PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
30048515-1	2018	Ticagrelor, a P2Y12 antagonist, is approved for prevention of thromboembolic events.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	14-19
29799992-12	2018	Conclusions and Relevance: Between 2008 and 2016, increased use of prasugrel and ticagrelor was accompanied by increased nonfilling of prescriptions for P2Y12 inhibitors within 30 days of discharge.	Ticagrelor	81-91	purinergic receptor P2Y12	Homo sapiens	153-158
29526833-1	2018	BACKGROUND: Switching between different classes of P2Y12 inhibitors, including de-escalation from ticagrelor to clopidogrel, commonly occurs in clinical practice.	Ticagrelor	98-108	purinergic receptor P2Y12	Homo sapiens	51-56
29686623-1	2018	Ticagrelor is one of the most powerful P2Y12 inhibitor.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	39-44
29150850-3	2018	Ticagrelor and prasugrel are two latest generation P2Y12 inhibitors with advantageous platelet inhibitory profiles.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	51-56
29150850-10	2018	WHAT IS NEW AND CONCLUSION: Although ticagrelor and prasugrel have similar platelet inhibitory effects in patients with T2DM, if a P2Y12 inhibitor is necessitated in patients with T2DM, ticagrelor might exert a more stable antiplatelet effect with 30-day short-term treatment.	Ticagrelor	186-196	purinergic receptor P2Y12	Homo sapiens	131-136
29050464-5	2018	RESULTS: In MEA analysis, adenosine diphosphate (ADP) and thrombin receptor activating peptide (TRAP)-induced platelet aggregations were lower in the CPD and the TCG groups; arachidonic acid (AA)-induced platelet aggregation was lower in the ASA group, whereas collagen (COL)-induced platelet aggregations were comparable among four groups.	Ticagrelor	162-165	TRAP	Homo sapiens	58-94
29050464-5	2018	RESULTS: In MEA analysis, adenosine diphosphate (ADP) and thrombin receptor activating peptide (TRAP)-induced platelet aggregations were lower in the CPD and the TCG groups; arachidonic acid (AA)-induced platelet aggregation was lower in the ASA group, whereas collagen (COL)-induced platelet aggregations were comparable among four groups.	Ticagrelor	162-165	TRAP	Homo sapiens	96-100
29381821-4	2018	It remains unknown whether the cardioprotective effects of ticagrelor are also mediated by modulating myocardial galectin-3 expression.	Ticagrelor	59-69	galectin 3	Rattus norvegicus	113-123
29381821-7	2018	RESULTS: Our results showed that ticagrelor treatment significantly reduced IA/AAR ratio at 3 and 7 days post I/R, downregulated mRNA and protein expression of galectin-3, as well as mRNA expression of TNF-alpha and IL-6 in infarct area at 24 h, 3 and 7 days post I/R.	Ticagrelor	33-43	galectin 3	Rattus norvegicus	160-170
29381821-7	2018	RESULTS: Our results showed that ticagrelor treatment significantly reduced IA/AAR ratio at 3 and 7 days post I/R, downregulated mRNA and protein expression of galectin-3, as well as mRNA expression of TNF-alpha and IL-6 in infarct area at 24 h, 3 and 7 days post I/R.	Ticagrelor	33-43	tumor necrosis factor	Rattus norvegicus	202-211
29381821-7	2018	RESULTS: Our results showed that ticagrelor treatment significantly reduced IA/AAR ratio at 3 and 7 days post I/R, downregulated mRNA and protein expression of galectin-3, as well as mRNA expression of TNF-alpha and IL-6 in infarct area at 24 h, 3 and 7 days post I/R.	Ticagrelor	33-43	interleukin 6	Rattus norvegicus	216-220
29381821-8	2018	CONCLUSIONS: Our results suggest that the cardioprotective effects of ticagrelor might partly be mediated by downregulating galectin-3 expression in infarct area in this rat model of myocardial I/R injury.	Ticagrelor	70-80	galectin 3	Rattus norvegicus	124-134
29686623-3	2018	In the present study, we showed that, in the same population, after 1 month treatment with ticagrelor, but not with clopidogrel, there is a decrease of the circulating levels of epidermal growth factor (EGF) and that these changes in circulating levels of EGF correlate with on-treatment platelet reactivity.	Ticagrelor	91-101	epidermal growth factor	Homo sapiens	178-201
29686623-3	2018	In the present study, we showed that, in the same population, after 1 month treatment with ticagrelor, but not with clopidogrel, there is a decrease of the circulating levels of epidermal growth factor (EGF) and that these changes in circulating levels of EGF correlate with on-treatment platelet reactivity.	Ticagrelor	91-101	epidermal growth factor	Homo sapiens	203-206
29686623-3	2018	In the present study, we showed that, in the same population, after 1 month treatment with ticagrelor, but not with clopidogrel, there is a decrease of the circulating levels of epidermal growth factor (EGF) and that these changes in circulating levels of EGF correlate with on-treatment platelet reactivity.	Ticagrelor	91-101	epidermal growth factor	Homo sapiens	256-259
29686623-7	2018	Taken together our data indicate that ticagrelor improves endothelial function by lowering circulating EGF that results in the activation of eNOS in the vascular endothelium.	Ticagrelor	38-48	epidermal growth factor	Homo sapiens	103-106
29355684-4	2018	We investigated the impact of rs5751876 C > T polymorphism of adenosine A2a receptor (ADORA2a) on platelet reactivity in patients during chronic treatment with ticagrelor.	Ticagrelor	163-173	adenosine A2a receptor	Homo sapiens	65-87
29344794-9	2018	The company submitted an individual patient simulation model to estimate the cost-effectiveness of ticagrelor 60 mg BID + ASA versus ASA only.	Ticagrelor	99-109	BH3 interacting domain death agonist	Homo sapiens	116-119
29344794-18	2018	In its final guidance, the AC recommended treatment with ticagrelor 60 mg BID + low-dose ASA for secondary prevention of atherothrombotic events in adults who have had an MI and are at increased risk of atherothrombotic events.	Ticagrelor	57-67	BH3 interacting domain death agonist	Homo sapiens	74-77
28982722-1	2018	OBJECTIVE: To estimate the absolute treatment effects of newer P2Y12 inhibitors (ticagrelor and prasugrel) compared with clopidogrel in men and women with acute coronary syndrome (ACS).	Ticagrelor	81-91	purinergic receptor P2Y12	Homo sapiens	63-68
29215418-1	2018	Ticagrelor and prasugrel are newer antiplatelet drugs which, like clopidogrel, block the P2Y12 platelet receptor to inhibit platelet aggregation.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	89-94
29215418-3	2018	Therefore, some institutions and providers switch patients from ticagrelor or prasugrel to clopidogrel in an effort to lower bleeding risk, stem costs, or otherwise ensure that patients can safely adhere to long-term P2Y12 inhibitor therapy.	Ticagrelor	64-74	purinergic receptor P2Y12	Homo sapiens	217-222
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.	Ticagrelor	148-158	purinergic receptor P2Y12	Homo sapiens	97-102
29355684-4	2018	We investigated the impact of rs5751876 C > T polymorphism of adenosine A2a receptor (ADORA2a) on platelet reactivity in patients during chronic treatment with ticagrelor.	Ticagrelor	163-173	adenosine A2a receptor	Homo sapiens	89-96
28503981-5	2018	We found that aspirin plus prasugrel or aspirin plus ticagrelor inhibited platelet responses to multiple agonists and reduced P-selectin expression.	Ticagrelor	53-63	selectin P	Homo sapiens	126-136
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.	Ticagrelor	49-59	purinergic receptor P2Y12	Homo sapiens	6-12
29534250-1	2018	Third-generation P2Y12 inhibitors (prasugrel, ticagrelor) are recommended in acute myocardial infarction (AMI).	Ticagrelor	46-56	purinergic receptor P2Y12	Homo sapiens	17-22
28945935-3	2018	Ticagrelor is a new oral antagonist of the adenosine diphosphate P2Y12 receptor.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	65-70
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).	Ticagrelor	395-405	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
29322294-3	2018	We examined the potential of the reversible P2Y12 inhibitor ticagrelor, an agent used clinically to prevent cardiovascular and cerebrovascular events, to reduce tumor growth and metastasis.	Ticagrelor	60-70	purinergic receptor P2Y12	Homo sapiens	44-49
29280403-8	2018	EXPERT OPINION: Introduction of ticagrelor, a first directly-acting and reversible P2Y12 inhibitor, gave some new possibilities as the efficacy of older drugs was often insufficient.	Ticagrelor	32-42	purinergic receptor P2Y12	Homo sapiens	83-88
29398917-2	2018	A P2Y12 receptor antagonist, ticagrelor, is unique among antiplatelet drugs, because ticagrelor inhibits the platelet P2Y12 receptor in a reversible manner, and because it demonstrates a wide palette of advantageous pleiotropic effects associated with the increased concentration of adenosine.	Ticagrelor	29-39	purinergic receptor P2Y12	Homo sapiens	2-7
29367102-9	2018	In contrast, the same concentration of ticagrelor, another P2Y12 inhibitor did not induce fibrillation events though it decreased the contractility of ventricular myocytes significantly.	Ticagrelor	39-49	purinergic receptor P2Y12	Rattus norvegicus	59-64
29398917-2	2018	A P2Y12 receptor antagonist, ticagrelor, is unique among antiplatelet drugs, because ticagrelor inhibits the platelet P2Y12 receptor in a reversible manner, and because it demonstrates a wide palette of advantageous pleiotropic effects associated with the increased concentration of adenosine.	Ticagrelor	29-39	purinergic receptor P2Y12	Homo sapiens	118-123
29398917-2	2018	A P2Y12 receptor antagonist, ticagrelor, is unique among antiplatelet drugs, because ticagrelor inhibits the platelet P2Y12 receptor in a reversible manner, and because it demonstrates a wide palette of advantageous pleiotropic effects associated with the increased concentration of adenosine.	Ticagrelor	85-95	purinergic receptor P2Y12	Homo sapiens	2-7
29398917-2	2018	A P2Y12 receptor antagonist, ticagrelor, is unique among antiplatelet drugs, because ticagrelor inhibits the platelet P2Y12 receptor in a reversible manner, and because it demonstrates a wide palette of advantageous pleiotropic effects associated with the increased concentration of adenosine.	Ticagrelor	85-95	purinergic receptor P2Y12	Homo sapiens	118-123
29393120-10	2018	In this patient population, year-to-year increases in P2Y12i prescriptions were observed with a dramatic increase in ticagrelor prescriptions.	Ticagrelor	117-127	purinergic receptor P2Y12	Homo sapiens	54-59
29345592-5	2018	This review aims to discuss potential benefits and highlight important pitfalls of prolonged treatment with P2Y12-inhibitors, with a focus on ticagrelor, an attractive reversible P2Y12-inhibitor in patients after myocardial infarction.	Ticagrelor	142-152	purinergic receptor P2Y12	Homo sapiens	179-184
29329963-13	2018	Six hours after daily dosing, VASP-PRI >50% was found in 42% of clopidogrel and 2% of ticagrelor treated patients.	Ticagrelor	89-99	vasodilator stimulated phosphoprotein	Homo sapiens	30-34
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.	Ticagrelor	184-194	purinergic receptor P2Y12	Homo sapiens	136-141
29075924-13	2018	In centers with high usage, ticagrelor is main newer generation P2Y12 inhibitor for precathlab and periprocedural administration.	Ticagrelor	28-38	purinergic receptor P2Y12	Homo sapiens	64-69
29894287-0	2018	Comparison of Ticagrelor with Clopidogrel in Reducing Interleukin-17 and Myeloperoxidase Expression in Thrombus and Improving Postprocedural Coronary Flow in ST-segment Elevation Myocardial Infarction Patients.	Ticagrelor	14-24	myeloperoxidase	Homo sapiens	73-88
29894287-1	2018	PURPOSE: This study aimed to explore the effects of ticagrelor (a P2Y12 receptor inhibitor) on interleukin (IL)-17 and myeloperoxidase (MPO) expression in coronary thrombus as well as on the coronary blood flow in ST-segment elevation myocardial infarction (STEMI) patients following percutaneous coronary intervention (PCI).	Ticagrelor	52-62	myeloperoxidase	Homo sapiens	119-134
29894287-1	2018	PURPOSE: This study aimed to explore the effects of ticagrelor (a P2Y12 receptor inhibitor) on interleukin (IL)-17 and myeloperoxidase (MPO) expression in coronary thrombus as well as on the coronary blood flow in ST-segment elevation myocardial infarction (STEMI) patients following percutaneous coronary intervention (PCI).	Ticagrelor	52-62	myeloperoxidase	Homo sapiens	136-139
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.	Ticagrelor	180-190	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.	Ticagrelor	180-190	myeloperoxidase	Homo sapiens	109-112
28117433-0	2018	Cost-effectiveness of cytochrome P450 2C19 *2 genotype-guided selection of clopidogrel or ticagrelor in Chinese patients with acute coronary syndrome.	Ticagrelor	90-100	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	22-42
29185103-2	2017	Statins and ticagrelor increase the production of 15-epi-lipoxin A4 via cyclooxygenase-2.	Ticagrelor	12-22	prostaglandin-endoperoxide synthase 2	Mus musculus	72-88
29185103-12	2017	Aspirin, ticagrelor, and rosuvastatin decreased serum IL-1beta and IL-6 levels.	Ticagrelor	9-19	interleukin 1 beta	Mus musculus	54-62
29185103-12	2017	Aspirin, ticagrelor, and rosuvastatin decreased serum IL-1beta and IL-6 levels.	Ticagrelor	9-19	interleukin 6	Mus musculus	67-71
29185103-14	2017	Aspirin, ticagrelor, and rosuvastatin all decreased TNF-alpha levels.	Ticagrelor	9-19	tumor necrosis factor	Mus musculus	52-61
29071332-2	2017	Ticagrelor is a direct-acting P2Y12 inhibitor and, unlike clopidogrel and prasugrel, does not require metabolic activation.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	30-35
29150806-1	2017	Ticagrelor (Brilique ) is an orally administered P2Y12 inhibitor.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	49-54
29150806-1	2017	Ticagrelor (Brilique ) is an orally administered P2Y12 inhibitor.	Ticagrelor	12-20	purinergic receptor P2Y12	Homo sapiens	49-54
29064388-9	2017	Thus ticagrelor, a P2Y12 inhibitor, was used to examine the potential therapeutic effect of an ADP receptor antagonist on cancer cells.	Ticagrelor	5-15	purinergic receptor P2Y12	Homo sapiens	19-24
29043405-4	2017	In patients with ACS the question arises when treatment with one of the more potent P2Y12 inhibitors, such as prasugrel and ticagrelor should be used instead of clopidogrel.	Ticagrelor	124-134	purinergic receptor P2Y12	Homo sapiens	84-89
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).	Ticagrelor	66-76	purinergic receptor P2Y12	Homo sapiens	20-25
27937053-0	2017	Association of PEAR1 rs12041331 polymorphism and pharmacodynamics of ticagrelor in healthy Chinese volunteers.	Ticagrelor	69-79	platelet endothelial aggregation receptor 1	Homo sapiens	15-20
27937053-3	2017	This study aimed to investigate whether PEAR1 polymorphism is associated with ticagrelor pharmacodynamics in healthy Chinese subjects.	Ticagrelor	78-88	platelet endothelial aggregation receptor 1	Homo sapiens	40-45
27937053-14	2017	PEAR1 polymorphism may influence ticagrelor pharmacodynamics in healthy Chinese subjects.	Ticagrelor	33-43	platelet endothelial aggregation receptor 1	Homo sapiens	0-5
29225903-7	2017	Results: Prasugrel or ticagrelor was given as the loading P2Y12 inhibitor in 49% of 2198 patients and as a maintenance therapy in 59%.	Ticagrelor	22-32	purinergic receptor P2Y12	Homo sapiens	58-63
29167415-2	2017	Yet combined therapeutic regimens have the potential of pharmacological interaction with both ticagrelor and simvastatin being metabolized by CYP3A4.	Ticagrelor	94-104	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	142-148
26752652-5	2017	Cyclopentyl-triazolo-pyrimidines, a newer pharmacological class from which ticagrelor is an example, also act at the P2Y12 platelet receptor, and like prasugrel, ticagrelor inhibits platelet aggregation in a fast and consistent manner, however, in a reversible way.	Ticagrelor	75-85	purinergic receptor P2Y12	Homo sapiens	117-122
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.	Ticagrelor	95-105	purinergic receptor P2Y12	Homo sapiens	50-55
28653184-5	2017	Compared to prasugrel- and clopidogrel-treated patients, the PRI-VASP of ticagrelor-treated patients showed no significant increase after in vitro administration of PP.	Ticagrelor	73-83	vasodilator stimulated phosphoprotein	Homo sapiens	65-69
28653184-7	2017	Surprisingly, PP with human serum or human serum alone were able to significantly increase PRI-VASP in samples of ticagrelor-treated patients (11.7 +- 10.9   61.3 +- 10.9%, p = 0.006; 11.7 +- 10.9   54.1 +- 2.7%, p < 0.001).	Ticagrelor	114-124	vasodilator stimulated phosphoprotein	Homo sapiens	95-99
29300792-9	2017	Newer oral P2Y12 inhibitors such as ticagrelor and prasugrel have demonstrated greater efficacy than clopidogrel in improving the cardiovascular outcomes of patients with ACS and diabetes.	Ticagrelor	36-46	purinergic receptor P2Y12	Homo sapiens	11-16
28150522-7	2017	In conclusion, in ACS patients undergoing PCI and treated with a P2Y12 receptor antagonist, dyspnea occurs commonly, particularly when ticagrelor is administered.	Ticagrelor	135-145	purinergic receptor P2Y12	Homo sapiens	65-70
29042978-7	2017	In addition, ticagrelor significantly decreased the ulcer-stimulated expression levels of EGF, VEGF, phosphorylated extracellular signal-regulated kinase (ERK), phosphorylated P38 mitogen-activated protein kinase and nuclear factor-kappaB P65 at the ulcer margin (P<0.05).	Ticagrelor	13-23	epidermal growth factor like 1	Rattus norvegicus	90-93
29042978-7	2017	In addition, ticagrelor significantly decreased the ulcer-stimulated expression levels of EGF, VEGF, phosphorylated extracellular signal-regulated kinase (ERK), phosphorylated P38 mitogen-activated protein kinase and nuclear factor-kappaB P65 at the ulcer margin (P<0.05).	Ticagrelor	13-23	vascular endothelial growth factor A	Rattus norvegicus	95-99
29042978-7	2017	In addition, ticagrelor significantly decreased the ulcer-stimulated expression levels of EGF, VEGF, phosphorylated extracellular signal-regulated kinase (ERK), phosphorylated P38 mitogen-activated protein kinase and nuclear factor-kappaB P65 at the ulcer margin (P<0.05).	Ticagrelor	13-23	Eph receptor B1	Rattus norvegicus	116-153
29042978-7	2017	In addition, ticagrelor significantly decreased the ulcer-stimulated expression levels of EGF, VEGF, phosphorylated extracellular signal-regulated kinase (ERK), phosphorylated P38 mitogen-activated protein kinase and nuclear factor-kappaB P65 at the ulcer margin (P<0.05).	Ticagrelor	13-23	Eph receptor B1	Rattus norvegicus	155-158
28833345-1	2017	STUDY OBJECTIVE: To describe contemporary trends of P2Y12 inhibitor use in patients with acute coronary syndrome (ACS) and comorbid diabetes mellitus (DM) and/or chronic kidney disease (CKD) who have a higher risk of recurring ACS and may benefit from treatment with higher efficacy third-generation agents (prasugrel and ticagrelor).	Ticagrelor	322-332	purinergic receptor P2Y12	Homo sapiens	52-57
28935927-1	2017	Ticagrelor is a direct acting and reversibly binding P2Y12 antagonist approved for the prevention of thromboembolic events.	Ticagrelor	0-10	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	53-58
28679740-2	2017	We showed that in murine models of ovarian cancer, a P2Y12 inhibitor (ticagrelor) reduced tumor growth by 60% compared with aspirin and by 75% compared with placebo.	Ticagrelor	70-80	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	53-58
28854078-4	2017	METHODS: This retrospective observational study of the MarketScan Commercial Claims and Encounters Database identified patients aged >= 18 years who were discharged from an ACS hospitalization in 2012-2014 and initiated P2Y12 APT (ticagrelor, prasugrel, or clopidogrel).	Ticagrelor	234-244	purinergic receptor P2Y12	Homo sapiens	223-228
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.	Ticagrelor	115-125	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	184-191
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.	Ticagrelor	210-220	purinergic receptor P2Y12	Homo sapiens	150-155
28776172-3	2017	As compared with clopidogrel, these newer P2Y12 agents-such as prasugrel and ticagrelor-allow for further reductions in ischemic end points, without the robust increases in bleeding seen in previous studies of antithrombotic therapies.	Ticagrelor	77-87	purinergic receptor P2Y12	Homo sapiens	42-47
28433569-0	2017	Vitamin D Binding Protein rs7041 polymorphism and high-residual platelet reactivity in patients receiving dual antiplatelet therapy with clopidogrel or ticagrelor.	Ticagrelor	152-162	GC vitamin D binding protein	Homo sapiens	0-25
28569920-4	2017	Under static conditions, GPVI-Fc inhibited plaque-induced platelet aggregation by 53 %, and increased platelet inhibition by ASA (51 %) and ticagrelor (64 %) to 66 % and 80 %, respectively.	Ticagrelor	140-150	glycoprotein VI platelet	Homo sapiens	25-29
28569920-5	2017	Under arterial flow, GPVI-Fc inhibited plaque-induced platelet aggregation by 57 %, and significantly increased platelet inhibition by ASA (28 %) and ticagrelor (47 %) to about 81 % each.	Ticagrelor	150-160	glycoprotein VI platelet	Homo sapiens	21-25
28750695-3	2017	METHODS: The authors performed a prospective economic substudy alongside the PEGASUS-TIMI 54 (Prevention of Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a Background of Aspirin-Thrombolysis In Myocardial Infarction 54) trial, which randomized 21,162 patients to ASA alone, ticagrelor 60 mg twice daily + low-dose ASA, or ticagrelor 90 mg twice daily + low-dose ASA.	Ticagrelor	172-182	IKAROS family zinc finger 5	Homo sapiens	77-92
28433569-5	2017	METHODS: Patients treated with DAPT (ASA and clopidogrel or ticagrelor) for an ACS or elective PCI were scheduled for platelet function assessment at 30-90days post-discharge.	Ticagrelor	60-70	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	79-82
28463894-7	2017	Pharmacokinetic/pharmacodynamic studies confirmed a more prompt and potent platelet inhibition after loading with the new P2Y12 inhibitors versus clopidogrel, and suggested the safety of switching from prasugrel to ticagrelor.	Ticagrelor	215-225	purinergic receptor P2Y12	Homo sapiens	122-127
28625369-1	2017	BACKGROUND: Among the 3 approved oral P2Y12 inhibitors for the treatment for patients with acute coronary syndrome (ACS), ticagrelor, but not prasugrel or clopidogrel, has been associated with off-target properties, such as improved endothelial-dependent vasomotion and increased adenosine plasma levels.	Ticagrelor	122-132	purinergic receptor P2Y12	Homo sapiens	38-43
28554486-9	2017	In conclusion, low-dose ticagrelor treatment, either with 90 mg QD or 45 mg BID, was associated with a more potent antiplatelet effect compared with clopidogrel treatment and once daily dose provided similar antiplatelet effect but favorable effect on optimal platelet inhibition compared with twice daily dose.	Ticagrelor	24-34	BH3 interacting domain death agonist	Homo sapiens	76-79
28683943-0	2017	In Vitro Pharmacodynamic Effects of Cangrelor on Platelet P2Y12 Receptor-Mediated Signaling in Ticagrelor-Treated Patients.	Ticagrelor	95-105	purinergic receptor P2Y12	Homo sapiens	58-63
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.	Ticagrelor	36-46	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	52-57
28562037-9	2017	The IC50 values of bicalutamide, ticagrelor, and meloxicam suggest that they might inhibit intestinal OATP2B1 at clinically relevant concentrations and therefore modulate the absorption of other concomitantly administered drugs.	Ticagrelor	33-43	solute carrier organic anion transporter family member 2B1	Homo sapiens	102-109
28604225-6	2017	CONCLUSION: Results of the current study showed that CYP4F2 rs3093135 TT variant carriers had a higher antiplatelet effect of ticagrelor, and more frequently had nonprocedural bleeding during ticagrelor therapy, as compared with AA and AT variant carriers.	Ticagrelor	126-136	cytochrome P450 family 4 subfamily F member 2	Homo sapiens	53-59
28611098-1	2017	BACKGROUND: In patients with non-ST-segment elevation acute coronary syndromes, inhibition of platelet aggregation (IPA) with a potent P2Y12 inhibitor, ticagrelor, was inferior to tirofiban infusion at 2 hours, indicating that glycoprotein IIb/IIIa inhibitors are still needed.	Ticagrelor	152-162	purinergic receptor P2Y12	Homo sapiens	135-140
28560235-1	2017	Ticagrelor is a potent, direct P2Y12 antagonist with rapid onset of action and intense platelet inhibition, indicated in patients with acute coronary syndromes (ACS).	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	31-36
28382371-1	2017	Dyspnoea may be induced by some reversibly-binding P2Y12 inhibitors, including cangrelor and ticagrelor.	Ticagrelor	93-103	purinergic receptor P2Y12	Homo sapiens	51-56
27885888-0	2017	Cangrelor in combination with ticagrelor provides consistent and potent P2Y12-inhibition during and after primary percutaneous coronary intervention in real-world patients with ST-segment-elevation myocardial infarction.	Ticagrelor	30-40	purinergic receptor P2Y12	Homo sapiens	72-77
28300867-2	2017	This study aimed to determine whether ticagrelor 60 mg twice daily (bid) provided potent and consistent platelet inhibition in patients with vs without diabetes in the PEGASUS-TIMI 54 platelet function substudy.	Ticagrelor	38-48	BH3 interacting domain death agonist	Homo sapiens	68-71
28300867-5	2017	In patients treated with ticagrelor 60 mg bid, on-treatment platelet reactivity to ADP, as determined by light transmission aggregometry (LTA), VerifyNow and VASP, was similar in patients with vs without diabetes (LTA post-dose, ADP 20 microM: 29 +- 14 vs 34 +- 10 %, respectively; p = 0.19).	Ticagrelor	25-35	BH3 interacting domain death agonist	Homo sapiens	42-45
28300867-6	2017	A consistent inhibitory effect of ticagrelor 60 mg bid was observed pre- and post-dose regardless of diabetes status, even in insulin-treated patients.	Ticagrelor	34-44	BH3 interacting domain death agonist	Homo sapiens	51-54
28300867-10	2017	In conclusion, ticagrelor 60 mg bid is equally effective at reducing platelet reactivity in patients with and without diabetes, yielding a consistently high level of platelet inhibition regardless of diabetes status.	Ticagrelor	15-25	BH3 interacting domain death agonist	Homo sapiens	32-35
28092426-10	2017	Longer exposure (24 h) to the drug decreased reversibility of activated GPIIb-IIIa by ticagrelor (65.1% [49.5-80.6], % of vehicle with 95% confidence interval [CI]) and T-AM (88.8% [79.2-98.3]), but not by cangrelor (101.4% [96.4-106.4]).	Ticagrelor	86-96	integrin subunit alpha 2b	Homo sapiens	72-77
28674626-6	2017	The use of ticagrelor in eligible patients not yet on a P2Y12 inhibitor at 1 year post-MI would cost an estimated US$885 000 per MI, stroke or cardiovascular death averted over a 3-year time horizon, while the use of clopidogrel would cost an estimated US$19 800 per ischaemic event averted.	Ticagrelor	11-21	purinergic receptor P2Y12	Homo sapiens	56-61
28150850-4	2017	Ticagrelor is a direct acting P2Y12 inhibitor and, unlike clopidogrel and prasugrel, does not require metabolic activation.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	30-35
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.	Ticagrelor	72-82	purinergic receptor P2Y12	Homo sapiens	163-169
28408884-0	2017	Effect of CYP3A4*1G and CYP3A5*3 Polymorphisms on Pharmacokinetics and Pharmacodynamics of Ticagrelor in Healthy Chinese Subjects.	Ticagrelor	91-101	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	10-16
28408884-0	2017	Effect of CYP3A4*1G and CYP3A5*3 Polymorphisms on Pharmacokinetics and Pharmacodynamics of Ticagrelor in Healthy Chinese Subjects.	Ticagrelor	91-101	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	24-30
28408884-6	2017	Genetic differences in CYP3A4 and CYP3A5 expression in human volunteers and patients might affect the clearance of ticagrelor or AR-C124910XX in vivo resulting in subsequent variable patient response.	Ticagrelor	115-125	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	23-29
