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Infarct+size

" in MedChemExpress (MCE) Product Catalog:

36

Inhibitors & Agonists

1

Biochemical Assay Reagents

4

Peptides

6

Natural
Products

2

Isotope-Labeled Compounds

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-B1218
    Sulfaphenazole
    Maximum Cited Publications
    14 Publications Verification

    		 Cytochrome P450 Antibiotic Bacterial Necroptosis Apoptosis Infection Cardiovascular Disease
    Sulfaphenazole is a selective inhibitor of human cytochrome P450 (CYP) 2C9 enzyme. Sulfaphenazole is a cytoprotective agent against light-induced death of photoreceptors. Sulfaphenazole inhibits light-induced necrosis and mitochondrial stress-initiated apoptosis. Sulfaphenazole is an off patent sulfonamide antibiotic and demonstrates bactericidal activity through enhanced M1 macrophage activity. Sulfaphenazole can significantly reduce infarct size and restore post-ischemic coronary flow following ischemia and reperfusion .
    Sulfaphenazole
  • HY-101415
    Coenzyme Q9
    1 Publications Verification

    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-17355A
    Dexpramipexole dihydrochloride
    2 Publications Verification

    (R)-Pramipexole dihydrochloride; R-(+)-Pramipexole dihydrochloride; KNS-760704 dihydrochloride

    		 ATP Synthase Sodium Channel Glutathione Peroxidase NOD-like Receptor (NLR) Mitophagy Ferroptosis PINK1/Parkin Autophagy Apoptosis Reactive Oxygen Species (ROS) Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more .
    Dexpramipexole dihydrochloride
  • HY-103445
    SSR69071

    		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-N0430
    Coptisine

    Coptisin

    		 Indoleamine 2,3-Dioxygenase (IDO) NF-κB p38 MAPK PI3K Akt Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism DNA/RNA Synthesis ROCK LDLR Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Coptisine is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine is a reversible, uncompetitive IDO inhibitor with a Ki of 5.8 μM and an IC50 of 6.3 μM. Coptisine suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine can be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .
    Coptisine
  • HY-N0430A
    Coptisine Sulfate
    5 Publications Verification

    		 Indoleamine 2,3-Dioxygenase (IDO) NF-κB p38 MAPK PI3K Akt Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism DNA/RNA Synthesis ROCK LDLR Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Coptisine Sulfate is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine Sulfate is a reversible, uncompetitive IDO inhibitor with a Ki of 5.8 μM and an IC50 of 6.3 μM. Coptisine Sulfate suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine Sulfate shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine Sulfate inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine Sulfate inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine Sulfate downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine Sulfate be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .
    Coptisine Sulfate
  • HY-W011082
    NLRP3-IN-2

    		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-17355B
    Dexpramipexole
    2 Publications Verification

    (R)-Pramipexole; R-(+)-Pramipexole; KNS-760704

    		 PINK1/Parkin Glutathione Peroxidase Sodium Channel ATP Synthase NOD-like Receptor (NLR) Mitophagy Ferroptosis Autophagy Apoptosis Reactive Oxygen Species (ROS) Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Dexpramipexole ((R)-Pramipexole) is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more .
    Dexpramipexole
  • HY-164304
    INF 195

    		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-103346
    MMPSI

    		Caspase Apoptosis Cardiovascular Disease
    MMPSI is a potent and selective small molecule caspase 3 and caspase 7 inhibitor with an IC50 of 1.7 μM for human caspase-3. MMPSI can significantly reduce ischemia-reperfusion-induced infarct size in the isolated rabbit heart, and reduce apoptosis in both the ischemic myocardium and isolated cardiomyocytes. MMPSI can be used for researching cardioprotection .
    MMPSI
  • HY-P1259A
    PR-39 TFA

    		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
    Coenzyme Q9 (Standard)

    Ubiquinone Q9 (Standard); CoQ9 (Standard); Ubiquinone 9 (Standard)

    		 Reference Standards 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-106150
    Eniporide

