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Results for "

myocardial function

" in MedChemExpress (MCE) Product Catalog:

53

Inhibitors & Agonists

2

Screening Libraries

1

Fluorescent Dye

1

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5

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10

Natural
Products

2

Isotope-Labeled Compounds

2

Oligonucleotides

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-16657
    TAPI-1
    Maximum Cited Publications
    15 Publications Verification

    		 MMP NF-κB Apoptosis TNF Receptor Inflammation/Immunology Cancer
    TAPI-1 is a broad-spectrum MMP inhibitor and NF-κB p65 inhibitor that targets ADAM17/TACE, ADAM10 and other proteins. TAPI-1 reduces the proteolytic cleavage of membrane-bound TNF-α, decreases TNF-α levels, inhibits NF-κB pathway activation, and downregulates profibrotic markers. TAPI-1 reduces the proportion of proinflammatory immune cells, alleviates cardiac and airway fibrosis, and improves cardiac function after myocardial infarction. Meanwhile, TAPI-1 inhibits the viability, migration and invasion of esophageal squamous cell carcinoma cells, enhances the chemosensitivity of Cisplatin (HY-17394), induces apoptosis, and shows low toxicity to normal esophageal epithelial cells. TAPI-1 can be widely used in studies related to myocardial infarction-induced heart failure, severe traumatic tracheal stenosis, esophageal squamous cell carcinoma and other conditions .
    TAPI-1
  • HY-B1409
    Isosorbide dinitrate

    ISDN

    		 NO Synthase Cardiovascular Disease
    Isosorbide dinitrate (ISDN) is an NO donor that prevents LV remodeling and degradation of cardiac function following myocardial infarction (MI) .
    Isosorbide dinitrate
  • HY-158426
    2-APQC
    1 Publications Verification

    		 Sirtuin Cardiovascular Disease
    2-APQC is an orally active and selective agonist of Sirtuin-3 (SIRT3) (Kd=2.756 μM), antagonizes Isoproterenol/ISO (HY-B0468)-induced cytotoxicity. 2-APQC activates the SIRT3-PYCR1 axis to enhance mitochondrial proline metabolism and inhibit the ROS-p38MAPK pathway by inhibiting signaling pathways such as mTOR-p70S6K, JNK, and TGF-β/Smad3. 2-APQC also activates the AMPK-Parkin axis to alleviate myocardial hypertrophy and fibrosis and protect cardiac function. 2-APQC can be used in the study of heart failure .
    2-APQC
  • 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-18100A
    PRE-084 hydrochloride
    10+ Cited Publications

    		 Sigma Receptor Akt NO Synthase Cardiovascular Disease Neurological Disease
    PRE-084 hydrochloride is a highly selective σ1 receptor (S1R) agonist, with an IC50 of 44 nM. PRE-084 hydrochloride exhibits good neuroprotective effects, can improve motor function and motor neuron survival in mice. PRE-084 hydrochloride also can ameliorate myocardial ischemia-reperfusion injury in rats by activating the Akt-eNOS pathway .
    PRE-084 hydrochloride
  • HY-121705
    Propionyl-L-carnitine

    		Endogenous Metabolite Apoptosis Bcl-2 Family NF-κB Survivin Src Akt AMPK NO Synthase Cardiovascular Disease Metabolic Disease Inflammation/Immunology
    Propionyl-L-carnitine is an orally active L-carnitine derivative. Propionyl-L-carnitine has a high affinity for muscle L-carnitine transferase. Propionyl-L-carnitine increases Apoptosis, Bax, and reduces NF-κB, VCAM-1, MCP-1, and survivin. Propionyl-L-carnitine activates Src kinase, Akt, induces p-AMPK and nitric oxide synthesis. Propionyl-L-carnitine alleviates cardiovascular disease, obesity, and colitis .
    Propionyl-L-carnitine
  • HY-173572
    SKLB-11A

    		Sirtuin Autophagy Cardiovascular Disease
    SKLB-11A is a selective, orally active and allosteric SIRT3 (sirtuin 3) agonist with a Kd value of 4.7 μM. SKLB-11A is highly selective for other members of the SIRT family. SKLB-11A activates autophagy-related signaling pathways, prevents mitochondrial dysfunction, improves cardiac function in Doxorubicin (HY-15142A)-induced cardiotoxicity and myocardial ischemia/reperfusion models .
    SKLB-11A
  • HY-159821
    Ulacamten

