Diethyl 1-benzyl-4-phenyl-1,4-dihydropyridine-3,5-dicarboxylate

Modify Date: 2024-02-04 12:36:09

Diethyl 1-benzyl-4-phenyl-1,4-dihydropyridine-3,5-dicarboxylate structure	Common Name	Diethyl 1-benzyl-4-phenyl-1,4-dihydropyridine-3,5-dicarboxylate
	CAS Number	120533-76-8	Molecular Weight	391.46
	Density	N/A	Boiling Point	N/A
	Molecular Formula	C₂₄H₂₅NO₄	Melting Point	N/A
	MSDS	N/A	Flash Point	N/A

Use of Diethyl 1-benzyl-4-phenyl-1,4-dihydropyridine-3,5-dicarboxylate

BML-278 is a SIRT1 activator (EC150: 1 μM). BML-278 increases H3K9 methylation and inhibits H3K9 acetylation in both the paternal and maternal pronucleus. BML-278 improves early embryonic development. BML-278 arrests the cell cycle at the G1/S phase, and reduces senescence in primary human mesenchymal cells. BML-278 reduces tubulin acetylation in U937 cells. BML-278 also increases mitochondrial density in murine C2C12 myoblasts[1][2].

Name	diethyl 1-benzyl-1,4-dihydro-4-phenylpyridine-3,5-dicarboxylate
Synonym	More Synonyms

Description	BML-278 is a SIRT1 activator (EC150: 1 μM). BML-278 increases H3K9 methylation and inhibits H3K9 acetylation in both the paternal and maternal pronucleus. BML-278 improves early embryonic development. BML-278 arrests the cell cycle at the G1/S phase, and reduces senescence in primary human mesenchymal cells. BML-278 reduces tubulin acetylation in U937 cells. BML-278 also increases mitochondrial density in murine C2C12 myoblasts[1][2].
Related Catalog	Signaling Pathways >> Epigenetics >> Sirtuin Research Areas >> Cancer Signaling Pathways >> Epigenetics >> Histone Methyltransferase Signaling Pathways >> Cell Cycle/DNA Damage >> Sirtuin
Target	SIRT1[1].
References	[1]. Adamkova K, et al. SIRT1-dependent modulation of methylation and acetylation of histone H3 on lysine 9 (H3K9) in the zygotic pronuclei improves porcine embryo development. J Anim Sci Biotechnol. 2017 Nov 1;8:83. [2]. Mai A, et al. Study of 1,4-dihydropyridine structural scaffold: discovery of novel sirtuin activators and inhibitors. J Med Chem. 2009 Sep 10;52(17):5496-504.