MT 63-78 |
カタログ番号GC60258 |
MT 63-78 は、EC50 が 25 μM の特異的かつ強力な直接 AMPK 活性化因子です。 MT 63-78 は、細胞有糸分裂の停止とアポトーシスも誘導します。 MT 63-78 は、脂質生成経路と mTORC1 経路を阻害することにより、前立腺がんの増殖をブロックします。 MT 63-78 には抗腫瘍効果があります。
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Cas No.: 1179347-65-9
Sample solution is provided at 25 µL, 10mM.
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.
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