    CK-4021586; CK-586

    		 Myosin Cardiovascular Disease
    Ulacamten (CK-4021586; CK-586) is an orally active cardiac myosin inhibitor and an inhibitor of the double-headed cardiac heavy meromyosin (HMM)ATPase (excluding single-headed myosin subfragment-1), with an EC50 of 2.9 μM. Ulacamten regulates cardiac myosin, reduces excessive myocardial contractility, and alleviates left ventricular outflow tract obstruction. Ulacamten increases the left ventricular short-axis systolic internal diameter, inhibits dobutamine-induced exacerbation of obstruction, and exerts only a mild reducing effect on left ventricular systolic function. Ulacamten also inhibits the fractional shortening of the short axis without altering calcium transients. Ulacamten shows good safety and tolerability in purpose-bred cats with naturally occurring obstructive hypertrophic cardiomyopathy .
    Ulacamten
  • HY-13660
    Mocravimod hydrochloride
    2 Publications Verification

    KRP-203

    		 LPL Receptor Reactive Oxygen Species (ROS) Akt GSK-3 JAK STAT Metabolic Disease Inflammation/Immunology Cancer
    Mocravimod (hydrochloride) is an orally active sphingosine-1-phosphate receptor (S1PR) modulator that blocks the signal required by T cells to egress from lymph nodes and other lymphoid organs. Mocravimod (hydrochloride) preferentially binds to S1PR1 over S1PR2 and S1PR3 in cardiomyocytes. Mocravimod (hydrochloride) significantly lowered the concentration of reactive oxygen species (ROS), prevented mitochondrial permeability transition pore opening, boosted mitochondrial membrane potential (MMP), and increased phosphorylation of AKT, EKR, GSK-3β, JAK2, and STAT3. Mocravimod (hydrochloride) retains T cell effector function. Mocravimod (hydrochloride) can be used for the study of acute myelogenous leukemia, diabetes and Myocardial Ischemia-Reperfusion Injury (MIRI) .
    Mocravimod hydrochloride
  • HY-109038
    Mocravimod
    2 Publications Verification

    KRP-203 free base

    		 LPL Receptor Reactive Oxygen Species (ROS) Mitochondrial Metabolism Akt GSK-3 JAK STAT Cardiovascular Disease Metabolic Disease Inflammation/Immunology Cancer
    Mocravimod (KRP-203 free base) is a sphingosine-1-phosphate receptor (S1PR) modulator that blocks the signal required by T cells to egress from lymph nodes and other lymphoid organs. Mocravimod preferentially binds to S1PR1 over S1PR2 and S1PR3 in cardiomyocytes. Mocravimod significantly lowered the concentration of reactive oxygen species (ROS), prevented mitochondrial permeability transition pore opening, boosted mitochondrial membrane potential (MMP), and increased phosphorylation of AKT, EKR, GSK-3β, JAK2, and STAT3. Mocravimod retains T cell effector function. Mocravimod can be used for the study of acute myelogenous leukemia, diabetes and Myocardial Ischemia-Reperfusion Injury (MIRI) .
    Mocravimod
  • HY-112205
    RR-11a
    3 Publications Verification

    		 Legumain Cancer
    RR-11a is a synthetic enzyme inhibitor of Legumain (IC50=31-55 nM). RR-11a can be used for the research of cancer and acute myocardial infarction (AMI) .
    RR-11a
  • HY-106844A
    (+)-EMD 57033

    		Phosphodiesterase (PDE) Cardiovascular Disease
    (+)-EMD 57033 is a cardiac troponin C (cTnC) activator, is a dominant Ca 2+ sensitizer. (+)-EMD 57033 binds the cardiac/slow skeletal troponin C isoform and exerts myocardial contractile promotion function .
    (+)-EMD 57033
  • HY-P3304
    MR 409

    		GHSR Neurological Disease Cancer
    MR 409 is a selected growth hormone-releasing hormone (GHRH) agonist. MR 409 has remarkable neuroprotective effects through enhancing endogenous neurogenesis in cerebral ischemic mice. MR 409 also inhibits the in vivo growth of lung cancer .
    MR 409
  • HY-108448
    N-Oleoyldopamine