28408884-6	2017	Genetic differences in CYP3A4 and CYP3A5 expression in human volunteers and patients might affect the clearance of ticagrelor or AR-C124910XX in vivo resulting in subsequent variable patient response.	Ticagrelor	115-125	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	34-40
28408884-7	2017	Thus, this study is designed to explore the effects of CYP3A4*1G and CYP3A5*3 polymorphisms on the pharmacokinetics and pharmcodynamics of ticagrelor in healthy Chinese subjects.	Ticagrelor	139-149	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	55-61
28408884-7	2017	Thus, this study is designed to explore the effects of CYP3A4*1G and CYP3A5*3 polymorphisms on the pharmacokinetics and pharmcodynamics of ticagrelor in healthy Chinese subjects.	Ticagrelor	139-149	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	69-75
28408884-8	2017	The results indicated that the CYP3A4*1G polymorphism significantly influenced the pharmacokinetics of AR-C124910XX, and it may be more important than CYP3A5*3 with respect to influencing ticagrelor pharmacokinetics by increasing CYP3A4 activity.	Ticagrelor	188-198	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	31-37
28408884-8	2017	The results indicated that the CYP3A4*1G polymorphism significantly influenced the pharmacokinetics of AR-C124910XX, and it may be more important than CYP3A5*3 with respect to influencing ticagrelor pharmacokinetics by increasing CYP3A4 activity.	Ticagrelor	188-198	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	151-157
28408884-8	2017	The results indicated that the CYP3A4*1G polymorphism significantly influenced the pharmacokinetics of AR-C124910XX, and it may be more important than CYP3A5*3 with respect to influencing ticagrelor pharmacokinetics by increasing CYP3A4 activity.	Ticagrelor	188-198	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	230-236
28065908-7	2017	Ticagrelor, unlike CAM, concentration dependently decreased TNF-alpha-induced TF expression and TF activity in LAA endocardial cells.	Ticagrelor	0-10	tumor necrosis factor	Homo sapiens	60-69
28065908-7	2017	Ticagrelor, unlike CAM, concentration dependently decreased TNF-alpha-induced TF expression and TF activity in LAA endocardial cells.	Ticagrelor	0-10	coagulation factor III, tissue factor	Homo sapiens	78-80
28065908-7	2017	Ticagrelor, unlike CAM, concentration dependently decreased TNF-alpha-induced TF expression and TF activity in LAA endocardial cells.	Ticagrelor	0-10	coagulation factor III, tissue factor	Homo sapiens	96-98
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.	Ticagrelor	65-75	purinergic receptor P2Y12	Homo sapiens	127-132
28062136-10	2017	Ticagrelor and prasugrel demonstrated a similar extent of P2Y12 receptor inhibition within 24h, although maximal platelet inhibition after these potent agents was not achieved for 6h.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	58-63
27922911-4	2017	The newer P2Y12 inhibitors include cangrelor, prasugrel, and ticagrelor.	Ticagrelor	61-71	purinergic receptor P2Y12	Homo sapiens	10-15
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.	Ticagrelor	101-111	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	16-23
27904901-6	2017	Ticagrelor, however, sensitised ECs for thrombin-induced hyperpermeability and potentiated the thrombin effect.	Ticagrelor	0-10	coagulation factor II, thrombin	Homo sapiens	40-48
27904901-6	2017	Ticagrelor, however, sensitised ECs for thrombin-induced hyperpermeability and potentiated the thrombin effect.	Ticagrelor	0-10	coagulation factor II, thrombin	Homo sapiens	95-103
27904901-9	2017	Accordingly, ticagrelor caused an increase in myosin light chain (MLC) phosphorylation, an important regulator of EC contractile machinery and thus permeability, which was abrogated by LaCl3.	Ticagrelor	13-23	modulator of VRAC current 1	Homo sapiens	46-64
27904901-9	2017	Accordingly, ticagrelor caused an increase in myosin light chain (MLC) phosphorylation, an important regulator of EC contractile machinery and thus permeability, which was abrogated by LaCl3.	Ticagrelor	13-23	modulator of VRAC current 1	Homo sapiens	66-69
28089137-11	2017	CONCLUSION: Despite rapid platelet inhibition provided by cangrelor, newer oral P2Y12 inhibitors such as ticagrelor and prasugrel have comparable clinical outcomes.	Ticagrelor	105-115	purinergic receptor P2Y12	Homo sapiens	80-85
26124456-8	2017	The powerful oral P2Y12 inhibitors, prasugrel and ticagrelor, have been clearly shown to prevent stent thrombosis and recurrent ischaemic events after emergency percutaneous coronary intervention in STEMI patients.	Ticagrelor	50-60	purinergic receptor P2Y12	Homo sapiens	18-23
27617370-3	2017	The new P2Y12 inhibitors, ticagrelor and prasugrel, have been shown to be superior to clopidogrel in STEMI patients undergoing primary percutaneous coronary intervention.	Ticagrelor	26-36	purinergic receptor P2Y12	Homo sapiens	8-13
27865197-3	2017	Ticagrelor is a direct-acting inhibitor of the adenosine diphosphate receptor P2Y12 that has a more rapid onset and offset than clopidogrel.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	78-83
27628008-7	2017	The antiplatelet effect of the new P2Y12 receptor antagonists, ticagrelor and prasugrel, seems less influenced by PPI co-treatment.Given the large number of patients treated with antithrombotic drugs and PPIs, even a minor reduction of platelet inhibition potentially carries considerable clinical impact.	Ticagrelor	63-73	purinergic receptor P2Y12	Homo sapiens	35-40
28049954-3	2017	Three genetic loci (SLCO1B1, CYP3A4, and UGT2B7) were reported to affect ticagrelor pharmacokinetics.	Ticagrelor	73-83	solute carrier organic anion transporter family member 1B1	Homo sapiens	20-27
28049954-3	2017	Three genetic loci (SLCO1B1, CYP3A4, and UGT2B7) were reported to affect ticagrelor pharmacokinetics.	Ticagrelor	73-83	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	29-35
28049954-3	2017	Three genetic loci (SLCO1B1, CYP3A4, and UGT2B7) were reported to affect ticagrelor pharmacokinetics.	Ticagrelor	73-83	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	41-47
27548273-8	2017	Patients discharged with ticagrelor versus thienopyridines demonstrated a higher rate of crossover to other P2Y12 inhibitors (11 vs. 5%, p = 0.03).	Ticagrelor	25-35	purinergic receptor P2Y12	Homo sapiens	108-113
28028070-0	2017	Ticagrelor, but not clopidogrel, reduces arterial thrombosis via endothelial tissue factor suppression.	Ticagrelor	0-10	coagulation factor III	Mus musculus	77-90
28028070-5	2017	Ticagrelor, but not CAM, reduced TNF-alpha-induced TF expression via proteasomal degradation and TF activity, independently of the P2Y12 receptor and the equilibrative nucleoside transporter 1 (ENT1), an additional target of ticagrelor.	Ticagrelor	0-10	tumor necrosis factor	Mus musculus	33-42
28028070-5	2017	Ticagrelor, but not CAM, reduced TNF-alpha-induced TF expression via proteasomal degradation and TF activity, independently of the P2Y12 receptor and the equilibrative nucleoside transporter 1 (ENT1), an additional target of ticagrelor.	Ticagrelor	0-10	coagulation factor III	Mus musculus	51-53
27886822-2	2017	Ticagrelor is a reversibly binding, potent oral P2Y12 inhibitor that also is a weak inhibitor of the equilibrative nucleoside transporter-1 pathway for cellular adenosine uptake.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	48-53
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.	Ticagrelor	191-201	purinergic receptor P2Y12	Homo sapiens	56-61
27511945-3	2016	Ticagrelor and dipyridamole inhibit platelet function by inhibiting P2Y12 receptors and platelet phosphodiesterase, respectively, but share the capacity to inhibit cellular uptake of adenosine and thereby increase extracellular adenosine levels.	Ticagrelor	0-10	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	68-73
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.	Ticagrelor	103-113	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).	Ticagrelor	120-130	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).	Ticagrelor	132-135	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	87-94
27694321-0	2016	Inverse agonism at the P2Y12 receptor and ENT1 transporter blockade contribute to platelet inhibition by ticagrelor.	Ticagrelor	105-115	purinergic receptor P2Y12	Homo sapiens	23-37
27694321-0	2016	Inverse agonism at the P2Y12 receptor and ENT1 transporter blockade contribute to platelet inhibition by ticagrelor.	Ticagrelor	105-115	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	42-46
27694321-1	2016	Ticagrelor is a potent antagonist of the P2Y12 receptor (P2Y12R) and consequently an inhibitor of platelet activity effective in the treatment of atherothrombosis.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	41-55
27694321-1	2016	Ticagrelor is a potent antagonist of the P2Y12 receptor (P2Y12R) and consequently an inhibitor of platelet activity effective in the treatment of atherothrombosis.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	57-63
27694321-4	2016	This additional effect of ticagrelor beyond P2Y12R antagonism was in part as a consequence of ticagrelor inhibiting the equilibrative nucleoside transporter 1 (ENT1) on platelets, leading to accumulation of extracellular adenosine and activation of Gs-coupled adenosine A2A receptors.	Ticagrelor	26-36	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	120-158
27694321-4	2016	This additional effect of ticagrelor beyond P2Y12R antagonism was in part as a consequence of ticagrelor inhibiting the equilibrative nucleoside transporter 1 (ENT1) on platelets, leading to accumulation of extracellular adenosine and activation of Gs-coupled adenosine A2A receptors.	Ticagrelor	26-36	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	160-164
27694321-4	2016	This additional effect of ticagrelor beyond P2Y12R antagonism was in part as a consequence of ticagrelor inhibiting the equilibrative nucleoside transporter 1 (ENT1) on platelets, leading to accumulation of extracellular adenosine and activation of Gs-coupled adenosine A2A receptors.	Ticagrelor	94-104	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	120-158
27694321-4	2016	This additional effect of ticagrelor beyond P2Y12R antagonism was in part as a consequence of ticagrelor inhibiting the equilibrative nucleoside transporter 1 (ENT1) on platelets, leading to accumulation of extracellular adenosine and activation of Gs-coupled adenosine A2A receptors.	Ticagrelor	94-104	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	160-164
27694321-8	2016	In these cells, ticagrelor blocked the constitutive agonist-independent activity of the P2Y12R, limiting basal Gi-coupled signaling and thereby increasing cAMP levels.	Ticagrelor	16-26	purinergic receptor P2Y12	Homo sapiens	88-94
27694321-11	2016	In summary, our studies describe 2 novel modes of action of ticagrelor, inhibition of platelet ENT1 and inverse agonism at the P2Y12R that contribute to its effective inhibition of platelet activation.	Ticagrelor	60-70	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	95-99
27694321-11	2016	In summary, our studies describe 2 novel modes of action of ticagrelor, inhibition of platelet ENT1 and inverse agonism at the P2Y12R that contribute to its effective inhibition of platelet activation.	Ticagrelor	60-70	purinergic receptor P2Y12	Homo sapiens	127-133
26757017-12	2016	In mice dosed to complete P2Y12 inhibition, boosting coagulation by administration of rhFVIIa or rhFII within 90s after bleeding initiation can partly reverse ticagrelor-enhanced bleeding.	Ticagrelor	159-169	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	26-31
27740874-3	2016	Ticagrelor is a reversibly binding oral P2Y12 receptor blocker that mediates potent inhibition of adenosine diphosphate-induced platelet function.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	40-45
27740874-6	2016	Expert commentary: Ongoing studies are now investigating the plausibility of removing aspirin therapy in the setting of potent P2Y12 receptor blockade via ticagrelor monotherapy or replacing aspirin with an oral anticoagulant.	Ticagrelor	155-165	purinergic receptor P2Y12	Homo sapiens	127-132
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.	Ticagrelor	52-62	translocated promoter region, nuclear basket protein	Homo sapiens	68-71
27830382-4	2016	HYPOTHESIS: Ticagrelor and rosuvastatin have additive effects on myocardial adenosine levels, and therefore, on IS and post-reperfusion activation of the NLRP3-inflammasome.	Ticagrelor	12-22	NLR family, pyrin domain containing 3	Rattus norvegicus	154-159
27416295-0	2016	Intestinal permeability and P-glycoprotein-mediated efflux transport of ticagrelor in Caco-2 monolayer cells.	Ticagrelor	72-82	ATP binding cassette subfamily B member 1	Homo sapiens	28-42
27416295-6	2016	Valspodar showed a significant inhibitory effect on the efflux of ticagrelor suggesting involvement of P-gp in its oral disposition.	Ticagrelor	66-76	ATP binding cassette subfamily B member 1	Homo sapiens	103-107
27416295-7	2016	Co-incubation of the P-gp inhibitor decreased the efflux Papp of ticagrelor from 1.60 x 10-5 to 1.13 x 10-5 cm/s and decreased its ER by 70%.	Ticagrelor	65-75	ATP binding cassette subfamily B member 1	Homo sapiens	21-25
27605392-1	2016	Ticagrelor is an antagonist of the platelet P2Y12 receptor for ADP, approved for the prevention of thromboembolic events in patients with acute coronary syndrome.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	44-49
27605392-6	2016	Ticagrelor, TAM, cangrelor and MRS2211, but not TIM, inhibited the cellular responses in P2Y13-transfected cells.	Ticagrelor	0-10	purinergic receptor P2Y13	Homo sapiens	89-94
27605392-9	2016	In conclusion, ticagrelor and TAM act as P2Y13 antagonists in a transfected cell system in vitro but this does not translate into any impact on pro-platelet formation in vitro or altered platelet count in patients.	Ticagrelor	15-25	purinergic receptor P2Y13	Homo sapiens	41-46
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).	Ticagrelor	95-105	purinergic receptor P2Y12	Homo sapiens	51-56
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.	Ticagrelor	0-10	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	88-93
27511945-6	2016	A2AR blockade abrogated the effects of ticagrelor and dipyridamole on osteoclast and osteoblast differentiation whereas A2BR blockade abrogated the effects of CAM.	Ticagrelor	39-49	adenosine A2a receptor	Mus musculus	0-4
27511945-7	2016	Ticagrelor and CAM, when applied to a 3-dimentional printed resorbable calcium-triphosphate/hydroxyapatite scaffold implanted in a calvarial bone defect, promoted significantly more bone regeneration than the scaffold alone and as much bone regeneration as BMP-2, a growth factor currently used to promote bone regeneration.	Ticagrelor	0-10	bone morphogenetic protein 2	Mus musculus	257-262
27576775-1	2016	BACKGROUND: In the PEGASUS-TIMI 54 trial (Prevention of Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a Background of Aspirin-Thrombolysis in Myocardial Infarction 54), ticagrelor reduced the risk of major adverse cardiovascular events when added to low-dose aspirin in stable patients with prior myocardial infarction, resulting in the approval of ticagrelor 60 mg twice daily for long-term secondary prevention.	Ticagrelor	401-411	IKAROS family zinc finger 5	Homo sapiens	19-34
27628615-5	2016	Analysis of 36 patients revealed high negative correlations between ticagrelor concentrations and platelet reactivity evaluated with all three platelet function tests (the VASP-assay: RS=-0.722; p<0.0001; the VerifyNow device: RS=-0.715; p<0.0001; the Multiplate analyzer: RS=-0.722; p<0.0001), with no significant differences between correlation coefficients.	Ticagrelor	68-78	vasodilator stimulated phosphoprotein	Homo sapiens	172-176
27086085-0	2016	Parathyroid Hormone Levels and High-Residual Platelet Reactivity in Patients Receiving Dual Antiplatelet Therapy With Acetylsalicylic Acid and Clopidogrel or Ticagrelor.	Ticagrelor	158-168	parathyroid hormone	Homo sapiens	0-19
27576775-1	2016	BACKGROUND: In the PEGASUS-TIMI 54 trial (Prevention of Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a Background of Aspirin-Thrombolysis in Myocardial Infarction 54), ticagrelor reduced the risk of major adverse cardiovascular events when added to low-dose aspirin in stable patients with prior myocardial infarction, resulting in the approval of ticagrelor 60 mg twice daily for long-term secondary prevention.	Ticagrelor	120-130	IKAROS family zinc finger 5	Homo sapiens	19-34
27576775-1	2016	BACKGROUND: In the PEGASUS-TIMI 54 trial (Prevention of Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a Background of Aspirin-Thrombolysis in Myocardial Infarction 54), ticagrelor reduced the risk of major adverse cardiovascular events when added to low-dose aspirin in stable patients with prior myocardial infarction, resulting in the approval of ticagrelor 60 mg twice daily for long-term secondary prevention.	Ticagrelor	221-231	IKAROS family zinc finger 5	Homo sapiens	19-34
25782570-9	2016	Newer P2Y12 inhibitors, especially ticagrelor, could be effective and safe alternatives if patients had a history of clopidogrel-associated neutropenia.	Ticagrelor	35-45	purinergic receptor P2Y12	Homo sapiens	6-11
27616880-3	2016	Ticagrelor is an oral P2Y12 antagonist that is used as a standard treatment in patients after acute myocardial infarction.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	22-27
27563870-3	2016	For this reason, ticagrelor-a new chemical class of P2Y12 receptor antagonist-was developed, but it can cause shortness of breath and various types of bleeding.	Ticagrelor	17-27	purinergic receptor P2Y12	Homo sapiens	52-57
27563870-4	2016	Moreover, ticagrelor is a cytochrome P450 3A4 substrate/inhibitor and, therefore, caution should be exercised when it is used concomitantly with strong CYP3A4 inducers/inhibitors.	Ticagrelor	10-20	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	152-158
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.	Ticagrelor	54-64	purinergic receptor P2Y12	Homo sapiens	25-30
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.	Ticagrelor	192-202	purinergic receptor P2Y12	Homo sapiens	132-137
28290914-1	2016	This review summarizes current knowledge concerning "nonplatelet effects of P2Y12 receptor antagonist ticagrelor.	Ticagrelor	102-112	purinergic receptor P2Y12	Homo sapiens	76-81
27399131-8	2016	CONCLUSION: Ticagrelor and apixaban with or without ASA inhibit platelet activation and thrombin formation in vivo in healthy subjects.	Ticagrelor	12-22	coagulation factor II, thrombin	Homo sapiens	88-96
26830862-1	2016	Ticagrelor is a novel direct-acting P2Y12 receptor antagonist used for preventing atherothrombotic events in patients with acute coronary syndromes (ACS).	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	36-41
27310147-2	2016	Administration of newer P2Y12 inhibitors (prasugrel and ticagrelor) combined with aspirin has been shown to reduce the incidence of sub-acute and late stent thrombosis, compared with clopidogrel.	Ticagrelor	56-66	purinergic receptor P2Y12	Homo sapiens	24-29
26857211-7	2016	Overall, the PEGASUS-TIMI 54 results demonstrate that patients with a history of ACS deemed to be at high risk of further ischaemic events, particularly those in whom the risks of ischaemic events and cardiovascular death outweigh the risk of life-threatening bleeding, may benefit from prolonged ticagrelor-based DAPT.	Ticagrelor	297-307	IKAROS family zinc finger 5	Homo sapiens	13-28
27385702-5	2016	Prasugrel was discontinued, and the patient was switched to another P2Y12 inhibitor (ticagrelor) for continued dual antiplatelet therapy.	Ticagrelor	85-95	purinergic receptor P2Y12	Homo sapiens	68-73
27385702-9	2016	Desensitization may be an option for thienopyridine-allergic patients undergoing PCI with stenting; alternatively, the nonthienopyridine P2Y12 inhibitor ticagrelor may be used in a dual antiplatelet therapy regimen.	Ticagrelor	153-163	purinergic receptor P2Y12	Homo sapiens	137-142
26751426-10	2016	The reversible binding of ticagrelor to the platelet P2Y12 receptor may be advantageous in patients with a high platelet turnover.	Ticagrelor	26-36	purinergic receptor P2Y12	Homo sapiens	53-58
27107082-8	2016	CONCLUSION: Ticagrelor dose-dependently inhibits platelet aggregation, increases cyclooxygenase-2 and also inhibits cellular uptake of adenosine all resulting in attenuation of I/R injury.	Ticagrelor	12-22	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	81-97
26491109-1	2016	AIMS: Ticagrelor reduced major adverse cardiovascular event (MACE) by 15-16% in patients with prior myocardial infarction (MI) in PEGASUS-TIMI 54.	Ticagrelor	6-16	IKAROS family zinc finger 5	Homo sapiens	130-145
26491109-8	2016	CONCLUSION: The benefit of ticagrelor for long-term secondary prevention in patients with prior MI and at least one additional risk factor appeared more marked in patients continuing on or re-starting after only a brief interruption of P2Y12 inhibition, when compared with patients who had proved themselves stable more than 2 years from their MI and off P2Y12 inhibitor therapy for more than a year.	Ticagrelor	27-37	purinergic receptor P2Y12	Homo sapiens	236-241
26491109-8	2016	CONCLUSION: The benefit of ticagrelor for long-term secondary prevention in patients with prior MI and at least one additional risk factor appeared more marked in patients continuing on or re-starting after only a brief interruption of P2Y12 inhibition, when compared with patients who had proved themselves stable more than 2 years from their MI and off P2Y12 inhibitor therapy for more than a year.	Ticagrelor	27-37	purinergic receptor P2Y12	Homo sapiens	355-360
26444255-9	2016	Ticagrelor is also a reversible direct-acting antagonist of the platelet P2Y12 receptor.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	73-78
26758983-3	2016	P2Y12 receptor antagonists, thienopyridines and ticagrelor, differ in their mode of action being prodrugs instead of direct acting and irreversibly instead of reversibly binding to P2Y12 .	Ticagrelor	48-58	purinergic receptor P2Y12	Homo sapiens	0-5
26758983-3	2016	P2Y12 receptor antagonists, thienopyridines and ticagrelor, differ in their mode of action being prodrugs instead of direct acting and irreversibly instead of reversibly binding to P2Y12 .	Ticagrelor	48-58	purinergic receptor P2Y12	Homo sapiens	181-186
26965534-1	2016	BACKGROUND: The PEGASUS-TIMI 54 (Prevention of Cardiovascular Events in Patients with Prior Heart Attack Using Ticagrelor Compared to Placebo on a Background of Aspirin-Thrombolysis In Myocardial Infarction 54) trial studied 2 doses of ticagrelor, 90 mg twice a day (bid) and 60 mg bid, for long-term prevention of ischemic events in patients with prior myocardial infarction.	Ticagrelor	111-121	IKAROS family zinc finger 5	Homo sapiens	16-31
26965534-1	2016	BACKGROUND: The PEGASUS-TIMI 54 (Prevention of Cardiovascular Events in Patients with Prior Heart Attack Using Ticagrelor Compared to Placebo on a Background of Aspirin-Thrombolysis In Myocardial Infarction 54) trial studied 2 doses of ticagrelor, 90 mg twice a day (bid) and 60 mg bid, for long-term prevention of ischemic events in patients with prior myocardial infarction.	Ticagrelor	236-246	IKAROS family zinc finger 5	Homo sapiens	16-31
26965534-14	2016	CONCLUSIONS: Ticagrelor 60 mg bid achieved high levels of peak and trough platelet inhibition in nearly all patients, similar to that with 90 mg bid, helping to explain the efficacy of the lower ticagrelor dose in PEGASUS-TIMI 54.	Ticagrelor	13-23	IKAROS family zinc finger 5	Homo sapiens	214-229
26965534-14	2016	CONCLUSIONS: Ticagrelor 60 mg bid achieved high levels of peak and trough platelet inhibition in nearly all patients, similar to that with 90 mg bid, helping to explain the efficacy of the lower ticagrelor dose in PEGASUS-TIMI 54.	Ticagrelor	195-205	IKAROS family zinc finger 5	Homo sapiens	214-229
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.	Ticagrelor	69-79	purinergic receptor P2Y12	Homo sapiens	14-19
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).	Ticagrelor	213-223	coagulation factor II, thrombin	Homo sapiens	0-8
26830177-3	2016	The focused updates to the guidelines contain updated recommendations for dual antiplatelet therapy, including use of the P2Y12 inhibitor ticagrelor, which was recently approved by the Food and Drug Administration.	Ticagrelor	138-148	purinergic receptor P2Y12	Homo sapiens	122-127
27262327-4	2016	RESULTS: Added to aspirin, clopidogrel, prasugrel and ticagrelor represent viable options regarding oral P2Y12 inhibition, with prasugrel and ticagrelor being preferred over clopidogrel, according to results of large randomized clinical trials.	Ticagrelor	54-64	purinergic receptor P2Y12	Homo sapiens	105-110
26542508-6	2015	Patients are randomly assigned to receive either clopidogrel or a more potent P2Y12 inhibitor (ticagrelor or prasugrel).	Ticagrelor	95-105	purinergic receptor P2Y12	Homo sapiens	78-83
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.	Ticagrelor	95-105	purinergic receptor P2Y12	Homo sapiens	65-70
26515417-3	2015	We therefore determined whether clopidogrel and the novel, more potent P2Y12 inhibitor, ticagrelor, modify these responses in an experimental human model.	Ticagrelor	88-98	purinergic receptor P2Y12	Homo sapiens	71-76
26515417-7	2015	In contrast to clopidogrel, ticagrelor also significantly reduced peak levels of IL-8 and growth colony-stimulating factor and increased peak levels of the anti-inflammatory cytokine IL-10.	Ticagrelor	28-38	C-X-C motif chemokine ligand 8	Homo sapiens	81-85
26515417-7	2015	In contrast to clopidogrel, ticagrelor also significantly reduced peak levels of IL-8 and growth colony-stimulating factor and increased peak levels of the anti-inflammatory cytokine IL-10.	Ticagrelor	28-38	interleukin 10	Homo sapiens	183-188
26083990-2	2015	Ticagrelor is the first reversible P2Y12 receptor antagonist that exhibits rapid antiplatelet effect.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	35-40
26083990-3	2015	Given that platelet aggregation varies among individuals, genetic polymorphisms in P2Y12 and subsequent signal molecular such as the G-protein beta 3 subunit (GNB3) are supposed to influence the antiplatelet effect of ticagrelor.	Ticagrelor	218-228	purinergic receptor P2Y12	Homo sapiens	83-88
26083990-3	2015	Given that platelet aggregation varies among individuals, genetic polymorphisms in P2Y12 and subsequent signal molecular such as the G-protein beta 3 subunit (GNB3) are supposed to influence the antiplatelet effect of ticagrelor.	Ticagrelor	218-228	G protein subunit beta 3	Homo sapiens	133-149
26083990-3	2015	Given that platelet aggregation varies among individuals, genetic polymorphisms in P2Y12 and subsequent signal molecular such as the G-protein beta 3 subunit (GNB3) are supposed to influence the antiplatelet effect of ticagrelor.	Ticagrelor	218-228	G protein subunit beta 3	Homo sapiens	159-163
26216931-10	2015	A time-dependent P-selectin expression was observed in prasugrel but not in ticagrelor-treated patients (prasugrel early 11.9 +- 9.4% vs. late 26.3 +- 19.0%, P = 0.031, ticagrelor early 9.6 +- 4.9% vs. late 13.5 +- 6.6%, P = 0.127).	Ticagrelor	169-179	selectin P	Homo sapiens	17-27
26386945-4	2016	In cardiovascular medicine, dyspnea has recently attracted attention because it has been reported that this symptom occurs more frequently with the administration of the new oral reversibly-binding platelet P2Y12 receptor inhibitors ticagrelor [1-6], cangrelor [7-10], and elinogrel [11].	Ticagrelor	233-243	purinergic receptor P2Y12	Homo sapiens	207-212
26542508-1	2015	RATIONALE: Dual antiplatelet therapy with acetylsalicylic acid in combination with a more potent P2Y12- inhibitor (ticagrelor or prasugrel) is recommended in patients with acute coronary syndrome without ST-segment elevation (NSTE-ACS) to prevent atherothrombotic complications.	Ticagrelor	115-125	purinergic receptor P2Y12	Homo sapiens	97-102
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.	Ticagrelor	451-461	purinergic receptor P2Y12	Homo sapiens	39-44
