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Results for "

myocardial ATP

" in MedChemExpress (MCE) Product Catalog:

By Targets:	ATP Synthase (8) Apoptosis (6) Autophagy (4) Calcium Channel (3) Creatine Kinase (1) Drug Derivative (1) Drug Metabolite (2) Endogenous Metabolite (2) Eukaryotic Initiation Factor (eIF) (2) Ferroptosis (4) Glutathione Peroxidase (6) Isotope-Labeled Compounds (2) Lactate Dehydrogenase (1) Mitochondrial Metabolism (1) Mitophagy (4) Myosin (1) NOD-like Receptor (NLR) (4) P2Y Receptor (1) PARP (2) PDHK (1) Phosphodiesterase (PDE) (2) PINK1/Parkin (4) PKA (1) Potassium Channel (6) Prostaglandin Receptor (1) Reactive Oxygen Species (ROS) (3) Reference Standards (1) Sodium Channel (4)
By Research Areas:	Cancer (4) Cardiovascular Disease (18) Infection (1) Inflammation/Immunology (9) Metabolic Disease (3) Neurological Disease (5)

By Targets:

ATP Synthase (8)

Apoptosis (6)

Autophagy (4)

Calcium Channel (3)

Creatine Kinase (1)

Drug Derivative (1)

Drug Metabolite (2)

Endogenous Metabolite (2)

Eukaryotic Initiation Factor (eIF) (2)

Ferroptosis (4)

Glutathione Peroxidase (6)

Isotope-Labeled Compounds (2)

Lactate Dehydrogenase (1)

Mitochondrial Metabolism (1)

Mitophagy (4)

Myosin (1)

NOD-like Receptor (NLR) (4)

P2Y Receptor (1)

PARP (2)

PDHK (1)

Phosphodiesterase (PDE) (2)

PINK1/Parkin (4)

PKA (1)

Potassium Channel (6)

Prostaglandin Receptor (1)

Reactive Oxygen Species (ROS) (3)

Reference Standards (1)

Sodium Channel (4)

By Research Areas:

Cancer (4)

Cardiovascular Disease (18)

Infection (1)

Inflammation/Immunology (9)

Metabolic Disease (3)

Neurological Disease (5)

Inhibitors & Agonists

Screening Libraries

Isotope-Labeled Compounds

Targets Recommended: ATP Synthase ATP-binding cassette (ABC) transporters ATP Citrate Lyase P-glycoprotein

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-112654

GCN2iB Maximum Cited Publications 60 Publications Verification	Eukaryotic Initiation Factor (eIF) Glutathione Peroxidase	Cardiovascular Disease Metabolic Disease Cancer
GCN2iB is an ATP-competitive, selective GCN2 inhibitor with an IC₅₀ of 2.4 nM. GCN2iB inhibits the activation of the GCN2 pathway and upregulates GPX4. GCN2iB enhances the anticancer effect of ASNase against acute lymphoblastic leukemia. GCN2iB increases left ventricular ejection fraction, while reducing fasting blood glucose and myocardial fibrosis. GCN2iB can be used in research related to acute lymphoblastic leukemia, acute myeloid leukemia and diabetic cardiomyopathy .

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 Na_v1.8 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 .

HY-121744

PS10 5+ Cited Publications	PDHK	Inflammation/Immunology
PS10 is a novel, potent and ATP-competitive pan-PDK inhibitor, inhibits all PDK isoforms with IC₅₀ of 0.8 μM, 0.76 μM, 2.1 μM and 21.3 μM for PDK2, PDK4, PDK1, and PDK3, respectively. PS10 shows high affinity for PDK2 (K_d= 239 nM) than for Hsp90 (K_d= 47 μM) . PS10 improves glucose tolerance, stimulates myocardial carbohydrate oxidation in diet-induced obesity. PS10 has the potential for the investigation of diabetic cardiomyopathy .PDK: pyruvate dehydrogenase kinase

HY-114869

DPQ 3 Publications Verification	PARP	Neurological Disease Cancer
DPQ is a selective PARP-1 inhibitor that blocks PARP-1-mediated DNA damage repair and NAD ⁺/ATP consumption, thereby inhibiting excessive inflammatory responses. DPQ inhibits NF-κB pathway activation, reduces the expression of pro-inflammatory factors (such as TNF-α, IL-6) and oxidative stress. DPQ can be used in inflammation-related studies of acute lung injury, myocardial infarction, and neurodegenerative diseases .