    OLDA

    		 TRP Channel Lipoxygenase Cardiovascular Disease Neurological Disease Metabolic Disease
    N-Oleoyldopamine (OLDA) is an orally active TRPV1 activator and 5-LOX inhibitor with blood-brain barrier permeability. N-Oleoyldopamine excites histaminergic neurons in the tuberomammillary nucleus via a dopamine receptor mechanism, a process independent of TRPV1 and cannabinoid receptors. On one hand, N-Oleoyldopamine promotes the release of insulin and glucose-dependent insulinotropic polypeptide through a GPR119-dependent pathway to improve glucose tolerance; on the other hand, N-Oleoyldopamine improves left ventricular function and reduces myocardial infarction size by triggering the release of substance P and calcitonin gene-related peptide. N-Oleoyldopamine is used in studies related to glycemic abnormalities and myocardial ischemia-reperfusion injury .
    N-Oleoyldopamine
  • HY-149662
    TMDJ-035

    		Calcium Channel ATP Synthase Myosin Cardiovascular Disease
    TMDJ-035 is a high-affinity, selective RyR2 inhibitor with an EC50 of 0.0130 μM. TMDJ-035 reduces RyR2 protein expression without affecting action potential-induced Ca 2+ transients. TMDJ-035 decreases ATP content and intracellular Ca 2+ levels. TMDJ-035 inhibits arrhythmias in a CPVT mouse model carrying mutant RyR2s. TMDJ-035 has no effect on electrocardiogram parameters or cardiac systolic function. TMDJ-035 exacerbates heart failure in mouse myocardial infarction models and hypoxic cardiomyocytes by altering cardiac function, causing tissue damage, promoting inflammatory infiltration, collagen deposition, and changes in Myosin heavy chain/actin expression. TMDJ-035 can be used in studies related to heart failure, catecholaminergic polymorphic ventricular tachycardia, and arrhythmias .
    TMDJ-035
  • 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-N6020B
    Butin
    1 Publications Verification

    		 Others Cardiovascular Disease Inflammation/Immunology
    Butin is a major biologically active flavonoid isolated from the heartwood of Dalbergia odorifera with oral activity, with strong antioxidant, antiplatelet and anti-inflammatory activities. Butin significantly alleviates myocardial infarction and improves heart function, together with prevents diabetes-induced cardiac oxidative damage in rat .
    Butin
  • 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-129763
    Di-4-ANEPPS

    		Fluorescent Dye Cardiovascular Disease
    Di-4-ANEPPS is a voltage-sensitive dye that acts on voltage-gated ion channels (such as sodium channels) and inhibits sodium current, significantly reducing sodium current density, although specific values like IC50 remain unclear. It mainly binds to the voltage-sensitive regions on the cell membrane, changing its fluorescence properties to reflect membrane potential changes and thus affecting the function of ion channels to exert its activity. This substance can be used in cardiovascular research, such as the electrophysiology of cardiomyocytes, myocardial ischemia, and the effects of drugs on cardiomyocytes. It is of great value in evaluating drug cardiotoxicity and exploring the mechanisms of arrhythmias .
    Di-4-ANEPPS
  • HY-174400
    SGLT2-IN-2

    		SGLT SOD Na+/H+ Exchanger (NHE) Autophagy Cardiovascular Disease
    SGLT2-IN-2 (Compound E9) is an inhibitor of SGLT2. SGLT2-IN-2 significantly enhances the inhibition of SGLT2, NHE1, and SOD enzyme activity. SGLT2-IN-2 has protective effect on the glucose-free DMEM-induced injured cardiomyocytes. SGLT2-IN-2 significantly improves cardiac function in TAC-induced HF mice and inhibits cardiomyocyte hypertrophy as well as collagen deposition. SGLT2-IN-2 can ameliorate myocardial tissue damage and enhance mitochondrial autophagy in injured cardiomyocytes, thereby increasing survival rates in HF mice .
    SGLT2-IN-2
  • HY-N6850
    Calenduloside E
    1 Publications Verification

    		 Apoptosis Pyroptosis AMPK Bcl-2 Family JAK STAT Calcium Channel Interleukin Related TNF Receptor SOD Reactive Oxygen Species (ROS) PPAR Cardiovascular Disease Inflammation/Immunology
    Calenduloside E is a pentacyclic triterpenoid saponin that can be extracted from the bark and roots of Aralia ovata, and has anti-inflammatory and anti-apoptotic activities. Calenduloside E alleviates atherosclerosis by regulating macrophage polarization, improves mitochondrial function by regulating the AMPK-SIRT3 pathway, and alleviates acute liver injury. In addition, Calenduloside E promotes the interaction between L-type calcium channels and Bcl-2 related apoptosis genes, inhibits calcium overload, and alleviates myocardial ischemia/reperfusion injury. Calenduloside E also improves non-alcoholic fatty liver disease by regulating heat shock-dependent pathways, and inhibits ROS mediated JAK1-STAT3 pathways to reduce cellular inflammatory responses .
    Calenduloside E
  • HY-177204
    DSPE-PEG2000-WLSEAGPVVTVRALRGTGSW