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 <0.0001).	Ticagrelor	339-349	purinergic receptor P2Y12	Homo sapiens	229-234
25848131-3	2015	MATERIALS AND METHODS: Thrombin generation was measured by the Calibrated Automated Thrombogram method (0.5 pmol/L tissue factor) using human platelet-rich plasma (PRP) spiked with rivaroxaban (15, 30, or 60 ng/mL), ticagrelor (1.0 microg/mL), and acetylsalicylic acid (ASA; 100 microg/mL).	Ticagrelor	216-226	coagulation factor II, thrombin	Homo sapiens	23-31
26063049-7	2015	Ticagrelor is an oral antiplatelet agent of the cyclopentyltriazolopyrimidine class and also acts through the P2Y12 receptor.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	110-115
26063049-8	2015	In contrast to clopidogrel and prasugrel, ticagrelor does not require metabolic activation and binds rapidly and reversibly to the P2Y12 receptor.	Ticagrelor	42-52	purinergic receptor P2Y12	Homo sapiens	131-136
25848131-6	2015	RESULTS: Rivaroxaban inhibited thrombin generation in a concentration-dependent manner and the effect was enhanced with ticagrelor and ticagrelor plus ASA.	Ticagrelor	120-130	coagulation factor II	Rattus norvegicus	31-39
25848131-6	2015	RESULTS: Rivaroxaban inhibited thrombin generation in a concentration-dependent manner and the effect was enhanced with ticagrelor and ticagrelor plus ASA.	Ticagrelor	135-145	coagulation factor II	Rattus norvegicus	31-39
26156883-9	2015	Ticagrelor is a more potent P2Y12 inhibitor than clopidogrel and also inhibits cellular adenosine uptake via equilibrative nucleoside transporter (ENT) 1, whereas clopidogrel does not.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	28-33
26447442-5	2015	Patients undergoing percutaneous coronary intervention for acute coronary syndromes who are known to be poor metabolizers of CYP2C19 should consider alternate antiplatelet therapy (e.g., ticagrelor, prasugrel).	Ticagrelor	187-197	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	125-132
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.	Ticagrelor	129-139	purinergic receptor P2Y12	Homo sapiens	77-82
26398625-4	2015	CYP2C19 LOF allele(s) carriers who were poor metabolizers received prasugrel or ticagrelor.	Ticagrelor	80-90	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
26119655-0	2015	Meta-Analysis of Comparison of the Newer Oral P2Y12 Inhibitors (Prasugrel or Ticagrelor) to Clopidogrel in Patients With Non-ST-Elevation Acute Coronary Syndrome.	Ticagrelor	77-87	purinergic receptor P2Y12	Homo sapiens	46-51
26113418-6	2015	Platelet function in response to ADP was normalized between five and 30 days after treatment cessation and in vitro addition of the reversible P2Y12 receptor antagonist ticagrelor fully suppressed the regained activation response.	Ticagrelor	169-179	purinergic receptor P2Y12	Homo sapiens	143-148
26354056-1	2015	BACKGROUND/AIMS: Newer P2Y12 inhibitors, such as prasugrel and ticagrelor, have greater antiplatelet efficacy but may increase the risk of bleeding.	Ticagrelor	63-73	purinergic receptor P2Y12	Homo sapiens	23-28
26156883-9	2015	Ticagrelor is a more potent P2Y12 inhibitor than clopidogrel and also inhibits cellular adenosine uptake via equilibrative nucleoside transporter (ENT) 1, whereas clopidogrel does not.	Ticagrelor	0-10	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	109-153
26044583-9	2015	Ticagrelor, but not clopidogrel, increased myocardial adenosine levels, increased phosphorylation of Akt, endothelial NO synthase, and extracellular-signal-regulated kinase 1/2 4 hours after reperfusion and decreased apoptosis.	Ticagrelor	0-10	AKT serine/threonine kinase 1	Rattus norvegicus	101-104
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.	Ticagrelor	116-126	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	151-158
26550258-4	2015	MATERIALS AND METHODS: We compared ticagrelor (180 mg loading dose, 90 mg twice daily thereafter) with clopidogrel (600 mg loading dose, 150 mg daily thereafter) for the prevention of cardiovascular events in CYP2C19*2 homozygotes patients admitted to the hospital with an acute coronary syndrome, with or without ST-segment elevation.	Ticagrelor	35-45	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	209-216
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.	Ticagrelor	300-310	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	74-81
26550258-10	2015	This study suggests that ticagrelor may be much better than doubling dose clopidogrel in patients with CYP2C19*2 in according to platelet reactivity monitoring.	Ticagrelor	25-35	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	103-110
26044583-13	2015	Ticagrelor, but not clopidogrel, attenuated the increase in proinflammatory tumor necrosis factor-alpha, interleukin-1beta, and interleukin-18, and increased anti-inflammatory 15-epi-lipoxin-A4 levels.	Ticagrelor	0-10	interleukin 1 beta	Rattus norvegicus	105-122
26044583-13	2015	Ticagrelor, but not clopidogrel, attenuated the increase in proinflammatory tumor necrosis factor-alpha, interleukin-1beta, and interleukin-18, and increased anti-inflammatory 15-epi-lipoxin-A4 levels.	Ticagrelor	0-10	interleukin 18	Rattus norvegicus	128-142
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.	Ticagrelor	208-218	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	115-122
25935875-12	2015	CONCLUSION: In patients with ACS, ticagrelor pharmacokinetics is influenced by three genetic loci (SLCO1B1, UGT2B7, and CYP3A4).	Ticagrelor	34-44	solute carrier organic anion transporter family member 1B1	Homo sapiens	99-106
25935875-12	2015	CONCLUSION: In patients with ACS, ticagrelor pharmacokinetics is influenced by three genetic loci (SLCO1B1, UGT2B7, and CYP3A4).	Ticagrelor	34-44	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	108-114
25935875-12	2015	CONCLUSION: In patients with ACS, ticagrelor pharmacokinetics is influenced by three genetic loci (SLCO1B1, UGT2B7, and CYP3A4).	Ticagrelor	34-44	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	120-126
26194851-5	2015	Supervised molecular dynamics (SuMD) of ticagrelor binding indicated interactions with the extracellular regions of P2Y12R, defining possible meta-binding sites.	Ticagrelor	40-50	purinergic receptor P2Y12	Homo sapiens	116-122
26108379-15	2015	CONCLUSIONS: Important financial benefits may be realized through use of genotype-guided antiplatelet therapy to reserve prasugrel or ticagrelor use for patients with reduced CYP2C19 activity to avoid costs associated with adverse cardiac events.	Ticagrelor	134-144	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	175-182
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.	Ticagrelor	165-175	purinergic receptor P2Y12	Homo sapiens	121-126
30524542-4	2015	Taking into account the bleeding risk associated with low on-treatment platelet reactivity, and to switch the patient from ticagrelor to a less potent P2Y12 inhibitor such as clopidogrel, cytochrome P450, genetic polymorphisms accounting for clopidogrel response variability were analyzed.	Ticagrelor	123-133	purinergic receptor P2Y12	Homo sapiens	151-156
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.	Ticagrelor	37-47	purinergic receptor P2Y12	Homo sapiens	12-17
25882759-8	2015	Ticagrelor represents a cost-effective alternative in the spectrum of P2Y12 inhibitors; however, further studies are required to enable the physician to choose the most appropriate antiplatelet agent for each patient.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	70-75
26149010-9	2015	New drugs, such as prasugrel and ticagrelor, which effectively inhibit P2Y12R in the vast majority of patients, have proved to be more efficacious than clopdidogrel in preventing major adverse cardiovascular events.	Ticagrelor	33-43	purinergic receptor P2Y12	Homo sapiens	71-77
25585230-5	2015	When combined with aspirin, the new P2Y12 receptor inhibitors prasugrel and ticagrelor provide superior efficacy for the diabetic patients with acute coronary syndromes.	Ticagrelor	76-86	purinergic receptor P2Y12	Homo sapiens	36-41
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).	Ticagrelor	168-178	purinergic receptor P2Y12	Homo sapiens	0-5
25641006-5	2015	RESULTS: Our results demonstrate that clopidogrel had no and prasugrel had only mild effects on donor PLT function, but the reversible P2Y12 inhibitor ticagrelor completely abolished adenosine diphosphate-mediated PLT activation in all assays tested.	Ticagrelor	151-161	purinergic receptor P2Y12	Homo sapiens	135-140
25788700-1	2015	Ticagrelor is a direct-acting reversibly binding P2Y12 antagonist and is widely used as an antiplatelet therapy for the prevention of cardiovascular events in acute coronary syndrome patients.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	49-54
25788700-3	2015	Here, we present data on the identification and the in vitro and in vivo pharmacology of an antigen-binding fragment (Fab) antidote for ticagrelor.	Ticagrelor	136-146	FA complementation group B	Homo sapiens	118-121
25732742-3	2015	Consequently, novel anti-platelets agents including the P2Y12 receptor antagonists, such as prasugrel and ticagrelor, have emerged.	Ticagrelor	106-116	purinergic receptor P2Y12	Homo sapiens	56-61
25440595-4	2015	Recently developed antiplatelet agents (prasugrel, ticagrelor, cangrelor and elinogrel) efficiently antagonize P2Y12 receptor, a key platelet activating signaling pathway, and thereby inhibit aggregation induced by mediators such as ADP, collagen, thrombin and TXA2.	Ticagrelor	51-61	purinergic receptor P2Y12	Homo sapiens	111-116
25791908-8	2015	Concomitant treatment with edoxaban and AM-clopidogrel or ticagrelor produced an additive inhibition of thrombin generation compared to the single treatments.	Ticagrelor	58-68	coagulation factor II, thrombin	Homo sapiens	104-112
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.	Ticagrelor	137-147	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	78-81
25697420-2	2015	Two novel antiplatelet agents, ticagrelor and prasugrel, have been shown to rapidly and more effectively inhibit the P2Y12 receptor compared with clopidogrel.	Ticagrelor	31-41	purinergic receptor P2Y12	Homo sapiens	117-122
25633751-8	2015	Prasugrel is currently challenged by ticagrelor, a P2Y12 receptor antagonist with different pharmacokinetic/pharmacodynamic properties.	Ticagrelor	37-47	purinergic receptor P2Y12	Homo sapiens	51-56
25440595-4	2015	Recently developed antiplatelet agents (prasugrel, ticagrelor, cangrelor and elinogrel) efficiently antagonize P2Y12 receptor, a key platelet activating signaling pathway, and thereby inhibit aggregation induced by mediators such as ADP, collagen, thrombin and TXA2.	Ticagrelor	51-61	coagulation factor II, thrombin	Homo sapiens	248-256
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.	Ticagrelor	42-52	purinergic receptor P2Y12	Homo sapiens	86-91
26224244-6	2015	EXPERT OPINION: Clinical trials studying newer P2Y12 inhibitors with increased potency have shown further reduction of cardiovascular events compared with clopidogrel, therefore suggesting the use of ticagrelor or prasugrel as a first-line agent for STEMI treatment.	Ticagrelor	200-210	purinergic receptor P2Y12	Homo sapiens	47-52
24798403-0	2015	The reversible P2Y12 inhibitor ticagrelor inhibits metastasis and improves survival in mouse models of cancer.	Ticagrelor	31-41	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	15-20
24798403-2	2015	Because platelet activation is largely mediated through ADP engagement of purinergic P2Y12 receptors on platelets, we investigated the potential of the reversible P2Y12 inhibitor ticagrelor, a clinical agent used in the prevention of cardiovascular and cerebrovascular events, to inhibit tumor adhesion and metastasis.	Ticagrelor	179-189	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	163-168
25350775-8	2015	ADP-induced platelet reactivity was decreased in the patients treated with prasugrel or ticagrelor compared with those on clopidogrel (mean +- SD: 139 +- 71 vs. 313 +- 162 arbitrary units [AU]*min, p = 0.006), due to a more potent antiplatelet activity of the novel P2Y12 antagonists.	Ticagrelor	88-98	purinergic receptor P2Y12	Homo sapiens	266-271
25846661-9	2015	On the contrary, when considering CD34+133+ PC and CD34+KDR+ EPC, we observed that patients treated by ticagrelor had a significantly higher increase in levels of these PC subtypes compared to those treated by clopidogrel (0.23 (-0.33; 0.79) vs 0.00 (-0.5; 0.34); p=0.04 and 0.01 (-0.04; 0.05) vs -0.01 (-0.06; 0.03); p=0.02).	Ticagrelor	103-113	CD34 molecule	Homo sapiens	34-38
25846661-9	2015	On the contrary, when considering CD34+133+ PC and CD34+KDR+ EPC, we observed that patients treated by ticagrelor had a significantly higher increase in levels of these PC subtypes compared to those treated by clopidogrel (0.23 (-0.33; 0.79) vs 0.00 (-0.5; 0.34); p=0.04 and 0.01 (-0.04; 0.05) vs -0.01 (-0.06; 0.03); p=0.02).	Ticagrelor	103-113	CD34 molecule	Homo sapiens	51-55
25846661-9	2015	On the contrary, when considering CD34+133+ PC and CD34+KDR+ EPC, we observed that patients treated by ticagrelor had a significantly higher increase in levels of these PC subtypes compared to those treated by clopidogrel (0.23 (-0.33; 0.79) vs 0.00 (-0.5; 0.34); p=0.04 and 0.01 (-0.04; 0.05) vs -0.01 (-0.06; 0.03); p=0.02).	Ticagrelor	103-113	kinase insert domain receptor	Homo sapiens	56-59
25823779-5	2015	CYP2C19 intermediate or poor metabolizer phenotype was among the strongest predictors for selecting prasugrel or ticagrelor as maintenance therapy (p < 0.001), and was the only significant predictor of a change in therapy (p < 0.001).	Ticagrelor	113-123	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
26677375-4	2015	Prasugrel (a third generation thienopyridine) and ticagrelor (a cyclopentyl-triazolo-pyrimidine) feature more potent and predictable P2Y12-inhibition compared to clopidogrel, which translates into improved ischemic outcomes.	Ticagrelor	50-60	purinergic receptor P2Y12	Homo sapiens	133-138
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.	Ticagrelor	129-139	serpin family A member 5	Homo sapiens	12-15
25516485-9	2014	In patients receiving pre-hospital ticagrelor, 50% were good responders at completion of PCI and average time to a VASP-value of <50% was 2.3 hours.	Ticagrelor	35-45	vasodilator stimulated phosphoprotein	Homo sapiens	115-119
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.	Ticagrelor	165-175	purinergic receptor P2Y12	Homo sapiens	121-126
25696877-7	2014	Alternatively, 2 third-generation P2Y12 inhibitors are available: prasugrel and ticagrelor.	Ticagrelor	80-90	purinergic receptor P2Y12	Homo sapiens	34-39
25211369-8	2014	CONCLUSION: A triple therapy at steady state with ticagrelor plus ASA in combination with dabigatran or rivaroxaban is as effective as a combination with phenprocoumon for platelet activation and thrombin generation in vivo.	Ticagrelor	50-60	coagulation factor II, thrombin	Homo sapiens	196-204
27122812-6	2014	The newer P2Y12 inhibitors, ticagrelor or prasugrel, have a more potent platelet inhibitory effect and can be used for STEMI patients prepared for primary PCI if there is no contraindication.	Ticagrelor	28-38	purinergic receptor P2Y12	Homo sapiens	10-15
25186974-2	2014	Recently, ticagrelor was licensed as the first perorally active and reversible P2Y12 -receptor antagonist.	Ticagrelor	10-20	purinergic receptor P2Y12	Homo sapiens	79-84
25211369-5	2014	Single doses of ticagrelor, dabigatran or rivaroxaban caused comparable decreases in shed blood beta-TG and were more pronounced than phenprocoumon at an INR of 2.0-3.0.	Ticagrelor	16-26	pro-platelet basic protein	Homo sapiens	96-103
24935072-6	2014	Mean final-extent IPA was greater with ticagrelor 90 mg bid versus ticagrelor 45 mg bid and with both ticagrelor doses versus clopidogrel.	Ticagrelor	39-49	BH3 interacting domain death agonist	Homo sapiens	56-59
25012137-10	2014	Adenosine-receptor antagonism blocked the ticagrelor effect and COX2 inhibition by SC5815, or high-dose aspirin attenuated the IS-limiting effect of ticagrelor, whereas cyclooxygenase-1 inhibition or low-dose aspirin had no effect.	Ticagrelor	149-159	prostaglandin-endoperoxide synthase 2	Homo sapiens	64-68
25012137-11	2014	Ticagrelor, but not clopidogrel, upregulated COX2 expression and activity.	Ticagrelor	0-10	prostaglandin-endoperoxide synthase 2	Homo sapiens	45-49
25012137-13	2014	Ticagrelor, but not clopidogrel, increased Akt and endothelial nitric oxide synthase phosphorylation.	Ticagrelor	0-10	AKT serine/threonine kinase 1	Homo sapiens	43-46
25012137-13	2014	Ticagrelor, but not clopidogrel, increased Akt and endothelial nitric oxide synthase phosphorylation.	Ticagrelor	0-10	nitric oxide synthase 3	Homo sapiens	51-84
25012137-15	2014	The protective effect of ticagrelor was dependent on adenosine-receptor activation with downstream upregulation of endothelial nitric oxide synthase and COX2 activity.	Ticagrelor	25-35	nitric oxide synthase 3	Homo sapiens	115-148
25012137-15	2014	The protective effect of ticagrelor was dependent on adenosine-receptor activation with downstream upregulation of endothelial nitric oxide synthase and COX2 activity.	Ticagrelor	25-35	prostaglandin-endoperoxide synthase 2	Homo sapiens	153-157
25069798-0	2014	Evaluation of the pharmacokinetic interaction between ticagrelor and venlafaxine, a cytochrome P-450 2D6 substrate, in healthy subjects.	Ticagrelor	54-64	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	84-104
25069798-2	2014	Ticagrelor has been shown in vitro to be a weak inhibitor of cytochrome P-450 (CYP) 2D6, a clinically important enzyme for the metabolism of many drugs.	Ticagrelor	0-10	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	61-87
25175921-1	2014	BACKGROUND: The direct-acting platelet P2Y12 receptor antagonist ticagrelor can reduce the incidence of major adverse cardiovascular events when administered at hospital admission to patients with ST-segment elevation myocardial infarction (STEMI).	Ticagrelor	65-75	purinergic receptor P2Y12	Homo sapiens	39-44
24958490-9	2014	Ticagrelor is a newer P2Y12 inhibitor that contains a cyclopentyltriazolopyrimidine structure.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	22-27
25071373-3	2014	Recently, introduction of new oral P2Y12 inhibitors (prasugrel, ticagrelor), with a faster and more pronounced antiplatelet effect, have decreased the use of abciximab even in patients with STEMI.	Ticagrelor	64-74	purinergic receptor P2Y12	Homo sapiens	35-40
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.	Ticagrelor	46-56	purinergic receptor P2Y12	Homo sapiens	28-33
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.	Ticagrelor	46-56	purinergic receptor P2Y12	Homo sapiens	174-179
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.	Ticagrelor	30-40	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	138-145
25163307-4	2014	New generation of P2Y12 ADP antagonists including prasugrel and ticagrelor are available, but only in patients with acute coronary syndrome.	Ticagrelor	64-74	purinergic receptor P2Y12	Homo sapiens	18-23
24768873-1	2014	This review constitutes a critical evaluation of recent publications that have described an additional mode of action of the P2Y12 receptor antagonist ticagrelor.	Ticagrelor	151-161	purinergic receptor P2Y12	Homo sapiens	125-130
24643079-2	2014	Clinical data show that ticagrelor, a direct-acting, reversibly binding P2Y12-receptor antagonist, reduces total cardiovascular events, including stroke.	Ticagrelor	24-34	purinergic receptor P2Y12	Rattus norvegicus	72-77
23771209-3	2014	Ticagrelor is a new reversible ADP P2Y12 platelet receptor inhibitor with no known resistance.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	35-40
24655690-3	2014	Ticagrelor is a potent, reversibly binding P2Y12 receptor-antagonist that has been shown to be superior to clopidogrel in patients with acute coronary syndromes for up to 1 year.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	43-48
24655690-4	2014	STUDY DESIGN: PEGASUS-TIMI 54 is a randomized, double-blind, placebo-controlled, multinational clinical trial designed to evaluate the efficacy and safety of ticagrelor in addition to aspirin (75-150 mg) for the prevention of major adverse cardiovascular events in patients with a history of myocardial infarction and risk factors.	Ticagrelor	158-168	IKAROS family zinc finger 5	Homo sapiens	14-29
24477376-7	2014	Ticagrelor is a recently approved P2Y12 receptor antagonist that is subject to drug-drug interactions involving the hepatic cytochrome P450-3A4 enzyme system because of its metabolic elimination pathway.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	34-39
24477376-7	2014	Ticagrelor is a recently approved P2Y12 receptor antagonist that is subject to drug-drug interactions involving the hepatic cytochrome P450-3A4 enzyme system because of its metabolic elimination pathway.	Ticagrelor	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	124-143
24477376-8	2014	This case demonstrates ticagrelor"s drug-drug interaction with phenytoin through a platelet aggregation study and supports the manufacturer recommendation to avoid the combination of ticagrelor with any known inducers of cytochrome P450-3A4 metabolism.	Ticagrelor	23-33	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	221-240
24477376-9	2014	CONCLUSION: The combination of ticagrelor and phenytoin may represent a potentially clinically significant drug-drug interaction because of phenytoin induction of ticagrelor metabolism and reduced P2Y12 receptor inhibition in patients who have recently undergone percutaneous coronary intervention and cardiac stent placement.	Ticagrelor	31-41	purinergic receptor P2Y12	Homo sapiens	197-202
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.	Ticagrelor	108-118	purinergic receptor P2Y12	Homo sapiens	65-70
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.	Ticagrelor	250-260	purinergic receptor P2Y12	Homo sapiens	0-6
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.	Ticagrelor	262-270	purinergic receptor P2Y12	Homo sapiens	0-6
24444280-2	2014	As bleeding events remain a hazard with antiplatelet therapy, this study investigated the effect of the vasopressin agonist, desmopressin, on ticagrelor-induced bleeding time prolongation.	Ticagrelor	142-152	arginine vasopressin	Homo sapiens	104-115
24643079-10	2014	Our results show that ticagrelor is protective against ischemia-induced cerebral injury and this effect is mediated, at least partly, by inhibition of P2Y12-mediated microglia activation and chemotaxis.	Ticagrelor	22-32	purinergic receptor P2Y12	Rattus norvegicus	151-156
24656538-12	2014	Consistent with the reversible binding of ticagrelor, this oral P2Y12 antagonist can be administered before, during, or after treatment with cangrelor.	Ticagrelor	42-52	purinergic receptor P2Y12	Homo sapiens	64-69
24529662-1	2014	Prasugrel and ticagrelor are next-generation antiplatelet agents that provide a rapider and more potent inhibition of platelet P2Y12 receptor than clopidogrel.	Ticagrelor	14-24	purinergic receptor P2Y12	Homo sapiens	127-132
24474638-1	2014	Ticagrelor (TIC) is the first reversible P2Y12 receptor antagonist that exhibits rapid antiplatelet effect by indirect inhibition of the GPIIb/IIIa complex.	Ticagrelor	0-10	integrin subunit alpha 2b	Homo sapiens	137-142
24309957-3	2014	In the Platelet Inhibition and Patients Outcome (PLATO) study, higher doses of aspirin appeared to neutralise the additional benefit of the potent P2Y12 inhibitor ticagrelor compared to clopidogrel (Circulation 124: 544-554, 2011).	Ticagrelor	163-173	purinergic receptor P2Y12	Homo sapiens	147-152
24414167-1	2014	INTRODUCTION: Studies have shown that ticagrelor has a further adenosine-mediated mechanism of action in addition to its potent inhibition of the P2Y12 receptor, which may explain some of ticagrelor"s clinical characteristics.	Ticagrelor	38-48	purinergic receptor P2Y12	Canis lupus familiaris	146-151
24414167-7	2014	Ticagrelor demonstrated high affinity (inhibition constant [Ki] = 41 nmol/L) for ENT1.	Ticagrelor	0-10	equilibrative nucleoside transporter 1	Canis lupus familiaris	81-85
24414167-10	2014	CONCLUSIONS: Ticagrelor inhibits cellular adenosine uptake selectively via ENT1 inhibition at concentrations of clinical relevance.	Ticagrelor	13-23	equilibrative nucleoside transporter 1	Canis lupus familiaris	75-79
24799926-5	2014	Currently, the most important role in the process of platelet inhibition is played by ADP P2Y12 blockers: clopidogrel, prasugrel and ticagrelor.	Ticagrelor	133-143	purinergic receptor P2Y12	Homo sapiens	90-95
24117220-13	2014	The increase in intracellular Ca(2+) evoked by Ft1 in HEK293 cells overexpressing P2Y12 receptors could be blocked by ticagrelor.	Ticagrelor	118-128	AKT interacting protein	Homo sapiens	47-50
24117220-13	2014	The increase in intracellular Ca(2+) evoked by Ft1 in HEK293 cells overexpressing P2Y12 receptors could be blocked by ticagrelor.	Ticagrelor	118-128	purinergic receptor P2Y12	Homo sapiens	82-87
23584598-3	2014	In recent years, newly developed P2Y12 antagonists, such as prasugrel and ticagrelor, have proven to be of higher efficacy and less resistance.	Ticagrelor	74-84	purinergic receptor P2Y12	Homo sapiens	33-38
24846362-11	2014	RESULTS: Total direct medical costs to the public payer at a one year horizon were 2,905 PLN higher with ticagrelor than with clopidogrel.	Ticagrelor	105-115	phospholamban	Homo sapiens	89-92
24111601-14	2014	Ticagrelor was associated with significantly greater P2Y12 inhibition than both clopidogrel and prasugrel during maintenance therapy.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	53-58
24127651-8	2014	C-reactive protein increased more at discharge in the ticagrelor group (28.0 +- 38.0 vs. 26.1 +- 36.6 mg/l; p < 0.001) and interleukin-6 remained higher during the first month of treatment with ticagrelor.	Ticagrelor	54-64	C-reactive protein	Homo sapiens	0-18
24071994-1	2014	In patients pretreated with P2Y12 receptor inhibitors who need to undergo non-emergent cardiac or major non-cardiac surgery, current guidelines of the European Society of Cardiology recommend postponing surgery for at least five days after last intake of clopidogrel or ticagrelor, and for seven days after last intake of prasugrel, unless there is high risk of ischemic events.	Ticagrelor	270-280	purinergic receptor P2Y12	Homo sapiens	28-33
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.	Ticagrelor	247-257	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.	Ticagrelor	190-200	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.	Ticagrelor	190-200	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	112-119
24112116-0	2013	Reversal strategy in antagonizing the P2Y12 -inhibitor ticagrelor.	Ticagrelor	55-65	purinergic receptor P2Y12	Homo sapiens	38-43
24112116-5	2013	MATERIALS AND METHODS: We report an ex vivo model to reverse the effects of the novel and highly effective P2Y12 -inhibitor ticagrelor in 20 healthy volunteers.	Ticagrelor	124-134	purinergic receptor P2Y12	Homo sapiens	107-112
23748750-2	2013	Previous in vitro studies showed that ticagrelor is a substrate and inhibitor of P-glycoprotein (ABCB1).	Ticagrelor	38-48	ATP binding cassette subfamily B member 1	Homo sapiens	97-102
24378838-5	2013	The new, more potent P2Y12 inhibitors, prasugrel and ticagrelor, have shown improved antithrombotic effects compared with clopidogrel in patients with ACS (with or without ST-segment elevation myocardial infarction) in landmark trials, even if they were associated with an increased risk of major bleeding.	Ticagrelor	53-63	purinergic receptor P2Y12	Homo sapiens	21-26
24378838-9	2013	In contrast, ticagrelor is not a prodrug (i.e., does not require hepatic metabolism to exert its antiplatelet effect) and represents the first oral P2Y12 receptor antagonist that is reversibly bound.	Ticagrelor	13-23	purinergic receptor P2Y12	Homo sapiens	148-153
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.	Ticagrelor	157-167	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	81-88
