54	acid phosphatase 5, tartrate resistant	Mus musculus	16-20
34840926-7	2021	The ADP-induced TRAP could be inhibited by clopidogrel a P2Y12 inhibitor.	clopidogrel	43-54	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	57-62
34851561-1	2021	OBJECTIVES: The cytochrome P450 2C19*2 (CYP2C19*2) genetic polymorphism is associated with reduced clopidogrel bioactivation, increasing the risk of atherothrombotic complications after percutaneous coronary intervention (PCI).	clopidogrel	99-110	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-36
34851561-1	2021	OBJECTIVES: The cytochrome P450 2C19*2 (CYP2C19*2) genetic polymorphism is associated with reduced clopidogrel bioactivation, increasing the risk of atherothrombotic complications after percutaneous coronary intervention (PCI).	clopidogrel	99-110	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-47
34851561-3	2021	The aim was to investigate the association between presence of the CYP2C19*2 allele and ISR within one-year after PCI in patients prescribed dual antiplatelet therapy with aspirin and clopidogrel.	clopidogrel	184-195	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	67-74
34851561-10	2021	CONCLUSIONS: The proportion of patients who were carriers of one or two CYP2C19*2 alleles who presented with DES-ISR within one-year post-PCI while on clopidogrel was significantly higher compared to patients with no documented ISR.	clopidogrel	151-162	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	72-79
34606835-9	2021	Analysis of middle cerebral arteries from clopidogrel treated rabbits showed that clopidogrel did not affect P2Y4, P2Y6, and P2Y14 receptor-mediated contraction but attenuated the contractile response after P2Y2 receptor activation.	clopidogrel	82-93	LOC100009486	Oryctolagus cuniculus	207-220
34165031-0	2021	Polymorphisms in the GCK gene increase the risk of clopidogrel resistance in stable coronary artery disease (SCAD) patients.	clopidogrel	51-62	glucokinase	Homo sapiens	21-24
34165031-1	2021	BACKGROUND: Diabetes mellitus is a major factor in clopidogrel resistance (CR), and the glucokinase (GCK) gene plays a pivotal role in glucose homeostasis.	clopidogrel	51-62	glucokinase	Homo sapiens	88-99
34165031-1	2021	BACKGROUND: Diabetes mellitus is a major factor in clopidogrel resistance (CR), and the glucokinase (GCK) gene plays a pivotal role in glucose homeostasis.	clopidogrel	51-62	glucokinase	Homo sapiens	101-104
34217665-1	2021	OBJECTIVES: This study sought to report the incidence of device-related thrombosis (DRT) and thromboembolic (TE) events when an alternative to clopidogrel is prescribed in loss-of-function (LOF) allele carriers of the cytochrome P450 2C19 (CYP2C19) gene.	clopidogrel	143-154	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	218-238
34217665-1	2021	OBJECTIVES: This study sought to report the incidence of device-related thrombosis (DRT) and thromboembolic (TE) events when an alternative to clopidogrel is prescribed in loss-of-function (LOF) allele carriers of the cytochrome P450 2C19 (CYP2C19) gene.	clopidogrel	143-154	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	240-247
34217665-2	2021	BACKGROUND: LOF polymorphisms of the CYP2C19 gene are associated with reduced hepatic bioactivation of clopidogrel.	clopidogrel	103-114	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-44
34106029-3	2021	The indication for one of the P2Y12 inhibitors (clopidogrel, prasugrel, ticagrelor) is dependent on the treatment strategy; whether the patients undergo coronary angiography or are treated medically only.	clopidogrel	48-59	purinergic receptor P2Y12	Homo sapiens	30-35
34606835-12	2021	These results suggest clopidogrel inhibits the endothelial P2Y2 receptor in the middle cerebral artery, which provides a mechanistic explanation for the adverse cerebral bleeding associated with the drug.	clopidogrel	22-33	LOC100009486	Oryctolagus cuniculus	59-72
34506827-11	2021	CONCLUSION: A genotype-guided escalation of P2Y12 inhibitor strategy is feasible in STEMI patients treated with clopidogrel and undergoing PCI and is associated with a reduction of primary outcomes compared to conventional antiplatelet therapy.	clopidogrel	112-123	purinergic receptor P2Y12	Homo sapiens	44-49
34690774-0	2021	The Dynamic Effect of Non-CYP3A4-Metabolized and CYP3A4-Metabolized Statins on Clopidogrel Resistance in Patients With Cerebral Infarction.	clopidogrel	79-90	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	26-32
34748146-2	2021	Prior studies indicated that insulin resistance may be correlated with low responsiveness to clopidogrel.	clopidogrel	93-104	insulin	Homo sapiens	29-36
34748146-3	2021	This study aimed to investigate the effects of beta-cell function on clopidogrel-induced platelet P2Y12 inhibition and the clinical outcomes of nondiabetic patients undergoing elective percutaneous coronary intervention (PCI).	clopidogrel	69-80	purinergic receptor P2Y12	Homo sapiens	98-103
34713722-15	2021	Conclusions GAS5 rs55829688 polymorphism might affect clopidogrel response in patients with CAD with the CYP2C19 poor metabolizer genotypes, and GAS5 regulates P2Y12 expression and clopidogrel response by acting as a competitive endogenous RNA for miR-223-3p.	clopidogrel	54-65	growth arrest specific 5	Homo sapiens	12-16
34713722-15	2021	Conclusions GAS5 rs55829688 polymorphism might affect clopidogrel response in patients with CAD with the CYP2C19 poor metabolizer genotypes, and GAS5 regulates P2Y12 expression and clopidogrel response by acting as a competitive endogenous RNA for miR-223-3p.	clopidogrel	54-65	growth arrest specific 5	Homo sapiens	145-149
34713722-15	2021	Conclusions GAS5 rs55829688 polymorphism might affect clopidogrel response in patients with CAD with the CYP2C19 poor metabolizer genotypes, and GAS5 regulates P2Y12 expression and clopidogrel response by acting as a competitive endogenous RNA for miR-223-3p.	clopidogrel	181-192	growth arrest specific 5	Homo sapiens	12-16
34713722-15	2021	Conclusions GAS5 rs55829688 polymorphism might affect clopidogrel response in patients with CAD with the CYP2C19 poor metabolizer genotypes, and GAS5 regulates P2Y12 expression and clopidogrel response by acting as a competitive endogenous RNA for miR-223-3p.	clopidogrel	181-192	growth arrest specific 5	Homo sapiens	145-149
34711749-1	2022	ABSTRACTION: The aim of this study was to investigate the association between CYP2C19 gene polymorphisms and the risk of cardiovascular events in the early stage and subsequent period after percutaneous coronary intervention (PCI) among patients who received clopidogrel.	clopidogrel	259-270	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	78-85
34711749-2	2022	Between October 2015 and January 2017, CYP2C19 genotyped patients who were treated with clopidogrel after PCI were enrolled in this study.	clopidogrel	88-99	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	39-46
34711749-11	2022	In conclusion, these data demonstrate a higher risk for ischemic events in patients with two CYP2C19 LOF alleles who are prescribed clopidogrel, seen at 3 months following PCI, that is not sustained for 12 months.	clopidogrel	132-143	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	93-100
34256091-5	2021	Clopidogrel is metabolised for a small amount by the polymorphic CYP2C19, which can have an impact on the overall pharmacokinetics, while the variability seen for dabigatran etexilate might be due to differences in the absorption, since this can be influenced by food intake.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	65-72
