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Pathways Recommended: Cell Cycle/DNA Damage
Results for "

cardiac tissue damage

" in MedChemExpress (MCE) Product Catalog:

6

Inhibitors & Agonists

2

Natural
Products

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-W018026
    Oxfenicine

    L-p-Hydroxyphenylglycine; 4-Hydroxy-L-phenylglycine; UK 25842

    		 Acyltransferase Apoptosis Cardiovascular Disease Metabolic Disease
    Oxfenicine (L-p-Hydroxyphenylglycine) is an orally active carnitine palmitoyltransferase-1 inhibitor. Oxfenicine inhibits the oxidation of fatty acids in the heart, protecting cardiac tissue from necrotic damage during ischemia, and also has an inhibitory effect on cardiac tissue apoptosis. In addition, Oxfenicine promotes lipolysis in a high-fat diet rat model. Oxfenicine can be used in the study of cardiovascular and metabolic diseases .
    Oxfenicine
  • 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-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-N6609
    Magnocurarine

    		nAChR Others
    Magnocurarine is a neuromuscular junction blocker that inhibits muscle contraction by functionally blocking signal transmission without directly damaging nerve or muscle tissues. In frog, mouse and rabbit models, Magnocurarine exerts a dose-dependent paralytic effect, which progresses gradually from limb weakness and loss of righting reflex to respiratory depression and even cardiac arrest. Although high doses cause complete cessation of movement, Magnocurarine does not affect the spinal multineuronal reflex in frogs. Magnocurarine exhibits biological activity similar to that of tubocurarine (HY-125901) in various animal models .
    Magnocurarine
  • HY-130272
    Anti-MI/R injury agent 1

    		Drug Derivative Cardiovascular Disease
    Anti-MI/R injury agent 1 (compound 18), a Panaxatriol derivative, is an orally active, potent anti-myocardial ischemia/reperfusion (anti-MI/R) injury agent. Anti-MI/R injury agent 1 enhances oxygen-glucose deprivation and reperfusion (OGD/R)-induced cardiomyocyte injury cell viability. Anti-MI/R injury agent 1 can markedly reduce myocardial infarction size, decrease circulating cardiac troponin I (cTnI) leakage, and alleviate cardiac tissue damage in the rats .
    Anti-MI/R injury agent 1
  • HY-N6609B
    Magnocurarine chloride

    		nAChR Cardiovascular Disease
    Magnocurarine chloride is a neuromuscular junction blocker that inhibits muscle contraction by functionally blocking signal transmission without directly damaging nerve or muscle tissues. In frog, mouse and rabbit models, Magnocurarine chloride exerts a dose-dependent paralytic effect, which progresses gradually from limb weakness and loss of righting reflex to respiratory depression and even cardiac arrest. Although high doses cause complete cessation of movement, Magnocurarine chloride does not affect the spinal multineuronal reflex in frogs. Magnocurarine chloride exhibits biological activity similar to that of tubocurarine (HY-125901) in various animal models .
    Magnocurarine chloride

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