Cardiomyopathy is a heterogeneous group of diseases characterized by abnormal structure or function of the heart muscle not caused by coronary artery disease, congenital heart disease, or other identifiable conditions. It impairs the heart's ability to pump blood effectively, leading to ventricular hypertrophy or dilatation, often with genetic origins. Major types include dilated cardiomyopathy (DCM), where the heart becomes enlarged and weakened, and hypertrophic cardiomyopathy, where the heart muscle thickens, reducing pumping efficiency. Symptoms commonly include shortness of breath, chest pain, fatigue, and arrhythmias, which may occur during exertion or even at rest. While the exact cause is frequently unknown, contributing factors include genetic mutations, hypertension, valvular heart disease, and certain medications. Dilated cardiomyopathy-2G (CMD2G) is a severe, early-onset autosomal recessive form caused by LMOD2 gene mutations on chromosome 7q31, marked by shortened thin filaments, disorganized myofibrils, and reduced contractile force, resulting in rapid progression to heart failure, arrhythmias, and premature death if untreated.
| Cat. No. |
Product Name |
CAS No. |
Purity |
Chemical Structure |
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- HY-44134
-
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Dimethyl 2-oxoglutarate
|
13192-04-6 |
|
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Dimethyl 2-oxoglutarate (Dimethyl α-ketoglutarate) is a cell-permeable derivative of 2-oxoglutarate and tricarboxylic acid cycle metabolite with antioxidant properties. Dimethyl 2-oxoglutarate inhibits Autophagy. Dimethyl 2-oxoglutarate prevents mitochondrial damage and reduces ROS production. Dimethyl 2-oxoglutarate alleviates Carbon tetrachloride (HY-Y0298)-induced liver fibrosis. Dimethyl-2-oxoglutaric acid can be used in the research of diseases such as Alzheimer's disease, diabetes, and cardiomyopathy.
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- HY-112654
-
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GCN2iB
|
2183470-12-2 |
99.83% |
|
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.
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- HY-123606
-
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GSK484
|
1652629-23-6 |
99.14% |
|
GSK484 is a PAD4 inhibitor that effectively inhibits protein citrullination and the formation of neutrophil extracellular traps (NETs) by blocking the catalytic activity of PAD4. GSK484 suppresses the production of histone H3, MHC-I expression, CD8+ T cell activation, proliferation and inflammatory cytokine release. GSK484 reduces inflammation and bone destruction in collagen-induced rheumatoid arthritis, alleviates pain and mast cell activation in sickle cell disease, and improves myocardial ischemia-reperfusion injury and experimental colitis. In addition, GSK484 restores intestinal microbial homeostasis by reversing ferroptosis-induced dysbiosis. GSK484 can be used to study the disease mechanisms of rheumatoid arthritis, sickle cell disease, thrombosis, myocardial injury, colitis and other conditions.
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-
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- HY-P99047
-
|
Simtuzumab
|
1318075-13-6 |
≥99.0% |
|
Simtuzumab (AB 0024; GS 6624) is a monoclonal antibody directed against Lysyl oxidase like-2 (LOXL2). Simtuzumab non-competitively blocks collagen cross-linking, reduces LOXL2 protein expression and attenuates extracellular matrix changes. Simtuzumab reduces myocardial fibrosis and prevents cardiac dysfunction. Simtuzumab lowers Myh7 and Nppa gene expression, reduces contraction heterogeneity, and cuts COL1A1 deposition. Simtuzumab can be used for the research of LMNA mutation-induced dilated cardiomyopathy, idiopathic pulmonary fibrosis, and primary sclerosing cholangitis.
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- HY-N9362
-
|
Emodinanthrone
|
491-60-1 |
98.66% |
|
Emodinanthrone (EmodAn) is a MARCH7 stabilizer that inhibits ferroptosis (EC50=70 nM). Emodinanthrone is also a precursor to Emodin (HY-14393) and possesses antibiotic activity. Emodinanthrone directly binds to MARCH7 and blocks its ubiquitination-mediated degradation at the K608 site; this action enhances MARCH7-mediated K48 ubiquitination and degradation of NCOA4, as well as its regulation of the intracellular localization of TFR1 via K63 ubiquitination, thereby reducing the intracellular labile iron pool and blocking ferroptosis. Emodinanthrone demonstrates in vivo cardioprotective effects and exhibits a favorable safety profile. Emodinanthrone is applicable to research on ferroptosis-related cardiovascular diseases, including Doxorubicin (HY-15142A)-induced cardiomyopathy and myocardial ischemia-reperfusion injury.
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- HY-182642
-
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MRS2339
|
436847-13-1 |
|
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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.