34622701-0	2021	Impact of Automated Best Practice Advisories on Provider Response to CYP2C19 Genotyping Results for Patients on Clopidogrel.	clopidogrel	112-123	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	69-76
34563718-5	2021	Hyper-response to clopidogrel was defined as P2Y12 Reaction Units (PRU) <= 60.	clopidogrel	18-29	purinergic receptor P2Y12	Homo sapiens	45-50
34764653-3	2021	Purpose: We aimed at investigating the association of PON1 p.Q192R with CAD and clopidogrel response in Colombian population.	clopidogrel	80-91	paraoxonase 1	Homo sapiens	54-58
34713722-0	2021	Influence of GAS5/MicroRNA-223-3p/P2Y12 Axis on Clopidogrel Response in Coronary Artery Disease.	clopidogrel	48-59	growth arrest specific 5	Homo sapiens	13-17
34713722-0	2021	Influence of GAS5/MicroRNA-223-3p/P2Y12 Axis on Clopidogrel Response in Coronary Artery Disease.	clopidogrel	48-59	purinergic receptor P2Y12	Homo sapiens	34-39
34713722-3	2021	This study aimed to investigate the roles of GAS5 (growth arrest-specific 5) and its rs55829688 polymorphism in clopidogrel response in patients with CAD.	clopidogrel	112-123	growth arrest specific 5	Homo sapiens	45-49
34713722-3	2021	This study aimed to investigate the roles of GAS5 (growth arrest-specific 5) and its rs55829688 polymorphism in clopidogrel response in patients with CAD.	clopidogrel	112-123	growth arrest specific 5	Homo sapiens	51-75
34415683-2	2021	Platelet reactivity was measured using the VerifyNow P2Y12 assay and clopidogrel resistance was defined as P2Y12 reaction units (PRUs) greater than or equal to 208.	clopidogrel	69-80	purinergic receptor P2Y12	Homo sapiens	107-112
34664214-10	2021	The P score displayed prasugrel (0.5871) as the best treatment for MACE, while clopidogrel (0.7701) was the best P2Y12 inhibitor to decrease the risk of major bleeding.	clopidogrel	79-90	purinergic receptor P2Y12	Homo sapiens	113-118
34164723-3	2021	Clopidogrel reduces the risk for recurrent cardiovascular events after PCI; however, its activity is influenced by cytochrome P450 (CYP450), ATP-binding cassette transporter B1 (ABCB1), and paraoxonase-1 (PON1).	clopidogrel	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	141-176
34164723-3	2021	Clopidogrel reduces the risk for recurrent cardiovascular events after PCI; however, its activity is influenced by cytochrome P450 (CYP450), ATP-binding cassette transporter B1 (ABCB1), and paraoxonase-1 (PON1).	clopidogrel	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	178-183
34164723-3	2021	Clopidogrel reduces the risk for recurrent cardiovascular events after PCI; however, its activity is influenced by cytochrome P450 (CYP450), ATP-binding cassette transporter B1 (ABCB1), and paraoxonase-1 (PON1).	clopidogrel	0-11	paraoxonase 1	Homo sapiens	190-203
34164723-3	2021	Clopidogrel reduces the risk for recurrent cardiovascular events after PCI; however, its activity is influenced by cytochrome P450 (CYP450), ATP-binding cassette transporter B1 (ABCB1), and paraoxonase-1 (PON1).	clopidogrel	0-11	paraoxonase 1	Homo sapiens	205-209
34609028-0	2021	Gene polymorphisms of insulin secretion signaling pathway associated with clopidogrel resistance in Han Chinese population.	clopidogrel	74-85	insulin	Homo sapiens	22-29
34609028-2	2021	Nevertheless, the relationship between the single-nucleotide polymorphisms (SNP) of the signal pathway gene of insulin secretion and the effect of clopidogrel is elusive.	clopidogrel	147-158	insulin	Homo sapiens	111-118
34609028-5	2021	RESULTS: Analysis of the study population showed that old age, lower plasma albumin (ALB) level, higher creatinine (CREA) level, higher uric acid (UA) level, lower platelet (PLT) count, and lower plateletcrit (PCT) potentially increased the risk of clopidogrel resistance.	clopidogrel	249-260	albumin	Homo sapiens	76-83
34609028-5	2021	RESULTS: Analysis of the study population showed that old age, lower plasma albumin (ALB) level, higher creatinine (CREA) level, higher uric acid (UA) level, lower platelet (PLT) count, and lower plateletcrit (PCT) potentially increased the risk of clopidogrel resistance.	clopidogrel	249-260	albumin	Homo sapiens	85-88
34609028-9	2021	In the RAPGEF4 gene polymorphism rs17746510, TG was the protective genotype, and the TT genotype was a risk factor for clopidogrel resistance.	clopidogrel	119-130	Rap guanine nucleotide exchange factor 4	Homo sapiens	7-14
34609028-11	2021	CONCLUSION: Single-nucleotide polymorphisms of insulin secretion signaling pathway genes trigger clopidogrel resistance.	clopidogrel	97-108	insulin	Homo sapiens	47-54
34690774-0	2021	The Dynamic Effect of Non-CYP3A4-Metabolized and CYP3A4-Metabolized Statins on Clopidogrel Resistance in Patients With Cerebral Infarction.	clopidogrel	79-90	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	49-55
34671655-3	2021	Aim: To investigate the association of inflammatory biomarkers such as leukocyte count and high-sensitivity C reactive proteins (hs-CRP) with platelet reactivity in PCI patients treated with clopidogrel.	clopidogrel	191-202	C-reactive protein	Homo sapiens	132-135
34671655-10	2021	Conclusions: This was the first large real-world study reporting that both leukocyte count and hs-CRP were the independent factors for platelet reactivity in PCI populations treated with clopidogrel, among which higher leukocyte count was associated with more LTPR while higher hs-CRP was associated with more HTPR, providing new insights on individualized antiplatelet therapy.	clopidogrel	187-198	C-reactive protein	Homo sapiens	98-101
34671655-10	2021	Conclusions: This was the first large real-world study reporting that both leukocyte count and hs-CRP were the independent factors for platelet reactivity in PCI populations treated with clopidogrel, among which higher leukocyte count was associated with more LTPR while higher hs-CRP was associated with more HTPR, providing new insights on individualized antiplatelet therapy.	clopidogrel	187-198	C-reactive protein	Homo sapiens	281-284
34661267-0	2021	The correlation between platelet responsiveness to clopidogrel and CYP2C19 polymorphism in patients with peripheral vascular disease.	clopidogrel	51-62	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	67-74
34661267-2	2021	We aimed to determine the frequency of the genetic polymorphism of CYP2C19*2 and the contribution of this polymorphism along with other clinical parameters to clopidogrel response in an Egyptian population.	clopidogrel	159-170	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	67-74
34661267-7	2021	Univariate analysis demonstrated that CYP2C19*2 genotype (p = 0.001), high body mass index (BMI; p = 0.025), diabetes (p = 0.037),  high fasting blood glucose (FBG) level (p = 0.037), and high glycosylated hemoglobin (HbA1c) level (p = 0.004) were significantly associated with clopidogrel resistance.	clopidogrel	278-289	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	38-45
34661267-8	2021	Multivariate analysis showed that CYP2C19*2 genotype (odds ratio (OR), 927.71; 95% confidence interval (CI), 1.915-449496.2; p = 0.030) and high BMI (OR, 1.789; 95% CI, 1.044-3.064; p = 0.034) were the most powerful predictors of clopidogrel resistance.	clopidogrel	230-241	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	34-41
