1. Epigenetics
    PI3K/Akt/mTOR
    Apoptosis
  2. AMPK
    mTOR
    Apoptosis
  3. MT 63-78

MT 63-78 

Cat. No.: HY-W058849
Handling Instructions

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.

For research use only. We do not sell to patients.

MT 63-78 Chemical Structure

MT 63-78 Chemical Structure

CAS No. : 1179347-65-9

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Description

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].

IC50 & Target[1]

AMPK

25 μM (EC50)

mTORC1

 

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[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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay[1]

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[1]

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[1]

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[1]

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.
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[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57 BL/6 male mice bearing LNCaP tumors[1]
Dosage: 30 mg/kg
Administration: Intraperitoneal injection; daily; for 14 days
Result: Led to a 33% inhibition of tumor growth.
Molecular Weight

326.35

Formula

C₂₁H₁₄N₂O₂

CAS No.

1179347-65-9

SMILES

N#CC1=CNC2=C1C=C(C3=CC=C(C4=C(O)C=CC=C4O)C=C3)C=C2

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

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Keywords:

MT 63-78AMPKmTORApoptosisAMP-activated protein kinaseMammalian target of RapamycinmTORC1directThr172dephosphorylationMcl-1BH3mitoticarrestp53RaptorlipogenesisantitumorInhibitorinhibitorinhibit

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