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 .

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 Na_v1.8 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 .

HY-135746

OR-1896 2 Publications Verification	Potassium Channel Phosphodiesterase (PDE) Drug Metabolite Apoptosis	Cardiovascular Disease
OR-1896 is an active long-lived metabolite of Levosimendan. OR-1896 is a highly selective phosphodiesterase (PDE) III isoform inhibitor and a powerful vasodilator. OR-1896 can open ATP-sensitive K ⁺ channels and has Ca ²⁺-sensitizing effect. OR-1896 mitigates cardiomyocyte apoptosis, cardiac remodeling and myocardial inflammation .

HY-108659

NF340	P2Y Receptor	Inflammation/Immunology
NF340 is a P2Y11 receptor inhibitor with a pIC₅₀ of 7.3-7.7 against human P2Y11 receptor, and it exhibits high selectivity over other P2Y family receptors. NF340 binds to the ATP-binding amino acid residues of the P2Y11 receptor to inhibit its activity, block nociceptive activity, and reduce spinal dorsal horn P2Y11 receptor upregulation induced by spinal cord injury. NF340 attenuates the NFκB signaling pathway activated by IL-1β by decreasing IκBα phosphorylation, nuclear p65 accumulation and NFκB promoter activity. NF340 inhibits IL-1β-induced pro-inflammatory cytokine expression, reduces intracellular ROS and 4-HNE levels, and suppresses IL-1β-induced matrix metalloproteinase expression in primary fibroblast-like synoviocytes. NF340 inhibits ATP-induced elevation of intracellular calcium ²⁺ concentration and cell migration in human hepatocellular carcinoma cells. NF340 is applicable to the research of neuropathic pain, myocardial ischemia/reperfusion injury, inflammatory pain, rheumatoid arthritis and hepatocellular carcinoma .

HY-12184

ONO-AE 248	Prostaglandin Receptor Endogenous Metabolite	Cardiovascular Disease
ONO-AE 248 is a selective EP3 receptor agonist with cardioprotective activity. ONO-AE 248 reduces myocardial infarction size by selectively binding to the EP3α receptor in mice. The cardioprotective effect of ONO-AE 248 is independent of hemodynamic effects. The mechanism of ONO-AE 248 may involve activation of protein kinase C and opening of K(ATP) channels .

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 Na_v1.8 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.

HY-172959

mPTP-IN-1	Mitochondrial Metabolism	Cardiovascular Disease
mPTP-IN-1 (Compound 14e) is a mitochondrial permeability transition pore (mPTP) inhibitor. mPTP-IN-1 blocks calcium-induced mPTP opening by targeting the C subunit of ATP synthase. mPTP-IN-1 can be used to study myocardial ischemia/reperfusion injury (IRI) .

HY-149736

ATP Synthesis-IN-3	PKA ATP Synthase	Cardiovascular Disease
ATP Synthesis-IN-3 (compound 31) is an ATP hydrolysis inhibitor with protective effects during myocardial ischemia. ATP Synthesis-IN-3 can increase the ATP content of ischemic cardiomyocytes, increase the phosphorylation of PKA and phospholamban, and inhibit ischemia-induced apoptosis .

HY-120540

BMS-182264	Potassium Channel	Cardiovascular Disease
BMS-182264 is a highly selective ATP-sensitive potassium channel agonist. BMS-182264 promotes potassium efflux and membrane hyperpolarization to induce smooth muscle relaxation and vasodilation. BMS-182264 is promising for research of cardiovascular diseases such as hypertension and myocardial ischemia .

HY-120554

RWJ 29009	Potassium Channel	Cardiovascular Disease
RWJ 29009 is a highly selective ATP-sensitive potassium channel agonist. RWJ 29009 activates potassium channel in vascular smooth muscle cells, promoting potassium efflux and membrane hyperpolarization to induce coronary and peripheral vasodilation. RWJ 29009 is promising for research of cardiovascular diseases such as acute myocardial ischemia and hypertension .