34661267-9	2021	CONCLUSIONS: Clopidogrel resistance in patients with peripheral vascular disease is associated with the presence of CYP2C19*2 allele, obesity, and diabetes; these factors should be considered prior to clopidogrel administration.	clopidogrel	13-24	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	116-123
34540909-2	2021	The present study aimed to explore the association between platelet endothelial aggregation receptor 1 (PEAR1) rs12041331 polymorphism and the outcomes in patients with acute ischemic stroke treated with aspirin or dual antiplatelet therapy (DAPT) with clopidogrel.	clopidogrel	253-264	platelet endothelial aggregation receptor 1	Homo sapiens	59-102
34589424-5	2021	Here, we aimed to (1) compare the effects of aspirin and clopidogrel on pancreatic cancer prevention, (2) characterize the effects of clopidogrel (platelet P2RY12 inhibitor) on cancer-associated thrombosis and cancer growth in vivo, (3) determine the effect of P2RY12 across different digestive-tract cancers in vitro, and (4) analyze the expression pattern of P2RY12 in two different cancer types affecting the digestive system.	clopidogrel	57-68	purinergic receptor P2Y12	Homo sapiens	361-367
34589424-5	2021	Here, we aimed to (1) compare the effects of aspirin and clopidogrel on pancreatic cancer prevention, (2) characterize the effects of clopidogrel (platelet P2RY12 inhibitor) on cancer-associated thrombosis and cancer growth in vivo, (3) determine the effect of P2RY12 across different digestive-tract cancers in vitro, and (4) analyze the expression pattern of P2RY12 in two different cancer types affecting the digestive system.	clopidogrel	134-145	purinergic receptor P2Y12	Homo sapiens	156-162
34117726-6	2021	The results showed that polymorphisms in CRY1, CACNA1C, and PRKCG changed the response to clopidogrel.	clopidogrel	90-101	cryptochrome circadian regulator 1	Homo sapiens	41-45
34117726-6	2021	The results showed that polymorphisms in CRY1, CACNA1C, and PRKCG changed the response to clopidogrel.	clopidogrel	90-101	calcium voltage-gated channel subunit alpha1 C	Homo sapiens	47-54
34117726-6	2021	The results showed that polymorphisms in CRY1, CACNA1C, and PRKCG changed the response to clopidogrel.	clopidogrel	90-101	protein kinase C gamma	Homo sapiens	60-65
34410542-6	2021	Combination antiplatelet therapy with aspirin and the P2Y12 inhibitors, clopidogrel and ticagrelor, reduced stroke recurrence in those presenting with mild ischemic stroke or high risk TIA.	clopidogrel	72-83	purinergic receptor P2Y12	Homo sapiens	54-59
34384383-0	2021	Association between cytochrome P450 2C19 polymorphism and clinical outcomes in clopidogrel-treated Uygur population with acute coronary syndrome: a retrospective study.	clopidogrel	79-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	20-40
34384383-9	2021	CONCLUSION: The CYP2C19*2 gene polymorphism contributes to the risk of MACE in dual clopidogrel-treated Uygur population with ACS with or without PCI (percutaneous coronary intervention).	clopidogrel	84-95	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
34638670-12	2021	Significant increases in plasma and kidney IL-1beta and IL-18 in response to CLP were decreased with Clopidogrel treatment.	clopidogrel	101-112	interleukin 1 alpha	Homo sapiens	43-51
34638670-12	2021	Significant increases in plasma and kidney IL-1beta and IL-18 in response to CLP were decreased with Clopidogrel treatment.	clopidogrel	101-112	interleukin 18	Homo sapiens	56-61
34501440-3	2021	Polymorphisms of the CYP2C19 gene have an impact on the metabolization of clopidogrel and, thereby, have an impact on on-treatment platelet reactivity.	clopidogrel	74-85	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	21-28
34803003-0	2021	Study on the effect of CYP2C19 genetic polymorphism and plasma concentration on clopidogrel resistance.	clopidogrel	80-91	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	23-30
34435480-0	2021	Expression of NLR and IL-1beta and their predictive efficacy value in acute myocardial infarction patients treated with aspirin combined with clopidogrel.	clopidogrel	142-153	interleukin 1 alpha	Homo sapiens	22-30
34471538-3	2021	Studies reported the genetic polymorphisms of CYP2C19*2, CYP2C19*17, and ITGB3 cause an alteration of the pharmacodynamic and pharmacokinetic profile of aspirin and clopidogrel.	clopidogrel	165-176	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	46-53
34471538-3	2021	Studies reported the genetic polymorphisms of CYP2C19*2, CYP2C19*17, and ITGB3 cause an alteration of the pharmacodynamic and pharmacokinetic profile of aspirin and clopidogrel.	clopidogrel	165-176	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	57-64
34471538-3	2021	Studies reported the genetic polymorphisms of CYP2C19*2, CYP2C19*17, and ITGB3 cause an alteration of the pharmacodynamic and pharmacokinetic profile of aspirin and clopidogrel.	clopidogrel	165-176	integrin subunit beta 3	Homo sapiens	73-78
34471538-7	2021	The PCR products of clopidogrel-treated patients were screened with agarose gel electrophoresis and then digested with SmaI and NsiI-HF for CYP2C19*2 and CYP2C19*17, respectively.	clopidogrel	20-31	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	140-147
34471538-7	2021	The PCR products of clopidogrel-treated patients were screened with agarose gel electrophoresis and then digested with SmaI and NsiI-HF for CYP2C19*2 and CYP2C19*17, respectively.	clopidogrel	20-31	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	154-161
34471538-10	2021	Results: Among the clopidogrel-treated patients, we observed 64.1% polymorphism (hetero + mutant) of CYP2C19*2 (loss-of-function allele) and 22.7% (hetero + mutant) of CYP2C19*17 (gain-of-function allele).	clopidogrel	19-30	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	101-108
34471538-10	2021	Results: Among the clopidogrel-treated patients, we observed 64.1% polymorphism (hetero + mutant) of CYP2C19*2 (loss-of-function allele) and 22.7% (hetero + mutant) of CYP2C19*17 (gain-of-function allele).	clopidogrel	19-30	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	168-175
34428831-12	2021	The main findings of this study support use of clopidogrel in CYP2C19 LOF noncarriers as an alternative P2Y12 inhibitor, which may reduce medical expenses and adverse reactions caused by more potent P2Y12 inhibitors in these patients.	clopidogrel	47-58	purinergic receptor P2Y12	Homo sapiens	104-109
34428831-12	2021	The main findings of this study support use of clopidogrel in CYP2C19 LOF noncarriers as an alternative P2Y12 inhibitor, which may reduce medical expenses and adverse reactions caused by more potent P2Y12 inhibitors in these patients.	clopidogrel	47-58	purinergic receptor P2Y12	Homo sapiens	199-204
34373244-3	2021	She had been on clopidogrel for 6 months for a carotid artery stent.	clopidogrel	16-27	Src homology 2 domain containing E	Homo sapiens	0-3
34447343-11	2021	Conclusions: HPR and clopidogrel resistance were more frequent in recurrent ischemic stroke patients receiving clopidogrel than in those receiving DAPT.	clopidogrel	111-122	haptoglobin-related protein	Homo sapiens	13-16
34527614-2	2021	Due to omeprazole"s inhibitory effects on the liver enzyme CYP2C19, its concomitant use with clopidogrel is argued to increase the risk of myocardial infarction (MI) recurrence, as CYP2C19 activates clopidogrel.	clopidogrel	93-104	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	59-66
34351918-0	2021	PON1 Q192R is associated with high platelet reactivity with clopidogrel in patients undergoing elective neurointervention: A prospective single-center cohort study.	clopidogrel	60-71	paraoxonase 1	Homo sapiens	0-4
