MT 63-78 是一种有效的直接 AMPK 激活剂，EC50 为 25 μM。M 63-78 还诱导细胞有丝分裂阻滞和细胞凋亡 (apoptosis)。MT 63-78 通过抑制脂肪生成和 mTORC1 途径来阻止前列腺癌的生长。MT 63-78 具有抗肿瘤作用。
货号:ajcx29528
CAS:1179347-65-9
分子式:C21H14N2O2
分子量：326.35
溶解度:N/A
纯度：98%
存储：Store at -20°C
库存：现货

Background:

MT 63-78 is a specific and potent direct AMPK activator with an EC50 of 25 μM. MT 63-78 also induces cell mitotic arrest and apoptosis. MT 63-78 blocks prostate cancer growth by inhibiting the lipogenesis and mTORC1 pathways. MT 63-78 has antitumor effects[1].

MT 63-78 (0-50 μM; 4 days; LNCaP and PC3 cells) treatment shows a dose-dependent decrease in cell number, and concomitant to the activation of AMPK signaling[1].MT 63-78 (25 μM; 24 hours; LNCaP and CRPC cells) treatment induces a significant enrichement in the G2/M population[1].MT 63-78 (0-50 μM; 24 hours; LNCaP, PC3, C4-4, C4-2B, CL1and 22RV1cells) treatment induces reduction of anti-apoptotic Mcl-1 in concert with accumulation of the pro-apoptotic BH3-only protein Puma[1].MT 63-78 (0-50 μM; 30 minutes; LNCaP and PC3 cells) treatment shows a dose-dependent phosphorylation of the two major AMPK targets Acetyl-CoA Carboxylase (ACC) on Ser79 and of Raptor on Ser792. And also increases Thr172 phosphorylation on the AMPK α subunit[1]. Cell Viability Assay[1] Cell Line: LNCaP and PC3 cells

MT 63-78 (30 mg/kg; intraperitoneal injection; daily; for 14 days; C57 BL/6 male mice) treatment leads to a 33% inhibition of tumor growth[1]. Animal Model: C57 BL/6 male mice bearing LNCaP tumors[1]

[1]. Zadra G, et al. A novel direct activator of AMPK inhibits prostate cancer growth by blocking lipogenesis. EMBO Mol Med. 2014 Apr;6(4):519-38.