    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-P1259
    PR-39

    		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-126049
    (S)-Oxiracetam

    (S)-(-)-Oxiracetam; (S)-ISF2522

    		 Apoptosis Neurological Disease
    (S)-oxiracetam (S-ORC) is an inhibitor targeting apoptosis. S-ORC reduces brain infarct size and lessens neurological dysfunction in middle cerebral artery occlusion/reperfusion (MCAO/R) models. S-ORC prevents neuronal apoptosis via activating PI3K/Akt/GSK3β signaling pathway via α7 nAChR after ischemic stroke. S-ORC can prevent neuronal death after ischemic stroke .
    (S)-Oxiracetam
  • HY-17355BS
    Dexpramipexole-d3 dihydrochloride

    (R)-Pramipexole-d3 dihydrochloride; R-(+)-Pramipexole-d3 dihydrochloride; KNS-760704-d3 dihydrochloride

    		 Isotope-Labeled Compounds ATP Synthase Sodium Channel Glutathione Peroxidase NOD-like Receptor (NLR) Mitophagy Ferroptosis PINK1/Parkin Autophagy Apoptosis Reactive Oxygen Species (ROS) Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Dexpramipexole-d3 ((R)-Pramipexole-d3) dihydrochloride is the deuterium labeled Dexpramipexole. Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more.
    Dexpramipexole-d3 dihydrochloride
  • HY-19230
    DY-9760e

    		Calmodulin NO Synthase CaMK Calcineurin Proteasome Caspase Cardiovascular Disease
    DY-9760e is a calmodulin (CaM) inhibitor. DY-9760e selectively inhibits the activity of various calmodulin-dependent enzymes by antagonizing the Ca²⁺/CaM complex, exhibiting the strongest inhibitory activity against nNOS, CaM kinase II, and calcineurin (Ki: 0.9, 1.4, and 2.0 μM, respectively). DY-9760e inhibits excessive nitric oxide production and protein tyrosine nitration, as well as the activation of calpain and caspase-3. DY-9760e reduces infarct size, improves cardiac function, and inhibits oxidative stress and cell death. DY-9760e can be used in research on the treatment of myocardial infarction, cerebral ischemia, and other diseases .
    DY-9760e
  • HY-175640
    Troponin-IN-1

    		Pyroptosis Reactive Oxygen Species (ROS) Interleukin Related Caspase Cardiovascular Disease
    Troponin-IN-1 is a troponin inhibitor. Troponin-IN-1 protects OGD/R-injured H9c2 cardiomyocytes by reducing LDH leakage, pyroptosis and ROS accumulation. Troponin-IN-1 inhibits NO production and IL-1β/TNF-α/IL-18 release in LPS (HY-D1056)-induced RAW264.7 cells. Troponin-IN-1 acts via caspase-1/GSDMD/IL-18 pathway. Troponin-IN-1 reduces myocardial infarct size in LAD-induced myocardial ischemia/reperfusion (MI/R) male rats. Troponin-IN-1 can be used for the study of myocardial ischemia/reperfusion (MI/R) injury .
    Troponin-IN-1
  • HY-N2638
    Ilexsaponin A

    		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-B1218R
    Sulfaphenazole (Standard)

    		Reference Standards Cytochrome P450 Antibiotic Bacterial Necroptosis Apoptosis Infection Cardiovascular Disease
    Sulfaphenazole (Standard) is the analytical standard of Sulfaphenazole. This product is intended for research and analytical applications. Sulfaphenazole is a selective inhibitor of human cytochrome P450 (CYP) 2C9 enzyme. Sulfaphenazole is a cytoprotective agent against light-induced death of photoreceptors. Sulfaphenazole inhibits light-induced necrosis and mitochondrial stress-initiated apoptosis. Sulfaphenazole is an off patent sulfonamide antibiotic and demonstrates bactericidal activity through enhanced M1 macrophage activity. Sulfaphenazole can significantly reduce infarct size and restore post-ischemic coronary flow following ischemia and reperfusion .
    Sulfaphenazole (Standard)
  • HY-P11124
    MGF24