34351918-1	2021	BACKGROUND AND PURPOSE: The impact of the paraoxonase-1 (PON1) polymorphism, Q192R, on platelet inhibition in response to clopidogrel remains controversial.	clopidogrel	122-133	paraoxonase 1	Homo sapiens	57-61
34351918-2	2021	We aimed to investigate the association between carrier status of PON1 Q192R and high platelet reactivity (HPR) with clopidogrel in patients undergoing elective neurointervention.	clopidogrel	117-128	paraoxonase 1	Homo sapiens	66-70
34351918-10	2021	CONCLUSIONS: Carrying >=1 PON1 192R allele is associated with HPR by original and corrected PRU with clopidogrel in patients undergoing elective neurointervention, although alternative results related to other genetic polymorphisms cannot be excluded.	clopidogrel	101-112	paraoxonase 1	Homo sapiens	26-30
34527614-2	2021	Due to omeprazole"s inhibitory effects on the liver enzyme CYP2C19, its concomitant use with clopidogrel is argued to increase the risk of myocardial infarction (MI) recurrence, as CYP2C19 activates clopidogrel.	clopidogrel	199-210	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	181-188
34092486-0	2021	Risk of stroke in CYP2C19 LoF polymorphism carrier coronary artery disease patients undergoing clopidogrel therapy: An ethnicity-based updated meta-analysis.	clopidogrel	95-106	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	18-25
34092486-2	2021	CYP2C19 loss-of-function (LoF) polymorphism is assumed to be responsible for the poor metabolism of clopidogrel that ultimately turns to resistance.	clopidogrel	100-111	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
34129280-10	2021	All intermediate clopidogrel metabolizers (CYP2C19*2 carriers) were correctly classified as clopidogrel resistant using Chrono-Par  , in contrast to the Agro-Bio ADP reagent.	clopidogrel	92-103	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	43-50
34319489-2	2021	Since purine receptor P2Y12 plays a crucial role in platelet activation, P2Y12 antagonists such as clopidogrel, prasugrel, and ticagrelor have been widely used in cardiovascular diseases worldwide in recent decades due to their potent antiplatelet and antithrombotic effects.	clopidogrel	99-110	purinergic receptor P2Y12	Homo sapiens	22-27
34092486-4	2021	AIM: To get clear evidence from an updated meta-analysis on CYP2C19 LoF polymorphism association with stroke risk in clopidogrel treated patients, this study has been performed.	clopidogrel	117-128	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	60-67
34092486-8	2021	CONCLUSION: Our meta-analysis confirmed that the presence of CYP2C19 LoF alleles increases the risk of stroke and composite events recurrence in the worldwide population, especially in Asians undergoing clopidogrel treatment.	clopidogrel	203-214	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	61-68
34234079-8	2021	Although the number of CYP2C19 loss-of-function alleles was clearly associated with a likelihood of HPR with clopidogrel, P2Y12 reactivity units with prasugrel treatment were also significantly and progressively higher in patients with more CYP2C19 loss-of-function alleles.	clopidogrel	109-120	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	23-30
34234079-9	2021	CONCLUSIONS: Clinical and genetic factors had a differential effect on a P2Y12 inhibitor reactivity with clopidogrel and prasugrel in patients with coronary artery disease.	clopidogrel	105-116	purinergic receptor P2Y12	Homo sapiens	73-78
34233065-2	2022	METHODS: GPI use was analyzed in this subanalysis of the POPular Genetics trial, which randomized STEMI patients to CYP2C19 genotype-guided treatment (clopidogrel or ticagrelor) or standard treatment with ticagrelor/prasugrel.	clopidogrel	151-162	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	116-123
34258380-5	2021	The trial will test, whether a DAT-regimen comprising clopidogrel plus the non-Vitamin-K-antagonist oral anticoagulant (NOAC) apixaban is superior to a TAT-regimen of vitamin-K-antagonist (VKA) plus dual anti-platelet therapy (APT) with respect to bleeding.	clopidogrel	54-65	solute carrier family 6 member 3	Homo sapiens	31-34
34447900-8	2021	In mild-grade CLP, clopidogrel- and vehicle-treated mice did not display a significant decrease in MAP, while thrombocytopenia and plasma concentrations of TNFalpha, IL6, IL10, MPO, TAT and organ damage reached similar levels in both groups, although lower than those reached in the high grade CLP.	clopidogrel	19-30	tumor necrosis factor	Mus musculus	156-164
34319489-2	2021	Since purine receptor P2Y12 plays a crucial role in platelet activation, P2Y12 antagonists such as clopidogrel, prasugrel, and ticagrelor have been widely used in cardiovascular diseases worldwide in recent decades due to their potent antiplatelet and antithrombotic effects.	clopidogrel	99-110	purinergic receptor P2Y12	Homo sapiens	73-78
34241731-1	2021	PURPOSE: Due to shared hepatic metabolism, concomitant medication with a proton pump inhibitor (PPI) and clopidogrel might reduce the effectiveness of clopidogrel in the prevention of cardiovascular events after percutaneous coronary intervention (PCI).	clopidogrel	151-162	ATPase H+/K+ transporting subunit alpha	Homo sapiens	73-84
34237806-2	2021	Clopidogrel is a prodrug and its bioactivation is catalyzed by cytochrome P450 (CYP)2C19.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	63-88
34237806-6	2021	Of the 27 patients with the CYP2C19*2 allele who were prescribed clopidogrel (18) or dual antiplatelet therapy (9), only 21 patients could be followed up for a period of six months post stroke event, in addition to 21 age- and sex-matched patients with the normal allele.	clopidogrel	65-76	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
34262326-8	2021	Compared with the clopidogrel group, the gastrin and motilin in the serum, the cyclooxygenase (COX)-1 and prostaglandin E2 in gastric tissue, and expression of vascular endothelial growth factor messenger ribonucleic acid in the serum were all significantly increased using TCM approach to protect against gastric mucosal injury (p < 0.05).	clopidogrel	18-29	gastrin	Rattus norvegicus	41-48
34262326-8	2021	Compared with the clopidogrel group, the gastrin and motilin in the serum, the cyclooxygenase (COX)-1 and prostaglandin E2 in gastric tissue, and expression of vascular endothelial growth factor messenger ribonucleic acid in the serum were all significantly increased using TCM approach to protect against gastric mucosal injury (p < 0.05).	clopidogrel	18-29	motilin	Rattus norvegicus	53-60
34262326-8	2021	Compared with the clopidogrel group, the gastrin and motilin in the serum, the cyclooxygenase (COX)-1 and prostaglandin E2 in gastric tissue, and expression of vascular endothelial growth factor messenger ribonucleic acid in the serum were all significantly increased using TCM approach to protect against gastric mucosal injury (p < 0.05).	clopidogrel	18-29	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	79-101
34430652-10	2021	Two retrospective observational studies determined clopidogrel resistance using measurement of P2Y12 reaction units, and one historical cohort study used genetic testing.	clopidogrel	51-62	purinergic receptor P2Y12	Homo sapiens	95-100
34430652-11	2021	Two studies concluded that clopidogrel resistance was a risk factor for thromboembolic complications, the other found higher values of P2Y12 reaction units in patients with thromboembolic events compared to those without.	clopidogrel	27-38	purinergic receptor P2Y12	Homo sapiens	135-140