24147518-1	2013	Ticagrelor is a potent P2Y12 adenosine diphosphate receptor antagonist characterized by a rapid onset, consistent and reversible antiplatelet effect, and an acceptable safety profile compared with existing adenosine diphosphate receptor blockers.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	23-28
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).	Ticagrelor	239-249	purinergic receptor P2Y12	Homo sapiens	172-177
24155721-3	2013	For next generation antiplatelet agents such as Ticagrelor and Prasugrel, these new P2Y12 receptor inhibitors form the cornerstone of therapy for patients with acute coronary syndrome (ACS) or undergoing percutaneous interventions.	Ticagrelor	48-58	purinergic receptor P2Y12	Homo sapiens	84-89
24088206-9	2013	High dose ticagrelor (375 mg bid) resulted in sufficient inhibition of platelet aggregation in 1/5 sheep, while acetylsalicylic acid did not show any antiplatelet effect.	Ticagrelor	10-20	BH3-interacting domain death agonist	Ovis aries	29-32
23476040-7	2013	Pharmacodynamic studies indicate the phosphodiesterase 3 inhibitor, cilostazol, the third generation thienopyridine prasugrel and the reversible P2Y12 antagonist ticagrelor to be potent strategies to overcome this biological resistance.	Ticagrelor	162-172	purinergic receptor P2Y12	Homo sapiens	145-150
23903326-1	2013	Prasugrel is the third generation thienopyridine prodrug, and ticagrelor is a non-competitive direct acting P2Y12 antagonist.	Ticagrelor	62-72	purinergic receptor P2Y12	Homo sapiens	108-113
24003163-6	2013	Platelet P2Y12 receptors are the targets of very widely used antithrombotic drugs such as clopidogrel, prasugrel, and ticagrelor.	Ticagrelor	118-128	purinergic receptor P2Y12	Homo sapiens	9-14
23751937-2	2013	Ticagrelor, an oral, direct, reversibly binding, P2Y12 receptor antagonist, is approved for the prevention of atherothrombotic events in adult patients with ACS.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	49-54
23751937-7	2013	A proposed hypothetical mechanism for the interaction between ticagrelor and higher aspirin dose is linked to the level of P2Y12 inhibition and the potential prothrombotic effects of high-dose aspirin through the suppression of prostacyclin.	Ticagrelor	62-72	purinergic receptor P2Y12	Homo sapiens	123-128
23890048-1	2013	BACKGROUND: Ticagrelor, a P2Y12 antagonist, is an antiplatelet agent approved for the treatment of acute coronary syndromes; it also inhibits adenosine uptake by erythrocytes and other cells.	Ticagrelor	12-22	purinergic receptor P2Y12	Homo sapiens	26-31
23476040-10	2013	Among these, the non-thienopyridine P2Y12 receptor antagonist ticagrelor, which does not require biotransformation, could be the drug of choice in CKD patients with ACS.	Ticagrelor	62-72	purinergic receptor P2Y12	Homo sapiens	36-41
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.	Ticagrelor	113-123	purinergic receptor P2Y12	Homo sapiens	55-60
23870610-1	2013	BACKGROUND: In vitro studies have demonstrated that ticagrelor, an oral antiplatelet agent, is a substrate, activator, and inhibitor of cytochrome P450 (CYP) 3A.	Ticagrelor	52-62	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	136-160
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.	Ticagrelor	87-97	purinergic receptor P2Y12	Homo sapiens	10-15
23474908-2	2013	A two-part decision model was adapted to compare treatment with ticagrelor or clopidogrel in a low-dose acetylsalicylic acid (ASA) cohort (<=150 mg) for all ACS patients and subtypes NSTEMI/IA and STEMI.	Ticagrelor	64-74	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	160-163
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.	Ticagrelor	40-50	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	20-23
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.	Ticagrelor	298-308	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.	Ticagrelor	298-308	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.	Ticagrelor	180-190	purinergic receptor P2Y12	Homo sapiens	143-148
23672863-3	2013	Ticagrelor, as the first approved direct and reversible oral P2Y12 blocker, still is limited clinically by its novel side-effect profile.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	61-66
23543615-4	2013	In order to reduce the incidence of HPR, the more potent P2Y12 receptor inhibitors prasugrel and ticagrelor are used.	Ticagrelor	97-107	purinergic receptor P2Y12	Homo sapiens	57-62
23380426-0	2013	Evaluation of the pharmacokinetic interaction between ticagrelor and tolbutamide, a cytochrome P450 2C9 substrate, in healthy volunteers.	Ticagrelor	54-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-103
23428385-5	2013	Two new drugs, prasugrel and ticagrelor, provide faster, greater, and more consistent platelet inhibition than clopidogrel, and have been shown to be more efficacious in preventing ischemic events after PCI in acute coronary syndrome patients.	Ticagrelor	29-39	serpin family A member 5	Homo sapiens	203-206
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.	Ticagrelor	240-250	purinergic receptor P2Y12	Homo sapiens	202-209
23093043-9	2013	Co-administration of strong CYP3A/P-glycoprotein inducers with ticagrelor should be discouraged.	Ticagrelor	63-73	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	28-33
23093043-9	2013	Co-administration of strong CYP3A/P-glycoprotein inducers with ticagrelor should be discouraged.	Ticagrelor	63-73	ATP binding cassette subfamily B member 1	Homo sapiens	34-48
24107485-2	2013	Additionally, novel P2Y12 receptor antagonists such as prasugrel and ticagrelor are even recommended over clopidogrel in certain clinical guidelines.	Ticagrelor	69-79	purinergic receptor P2Y12	Homo sapiens	20-25
23402441-1	2013	Ticagrelor is a reversibly binding oral P2Y(12) inhibitor, which belongs to a novel chemical class of antiplatelet agents named cyclopentyl-triazolo-pyrimidines.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	40-47
23407140-9	2013	However, this benefit may in part be driven by an increased efficacy of CYP3A4-metabolized statins on top of ticagrelor and/or from the inappropriate dose restriction of simvastatin and lovastatin in the clopidogrel arm.	Ticagrelor	109-119	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	72-78
23594617-1	2013	OBJECTIVE: The novel P2Y12 antagonist ticagrelor inhibits adenosine diphosphate (ADP)-induced platelet aggregation more potently than clopidogrel and reduces the incidence of myocardial infarction and total death in patients with an acute coronary syndrome (ACS).	Ticagrelor	38-48	purinergic receptor P2Y12	Homo sapiens	21-26
22795280-0	2012	Usefulness of the VerifyNow P2Y12 assay to evaluate the antiplatelet effects of ticagrelor and clopidogrel therapies.	Ticagrelor	80-90	purinergic receptor P2Y12	Homo sapiens	28-33
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.	Ticagrelor	67-77	cytochrome P450 family 8 subfamily B member 1	Homo sapiens	35-40
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.	Ticagrelor	162-172	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.	Ticagrelor	86-96	purinergic receptor P2Y12	Homo sapiens	41-46
22836596-4	2012	CAMI numbers showed a remarkable discrepancy to SRMI"s by more than a doubling of the difference: from 72 to 145 events in TRITON favoring prasugrel (from a hazard ratio [HR]=0.76, p=0.08; to a HR=0.76, p<0.001), and from 44 to 89 events in favour of ticagrelor in PLATO (from a HR=0.94, p=0.095; to a HR=0.84, p<0.001).	Ticagrelor	254-264	calmodulin 1	Homo sapiens	0-4
22795280-10	2012	CONCLUSIONS: The VerifyNow P2Y12 assay is effective in assessing the antiplatelet effects and in identifying HPR during clopidogrel or ticagrelor therapy.	Ticagrelor	135-145	purinergic receptor P2Y12	Homo sapiens	27-32
22339257-1	2012	Ticagrelor is a new oral antagonist of the platelet P2Y12 receptor that offers several potential advantages compared to clopidogrel including faster and more effective inhibition of platelet aggregation.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	52-57
22546677-1	2012	Ticagrelor (1) is the first reversible P2Y12 receptor antagonist blocking adenine diphosphate (ADP)-induced platelet aggregation with rapid onset and offset of effects.	Ticagrelor	0-10	purinergic receptor P2Y12	Rattus norvegicus	39-44
22565140-1	2012	PURPOSE OF REVIEW: Ticagrelor is a new, direct acting, reversibly binding P2Y12 receptor antagonist with more potent inhibition of platelets than clopidogrel and which does not require metabolic activation.	Ticagrelor	19-29	purinergic receptor P2Y12	Homo sapiens	74-79
22906899-3	2012	P2Y(12) inhibitors include ticlopidine (now rarely used), clopidogrel, prasugrel, and ticagrelor.	Ticagrelor	86-96	purinergic receptor P2Y12	Homo sapiens	0-7
22392457-4	2012	We provide an overview of emerging agents for the treatment of CAD and ACS, including the reversible P2Y(12) antagonists ticagrelor, cangrelor, and elinogrel, and a new class of oral protease-activated receptor-1 (PAR-1) inhibitors, vorapaxar and atopaxar.The recently approved P2Y(12) antagonists prasugrel and ticagrelor demonstrate enhanced ability to prevent adverse cardiac outcomes.	Ticagrelor	312-322	coagulation factor II thrombin receptor	Homo sapiens	183-212
22168538-16	2012	Two subjects discontinued in the ticagrelor 90 mg group due to elevated serum levels of ALT and AST.	Ticagrelor	33-43	solute carrier family 17 member 5	Homo sapiens	96-99
21895760-5	2012	Ticagrelor is a direct-acting and reversible inhibitor of the P2Y12 receptor with potentially more pleiotropic effects.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	62-67
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.	Ticagrelor	19-29	purinergic receptor P2Y12	Homo sapiens	80-85
21812912-0	2011	Antiplatelet effects of aspirin vary with level of P2Y12 receptor blockade supplied by either ticagrelor or prasugrel.	Ticagrelor	94-104	purinergic receptor P2Y12	Homo sapiens	51-56
22918731-3	2012	Non-thienopyridine derivatives including ticagrelor, cangrelor and elinogrel do not require metabolic activation and lead to a reversible P2Y12 receptor inhibition in contrast to thienopyridines.	Ticagrelor	41-51	purinergic receptor P2Y12	Homo sapiens	138-143
22071958-2	2011	Both irreversibly (clopidogrel) and reversibly binding (ticagrelor, AZD6140) P2Y12 antagonists are clinically used for restricted periods, but possible differences in platelet function recovery after drug cessation have not been investigated.	Ticagrelor	56-66	purinergic receptor P2Y12	Rattus norvegicus	77-82
22071958-2	2011	Both irreversibly (clopidogrel) and reversibly binding (ticagrelor, AZD6140) P2Y12 antagonists are clinically used for restricted periods, but possible differences in platelet function recovery after drug cessation have not been investigated.	Ticagrelor	68-75	purinergic receptor P2Y12	Rattus norvegicus	77-82
22360514-2	2012	Ticlopidine, Clopidogrel, Prasugrel, Ticagrelor, Cangrelor and Elinogrel are the P2Y12 inhibitors that act as antiplatelet drugs.	Ticagrelor	37-47	purinergic receptor P2Y12	Homo sapiens	81-86
22839520-4	2012	The purpose of this article is to define the developing role of novel non-thienopyridine reversible P2Y12 inhibitor ticagrelor  to present its pharmacokinetic, pharmacodynamic, and pharmacogenetic characteristics, based on current evidence.	Ticagrelor	116-126	purinergic receptor P2Y12	Homo sapiens	100-105
21970081-18	2011	Ticagrelor and its active metabolite are substrates and inhibitors of cytochrome P450 isoenzymes and P-glycoprotein, creating a risk of multiple pharmacokinetic interactions.	Ticagrelor	0-10	ATP binding cassette subfamily B member 1	Homo sapiens	101-115
21709065-11	2011	In adjusted analyses, both Cox regression with median maintenance dose and landmark techniques showed that, in patients taking low-dose maintenance aspirin, ticagrelor was associated with better outcomes compared with clopidogrel, with statistical superiority in the rest of the world and similar outcomes in the US cohort.	Ticagrelor	157-167	cytochrome c oxidase subunit 8A	Homo sapiens	27-30
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.	Ticagrelor	97-107	coagulation factor II, thrombin	Homo sapiens	216-224
21479342-8	2011	Compared to clopidogrel, new drugs inhibiting P2Y12, such as prasugrel and ticagrelor, decrease the risk of cardiovascular events and increase the risk of bleeding complications, because they adequately inhibit P2Y12-dependent platelet function in the vast majority of treated patients.	Ticagrelor	75-85	purinergic receptor P2Y12	Homo sapiens	46-51
21198849-5	2011	Finally, a novel reversible and direct-acting oral adenosine diphosphate (ADP) receptor antagonist, ticagrelor was developed that showed consistent and increased P2Y12 inhibition with similar incidence of bleeding but greater reduction in cardiac events compared to clopidogrel.	Ticagrelor	100-110	purinergic receptor P2Y12	Homo sapiens	162-167
21198849-6	2011	The focus of this article is to review ticagrelor as a new class of P2Y12 inhibitor.	Ticagrelor	39-49	purinergic receptor P2Y12	Homo sapiens	68-73
21545948-2	2011	BACKGROUND: Ticagrelor, an oral reversibly binding P2Y(12) inhibitor, provides more potent and consistent inhibition of platelet aggregation than clopidogrel but in a phase II study was associated with increased risk for ventricular pauses.	Ticagrelor	12-22	purinergic receptor P2Y12	Homo sapiens	51-58
21479342-8	2011	Compared to clopidogrel, new drugs inhibiting P2Y12, such as prasugrel and ticagrelor, decrease the risk of cardiovascular events and increase the risk of bleeding complications, because they adequately inhibit P2Y12-dependent platelet function in the vast majority of treated patients.	Ticagrelor	75-85	purinergic receptor P2Y12	Homo sapiens	211-216
21479343-2	2011	Three reversibly-binding P2Y12 inhibitors are in phase 3 development, ticagrelor, cangrelor and elinogrel.	Ticagrelor	70-80	purinergic receptor P2Y12	Homo sapiens	25-30
21071697-0	2010	Ticagrelor effectively and reversibly blocks murine platelet P2Y12-mediated thrombosis and demonstrates a requirement for sustained P2Y12 inhibition to prevent subsequent neointima.	Ticagrelor	0-10	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	61-66
21177984-5	2011	Ticagrelor moderately inhibited CYP2C9 activity in human liver microsomes with an IC(50) of 10.5 muM, while exhibiting little or no inhibition of CYP1A2, CYP2B6, CYP2C8, CYP2C19, CYP2D6, and CYP2E1.	Ticagrelor	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
21177984-5	2011	Ticagrelor moderately inhibited CYP2C9 activity in human liver microsomes with an IC(50) of 10.5 muM, while exhibiting little or no inhibition of CYP1A2, CYP2B6, CYP2C8, CYP2C19, CYP2D6, and CYP2E1.	Ticagrelor	0-10	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	170-177
21177984-5	2011	Ticagrelor moderately inhibited CYP2C9 activity in human liver microsomes with an IC(50) of 10.5 muM, while exhibiting little or no inhibition of CYP1A2, CYP2B6, CYP2C8, CYP2C19, CYP2D6, and CYP2E1.	Ticagrelor	0-10	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	179-185
21177984-5	2011	Ticagrelor moderately inhibited CYP2C9 activity in human liver microsomes with an IC(50) of 10.5 muM, while exhibiting little or no inhibition of CYP1A2, CYP2B6, CYP2C8, CYP2C19, CYP2D6, and CYP2E1.	Ticagrelor	0-10	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	191-197
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.	Ticagrelor	55-65	purinergic receptor P2Y12	Homo sapiens	15-20
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.	Ticagrelor	55-65	purinergic receptor P2Y12	Homo sapiens	92-97
21392598-4	2011	The second-generation P2Y(12) inhibitor ticagrelor plus aspirin demonstrated superior ischemic outcomes, including reduction in total mortality, versus clopidogrel plus aspirin, but event rates remain high, and major bleeding not related to coronary artery bypass grafting is increased.	Ticagrelor	40-50	purinergic receptor P2Y12	Homo sapiens	22-29
20966167-8	2011	New drugs, such as prasugrel and ticagrelor, which effectively inhibit P2Y12 in the majority of patients, proved to be more efficacious than clopdidogrel in preventing major cardiovascular events.	Ticagrelor	33-43	purinergic receptor P2Y12	Homo sapiens	71-76
21071697-5	2010	Ticagrelor inhibited platelet aggregation and P-selectin expression in a dose-dependent, reversible manner.	Ticagrelor	0-10	selectin, platelet	Mus musculus	46-56
19176251-0	2010	The reversible oral P2Y12 antagonist AZD6140 inhibits ADP-induced contractions in murine and human vasculature.	Ticagrelor	37-44	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	20-25
21079055-0	2010	First analysis of the relation between CYP2C19 genotype and pharmacodynamics in patients treated with ticagrelor versus clopidogrel: the ONSET/OFFSET and RESPOND genotype studies.	Ticagrelor	102-112	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	39-46
21079055-1	2010	BACKGROUND: The influence of cytochrome P450 (CYP) 2C19 genotype on platelet function in patients treated with ticagrelor versus clopidogrel is unknown.	Ticagrelor	111-121	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	29-55
21142630-1	2010	Ticagrelor (AZD6140), a cyclopentyl-triazolo-pyrimidine, is the first orally available antagonist of the ADP receptor of the P2Y12 subtype.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	125-130
21142630-1	2010	Ticagrelor (AZD6140), a cyclopentyl-triazolo-pyrimidine, is the first orally available antagonist of the ADP receptor of the P2Y12 subtype.	Ticagrelor	12-19	purinergic receptor P2Y12	Homo sapiens	125-130
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.	Ticagrelor	18-28	purinergic receptor P2Y12	Homo sapiens	122-127
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).	Ticagrelor	96-106	ATP binding cassette subfamily B member 1	Homo sapiens	8-13
19485932-7	2010	Two additional P2Y12 agents, ticagrelor and cangrelor are in advanced stages of development.	Ticagrelor	29-39	purinergic receptor P2Y12	Homo sapiens	15-20
20333345-8	2010	Newer developments are focusing on ticagrelor, a new ADP-receptor antagonist, which has been proven superior to clopidogrel in clinical studies and triple therapy utilizing ASS, clopidogrel, and one of the new highly specific antithrombotics (e.g. factors Xa-antagonists or direct thrombin inhibitors).	Ticagrelor	35-45	coagulation factor II, thrombin	Homo sapiens	281-289
20372759-4	2010	Recently, 2 novel third generation oral inhibitors of P2Y12 receptors, prasugrel and ticagrelor, have undergone clinical evaluation with promising results.	Ticagrelor	85-95	purinergic receptor P2Y12	Homo sapiens	54-59
20124464-1	2010	OBJECTIVE: To summarize the pharmacokinetic and pharmacodynamic properties of ticagrelor, a selective P2Y12 receptor antagonist, and evaluate its role in the treatment of patients with acute coronary syndromes (ACS).	Ticagrelor	78-88	purinergic receptor P2Y12	Homo sapiens	102-107
20124464-4	2010	DATA SYNTHESIS: Ticagrelor selectively and reversibly blocks the P2Y12 receptor, inhibiting platelet aggregation and preventing amplification of platelet activation.	Ticagrelor	16-26	purinergic receptor P2Y12	Homo sapiens	65-70
19846210-0	2010	The novel P2Y 12 antagonist AZD6140 rapidly and reversibly reduces platelet activation in diabetic rats.	Ticagrelor	28-35	purinergic receptor P2Y12	Rattus norvegicus	10-16
19846210-7	2010	RESULTS: At 0.5 hour, AZD6140 strongly reduced ADP-induced P-selectin surface expression, inhibited ADP-induced platelet aggregation, and significantly reduced platelet adhesion to fibrinogen under arterial flow conditions.	Ticagrelor	22-29	selectin P	Rattus norvegicus	59-69
19846210-8	2010	Chronic treatment with AZD6140 (10mg/kg bid for 2 weeks, based on data obtained in the acute study) starting at day 14 reduced P-selectin surface expression on circulating platelets, indicating lower in vivo platelet activation.	Ticagrelor	23-30	selectin P	Rattus norvegicus	127-137
19485932-9	2010	Ticagrelor is an oral reversible P2Y12 antagonist with greater platelet inhibition compared with clopidogrel.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	33-38
19946242-8	2009	Promising results have been reported with ticagrelor, an oral first reversible, direct-acting inhibitor of the P2Y12 receptor.	Ticagrelor	42-52	purinergic receptor P2Y12	Homo sapiens	111-116
22282698-5	2010	Recent investigations have included ticagrelor, a reversible inhibitor of the P2Y12 platelet receptor, which appears to have overcome several drawbacks of the current thienopyridines.	Ticagrelor	36-46	purinergic receptor P2Y12	Homo sapiens	78-83
20659022-16	2010	Direct P2Y12 antagonist ticagrelor seems to be especially attractive because of effect on total mortality and acceptable rate of bleeding.	Ticagrelor	24-34	purinergic receptor P2Y12	Homo sapiens	7-12
19892299-4	2009	These include prasugrel, a thienopyridine prodrug which has a mechanism similar to that of clopidogrel but superior pharmacokinetic features; ticagrelor, a non-thienopyridine that binds reversibly to the platelet P2Y(12) receptor; cangrelor, an intravenously administered analog of ticagrelor; the thrombin receptor antagonist SCH 53048; and terutroban (S18886), a thromboxane A(2) receptor inhibitor.	Ticagrelor	142-152	thromboxane A2 receptor	Homo sapiens	365-390
19946242-9	2009	Ticagrelor is the first oral P2Y12 receptor binding antagonist that does not require metabolic activation.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	29-34
19692114-1	2009	Ticagrelor (AZD6140), the first reversibly binding oral P2Y(12) receptor antagonist, blocks adenosine diphosphate (ADP)-induced platelet aggregation via a mode of action distinct from that of thienopyridine antiplatelet agents.	Ticagrelor	0-10	purinergic receptor P2Y1	Rattus norvegicus	56-59
19692114-1	2009	Ticagrelor (AZD6140), the first reversibly binding oral P2Y(12) receptor antagonist, blocks adenosine diphosphate (ADP)-induced platelet aggregation via a mode of action distinct from that of thienopyridine antiplatelet agents.	Ticagrelor	12-19	purinergic receptor P2Y1	Rattus norvegicus	56-59
19630813-6	2009	Ticagrelor is the first of a new class of orally available antiplatelet agents antagonizing the effects of ADP mediated by P2Y12; it is currently being studied in a phase III trial in patients with ACS.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	123-128
19717846-1	2009	BACKGROUND: Ticagrelor is an oral, reversible, direct-acting inhibitor of the adenosine diphosphate receptor P2Y12 that has a more rapid onset and more pronounced platelet inhibition than clopidogrel.	Ticagrelor	12-22	purinergic receptor P2Y12	Homo sapiens	109-114
19678800-6	2009	Currently, several studies are continuing to test new direct P2Y12 receptor antagonists, such as cangrelor and AZD6140, characterised by a faster reversal of platelet inhibition.	Ticagrelor	111-118	purinergic receptor P2Y12	Homo sapiens	61-66
19552634-0	2009	Ticagrelor binds to human P2Y(12) independently from ADP but antagonizes ADP-induced receptor signaling and platelet aggregation.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	26-33
19552634-3	2009	OBJECTIVE: To characterize the receptor biology of the first reversibly binding oral P2Y(12) antagonist, ticagrelor (AZD6140), a member of the new cyclopentyltriazolopyrimidine (CPTP) class currently in phase III development.	Ticagrelor	105-115	purinergic receptor P2Y12	Homo sapiens	85-92
19552634-3	2009	OBJECTIVE: To characterize the receptor biology of the first reversibly binding oral P2Y(12) antagonist, ticagrelor (AZD6140), a member of the new cyclopentyltriazolopyrimidine (CPTP) class currently in phase III development.	Ticagrelor	117-124	purinergic receptor P2Y12	Homo sapiens	85-92
19552634-7	2009	RESULTS: Radioligand-binding studies demonstrated that ticagrelor binds potently and reversibly to human P2Y(12) with K(on) and K(off) of (1.1 +/- 0.2) x 10(-4) nm(-1) s(-1) and (8.7 +/- 1.4) x 10(-4) s(-1), respectively.	Ticagrelor	55-65	purinergic receptor P2Y12	Homo sapiens	105-112
19550317-6	2009	Novel P2Y12 antagonists (prasugrel, ticagrelor, cangrelor, and elinogrel) that have advantages over clopidogrel - including more rapid, less variable, and more complete inhibition of platelet function - are in various phases of development.	Ticagrelor	36-46	purinergic receptor P2Y12	Homo sapiens	6-11
19028049-9	2009	MMP-9 expression correlated with mural thrombus area and was significantly reduced by AZD6140 (P < .05).	Ticagrelor	86-93	matrix metallopeptidase 9	Rattus norvegicus	0-5
18506123-22	2008	Prasugrel, a novel thienopyridine, Cangrelor and AZD 6140 represent newer P2Y12 antagonists.	Ticagrelor	49-57	purinergic receptor P2Y12	Homo sapiens	74-79
19267766-7	2009	AZD6140, the first reversible oral P2Y(12) inhibitor, provides more rapid onset of effect and greater and more consistent platelet inhibition than clopidogrel.	Ticagrelor	0-7	purinergic receptor P2Y12	Homo sapiens	35-42
18574020-9	2008	AZD6140, a novel, potent oral P2Y12 antagonist, demonstrated more effective platelet inhibition versus clopidogrel in a large randomized trial of patients with acute coronary syndrome.	Ticagrelor	0-7	purinergic receptor P2Y12	Homo sapiens	30-35
17187456-8	2007	Two direct and reversible P2Y12 antagonists, cangrelor and AZD6140, have very rapid onset and reversal of platelet inhibition, which make them attractive alternatives to thienopyridines, especially when rapid inhibition of platelet aggregation or its quick reversal are required.	Ticagrelor	59-66	purinergic receptor P2Y12	Homo sapiens	26-31
18174449-3	2008	Novel P2Y12 antagonists, including prasugrel, AZD6140, and cangrelor, have a faster onset of action, as well as more potent, and less variable, inhibition of platelet function ex vivo.	Ticagrelor	46-53	purinergic receptor P2Y12	Homo sapiens	6-11
16941047-8	2006	Two direct and reversible P2Y(12) antagonists, cangrelor and AZD6140, feature very rapid onset and reversal of platelet inhibition, which make them attractive alternatives to thienopyridines, especially when rapid inhibition of platelet aggregation or its quick reversal are required.	Ticagrelor	61-68	purinergic receptor P2Y12	Homo sapiens	26-33
17066149-8	2006	Two direct and reversible P2Y12 antagonists, cangrelor and AZD6140, feature very rapid onset and reversal of platelet inhibition, which make them attractive alternatives to thienopyridines, especially when rapid inhibition of platelet aggregation or its quick reversal are required.	Ticagrelor	59-66	purinergic receptor P2Y12	Homo sapiens	26-31
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.	Ticagrelor	117-125	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	157-162
16476694-0	2006	Pharmacodynamics, pharmacokinetics, and safety of the oral reversible P2Y12 antagonist AZD6140 with aspirin in patients with atherosclerosis: a double-blind comparison to clopidogrel with aspirin.	Ticagrelor	87-94	purinergic receptor P2Y12	Homo sapiens	70-75
33767770-6	2021	In addition, ticagrelor treatment reduced SCr, CD62P and IL-1beta expression levels, renal tissue MPO activity and renal cell apoptosis in rats with sepsis-induced AKI (P<0.05).	Ticagrelor	13-23	interleukin 1 alpha	Rattus norvegicus	57-65
33767770-6	2021	In addition, ticagrelor treatment reduced SCr, CD62P and IL-1beta expression levels, renal tissue MPO activity and renal cell apoptosis in rats with sepsis-induced AKI (P<0.05).	Ticagrelor	13-23	myeloperoxidase	Rattus norvegicus	98-101
33819246-2	2021	The potent P2Y12 blocker, Ticagrelor has greater anti-platelet effects than Clopidogrel.	Ticagrelor	26-36	purinergic receptor P2Y12	Homo sapiens	11-16
33234137-4	2020	Moreover, there are limited head-to-head comparisons of the two P2Y12 inhibitors-ticagrelor and prasugrel-currently recommended by the guidelines.	Ticagrelor	81-91	purinergic receptor P2Y12	Homo sapiens	64-69
33760801-2	2021	This meta-analysis investigated whether ticagrelor, a novel P2Y12 inhibitor, was superior to clopidogrel and prasugrel in efficacy and safety for DM patients undergoing PCI.	Ticagrelor	40-50	purinergic receptor P2Y12	Homo sapiens	60-65
