2. Disease Areas
  3. Blood or Cardio-cerebrovascular Disease
  4. Heart Disease
  5. Myocardial Infarction

Myocardial Infarction

Myocardial infarction, commonly known as a heart attack, is a critical cardiovascular event characterized by the irreversible necrosis of heart muscle tissue due to prolonged ischemia resulting from blocked blood flow in one or more coronary arteries. The most frequent cause is atherosclerosis, where plaque buildup in the arterial walls ruptures and triggers thrombus formation, leading to acute obstruction. This blockage deprives the myocardium of oxygen and nutrients, causing chest pain—typically retrosternal and radiating to the left shoulder, arm, or jaw—that may mimic heartburn or indigestion. Additional symptoms include shortness of breath, nausea, vomiting, lightheadedness, dizziness, cold sweats, and in severe cases, cardiac arrest. Prompt medical intervention with thrombolytic agents (clot-busters), antiplatelet drugs, angioplasty, or coronary artery bypass grafting is essential to restore perfusion and minimize myocardial damage. Delayed treatment can result in permanent heart muscle injury, heart failure, or death. Recognition of warning signs and immediate activation of emergency services are crucial for improving outcomes.

Myocardial Infarction (24):

Cat. No. Product Name CAS No. Purity Chemical Structure
  • HY-Y1322
    Triphenyl phosphate 115-86-6 99.67%
    Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring.
    Triphenyl phosphate
  • HY-103185
    CCPA 37739-05-2 99.77%
    CCPA (2-Chloro-N6-cyclopentyladenosine) a highly selective A1 adenosine receptors agonist with a Ki of 0.4 nM. CCPA inhibits adenylate cyclase with an IC50 of 33 nM. CCPA exhibits anti-seizure and cardiacprotective activity. CCPA can be used for the research of seizure and myocardial infarction.
    CCPA
  • HY-159821
    Ulacamten 2830607-59-3 99.22%
    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-125972
    zr17-2 1263893-98-6 98.01%
    zr17-2 is a cold inducible RNA-binding protein (CIRBP) agonist. zr17-2 has anti-inflammatory and anti-oxidant and can be used for the study of myocardial infarction. zr17-2 is a hypothermia mimetic molecule that reduces oxidative stress-induced retinal cell death.
    zr17-2
  • HY-117200
    Necrostatin-7 351062-08-3 99.64%
    Necrostatin-7 (Nec-7) is a Necroptosis inhibitor with an EC50 of 10.6 μM. Necrostatin-7 inhibits signal transduction from RANK to NFATc1 without affecting the activation of MAPK or NF-κB. Necrostatin-7 suppresses the expression levels of Acp5, Atp6v0d2, Ctsk and Dcstamp. Necrostatin-7 reduces myocardial infarction size, ameliorates adverse left ventricular remodeling, decreases myocardial wall stress, reduces the amount and length of scar tissue, and improves left ventricular function. Necrostatin-7 exerts cardioprotective effects in a rat model of permanent coronary artery occlusion. Necrostatin-7 can be used in research related to osteolytic bone diseases and myocardial infarction.
    Necrostatin-7
  • HY-P11751A
    RES-701-3 peptide TFA
    RES-701-3 peptide TFA is a class II lasso peptide. RES-701-3 peptide TFA can be isolated from the fermentation broth of Streptomyces species. RES-701-3 peptide TFA potently inhibits the binding of ET-1 to ETB, with an IC50 of approximately 5-10 nM. RES-701-3 peptide TFA is applicable to research related to systemic hypertension, myocardial infarction, and myocardial ischemia.
    RES-701-3 peptide TFA
  • HY-P991895
    PLG-101
    PLG-101 is a human anti-CD8 antibody. PLG-101 can be used in research on acute myocardial infarction .
    PLG-101
  • HY-118945
    FR191413 194928-55-7
    FR191413 is a selective bradykinin B2 receptor agonist that stimulates prostaglandin E2 production in WI-38 cells and activates BK B2 receptor-mediated pathways such as vasodilation and organ protection. FR191413 competitively binds to [3H]-BK in guinea pig ileum (GPI) membranes and CHO cells transfected with the human BK B2 receptor, with IC50 values ​​of 20.0 nM and 2.60 nM, respectively. FR191413 can be used in research related to cardiovascular diseases and diabetes, including hypertension, myocardial hypertrophy, myocardial infarction, arrhythmias, and diabetic nephropathy.
    FR191413
  • HY-19664
    Pranidipine 99522-79-9 99.52%
    Pranidipine (OPC-13340) is an orally active L-type voltage-dependent calcium channel (L-VDCC) blocker with a Ki value of 0.16 nM. Pranidipine inhibits calcium-induced contraction, suppresses slow-response action potentials, shortens action potential duration, reduces systolic and diastolic blood pressure, and exerts vasodilatory effects. Pranidipine enhances its vasodilatory effect by blocking NO decomposition. Pranidipine can be used in research related to essential hypertension, angina pectoris, myocardial infarction, and dilated cardiomyopathy.
