169181-28-6

Basic information

• Product Name: amidepsine A
• Synonyms: amidepsine A;2,4-Dimethoxy-6-methyl-benzoic acid 4-[[4-[[(1-carboxyethyl)amino]carbonyl]-3-hydroxy-5-methylphenoxy]carbonyl]-3-hydroxy-5-methylphenyl ester;FO 2942A
• CAS NO: 169181-28-6
• Molecular Formula: C29H29NO11
• Molecular Weight: 567.54066
• Mol File: 169181-28-6.mol
• Article Data: 0

Chemical Properties

• Boiling Point: 773.3±60.0 °C(Predicted)
• Appearance: /
• Density: 1.356±0.06 g/cm3(Predicted)
• Solubility: Soluble in methanol
• PKA: 3.53±0.10(Predicted)
• CAS DataBase Reference: amidepsine A(CAS DataBase Reference)
• NIST Chemistry Reference: amidepsine A(169181-28-6)
• EPA Substance Registry System: amidepsine A(169181-28-6)

Safety Data

• Hazardous Substances Data: 169181-28-6(Hazardous Substances Data)

Usage

Uses

Amidepsine A is a fungal metabolite, isolated from the culture broth of Humicola sp. FO-2942 that inhibits DGAT activity.

Biological Activity

amidepsine a is a fungal metabolite isolated from the culture broth of humicola sp fo-2942. amidepsine a is an inhibitor of dylglycerol acyltransferase (dgat).dylglycerol acyltransferase (dgat) has been involved in catalyzing the formation of triglycerides from diacylglycerol and acyl-coa. the reaction is considered the terminal and only committed step in triglyceride synthesis and is essential for the formation of adipose tissue. there are two isozymes of dgat have been identified: dgat1 and dgat2. dgat-1 deficient mice are lean and resistant to the development of diet-induced obesity or insulin resistance [1]. dgat2-/- mice demonstrate reduced triglyceride levels and suffer from skin barrier abnormalities [2].fo-2942 inhibited dgat activity with an ic50 of 10.2 μm in rat liver microsomes. fo-2942 inhibited triacylglycerol formation in raji cells with the ic50 value of 15.5 μm [1].

references

[1] tomoda h, tabata n, ito m, et al. amidepsines, inhibitors of diacylglycerol acyltransferase produced by humicola sp. fo-2942[j]. the journal of antibiotics, 1995, 48(9): 942-947.[2] smith s j, cases s, jensen d r, et al. obesity resistance and multiple mechanisms of triglyceride synthesis in mice lacking dgat[j]. nature genetics, 2000, 25(1): 87-90.[3] stone s j, myers h m, watkins s m, et al. lipopenia and skin barrier abnormalities in dgat2-deficient mice[j]. journal of biological chemistry, 2004, 279(12): 11767-11776.