Delving into the Latest Updates on MPT0B392 with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

Target

Mechanism

Akt inhibitors(Proto-oncogene proteins c-akt inhibitors), JNK stimulants(c-Jun N-terminal kinase stimulants), Mcl-1 inhibitors(Induced myeloid leukemia cell differentiation protein Mcl-1 inhibitors)

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Therapeutic Areas

NeoplasmsHemic and Lymphatic Diseases

Active Indication

acute leukemia

Inactive Indication-

Originator Organization

Taipei Medical University

Active Organization

Taipei Medical University

Inactive Organization-

Drug Highest PhasePreclinical

First Approval Date-

Regulation-

Despite great advances in the treatment of acute leukemia, a renaissance of current chemotherapy needs to be improved. The present study elucidates the underlying mechanism of a new synthetic quinoline derivative, MPT0B392 (B392) against acute leukemia and its potential anticancer effect in drug resistant cells. B392 caused mitotic arrest and ultimately led to apoptosis. It was further demonstrated to be a novel microtubule-depolymerizing agent. The effects of oral administration of B392 showed relative potent anti-leukemia activity in an in vivo xenograft model. Further investigation revealed that B392 triggered induction of the mitotic arrest, followed by mitochondrial membrane potential loss and caspases cleavage by activation of c-Jun N-terminal kinase (JNK). In addition, B392 enhanced the cytotoxicity of sirolimus in sirolimus-resistant acute leukemic cells through inhibition of Akt/mTOR pathway and Mcl-1 protein expression, and also was active in the p-glycoprotein (p-gp)-overexpressing National Cancer Institute/Adriamycin-Resistant cells with little susceptibility to p-gp. Taken together, B392 has potential as an oral mitotic drug and adjunct treatment for drug resistant cancer cells.

100 Deals associated with MPT0B392

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