Entinostat

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

一种有效的选择性 I 类 HDAC 抑制剂，对 HDAC1/2/3 的 IC50 为 243/453/248 nM。

A potent and selective class I HDACs inhibitor with IC50 of 243/453/248 nM for HDAC1/2/3; no inhibition on HDAC8/4/5/7/9/6/10 (IC50>10 uM); induces accumulation of p21WAF1/CIP1 and gelsolin in K562 cell; reduce S-phase cells and induce G1-phase cells in A2780 cell.Breast Cancer Phase 3 Clinical(In Vitro):Binding affinity of Entinostat (MS-275) against HDAC1 and HDAC2 is 282 nM and 156 nM, respectively. Effects of the HDAC inhibitor Entinostat (MS-275) have been examined in human leukemia and lymphoma cells (U937, HL-60, K562, and Jurkat) as well as in primary acute myelogenous leukemia blasts in relation to differentiation and apoptosis. MS-275 displays dose-dependent effects in each of the cell lines. When administered at a low concentration (e.g., 1 μM), MS-275 exhibits potent antiproliferative activity, inducing p21CIP1/WAF1-mediated growth arrest and expression of differentiation markers (CD11b) in U937 cells. Entinostat (MS-275) potently induces cell death, triggering apoptosis in ~70% of cells at 48 h. (In Vivo):Entinostat (MS-27-275) at 49 mg/kg shows marked antitumor effects against KB-3-1, 4-1St, and St-4 tumor lines, and a moderate effect against Capan-1 tumor. Entinostat at 24.5 mg/kg and 12.3 mg/kg also shows significant effects against these tumors. In addition, oral administration of Entinostat apparently increases the level of histone acetylation in HT-29 tumor xenografts 4-24 h after the administration. MS-275 administration (3.5 mg/kg i.p.) to Experimental autoimmune neuritis (EAN) rats once daily from the appearance of first neurological signs greatly reduces the severity and duration of EAN and attenuated local accumulation of macrophages, T cells and B cells, anddemyelination of sciatic nerves. In addition, MS-275 treatment increases proportion of infiltrated Foxp3+ cells and anti-inflammatory M2 macrophages in sciatic nerves of EAN rats.

Binding affinity of Entinostat (MS-275) against HDAC1 and HDAC2 is 282 nM and 156 nM, respectively. Effects of the HDAC inhibitor Entinostat (MS-275) have been examined in human leukemia and lymphoma cells (U937, HL-60, K562, and Jurkat) as well as in primary acute myelogenous leukemia blasts in relation to differentiation and apoptosis. MS-275 displays dose-dependent effects in each of the cell lines. When administered at a low concentration (e.g., 1 μM), MS-275 exhibits potent antiproliferative activity, inducing p21CIP1/WAF1-mediated growth arrest and expression of differentiation markers (CD11b) in U937 cells. Entinostat (MS-275) potently induces cell death, triggering apoptosis in ~70% of cells at 48 h.

Entinostat (MS-27-275) at 49 mg/kg shows marked antitumor effects against KB-3-1, 4-1St, and St-4 tumor lines, and a moderate effect against Capan-1 tumor. Entinostat at 24.5 mg/kg and 12.3 mg/kg also shows significant effects against these tumors. In addition, oral administration of Entinostat apparently increases the level of histone acetylation in HT-29 tumor xenografts 4-24 h after the administration. MS-275 administration (3.5 mg/kg i.p.) to Experimental autoimmune neuritis (EAN) rats once daily from the appearance of first neurological signs greatly reduces the severity and duration of EAN and attenuated local accumulation of macrophages, T cells and B cells, anddemyelination of sciatic nerves. In addition, MS-275 treatment increases proportion of infiltrated Foxp3+ cells and anti-inflammatory M2 macrophages in sciatic nerves of EAN rats.

MS-275 | SNDX-275 | MS 275 | SNDX 275

Cell Cycle/DNA Damage

HDAC

HDAC1|HDAC3

Cancer

Breast Cancer

209783-80-2

376.4085

C21H20N4O3

>98% (HPLC)

10 mM in DMSO

O=C(OCC1=CC=CN=C1)NCC2=CC=C(C(NC3=CC=CC=C3N)=O)C=C2

Carbamic acid, N-[[4-[[(2-aminophenyl)amino]carbonyl]phenyl]methyl]-, 3-pyridinylmethyl ester

(-20℃)

With Ice Pack

≥ 2 years