    Pranidipine
  • HY-P991422
    Stromab 99.28%
    Stromab (DS9231) is a human IgG1 monoclonal antibody (mAb) targeting Serpin F2. Recommended isotype control: Human IgG1 kappa, Isotype Control (HY-P99001).
    Stromab
  • HY-P2807A
    Lactate Dehydrogenase (LDH), Porcine Heart 9001-60-9
    Lactate Dehydrogenase (LDH), Porcine Heart, is an isoenzyme of lactate dehydrogenase derived from porcine heart. Lactate Dehydrogenase (LDH), Porcine Heart, is primarily used in life science research, tissue damage diagnosis, and as an enzyme marker.
    Lactate Dehydrogenase (LDH), Porcine Heart
  • HY-P4866
    Q-Peptide 1361235-89-3 99.46%
    Q-Peptide is an angiopoietin-1 derived peptide (QHREDGS). Q-Peptide interacts with β1-integrin, binds to integrins on the surface of osteoblasts, and serves as an acyl donor substrate for Streptomyces mobaraensis transglutaminase. Q-Peptide activates Akt, MAPKp42/44, ILK, ERK1/2, and downregulates caspase-3/7. Q-Peptide inhibits cell apoptosis, enhances cell adhesion and migration, and promotes osteoblast differentiation, bone matrix deposition and mineralization. Q-Peptide can be used in studies related to myocardial infarction, bone regeneration, diabetic wound repair and human induced pluripotent stem cells.
    Q-Peptide
  • HY-P6437A
    Drp1 peptide inhibitor P110 TFA 99.11%
    Drp1 peptide inhibitor P110 (Compound P110) TFA is a selective Drp1 peptide inhibitor with neuroprotective properties. Drp1 peptide inhibitor P110 TFA can inhibit the activation of Drp1, prevent MPTP (HY-15608)-induced Drp1 mitochondrial translocation, and alleviate MPTP-induced dopaminergic neuron loss, dopaminergic nerve terminal damage, and behavioral deficits, and can be used in the study of Alzheimer's disease. Additionally, Drp1 peptide inhibitor P110 TFA can reduce mitochondrial damage and organ injury in animal models of Huntington's disease, cerebral ischemic injury, and myocardial infarction.
    Drp1 peptide inhibitor P110 TFA
  • HY-120148A
    SM19712 194542-56-8 99.0%
    SM19712 is an orally active, selective endothelin converting enzyme (ECE) inhibitor. SM19712 inhibits conversion of big ET-1 to ET-1. SM19712 attenuates colonic angiogenesis, tissue injury, inflammation, without altering colon shortening or myeloperoxidase levels in mice. SM19712 can be used for the research of inflammatory bowel disease (colitis), ischemic acute renal failure, acute myocardial infarction, and myocardial ischemia/reperfusion injury.
    SM19712
  • HY-14240
    PG 116800 291533-11-4 99.81%
    PG 116800 (PGE 530742; PGE 7113313) is an orally active, selective and high-affinity inhibitor of MMP. PG 116800 acts as an inhibitor of ventricular remodeling, reduces left ventricular volumes and infarct zone collagen content, and improves ejection fraction. PG 116800 is generally well tolerated, but is associated with higher rates of arthralgia, joint stiffness, and dyspepsia. PG 116800 can be used for the research of myocardial infarction.
    PG 116800
  • HY-125404
    DAPK-IN-1 313971-05-0
    DAPK-IN-1 is a DAPK1 and DAPK3 inhibitor. DAPK-IN-1 is applicable to research related to cerebral infarction, myocardial infarction and renal failure.
    DAPK-IN-1
  • HY-W207224
    F1386-0303 287177-12-2
    F1386-0303 is a highly selective MAP4K4 inhibitor with an IC50 of 34 nM against human targets. F1386-0303 exerts cardiomyocyte protective and function-preserving effects through mechanisms such as alleviating oxidative stress, inhibiting caspases, and maintaining mitochondrial membrane potential, while it does not interfere with the activity of Doxorubicin (HY-15142A) in cancer cells. F1386-0303 is rapidly cleared and has no bioavailability in mice, but it is well-suited as a tool compound for target validation. F1386-0303 can be applied to studies related to cardiac ischemia-reperfusion injury, Doxorubicin-induced cardiotoxicity, myocardial infarction and other related conditions.
    F1386-0303
  • HY-186074
    ERβ agonist-2 628321-25-5
    ERβ agonist-2 (Page 72) is a selective ERβ agonist with an EC50 of 800 nM or lower. ERβ agonist-2 selectively inhibits T cell activation and/or proliferation, thereby reducing circulating T cell levels in subjects, without exerting significant effects on circulating neutrophil, monocyte or B cell levels. ERβ agonist-2 is applicable to studies of chronic heart failure after myocardial infarction, as well as graft-versus-host disease, multiple sclerosis and experimental autoimmune encephalomyelitis.
    ERβ agonist-2
  • HY-19224
    Fonsartan 153235-15-5
    Fonsartan (HR720) is an AT1 receptor antagonist. Fonsartan can be used for the study of myocardial infarction (MI).
    Fonsartan
  • HY-106150A
    Eniporide mesylate 190368-98-0
    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