    		Apoptosis PKC Keap1-Nrf2 Heme Oxygenase (HO) Drug Derivative Neurological Disease
    MGF24 is a modified protease-resistant MGF derivative. MGF24 protects dopaminergic neurons from 6-Hydroxydopamine (6-OHDA) (HY-113028)-induced apoptosis by inducing Heme oxygenase-1 (HO-1). MGF24 activates PKC-ε, which in turn activates Nrf2, up-regulating HO-1. MGF24 has neuroprotective activity and reduces myocardial infarct size in sheep models of myocardial ischemia. MGF24 can be used for neurological diseases like stroke, nerve injury and amyotrophic lateral sclerosis research .
    MGF24
  • HY-175675
    P2Y1 antagonist 4

    		P2Y Receptor Keap1-Nrf2 Cardiovascular Disease Neurological Disease
    P2Y1 antagonist 4 is a selective P2Y1 receptor antagonist with excellent blood-brain barrier (BBB) penetration. P2Y1 antagonist 4 inhibits P2Y1 receptor-mediated cytosolic Ca 2+ increase (IC50 = 1.95 μM) and platelet aggregation (IC50 = 3.24 μM) induced by ADP in rabbit washed platelets. P2Y1 antagonist 4 significantly upregulates the level of nuclear Nrf2 protein in H2O2-treated HT22 cells. P2Y1 antagonist 4 reduces myocardial infarct size in a mouse acute myocardial infarction (MI) model. P2Y1 antagonist 4 can be used for the study of ischemic stroke and myocardial infarction .
    P2Y1 antagonist 4
  • HY-121726
    3HOI-BA-01

    		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-19862
    TY-51924 ethanol sodium

    		Na+/H+ Exchanger (NHE) Cardiovascular Disease
    TY-51924 ethanol sodium is a highly selective NHE-1 inhibitor (IC50 = 0.095 μM). TY-51924 ethanol sodium can significantly reduce the infarct size and myocardial enzyme release. TY-51924 ethanol sodium is commonly used in the study of ischemia-reperfusion injury .
    TY-51924 ethanol sodium
  • HY-106150A
    Eniporide mesylate

    		Na+/H+ Exchanger (NHE) Cardiovascular Disease
    Eniporide mesylate (EMD 96785 mesylate) is a Na(+)/H(+) exchange (NHE) inhibitor. Eniporide mesylate specifically inhibits the NHE-1 isoform. Eniporide mesylate improves cardiac performance inhibition associated with myocardial ischemia/reperfusion in animals, and limits infarct size in experimental models. Eniporide mesylate regulates cardiac performance and high-energy phosphate content .
    Eniporide mesylate
  • HY-W011082R
    NLRP3-IN-2 (Standard)

    		Reference Standards 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-N2638R
    Ilexsaponin A (Standard)

    		Reference Standards 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-19129
    KT2-962

    		Prostaglandin Receptor Cardiovascular Disease
    KT2-962 is a thromboxane A2 (TXA2) receptor antagonist and potent hydroxyl radical scavenger (IC50=500 nM). KT2-962 reduces myocardial infarct size and ventricular fibrillation. KT2-962 demonstrates cardioprotective effect in a canine ischemia/reperfusion model. KT2-962 is promising for research of myocardial ischemia-reperfusion injury and TXA2-mediated vascular diseases .
    KT2-962
  • HY-P5947
    Tat-HA-NR2B9c

    		HIV Neurological Disease
    Tat-HA-NR2B9 contains a fragment of the cellmembrane transduction domain of HIV-1 Tat, a influenza virus hemagglutinin (HA) epitope-tag, and the C-terminal 9 amino acids of NR2B (NR2B9c). Tat-HA-NR2B9 reduces infarct size and improves neurological functions in ischemia-induced cerebral injury in the rats
    Tat-HA-NR2B9c
  • HY-168770
    Cl-Necrostatin-1