34182941-5	2021	Platelet reactivity for clopidogrel was measured by VerifyNow assay system, and we defined the cut off value of P2Y12 Reaction Units (PRU) at 208 and classified patients as hypo-responders (PRU 208) or responders (PRU<208).	clopidogrel	24-35	purinergic receptor P2Y12	Homo sapiens	112-117
34195679-3	2021	To monitor their differential response to treatment, we performed untargeted plasma metabolomics on 175 patients from the platelet inhibition and patient outcomes (PLATO) trial treated with ticagrelor and clopidogrel, two common P2Y12 inhibitors.	clopidogrel	205-216	purinergic receptor P2Y12	Homo sapiens	229-234
34131167-0	2021	A genetic polymorphism in P2RY1 impacts response to clopidogrel in cats with hypertrophic cardiomyopathy.	clopidogrel	52-63	purinergic receptor P2Y1	Felis catus	26-31
34131167-7	2021	Whole blood platelet aggregometry revealed a significant reduction of platelet inhibition by clopidogrel in cats with the P2RY1:A236G and the P2RY12:V34I variants.	clopidogrel	93-104	purinergic receptor P2Y1	Felis catus	122-127
34131167-7	2021	Whole blood platelet aggregometry revealed a significant reduction of platelet inhibition by clopidogrel in cats with the P2RY1:A236G and the P2RY12:V34I variants.	clopidogrel	93-104	purinergic receptor P2Y12	Felis catus	142-148
34131167-8	2021	The association with the P2RY1:A236G variant and clopidogrel resistance remained significant after adjustment for multiple comparisons.	clopidogrel	49-60	purinergic receptor P2Y1	Felis catus	25-30
34131167-9	2021	This study demonstrated that a genetic polymorphism in the P2RY1 gene altered response to clopidogrel therapy and suggests that clinicians may consider alternative or additional thromboprophylactic therapy in cats with the P2RY1:A236G variant.	clopidogrel	90-101	purinergic receptor P2Y1	Felis catus	59-64
34202960-8	2021	RESULTS: Clopidogrel vs. aspirin monotherapy was associated with better endothelial function (RHI: 2.11 +- 0.77% vs. 1.87 +- 0.72%, p = 0.045), lower platelet reactivity (130 +- 64 vs. 214 +- 50 P2Y12 reaction unit (PRU), p < 0.001) and prolonged reaction time (TEG R: 5.5 +- 1.2 vs. 5.1 +- 1.1 min, p = 0.037).	clopidogrel	9-20	purinergic receptor P2Y12	Homo sapiens	195-200
34098766-8	2021	Modulating miR-223 or miR-126 in platelets in vitro significantly changed the response to clopidogrel by regulating platelet aggregation.	clopidogrel	90-101	microRNA 223	Homo sapiens	11-18
34098766-8	2021	Modulating miR-223 or miR-126 in platelets in vitro significantly changed the response to clopidogrel by regulating platelet aggregation.	clopidogrel	90-101	microRNA 126	Homo sapiens	22-29
34071189-10	2021	Furthermore, miR-126, Let-7e and miR-223 expressions in the clopidogrel group were significantly higher than in the ASA group (p = 0.014; p = 0.013; p = 0.028, respectively).	clopidogrel	60-71	microRNA 126	Homo sapiens	13-20
34400920-3	2021	Patients were assessed for the presence of the most common genetic polymorphisms that reduce the absorption (ABCB1) and activation (CYP2C19*2 and CYP2C19*3) of clopidogrel to exclude the effect of genetic variability on drug concentrations and activity.	clopidogrel	160-171	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	132-139
34400920-3	2021	Patients were assessed for the presence of the most common genetic polymorphisms that reduce the absorption (ABCB1) and activation (CYP2C19*2 and CYP2C19*3) of clopidogrel to exclude the effect of genetic variability on drug concentrations and activity.	clopidogrel	160-171	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	146-153
34071189-10	2021	Furthermore, miR-126, Let-7e and miR-223 expressions in the clopidogrel group were significantly higher than in the ASA group (p = 0.014; p = 0.013; p = 0.028, respectively).	clopidogrel	60-71	microRNA let-7e	Homo sapiens	22-28
34071189-10	2021	Furthermore, miR-126, Let-7e and miR-223 expressions in the clopidogrel group were significantly higher than in the ASA group (p = 0.014; p = 0.013; p = 0.028, respectively).	clopidogrel	60-71	microRNA 223	Homo sapiens	33-40
34065778-0	2021	A Pharmacogenetic Study of CYP2C19 in Acute Coronary Syndrome Patients of Colombian Origin Reveals New Polymorphisms Potentially Related to Clopidogrel Therapy.	clopidogrel	140-151	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	27-34
35334330-1	2022	Single nucleotide variants in CYP2C19*2 are associated with clopidogrel resistance in coronary heart disease.	clopidogrel	60-71	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	30-37
35525324-0	2022	P2Y12 inhibition by clopidogrel increases adverse clinical events after transcatheter aortic valve replacement.	clopidogrel	20-31	purinergic receptor P2Y12	Homo sapiens	0-5
35525324-2	2022	In the present study, we sought to assess whether P2Y12 inhibition by clopidogrel impacts clinical outcomes in TAVR patients.	clopidogrel	70-81	purinergic receptor P2Y12	Homo sapiens	50-55
35525324-11	2022	CONCLUSIONS: In conclusion, appropriate P2Y12 inhibition by clopidogrel is a major determinant of MACCE at 90 days after TAVR.	clopidogrel	60-71	purinergic receptor P2Y12	Homo sapiens	40-45
35176816-0	2022	Increased frequency of CYP2C19 loss-of-function alleles in clopidogrel-treated patients with recurrent cerebral ischemia.	clopidogrel	59-70	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	23-30
35176816-2	2022	Previous - mainly Asian - studies have shown that genetic variations in CYP2C19 are associated with an increased risk of recurrent stroke in clopidogrel-treated patients.	clopidogrel	141-152	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	72-79
35176816-5	2022	METHODS: CYP2C19-genotyping (*2 and *3) was performed in clopidogrel-treated patients who presented with a recurrent ischemic stroke/TIA.	clopidogrel	57-68	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	9-16
35176816-10	2022	CONCLUSION: In this clopidogrel-treated population with recurrent cerebral ischemia the frequency of CYP2C19 LoF alleles was significantly higher than in reference groups, especially in early recurrent events.	clopidogrel	20-31	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	101-108
35389962-3	2022	Several studies have shown that polymorphisms in the gene encoding the CYP2C19 contribute to the variability in response to clopidogrel.	clopidogrel	124-135	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
35331593-2	2022	OBJECTIVE: This systematic review aimed to compare early use of P2Y12 inhibitors (clopidogrel/ticagrelor) plus aspirin to aspirin alone for acute treatment and secondary prevention in acute non-cardioembolic minor ischemic stroke or TIA.	clopidogrel	82-93	purinergic receptor P2Y12	Homo sapiens	64-69
34065778-4	2021	We analyzed the coding and regulatory regions of CYP2C19 in 166 patients with acute coronary syndrome (ACS) treated with clopidogrel.	clopidogrel	121-132	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	49-56
35595172-2	2022	OBJECTIVE: In the present work, we report a method based on micellar liquid chromatography coupled with ultraviolet detection (MLC/UV), for the simultaneous quantification of combined anti-platelet therapy namely, clopidogrel bisulphate (CPS), aspirin (ASP), together with salicylic acid (SA), in their pharmaceutical dosage form.	clopidogrel	214-236	assembly factor for spindle microtubules	Homo sapiens	253-256