HY-165363

AK-135 hydrochloride	Drug Derivative Lactate Dehydrogenase ATP Synthase	Cardiovascular Disease
AK-135 hydrochloride is a Menadione (HY-B0332) derivative. AK-135 hydrochloride restores the electron flow in defective respiratory chain systems. AK-135 hydrochloride decreases LDH release, increases the amount of *ATP. AK-135 hydrochloride has a protective effect against myocardial* injury .

HY-W010902

Calcium fructose diphosphate Dicalcium 1,6-di-O-phosphonato-L-tagatose	Endogenous Metabolite ATP Synthase	Metabolic Disease
Calcium fructose diphosphate (Dicalcium 1,6-di-O-phosphonato-L-tagatose) is a crucial intermediate in the glycolysis process and is closely related to ATP synthesis. Calcium fructose diphosphate can be used to regulate calcium and phosphorus balance, protect myocardial tissue from ischemia/reperfusion injury, counteract the effects of alcohol, and serve as a safer source of phosphate in parenteral nutrition .

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 Na_v1.8 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.

HY-W424851

DPQ hydrochloride 6,7-Dimethoxy-2-(1-piperazinyl)-4-quinazolinamine hydrochloride	PARP	Infection Inflammation/Immunology
DPQ hydrochloride is a blood-brain barrier permeable and selective PARP-1 inhibitor that blocks PARP-1-mediated DNA damage repair and NAD ⁺/ATP consumption, thereby inhibiting excessive inflammatory responses. DPQ hydrochloride inhibits NF-κB pathway activation, reduces the expression of pro-inflammatory factors (such as TNF-α, IL-6) and oxidative stress. DPQ hydrochloride can be used in inflammation-related studies of acute lung injury, myocardial infarction, and neurodegenerative diseases .

HY-112654A

GCN2iB acetate	Eukaryotic Initiation Factor (eIF) Glutathione Peroxidase	Cardiovascular Disease Metabolic Disease Cancer
GCN2iB acetate is an ATP-competitive, selective GCN2 inhibitor with an IC₅₀ of 2.4 nM. GCN2iB acetate inhibits the activation of the GCN2 pathway and upregulates GPX4. GCN2iB acetate enhances the anticancer effect of ASNase against acute lymphoblastic leukemia. GCN2iB acetate increases left ventricular ejection fraction, while reducing fasting blood glucose and myocardial fibrosis. GCN2iB acetate can be used in research related to acute lymphoblastic leukemia, acute myeloid leukemia and diabetic cardiomyopathy .

HY-165486

AWD 122-60	Potassium Channel Calcium Channel	Cardiovascular Disease
AWD 122-60 is a potassium channel blocker and calcium sensitizer, with IC₅₀ values of 11 μM and 29 μM, respectively, against mouse skeletal muscle ATP-sensitive potassium (K_ATP) channels. AWD 122-60 exerts potent positive inotropic activity. AWD 122-60 exhibits antiarrhythmic activity in vivo and prolongs myocardial refractory period in vitro. AWD 122-60 can be used for research related to arrhythmias .

HY-135746S

OR-1896-d3	Isotope-Labeled Compounds Phosphodiesterase (PDE) Apoptosis Potassium Channel Drug Metabolite	Cardiovascular Disease
OR-1896-d₃ is the deuterium labeled OR-1896 (HY-135746). OR-1896 is an active long-lived metabolite of Levosimendan. OR-1896 is a highly selective phosphodiesterase (PDE) III isoform inhibitor and a powerful vasodilator. OR-1896 can open ATP-sensitive K+ channels and has Ca2+-sensitizing effect. OR-1896 mitigates cardiomyocyte apoptosis, cardiac remodeling and myocardial inflammation .

