PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 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 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 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 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 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 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 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 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 35040887-6 2022 Ticagrelor was the preferred P2Y12 inhibitor. Ticagrelor 0-10 purinergic receptor P2Y12 Homo sapiens 29-34 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 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 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 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 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 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 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 32523112-5 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 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 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 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 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 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 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 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 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 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 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 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 122-132 purinergic receptor P2Y12 Homo sapiens 195-200 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 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 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 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 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 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 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 33563204-0 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 33563204-10 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 33563204-0 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 32152791-8 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 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 32960097-1 2021 Ticagrelor is a potent and orally active P2Y12 inhibitor. Ticagrelor 0-10 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 32106619-5 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 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 32062795-9 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 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 32062795-7 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 32062795-8 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 0-10 vasodilator stimulated phosphoprotein Homo sapiens 144-148 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 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 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 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 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 31351022-13 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 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 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 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 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 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 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 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 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 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 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 31445718-2 2019 The oral P2Y12 inhibitors comprise clopidogrel, prasugrel, and ticagrelor. Ticagrelor 63-73 purinergic receptor P2Y12 Homo sapiens 9-14 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 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 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 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 31003796-7 2019 In this analysis, administration of Ticagrelor was associated with lower MPA percentage of CD14high monocyte subpopulations than Clopidogrel (p < 0.01) or Prasugrel (p < 0.05). Ticagrelor 36-46 CD14 molecule Homo sapiens 91-95 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 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 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 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 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 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 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 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 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 113-123 purinergic receptor P2Y12 Homo sapiens 83-88 31198410-3 2019 The most used P2Y12-antagonists are clopidogrel, prasugrel and ticagrelor. Ticagrelor 63-73 purinergic receptor P2Y12 Homo sapiens 14-19 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 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 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 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 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 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 30721704-7 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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<0.05), while CD42+ PMVs were significantly reduced on ticagrelor (by about 6-fold, p<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 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 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 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 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 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 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 30500673-5 2019 Platelet reactivity was reduced by all P2Y12 inhibitors, demonstrated by OT prolongation (clopidogrel 378 +- 87 s vs. 491 +- 93 s, p < 0.001; ticagrelor 416 +- 122 s vs. 549 +- 121 s, p < 0.001; cangrelor 381 +- 146 s vs. 613 +- 210 s, p < 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 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 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 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 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 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 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 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 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 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 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 < 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 < 0.05). Ticagrelor 0-10 mitogen-activated protein kinase 8 Mus musculus 38-41 30048515-1 2018 Ticagrelor, a P2Y12 antagonist, is approved for prevention of thromboembolic events. Ticagrelor 0-10 purinergic receptor P2Y12 Homo sapiens 14-19 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 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 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 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 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 29686623-1 2018 Ticagrelor is one of the most powerful P2Y12 inhibitor. Ticagrelor 0-10 purinergic receptor P2Y12 Homo sapiens 39-44 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 29150806-1 2017 Ticagrelor (Brilique ) is an orally administered P2Y12 inhibitor. Ticagrelor 0-10 purinergic receptor P2Y12 Homo sapiens 49-54 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 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 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 29150806-1 2017 Ticagrelor (Brilique ) is an orally administered P2Y12 inhibitor. Ticagrelor 12-20 purinergic receptor P2Y12 Homo sapiens 49-54 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 27922911-4 2017 The newer P2Y12 inhibitors include cangrelor, prasugrel, and ticagrelor. Ticagrelor 61-71 purinergic receptor P2Y12 Homo sapiens 10-15 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 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 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 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 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 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 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 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 28028070-5 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 25848131-6 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 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 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 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 purinergic receptor P2Y12 Homo sapiens 28-33 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 25696877-7 2014 Alternatively, 2 third-generation P2Y12 inhibitors are available: prasugrel and ticagrelor. Ticagrelor 80-90 purinergic receptor P2Y12 Homo sapiens 34-39 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 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 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 24958490-9 2014 Ticagrelor is a newer P2Y12 inhibitor that contains a cyclopentyltriazolopyrimidine structure. Ticagrelor 0-10 purinergic receptor P2Y12 Homo sapiens 22-27 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 24112116-0 2013 Reversal strategy in antagonizing the P2Y12 -inhibitor ticagrelor. Ticagrelor 55-65 purinergic receptor P2Y12 Homo sapiens 38-43 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 23474908-12 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 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 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 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 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 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 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 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 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 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 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 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 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 22795280-0 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 19552634-3 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 1 Homo sapiens 25-30 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 34238553-1 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 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 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 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 34163168-0 2021 Ticagrelor Use in Stroke Patients: Past, Present, and Future. Ticagrelor 0-10 EH domain containing 1 Homo sapiens 35-39 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 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 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 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 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 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 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 35595877-15 2022 The P2Y12 inhibitor ticagrelor per se induces a humoral cardioprotective signal. Ticagrelor 20-30 purinergic receptor P2Y12 Rattus norvegicus 4-9 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 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 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 nuclear receptor subfamily 1 group I member 2 Homo sapiens 57-60 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 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 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 coagulation factor II, thrombin Homo sapiens 126-134 35353154-6 2022 As compared to DAPT, on a background of the same P2Y12 inhibitor (clopidogrel or ticagrelor), DPI was associated with reduced thrombin generation, increased markers of cyclooxygenase-1 activity and TRAP-induced platelet aggregation and no differences in markers of P2Y12 signaling, platelet-mediated global thrombogenicity and TF-induced platelet aggregation. 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 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 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 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 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