    		Ferroptosis Apoptosis Glutathione Peroxidase Cardiovascular Disease
    DSPE-PEG2000-WLSEAGPVVTVRALRGTGSW is a polypeptide targeting tenascin-X (Tenascin-X) that can be conjugated with liposomes and exosomes. DSPE-PEG2000-WLSEAGPVVTVRALRGTGSW specifically binds to Tenascin-X on the surface of cardiomyocytes, mediates receptor-dependent uptake of nanocarriers, enhances targeted drug delivery of cargo to cardiomyocytes, and increases drug accumulation in cardiac tissue. DSPE-PEG2000-WLSEAGPVVTVRALRGTGSW protects cardiomyocytes treated with LPS, alleviates oxidative stress, repairs mitochondrial function, inhibits ferroptosis and apoptosis, and downregulates the secretion of pro-inflammatory cytokines at the same time. DSPE-PEG2000-WLSEAGPVVTVRALRGTGSW improves cardiac injury and pathological morphology in mice with sepsis-induced cardiomyopathy, restores GPX4 expression, and promotes the internalization of cardiomyocyte-derived exosomes, making it suitable for related research on sepsis-induced cardiomyopathy, myocardial ischemia-reperfusion injury, and other conditions .
    DSPE-PEG2000-WLSEAGPVVTVRALRGTGSW
  • HY-176716
    ALDH2 activator 1

    		Aldehyde Dehydrogenase (ALDH) Cardiovascular Disease
    ALDH2 activator 1 (Compound Z17) is an allosteric aldehyde dehydrogenase 2 (ALDH2) agonist. ALDH2 activator 1 enhances cardiac function and reduces myocardial necrosis in a mouse model of myocardial ischemia-reperfusion. ALDH2 activator 1 is promising for research of cardiovascular diseases such as myocardial infarction (MI) .
    ALDH2 activator 1
  • HY-170538
    SNT-5382

    		Lysyl Oxidase Cytochrome P450 Cardiovascular Disease Metabolic Disease
    SNT-5382 is a lysyl oxidase family (LOX) inhibitor and anti-fibrotic agent. SNT-5382 binds to the LTQ cofactor of LOXL2 and inhibits the enzymatic activities of LOXL3, LOXL4, LOXL1, CYP2C9, and CYP2C19. SNT-5382 reduces cardiac and liver fibrosis as well as collagen crosslinks, and improves cardiac function. SNT-5382 can be used for the research of heart failure, myocardial infarction, and nonalcoholic steatohepatitis-related liver fibrosis .
    SNT-5382
  • HY-P10336
    Serpinin

    		Serpin Neurological Disease Endocrinology
    Serpinin is an agonist of the protease inhibitor Nexin-1 (PN-1). Serpinin upregulates the expression of PN-1 through the cAMP-PKA-Sp1 signaling pathway, promoting granule biogenesis in endocrine cells. Serpinin is used in research related to the regulation of secretory function . Serpinin is a selective agonist for β-adrenergic receptors. Serpinin interacts with β1-adrenergic receptors to activate the AC-cAMP-PKA pathway, which regulates myocardial systolic and diastolic function. pGlu-serpinin upregulates Bcl2 mRNA transcription and exerts neuroprotective effects .
    Serpinin
  • HY-N2026A
    Propylparaben sodium
    1 Publications Verification

    Propyl parahydroxybenzoate sodium; Propyl 4-hydroxybenzoate sodium

    		 Estrogen Receptor/ERR Cardiovascular Disease Neurological Disease
    Propylparaben sodium is an orally active weak estrogen receptor agonist. Propylparaben sodium regulates the PI3K-AKT and JNK signaling pathways, induces oxidative stress, and alters the estrous cycle, hormone levels and ovarian reserve function. Propylparaben sodium inhibits the growth of antral follicles and alters the accumulation of steroid hormones in follicle culture media. Propylparaben sodium can be used in studies related to ovarian aging and myocardial ischemia-reperfusion injury[1][2][3][4][5].
    Propylparaben sodium
  • 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-121259
    Doxorubicinol

