Heart Disease

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.

DMH-1 is a selective BMP inhibitor. DMH-1 upregulates the expression of SOX1. DMH-1 increases cardiomyocyte progenitor cells and promotes the differentiation of mouse embryonic stem cells into cardiomyocytes. DMH-1 induces the differentiation of hiPSC-derived neural progenitor cells into β3-tubulin-positive neurons.

Prostaglandin E1 (Alprostadil) is a prostanoid receptor ligand, with K_is of 1.1 nM, 2.1 nM, 10 nM, 33 nM and 36 nM for mouse EP3, EP4, EP2, IP and EP1, respectively. Prostaglandin E1 induces vasodilation and inhibits platelet aggregation. Prostaglandin E1 can be used as a vasodilator for the research of peripheral vascular diseases.

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.

Aldosterone is the primary mineralocorticoid. Aldosterone is a steroid hormone, and it is synthesized and secreted in response to renin-angiotensin system activation (RAS) or high dietary potassium by the zona glomerulosa (ZG) of the adrenal cortex. Aldosterone activity is dependent by the binding and activation of the cytoplasmic/nuclear mineralocorticoid receptor (MR) at cellular level.

Furosemide is an orally active GABAA receptor antagonist. Furosemide inhibits carbonic anhydrase, the sodium-chloride cotransporter, sodium reabsorption, tubuloglomerular feedback, and GABA-induced chloride flux. Furosemide can be used as a diuretic reagent. Furosemide is applied in the research of hepatic necrosis, sepsis-associated acute kidney injury, hypoalbuminemia-related fluid retention, and congestive heart failure.

Conivaptan hydrochloride (YM 087) is an orally active dual vasopressin V_1a/V₂ receptor antagonist with K_i values of 0.48 nM and 3.04 nM for vasopressin V_1a receptor and V₂ receptor, respectively. Conivaptan hydrochloride competitively and reversibly blocks vasopressin-mediated antidiuresis, vasoconstriction, and cellular hypertrophy, while inhibiting CYP3A4. Conivaptan hydrochloride inhibits vasopressin-induced intracellular calcium, cAMP, and mitogen-activated kinase activation in vascular smooth muscle cells and cardiomyocytes. Conivaptan hydrochloride induces water diuresis while improving hemodynamics in heart failure models, reducing left ventricular end-diastolic pressure, vascular resistance, and organ weight. Conivaptan hydrochloride is used for research on hyponatremia and congestive heart failure.

Alagebrium chloride (ALT711) is an advanced glycation end product (AGE) inhibitor.

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.

Amiodarone, a benzofuran-based Class III antiarrhythmic agent, inhibits WT outward ionic current (IhERG) tails with an IC₅₀ of ∼45 nM. Amiodarone induces cell proliferation and myofibroblast differentiation via ERK1/2 and p38 MAPK signaling in fibroblasts. Amiodarone can be used in the research of both supraventricular and ventricular arrhythmias.

N1-Methylpseudouridine-5′-triphosphate (1-Methylpseudouridine-5′-triphosphate) trisodium solution (100 mM) is a nucleobase-modified nucleotide. N1-Methylpseudouridine-5′-triphosphate (1-Methylpseudouridine-5′-triphosphate) trisodium solution (100 mM) is used for synthesizing mRNA with reduced immunogenicity and improved stability.

Losmapimod (GSK-AHAB; GW856553X) is an orally active p38α/β MAPK inhibitor, with pK_i values of 8.1 and 7.6 for p38α and p38β, respectively. Losmapimod reduces DUX4 expression, thus exerting efficacy in facioscapulohumeral muscular dystrophy. By inhibiting MAPK/NF-κB, Losmapimod reduces apoptosis of epileptiform hippocampal neurons, and exhibits anti-allodynia and anti-hyperalgesic activities. Losmapimod blocks the entry and fusion of Lassa fever virus (LASV). Losmapimod overcomes tyrosine kinase inhibitor resistance in non-small cell lung cancer (NSCLC). Losmapimod inhibits myocardial senescence and inflammation, and possesses cardioprotective activity against cardiotoxicity.