34876147-9	2021	The platelet reactivity index (PRI) level in the VASP test was also markedly lower in the group given aspirin and ticagrelor (P <  0.001).	Ticagrelor	114-124	vasodilator stimulated phosphoprotein	Homo sapiens	49-53
34993242-1	2021	Background: Current guidelines recommend ticagrelor as the preferred P2Y12 inhibitor on top of aspirin in patients after an acute coronary syndrome.	Ticagrelor	41-51	purinergic receptor P2Y12	Homo sapiens	69-74
29992382-6	2018	Ticagrelor, a P2Y12 antagonist, and VX-765 decreased infarct size to 42.8 +- 3.3 and 29.2 +- 4.9%, respectively.	Ticagrelor	0-10	purinergic receptor P2Y12	Rattus norvegicus	14-19
34873925-0	2021	Age-Dependent Effect of Ticagrelor Monotherapy Versus Ticagrelor With Aspirin on Major Bleeding and Cardiovascular Events: A Post Hoc Analysis of the TICO Randomized Trial.	Ticagrelor	24-34	renin binding protein	Homo sapiens	0-3
34873925-0	2021	Age-Dependent Effect of Ticagrelor Monotherapy Versus Ticagrelor With Aspirin on Major Bleeding and Cardiovascular Events: A Post Hoc Analysis of the TICO Randomized Trial.	Ticagrelor	54-64	renin binding protein	Homo sapiens	0-3
34873925-1	2021	Background We aimed to evaluate the age-dependent effect of ticagrelor monotherapy after 3-month dual-antiplatelet therapy (DAPT) versus ticagrelor-based 12-month DAPT on major bleeding and cardiovascular events in patients with acute coronary syndrome.	Ticagrelor	60-70	renin binding protein	Homo sapiens	36-39
34873925-1	2021	Background We aimed to evaluate the age-dependent effect of ticagrelor monotherapy after 3-month dual-antiplatelet therapy (DAPT) versus ticagrelor-based 12-month DAPT on major bleeding and cardiovascular events in patients with acute coronary syndrome.	Ticagrelor	137-147	renin binding protein	Homo sapiens	36-39
34873925-4	2021	The risk reduction effect of ticagrelor monotherapy after 3-month DAPT versus ticagrelor-based 12-month DAPT on the primary end point gradually increased with age and was more marked from the subpopulation of age 64 years with the change point.	Ticagrelor	29-39	renin binding protein	Homo sapiens	159-162
34873925-4	2021	The risk reduction effect of ticagrelor monotherapy after 3-month DAPT versus ticagrelor-based 12-month DAPT on the primary end point gradually increased with age and was more marked from the subpopulation of age 64 years with the change point.	Ticagrelor	29-39	renin binding protein	Homo sapiens	209-212
34873925-6	2021	Conclusions The age-dependent increase in the benefit of ticagrelor monotherapy after 3-month DAPT versus ticagrelor-based 12-month DAPT was observed in the patients with acute coronary syndrome.	Ticagrelor	57-67	renin binding protein	Homo sapiens	16-19
34873925-6	2021	Conclusions The age-dependent increase in the benefit of ticagrelor monotherapy after 3-month DAPT versus ticagrelor-based 12-month DAPT was observed in the patients with acute coronary syndrome.	Ticagrelor	106-116	renin binding protein	Homo sapiens	16-19
34918066-5	2022	METHODS AND RESULTS: We performed a network meta-analysis of randomized controlled trials (RCTs) comparing different oral P2Y12 inhibitors currently recommended for the treatment of patients with ACS (clopidogrel, prasugrel, and ticagrelor).	Ticagrelor	229-239	purinergic receptor P2Y12	Homo sapiens	122-127
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.	Ticagrelor	72-82	purinergic receptor P2Y12	Homo sapiens	30-35
34748820-13	2021	Prasugrel and ticagrelor are potent P2Y12 inverse agonists, and exhibit superior antiplatelet and antithrombotic efficacy over clopidogrel in mice and rats with sepsis.	Ticagrelor	14-24	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	36-41
34748820-15	2021	Compared to clopidogrel, prasugrel and ticagrelor are potent P2Y12 inverse agonists with superior antiplatelet and antithrombotic efficacy in experimental sepsis.	Ticagrelor	39-49	purinergic receptor P2Y12	Rattus norvegicus	61-66
34383973-4	2021	We therefore examined the effects on platelet activation of adenosine signalling activators in combination with the P2Y12 receptor antagonists ticagrelor and prasugrel.	Ticagrelor	143-153	purinergic receptor P2Y12	Homo sapiens	116-121
34814698-0	2021	Incidence of Myocardial Infarction Types in Patients Treated With Ticagrelor in the THEMIS Trial.	Ticagrelor	66-76	thymocyte selection associated	Homo sapiens	84-90
34867774-9	2021	Ticagrelor inhibits both VPAC1 and VPAC2 receptors which was confirmed in VIP-binding and calcium mobilization assays.	Ticagrelor	0-10	vasoactive intestinal peptide receptor 1	Homo sapiens	25-30
34242414-6	2021	Alternative P2Y12 inhibitors (prasugrel or ticagrelor) were used less often in the older group than the younger group in patients with a CYP2C19 no function allele (55% vs. 67%; p=0.02) and in patients without a no function allele (10% vs. 35%, p<0.001).	Ticagrelor	43-53	purinergic receptor P2Y12	Homo sapiens	12-17
34283374-2	2021	Ticagrelor is metabolized mainly by CYP3A4 and produces a rapid blood concentration-dependent platelet inhibitory effect.	Ticagrelor	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	36-42
34283374-7	2021	RESULTS: Many studies have shown that ticagrelor can inhibit equilibrative nucleoside transporter 1 (ENT1).	Ticagrelor	38-48	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	61-99
34283374-7	2021	RESULTS: Many studies have shown that ticagrelor can inhibit equilibrative nucleoside transporter 1 (ENT1).	Ticagrelor	38-48	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	101-105
34283374-9	2021	CONCLUSIONS: Based on the studies reviewed, it was found that ticagrelor essentially inhibits adenosine absorption of adenosine into cells through ENT1, which increases the concentration in the blood and subsequently increases the protection of the heart muscle by adenosine.	Ticagrelor	62-72	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	147-151
34867774-9	2021	Ticagrelor inhibits both VPAC1 and VPAC2 receptors which was confirmed in VIP-binding and calcium mobilization assays.	Ticagrelor	0-10	vasoactive intestinal peptide receptor 2	Homo sapiens	35-40
34867774-9	2021	Ticagrelor inhibits both VPAC1 and VPAC2 receptors which was confirmed in VIP-binding and calcium mobilization assays.	Ticagrelor	0-10	vasoactive intestinal peptide	Homo sapiens	74-77
34768623-9	2021	BMS were associated with a significantly higher rate of primary EP whether treated with prasugrel or ticagrelor.	Ticagrelor	101-111	epiregulin	Homo sapiens	64-66
34815751-3	2021	Previous guidance has been provided regarding the classification of high-risk CCS and the use of newer-generation P2Y12 inhibitors (i.e. ticagrelor and prasugrel) after acute coronary syndromes (ACS) in Asia.	Ticagrelor	137-147	purinergic receptor P2Y12	Homo sapiens	114-119
34871206-2	2021	Although the potent oral P2Y12 inhibitor, ticagrelor is clinically beneficial, its association with bleeding events in elderly ACS patients (>=75 years) is poorly understood.	Ticagrelor	42-52	purinergic receptor P2Y12	Homo sapiens	25-30
34633479-10	2021	Following the early termination of DAPT, continuing antithrombotic monotherapy with the P2Y12 inhibitor ticagrelor may be indicated to prevent further ischemic events without the risk of bleeding complications comparable to DAPT.	Ticagrelor	104-114	purinergic receptor P2Y12	Homo sapiens	88-93
34736855-0	2022	Rationale and Design of the Safe and Timely Antithrombotic Removal - Ticagrelor (STAR-T) Trial: A Prospective, Multi-center, Double-blind, Randomized Controlled Trial Evaluating Reductions in Postoperative Bleeding with Intraoperative Removal of Ticagrelor by the DrugSorb -ATR Device in Patients Undergoing Cardiothoracic Surgery within 48hrs from Last Ticagrelor Dose.	Ticagrelor	246-256	ATR serine/threonine kinase	Homo sapiens	274-277
34736855-3	2022	The goal of the current trial is to evaluate the effectiveness and safety of the DrugSorb -ATR hemoadsorption device for the intraoperative removal of ticagrelor to reduce postoperative bleeding in the above patient population.	Ticagrelor	151-161	ATR serine/threonine kinase	Homo sapiens	91-94
34236915-7	2021	Forty-six patients were included in the primary analysis, of which 26 were discharged on triple antithrombotic therapy with clopidogrel and 20 discharged on potent P2Y12 inhibitors (ticagrelor or prasugrel).	Ticagrelor	182-192	purinergic receptor P2Y12	Homo sapiens	164-169
34275780-8	2021	Median VASP index was significantly lower with the newer P2Y12 inhibitors (14% under ticagrelor, 14% under prasugrel) than with clopidogrel (42%).	Ticagrelor	85-95	purinergic receptor P2Y12	Homo sapiens	57-62
34676463-1	2021	Ticagrelor (TG) suffers from low peroral bioabsorption (36%) due to P-gp efflux and poor solubility (10 microg/mL).	Ticagrelor	0-10	phosphoglycolate phosphatase	Rattus norvegicus	68-72
34676463-1	2021	Ticagrelor (TG) suffers from low peroral bioabsorption (36%) due to P-gp efflux and poor solubility (10 microg/mL).	Ticagrelor	12-14	phosphoglycolate phosphatase	Rattus norvegicus	68-72
34676463-9	2021	Enhanced oral bioavailability of TG-SDAs can be attributed to inhibition of P-gp efflux by PEG 4000, increased wettability, and reduced crystallinity of drug leading to improved drug solubility and dissolution.	Ticagrelor	33-35	phosphoglycolate phosphatase	Rattus norvegicus	76-80
34721047-7	2021	Study with recombinant human UGTs suggested that multiple UGT isoforms including UGT1A9, UGT1A7, UGT1A3, UGT1A4, UGT1A1, UGT2B7 and UGT1A8 are involved in the conversion of ticagrelor to ticagrelor-O-glucuronide with UGT1A9 showing highest catalytic activity.	Ticagrelor	173-183	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	58-61
34721047-7	2021	Study with recombinant human UGTs suggested that multiple UGT isoforms including UGT1A9, UGT1A7, UGT1A3, UGT1A4, UGT1A1, UGT2B7 and UGT1A8 are involved in the conversion of ticagrelor to ticagrelor-O-glucuronide with UGT1A9 showing highest catalytic activity.	Ticagrelor	173-183	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	81-87
34721047-7	2021	Study with recombinant human UGTs suggested that multiple UGT isoforms including UGT1A9, UGT1A7, UGT1A3, UGT1A4, UGT1A1, UGT2B7 and UGT1A8 are involved in the conversion of ticagrelor to ticagrelor-O-glucuronide with UGT1A9 showing highest catalytic activity.	Ticagrelor	173-183	UDP glucuronosyltransferase family 1 member A7	Homo sapiens	89-95
34721047-7	2021	Study with recombinant human UGTs suggested that multiple UGT isoforms including UGT1A9, UGT1A7, UGT1A3, UGT1A4, UGT1A1, UGT2B7 and UGT1A8 are involved in the conversion of ticagrelor to ticagrelor-O-glucuronide with UGT1A9 showing highest catalytic activity.	Ticagrelor	173-183	UDP glucuronosyltransferase family 1 member A3	Homo sapiens	97-103
34721047-7	2021	Study with recombinant human UGTs suggested that multiple UGT isoforms including UGT1A9, UGT1A7, UGT1A3, UGT1A4, UGT1A1, UGT2B7 and UGT1A8 are involved in the conversion of ticagrelor to ticagrelor-O-glucuronide with UGT1A9 showing highest catalytic activity.	Ticagrelor	173-183	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	105-111
34721047-7	2021	Study with recombinant human UGTs suggested that multiple UGT isoforms including UGT1A9, UGT1A7, UGT1A3, UGT1A4, UGT1A1, UGT2B7 and UGT1A8 are involved in the conversion of ticagrelor to ticagrelor-O-glucuronide with UGT1A9 showing highest catalytic activity.	Ticagrelor	173-183	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	113-119
34721047-7	2021	Study with recombinant human UGTs suggested that multiple UGT isoforms including UGT1A9, UGT1A7, UGT1A3, UGT1A4, UGT1A1, UGT2B7 and UGT1A8 are involved in the conversion of ticagrelor to ticagrelor-O-glucuronide with UGT1A9 showing highest catalytic activity.	Ticagrelor	173-183	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	121-127
34721047-7	2021	Study with recombinant human UGTs suggested that multiple UGT isoforms including UGT1A9, UGT1A7, UGT1A3, UGT1A4, UGT1A1, UGT2B7 and UGT1A8 are involved in the conversion of ticagrelor to ticagrelor-O-glucuronide with UGT1A9 showing highest catalytic activity.	Ticagrelor	173-183	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	132-138
34721047-7	2021	Study with recombinant human UGTs suggested that multiple UGT isoforms including UGT1A9, UGT1A7, UGT1A3, UGT1A4, UGT1A1, UGT2B7 and UGT1A8 are involved in the conversion of ticagrelor to ticagrelor-O-glucuronide with UGT1A9 showing highest catalytic activity.	Ticagrelor	173-183	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	217-223
34721047-8	2021	The results were further supported by the inhibition studies on ticagrelor glucuronidation with typical UGT inhibitors in pooled HLM and HIM.	Ticagrelor	64-74	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	104-107
34721047-9	2021	Little or no inhibition of UGT1A1, UGT1A3, UGT1A4, UGT1A6, UGT1A9 and UGT2B7 by ticagrelor and ticagrelor-O-glucuronide was noted.	Ticagrelor	80-90	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	70-76
34604694-6	2021	Results  RUC-4 inhibited all three VN assays, aspirin did not affect the assays, and ticagrelor markedly inhibited the ADP + PGE 1 assay, slightly inhibited the iso-TRAP assay, and did not inhibit the base channel assay.	Ticagrelor	85-95	TRAP	Homo sapiens	165-169
34581430-0	2021	Modified ticagrelor loading doses according to the vasodilator-stimulated phosphoprotein phosphorylation index improve the clinical outcome in ST-elevation myocardial infarction patients with high on-treatment platelet reactivity.	Ticagrelor	9-19	vasodilator stimulated phosphoprotein	Homo sapiens	51-88
34581430-3	2021	The study was conducted to validate whether vasodilator-stimulated phosphoprotein (VASP)-guided ticagrelor dosing individual therapy may result in more effective platelet inhibition and better clinical outcomes.	Ticagrelor	96-106	vasodilator stimulated phosphoprotein	Homo sapiens	44-81
34581430-3	2021	The study was conducted to validate whether vasodilator-stimulated phosphoprotein (VASP)-guided ticagrelor dosing individual therapy may result in more effective platelet inhibition and better clinical outcomes.	Ticagrelor	96-106	vasodilator stimulated phosphoprotein	Homo sapiens	83-87
34570197-8	2021	MTA, coronary angiography, cerebrovascular disease, diabetes with complications, previous bleeding, antidiabetics, and ticagrelor as P2Y12 inhibitor were associated with non-persistence, whereas female sex, advanced age, and concomitant pharmacotherapy with angiotensin-converting enzyme inhibitors, beta-blockers, statins, oral anticoagulants, and aspirin were associated with high persistence.	Ticagrelor	119-129	purinergic receptor P2Y12	Homo sapiens	133-138
34781659-1	2021	Ticagrelor is a potent, oral P2Y12 inhibitor used as a part of dual antiplatelet therapy (DAPT) in acute coronary syndromes (ACS).	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	29-34
34510337-5	2022	The results suggest the effectiveness of vorapaxar, ticagrelor, cilostazol, cangrelor, and prasugrel in binding the main protease (Mpro) of SARS-CoV-2.	Ticagrelor	52-62	NEWENTRY	Severe acute respiratory syndrome-related coronavirus	131-135
34232433-1	2021	PURPOSE: Ticagrelor and dapagliflozin can suppress the activation of the NOD-like receptor 3 (NLRP3)-inflammasome and activate AMP-activated protein kinase (AMPK).	Ticagrelor	9-19	NLR family, pyrin domain containing 3	Mus musculus	73-92
34510337-6	2022	At the same time, vorapaxar, ticagrelor, and cilostazol are the best binders of the spike protein.	Ticagrelor	29-39	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	84-89
34244132-1	2021	BACKGROUND AND PURPOSE: Ticagrelor is a novel P2Y12 antagonist, and little is known about its efficacy and safety in the endovascular treatment of aneurysms.	Ticagrelor	24-34	purinergic receptor P2Y12	Homo sapiens	46-51
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.	Ticagrelor	127-137	purinergic receptor P2Y12	Homo sapiens	22-27
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.	Ticagrelor	127-137	purinergic receptor P2Y12	Homo sapiens	73-78
34238553-0	2021	Impact of Age on the Safety and Efficacy of Ticagrelor Monotherapy in Patients Undergoing PCI.	Ticagrelor	44-54	renin binding protein	Homo sapiens	10-13
34238553-1	2021	OBJECTIVES: The aim of this study was to assess the impact of age on the safety and efficacy of ticagrelor monotherapy after percutaneous coronary intervention (PCI).	Ticagrelor	96-106	renin binding protein	Homo sapiens	62-65
34238553-9	2021	At 1 year after randomization, ticagrelor monotherapy significantly reduced BARC type 2, 3, or 5 bleeding (4.5% vs. 8.2%; hazard ratio: 0.53; 95% confidence interval: 0.40 to 0.71) without increasing ischemic events (4.2% vs. 4.4%; hazard ratio: 0.96; 95% confidence interval: 0.68 to 1.35) compared with ticagrelor plus aspirin among patients >=65 years of age.	Ticagrelor	31-41	renin binding protein	Homo sapiens	358-361
34233865-0	2021	Severe diarrhoea due to use of P2Y12 inhibitor ticagrelor: a rarely reported adverse event.	Ticagrelor	47-57	purinergic receptor P2Y12	Homo sapiens	31-36
34423649-0	2021	Long-Term Ticagrelor in Patients With Prior Coronary Stenting in the PEGASUS-TIMI 54 Trial.	Ticagrelor	10-20	IKAROS family zinc finger 5	Homo sapiens	69-84
34424771-0	2021	Applying Decision Analysis to Inform the US Food and Drug Administration"s Benefit-Risk Assessment of Ticagrelor for Primary Prevention of Myocardial Infarction or Stroke Based on THEMIS.	Ticagrelor	102-112	thymocyte selection associated	Homo sapiens	180-186
34137238-1	2021	BACKGROUND: The use of potent P2Y12 inhibitors (ticagrelor & prasugrel) in acute coronary syndrome (ACS) patients undergoing percutaneous coronary interventions (PCI) is a class I recommendation.	Ticagrelor	48-58	purinergic receptor P2Y12	Homo sapiens	30-35
34232433-1	2021	PURPOSE: Ticagrelor and dapagliflozin can suppress the activation of the NOD-like receptor 3 (NLRP3)-inflammasome and activate AMP-activated protein kinase (AMPK).	Ticagrelor	9-19	NLR family, pyrin domain containing 3	Mus musculus	94-99
34232433-3	2021	Dapagliflozin and ticagrelor have been shown to have additive effects on the progression of diabetic cardiomyopathy in BTBR ob/ob mice with type-2 diabetes.	Ticagrelor	18-28	leptin	Mus musculus	124-126
34232433-3	2021	Dapagliflozin and ticagrelor have been shown to have additive effects on the progression of diabetic cardiomyopathy in BTBR ob/ob mice with type-2 diabetes.	Ticagrelor	18-28	leptin	Mus musculus	127-129
34232433-4	2021	We assessed whether dapagliflozin and ticagrelor have additive effects on the activation of the NLRP3-inflammasome and the progression of diabetic nephropathy in mice with type-2 diabetes.	Ticagrelor	38-48	NLR family, pyrin domain containing 3	Mus musculus	96-101
34232433-10	2021	RESULTS: Both ticagrelor and dapagliflozin reduced serum creatinine and cystatin C levels and urinary albumin.	Ticagrelor	14-24	cystatin C	Mus musculus	72-82
34377702-10	2021	LEARNING POINTS: Ticagrelor is a pro-drug and directly inhibits P2Y12 receptors.This makes ticagrelor less susceptible to drug-drug interactions or pharmacogenetic influences.Thromboelastography platelet mapping measures the physical properties of clot formation and can reveals platelet resistance to various P2Y12 inhibitors, including ticagrelor.	Ticagrelor	17-27	purinergic receptor P2Y12	Homo sapiens	64-69
34232433-15	2021	CONCLUSIONS: Dapagliflozin and ticagrelor attenuated the progression of diabetic nephropathy in BTBR ob/ob mice with additive effects of the combination.	Ticagrelor	31-41	leptin	Mus musculus	101-103
34377702-10	2021	LEARNING POINTS: Ticagrelor is a pro-drug and directly inhibits P2Y12 receptors.This makes ticagrelor less susceptible to drug-drug interactions or pharmacogenetic influences.Thromboelastography platelet mapping measures the physical properties of clot formation and can reveals platelet resistance to various P2Y12 inhibitors, including ticagrelor.	Ticagrelor	17-27	purinergic receptor P2Y12	Homo sapiens	310-315
34377702-10	2021	LEARNING POINTS: Ticagrelor is a pro-drug and directly inhibits P2Y12 receptors.This makes ticagrelor less susceptible to drug-drug interactions or pharmacogenetic influences.Thromboelastography platelet mapping measures the physical properties of clot formation and can reveals platelet resistance to various P2Y12 inhibitors, including ticagrelor.	Ticagrelor	91-101	purinergic receptor P2Y12	Homo sapiens	64-69
34232433-15	2021	CONCLUSIONS: Dapagliflozin and ticagrelor attenuated the progression of diabetic nephropathy in BTBR ob/ob mice with additive effects of the combination.	Ticagrelor	31-41	leptin	Mus musculus	104-106
34163168-0	2021	Ticagrelor Use in Stroke Patients: Past, Present, and Future.	Ticagrelor	0-10	EH domain containing 1	Homo sapiens	35-39
34207339-1	2021	East Asians treated with potent P2Y12 inhibitors (prasugrel or ticagrelor) generally experience more intense platelet inhibitory responses resulting in an increased risk of major bleeding.	Ticagrelor	63-73	purinergic receptor P2Y12	Homo sapiens	32-37
34114623-12	2021	CONCLUSION: In patients with DM, although ticagrelor maintenance dose regimens (60 mg and 90 mg) yield potent P2Y12 inhibition, levels of platelet reactivity tended to be higher and subject to broader variability in non-CKD compared with CKD patients.	Ticagrelor	42-52	purinergic receptor P2Y12	Homo sapiens	110-115
35596184-8	2022	In diabetic patients receiving ticagrelor, PCSK9 levels were positively correlated with maximal platelet aggregation measured by light transmittance aggregometry and maximum amplitude of adenosine diphosphate-induced platelet-fibrin clots measured by thrombelastography in the maintenance phase of treatment, whereas no correlations were found in non-diabetic patients.	Ticagrelor	31-41	proprotein convertase subtilisin/kexin type 9	Homo sapiens	43-48
35618653-8	2022	TPTS/C/T realized targeted drug release to plaques and synergistic therapeutic effects of simvastatin and ticagrelor on atherosclerosis treatment in an ApoE-/- mouse model, resulting in excellent atherosclerosis therapeutic efficacy and a promising biosafety profile.	Ticagrelor	106-116	apolipoprotein E	Mus musculus	152-156
35595877-15	2022	The P2Y12 inhibitor ticagrelor per se induces a humoral cardioprotective signal.	Ticagrelor	20-30	purinergic receptor P2Y12	Rattus norvegicus	4-9
35321823-1	2022	BACKGROUND: The THEMIS trial demonstrated that in high-risk patients with stable coronary artery disease and diabetes without previous myocardial infarction or stroke, ticagrelor, in addition to aspirin, reduced the incidence of ischemic events but increased major bleeding.	Ticagrelor	168-178	thymocyte selection associated	Homo sapiens	16-22
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.	Ticagrelor	94-104	purinergic receptor P2Y12	Homo sapiens	64-69
35514270-6	2022	We sought to compare the in vitro efficacy of prasugrel (n=121) and ticagrelor (n=99) to inhibit PAR-mediated platelet aggregation in individuals with type 2 diabetes (prasugrel n=26, ticagrelor n=29).	Ticagrelor	68-78	nuclear receptor subfamily 1 group I member 2	Homo sapiens	97-100
35514270-12	2022	CONCLUSION: Prasugrel and ticagrelor inhibit P2Y12 - and PAR-mediated platelet aggregation in individuals with diabetes to a similar extent, irrespective of HbA1c levels and BMI.	Ticagrelor	26-36	purinergic receptor P2Y12	Homo sapiens	45-50
35514270-12	2022	CONCLUSION: Prasugrel and ticagrelor inhibit P2Y12 - and PAR-mediated platelet aggregation in individuals with diabetes to a similar extent, irrespective of HbA1c levels and BMI.	Ticagrelor	26-36	nuclear receptor subfamily 1 group I member 2	Homo sapiens	57-60
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.	Ticagrelor	155-165	purinergic receptor P2Y12	Homo sapiens	109-114
35501592-0	2022	Effect of Genetic Polymorphism Including NUP153 and SVEP1 on the Pharmacokinetics and Pharmacodynamics of Ticagrelor in Healthy Chinese Subjects.	Ticagrelor	106-116	nucleoporin 153	Homo sapiens	41-47
35501592-0	2022	Effect of Genetic Polymorphism Including NUP153 and SVEP1 on the Pharmacokinetics and Pharmacodynamics of Ticagrelor in Healthy Chinese Subjects.	Ticagrelor	106-116	sushi, von Willebrand factor type A, EGF and pentraxin domain containing 1	Homo sapiens	52-57
35529262-2	2022	This study is aimed at investigating the efficacy of tirofiban combined with ticagrelor in AMI patients after percutaneous coronary intervention (PCI) and its effects on plasma activated partial thromboplastin time (APTT), fibrinogen (FIB), D-dimer (D-D) levels, myocardial injury markers, and inflammatory factors.	Ticagrelor	77-87	fibrinogen beta chain	Homo sapiens	223-233
35482455-5	2022	Platelet-induced tumor cell PD-L1 upregulation was reduced by anti-platelet agents, such as aspirin and ticagrelor.	Ticagrelor	104-114	CD274 molecule	Homo sapiens	28-33
35566604-1	2022	BACKGROUND: East Asian patients receiving treatment with the potent P2Y12 inhibitors prasugrel or ticagrelor experience more potent platelet inhibition than with clopidogrel.	Ticagrelor	98-108	purinergic receptor P2Y12	Homo sapiens	68-73
35090983-1	2022	BACKGROUND: The safety and efficacy of potent P2Y12 inhibitors (Ticagrelor and Prasugrel) in dual antiplatelet therapy (DAPT) with aspirin in elderly acute coronary syndrome (ACS) patients remains unclear.	Ticagrelor	64-74	purinergic receptor P2Y12	Homo sapiens	46-51
35466828-17	2022	CONCLUSIONS: A lower dose of ticagrelor (45 mg twice daily) appears to be safe and effective in this small cohort of patients who are resistant to clopidogrel per P2Y12 testing and who have increased risk of ischemic or hemorrhagic strokes due to neurovascular pathologies and implants.	Ticagrelor	29-39	purinergic receptor P2Y12	Homo sapiens	163-168
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.	Ticagrelor	81-91	coagulation factor II, thrombin	Homo sapiens	126-134
35396752-12	2022	WHAT IS NEW AND CONCLUSIONS: For patients carrying CYP2C19 LOF alleles after PCI, ticagrelor may be better than high-dose clopidogrel in reducing the risk of MACEs, while dyspnoea incidents should be alerted.	Ticagrelor	82-92	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	51-58
35456184-5	2022	An agreement was reached on the indication of ticagrelor as the first choice P2Y12 inhibitor in MI patients, irrespective of the presentation (ST elevation MI (STEMI), 72%, vs. non-ST elevation MI (NSTEMI), 71%) or the management (invasive vs. conservative (75%)).	Ticagrelor	46-56	purinergic receptor P2Y12	Homo sapiens	77-82
35428703-1	2022	BACKGROUND: Currently, potent P2Y12 inhibition with the use of prasugrel or ticagrelor is the mainstay of treatment after an acute coronary syndrome (ACS).	Ticagrelor	76-86	purinergic receptor P2Y12	Homo sapiens	30-35
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.	Ticagrelor	81-91	prostaglandin-endoperoxide synthase 1	Homo sapiens	168-184
35353154-7	2022	In an analysis according to P2Y12 inhibitor type, ticagrelor reduced markers of platelet-mediated global thrombogenicity, P2Y12 signaling and rates of high platelet reactivity compared to clopidogrel.	Ticagrelor	50-60	purinergic receptor P2Y12	Homo sapiens	28-33
35353154-7	2022	In an analysis according to P2Y12 inhibitor type, ticagrelor reduced markers of platelet-mediated global thrombogenicity, P2Y12 signaling and rates of high platelet reactivity compared to clopidogrel.	Ticagrelor	50-60	purinergic receptor P2Y12	Homo sapiens	122-127
35300607-0	2022	Effect of CYP2C19 genetic polymorphism on the pharmacodynamics and clinical outcomes for patients treated with ticagrelor: a systematic review with qualitative and quantitative meta-analysis.	Ticagrelor	111-121	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-17
35300607-1	2022	BACKGROUND: Studies show inconsistent results regarding the impact of CYP2C19 genotype on the pharmacodynamics (PD) and clinical outcomes of ticagrelor.	Ticagrelor	141-151	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	70-77
35300607-2	2022	With the implementation of genotype-guided individualized antiplatelet therapy, the association between CYP2C19 polymorphism and the efficacy and safety of ticagrelor for patients is still worthy of exploring and studying.	Ticagrelor	156-166	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	104-111