35616671-0	2022	The Cytochrome P450 2C19 Polymorphism is Associated with Major Adverse Cardiovascular Events Risk in Kazak Patients Undergoing Percutaneous Coronary Intervention and Receiving Clopidogrel.	clopidogrel	176-187	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	4-24
35616671-9	2022	CONCLUSION: The CYP2C19*2 allele variants and poor metabolizers are associated with MACE in a clopidogrel-treated Kazak population with acute coronary syndrome following PCI.	clopidogrel	94-105	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
35595172-8	2022	CONCLUSION: The developed MLC/UV method was successfully applied for quantitative analysis of CPS, ASP together with SA-as a main degradation product of ASP-in their pharmaceutical dosage form.	clopidogrel	94-97	assembly factor for spindle microtubules	Homo sapiens	153-156
35600474-7	2022	In comparison, ASA plus clopidogrel treatment presented a significant reduction of the thrombin peak in PRP, which was less pronounced than during subsequent ASA plus rivaroxaban therapy.	clopidogrel	24-35	coagulation factor II, thrombin	Homo sapiens	87-95
35416588-12	2022	Likelihood of death following a COVID-19 infection was also higher in those people with a diagnosis of chronic obstructive pulmonary disease (COPD) or severe enduring mental illness but not with asthma, and in people taking aspirin/clopidogrel/insulin.	clopidogrel	232-243	insulin	Homo sapiens	244-251
35380455-4	2022	The most studied gene-drug pairs were clopidogrel and warfarin associated with cytochrome p450 and vitamin K epoxide reductase complex subunit 1 genes (CYP2C19, CYP2C9 and VKORC1), classified as critically low quality.	clopidogrel	38-49	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	152-159
35380455-4	2022	The most studied gene-drug pairs were clopidogrel and warfarin associated with cytochrome p450 and vitamin K epoxide reductase complex subunit 1 genes (CYP2C19, CYP2C9 and VKORC1), classified as critically low quality.	clopidogrel	38-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
35380455-4	2022	The most studied gene-drug pairs were clopidogrel and warfarin associated with cytochrome p450 and vitamin K epoxide reductase complex subunit 1 genes (CYP2C19, CYP2C9 and VKORC1), classified as critically low quality.	clopidogrel	38-49	vitamin K epoxide reductase complex subunit 1	Homo sapiens	172-178
35631502-0	2022	Physiologically Based Pharmacokinetic (PBPK) Modeling of Clopidogrel and Its Four Relevant Metabolites for CYP2B6, CYP2C8, CYP2C19, and CYP3A4 Drug-Drug-Gene Interaction Predictions.	clopidogrel	57-68	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	107-113
35365779-2	2022	We defaulted that 20% of 500,000 health-system members between the ages of 55 and 65 received PGx testing for CYP2C19 (ACS-clopidogrel) and CYP2C9, CYP4F2 and VKORC1 (AF-warfarin) annually.	clopidogrel	123-134	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	110-117
35571182-4	2022	Methods: The randomized controlled trials with available comparisons between early and delayed initiation of P2Y12 inhibitors (clopidogrel, prasugrel, and ticagrelor) in patients with NSTE-ACS until January 2021 were reviewed.	clopidogrel	127-138	purinergic receptor P2Y12	Homo sapiens	109-114
35466828-5	2022	Patients were placed on ticagrelor if their measured P2Y12 reaction units (PRU) responses to clopidogrel were outside the expected range in our center using the VerifyNow  P2Y12 test.	clopidogrel	93-104	purinergic receptor P2Y12	Homo sapiens	53-58
35631502-0	2022	Physiologically Based Pharmacokinetic (PBPK) Modeling of Clopidogrel and Its Four Relevant Metabolites for CYP2B6, CYP2C8, CYP2C19, and CYP3A4 Drug-Drug-Gene Interaction Predictions.	clopidogrel	57-68	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	115-121
35631502-0	2022	Physiologically Based Pharmacokinetic (PBPK) Modeling of Clopidogrel and Its Four Relevant Metabolites for CYP2B6, CYP2C8, CYP2C19, and CYP3A4 Drug-Drug-Gene Interaction Predictions.	clopidogrel	57-68	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	123-130
35438151-1	2022	AIMS: Vicagrel, a novel antiplatelet prodrug to overcome the residual high platelet reactivity of clopidogrel induced by inactive metabolism and cytochrome P450 (CYP) 2C19 polymorphisms, provides favorable antiplatelet inhibition in healthy volunteers.	clopidogrel	98-109	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	145-171
35418564-0	2022	Antiplatelet response to clopidogrel is associated with a haplotype in CYP2C19 gene in Pakistani patients.	clopidogrel	25-36	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
35449399-1	2022	Loss-of-function CYP2C19 variants are associated with increased cumulative ischemic outcomes warranting CYP2C19 genotyping prior to clopidogrel administration.	clopidogrel	132-143	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-24
35405265-3	2022	METHODS: We retrospectively identified 158 patients taking clopidogrel prior to undergoing elective total hip or knee arthroplasty.	clopidogrel	59-70	hedgehog interacting protein	Homo sapiens	106-109
35480401-1	2022	This study aimed to investigate the possible influence of genetic and non-genetic factors on the incidence of clopidogrel adverse drug reactions (ADRs) in cardiology patients, including the most important CYP2C19 alleles, namely *2 and *17, as well as compliance, dose, drug interactions, and clinical factors.	clopidogrel	110-121	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	205-212
35480401-9	2022	Our study, which is the first to report the frequency of CYP2C19 polymorphism in the Montenegrin population, as well as to link the pharmacovigilance of clopidogrel with CYP2C19 gene variability, shows that the incidence of ADRs of clopidogrel in cardiac patients is high and depends on CYP2C19 polymorphisms, comedication/drug interactions, and gastrointestinal comorbidity.	clopidogrel	153-164	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	170-177
35480401-9	2022	Our study, which is the first to report the frequency of CYP2C19 polymorphism in the Montenegrin population, as well as to link the pharmacovigilance of clopidogrel with CYP2C19 gene variability, shows that the incidence of ADRs of clopidogrel in cardiac patients is high and depends on CYP2C19 polymorphisms, comedication/drug interactions, and gastrointestinal comorbidity.	clopidogrel	153-164	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	287-294
35407624-2	2022	In Japan, clopidogrel was the major P2Y12 inhibitor used for a decade until the new P2Y12 inhibitor, prasugrel, was introduced.	clopidogrel	10-21	purinergic receptor P2Y12	Homo sapiens	36-41
35631502-0	2022	Physiologically Based Pharmacokinetic (PBPK) Modeling of Clopidogrel and Its Four Relevant Metabolites for CYP2B6, CYP2C8, CYP2C19, and CYP3A4 Drug-Drug-Gene Interaction Predictions.	clopidogrel	57-68	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	136-142
35631502-1	2022	The antiplatelet agent clopidogrel is listed by the FDA as a strong clinical index inhibitor of cytochrome P450 (CYP) 2C8 and weak clinical inhibitor of CYP2B6.	clopidogrel	23-34	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	96-121
35631502-1	2022	The antiplatelet agent clopidogrel is listed by the FDA as a strong clinical index inhibitor of cytochrome P450 (CYP) 2C8 and weak clinical inhibitor of CYP2B6.	clopidogrel	23-34	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	153-159
35631502-2	2022	Moreover, clopidogrel is a substrate of-among others-CYP2C19 and CYP3A4.	clopidogrel	10-21	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-60
