2. Disease Areas
  3. Blood or Cardio-cerebrovascular Disease
  4. Cardiovascular Disease Heart Disease
  5. Heart Failure

Heart Failure

Heart failure is a chronic condition in which the heart is unable to pump blood effectively to meet the body's needs, leading to symptoms such as fatigue, shortness of breath, and fluid retention. It can result from various underlying causes including coronary artery disease, hypertension, cardiomyopathy, and valvular heart disease. Heart failure is classified based on left ventricular ejection fraction into heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). Management involves lifestyle modifications, pharmacological therapies such as ACE inhibitors, beta-blockers, and diuretics, and in some cases, device implantation or cardiac transplantation. Early diagnosis and comprehensive treatment are crucial to improving outcomes and quality of life.

Heart Failure (51):

Cat. No. Product Name CAS No. Purity Chemical Structure
  • HY-112537
    D-Glucose 6-phosphate 56-73-5 99.90%
    D-Glucose 6-phosphate is a key central node metabolite in glucose metabolism. It serves as the initiating metabolite for glycolysis and the pentose phosphate pathway, as well as a substrate for glycogen synthesis. D-Glucose 6-phosphate acts as a metabolic stress signal, which activates the mTOR pathway to promote protein synthesis, especially when phosphoglucose isomerase (PGI) is inhibited, thereby participating in cardiac remodeling processes. D-Glucose 6-phosphate can be used in research related to non-insulin-dependent diabetes mellitus and heart failure.
    D-Glucose 6-phosphate
  • HY-149662
    TMDJ-035 2681302-83-8 99.92%
    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 Ca2+ transients. TMDJ-035 decreases ATP content and intracellular Ca2+ 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-P1181A
    Pam2CSK4 TFA 99.46%
    Pam2CSK4 TFA is a TLR2 agonist. Pam2CSK4 TFA induces the expression of iNOS and NO in macrophage cell lines via TBK1 and MyD88 molecules. Pam2CSK4 TFA activates the NF-κB and Bruton's tyrosine kinase signaling pathways in platelets, and promotes platelet-endothelial cell interactions. TLR2 activation triggered by Pam2CSK4 TFA expands myeloid-derived suppressor cells (MDSCs) and suppresses anti-tumor immune responses in the tumor microenvironment. Pam2CSK4 TFA acts as a Th2-polarizing adjuvant in mouse vaccine models against Leishmania major and Brugia malayi. Pam2CSK4 TFA can be used in the research of various diseases, including thromboinflammatory diseases, sepsis, atherosclerosis, heart failure, influenza, lymphoma, melanoma, cutaneous leishmaniasis and lymphatic filariasis.
    Pam2CSK4 TFA
  • HY-N0559
    Kirenol 52659-56-0 99.82%
    Kirenol is a diterpenoid compound, an orally active apoptosis inducer and signaling pathway regulator, with a Kd value of 5.47 μM against the target CK2. Kirenol promotes the cleavage of Bid into tBid, regulates the protein levels/phosphorylation of Bax, Bcl-2, p53 and p21, and induces caspase-independent apoptosis, S-phase cell cycle arrest, ROS accumulation and cytotoxicity in cancer cells. Kirenol activates the CK2/AKT and AMPK-mTOR-ULK1 pathways, inhibits the signaling of NF-κB, TGF-β/Smads and NLRP3 inflammasome, and regulates the GSK3β, BMP and Wnt/β-catenin pathways. Kirenol induces autophagy, mitophagy and osteoblast differentiation, promotes mitochondrial fusion, and exerts antioxidant, anti-inflammatory, antifibrotic, renoprotective, cardioprotective, neuroprotective and analgesic effects. Kirenol is applicable to research related to chronic myeloid leukemia, ischemic stroke, diabetic nephropathy, heart failure, acute lung injury and osteoporosis.
    Kirenol
  • HY-101327A
    Xamoterol hemifumarate 73210-73-8 ≥99.0%
    Xamoterol (Corwin; ICI 118587) hemifumarate is an orally active and selective β1-adrenoceptor partial agonist. Xamoterol hemifumarate acts as agonist at low sympathetic tone, antagonist at high sympathetic tone, with context-dependent cardiovascular effects including modulated heart rate, blood pressure, and cardiac output. Xamoterol hemifumarate can be used for the research of heart failure, postural hypotension, and ischemic heart disease.