35300607-13	2022	CONCLUSIONS: This qualitative and quantitative study suggested Asian patients carrying any CYP2C19 LOF allele might have a lower risk of bleeding events comparing with no LOF allele carriers when treated with ticagrelor.	Ticagrelor	209-219	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	91-98
35369358-13	2022	These findings suggest that clopidogrel is an effective alternative to the more potent P2Y12 inhibitor ticagrelor in older patients.	Ticagrelor	103-113	purinergic receptor P2Y12	Homo sapiens	87-92
35000152-6	2022	Itching and pain behaviours of the mice in the type 2 diabetes mellitus + itch group were significantly increased, and the expression of P2Y12 and NLRP3 as well as the content of ROS increased, and these changes were significantly reversed by treatment with P2Y12 short hairpin RNA (shRNA) or P2Y12 antagonist ticagrelor.	Ticagrelor	310-320	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	137-142
35157607-8	2022	Ticagrelor was the most common P2Y12 inhibitor administered (41.9%), followed by clopidogrel (12.2%) and prasugrel (1.2%).	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	31-36
35226525-0	2022	In patients with stroke or TIA and CYP2C19 loss-of-function alleles, ticagrelor vs. clopidogrel reduced 90-d stroke.	Ticagrelor	69-79	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	35-42
35294730-4	2022	The benefit of more potent P2Y12 inhibitors such as ticagrelor or prasugrel in stable patients is unproven, but their use might be reasonable in those with high clinical or angiographic features of increased ischemic risk without increased risk of bleeding.	Ticagrelor	52-62	purinergic receptor P2Y12	Homo sapiens	27-32
35000152-6	2022	Itching and pain behaviours of the mice in the type 2 diabetes mellitus + itch group were significantly increased, and the expression of P2Y12 and NLRP3 as well as the content of ROS increased, and these changes were significantly reversed by treatment with P2Y12 short hairpin RNA (shRNA) or P2Y12 antagonist ticagrelor.	Ticagrelor	310-320	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	258-263
35000152-12	2022	Treatment with P2Y12 receptor shRNA or P2Y12 antagonist ticagrelor can inhibit these pathological changes and improve itching behaviour.	Ticagrelor	56-66	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	39-44
35280252-12	2021	Conclusion: This study is the first to show that the CYP4F2 rs2074900 SNP had a remarkable effect on ticagrelor PK, which is significant since it adds to the limited pharmacogenetic information on ticagrelor.	Ticagrelor	101-111	cytochrome P450 family 4 subfamily F member 2	Homo sapiens	53-59
35280252-12	2021	Conclusion: This study is the first to show that the CYP4F2 rs2074900 SNP had a remarkable effect on ticagrelor PK, which is significant since it adds to the limited pharmacogenetic information on ticagrelor.	Ticagrelor	197-207	cytochrome P450 family 4 subfamily F member 2	Homo sapiens	53-59
35192075-14	2022	One hour after reperfusion, AZD3366 and ticagrelor equally attenuated the increase in interleukin-15 (an early inflammatory marker after ischemic cell death) levels, and their combined effects were additive.	Ticagrelor	40-50	interleukin 15	Rattus norvegicus	86-100
35048203-5	2022	STUDY DESIGN: PLINY THE ELDER (PLatelet INhibition with two different doses of potent P2y12 inhibitors in THE ELDERly population) (NCT04739384) is a prospective, randomized, open-label, crossover trial to evaluate the non-inferiority of a lower dose of ticagrelor (60 mg twice daily) compared with a standard dose (90 mg twice daily) among elderly patients with ACS undergoing percutaneous coronary intervention (PCI).	Ticagrelor	253-263	purinergic receptor P2Y12	Homo sapiens	86-91
35040887-6	2022	Ticagrelor was the preferred P2Y12 inhibitor.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	29-34
35082514-2	2022	Ticagrelor is a new class of receptor inhibitors receptor antagonist of P2Y12 and is used as an antiplatelet agents.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	72-77
35082514-9	2022	Results: DNAH17, PGS1 and ABCA1 as the potential variant genes are associated with the expected antiplatelet effect to ticagrelor.	Ticagrelor	119-129	dynein axonemal heavy chain 17	Homo sapiens	9-15
35082514-9	2022	Results: DNAH17, PGS1 and ABCA1 as the potential variant genes are associated with the expected antiplatelet effect to ticagrelor.	Ticagrelor	119-129	phosphatidylglycerophosphate synthase 1	Homo sapiens	17-21
35082514-9	2022	Results: DNAH17, PGS1 and ABCA1 as the potential variant genes are associated with the expected antiplatelet effect to ticagrelor.	Ticagrelor	119-129	ATP binding cassette subfamily A member 1	Homo sapiens	26-31
35040887-11	2022	In the P2Y12 inhibitor group, ticagrelor was used in 63% of patients and clopidogrel in 37%.	Ticagrelor	30-40	purinergic receptor P2Y12	Homo sapiens	7-12
32664772-0	2021	Risk of major adverse cardiovascular events of CYP2C19 loss-of-function genotype guided prasugrel/ticagrelor vs clopidogrel therapy for acute coronary syndrome patients undergoing percutaneous coronary intervention: a meta-analysis.	Ticagrelor	98-108	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	47-54
35396017-1	2022	Ticagrelor is one of the most recent antiplatelet agents used to inhibit platelet aggregation via blocking the ADP receptors of the subtype P2Y12.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	140-145
32664772-6	2021	It was demonstrated that patients treated with prasugrel or ticagrelor significantly reduced the risk of MACEs (RR 0.58; 95% CI 0.45-0.76; P<0.0001) as compared to patients with clopidogrel where both groups carrying CYP2C19 LoF alleles.	Ticagrelor	60-70	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	217-224
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.	Ticagrelor	233-243	purinergic receptor P2Y12	Homo sapiens	194-199
32523112-5	2021	Further mechanistic studies demonstrate that ticagrelor attenuates the oligomerization of apoptosis-associated speck-like protein containing a CARD (ASC) by blocking chloride efflux, an effect achieved through the degradation of chloride intracellular channel proteins (CLICs) and blockade of the translocation of CLICs to the plasma membrane.	Ticagrelor	45-55	PYD and CARD domain containing	Homo sapiens	90-147
33985681-10	2021	CONCLUSION: Ticagrelor plus aspirin yielded generally consistent and favorable net clinical benefit across the diabetes-related factors in THEMIS-PCI but not in the overall THEMIS population.	Ticagrelor	12-22	thymocyte selection associated	Homo sapiens	139-145
33955698-4	2021	Long-term benefit is provided by oral P2Y12 receptor antagonists such as clopidogrel, prasugrel, and ticagrelor.	Ticagrelor	101-111	purinergic receptor P2Y12	Homo sapiens	38-43
33957564-0	2021	Epac-1/Rap-1 signaling pathway orchestrates the reno-therapeutic effect of ticagrelor against renal ischemia/reperfusion model.	Ticagrelor	75-85	Rap guanine nucleotide exchange factor 3	Rattus norvegicus	0-6
33957564-7	2021	On the molecular level, ticagrelor enhanced renal Epac-1 mRNA expression, Rap-1 activation (Rap-1-GTP) and SOCS-3 level.	Ticagrelor	24-34	Rap guanine nucleotide exchange factor 3	Rattus norvegicus	50-56
33957564-7	2021	On the molecular level, ticagrelor enhanced renal Epac-1 mRNA expression, Rap-1 activation (Rap-1-GTP) and SOCS-3 level.	Ticagrelor	24-34	suppressor of cytokine signaling 3	Rattus norvegicus	107-113
33957564-11	2021	In conclusion, ticagrelor reno-therapeutic effect is partly mediated through modulating the Epac-1/Rap-1-GTP, AKT/Nrf-2/HO-1 and JAK-2/STAT-3/SOCS-3 trajectories, pathways that integrate to afford novel explanations to its anti-inflammatory, anti-oxidant, and anti-apoptotic potentials.	Ticagrelor	15-25	Rap guanine nucleotide exchange factor 3	Rattus norvegicus	92-98
33957564-11	2021	In conclusion, ticagrelor reno-therapeutic effect is partly mediated through modulating the Epac-1/Rap-1-GTP, AKT/Nrf-2/HO-1 and JAK-2/STAT-3/SOCS-3 trajectories, pathways that integrate to afford novel explanations to its anti-inflammatory, anti-oxidant, and anti-apoptotic potentials.	Ticagrelor	15-25	AKT serine/threonine kinase 1	Rattus norvegicus	110-113
33957564-11	2021	In conclusion, ticagrelor reno-therapeutic effect is partly mediated through modulating the Epac-1/Rap-1-GTP, AKT/Nrf-2/HO-1 and JAK-2/STAT-3/SOCS-3 trajectories, pathways that integrate to afford novel explanations to its anti-inflammatory, anti-oxidant, and anti-apoptotic potentials.	Ticagrelor	15-25	NFE2 like bZIP transcription factor 2	Rattus norvegicus	114-119
33957564-11	2021	In conclusion, ticagrelor reno-therapeutic effect is partly mediated through modulating the Epac-1/Rap-1-GTP, AKT/Nrf-2/HO-1 and JAK-2/STAT-3/SOCS-3 trajectories, pathways that integrate to afford novel explanations to its anti-inflammatory, anti-oxidant, and anti-apoptotic potentials.	Ticagrelor	15-25	heme oxygenase 1	Rattus norvegicus	120-124
33957564-11	2021	In conclusion, ticagrelor reno-therapeutic effect is partly mediated through modulating the Epac-1/Rap-1-GTP, AKT/Nrf-2/HO-1 and JAK-2/STAT-3/SOCS-3 trajectories, pathways that integrate to afford novel explanations to its anti-inflammatory, anti-oxidant, and anti-apoptotic potentials.	Ticagrelor	15-25	Janus kinase 2	Rattus norvegicus	129-134
33957564-11	2021	In conclusion, ticagrelor reno-therapeutic effect is partly mediated through modulating the Epac-1/Rap-1-GTP, AKT/Nrf-2/HO-1 and JAK-2/STAT-3/SOCS-3 trajectories, pathways that integrate to afford novel explanations to its anti-inflammatory, anti-oxidant, and anti-apoptotic potentials.	Ticagrelor	15-25	signal transducer and activator of transcription 3	Rattus norvegicus	135-141
33957564-11	2021	In conclusion, ticagrelor reno-therapeutic effect is partly mediated through modulating the Epac-1/Rap-1-GTP, AKT/Nrf-2/HO-1 and JAK-2/STAT-3/SOCS-3 trajectories, pathways that integrate to afford novel explanations to its anti-inflammatory, anti-oxidant, and anti-apoptotic potentials.	Ticagrelor	15-25	suppressor of cytokine signaling 3	Rattus norvegicus	142-148
33993817-2	2021	The potent P2Y12 inhibitors, prasugrel and ticagrelor, can overcome this limitation but at the expense of an increased risk of bleeding.	Ticagrelor	43-53	purinergic receptor P2Y12	Homo sapiens	11-16
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.	Ticagrelor	57-67	purinergic receptor P2Y12	Homo sapiens	27-32
32523112-0	2021	Ticagrelor inhibits the NLRP3 inflammasome to protect against inflammatory disease independent of the P2Y12 signaling pathway.	Ticagrelor	0-10	NLR family pyrin domain containing 3	Homo sapiens	24-29
32523112-4	2021	In this study, we systematically examined the effects of ticagrelor on the NLRP3 inflammasome and found that ticagrelor inhibits NLRP3 inflammasome activation in macrophages independent of its classic inhibitory effect on the P2Y12 signaling pathway.	Ticagrelor	109-119	NLR family pyrin domain containing 3	Homo sapiens	129-134
32523112-5	2021	Further mechanistic studies demonstrate that ticagrelor attenuates the oligomerization of apoptosis-associated speck-like protein containing a CARD (ASC) by blocking chloride efflux, an effect achieved through the degradation of chloride intracellular channel proteins (CLICs) and blockade of the translocation of CLICs to the plasma membrane.	Ticagrelor	45-55	PYD and CARD domain containing	Homo sapiens	149-152
32523112-7	2021	Importantly, oral administration of ticagrelor rapidly and strongly inhibited NLRP3 inflammasome activation in peripheral blood mononuclear cells from patients with acute coronary syndrome.	Ticagrelor	36-46	NLR family pyrin domain containing 3	Homo sapiens	78-83
32523112-8	2021	Overall, our study reveals a novel pharmacological function of ticagrelor in addition to its classic antiplatelet properties, which suggests that ticagrelor may serve as a potential therapeutic agent for use in NLRP3-associated diseases.	Ticagrelor	63-73	NLR family pyrin domain containing 3	Homo sapiens	211-216
32523112-8	2021	Overall, our study reveals a novel pharmacological function of ticagrelor in addition to its classic antiplatelet properties, which suggests that ticagrelor may serve as a potential therapeutic agent for use in NLRP3-associated diseases.	Ticagrelor	146-156	NLR family pyrin domain containing 3	Homo sapiens	211-216
33744207-14	2021	CONCLUSIONS: The effect of ticagrelor or prasugrel compared with clopidogrel in reducing ischemic events in patients with CAD who predominantly undergo PCI is based primarily on the presence of CYP2C19 loss-of-function carrier status.	Ticagrelor	27-37	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	194-201
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.	Ticagrelor	43-53	purinergic receptor P2Y12	Homo sapiens	11-16
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.	Ticagrelor	247-257	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	63-70
33744207-2	2021	BACKGROUND: The effect of CYP2C19 genotype on treatment outcomes with ticagrelor or prasugrel compared with clopidogrel is unclear.	Ticagrelor	70-80	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
33877270-2	2021	Dual antiplatelet therapy (DAPT), consisting of aspirin and a P2Y12 inhibitor (clopidogrel, ticagrelor, or prasugrel) reduces cardiovascular event rates after ACS.	Ticagrelor	92-102	purinergic receptor P2Y12	Homo sapiens	62-67
33898623-7	2021	Ticagrelor inhibited angiogenesis and blood reperfusion recovery significantly elevated the levels of IL-10 and decreased the expression of VEGF in the IL-10+/+ mouse ischemic hindlimb, which were abolished in IL-10-deficient (IL-10-/-) C57BL/6J mice.	Ticagrelor	0-10	interleukin 10	Mus musculus	102-107
33744207-3	2021	METHODS: Databases through February 19, 2020, were searched for studies reporting the effect of CYP2C19 genotype on ischemic outcomes during ticagrelor or prasugrel versus clopidogrel treatment.	Ticagrelor	141-151	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	96-103
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).	Ticagrelor	0-10	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	170-177
33898623-7	2021	Ticagrelor inhibited angiogenesis and blood reperfusion recovery significantly elevated the levels of IL-10 and decreased the expression of VEGF in the IL-10+/+ mouse ischemic hindlimb, which were abolished in IL-10-deficient (IL-10-/-) C57BL/6J mice.	Ticagrelor	0-10	vascular endothelial growth factor A	Mus musculus	140-144
33898623-7	2021	Ticagrelor inhibited angiogenesis and blood reperfusion recovery significantly elevated the levels of IL-10 and decreased the expression of VEGF in the IL-10+/+ mouse ischemic hindlimb, which were abolished in IL-10-deficient (IL-10-/-) C57BL/6J mice.	Ticagrelor	0-10	interleukin 10	Mus musculus	152-157
33898623-7	2021	Ticagrelor inhibited angiogenesis and blood reperfusion recovery significantly elevated the levels of IL-10 and decreased the expression of VEGF in the IL-10+/+ mouse ischemic hindlimb, which were abolished in IL-10-deficient (IL-10-/-) C57BL/6J mice.	Ticagrelor	0-10	interleukin 10	Mus musculus	152-157
33898623-7	2021	Ticagrelor inhibited angiogenesis and blood reperfusion recovery significantly elevated the levels of IL-10 and decreased the expression of VEGF in the IL-10+/+ mouse ischemic hindlimb, which were abolished in IL-10-deficient (IL-10-/-) C57BL/6J mice.	Ticagrelor	0-10	interleukin 10	Mus musculus	152-157
33706987-7	2021	The first one maintains DAPT but switches from the potent P2Y12 inhibitors ticagrelor or prasugrel to either a lower dose or to clopidogrel, while maintaining ASA.	Ticagrelor	75-85	purinergic receptor P2Y12	Homo sapiens	58-63
33558152-1	2021	AIMS: THEMIS (NCT01991795) demonstrated cardioprotective benefits of ticagrelor plus acetylsalicylic acid (ASA) compared with placebo plus ASA in patients with type 2 diabetes (T2D), stable coronary artery disease (CAD) and no history of myocardial infarction (MI) or stroke.	Ticagrelor	69-79	thymocyte selection associated	Homo sapiens	6-12
33758122-6	2021	Another recently published VORA-PRATIC (Vorapaxar in Patients with Prior Myocardial Infarction Treated with prasugrel and ticagrelor) study showed that among post-MI patients treated with potent P2Y12 inhibitors (prasugrel or ticagrelor), vorapaxar reduced platelet-driven global thrombogenicity, an effect that persisted, albeit attenuated, in the absence of aspirin.	Ticagrelor	122-132	purinergic receptor P2Y12	Homo sapiens	195-200
33582955-1	2021	Prasugrel and ticagrelor are potent oral platelet P2Y12 inhibitors and are recommended over clopidogrel in patients with acute coronary syndrome (ACS).	Ticagrelor	14-24	purinergic receptor P2Y12	Homo sapiens	50-55
33758122-6	2021	Another recently published VORA-PRATIC (Vorapaxar in Patients with Prior Myocardial Infarction Treated with prasugrel and ticagrelor) study showed that among post-MI patients treated with potent P2Y12 inhibitors (prasugrel or ticagrelor), vorapaxar reduced platelet-driven global thrombogenicity, an effect that persisted, albeit attenuated, in the absence of aspirin.	Ticagrelor	226-236	purinergic receptor P2Y12	Homo sapiens	195-200
33736607-10	2021	In the unadjusted analysis, survival was greater in patients discharged on ticagrelor than on another P2Y12 inhibitor (90.2% vs. 76.7%, Log-rank = 0.001), and the difference was particularly evident in PG-l patients.	Ticagrelor	75-85	purinergic receptor P2Y12	Homo sapiens	102-107
33408862-2	2021	Ticagrelor, a direct-acting potent P2Y12 inhibitor, is superior to clopidogrel in the acute setting of ACS: due to its faster onset and potent antiplatelet inhibition.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	35-40
33668076-1	2021	Dual antiplatelet therapy (DAPT) and subsequent P2Y12 inhibitor monotherapy, particularly ticagrelor, is an emerging treatment strategy in patients undergoing percutaneous coronary intervention (PCI).	Ticagrelor	90-100	purinergic receptor P2Y12	Homo sapiens	48-53
33708263-2	2021	Newer generation P2Y12 inhibitors (i.e. ticagrelor and prasugrel) have demonstrated improved clinical outcomes compared with clopidogrel.	Ticagrelor	40-50	purinergic receptor P2Y12	Homo sapiens	17-22
33563204-0	2022	Ticagrelor Ameliorates Bleomycin-Induced Pulmonary Fibrosis in Rats by Inhibition of TGF-beta1/Smad3 and PI3K/AKT/mTOR Pathways.	Ticagrelor	0-10	transforming growth factor, beta 1	Rattus norvegicus	85-94
33563204-0	2022	Ticagrelor Ameliorates Bleomycin-Induced Pulmonary Fibrosis in Rats by Inhibition of TGF-beta1/Smad3 and PI3K/AKT/mTOR Pathways.	Ticagrelor	0-10	SMAD family member 3	Rattus norvegicus	95-100
33563204-0	2022	Ticagrelor Ameliorates Bleomycin-Induced Pulmonary Fibrosis in Rats by Inhibition of TGF-beta1/Smad3 and PI3K/AKT/mTOR Pathways.	Ticagrelor	0-10	AKT serine/threonine kinase 1	Rattus norvegicus	110-113
32564571-9	2021	However, P-selectin was lower in the ticagrelor group compared with clopidogrel group.	Ticagrelor	37-47	selectin P	Homo sapiens	9-19
33738162-1	2021	Ticagrelor is a potent P2Y12 inhibitor that is increasingly used in acute coronary syndrome.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	23-28
33563204-0	2022	Ticagrelor Ameliorates Bleomycin-Induced Pulmonary Fibrosis in Rats by Inhibition of TGF-beta1/Smad3 and PI3K/AKT/mTOR Pathways.	Ticagrelor	0-10	mechanistic target of rapamycin kinase	Rattus norvegicus	114-118
33563204-10	2022	We found that ticagrelor inhibited TGF-beta1 production and suppressed Smad3 activation and signaling pathway with subsequent inhibition of Slug and Snail.	Ticagrelor	14-24	transforming growth factor, beta 1	Rattus norvegicus	35-44
33563204-10	2022	We found that ticagrelor inhibited TGF-beta1 production and suppressed Smad3 activation and signaling pathway with subsequent inhibition of Slug and Snail.	Ticagrelor	14-24	SMAD family member 3	Rattus norvegicus	71-76
33563204-10	2022	We found that ticagrelor inhibited TGF-beta1 production and suppressed Smad3 activation and signaling pathway with subsequent inhibition of Slug and Snail.	Ticagrelor	14-24	snail family transcriptional repressor 2	Rattus norvegicus	140-144
33563204-11	2022	In addition, ticagrelor antagonized PI3K/AKT/mTOR pathway signaling.	Ticagrelor	13-23	AKT serine/threonine kinase 1	Rattus norvegicus	41-44
33563204-11	2022	In addition, ticagrelor antagonized PI3K/AKT/mTOR pathway signaling.	Ticagrelor	13-23	mechanistic target of rapamycin kinase	Rattus norvegicus	45-49
33563204-12	2022	Moreover, ticagrelor inhibited the EMT that revealed by its ability to up-regulate the epithelial markers as E-cadherin (E-cad) and to decrease the expression of the mesenchymal markers as vimentin (VIM) and alpha-smooth muscle actin (alpha-SMA).	Ticagrelor	10-20	cadherin 1	Rattus norvegicus	109-119
33563204-12	2022	Moreover, ticagrelor inhibited the EMT that revealed by its ability to up-regulate the epithelial markers as E-cadherin (E-cad) and to decrease the expression of the mesenchymal markers as vimentin (VIM) and alpha-smooth muscle actin (alpha-SMA).	Ticagrelor	10-20	cadherin 1	Rattus norvegicus	109-114
33563204-12	2022	Moreover, ticagrelor inhibited the EMT that revealed by its ability to up-regulate the epithelial markers as E-cadherin (E-cad) and to decrease the expression of the mesenchymal markers as vimentin (VIM) and alpha-smooth muscle actin (alpha-SMA).	Ticagrelor	10-20	vimentin	Rattus norvegicus	189-197
33563204-12	2022	Moreover, ticagrelor inhibited the EMT that revealed by its ability to up-regulate the epithelial markers as E-cadherin (E-cad) and to decrease the expression of the mesenchymal markers as vimentin (VIM) and alpha-smooth muscle actin (alpha-SMA).	Ticagrelor	10-20	vimentin	Rattus norvegicus	199-202
33563204-12	2022	Moreover, ticagrelor inhibited the EMT that revealed by its ability to up-regulate the epithelial markers as E-cadherin (E-cad) and to decrease the expression of the mesenchymal markers as vimentin (VIM) and alpha-smooth muscle actin (alpha-SMA).	Ticagrelor	10-20	actin gamma 2, smooth muscle	Rattus norvegicus	208-233
33563204-13	2022	CONCLUSION: Our results suggest that the P2Y12 inhibitor, ticagrelor may have a therapeutic potential in reducing the progression of PF.	Ticagrelor	58-68	purinergic receptor P2Y12	Rattus norvegicus	41-46
33400617-1	2021	This study was to evaluate the effect of resveratrol on the pharmacokinetics of ticagrelor in rats and the metabolism of ticagrelor in human CYP3A4 and liver microsomes.	Ticagrelor	121-131	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	141-147
32915088-4	2021	Pharmacokinetic exposure (AUCinf = 1472 ng h/mL) associated with administration of 10 mg/kg of dronedarone increased significantly, with delayed T max in the group that received ticagrelor-pretreatment when compared to the dronedarone only group (AUCinf = 723 ng h/mL).	Ticagrelor	178-188	thrombopoietin	Mus musculus	45-47
32915088-4	2021	Pharmacokinetic exposure (AUCinf = 1472 ng h/mL) associated with administration of 10 mg/kg of dronedarone increased significantly, with delayed T max in the group that received ticagrelor-pretreatment when compared to the dronedarone only group (AUCinf = 723 ng h/mL).	Ticagrelor	178-188	thrombopoietin	Mus musculus	265-267
32915088-5	2021	In addition, pharmacokinetic exposure (AUCinf = 2391 ng h/mL) associated with administration of 10 mg/kg of ticagrelor increased significantly, with increased K el (0.31 h-1) and decreased V z/F (14.6 L/kg) in the dronedarone-pretreatment group when compared to the ticagrelor only group (AUCinf = 1616 ng h/mL; K el = 0.21 h-1; V z/F  =  31.3 L/kg).	Ticagrelor	108-118	thrombopoietin	Mus musculus	58-60
32915088-5	2021	In addition, pharmacokinetic exposure (AUCinf = 2391 ng h/mL) associated with administration of 10 mg/kg of ticagrelor increased significantly, with increased K el (0.31 h-1) and decreased V z/F (14.6 L/kg) in the dronedarone-pretreatment group when compared to the ticagrelor only group (AUCinf = 1616 ng h/mL; K el = 0.21 h-1; V z/F  =  31.3 L/kg).	Ticagrelor	108-118	thrombopoietin	Mus musculus	59-60
32915088-5	2021	In addition, pharmacokinetic exposure (AUCinf = 2391 ng h/mL) associated with administration of 10 mg/kg of ticagrelor increased significantly, with increased K el (0.31 h-1) and decreased V z/F (14.6 L/kg) in the dronedarone-pretreatment group when compared to the ticagrelor only group (AUCinf = 1616 ng h/mL; K el = 0.21 h-1; V z/F  =  31.3 L/kg).	Ticagrelor	108-118	thrombopoietin	Mus musculus	308-310
32915088-5	2021	In addition, pharmacokinetic exposure (AUCinf = 2391 ng h/mL) associated with administration of 10 mg/kg of ticagrelor increased significantly, with increased K el (0.31 h-1) and decreased V z/F (14.6 L/kg) in the dronedarone-pretreatment group when compared to the ticagrelor only group (AUCinf = 1616 ng h/mL; K el = 0.21 h-1; V z/F  =  31.3 L/kg).	Ticagrelor	108-118	thrombopoietin	Mus musculus	201-202
33262250-7	2021	Twenty-one compounds inhibited uridine uptake and abacavir, nevirapine, ticagrelor, and uridine triacetate had different IC50 values for ENT1 and ENT2.	Ticagrelor	72-82	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	137-141
33262250-7	2021	Twenty-one compounds inhibited uridine uptake and abacavir, nevirapine, ticagrelor, and uridine triacetate had different IC50 values for ENT1 and ENT2.	Ticagrelor	72-82	solute carrier family 29 member 2	Homo sapiens	146-150
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.	Ticagrelor	81-91	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.	Ticagrelor	126-136	NLR family, pyrin domain containing 3	Rattus norvegicus	186-191
33551797-17	2020	Conclusion: This study confirms that efficiently returned CYP2C19 genotype results did partially guide cardiologists to prescribe ticagrelor for patients with a LOF allele, and that clopidogrel had a higher risk of MACCE than ticagrelor in these patients, which provides support for the implementation of CYP2C19 gene-guided antiplatelet therapy in clinical practice.	Ticagrelor	130-140	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	58-65
33400617-4	2021	The vitro experiment was performed to examine the influence of resveratrol on ticagrelor metabolism in CYP3A4*1, human, and rat liver microsomes.	Ticagrelor	78-88	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	103-109
33302757-0	2020	When Less Becomes More: Insights on the Pharmacodynamic Effects of Aspirin Withdrawal in Patients With Potent Platelet P2Y12 Inhibition Induced by Ticagrelor.	Ticagrelor	147-157	purinergic receptor P2Y12	Homo sapiens	119-124
33411687-8	2020	Our findings showed that ticagrelor/aspirin therapy possessed greater platelet inhibition and more rapid onset in platelet inhibition compared with clopidogrel/aspirin therapy both in carriers and non-carriers of CYP2C19 lose-of-function alleles with acute minor stroke or TIA.	Ticagrelor	25-35	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	213-220
33334129-1	2021	Ticagrelor is a potent reversible P2Y12 inhibitor with proven superiority over clopidogrel.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	34-39
32853794-6	2020	ASA alone or in combination with ticagrelor(a P2Y12 blocker) affected platelet aggregation associated with profound inhibition of TXB2 generation.	Ticagrelor	33-43	purinergic receptor P2Y12	Homo sapiens	46-51
32513604-2	2020	Prasugrel and ticagrelor are commonly used P2Y12 inhibitors, and a few head-to-head randomized control trials (RCTs) have been performed.	Ticagrelor	14-24	purinergic receptor P2Y12	Homo sapiens	43-48
33114045-7	2020	Ticagrelor was the most frequently prescribed P2Y12 inhibitor among patients below 70 years old, and clopidogrel in those aged >=70 years.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	46-51
33306876-0	2020	Ticagrelor monotherapy: When is mono-antiplatelet therapy (MAPT) equivalent or better?	Ticagrelor	0-10	microtubule associated protein tau	Homo sapiens	59-63