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- HY-D3250
-
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PYSNO
|
2445485-84-5 |
|
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PYSNO is a lysosome-targeted fluorescent probe based on a pyridazinone skeleton (λem=515-565 nm, λex=405 nm) that can be used to track nitric oxide (NO) production in vivo. PYSNO exhibits a rapid, highly sensitive and highly selective "turn-on" response to endogenous and exogenous NO by blocking photoinduced electron transfer and regulating radiative decay rates. PYSNO enables precise in vivo monitoring in a mouse model of myocardial fibrosis and can be applied to the research of related diseases.
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- HY-P11373
-
|
α-Myosin (614-643)
|
176373-77-6 |
|
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α-Myosin (614-643) is a segment of polypeptide of the heavy chain of cardiac α-myosin. α-Myosin has a strong ability to induce autoimmune myocarditis.
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- HY-W092043
-
|
TLR4-IN-C34-C2-COOH
|
1159408-54-4 |
99.94% |
|
TLR4-IN-C34-C2-COO is a linker that incorporates TLR4 inhibitor TLR4-IN-C34. TLR4-IN-C34-C2-COOH can be used in the research of inflammation and acute myocardial injury. TLR4-IN-C34 inhibits TLR4 in enterocytes and macrophages, and reduces systemic inflammation in mouse models of endotoxemia and necrotizing enterocolitis.
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- HY-N1990
-
|
Gypenoside XLIX
|
94987-08-3 |
99.88% |
|
Gypenoside XLIX is a multifunctional bioactive compound that can be isolated from Gynostemma pentaphyllum, with a Ka value of 1.58 μM for its binding to SIRT1. Gypenoside XLIX acts as a PPAR-α agonist. It inhibits the activation of TLR4-mediated NF-κB signaling pathway by activating the Sirt1/Nrf2 signaling pathway, reduces ROS accumulation, and alleviates hepatic inflammatory injury in mice with sepsis-induced liver disease. Gypenoside XLIX targets SIRT1 to block YAP-NLRP3 activation and improve sepsis-induced cardiomyopathy. Gypenoside XLIX inhibits apoptosis (Apoptosis), pyroptosis (Pyroptosis), autophagy (Autophagy), lipid peroxidation, pro-inflammatory cytokines and anti-inflammatory cytokines. Gypenoside XLIX alleviates sepsis-induced splenic injury by inhibiting inflammation and oxidative stress, and mitigates sepsis-associated encephalopathy by targeting PPAR-α. Gypenoside XLIX prevents acute kidney injury by inhibiting IGFBP7/IGF1R-mediated programmed cell death and inflammation. Gypenoside XLIX inhibits the expression and activity of vascular cell adhesion molecule-1 in cytokine-induced human endothelial cells. Gypenoside XLIX is applicable to research related to acute liver injury, lung injury, cardiomyopathy, acute splenic injury, sepsis-associated encephalopathy, acute kidney injury, atherosclerosis and chronic inflammation.
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- HY-N0657
-
|
Pinoresinol Diglucoside
|
63902-38-5 |
99.84% |
|
Pinoresinol Diglucoside is an orally active lignan with multifunctional bioactivity. Pinoresinol Diglucoside interacts with targets including ALB, HIF1A, GSK3B, BCL2, MARK3, IL6, NF-κB p65, Nrf2, HO-1, and TLR4, and modulates pathways including PI3K-Akt, estrogen, MAPK, Rap1, AKT/mTOR/NF-κB, and TGF-β1/Smads. Pinoresinol Diglucoside regulates osteogenesis, bone resorption, oxidative stress, inflammation, apoptosis, ferroptosis, ferritinophagy, cardiac fibrosis, and vasorelaxation. Pinoresinol Diglucoside can be used for the research of osteoporosis, ischemia/reperfusion-induced brain injury, Alzheimer’s disease, myocardial ischemia-reperfusion injury, chondrodysplasia, diabetic cardiomyopathy, cardiac hypertrophy, hypertension, cisplatin-induced hearing loss, atherosclerotic cardiovascular diseases, and disuse osteoporosis.
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- HY-B0298
-
|
Clemastine
|
15686-51-8 |
99.26% |
|
Clemastine (HS-592; Meclastine) is an orally active, blood-brain barrier-permeable H1 histamine receptor (H1 histamine receptor) antagonist with potent antiallergic effects. Clemastine also antagonizes muscarinic acetylcholine receptors (mAChR), particularly the M1 and M4 subtypes. In addition to antihistamine effects, Clemastine exhibits multiple pharmacological activities, especially in promoting central nervous system remyelination, activating autophagy and pyroptosis, exerting anti-apoptotic and neuroprotective effects, and suppressing inflammation.
