MT 63-78

SKU: orb1219728

Description

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.

Key Properties

• CAS Number: 1179347-65-9
• MW: 326.35
• Purity: >98% (HPLC)
• Formula: C₂₁H₁₄N₂O₂
• SMILES: Oc1cccc(O)c1-c1ccc(cc1)-c1ccc2[nH]cc(C#N)c2c1
• Target: AMPK
• Solubility: In Vitro: DMSO : 125 mg/mL (383.02 mM)

Bioactivity

• In Vivo:
  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.
• In Vitro:
  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 hours. Result: 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.

Storage & Handling

• Storage: Storage temperature: -20°C. Stability: ≥ 2 years
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Quick Database Links

Gene Symbol

AMPK