    Xamoterol hemifumarate
  • HY-101327
    Xamoterol 81801-12-9
    Xamoterol (Corwin; ICI 118587) is an orally active and selective β1-adrenoceptor partial agonist. Xamoterol acts as agonist at low sympathetic tone, antagonist at high sympathetic tone, with context-dependent cardiovascular effects including modulated heart rate, blood pressure, and cardiac output. Xamoterol can be used for the research of heart failure, postural hypotension, and ischemic heart disease.
    Xamoterol
  • HY-182642
    MRS2339 436847-13-1
    MRS2339 is a ribose-modified nucleotide and a nucleotidase-resistant P2 receptor agonist. MRS2339 activates P2X4R. MRS2339 induces ionic currents via P2X receptors, reduces cardiomyocyte cross-sectional area and heart weight/body weight ratio, lacks vasodilatory activity, and extends the lifespan of mice with cardiomyopathy. MRS2339 can be used in research related to heart failure and cardiomyopathy.
    MRS2339
  • HY-W589560
    TMA-IN-1 160172-20-3
    TMA-IN-1 (Compound 7) is a highly potent, orally active and selective TMA Lyase inhibitor with an estimated Kd value of 3.2 μM. TMA-IN-1 reduces Trimethylamine oxide (TMAO) levels. TMA-IN-1 can be used for the research of heart failure.
    TMA-IN-1
  • HY-137750
    MANT-cGMP 83707-15-7
    MANT-cGMP, a ribose-substituted nucleotide, is an adenylyl cyclase (AC) inhibitor with a Ki of 100 μM and a pKi of 4. MANT-cGMP can be used for the study of heart failure, cancer, and neurological disorders.
    MANT-cGMP
  • HY-132187
    Sphingosylphosphorylcholine 1670-26-4 99.50%
    Sphingosylphosphorylcholine is a bioactive lipid and a major component of plasma high-density lipoprotein that binds to OGR1 with a Kd of 33.3 nM. Sphingosylphosphorylcholine triggers delayed phosphorylation of Smad2, upregulates α-SMA expression, and activates TRPM3. Sphingosylphosphorylcholine reduces Apoptosis and upregulates the expression of uPA and its receptor uPA-R. Sphingosylphosphorylcholine exerts anti-apoptotic, anti-cardiac hypertrophy and pro-wound healing effects. Sphingosylphosphorylcholine induces scratching behavior in mice. Sphingosylphosphorylcholine is used in studies related to atopic dermatitis, promyelocytic leukemia, heart failure, myocardial ischemia/reperfusion injury, ovarian cancer, breast cancer, pancreatic cancer, and skin wound healing disorders in genetically impaired healing diabetes.
    Sphingosylphosphorylcholine
  • HY-12502
    Efonidipine 111011-63-3 99.88%
    Efonidipine (NZ-105) is an orally active dual L-type and T-type calcium channel blocker (CCB) with IC50 values of 1.8 and 350 nM, respectively. Efonidipine inhibits SARS-CoV-2 main protease. Efonidipine modulates adrenal steroidogenesis by increasing the expression of steroidogenic acute regulatory protein (StAR), dbcAMP-or angiotensin II-induced StAR mRNA expression and DHEA-S production, while suppressing the biosynthesis of aldosterone and cortisol. Efonidipine reduces plasma aldosterone levels in vivo. Efonidipine improves cardiac function in heart failure models by inhibiting T-type calcium channels (via both tonic and use-dependent blockade), independently of blood pressure reduction. Efonidipine can be used for research in hypertension, heart failure, and disorders involving dysregulated steroid hormone synthesis.
    Efonidipine
  • HY-12502A
    Efonidipine hydrochloride monoethanolate 111011-76-8 99.83%
    Efonidipine (NZ-105) hydrochloride monoethanolate is an orally active dual L-type and T-type calcium channel blocker (CCB) with IC50 values of 1.8 and 350 nM, respectively. Efonidipine hydrochloride monoethanolate inhibits SARS-CoV-2 main protease. Efonidipine hydrochloride monoethanolate modulates adrenal steroidogenesis by increasing the expression of steroidogenic acute regulatory protein (StAR), dbcAMP-or angiotensin II-induced StAR mRNA expression and DHEA-S production, while suppressing the biosynthesis of aldosterone and cortisol. Efonidipine hydrochloride monoethanolate reduces plasma aldosterone levels in vivo. Efonidipine hydrochloride monoethanolate improves cardiac function in heart failure models by inhibiting T-type calcium channels (via both tonic and use-dependent blockade), independently of blood pressure reduction. Efonidipine hydrochloride monoethanolate can be used for research in hypertension, heart failure, and disorders involving dysregulated steroid hormone synthesis.