Eplerenone (Epoxymexrenone) is a selective, highly specific and orally active aldosterone blocker (SAB). Eplerenone also is a selective mineralocorticoid receptor antagonist (MRA) with IC₅₀ value of 0.081 μM. Eplerenone can be used for the research of hypertension, atherosclerosis, chronic systolic heart failure (HF) and cardiovascular (CV).

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.

9''-Methyl salvianolate B (MSB) is a blood-brain barrier-permeable inhibitor with high affinity for g5Rp, with a K_d value of 117 nM against African swine fever virus (ASFV) g5Rp. 9''-Methyl salvianolate B also acts as a ZBP1 inhibitor. It exhibits strong binding affinity to key proteins in the PPARγ/NF-κB pathway. 9''-Methyl salvianolate B blocks the interaction between ASFV g5Rp and host proteins eIF5A or RPS15. It restores hypusination modification of eIF5A, promotes autophagy (Autophagy), and inhibits ASFV replication. 9''-Methyl salvianolate B effectively disrupts ZBP1-mediated PANoptosome assembly. It effectively alleviates myocardial ischemia/reperfusion injury. 9''-Methyl salvianolate B can be used in studies related to African swine fever.

Enalapril (MK-421) is an orally active angiotensin-converting enzyme inhibitor. Enalapril blocks the conversion of angiotensin I to angiotensin II, regulates the renin-angiotensin system, reduces preload and afterload, and decreases plasma angiotensin II levels. Enalapril inhibits apoptosis, reduces nitric oxide metabolite levels, stabilizes endothelial cells, enhances endothelial antioxidant defense, scavenges reactive oxygen species (ROS), and alleviates neuronal damage. Enalapril attenuates glutathione depletion, protein/lipid oxidation, tissue damage, and type III collagen immunolabeling in organs of diabetic rats. Enalapril reduces systolic blood pressure and urinary albumin excretion, and delays the progression of diabetic cardiac/renal injury. Enalapril is used in research related to asymptomatic left ventricular dysfunction, congestive heart failure, Alzheimer's disease, diabetes mellitus, acute myocardial infarction, atrial fibrillation, hypertension, cerebral ischemia, chronic heart failure, and single-ventricle physiology.

Enalapril maleate (MK-421 maleate) is an orally active angiotensin-converting enzyme inhibitor. Enalapril maleate blocks the conversion of angiotensin I to angiotensin II, regulates the renin-angiotensin system, reduces preload and afterload, and decreases plasma angiotensin II levels. Enalapril maleate inhibits apoptosis, reduces nitric oxide metabolite levels, stabilizes endothelial cells, enhances endothelial antioxidant defense, scavenges reactive oxygen species (ROS), and alleviates neuronal damage. Enalapril maleate attenuates glutathione depletion, protein/lipid oxidation, tissue damage, and type III collagen immunolabeling in organs of diabetic rats. Enalapril maleate reduces systolic blood pressure and urinary albumin excretion, and delays the progression of diabetic cardiac/renal injury. Enalapril maleate is used in research related to asymptomatic left ventricular dysfunction, congestive heart failure, Alzheimer's disease, diabetes mellitus, acute myocardial infarction, atrial fibrillation, hypertension, cerebral ischemia, chronic heart failure, and single-ventricle physiology.

Cysteinylglycine (L-Cysteinylglycine; Cys-Gly) is a dipeptide formed by the peptide bond linkage between cysteine (Cysteine) and glycine (Glycine). Cysteinylglycine is an important metabolic intermediate in the human body, mainly derived from the degradation of glutathione (GSH). Cysteinylglycine reduces ferric iron to ferrous iron, drives the redox cycle of iron, generates reactive oxygen species (ROS), stimulates oxidative reactions, induces lipid peroxidation of human plasma LDL lipoproteins, and causes oxidative damage to DNA bases. Cysteinylglycine can be used as a biomarker to evaluate ischemic heart disease, breast cancer and other conditions.

Levosimendan (Simsndan; OR-1259) is a calcium sensitiser used in the management of acutely decompensated congestive heart failure.

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).