    Adriamycinol; DXR-OL

    		 Endogenous Metabolite Cardiovascular Disease
    Doxorubicinol, a potent inhibitor of the cardiac sarcoplasmic reticulum calcium pump, inhibits systolic myocardial function in isolated heart muscle. Doxorubicinol inhibits tumor cell growth and has cardiotoxicity.
    Doxorubicinol
  • HY-B1409S
    Isosorbide dinitrate-13C6

    ISDN-13C6

    		 NO Synthase Cardiovascular Disease
    Isosorbide dinitrate- 13C6 is the 13C labeled Isosorbide dinitrate . Isosorbide dinitrate (ISDN) is an NO donor that prevents LV remodeling and degradation of cardiac function following myocardial infarction (MI) .
    Isosorbide dinitrate-13C6
  • HY-18100
    PRE-084

    		Sigma Receptor Akt NO Synthase Cardiovascular Disease Neurological Disease
    PRE-084 is a highly selective σ1 receptor (S1R) agonist, with an IC50 of 44 nM. PRE-084 exhibits good neuroprotective effects, can improve motor function and motor neuron survival in mice. PRE-084 also can ameliorate myocardial ischemia-reperfusion injury in rats by activating the Akt-eNOS pathway .
    PRE-084
  • 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-105362
    PD 155080

    		Endothelin Receptor Cardiovascular Disease
    PD 155080 is a selective endothelin A receptor (ETA receptor) antagonist. PD 155080 reduces coronary resistance in the isolated rat heart model. PD 155080 improves myocardial systolic function and diastolic function in the ischemia/reperfusion model. PD 155080 can be used for the study of cardiovascular diseases .
    PD 155080
  • HY-123721
    Tiracizine hydrochloride

    AWD-19-166; GS 015

    		 Endogenous Metabolite Cardiovascular Disease
    Tiracizine hydrochloride (AWD-19-166) is a Class I antiarrhythmic drug with activity that reduces myocardial contractile function. Tiracizine hydrochloride was studied in patients with ischemic heart disease, showing its effects on the myocardium. Tiracizine hydrochloride reduces myocardial contractility and may have potential use in the management of heart disease .
    Tiracizine hydrochloride
  • HY-106987
    SP/W 5186

    		NO Synthase Cardiovascular Disease Inflammation/Immunology
    SP/W-5186 is a nitric oxide (NO) donor agent containing a cysteine structure. SP/W-5186 can improve cardiac function, reduce myocardial damage, protect vascular endothelial function and inhibit inflammation and oxidative stress. SP/W-5186 has the ability to inhibit oxidative damage induced by peroxynitrite (ONOO⁻). SP/W-5186 can be used in the research of myocardial ischemia-reperfusion injury .
    SP/W 5186
  • HY-106045
    Imazodan

    CI 914 free base

    		 Phosphodiesterase (PDE) Cardiovascular Disease
    Imazodan is a selective inhibitor for phosphodiesterase III (PDE III), which increases myocardial contractility by blocking the cAMP degradation, and improves the contractile function of heart. Imazodan serves also as a peripheral vasodilator .
    Imazodan
  • HY-B1409R
    Isosorbide dinitrate (Standard)

    ISDN (Standard)

    		 Reference Standards NO Synthase Cardiovascular Disease
    Isosorbide dinitrate (Standard) is the analytical standard of Isosorbide dinitrate. This product is intended for research and analytical applications. Isosorbide dinitrate (ISDN) is an NO donor that prevents LV remodeling and degradation of cardiac function following myocardial infarction (MI) .
    Isosorbide dinitrate (Standard)
  • HY-106045A
    Imazodan hydrochloride

    CI 914

    		 Phosphodiesterase (PDE) Cardiovascular Disease
    Imazodan hydrochloride is the hydrochloride form of Imazodan (HY-106045). Imazodan hydrochloride is a selective inhibitor for phosphodiesterase III (PDE III), which increases myocardial contractility by blocking the cAMP degradation, and improves the contractile function of heart. Imazodan hydrochloride serves also as a peripheral vasodilator .
    Imazodan hydrochloride
  • HY-W803860
    N-Depropylpropafenone

    		Drug Metabolite Sodium Channel Cardiovascular Disease
    N-Depropylpropafenone is an active metabolite of Propafenone (HY-B0432), generated through the CYP450 enzyme system (mainly CYP2D6). It functions by blocking sodium ion channels, slowing myocardial conduction and exhibiting certain antiarrhythmic effects .
    N-Depropylpropafenone
  • HY-171336
    TRC4186

