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myocardial infarct size

" in MedChemExpress (MCE) Product Catalog:

14

Inhibitors & Agonists

1

Biochemical Assay Reagents

2

Peptides

4

Natural
Products

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-103445

    Elastase Cardiovascular Disease
    SSR69071 is a potent, orally active and selective inhibitor of neutrophil elastase. SSR69071 reduces myocardial infarct size following ischemia-reperfusion injury . SSR69071 displays a higher affinity for human elastase (Ki=0.0168 nM) than for rat (Ki=3 nM), mouse (Ki=1.8 nM), and rabbit (Ki= 58 nM) elastases .
    SSR69071
  • HY-W011082

    NOD-like Receptor (NLR) Cardiovascular Disease
    NLRP3-IN-2, an intermediate substrate in the synthesis of glyburide, inhibits the formation of the NLRP3 inflammasome in cardiomyocytes and limits the infarct size following myocardial ischemia/reperfusion in the mouse, without affecting glucose metabolism .
    NLRP3-IN-2
  • HY-N2638

    Apoptosis Cardiovascular Disease
    Ilexsaponin A, isolated from the root of Ilex pubescens, attenuates ischemia-reperfusion-induced myocardial injury through anti-apoptotic pathway. Ilexsaponin A can reduce myocardial infarct size, lower the serum levels of LDH, AST and CK-MB, increase cellular viability and inhibit apoptosis in hypoxia/reoxygenation cardiomyocytes .
    Ilexsaponin A
  • HY-164304

    Pyroptosis Interleukin Related NOD-like Receptor (NLR) Cardiovascular Disease Inflammation/Immunology
    INF 195 is an NLRP3 inhibitor. INF 195 can inhibit NLRP3 driven macrophage pyroptosis and IL-1β release, with an EC50 value of 0.15 μM. INF 195 can reduce the infarct size of isolated mouse hearts at low doses, effectively preventing myocardial ischemia/reperfusion injury .
    INF 195
  • HY-101415

    Ubiquinone Q9; CoQ9; Ubiquinone 9

    Apoptosis Endogenous Metabolite Cardiovascular Disease
    Coenzyme Q9 (Ubiquinone Q9), the major form of ubiquinone in rodents, is an amphipathic molecular component of the electron transport chain that functions as an endogenous antioxidant. Coenzyme Q9 attenuates the diabetes-induced decreases in antioxidant defense mechanisms. Coenzyme Q9 improves left ventricular performance and reduces myocardial infarct size and cardiomyocyte apoptosis .
    Coenzyme Q9
  • HY-128090

    Aminopeptidase Cardiovascular Disease
    Apstatin is a potent aminopeptidase P (APP) inhibitor with Ki values of 2.6, 0.64 µM for rat and human APP, respectively. Apstatin shows cardioprotection .
    Apstatin
  • HY-121726

    mTOR Autophagy Cardiovascular Disease
    3HOI-BA-01 is amTORinhibitor.3HOI-BA-01reduces infarct size and inducedautophagyin a murine myocardial ischemia/reperfusion injury model .
    3HOI-BA-01
  • HY-N2638R

    Apoptosis Cardiovascular Disease
    Ilexsaponin A (Standard) is the analytical standard of Ilexsaponin A. This product is intended for research and analytical applications. Ilexsaponin A, isolated from the root of Ilex pubescens, attenuates ischemia-reperfusion-induced myocardial injury through anti-apoptotic pathway. Ilexsaponin A can reduce myocardial infarct size, lower the serum levels of LDH, AST and CK-MB, increase cellular viability and inhibit apoptosis in hypoxia/reoxygenation cardiomyocytes .
    Ilexsaponin A (Standard)
  • HY-106150

    EMD-96785

    Na+/H+ Exchanger (NHE) Others
    Eniporide (EMD 96785) is a Na(+)/H(+) exchange (NHE) inhibitor. Eniporide specifically inhibits the NHE-1 isoform. Eniporide improves cardiac performance inhibition associated with myocardial ischemia/reperfusion in animals, and limits infarct size in experimental models. Eniporide regulates cardiac performance and high-energy phosphate content in clinically relevant pig models of CPB and cardiac arrest .
    Eniporide
  • HY-W011082R

    NOD-like Receptor (NLR) Cardiovascular Disease
    NLRP3-IN-2 (Standard) is the analytical standard of NLRP3-IN-2. This product is intended for research and analytical applications. NLRP3-IN-2, an intermediate substrate in the synthesis of glyburide, inhibits the formation of the NLRP3 inflammasome in cardiomyocytes and limits the infarct size following myocardial ischemia/reperfusion in the mouse, without affecting glucose metabolism .
    NLRP3-IN-2 (Standard)
  • HY-P1259

    Proteasome Bacterial Inflammation/Immunology
    PR-39, a natural proline- and arginine-rich antibacterial peptide, is a noncompetitive, reversible and allosteric proteasome inhibitor. PR-39 reversibly binds to the α7 subunit of the proteasome and blocks degradation of NF-κB inhibitor IκBα by the ubiquitin-proteasome pathway. PR-39 stimulates angiogenesis, inhibits inflammatory responses and significant reduces myocardial infarct size in mice .
    PR-39
  • HY-P1259A

    Proteasome Bacterial Inflammation/Immunology
    PR-39 TFA, a natural proline- and arginine-rich antibacterial peptide, is a noncompetitive, reversible and allosteric proteasome inhibitor. PR-39 TFAreversibly binds to the α7 subunit of the proteasome and blocks degradation of NF-κB inhibitor IκBα by the ubiquitin-proteasome pathway. PR-39 TFA stimulates angiogenesis, inhibits inflammatory responses and significant reduces myocardial infarct size in mice .
    PR-39 TFA
  • HY-101415R

    Apoptosis Endogenous Metabolite Cardiovascular Disease
    Coenzyme Q9 (Standard) is the analytical standard of Coenzyme Q9. This product is intended for research and analytical applications. Coenzyme Q9 (Ubiquinone Q9), the major form of ubiquinone in rodents, is an amphipathic molecular component of the electron transport chain that functions as an endogenous antioxidant. Coenzyme Q9 attenuates the diabetes-induced decreases in antioxidant defense mechanisms. Coenzyme Q9 improves left ventricular performance and reduces myocardial infarct size and cardiomyocyte apoptosis .
    Coenzyme Q9 (Standard)
  • HY-121586

    Bay g 6575

    Others 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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