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.
| Cat. No. |
Product Name |
CAS No. |
Purity |
Chemical Structure |
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- HY-112537
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D-Glucose 6-phosphate
|
56-73-5 |
99.90% |
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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.
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- HY-18341B
-
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L-Thyroxine sodium
|
55-03-8 |
99.75% |
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L-Thyroxine sodium (Levothyroxine sodium) is a synthetic hormone for the research of hypothyroidism. DIO enzymes convert biologically active thyroid hormone (Triiodothyronine,T3) from L-Thyroxine (T4).
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- HY-P10284
-
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S7
|
853248-13-2 |
98.25% |
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S7 is an inhibitory polypeptide targeting IL-6R, which specifically binds to IL-6R and its A chain (gp80/IL-6RA) to block its signal transduction. S7 inhibits IL-6-mediated anti-apoptosis (apoptosis), angiogenesis and the expression of VEGF-A, blocks related survival signaling pathways, and enhances the sensitivity of cancer cells to chemotherapeutic drugs. S7 can be applied to the research of related diseases such as cervical cancer, multiple myeloma, Kaposi's sarcoma, prostate cancer and basal cell carcinoma.
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- HY-149662
-
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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.
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- HY-P1181A
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Pam2CSK4 TFA
|
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99.46% |
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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.
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- HY-124470
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Amisometradine
|
550-28-7 |
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Amisometradine is an orally active aminouracil diuretic with a diuretic potency approximately 40% that of Mersalyl (HY-108868) (when administered intramuscularly). Amisometradine exerts its effects by promoting the excretion of sodium, chloride and a small amount of potassium, exhibits significant therapeutic effects in heart failure models, and has good tolerance with long-term administration. Compared with drugs of the same class, Amisometradine causes fewer gastrointestinal reactions; its minor side effects mainly include nausea, vomiting, diarrhea, tinnitus and deafness, and are usually not accompanied by proteinuria or abnormalities in blood and urine indicators. Amisometradine is an important tool for the study of heart failure and related diuretic mechanisms.
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- HY-182252
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SAR296968
|
1426899-28-6 |
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SAR296968 is a Na+/Ca2+ exchanger (NCX) subtype inhibitor with an IC50 value of 74 nM against hNCX1. SAR296968 inhibits both forward and reverse modes of NCX current. SAR296968 enhances cardiac contractility and stroke volume. SAR296968 exerts antiarrhythmic effects. SAR296968 is applicable to research related to heart failure.
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- HY-120168
-
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CCG 258001
|
2055990-96-8 |
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CCG 258001 is a GRK inhibitor with IC50 values of 0.29, 51.8, and 33 µM against GRK2, GRK1, and GRK5, respectively. CCG 258001 inhibits GRK activity in cardiomyocytes and other muscle cells. CCG 258001 is applicable to the research of heart diseases, including heart failure, myocardial hypertrophy, and hypertension.
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- HY-N0559
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Kirenol
|
52659-56-0 |
99.82% |
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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.
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- HY-101327A
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Xamoterol hemifumarate
|
73210-73-8 |
≥99.0% |
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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.
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- HY-101327
-
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Xamoterol
|
81801-12-9 |
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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.
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- HY-132187
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Sphingosylphosphorylcholine
|
1670-26-4 |
99.50% |
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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.
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- HY-12502
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Efonidipine
|
111011-63-3 |
99.88% |
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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.
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- HY-12502A
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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.
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- HY-13101
-
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MCOPPB trihydrochloride
|
1108147-88-1 |
99.98% |
|
MCOPPB trihydrochloride is a NOP/ORL1 G protein-coupled receptor agonist and autophagy inhibitor that can cross the blood-brain barrier. MCOPPB trihydrochloride clears senescent cells, regulates locomotion, lipid storage and immune responses, and inhibits fibrosis and angiogenesis. MCOPPB trihydrochloride blocks autophagic flux, induces changes in locomotion and lipid storage, and activates the stress-responsive immune transcription network, thereby improving post-infarction cardiac function and exerting anxiolytic effects. MCOPPB trihydrochloride can be applied to research fields such as aging-related diseases and ischemic heart failure.
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- HY-P990951
-
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Vixticibart
|
2845128-05-2 |
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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.
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- HY-136933
-
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Gitoxin
|
4562-36-1 |
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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.
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- HY-171978
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LM-189
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|
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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.
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- HY-N6065
-
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Praeruptorin A
|
73069-27-9 |
99.57% |
|
Praeruptorin A ((+)-Praeruptorin A) is an orally active isomer of (±)-Praeruptorin A (HY-N0081). Praeruptorin A also acts as a Calcium channel blocker. Praeruptorin A can be isolated from Peucedanum. Praeruptorin A serves as a substrate for CYP3A4. Praeruptorin A downregulates NMDA receptors containing GluN2B and inhibits neuronal Apoptosis. Praeruptorin A mediates vasodilation, inhibits vascular hypertrophy and reduces blood pressure. Praeruptorin A can be used in research related to neurological diseases, myocardial ischemia, heart failure, exertional angina, renovascular hypertension and spontaneous hypertension.
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- HY-133829
-
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Zofenoprilat
|
75176-37-3 |
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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.
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