32916566-0	2020	Impact of the rs73598374 polymorphism of the adenosine deaminase gene on platelet reactivity and long-term outcomes among patients with acute coronary syndrome treated with ticagrelor.	Ticagrelor	173-183	adenosine deaminase	Homo sapiens	45-64
32916566-3	2020	Therefore, the aim of our study was to explore the impact of the rs73598374 polymorphism of ADA gene on platelet reactivity in ACS patients treated with ticagrelor.	Ticagrelor	153-163	adenosine deaminase	Homo sapiens	92-95
32390477-3	2020	The newer P2Y12 inhibitors (prasugrel and ticagrelor) have better efficacy than clopidogrel.	Ticagrelor	42-52	purinergic receptor P2Y12	Homo sapiens	10-15
33142937-3	2020	Using in vitro methods, we show that inhibition of P2Y12 with ticagrelor enhances tumor cell phagocytosis by macrophages and induces an anti-tumoral phenotype.	Ticagrelor	62-72	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	51-56
33142937-5	2020	Inhibiting the UPR with tauroursodeoxycholic acid (Tudca) diminishes the pro-phagocytotic effect of ticagrelor, thereby indicating that P2Y12 mediates macrophage function through activation of ER stress pathways.	Ticagrelor	100-110	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	136-141
32766961-5	2020	RESULTS: The mean P2Y12 reaction units (PRU) score on ticagrelor was significantly less compared to that of clopidogrel (50.4, 95% confidence interval (CI) 29-73.9; vs. 149.6, 95% CI 129.4-169.9; p value < 0.001).	Ticagrelor	54-64	purinergic receptor P2Y12	Homo sapiens	18-23
33336751-1	2020	OBJECTIVE: To investigate the therapeutic effects of ticagrelor and clopidogrel on patients with acute myocardial infarction (AMI) and its effect of lncRNA BANCR.	Ticagrelor	53-63	BRAF-activated non-protein coding RNA	Homo sapiens	156-161
33275460-0	2020	Effects of atorvastatin and ticagrelor combination therapy on renal function and the levels of suppression of tumorigenicity 2 and interleukin-33 in patients with ST-segment elevation myocardial infarction.	Ticagrelor	28-38	ST2	Homo sapiens	95-126
33275460-0	2020	Effects of atorvastatin and ticagrelor combination therapy on renal function and the levels of suppression of tumorigenicity 2 and interleukin-33 in patients with ST-segment elevation myocardial infarction.	Ticagrelor	28-38	interleukin 33	Homo sapiens	131-145
33654473-2	2020	In the last decade, the arrival of prasugrel and ticagrelor, faster and more powerful oral platelet receptor P2Y12 inhibitors compared to clopidogrel, significantly improved platelet inhibition in patients with ACS.	Ticagrelor	49-59	purinergic receptor P2Y12	Homo sapiens	109-114
33313086-9	2020	Ticagrelor treatment led to significant increases in circulating miR-223 levels compared with clopidogrel treatment.	Ticagrelor	0-10	microRNA 223	Homo sapiens	65-72
33313086-11	2020	Circulating miR-223 levels were significantly elevated with ticagrelor treatment compared with clopidogrel treatment.	Ticagrelor	60-70	microRNA 223	Homo sapiens	12-19
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.	Ticagrelor	114-124	microRNA 223	Homo sapiens	0-7
33107944-1	2020	Importance: Current guidelines recommend ticagrelor as the preferred P2Y12 platelet inhibitor for patients with acute coronary syndrome (ACS), primarily based on a single large randomized clinical trial.	Ticagrelor	41-51	purinergic receptor P2Y12	Homo sapiens	69-74
32856376-7	2020	Ticagrelor treatment in diabetic mice lowered urinary albumin excretion, it prevented diabetes-induced mesangial matrix expansion, podocyte effacement, and glomerular endothelial cell injury, which includes loss of endothelial fenestrations, ICAM-1 expression, and PECAM expression.	Ticagrelor	0-10	albumin	Mus musculus	54-61
31893974-1	2020	Ticagrelor is an antagonist of both platelet adenosine diphosphate (ADP) receptor P2Y12 and equilibrative nucleoside transporter-1.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	82-87
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.	Ticagrelor	44-54	purinergic receptor P2Y12	Homo sapiens	4-10
32822211-6	2020	In addition to targeting platelets, ticagrelor may exert P2Y12R-independent effect by targeting erythrocyte-mediated purinergic activation.	Ticagrelor	36-46	purinergic receptor P2Y12	Homo sapiens	57-63
33065552-10	2020	Ticagrelor was superior to clopidogrel in inhibiting platelet reactivity measured by TEG platelet mapping among patients with acute minor stroke or TIA, particularly in carriers of the CYP2C19 LOF alleles.	Ticagrelor	0-10	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	185-192
32856376-7	2020	Ticagrelor treatment in diabetic mice lowered urinary albumin excretion, it prevented diabetes-induced mesangial matrix expansion, podocyte effacement, and glomerular endothelial cell injury, which includes loss of endothelial fenestrations, ICAM-1 expression, and PECAM expression.	Ticagrelor	0-10	intercellular adhesion molecule 1	Mus musculus	242-248
32856376-7	2020	Ticagrelor treatment in diabetic mice lowered urinary albumin excretion, it prevented diabetes-induced mesangial matrix expansion, podocyte effacement, and glomerular endothelial cell injury, which includes loss of endothelial fenestrations, ICAM-1 expression, and PECAM expression.	Ticagrelor	0-10	platelet/endothelial cell adhesion molecule 1	Mus musculus	265-270
32856376-9	2020	This tubular protection is likely to be a result of protection to the glomerular endothelium by ticagrelor, which reduces albuminuria and albumin toxicity to the tubules and reduced tubular and interstitial inflammation and fibrosis.	Ticagrelor	96-106	albumin	Mus musculus	122-129
32152791-8	2020	Risk of recurrent 1-year primary endpoint remained higher for HPR patients switched to either ticagrelor or prasugrel as compared to subjects who had low on treatment platelet reactivity (n = 144) (LPR) on clopidogrel [Hazard Ratio: 3.5 (95% CI 1.1-11.1); p = 0.036)].	Ticagrelor	94-104	haptoglobin-related protein	Homo sapiens	62-65
32960097-1	2021	Ticagrelor is a potent and orally active P2Y12 inhibitor.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	41-46
32675750-0	2020	Diabetes and CYP2C19 Polymorphism Synergistically Impair the Antiplatelet Activity of Clopidogrel Compared to Ticagrelor in PCI-Treated ACS Patients.	Ticagrelor	110-120	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
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.	Ticagrelor	153-163	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	43-50
32152791-3	2020	Prasugrel and ticagrelor are more potent P2Y12 inhibitors than clopidogrel and commonly substituted for clopidogrel when HPR is documented, however benefit of VN guided intensified antiplatelet therapy is uncertain.	Ticagrelor	14-24	purinergic receptor P2Y12	Homo sapiens	41-46
32960097-3	2021	The pharmacokinetics and pharmacodynamics of Ticagrelor result in more rapid and effective inhibition of platelet activation compared with other P2Y12 inhibitors.	Ticagrelor	45-55	purinergic receptor P2Y12	Homo sapiens	145-150
32679592-7	2020	Plasma levels of VWF activity predicted 1-year (hazard ratio [HR]: 2.68; 95% CI: 1.14-6.31; p < 0.024) and long-term (HR: 2.59; 95% CI: 1.10-6.09) mortality despite treatment with potent platelet inhibitors (dual-antiplatelet therapy with aspirin and prasugrel or ticagrelor).	Ticagrelor	264-274	von Willebrand factor	Homo sapiens	17-20
32772110-7	2020	DAPT with low-dose ASA and ticagrelor [odds ratio (OR) 2.53, 95% credible interval (CrI) 1.35-4.72; I2 = 55; low certainty] or clopidogrel (OR 1.56, 95% CrI 1.02-2.39; I2 = 55; very low certainty) improved saphenous vein graft patency when compared to low-dose ASA monotherapy.	Ticagrelor	27-37	EP300 interacting inhibitor of differentiation 1	Homo sapiens	65-90
32942754-1	2020	In acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI), treatment with the P2Y12 inhibitors ticagrelor or prasugrel is recommended over clopidogrel due to a better efficacy, albeit having more bleeding complication.	Ticagrelor	131-141	purinergic receptor P2Y12	Homo sapiens	114-119
32832010-2	2020	Here, we investigate whether direct NLRP3 inflammasome inhibition exerts additive effects on myocardial protection induced by the P2Y12 receptor antagonist Ticagrelor.	Ticagrelor	156-166	NLR family, pyrin domain containing 3	Rattus norvegicus	36-41
32840598-7	2020	CYP2C19 LOF carriers were prescribed ticagrelor and noncarriers clopidogrel.	Ticagrelor	37-47	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
33204945-1	2020	Background: Ticagrelor is a widely used P2Y12 inhibitor and represents a fundamental therapeutic agent in acute coronary syndrome treatment and selected post-percutaneous coronary intervention (PCI) cases.	Ticagrelor	12-22	purinergic receptor P2Y12	Homo sapiens	40-45
32353222-11	2020	VWF staining was significantly lower in the ASA+Ticagrelor+UFH group compared with that in the other groups on the 3rd day (p=0.005).	Ticagrelor	48-58	von Willebrand factor	Homo sapiens	0-3
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.	Ticagrelor	97-107	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-20
32832010-2	2020	Here, we investigate whether direct NLRP3 inflammasome inhibition exerts additive effects on myocardial protection induced by the P2Y12 receptor antagonist Ticagrelor.	Ticagrelor	156-166	purinergic receptor P2Y12	Rattus norvegicus	130-135
32832010-9	2020	Myocardial IR induced the NLRP3 inflammasome complex formation, which was attenuated by either INF pretreatment ex vivo, or by repeated oral treatment with Ticagrelor.	Ticagrelor	156-166	NLR family, pyrin domain containing 3	Rattus norvegicus	26-31
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.	Ticagrelor	56-66	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	122-129
31542850-1	2020	INTRODUCTION: Despite the use of the new generation P2Y12 inhibitors (Ticagrelor and Prasugrel) with aspirin is the recommended therapy in acute NSTE-ACS patients, their current use in clinical practice remains quite low and might be related, among several variables, with increased comorbidity burden.	Ticagrelor	70-80	purinergic receptor P2Y12	Homo sapiens	52-57
31542850-6	2020	RESULTS: A total of 629 patients were included, median age 67 years, 23.2% women, 359 patients (57.1%) treated with clopidogrel and 40.6% with new P2Y12 inhibitors: ticagrelor (228 patients, 36.2%) and prasugrel (30 patients, 4.8%).	Ticagrelor	165-175	purinergic receptor P2Y12	Homo sapiens	147-152
32784868-1	2020	In the current era, the antithrombotic treatment of patients with non-ST segment elevation acute coronary syndrome (NSTE-ACS) includes standard aspirin, and one of the potent P2Y12 inhibitors ticagrelor or prasugrel.	Ticagrelor	192-202	purinergic receptor P2Y12	Homo sapiens	175-180
32320492-12	2020	CONCLUSION: CYP2C19 reduced-metabolizers can expect better clinical outcome on using prasugrel or ticagrelor rather than clopidogrel.	Ticagrelor	98-108	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
32335797-0	2020	Dapagliflozin and Ticagrelor Have Additive Effects on the Attenuation of the Activation of the NLRP3 Inflammasome and the Progression of Diabetic Cardiomyopathy: an AMPK-mTOR Interplay.	Ticagrelor	18-28	NLR family, pyrin domain containing 3	Mus musculus	95-100
32335797-0	2020	Dapagliflozin and Ticagrelor Have Additive Effects on the Attenuation of the Activation of the NLRP3 Inflammasome and the Progression of Diabetic Cardiomyopathy: an AMPK-mTOR Interplay.	Ticagrelor	18-28	mechanistic target of rapamycin kinase	Mus musculus	170-174
32335797-1	2020	PURPOSE: Ticagrelor, a P2Y12 receptor antagonist, and dapagliflozin, a sodium-glucose-cotransporter-2 inhibitor, suppress the activation of the NLRP3 inflammasome.	Ticagrelor	9-19	NLR family, pyrin domain containing 3	Mus musculus	144-149
32335797-13	2020	CONCLUSIONS: Both dapagliflozin and ticagrelor attenuated the progression of diabetic cardiomyopathy, the activation of the NLRP3 inflammasome, and fibrosis in BTBR mice with additive effects of the combination.	Ticagrelor	36-46	NLR family, pyrin domain containing 3	Mus musculus	124-129
32662726-5	2020	EXPERT OPINION: The results of the THEMIS trial, conducted in DM patients with stable coronary artery disease and no prior stroke or myocardial infarction, showed that although ticagrelor in addition to aspirin reduced the risk of ischemic events, this was associated with a parallel increase in bleeding complications.	Ticagrelor	177-187	thymocyte selection associated	Homo sapiens	35-41
32821149-2	2020	Current clinical practice guidelines now recommend more potent P2Y12 inhibitors (prasugrel or ticagrelor) over clopidogrel in acute coronary syndrome (ACS).	Ticagrelor	94-104	purinergic receptor P2Y12	Homo sapiens	63-68
32585929-2	2020	Current clinical guidelines recommend novel P2Y12 inhibitors (e.g., prasugrel or ticagrelor) in addition to aspirin based on the results of representative randomized controlled trials conducted predominantly in Western countries.	Ticagrelor	81-91	purinergic receptor P2Y12	Homo sapiens	44-49
32473356-4	2020	METHODS: Assessment of Loading with the P2Y12 inhibitor ticagrelor or clopidogrel to Halt ischemic Events in patients Undergoing elective coronary Stenting (ALPHEUS) (NCT02617290) is an international, multicenter, randomized, parallel-group, open-label study in patients with stable coronary artery disease who are planned for an elective PCI.	Ticagrelor	56-66	purinergic receptor P2Y12	Homo sapiens	40-45
32546773-1	2020	Dabigatran etexilate (DABE) is a direct oral anticoagulant (DOAC) and may be combined with ticagrelor, a P2Y12 inhibitor with antiplatelet effects.	Ticagrelor	91-101	purinergic receptor P2Y12	Homo sapiens	105-110
32493215-7	2020	Carriers of a CYP2C19*2 loss-of-function allele receive prasugrel or ticagrelor, while non-carriers are treated with clopidogrel.	Ticagrelor	69-79	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
32240760-1	2020	BACKGROUND: P2Y12 inhibitor monotherapy with ticagrelor after a brief period of dual antiplatelet therapy can reduce bleeding without increasing ischemic harm after percutaneous coronary intervention (PCI).	Ticagrelor	45-55	purinergic receptor P2Y12	Homo sapiens	12-17
32704557-1	2020	Background: THEMIS (NCT01991795) showed that in patients with type 2 diabetes (T2D) and stable coronary artery disease (CAD) but with no prior myocardial infarction (MI) or stroke, ticagrelor plus acetylsalicylic acid (ASA) decreased the incidence of ischaemic cardiovascular events compared with placebo plus ASA.	Ticagrelor	181-191	thymocyte selection associated	Homo sapiens	12-18
32301059-0	2020	Ticagrelor reverses the mitochondrial dysfunction through preventing accumulated autophagosomes-dependent apoptosis and ER stress in insulin-resistant H9c2 myocytes.	Ticagrelor	0-10	insulin	Homo sapiens	133-140
32301059-5	2020	We found that ticagrelor treatment significantly prevented depolarization of mitochondrial membrane potential and increases in reactive oxygen species with a marked increase in the ATP level in insulin-resistant H9c2 cells.	Ticagrelor	14-24	insulin	Homo sapiens	194-201
32301059-6	2020	Ticagrelor treatment also reversed the increases in the resting level of free Ca2+ and mRNA level of P2Y12 receptors as well as preserved ER stress and apoptosis in insulin-resistant H9c2 cells.	Ticagrelor	0-10	purinergic receptor P2Y12	Rattus norvegicus	101-106
32301059-6	2020	Ticagrelor treatment also reversed the increases in the resting level of free Ca2+ and mRNA level of P2Y12 receptors as well as preserved ER stress and apoptosis in insulin-resistant H9c2 cells.	Ticagrelor	0-10	insulin	Homo sapiens	165-172
32301059-7	2020	Furthermore, we determined marked repression with ticagrelor treatment in the increased number of autophagosomes and degeneration of mitochondrion, including swelling and loss of crista besides recoveries in enlargement and irregularity seen in SER in insulin-resistant H9c2 cells.	Ticagrelor	50-60	insulin	Homo sapiens	252-259
32301059-8	2020	Moreover, ticagrelor treatment could prevent the altered mRNA levels of Becklin-1 and type 1 equilibrative nucleoside transporter (ENT1), which are parallel to the preservation of ultrastructural ones.	Ticagrelor	10-20	solute carrier family 29 member 1	Rattus norvegicus	131-135
32301059-9	2020	Our overall data demonstrated that ticagrelor can directly affect cardiomyocytes and provide marked protection against ER stress and dramatic induction of autophagosomes, and therefore, can alleviate the ER stress-induced oxidative stress increase and cell apoptosis during insulin resistance.	Ticagrelor	35-45	insulin	Homo sapiens	274-281
32100736-6	2020	In addition, whether the use of PPIs may affect the clinical efficacy of the new P2Y12 receptor antagonists, ticagrelor and prasugrel, remains less known.	Ticagrelor	109-119	purinergic receptor P2Y12	Homo sapiens	81-86
32266041-1	2020	The aim of the study was to compare the clinical efficacy and safety of ticagrelor and clopidogrel in patients with coronary heart disease one year after percutaneous coronary intervention (PCI), and to explore their association with the CYP2C19 gene polymorphism.	Ticagrelor	72-82	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	238-245
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.	Ticagrelor	170-180	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	143-150
32373308-2	2020	Ticagrelor, a reversibly binding P2Y12 antiplatelet agent, has shown superiority to clopidogrel in prevention of ischemic events and death, but is also associated with a small increase in the incidence of intracranial bleeding.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	33-38
32140798-0	2020	Ticagrelor Versus Clopidogrel in Patients with Two CYP2C19 Loss-of-Function Alleles Undergoing Percutaneous Coronary Intervention.	Ticagrelor	0-10	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	51-58
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).	Ticagrelor	133-143	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	80-87
32140798-11	2020	CONCLUSIONS: In patients with two CYP2C19 loss-of-function alleles, ticagrelor was more effective than clopidogrel in preventing cardiovascular events, while the two antiplatelet agents were associated with similar incidences of major bleeding.	Ticagrelor	68-78	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	34-41
32074647-2	2020	The past 30 years has seen the progress from early trials of clopidogrel and glycoprotein IIb/IIIa inhibitors to the application of more potent P2Y12 inhibitors prasugrel and ticagrelor.	Ticagrelor	175-185	purinergic receptor P2Y12	Homo sapiens	144-149
31665395-8	2020	Unlike clopidogrel, ticagrelor is a direct P2Y12 inhibitor that does not require metabolism to an active metabolite.	Ticagrelor	20-30	purinergic receptor P2Y12	Homo sapiens	43-48
31302083-2	2020	This report describes a case of stent thrombosis in a patient who discontinued a P2Y12 inhibitor (ticagrelor) for 3 days before coronary artery bypass grafting.	Ticagrelor	98-108	purinergic receptor P2Y12	Homo sapiens	81-86
31833175-1	2020	BACKGROUND: Platelet P2Y12 antagonist ticagrelor reduces mortality after acute myocardial infarction (AMI) compared to clopidogrel, but the underlying mechanism is unknown.	Ticagrelor	38-48	purinergic receptor P2Y12	Homo sapiens	21-26
32106619-1	2020	Ticagrelor is a powerful P2Y12 inhibitor with pleiotropic effects in the cardiovascular system.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	25-30
32106619-5	2020	We found that 1-month treatment with ticagrelor, but not clopidogrel, led to increased levels of SIRT1 and HES1 mRNAs.	Ticagrelor	37-47	sirtuin 1	Homo sapiens	97-102
32106619-5	2020	We found that 1-month treatment with ticagrelor, but not clopidogrel, led to increased levels of SIRT1 and HES1 mRNAs.	Ticagrelor	37-47	hes family bHLH transcription factor 1	Homo sapiens	107-111
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.	Ticagrelor	25-35	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.	Ticagrelor	25-35	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.	Ticagrelor	25-35	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.	Ticagrelor	25-35	epidermal growth factor	Homo sapiens	174-177
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.	Ticagrelor	239-249	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.	Ticagrelor	239-249	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.	Ticagrelor	239-249	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.	Ticagrelor	141-151	vasodilator stimulated phosphoprotein	Homo sapiens	55-92
32051439-2	2020	Here, we identify how release of pro-survival exosomes from human cardiac-derived mesenchymal progenitor cells (hCPCs) is regulated by clinically relevant dose of ticagrelor (1 muM), an oral selective and reversible non-thienopyridine P2Y12 inhibitor.	Ticagrelor	163-173	purinergic receptor P2Y12	Homo sapiens	235-240
32051439-5	2020	While it is known that pan-Aurora kinase inhibitor halts cell proliferation through dephosphorylation of histone H3 residue Ser10, we demonstrate that it also prevents ticagrelor-induced effects on release of cardiac progenitor cell-derived exosomes delivering anti-apoptotic HSP70.	Ticagrelor	168-178	heat shock protein family A (Hsp70) member 4	Homo sapiens	276-281
32062795-7	2020	In contrast, Pam3CSK4-induced platelet surface expression of P-selectin and activated GPIIb/IIIa were significantly lower in ticagrelor-treated patients (both p <= 0.005).	Ticagrelor	125-135	selectin P	Homo sapiens	61-71
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.	Ticagrelor	141-151	vasodilator stimulated phosphoprotein	Homo sapiens	94-98
32062795-7	2020	In contrast, Pam3CSK4-induced platelet surface expression of P-selectin and activated GPIIb/IIIa were significantly lower in ticagrelor-treated patients (both p <= 0.005).	Ticagrelor	125-135	integrin subunit alpha 2b	Homo sapiens	86-91
32062795-9	2020	Finally, PAR-4 mediated platelet activation as assessed by platelet surface expression of activated GPIIb/IIIa following stimulation with AYPGKF was significantly lower in patients receiving ticagrelor (p = 0.02).	Ticagrelor	191-201	F2R like thrombin or trypsin receptor 3	Homo sapiens	9-14
31442298-3	2020	Ticagrelor-based DAPT and ticagrelor-monotherapy significantly decreased MEA-ADP (Deltamean: -51.4 (-56.9; -45.8) and -46.2 (-51.7; -40.7)) and VASP (Deltamean: -70.3 (-76.2; -64.4) and -69.6 (-75.5; -63.7)) at 2 hours and over 24 hours.	Ticagrelor	0-10	vasodilator stimulated phosphoprotein	Homo sapiens	144-148
32062795-9	2020	Finally, PAR-4 mediated platelet activation as assessed by platelet surface expression of activated GPIIb/IIIa following stimulation with AYPGKF was significantly lower in patients receiving ticagrelor (p = 0.02).	Ticagrelor	191-201	integrin subunit alpha 2b	Homo sapiens	100-105
32062795-10	2020	CONCLUSION: Ticagrelor inhibits TLR-1/2 and PAR mediated platelet activation in ACS patients more strongly than prasugrel.	Ticagrelor	12-22	toll like receptor 1	Homo sapiens	32-39
32062795-10	2020	CONCLUSION: Ticagrelor inhibits TLR-1/2 and PAR mediated platelet activation in ACS patients more strongly than prasugrel.	Ticagrelor	12-22	nuclear receptor subfamily 1 group I member 2	Homo sapiens	44-47
32062795-8	2020	Moreover, SFLLRN-induced platelet surface expression of P-selectin and activated GPIIb/IIIa were significantly less pronounced in patients on ticagrelor therapy compared to prasugrel-treated patients (both p < 0.03).	Ticagrelor	142-152	selectin P	Homo sapiens	56-66
32062795-8	2020	Moreover, SFLLRN-induced platelet surface expression of P-selectin and activated GPIIb/IIIa were significantly less pronounced in patients on ticagrelor therapy compared to prasugrel-treated patients (both p < 0.03).	Ticagrelor	142-152	integrin subunit alpha 2b	Homo sapiens	81-86
31442298-3	2020	Ticagrelor-based DAPT and ticagrelor-monotherapy significantly decreased MEA-ADP (Deltamean: -51.4 (-56.9; -45.8) and -46.2 (-51.7; -40.7)) and VASP (Deltamean: -70.3 (-76.2; -64.4) and -69.6 (-75.5; -63.7)) at 2 hours and over 24 hours.	Ticagrelor	26-36	vasodilator stimulated phosphoprotein	Homo sapiens	144-148
30585111-12	2020	We expect that plasma from patients treated with ticagrelor (1) contains lower concentrations of EVs from activated platelets, exposing fibrinogen, exposing PS, from leukocytes and from endothelial cells and (2) has lower procoagulant activity, when compared to patients treated with clopidogrel.	Ticagrelor	49-59	fibrinogen beta chain	Homo sapiens	136-146
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.	Ticagrelor	47-57	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.	Ticagrelor	69-79	interleukin 6	Homo sapiens	195-199
31738933-9	2020	In the presence of ticagrelor, blockage of the P2Y1 receptor prevented restoration of platelet aggregation by the combination of epinephrine and ADP, as well as intracellular Ca2+ mobilisation.	Ticagrelor	19-29	purinergic receptor P2Y1	Homo sapiens	47-60
31738933-10	2020	In combination with ADP, epinephrine induced platelet aggregation of ticagrelor-treated platelets through inhibition of the cAMP pathway and activation of the PI3K pathway, thus enabling the P2Y1 receptor signalling and subsequent Ca2+ mobilisation.	Ticagrelor	69-79	purinergic receptor P2Y1	Homo sapiens	191-204
30585111-3	2020	The more potent P2Y12 antagonist ticagrelor improves cardiovascular outcome in patients after AMI compared to the less potent clopidogrel, suggesting that greater inhibition of platelet aggregation is associated with better prognosis.	Ticagrelor	33-43	purinergic receptor P2Y12	Homo sapiens	16-21
31351022-5	2019	The VASP index was used to assess PR after ticagrelor loading dose (LD).	Ticagrelor	43-53	vasodilator stimulated phosphoprotein	Homo sapiens	4-8
31888640-0	2019	Ticagrelor and clopidogrel suppress NF-kappaB signaling pathway to alleviate LPS-induced dysfunction in vein endothelial cells.	Ticagrelor	0-10	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.	Ticagrelor	24-34	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.	Ticagrelor	9-19	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.	Ticagrelor	9-19	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.	Ticagrelor	9-19	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.	Ticagrelor	9-19	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.	Ticagrelor	9-19	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.	Ticagrelor	9-19	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.	Ticagrelor	9-19	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.	Ticagrelor	9-19	interleukin 2	Homo sapiens	199-203
31888640-8	2019	CONCLUSIONS: Ticagrelor and clopidogrel alleviate cellular dysfunction through suppressing NF-KappaB signaling pathway.	Ticagrelor	13-23	nuclear factor kappa B subunit 1	Homo sapiens	91-100
31351022-13	2019	CONCLUSION: In patients receiving a ticagrelor LD while undergoing PCI for ACS, PR using the VASP did not predict MACE or bleeding, but it was significantly associated with the occurrence of definite acute stent thrombosis.	Ticagrelor	36-46	vasodilator stimulated phosphoprotein	Homo sapiens	93-97
31500011-6	2019	As a result of the statistical approach, TCG-SM (490 mg) was successfully solidified with Nesulin US2 (167.8 mg) and Florite R (82.2 mg), which showed good powder properties and improved dissolution of TCG.	Ticagrelor	41-44	usherin	Homo sapiens	98-101
31600634-6	2019	RESULTS: Ticagrelor, empagliflozin and tamoxifen significantly increased aorta tissue AMPK and eNOS and decreased Ang-II, ET-1, P-selectin, VCAM-1 and VIP levels compared with RA/DM-co-morbidity, coupled with improved acetylcholine vasorelaxation in vitro.	Ticagrelor	9-19	angiotensinogen	Rattus norvegicus	114-120
31600634-6	2019	RESULTS: Ticagrelor, empagliflozin and tamoxifen significantly increased aorta tissue AMPK and eNOS and decreased Ang-II, ET-1, P-selectin, VCAM-1 and VIP levels compared with RA/DM-co-morbidity, coupled with improved acetylcholine vasorelaxation in vitro.	Ticagrelor	9-19	endothelin 1	Rattus norvegicus	122-126
31600634-6	2019	RESULTS: Ticagrelor, empagliflozin and tamoxifen significantly increased aorta tissue AMPK and eNOS and decreased Ang-II, ET-1, P-selectin, VCAM-1 and VIP levels compared with RA/DM-co-morbidity, coupled with improved acetylcholine vasorelaxation in vitro.	Ticagrelor	9-19	selectin P	Rattus norvegicus	128-138