    		RIP kinase TNF Receptor Apoptosis Cardiovascular Disease
    Cl-Necrostatin-1 is a RIPK1 inhibitor. Cl-Necrostatin-1 can also inhibit TNF-α-induced necroptosis in Jurkat cells deficient in Fas-associated death domain protein (FADD; EC50 = 180 nM), a modification that prevents caspase activation in response to death-domain receptor signaling. Cl-Necrostatin-1 can also reduce infarct size in a mouse model of middle cerebral artery occlusion (MCAO). Cl-Necrostatin-1 is used for research in cardiovascular and cerebrovascular diseases .
    Cl-Necrostatin-1
  • 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
  • HY-17355AR
    Dexpramipexole dihydrochloride (Standard)

    (R)-Pramipexole dihydrochloride (Standard); R-(+)-Pramipexole dihydrochloride (Standard); KNS-760704 dihydrochloride (Standard)

    		 Reference Standards ATP Synthase Sodium Channel Glutathione Peroxidase NOD-like Receptor (NLR) Mitophagy Ferroptosis PINK1/Parkin Autophagy Apoptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Dexpramipexole ((R)-Pramipexole) dihydrochloride (Standard) is the analytical standard of Dexpramipexole (dihydrochloride). This product is intended for research and analytical applications. Dexpramipexole dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more.
    Dexpramipexole dihydrochloride (Standard)
  • HY-133931
    Bimakalim

    EMD-52692; SR-44866

    		 Potassium Channel Glutathione Peroxidase Cardiovascular Disease
    Bimakalim (EMD-52692) is an ATP-sensitive potassium channel opener. Bimakalim reduces transmural MPO activity. Bimakalim mimics the effects of ischemic preconditioning to reduce infarct size, adenosine release, and neutrophil function in dogs .
    Bimakalim
  • HY-103346R
    MMPSI (Standard)

    		Reference Standards Caspase Apoptosis Cardiovascular Disease
    MMPSI (Standard) is the analytical standard of MMPSI (HY-103346). This product is intended for research and analytical applications. MMPSI is a potent and selective small molecule caspase 3 and caspase 7 inhibitor with an IC50 of 1.7 μM for human caspase-3. MMPSI can significantly reduce ischemia-reperfusion-induced infarct size in the isolated rabbit heart, and reduce apoptosis in both the ischemic myocardium and isolated cardiomyocytes. MMPSI can be used for researching cardioprotection .
    MMPSI (Standard)
  • HY-B1218S
    Sulfaphenazole-d4

    		Isotope-Labeled Compounds Cytochrome P450 Antibiotic Bacterial Necroptosis Apoptosis Infection
    Sulfaphenazole-d4 is the deuterium labeled Sulfaphenazole (HY-B1218). Sulfaphenazole is a selective inhibitor of human cytochrome P450 (CYP) 2C9 enzyme. Sulfaphenazole is a cytoprotective agent against light-induced death of photoreceptors. Sulfaphenazole inhibits light-induced necrosis and mitochondrial stress-initiated apoptosis. Sulfaphenazole is an off patent sulfonamide antibiotic and demonstrates bactericidal activity through enhanced M1 macrophage activity. Sulfaphenazole can significantly reduce infarct size and restore post-ischemic coronary flow following ischemia and reperfusion .
    Sulfaphenazole-d4
  • HY-182548
    BTS 72664

    		GABA Receptor Sodium Channel iGluR Cardiovascular Disease Neurological Disease
    BTS 72664 is a broad-spectrum, non-sedating, orally effective anticonvulsant. Its anticonvulsant effect mainly arises from enhancing GABAA receptor (GABAA receptor)-mediated chloride channel currents, while it exerts weak blocking effects on Na + channels (Ki = 350 μM) and NMDA receptors (NMDA receptor) (IC50 = 43 μM). BTS 72664 prevents the elevation of extracellular glutamate, glycine and serine concentrations in neurons, reduces cerebral infarct size, promotes functional recovery, prevents multiple types of epileptic seizures, and has low sedative potential. BTS 72664 can be used for the research of epilepsy, stroke and migraine .
    BTS 72664

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