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Results for "

dog. platelet

" in MedChemExpress (MCE) Product Catalog:

6

Inhibitors & Agonists

1

Peptides

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-113331
    Thromboxane B2

    		Prostaglandin Receptor Cardiovascular Disease Inflammation/Immunology
    Thromboxane B2 is a prostaglandin derivative that is released during anaphylaxis. Thromboxane B2 induces arterial contraction and platelet aggregation. Thromboxane B2 is a biological inactive product and circulating catabolite of thromboxane A2. Thromboxane B2 levels in peripheral venous blood and coronary sinus blood can be used as a diagnostic marker for angina. Thromboxane B2 level in serum is also associated with inhibition of COX-1 activity inhibition in platelets. Thromboxane B2 is a major product of prostaglandin endoperoxide metabolism. Thromboxane B2 produces dose-related decreases in airflow rate, tidal volume and dynamic lung compliance, whilst simultaneously increasing pulmonary airway resistance in dog model. Thromboxane B2 appears to be a naturally occurring bronchoactive metabolite in the bioconversion of arachidonic acid .
    Thromboxane B2
  • HY-18071A
    BI-9627 hydrochloride
    2 Publications Verification

    		 Na+/H+ Exchanger (NHE) Autophagy Cardiovascular Disease
    BI-9627 hydrochloride is a potent sodium-hydrogen exchanger isoform 1 (NHE1) inhibitor (IC50 = 6 and 31 nM in intracellular pH recovery (pHi) and human platelet swelling assays). BI-9627 hydrochloride displays >30-fold selectivity against NHE2 and with no measurable inhibitory activity against the NHE3 isoform. BI-9627 hydrochloride decreases autophagy in HTR-8/SVneo cells. BI-9627 hydrochloride can significantly reduce the pHi of human sperm and partially reverse the effect of DMA. BI-9627 hydrochloride prolongs Ca 2+ recovery time in KO hiPSC-CMs. BI-9627 hydrochloride shows low DDI (agent-agent interaction) potential, excellent pharmacokinetics in rat and dog, and remarkably potent activity in the isolated heart model of ischemia-reperfusion injury .
    BI-9627 hydrochloride
  • HY-18071
    BI-9627
    2 Publications Verification

    		 Na+/H+ Exchanger (NHE) Autophagy Cardiovascular Disease
    BI-9627 is a potent sodium-hydrogen exchanger isoform 1 (NHE1) inhibitor (IC50 = 6 and 31 nM in intracellular pH recovery (pHi) and human platelet swelling assays). BI-9627 displays >30-fold selectivity against NHE2 and with no measurable inhibitory activity against the NHE3 isoform. BI-9627 decreases autophagy in HTR-8/SVneo cells. BI-9627 can significantly reduce the pHi of human sperm and partially reverse the effect of DMA. BI-9627 prolongs Ca 2+ recovery time in KO hiPSC-CMs. BI-9627 shows low DDI (agent-agent interaction) potential, excellent pharmacokinetics in rat and dog, and remarkably potent activity in the isolated heart model of ischemia-reperfusion injury .
    BI-9627
  • HY-169836
    Des-ethyl-carafiban

    		Integrin Cardiovascular Disease
    Des-ethyl-carafiban (Compound 44) is a fibrinogen receptor antagonist that can effectively inhibit platelet aggregation induced by multiple agonists. Des-ethyl-carafiban can be used in the research of thrombotic diseases .
    Des-ethyl-carafiban
  • HY-W419570
    (Rac)-BX 048

    		P2Y Receptor Cardiovascular Disease
    (Rac)-BX 048 is a BX 048 racemate. BX 048 is a P2Y12 receptor antagonist. BX 048 inhibits ADP-induced platelet aggregation in human, dog and rat whole blood. BX 048 also inhibits Arachidonic acid (HY-109590) induced platelet aggregation (IC50 of 15 μM) .
    (Rac)-BX 048
  • HY-121586
    Nafazatrom

    Bay g 6575

    		 Lipoxygenase Cardiovascular Disease
    Nafazatrom (Bay g 6575) is an orally active cardioprotective agent that protects against ischemic damage. Nafazatrom dose-dependently inhibits neutrophil aggregation, superoxide anion generation, arachidonic acid metabolism, and to a lesser extent the release of β-glucosidase, platelet aggregation or arachidonic acid in vitro. Acid metabolism has no significant effect. In a dog ischemia-reperfusion model, Nafazatrom (10 mg/kg; po) reduced infarct size and the occurrence of arrhythmias and rescued ischemic myocardial function without affecting any hemodynamic changes. The basis of Nafazatrom's cardioprotection may be inhibition of neutrophil function and cellular infiltration in vitro .
    Nafazatrom

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