35631502-2	2022	Moreover, clopidogrel is a substrate of-among others-CYP2C19 and CYP3A4.	clopidogrel	10-21	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	65-71
35396752-2	2022	Because the genetic polymorphism of CYP2C19 gene leads to clopidogrel resistance, guidelines for antiplatelet recommendations in CYP2C19 of ultrarapid metabolizers (UM), extended metabolizers (EM) and poor metabolizers (PM) are clear.	clopidogrel	58-69	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	36-43
35480401-9	2022	Our study, which is the first to report the frequency of CYP2C19 polymorphism in the Montenegrin population, as well as to link the pharmacovigilance of clopidogrel with CYP2C19 gene variability, shows that the incidence of ADRs of clopidogrel in cardiac patients is high and depends on CYP2C19 polymorphisms, comedication/drug interactions, and gastrointestinal comorbidity.	clopidogrel	232-243	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	170-177
35059789-5	2022	CASE PRESENTATION: We present a case of a Caucasian male with mCRPC who was treated with enzalutamide and a moderate CYP2C8 inhibitor, clopidogrel, concomitantly.	clopidogrel	135-146	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	117-123
35428703-4	2022	METHODS: We systematically searched PubMed, Cochrane Central Register of Controlled Trials and Web of Science to identify studies that compared different oral P2Y12 inhibitors (clopidogrel, prasugrel and ticagrelor) in patients with NSTE-ACS.	clopidogrel	177-188	purinergic receptor P2Y12	Homo sapiens	159-164
35307978-1	2022	Treatment response to clopidogrel is associated with CYP2C19 activity through the formation of the active H4 metabolite.	clopidogrel	22-33	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	53-60
35307978-2	2022	The aims of this study were to develop a physiologically based pharmacokinetic (PBPK) model of clopidogrel and its metabolites for populations of European ancestry, to predict the pharmacokinetics in the Japanese population by CYP2C19 phenotype, and to investigate the effect of clinical and demographic factors.	clopidogrel	95-106	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	227-234
35307978-9	2022	This is the first PBPK model describing the two major metabolic pathways of clopidogrel, which can be applied to populations of European and Japanese ancestry by CYP2C19 phenotype.	clopidogrel	76-87	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	162-169
35418564-3	2022	This study aims to investigate the association of cytochrome P450 2C19 (CYP2C19) loss-of-function polymorphisms, haplotypes as well as a wide range of clinical and demographic variables with platelet aggregation phenotypes to clopidogrel in a Pakistani cohort.	clopidogrel	226-237	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	50-70
35418564-3	2022	This study aims to investigate the association of cytochrome P450 2C19 (CYP2C19) loss-of-function polymorphisms, haplotypes as well as a wide range of clinical and demographic variables with platelet aggregation phenotypes to clopidogrel in a Pakistani cohort.	clopidogrel	226-237	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	72-79
35387342-1	2022	Aim: Growing evidence indicated that CYP2C19 genotypes could only explain a fraction of the pharmacodynamic response to clopidogrel, while a number of clinical factors also have contributing roles.	clopidogrel	120-131	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-44
35399851-0	2022	Clinical Study of Clopidogrel Combined with Huoxue Tongluo Prescription in Improving Transient Ischemic Attack and the Effect on MMP-9, Hcy, and CRP.	clopidogrel	18-29	matrix metallopeptidase 9	Homo sapiens	129-134
35399851-0	2022	Clinical Study of Clopidogrel Combined with Huoxue Tongluo Prescription in Improving Transient Ischemic Attack and the Effect on MMP-9, Hcy, and CRP.	clopidogrel	18-29	C-reactive protein	Homo sapiens	145-148
35399851-1	2022	Background: This study aimed to explore the clinical study of clopidogrel combined with Huoxue Tongluo prescription in improving transient ischemic attack (TIA) and the effect on MMP-9, Hcy, and CRP.	clopidogrel	62-73	matrix metallopeptidase 9	Homo sapiens	179-184
35399851-1	2022	Background: This study aimed to explore the clinical study of clopidogrel combined with Huoxue Tongluo prescription in improving transient ischemic attack (TIA) and the effect on MMP-9, Hcy, and CRP.	clopidogrel	62-73	C-reactive protein	Homo sapiens	195-198
35399851-12	2022	Conclusion: Clopidogrel combined with Huoxue Tongluo prescription can significantly improve the therapeutic effect and reduce the levels of MMP-9, Hcy, and CRP in patients with TIA.	clopidogrel	12-23	matrix metallopeptidase 9	Homo sapiens	140-145
35399851-12	2022	Conclusion: Clopidogrel combined with Huoxue Tongluo prescription can significantly improve the therapeutic effect and reduce the levels of MMP-9, Hcy, and CRP in patients with TIA.	clopidogrel	12-23	C-reactive protein	Homo sapiens	156-159
35353154-6	2022	As compared to DAPT, on a background of the same P2Y12 inhibitor (clopidogrel or ticagrelor), DPI was associated with reduced thrombin generation, increased markers of cyclooxygenase-1 activity and TRAP-induced platelet aggregation and no differences in markers of P2Y12 signaling, platelet-mediated global thrombogenicity and TF-induced platelet aggregation.	clopidogrel	66-77	purinergic receptor P2Y12	Homo sapiens	49-54
35353154-6	2022	As compared to DAPT, on a background of the same P2Y12 inhibitor (clopidogrel or ticagrelor), DPI was associated with reduced thrombin generation, increased markers of cyclooxygenase-1 activity and TRAP-induced platelet aggregation and no differences in markers of P2Y12 signaling, platelet-mediated global thrombogenicity and TF-induced platelet aggregation.	clopidogrel	66-77	coagulation factor II, thrombin	Homo sapiens	126-134
35353154-6	2022	As compared to DAPT, on a background of the same P2Y12 inhibitor (clopidogrel or ticagrelor), DPI was associated with reduced thrombin generation, increased markers of cyclooxygenase-1 activity and TRAP-induced platelet aggregation and no differences in markers of P2Y12 signaling, platelet-mediated global thrombogenicity and TF-induced platelet aggregation.	clopidogrel	66-77	prostaglandin-endoperoxide synthase 1	Homo sapiens	168-184
35353154-6	2022	As compared to DAPT, on a background of the same P2Y12 inhibitor (clopidogrel or ticagrelor), DPI was associated with reduced thrombin generation, increased markers of cyclooxygenase-1 activity and TRAP-induced platelet aggregation and no differences in markers of P2Y12 signaling, platelet-mediated global thrombogenicity and TF-induced platelet aggregation.	clopidogrel	66-77	TRAP	Homo sapiens	198-202
35407361-0	2022	The Risk of Bleeding and Adverse Events with Clopidogrel in Elective Hip and Knee Arthroplasty Patients.	clopidogrel	45-56	hedgehog interacting protein	Homo sapiens	69-72
35264399-10	2022	Compared with clopidogrel, potent P2Y12 inhibitors were associated with a lower risk of ischaemic stroke (HR 0.57; 95% CI 0.37 to 0.87; p=0.008) and a lower risk of thrombotic events (HR 0.77; 95% CI 0.66 to 0.90; p=0.001).	clopidogrel	14-25	purinergic receptor P2Y12	Homo sapiens	34-39
35294730-3	2022	RECENT FINDINGS: Clopidogrel is the recommended P2Y12 inhibitor in the elective PCI setting.	clopidogrel	17-28	purinergic receptor P2Y12	Homo sapiens	48-53