    		Interleukin Related Metabolic Disease
    TRC4186 is a potent advanced glycation end-product (AGE) inhibitor. TRC4186 demonstrates AGE-breaking activities in vitro and improvement in the endothelial and myocardial function in animal models of diabetes mellitus. TRC4186 can be used for complications associated with diabetes research .
    TRC4186
  • HY-174673
    Human GATA4 mRNA

    		mRNA Cancer
    Human GATA4 mRNA encodes the human GATA binding protein 4 (GATA4) protein, a member of the GATA family of zinc-finger transcription factors. GATA4 is thought to regulate genes involved in embryogenesis and in myocardial differentiation and function. It is also necessary for normal testicular development.
    Human GATA4 mRNA
  • HY-N6020BR
    Butin (Standard)

    		Reference Standards Others Cardiovascular Disease Inflammation/Immunology
    Butin is a major biologically active flavonoid isolated from the heartwood of Dalbergia odorifera with oral activity, with strong antioxidant, antiplatelet and anti-inflammatory activities. Butin significantly alleviates myocardial infarction and improves heart function, together with prevents diabetes-induced cardiac oxidative damage in rat .
    Butin (Standard)
  • HY-101390B
    Niguldipine

    		Calcium Channel Cardiovascular Disease
    Niguldipine is a calcium channel blocker with activity in regulating cardiovascular function. Niguldipine can reduce systolic and diastolic blood pressure, thereby increasing heart rate and cardiac output. Niguldipine exhibits dose-dependent and sustained increases in coronary blood flow. Niguldipine also increases perfusion in the kidneys and femoral arteries, but the effect is temporary and to a lesser extent. The effect of Niguldipine on myocardial metabolism is not significant .
    Niguldipine
  • 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-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-E70759
    MKK6 SDTD Recombinant Human Active Protein Kinase

    		p38 MAPK Cancer
    The mitogen-activated protein kinase kinase 6 (MKK6) is one of the upstream activators of p38 MAPK. MKK6 activates myocardial cell NF-κB and inhibits apoptosis in a p38 MAPK-dependent manner. MKK6 SDTD is a mutant of MKK6. MKK6 SDTD Recombinant Human Active Protein Kinase is a recombinant MKK6 SDTD protein that can be used to study MKK6 SDTD-related functions .
    MKK6 SDTD Recombinant Human Active Protein Kinase
  • HY-18100AR
    PRE-084 hydrochloride (Standard)

    		Reference Standards Sigma Receptor Akt NO Synthase Cardiovascular Disease Neurological Disease
    PRE-084 (hydrochloride) (Standard) is the analytical standard of PRE-084 (hydrochloride). This product is intended for research and analytical applications. PRE-084 hydrochloride is a highly selective σ1 receptor (S1R) agonist, with an IC50 of 44 nM. PRE-084 hydrochloride exhibits good neuroprotective effects, can improve motor function and motor neuron survival in mice. PRE-084 hydrochloride also can ameliorate myocardial ischemia-reperfusion injury in rats by activating the Akt-eNOS pathway .
    PRE-084 hydrochloride (Standard)
  • HY-P5762A
    Phoenixin-14 TFA

    PNX-14 TFA

    		 Orphan GPCR Glutathione Peroxidase Ferroptosis ERK Toll-like Receptor (TLR) Sirtuin FOXO Akt PKA MyD88 Reactive Oxygen Species (ROS) Apoptosis NF-κB Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    Phoenixin-14 (PNX-14) TFA is an endogenous neuropeptide with multiple biological activities, and serves as the endogenous ligand of GPR173. Phoenixin-14 TFA reduces ROS production by inhibiting the HMGB1/TLR4/MyD88/NF-κB signaling axis, thereby exerting antioxidant and mitochondrial protective effects. Phoenixin-14 TFA inhibits FOXO3 phosphorylation by upregulating SIRT3 expression, suppresses apoptosis, and improves myocardial systolic/diastolic function. Phoenixin-14 TFA resists ferroptosis by activating the ATF4/SLC7A11/GPX4 axis; it activates ERK1/2 phosphorylation via GPR173. Phoenixin-14 TFA can be used in researches on neuroprotection, diabetes, cardiomyopathy, reproductive protection and so on .
    Phoenixin-14 TFA

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