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Enoxolone (Glycyrrhetin) is a β -aromatic resin alcohol pentacyclic triterpenoid derivative obtained by Glycyrrhetin hydrolysis, with anti-ulcer, anti-inflammatory and anti-proliferation properties.
| Molecular Weight | 470.69 |
| Formula | C30H46O4 |
| CAS Number | 471-53-4 |
| Solubility (25°C) | DMSO ≥ 60 mg/mL |
| Storage | 2-8°C |
[3] S Tanaka, et al. Contact Dermatitis. Allergic contact dermatitis from enoxolone
[4] F Villas Martnez, et al. Contact Dermatitis. Sensitization to oral enoxolone
| Related Metabolite/Endogenous Metabolite Products |
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| Myristoyl coenzyme A lithium
Myristoyl coenzyme A lithium is lithium-labeled myristoylated coenzyme A (CoA). Myristoylation is an essential process in viruses and is generally controlled by N-myristoyltransferase (NMT). Myristoyl coenzyme A blocks the demyristoylation process and has potential anticancer and antiviral mechanisms. |
| Lithium acetoacetate
Lithium acetoacetate (Acetoacetic acid lithium) is an oxidative stress inducer that affects the antioxidant enzyme system and lipoprotein metabolism. Lithium acetoacetate induces oxidative stress by decreasing the mRNA expression and activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), increasing MDA content, and inhibiting very low density lipoprotein (VLDL) assembly by downregulating apolipoprotein ApoB100, ApoE, and low density lipoprotein receptor (LDLR), leading to triglyceride (TG) accumulation in hepatocytes. |
| Gentisuric Acid
Gentisuric Acid is a metabolite of Aspirin, it is a substrate of α-amidating monooxygenase (PAM). Gentisuric acid prevents DNA-damage by Mitomycin C. |
| 5α-Dihydroprogesterone
5α-Dihydroprogesterone (5a-Pregnane-3,20-dione) is the endogenous progesterone metabolite. 5α-Dihydroprogesterone (5a-Pregnane-3,20-dione) decreases cell-substrate attachment, adhesion plaques, vinculin expression, and polymerizes F-actin in MCF-7 breast cancer cells. |
| Adenosine 2',3'-cyclic phosphate sodium
Adenosine 2',3'-cyclic phosphate sodium serves as an extracellular source of adenosine. The release of extracellular 2′,3′-cAMP occurs in response to injury. 2′,3′-cAMP may be used to study the distribution and specificity of its degrading enzymes in the context of unique biological activities. 2′,3′-cAMP may also be used to study apoptosis induced at the level of mitochondrial permeability transition pores. 2′,3′-cAMP is converted into 2′-AMP and 3′-AMP which inhibit proliferation of preglomerular vascular smooth muscle cells and glomerular mesangial cells via A2B receptors. |
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