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- HY-112974
-
|
Inotersen
|
1492984-65-2 |
|
|
Inotersen (GSK-2998728; ISIS-420915) is a 2'-O-methoxyethyl-modified antisense oligonucleotide and transthyretin (TTR) inhibitor with low genotoxicity. Inotersen triggers RNase H1-mediated degradation by binding to TTR mRNA, thereby effectively reducing the production of both mutant and wild-type transthyretin in the liver. Inotersen significantly reduces amyloid fiber deposition, yet specific toxicities such as inflammation or tumors are observed at high doses in some animal models. Inotersen is used in studies of hereditary transthyretin amyloidosis and the associated polyneuropathy and cardiomyopathy.
|
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- HY-B1016
-
|
Trapidil
|
15421-84-8 |
98.0% |
|
Trapidil (AR-12008) is an orally active vasodilator and antiplatelet agent. Trapidil antagonizes platelet-derived growth factor (PDGF), inhibits phosphodiesterase, thromboxane A2 synthesis and pro-inflammatory cytokine production. Trapidil promotes prostacyclin biosynthesis, reduces lipid peroxidation, regulates nitric oxide metabolism, and inhibits cell proliferation and migration. Trapidil exerts tissue-protective effects, regulates bone turnover, and inhibits pyroptosis via the GPX3/Nrf2 pathway. Trapidil is applicable to research related to renal ischemia-reperfusion injury, chronic stable angina, restenosis, meningioma, diabetic cardiomyopathy and peripheral nerve crush injury.
|
-
-
- HY-W145695
-
|
Chitoheptaose
|
68232-35-9 |
≥98.0% |
|
Chitoheptaose is an orally active chitooligosaccharide (degree of polymerization = 7). Chitoheptaose can be extracted from the exoskeletons of crustaceans, such as the shells of crabs, shrimps and lobsters. Chitoheptaose reduces pro-inflammatory cytokines while increasing the levels of anti-inflammatory cytokines (decreasing the levels of pro-inflammatory cytokines IL-1β, IL-17A and IFN-γ, and increasing the level of the anti-inflammatory cytokine IL-10). Chitoheptaose possesses antioxidant, anti-inflammatory and anti-Apoptotic activities. Chitoheptaose improves cardiac parameters, alleviates myocarditis injury, and exerts cardioprotective effects in a rat model of myocarditis. Chitoheptaose can be used in studies related to myocarditis.
|
-
-
- HY-182103
-
|
ZAK-IN-2
|
3033697-19-4 |
|
|
ZAK-IN-2 (Compound 8) is a selective, covalent ZAK inhibitor with an IC50 of 11.5 nM. ZAK-IN-2 forms a covalent bond with Cys22 in the P-loop of ZAK to inhibit its kinase activity. ZAK-IN-2 inhibits the phosphorylation of the downstream target p38. ZAK-IN-2 blocks Doxorubicin (HY-15142A)-induced cleavage of Caspase 3. ZAK-IN-2 is applicable to research related to myocardial hypertrophy.
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-
- HY-181548
-
|
YL3147
|
|
|
|
YL3147 is a ferroptosis inhibitor. YL3147 also acts as a radical-trapping antioxidant that directly prevents the spread of lipid peroxidation and blocks ferroptosis. YL3147 exerts significant cardioprotective effects in mouse cardiomyopathy models. YL3147 can be used in studies related to cardiomyopathy.
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-
-
- HY-17681
-
|
Myosin-IN-5
|
2839464-02-5 |
|
|
Myosin-IN-5 (example 3) is a selective cardiac myosin inhibitor with an IC50 of 1.5 μM. Myosin-IN-5 shows much less effective in inhibiting skeletal myofibril activity (IC50 of 43.4 μM). Myosin-IN-5 can be used for the study of hypertrophic cardiomyopathy (HCM) and cardiac diseases.
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-
- HY-112654A
-
|
GCN2iB acetate
|
2183470-13-3 |
|
|
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-110067
-
|
VO-OHPic
|
675848-25-6 |
|
|
VO-OHPic is a reversible, noncompetitive PTEN inhibitor with an human IC50 value of 46 nM. VO-OHPic inhibits PTEN signaling, activates Akt-GSK3β and Nrf-2/HO-1 pathways, induces apoptosis resistance and elevates IL-10 levels. VO-OHPic inhibits autophagy, ferroptosis and oxidative stress. VO-OHPic can be used for the research of acute myocardial infarction, intervertebral disc degeneration, cardiomyopathy and cancer.
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