    Efonidipine hydrochloride monoethanolate
  • HY-P990951
    Vixticibart 2845128-05-2
    Vixticibart (REGN-5381) is a fully human IgG4 monoclonal antibody and NPR1 agonist that targets NPR1. Vixticibart stabilizes the receptor in an activated conformation by binding to the N-terminal domain of NPR1, and enhances the activity of endogenous ligands ANP and BNP without blocking ligand binding when these ligands are present. Vixticibart exerts vasodilatory and hypotensive effects by inducing cGMP production, preferentially dilating venous vessels to reduce systolic and venous pressure, but does not induce diuresis and may trigger a compensatory increase in heart rate. Vixticibart produces a synergistic hypotensive effect when combined with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, and is currently mainly used in research related to heart failure and hypertension.
    Vixticibart
  • HY-136933
    Gitoxin 4562-36-1
    Gitoxin is a degradation metabolite of Digitoxin (HY-B1357) and a non-competitive Na+/K+-ATPase inhibitor, with an IC50 of 1.18e-6 M against the porcine high-affinity subtype and an IC50 of 2.85e-5 M against the porcine low-affinity subtype. Gitoxin regulates atrial contractility and rhythmicity. Gitoxin is applicable to research related to congestive heart failure.
    Gitoxin
  • HY-171978
    LM-189
    LM-189 is a β2-adrenergic receptor (β2AR) ligand and G protein-biased modulator with a human β2AR Ki of 0.063 nM.LM-189 promotes β2AR coupling to Gαs and Gαi heterotrimers, stabilizes distinct β2AR conformations including a TM6 outward state, and increases β2AR ICL2 dynamics.LM-189 restricts β2AR ligand-binding pocket conformational heterogeneity, stabilizes polar ligand-receptor interaction networks, and exhibits bias toward Gαi signaling over Gαs signaling.LM-189 enabled cryo-EM structural characterization of the β2AR-Gi complex.LM-189 can be used for the research of congestive heart failure.
    LM-189
  • HY-133829
    Zofenoprilat 75176-37-3
    Zofenoprilat is an angiotensin-converting enzyme (ACE) inhibitor with an IC50 of 1.7 nM. Zofenoprilat exerts cardioprotective and renoprotective effects by inhibiting angiotensin II expression and lowering blood pressure. Zofenoprilat promotes NO production and reduces endothelin-1 (ET-1) expression. Zofenoprilat decreases TNFα-induced ROS production and protects vascular endothelial function. Zofenoprilat regulates oxidative stress-related molecules and possesses antioxidant activity. Zofenoprilat can be used in studies related to hypertension and congestive heart failure.
    Zofenoprilat
  • HY-183906
    GSK3491943 2215853-96-4
    GSK3491943 is an antagonist of the transient receptor potential vanilloid subtype 4 (TRPV4) ion channel. GSK3491943 is applicable to research related to pulmonary edema induced by heart failure.
    GSK3491943
  • HY-183777
    B-007
    B-007 is an AplnR agonist with G protein-biased signaling (EC50 = 11.6 nM). B-007 activates the G protein pathway while abolishing β-arrestin1 and β-arrestin2 signaling. B-007 serves as a scaffold for development of G protein-biased apelin receptor agonists. B-007 can be used for the research of heart failure.
    B-007
  • HY-148150A
    Cyclocreatine phosphate dilithium 63784-08-7
    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.
    Cyclocreatine phosphate dilithium
  • HY-183636
    M353-0039 1185074-29-6
    M353-0039 is a selective UT-A2 inhibitor with a human IC50 of 0.35 μM. M353-0039 blocks urea transport mediated by UT-A2. M353-0039 can be used for the study of hyponatremia and edema associated with congestive heart failure, nephrotic syndrome, and cirrhosis.
    M353-0039