MT 63-78

Research use only, not for human use.

MT 63-78 is a specific and effective direct AMPK activator (EC50: 25 μM). MT 63-78 blocks prostate cancer growth by inhibiting the lipogenesis and mTORC1 pathways.

MT 63-78 is a specific and effective direct AMPK activator (EC50: 25 μM). MT 63-78 blocks prostate cancer growth by inhibiting the lipogenesis and mTORC1 pathways. MT 63-78 has antitumor effects. MT 63–78 also causes cell mitotic arrest and apoptosis.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 an accumulation of the pro-apoptotic BH3-only protein Puma. MT 63-78 (0-50 μM; 4 days; LNCaP and PC3 cells) treatment displays a dose-dependent decrease in cell number and concomitant to the activation of AMPK signaling. MT 63-78 (0-50 μM; 30 minutes; LNCaP and PC3 cells) treatment shows 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. MT 63-78 (25 μM; 24 hours; LNCaP and CRPC cells) treatment causes a significant enrichment in the G2/M population .MT 63-78 (30 mg/kg; intraperitoneal injection; daily; for 14 days; C57 BL/6 male mice) treatment causes a 33% inhibition of tumor growth.

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.MT 63-78 (25 μM; 24 hours; LNCaP and CRPC cells) treatment induces a significant enrichement in the G2/M population.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.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.Cell Viability Assay Cell Line:LNCaP and PC3 cells Concentration:0 μM, 1 μM, 5 μM, 10 μM, 25 μM, 50 μM Incubation Time:4 days Result:A dose-dependent decrease in cell number, concomitant to the activation of AMPK signaling was observed.Cell Cycle Analysis Cell Line:LNCaP and CRPC cells Concentration:25 μM Incubation Time:24 hours Result:Induced a significant enrichement in the G2/M population in both androgen sensitive and CRPC cell models.Apoptosis Analysis Cell Line:LNCaP, PC3, C4-4, C4-2B, CL1and 22RV1cells Concentration:0 μM, 10 μM, 25 μM, 50 μM Incubation Time:24 hoursResult:Induced reduction of anti-apoptotic Mcl-1 in concert with accumulation of the pro-apoptotic BH3-only protein Puma in all PCa cells.Western Blot Analysis Cell Line:LNCaP and PC3 cells Concentration:0 μM, 0.25 μM, 0.5 μM, 1 μM, 5 μM, 25 μM, 50 μM Incubation Time:30 minutes Result:Observed a dose-dependent phosphorylation of the two major AMPK targets Acetyl-CoA Carboxylase (ACC) on Ser79 and of Raptor on Ser792. A corresponding increase in Thr172 phosphorylation on the AMPK α subunit was also observed.

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. Animal Model:C57 BL/6 male mice bearing LNCaP tumors Dosage:30 mg/kg Administration:Intraperitoneal injection; daily; for 14 days Result:Led to a 33% inhibition of tumor growth.

——

Membrane Transporter/Ion Channel

AMPK

AMPK|mTORC1

——

——

1179347-65-9

326.35

C21H14N2O2

>98% (HPLC)

In Vitro:?DMSO : 125 mg/mL (383.02 mM)

Oc1cccc(O)c1-c1ccc(cc1)-c1ccc2[nH]cc(C#N)c2c1

——

(-20℃)

With Ice Pack

≥ 2 years