HY-183206

UR 8225	Potassium Channel Calcium Channel	Cardiovascular Disease Inflammation/Immunology
UR 8225 is an orally active ATP-sensitive K ⁺ channel activator with vasodilator, smooth muscle relaxant, antihypertensive, and bronchodilator activities. UR 8225 induces membrane hyperpolarization by increasing outward K ⁺ conductance and reduces Ca ²⁺ influx through voltage-gated L-type Ca ²⁺ channels. UR 8225 reduces total peripheral vascular resistance, shortens cardiac action potential duration, inhibits agonist-induced Ca ²⁺ influx, and stimulates renin release. UR 8225 induces reflex tachycardia but lacks β-adrenergic receptor blocking activity. UR 8225 is widely applicable to research in fields related to hypertension, myocardial ischemia, ventricular fibrillation, and other conditions .

HY-148150A

Cyclocreatine phosphate dilithium	Creatine Kinase	Cardiovascular Disease Inflammation/Immunology Cancer
Cyclocreatine phosphate dilithium is a synthetic intracellular energy buffer. Cyclocreatine phosphate dilithium mediates antiproliferative activity in cells with high creatine kinase levels and inhibits solid tumor growth. Cyclocreatine phosphate dilithium maintains adenosine triphosphate (ATP) levels and protects tissues from hypoxia, cellular damage and inflammation during ischemic events. Cyclocreatine phosphate dilithium accumulates in skeletal muscle, reduces muscle phosphocreatine and total creatine levels, and acts both as a bioenergetic/anti-inflammatory agent and an experimental tool for the assessment of ischemic injury. Cyclocreatine phosphate dilithium can be used in studies related to solid tumors, heart failure and ischemia .

Cat. No.	Product Name

HY-L227

Amino Acid Metabolite Compound Library	198 compounds
Amino acids are the fundamental components that sustain life activities, playing roles in ATP generation, promoting nucleotide synthesis, and maintaining cellular redox balance. Moreover, dysregulation of amino acid consumption is a significant potential regulatory mechanism leading to impaired anti-tumor immunity in immune cells. The normal functioning of immune cells relies on amino acid metabolic pathways to obtain energy and materials, and upon activation, they reprogram their metabolism to support growth, proliferation, and effector functions. Additionally, metabolic disorders of specific amino acids (such as branched-chain amino acids, glutamine, and arginine) can exacerbate mitochondrial dysfunction and oxidative stress, thereby promoting myocardial fibrosis and cardiac cell damage. Therefore, conducting research related to amino acid metabolism holds promise for discovering potential drugs for diseases related to cancer, immunity, and metabolism. MCE can provide 198 kinds of metabolites of amino acid metabolic pathways, which can be used for drug screening in various diseases such as cancer, immune disorders, metabolic diseases, mitochondrial-targeted diseases

Amino Acid Metabolite Compound Library

198 compounds

Amino acids are the fundamental components that sustain life activities, playing roles in ATP generation, promoting nucleotide synthesis, and maintaining cellular redox balance. Moreover, dysregulation of amino acid consumption is a significant potential regulatory mechanism leading to impaired anti-tumor immunity in immune cells. The normal functioning of immune cells relies on amino acid metabolic pathways to obtain energy and materials, and upon activation, they reprogram their metabolism to support growth, proliferation, and effector functions. Additionally, metabolic disorders of specific amino acids (such as branched-chain amino acids, glutamine, and arginine) can exacerbate mitochondrial dysfunction and oxidative stress, thereby promoting myocardial fibrosis and cardiac cell damage. Therefore, conducting research related to amino acid metabolism holds promise for discovering potential drugs for diseases related to cancer, immunity, and metabolism.

MCE can provide 198 kinds of metabolites of amino acid metabolic pathways, which can be used for drug screening in various diseases such as cancer, immune disorders, metabolic diseases, mitochondrial-targeted diseases

Cat. No.	Product Name	Chemical Structure

HY-17355BS

Dexpramipexole-d3 dihydrochloride
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 Na_v1.8 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

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 Na_v1.8 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.

HY-135746S

OR-1896-d3
OR-1896-d₃ is the deuterium labeled OR-1896 (HY-135746). OR-1896 is an active long-lived metabolite of Levosimendan. OR-1896 is a highly selective phosphodiesterase (PDE) III isoform inhibitor and a powerful vasodilator. OR-1896 can open ATP-sensitive K+ channels and has Ca2+-sensitizing effect. OR-1896 mitigates cardiomyocyte apoptosis, cardiac remodeling and myocardial inflammation .

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