Delving into the Latest Updates on HS-438 with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

Target

Bcr-Abl T315I

Mechanism

Bcr-Abl T315I inhibitors(BCR-ABL T315I mutation inhibitors)

Therapeutic Areas

NeoplasmsHemic and Lymphatic DiseasesOther Diseases

Active Indication

BCR-ABL Negative Atypical Chronic Myeloid Leukemia

Inactive Indication-

Originator Organization

Inha University

Active Organization

Inha University

Inactive Organization-

Drug Highest PhasePreclinical

First Approval Date-

Regulation-

Structure

Molecular FormulaC17H17N3O3S

InChIKeyLAAHHHDILCOULN-UHFFFAOYSA-N

CAS Registry1430720-10-7

Imatinib is a selective breakpoint cluster region-Abelson (BCR-ABL) tyrosine kinase inhibitor (TKI) that has significantly improved the prognosis of patients with chronic myeloid leukemia (CML). However, T315I gene mutations of the BCR-ABL kinase domain have been shown to confer resistance to imatinib. In the present study, we synthesized a novel BCR-ABL inhibitor, HS-438, and identified its anti-leukemic effects in vitro and in vivo. We found that HS-438 strongly inhibited the expression of BCR-ABL signaling pathways in wild-type BCR-ABL (BaF3/WT) cells as well as T315I-mutated BCR-ABL (BaF3/T315I) cells with resistance to imatinib. HS-438 induced cell cycle arrest, particularly during the G0/G1 cell cycle phase, and induced apoptosis. In BaF3/T315I xenograft models, HS-438 significantly delayed tumor growth, unlike imatinib. In summary, we suggest that HS-438 may be a novel drug candidate with the therapeutic potential to target BCR-ABL and overcome imatinib resistance in patients with CML.

100 Deals associated with HS-438

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