35101369-1	2022	BACKGROUND: High on-clopidogrel platelet reactivity could be partially explained by loss-of-function alleles of CYP2C19, the enzyme that converts clopidogrel into its active form.	clopidogrel	20-31	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	112-119
35101369-1	2022	BACKGROUND: High on-clopidogrel platelet reactivity could be partially explained by loss-of-function alleles of CYP2C19, the enzyme that converts clopidogrel into its active form.	clopidogrel	146-157	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	112-119
35484746-8	2022	Two clopidogrel related SNPs CYP2C19*2 and CYP2C19*3 of 56 clinical samples were correctly genotyped by using this rapid visualized genotyping assay.	clopidogrel	4-15	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	29-36
35121011-13	2022	We confirmed that alphaII-spectrin cleavage increased post-TBI, with the highest cleavage detected in CLOP-treated rats.	clopidogrel	102-106	spectrin, alpha, non-erythrocytic 1	Rattus norvegicus	18-34
35387902-6	2022	After optimizing the condition of LC-MS/MS, a stable linearity was observed in the standard curves over the concentration ranges of 0.05 to 50.0 ng/mL for clopidogrel, 0.5 to 50.0 ng/mL for 2-Oxo-CLP, and 0.5 to 100 ng/mL for clopidogrel active metabolite derivative (CAMD).	clopidogrel	155-166	calmodulin like 3	Homo sapiens	196-199
35231553-4	2022	The Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) trial demonstrated that the P2Y12 inhibitor clopidogrel, when added to aspirin, reduced major cardiovascular events.	clopidogrel	114-125	purinergic receptor P2Y12	Homo sapiens	98-103
35181265-2	2022	However, in clinical practice, patients are often switched from a potent P2Y12 inhibitor to clopidogrel prior to or at discharge ("de-escalation").	clopidogrel	92-103	purinergic receptor P2Y12	Homo sapiens	73-78
35140503-11	2022	Conclusion: In this hospital-wide cohort, 8.2% were clopidogrel users, of which 14.9% were CYP2C19 PMs.	clopidogrel	52-63	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	91-98
35484746-8	2022	Two clopidogrel related SNPs CYP2C19*2 and CYP2C19*3 of 56 clinical samples were correctly genotyped by using this rapid visualized genotyping assay.	clopidogrel	4-15	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	43-50
35042400-0	2022	Effects of CYP2C19 LoF allele on major adverse cardiovascular events associated with clopidogrel in acute coronary syndrome patients undergoing percutaneous coronary intervention: meta-analysis.	clopidogrel	85-96	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	11-18
35063138-6	2022	On the other hand, a P2Y12 inhibitor, clopidogrel significantly improved survival outcomes at the higher dose but caused massive bleeding in the brain at both low and high doses.	clopidogrel	38-49	purinergic receptor P2Y12	Rattus norvegicus	21-26
35042400-1	2022	The aggregated risk of major adverse cardiovascular events (MACE) in acute coronary syndrome (ACS) patients inheriting CYP2C19 loss-of function (LoF) alleles who underwent percutaneous coronary intervention (PCI) and were treated with clopidogrel is controversial.	clopidogrel	235-246	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	119-126
35042400-8	2022	The ACS patients inheriting CYP2C19 LoF alleles, who underwent PCI and were treated with clopidogrel were correlated with significantly increased risk of MACE compared with noncarriers.	clopidogrel	89-100	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
35068171-1	2022	To investigate the differences in the correlation between multidrug resistance protein 1 (MDR1) (ABCB1) gene polymorphism and clopidogrel resistance in patients of the Hui and Han nationalities with percutaneous coronary intervention (PCI).	clopidogrel	126-137	ATP binding cassette subfamily B member 1	Homo sapiens	58-88
35112572-1	2022	Clopidogrel is a prodrug chiefly metabolized by the hepatic isoenzyme CYP2C19 to its active metabolite that inhibits the platelet aggregation.	clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	70-77
35112572-3	2022	As CYP2C19 genetic polymorphism is highly prevalent among the Asian population, the influence of the same on the pharmacokinetics and; thereby, the pharmacodynamics of clopidogrel needs more attention.	clopidogrel	168-179	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	3-10
35138719-5	2022	In patients with coronary artery disease and a higher bleeding risk, it is valuable to determine the CYP2C19 genotype prior to treatment with clopidogrel.	clopidogrel	142-153	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	101-108
35138719-6	2022	Pending further studies, we recommend that specialists prescribing clopidogrel should determine the CYP2C19 genotype in patients at high risk of recurrent ischemic events.	clopidogrel	67-78	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	100-107
35156424-1	2022	Background Studies have demonstrated increased risk of major atherothrombotic events in CYP2C19 loss-of-function (LOF) variant carriers versus non-carriers treated with clopidogrel after percutaneous coronary intervention (PCI).	clopidogrel	169-180	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	88-95
34983074-8	2022	Clopidogrel-based treatments reduced markers of P2Y12 signaling and TRAP-induced platelet aggregation.	clopidogrel	0-11	purinergic receptor P2Y12	Homo sapiens	48-53
34983074-8	2022	Clopidogrel-based treatments reduced markers of P2Y12 signaling and TRAP-induced platelet aggregation.	clopidogrel	0-11	TRAP	Homo sapiens	68-72
35275501-5	2022	Patients in the clopidogrel-resistant group carried more CYP2C19*3 or *2, which was associated with higher clopidogrel resistance in this group (69.11%, 47/68) than in the control group (64.29%, 36/56).	clopidogrel	16-27	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	57-64
35275501-5	2022	Patients in the clopidogrel-resistant group carried more CYP2C19*3 or *2, which was associated with higher clopidogrel resistance in this group (69.11%, 47/68) than in the control group (64.29%, 36/56).	clopidogrel	107-118	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	57-64
35073541-2	2022	A lot of genotype-oriented studies have concentrated on the impact of CYP2C19 gene polymorphisms on platelet aggregation in patients receiving clopidogrel.	clopidogrel	143-154	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	70-77
35068171-1	2022	To investigate the differences in the correlation between multidrug resistance protein 1 (MDR1) (ABCB1) gene polymorphism and clopidogrel resistance in patients of the Hui and Han nationalities with percutaneous coronary intervention (PCI).	clopidogrel	126-137	ATP binding cassette subfamily B member 1	Homo sapiens	90-94
35068171-1	2022	To investigate the differences in the correlation between multidrug resistance protein 1 (MDR1) (ABCB1) gene polymorphism and clopidogrel resistance in patients of the Hui and Han nationalities with percutaneous coronary intervention (PCI).	clopidogrel	126-137	ATP binding cassette subfamily B member 1	Homo sapiens	97-102
35068171-8	2022	Patients with a T allele at MDR1 C3435 T are more likely to show clopidogrel resistance, and no significant differences were identified in C3435 T gene polymorphism between the two nationalities.	clopidogrel	65-76	ATP binding cassette subfamily B member 1	Homo sapiens	28-32
35040887-11	2022	In the P2Y12 inhibitor group, ticagrelor was used in 63% of patients and clopidogrel in 37%.	clopidogrel	73-84	purinergic receptor P2Y12	Homo sapiens	7-12