31600634-6	2019	RESULTS: Ticagrelor, empagliflozin and tamoxifen significantly increased aorta tissue AMPK and eNOS and decreased Ang-II, ET-1, P-selectin, VCAM-1 and VIP levels compared with RA/DM-co-morbidity, coupled with improved acetylcholine vasorelaxation in vitro.	Ticagrelor	9-19	vascular cell adhesion molecule 1	Rattus norvegicus	140-146
31600634-6	2019	RESULTS: Ticagrelor, empagliflozin and tamoxifen significantly increased aorta tissue AMPK and eNOS and decreased Ang-II, ET-1, P-selectin, VCAM-1 and VIP levels compared with RA/DM-co-morbidity, coupled with improved acetylcholine vasorelaxation in vitro.	Ticagrelor	9-19	vasoactive intestinal peptide	Rattus norvegicus	151-154
31600634-7	2019	CONCLUSION: Ticagrelor, empagliflozin and tamoxifen may correct vascular reactivity defects, where modulation of vascular AMPK, eNOS, Ang-II, ET-1, P-selectin, VCAM-1 and MMP-2 underline their protective effects.	Ticagrelor	12-22	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	122-126
31600634-7	2019	CONCLUSION: Ticagrelor, empagliflozin and tamoxifen may correct vascular reactivity defects, where modulation of vascular AMPK, eNOS, Ang-II, ET-1, P-selectin, VCAM-1 and MMP-2 underline their protective effects.	Ticagrelor	12-22	nitric oxide synthase 3	Rattus norvegicus	128-132
31600634-7	2019	CONCLUSION: Ticagrelor, empagliflozin and tamoxifen may correct vascular reactivity defects, where modulation of vascular AMPK, eNOS, Ang-II, ET-1, P-selectin, VCAM-1 and MMP-2 underline their protective effects.	Ticagrelor	12-22	vascular cell adhesion molecule 1	Rattus norvegicus	160-166
31600634-7	2019	CONCLUSION: Ticagrelor, empagliflozin and tamoxifen may correct vascular reactivity defects, where modulation of vascular AMPK, eNOS, Ang-II, ET-1, P-selectin, VCAM-1 and MMP-2 underline their protective effects.	Ticagrelor	12-22	matrix metallopeptidase 2	Rattus norvegicus	171-176
31600634-6	2019	RESULTS: Ticagrelor, empagliflozin and tamoxifen significantly increased aorta tissue AMPK and eNOS and decreased Ang-II, ET-1, P-selectin, VCAM-1 and VIP levels compared with RA/DM-co-morbidity, coupled with improved acetylcholine vasorelaxation in vitro.	Ticagrelor	9-19	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	86-90
31600634-6	2019	RESULTS: Ticagrelor, empagliflozin and tamoxifen significantly increased aorta tissue AMPK and eNOS and decreased Ang-II, ET-1, P-selectin, VCAM-1 and VIP levels compared with RA/DM-co-morbidity, coupled with improved acetylcholine vasorelaxation in vitro.	Ticagrelor	9-19	nitric oxide synthase 3	Rattus norvegicus	95-99
31218354-0	2019	Efficacy and safety with ticagrelor in patients with prior myocardial infarction in the approved European label: insights from PEGASUS-TIMI 54.	Ticagrelor	25-35	IKAROS family zinc finger 5	Homo sapiens	127-142
30972696-1	2019	BACKGROUND AND OBJECTIVE: Ticagrelor, a reversible P2Y12 platelet inhibitor, is under investigation as a sickle cell disease (SCD) therapy in children.	Ticagrelor	26-36	purinergic receptor P2Y12	Homo sapiens	51-56
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).	Ticagrelor	143-153	purinergic receptor P2Y12	Homo sapiens	112-117
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).	Ticagrelor	76-86	purinergic receptor P2Y12	Homo sapiens	7-12
31218354-1	2019	AIMS: In PEGASUS-TIMI 54, ticagrelor significantly reduced the risk of the composite of major adverse cardiovascular (CV) events by 15-16% in stable patients with a prior myocardial infarction (MI) 1-3 years earlier.	Ticagrelor	26-36	IKAROS family zinc finger 5	Homo sapiens	9-24
31218354-10	2019	CONCLUSION: In PEGASUS-TIMI 54, treatment with ticagrelor 60 mg as recommended in the EU label, was associated with a relative risk reduction of 20% in CV death, MI, or stroke.	Ticagrelor	47-57	IKAROS family zinc finger 5	Homo sapiens	15-30
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.	Ticagrelor	24-34	purinergic receptor P2Y12	Homo sapiens	146-151
31445718-2	2019	The oral P2Y12 inhibitors comprise clopidogrel, prasugrel, and ticagrelor.	Ticagrelor	63-73	purinergic receptor P2Y12	Homo sapiens	9-14
31389599-7	2019	RESULTS: The results showed that CK, CK-MB, cTnI, and BNP levels in ticagrelor group were lower than those in clopidogrel group, and the differences were statistically significant (p<0.05).	Ticagrelor	68-78	cytidine/uridine monophosphate kinase 1	Homo sapiens	33-35
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.	Ticagrelor	81-91	purinergic receptor P2Y12	Homo sapiens	30-35
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.	Ticagrelor	81-91	purinergic receptor P2Y12	Homo sapiens	246-251
31402681-11	2019	CONCLUSION: Our study shows that higher PRU and the subsequent HPR at the time of primary PCI, after pretreatment with ticagrelor, are the only correlates of post PCI MBG.	Ticagrelor	119-129	haptoglobin-related protein	Homo sapiens	63-66
31377269-2	2019	BACKGROUND: Morphine delays the onset of action of oral P2Y12 receptor inhibitors, including ticagrelor, by inhibiting gastric emptying and leading to delayed drug absorption.	Ticagrelor	93-103	purinergic receptor P2Y12	Homo sapiens	56-61
33609114-11	2019	CONCLUSION: Our study shows that higher PRU and the subsequent HPR at the time of primary PCI, after pretreatment with ticagrelor, are the only correlates of post PCI MBG.	Ticagrelor	119-129	haptoglobin-related protein	Homo sapiens	63-66
31172515-6	2019	However, in ticagrelor-treated patients, miRNA levels were significantly increased at baseline (miRNA-223 and -21), day 10 (miRNA-223, -150, -21, -126) and day 30 (miRNA-223, -150, -21, -126) as compared to prasugrel, and at day 10 (miRNA-150 and -21) and day 30 (miRNA-150) as compared to clopidogrel (all P < 0.05).	Ticagrelor	12-22	microRNA 223	Homo sapiens	96-105
31172515-6	2019	However, in ticagrelor-treated patients, miRNA levels were significantly increased at baseline (miRNA-223 and -21), day 10 (miRNA-223, -150, -21, -126) and day 30 (miRNA-223, -150, -21, -126) as compared to prasugrel, and at day 10 (miRNA-150 and -21) and day 30 (miRNA-150) as compared to clopidogrel (all P < 0.05).	Ticagrelor	12-22	microRNA 223	Homo sapiens	124-133
31172515-6	2019	However, in ticagrelor-treated patients, miRNA levels were significantly increased at baseline (miRNA-223 and -21), day 10 (miRNA-223, -150, -21, -126) and day 30 (miRNA-223, -150, -21, -126) as compared to prasugrel, and at day 10 (miRNA-150 and -21) and day 30 (miRNA-150) as compared to clopidogrel (all P < 0.05).	Ticagrelor	12-22	microRNA 223	Homo sapiens	124-133
31172515-6	2019	However, in ticagrelor-treated patients, miRNA levels were significantly increased at baseline (miRNA-223 and -21), day 10 (miRNA-223, -150, -21, -126) and day 30 (miRNA-223, -150, -21, -126) as compared to prasugrel, and at day 10 (miRNA-150 and -21) and day 30 (miRNA-150) as compared to clopidogrel (all P < 0.05).	Ticagrelor	12-22	microRNA 150	Homo sapiens	233-242
31172515-6	2019	However, in ticagrelor-treated patients, miRNA levels were significantly increased at baseline (miRNA-223 and -21), day 10 (miRNA-223, -150, -21, -126) and day 30 (miRNA-223, -150, -21, -126) as compared to prasugrel, and at day 10 (miRNA-150 and -21) and day 30 (miRNA-150) as compared to clopidogrel (all P < 0.05).	Ticagrelor	12-22	microRNA 150	Homo sapiens	264-273
31389599-7	2019	RESULTS: The results showed that CK, CK-MB, cTnI, and BNP levels in ticagrelor group were lower than those in clopidogrel group, and the differences were statistically significant (p<0.05).	Ticagrelor	68-78	troponin I3, cardiac type	Homo sapiens	44-48
31389599-7	2019	RESULTS: The results showed that CK, CK-MB, cTnI, and BNP levels in ticagrelor group were lower than those in clopidogrel group, and the differences were statistically significant (p<0.05).	Ticagrelor	68-78	natriuretic peptide B	Homo sapiens	54-57
31319418-7	2019	Results: Protection by ticagrelor was demonstrated functionally by using the electroretinogram, as ticagrelor-treated ABCA4-/- mice had increased a- and b-waves compared to untreated mice.	Ticagrelor	23-33	ATP-binding cassette, sub-family A (ABC1), member 4	Mus musculus	118-123
31003796-7	2019	In this analysis, administration of Ticagrelor was associated with lower MPA percentage of CD14high monocyte subpopulations than Clopidogrel (p &lt; 0.01) or Prasugrel (p &lt; 0.05).	Ticagrelor	36-46	CD14 molecule	Homo sapiens	91-95
31319418-11	2019	Conclusions: Oral treatment with ticagrelor protected photoreceptors in the ABCA4-/- mouse, which is consistent with enhanced lysosomal function.	Ticagrelor	33-43	ATP-binding cassette, sub-family A (ABC1), member 4	Mus musculus	76-81
31198410-3	2019	The most used P2Y12-antagonists are clopidogrel, prasugrel and ticagrelor.	Ticagrelor	63-73	purinergic receptor P2Y12	Homo sapiens	14-19
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).	Ticagrelor	192-202	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	48-55
31141104-11	2019	P2Y12 inhibitor switching for any reason occurred in 197 patients and was more common in patients treated with ticagrelor (146 of 1704 [8.6%]) compared with clopidogrel (51 of 1333 [3.8%]).	Ticagrelor	111-121	purinergic receptor P2Y12	Homo sapiens	0-5
31141104-12	2019	Of patients initially treated with ticagrelor, only 1 (0.1% overall; 0.7% of all who switched) was switched based on CYP2C19 status.	Ticagrelor	35-45	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	117-124
31242230-0	2019	Ticagrelor induces paraoxonase-1 (PON1) and better protects hypercholesterolemic mice against atherosclerosis compared to clopidogrel.	Ticagrelor	0-10	paraoxonase 1	Mus musculus	19-32
31242230-0	2019	Ticagrelor induces paraoxonase-1 (PON1) and better protects hypercholesterolemic mice against atherosclerosis compared to clopidogrel.	Ticagrelor	0-10	paraoxonase 1	Mus musculus	34-38
31242230-1	2019	Ticagrelor (TIC), a P2Y purinoceptor 12 (P2Y12)-receptor antagonist, has been widely used to treat patients with acute coronary syndrome.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	20-39
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).	Ticagrelor	192-202	purinergic receptor P2Y12	Homo sapiens	83-88
31171523-13	2019	CONCLUSION: Patients with minor stroke or transient ischaemic attack who are treated with ticagrelor plus aspirin have a lower proportion of high platelet reactivity than those who are treated with clopidogrel plus aspirin, particularly for those who are carriers of the CYP2C19 loss-of-function allele.	Ticagrelor	90-100	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	271-278
31070112-5	2019	Higher potency P2Y12 inhibitors (prasugrel or ticagrelor) were prescribed at discharge in 39%, 35%, 23%, and 15% ( P<0.01) of patients with stages 1, 2, 3, and >=4, respectively.	Ticagrelor	46-56	purinergic receptor P2Y12	Homo sapiens	15-20
31274838-1	2019	We recently showed that ticagrelor reduced myocardial ischemia-reperfusion injury (IRI) and downregulated galectin-3 in the ischemic myocardium.	Ticagrelor	24-34	galectin 3	Rattus norvegicus	106-116
31274838-4	2019	Ticagrelor significantly reduced the infarct size and plasma cTnI at 3 and 7 days after IRI, significantly downregulated protein and mRNA expressions of NF-kappaB and galectin-3, and mRNA expressions of IL-6 and TNF-alpha in the ischemic area at 24 hours, 3 and 7 days after IRI.	Ticagrelor	0-10	troponin I3, cardiac type	Rattus norvegicus	61-65
31274838-4	2019	Ticagrelor significantly reduced the infarct size and plasma cTnI at 3 and 7 days after IRI, significantly downregulated protein and mRNA expressions of NF-kappaB and galectin-3, and mRNA expressions of IL-6 and TNF-alpha in the ischemic area at 24 hours, 3 and 7 days after IRI.	Ticagrelor	0-10	galectin 3	Rattus norvegicus	167-177
31274838-4	2019	Ticagrelor significantly reduced the infarct size and plasma cTnI at 3 and 7 days after IRI, significantly downregulated protein and mRNA expressions of NF-kappaB and galectin-3, and mRNA expressions of IL-6 and TNF-alpha in the ischemic area at 24 hours, 3 and 7 days after IRI.	Ticagrelor	0-10	interleukin 6	Rattus norvegicus	203-207
31274838-4	2019	Ticagrelor significantly reduced the infarct size and plasma cTnI at 3 and 7 days after IRI, significantly downregulated protein and mRNA expressions of NF-kappaB and galectin-3, and mRNA expressions of IL-6 and TNF-alpha in the ischemic area at 24 hours, 3 and 7 days after IRI.	Ticagrelor	0-10	tumor necrosis factor	Rattus norvegicus	212-221
31274838-5	2019	Ticagrelor also significantly decreased plasma high-sensitivity C-reactive protein and NT-proBNP levels at 24 hours and 3 days after IRI.	Ticagrelor	0-10	C-reactive protein	Rattus norvegicus	64-82
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).	Ticagrelor	113-123	purinergic receptor P2Y12	Homo sapiens	83-88
31221073-0	2019	[Double antiplatelet therapy in patients with acute coronary syndrome after percutaneous coronary intervention: individual efficacy and hemorrhagic safety of P2Y12 blockers of ticagrelor and clopidogrel in actual clinical practice].	Ticagrelor	176-186	purinergic receptor P2Y12	Homo sapiens	158-163
31294325-8	2019	Among the 80 ticagrelor-treated patients with adequate P2Y12 inhibition, 25 patients (31%) still had a normal response to SFLLRN, and 50 (63%) still had a normal response to AYPGKF.	Ticagrelor	13-23	purinergic receptor P2Y12	Homo sapiens	55-60
30721704-7	2019	To explore this hypothesis, we analyzed the expression, localization and activity of NCX1 in the heart derived H9c2-NCX1 cells following ticagrelor exposure.	Ticagrelor	137-147	solute carrier family 8 member A1	Rattus norvegicus	85-89
30883047-1	2019	BACKGROUND: Ticagrelor is an oral P2Y12 inhibitor that is used with aspirin to reduce the risk of ischemic events among patients with acute coronary syndromes or previous myocardial infarction.	Ticagrelor	12-22	purinergic receptor P2Y12	Homo sapiens	34-39
30721704-1	2019	Ticagrelor is a direct acting and reversibly binding P2Y12 antagonist approved for the prevention of thromboembolic events.	Ticagrelor	0-10	purinergic receptor P2Y12	Rattus norvegicus	53-58
30721704-8	2019	We found that ticagrelor concentration- and time-dependently reduced the activity of the cardiac NCX1 in H9c2 cells.	Ticagrelor	14-24	solute carrier family 8 member A1	Rattus norvegicus	97-101
30721704-9	2019	In particular, the inhibitory effect of ticagrelor on the Ca2+-influx mode of NCX1 was evident within 1 h and further developed after 24 h, when NCX1 activity was suppressed by about 55% in cells treated with 1 muM ticagrelor.	Ticagrelor	40-50	solute carrier family 8 member A1	Rattus norvegicus	78-82
30721704-9	2019	In particular, the inhibitory effect of ticagrelor on the Ca2+-influx mode of NCX1 was evident within 1 h and further developed after 24 h, when NCX1 activity was suppressed by about 55% in cells treated with 1 muM ticagrelor.	Ticagrelor	40-50	solute carrier family 8 member A1	Rattus norvegicus	145-149
30721704-9	2019	In particular, the inhibitory effect of ticagrelor on the Ca2+-influx mode of NCX1 was evident within 1 h and further developed after 24 h, when NCX1 activity was suppressed by about 55% in cells treated with 1 muM ticagrelor.	Ticagrelor	215-225	solute carrier family 8 member A1	Rattus norvegicus	78-82
30721704-9	2019	In particular, the inhibitory effect of ticagrelor on the Ca2+-influx mode of NCX1 was evident within 1 h and further developed after 24 h, when NCX1 activity was suppressed by about 55% in cells treated with 1 muM ticagrelor.	Ticagrelor	215-225	solute carrier family 8 member A1	Rattus norvegicus	145-149
31124413-4	2019	CYP4F2 T allele significantly increased odds for bleeding in ticagrelor users (OR: 8.270, 95% CI: 3.917-17.462; p < 0.001).	Ticagrelor	61-71	cytochrome P450 family 4 subfamily F member 2	Homo sapiens	0-6
30788847-3	2019	The Effect of Ticagrelor on Health Outcomes in diabEtes Mellitus patients Intervention Study (THEMIS, NCT01991795) is a Phase 3b randomized, double-blinded, placebo-controlled trial of ticagrelor vs placebo, on top of low dose aspirin.	Ticagrelor	14-24	thymocyte selection associated	Homo sapiens	94-100
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.	Ticagrelor	117-127	purinergic receptor P2Y12	Homo sapiens	75-80
31551217-1	2019	The main aim of the current work was to investigate the application of ticagrelor in patients with coronary atherosclerotic heart disease (CAHD) and its effects on brain natriuretic peptide (BNP), heart rate (HR) and myocardial enzymes.	Ticagrelor	71-81	natriuretic peptide B	Homo sapiens	164-189
31551217-1	2019	The main aim of the current work was to investigate the application of ticagrelor in patients with coronary atherosclerotic heart disease (CAHD) and its effects on brain natriuretic peptide (BNP), heart rate (HR) and myocardial enzymes.	Ticagrelor	71-81	natriuretic peptide B	Homo sapiens	191-194
31551217-7	2019	The utilization of ticagrelor in patients with postoperative stenting for CAHD improved the BNP, HR and myocardial enzyme level in patients, and also reduced the incidence of adverse cardiac events.	Ticagrelor	19-29	natriuretic peptide B	Homo sapiens	92-95
30630341-14	2019	CONCLUSIONS: In patients undergoing primary percutaneous coronary intervention, cangrelor is an effective strategy to bridge the gap in platelet inhibition associated with the use of oral P2Y12 inhibition induced by ticagrelor.	Ticagrelor	216-226	purinergic receptor P2Y12	Homo sapiens	188-193
30456635-2	2019	New generation P2Y12 inhibitors (ticagrelor and prasugrel) might potentially replace clopidogrel for the treatment of post-interventional acute coronary syndrome (ACS).	Ticagrelor	33-43	purinergic receptor P2Y12	Homo sapiens	15-20
30592271-0	2019	Ticagrelor suppresses oxidized low-density lipoprotein-induced endothelial cell apoptosis and alleviates atherosclerosis in ApoE-/- mice via downregulation of PCSK9.	Ticagrelor	0-10	apolipoprotein E	Mus musculus	124-128
30592271-0	2019	Ticagrelor suppresses oxidized low-density lipoprotein-induced endothelial cell apoptosis and alleviates atherosclerosis in ApoE-/- mice via downregulation of PCSK9.	Ticagrelor	0-10	proprotein convertase subtilisin/kexin type 9	Mus musculus	159-164
30592271-12	2019	The present results suggested that ticagrelor may alleviate AS via downregulation of PCSK9-mediated endothelial cell apoptosis, which may be JNK-dependent.	Ticagrelor	35-45	proprotein convertase subtilisin/kexin type 9	Mus musculus	85-90
30592271-12	2019	The present results suggested that ticagrelor may alleviate AS via downregulation of PCSK9-mediated endothelial cell apoptosis, which may be JNK-dependent.	Ticagrelor	35-45	mitogen-activated protein kinase 8	Mus musculus	141-144
29998574-5	2019	CYP3A4*22 carriers also showed more pronounced platelet inhibition at 24 hours after ticagrelor ingestion than the controls (43% vs. 21%; P = 0.029).	Ticagrelor	85-95	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
29954720-0	2019	Annual Incidence of Confirmed Stent Thrombosis and Clinical Predictors in Patients With ACS Treated With Ticagrelor or Prasugrel.	Ticagrelor	105-115	1-aminocyclopropane-1-carboxylate synthase homolog (inactive)	Homo sapiens	88-91
30936830-10	2019	Although CYP2C19 and SLCO1B1 genetic variants were related to the pharmacokinetics of ticagrelor or M8, they did not show a significant effect on the platelet function recovery in this study.	Ticagrelor	86-96	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	9-16
30936830-10	2019	Although CYP2C19 and SLCO1B1 genetic variants were related to the pharmacokinetics of ticagrelor or M8, they did not show a significant effect on the platelet function recovery in this study.	Ticagrelor	86-96	solute carrier organic anion transporter family member 1B1	Homo sapiens	21-28
30882670-1	2019	Although the new oral P2Y12 inhibitors, prasugrel/ticagrelor have shown greater efficacy than clopidogrel in patients with the acute coronary syndrome, but they have not shown better efficacy in Korean patients.	Ticagrelor	50-60	purinergic receptor P2Y12	Homo sapiens	22-27
30723937-5	2019	Recently, more data have emerged using alternative P2Y12 inhibitors such as prasugrel and ticagrelor.	Ticagrelor	90-100	purinergic receptor P2Y12	Homo sapiens	51-56
30580572-8	2019	A modifying effect of ticagrelor on DKK1 discharge levels was observed but not associated with prognosis.	Ticagrelor	22-32	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	36-40
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.	Ticagrelor	148-158	purinergic receptor P2Y12	Homo sapiens	29-36
30580183-2	2019	Concomitant treatment with ticagrelor, a moderate CYP3A4 inhibitor, and CYP3A4-metabolized statins such as atorvastatin, might lead to an increased risk of muscle-related adverse events.	Ticagrelor	27-37	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	50-56
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.	Ticagrelor	128-138	purinergic receptor P2Y12	Homo sapiens	98-103
29671861-0	2019	P2Y12 antagonist ticagrelor inhibits the release of procoagulant extracellular vesicles from activated platelets.	Ticagrelor	17-27	purinergic receptor P2Y12	Homo sapiens	0-5
30899625-1	2019	The P2Y12 inhibitor, ticagrelor, has been shown to prevent thrombotic events and hence, improve morbidity and mortality in patients with acute coronary syndrome following coronary artery stent placement.	Ticagrelor	21-31	purinergic receptor P2Y12	Homo sapiens	4-9
29451832-9	2019	Short-term dual antiplatelet therapy in ACS patients restores the low platelet/KDR+ conjugates and CD34+ cell levels and improves the low membrane expression levels of KDR in these cells, an effect being more pronounced in ticagrelor-treated patients.	Ticagrelor	223-233	kinase insert domain receptor	Homo sapiens	168-171
29412111-2	2019	Of them, adenosine diphosphate receptor P2Y12 inhibitors clopidogrel, prasugrel and ticagrelor are currently used for post-ACS long-term treatment.	Ticagrelor	84-94	purinergic receptor P2Y12	Homo sapiens	40-45
29412111-9	2019	Ticagrelor is metabolized mainly by CYP3A4, which does not show functionally relevant genetic variability.	Ticagrelor	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	36-42
31280824-3	2019	OBJECTIVE: We performed a meta-analysis of all available studies in AMI patients treated with prasugrel or ticagrelor (P2Y12 inhibitors) that reported use of morphine prior to loading the antiplatelet agents to critically assess the safety of co-administration of morphine and the newer P2Y12 inhibitors.	Ticagrelor	107-117	purinergic receptor P2Y12	Homo sapiens	119-124
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.	Ticagrelor	47-57	purinergic receptor P2Y12	Homo sapiens	0-5
29370574-3	2019	In the present study, ticagrelor was used to induce a mouse model of SAKI by cecal ligation and puncture.	Ticagrelor	22-32	NOP2/Sun RNA methyltransferase 2	Homo sapiens	69-73
30745807-7	2019	Compared to clopidogrel-treated patients, CD42+/CD62P+ PMVs counts were 3-4-fold lower in subjects receiving ticagrelor (p=0.001) or prasugrel (p&lt;0.05), while CD42+ PMVs were significantly reduced on ticagrelor (by about 6-fold, p&lt;0.001), but not prasugrel (p=0.3).	Ticagrelor	109-119	selectin P	Homo sapiens	48-53
30745807-10	2019	Conclusions: Higher antiplatelet potency of prasugrel and ticagrelor versus clopidogrel is associated with decreased plasma CD42+/CD62P+ PMVs numbers.	Ticagrelor	58-68	selectin P	Homo sapiens	130-135
30252571-11	2019	The concentration of IL-8 and IL-10 were decreased in patients with half and standard-dose ticagrelor group.	Ticagrelor	91-101	C-X-C motif chemokine ligand 8	Homo sapiens	21-25
30252571-11	2019	The concentration of IL-8 and IL-10 were decreased in patients with half and standard-dose ticagrelor group.	Ticagrelor	91-101	interleukin 10	Homo sapiens	30-35
29370574-4	2019	It was found that ticagrelor could inhibit platelet activity, decrease the levels of interleukin-1beta and serum creatinine, reduce infiltration of neutrophils in renal tissue, and attenuate cell apoptosis in the kidney.	Ticagrelor	18-28	interleukin 1 beta	Mus musculus	85-102
29851527-1	2019	In the PLATelet inhibition and patient Outcomes (PLATO) study, the P2Y12 inhibitors ticagrelor and clopidogrel were compared in the treatment of acute coronary syndromes (ACS).	Ticagrelor	84-94	purinergic receptor P2Y12	Homo sapiens	67-72
30074112-5	2018	Ticagrelor is a P2Y12 receptor antagonist with evidence of cardiovascular event reduction in patients with acute coronary syndromes and those with a previous myocardial infarction.	Ticagrelor	0-10	purinergic receptor P2Y12	Homo sapiens	16-21
30359421-4	2018	A number of approved drugs, including the P2Y12 antagonist ticagrelor, have been described to increase extracellular adenosine.	Ticagrelor	59-69	purinergic receptor P2Y12	Homo sapiens	42-47
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).	Ticagrelor	145-155	purinergic receptor P2Y12	Homo sapiens	39-44
30124783-11	2018	Only ticagrelor enhanced myocardial AMPK and Akt/PKB activation and reduced aquaporin-4 levels (P < 0.05 vs. control and clopidogrel).	Ticagrelor	5-15	protein kinase AMP-activated catalytic subunit alpha 1	Sus scrofa	36-40
30124783-11	2018	Only ticagrelor enhanced myocardial AMPK and Akt/PKB activation and reduced aquaporin-4 levels (P < 0.05 vs. control and clopidogrel).	Ticagrelor	5-15	AKT serine/threonine kinase 1	Sus scrofa	45-52
30124783-11	2018	Only ticagrelor enhanced myocardial AMPK and Akt/PKB activation and reduced aquaporin-4 levels (P < 0.05 vs. control and clopidogrel).	Ticagrelor	5-15	aquaporin 4	Sus scrofa	76-87
30347494-14	2018	Ticagrelor, but not vorapaxar, abolished the PAR4 variant effect on thrombin-induced platelet aggregation.	Ticagrelor	0-10	F2R like thrombin or trypsin receptor 3	Homo sapiens	45-49
30347494-14	2018	Ticagrelor, but not vorapaxar, abolished the PAR4 variant effect on thrombin-induced platelet aggregation.	Ticagrelor	0-10	coagulation factor II, thrombin	Homo sapiens	68-76
30478067-12	2018	CONCLUSION: P2Y12 inhibition with ticagrelor reduced MHA symptoms similarly to our previous thienopyridine experience, but participants seemed to have a less robust MHA benefit and more frequent side effects than with the thienopyridines, making it an inferior choice for a randomized trial.	Ticagrelor	34-44	purinergic receptor P2Y12	Homo sapiens	12-17
29805112-8	2018	P2Y12 platelet reactivity units were lower after ticagrelor as compared with clopidogrel at all time points and after maintenance dose as compared with prasugrel.	Ticagrelor	49-59	purinergic receptor P2Y12	Homo sapiens	0-5
29958560-8	2018	Ticagrelor blocked the activation of phosphatidylinositol 3-kinase (PI3K) and extracellular signal-regulated kinase 1/2 (ERK1/2) in ADPbetaS-treated DCs.	Ticagrelor	0-10	phosphoinositide-3-kinase regulatory subunit 1	Mus musculus	37-66
29958560-8	2018	Ticagrelor blocked the activation of phosphatidylinositol 3-kinase (PI3K) and extracellular signal-regulated kinase 1/2 (ERK1/2) in ADPbetaS-treated DCs.	Ticagrelor	0-10	mitogen-activated protein kinase 3	Mus musculus	78-119
29958560-8	2018	Ticagrelor blocked the activation of phosphatidylinositol 3-kinase (PI3K) and extracellular signal-regulated kinase 1/2 (ERK1/2) in ADPbetaS-treated DCs.	Ticagrelor	0-10	mitogen-activated protein kinase 3	Mus musculus	121-127
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.	Ticagrelor	114-124	purinergic receptor P2Y12	Homo sapiens	23-28
29902700-0	2018	Ticagrelor, a P2Y12 antagonist, attenuates vascular dysfunction and inhibits atherogenesis in apolipoprotein-E-deficient mice.	Ticagrelor	0-10	purinergic receptor P2Y, G-protein coupled 12	Mus musculus	14-19
29902700-12	2018	Ticagrelor decreased the phosphorylation of JNK in the aorta compared with control (p &lt; 0.05).	Ticagrelor	0-10	mitogen-activated protein kinase 8	Mus musculus	44-47
29902700-15	2018	Ticagrelor also inhibited ADP-induced JNK activation in HUVEC (p &lt; 0.05).	Ticagrelor	0-10	mitogen-activated protein kinase 8	Mus musculus	38-41