Application of SGI-7079 in treatment of FLT3 mutant acute myelogenous leukemia

By developing the selective drug SGI-7079, the limitations of existing FLT3 inhibitors in treating FLT3-mutant acute myeloid leukemia have been addressed. This drug effectively inhibits FLT3-mutant leukemia and overcomes drug resistance mutations, significantly improving patient prognosis.

CN122140719AActive Publication Date: 2026-06-05GUANGZHOU FIRST PEOPLES HOSPITAL (GUANGZHOU DIGESTIVE DISEASE CENT GUANGZHOU FIRST PEOPLES HOSPITAL GUANGZHOU MEDICAL UNIV THE SECOND AFFILIATED HOSPITAL OF SOUTH CHINA UNIV OF TECH)
3 Cites 0 Cited by

Patent Information

Application Number
CN202610493117.0
Authority / Receiving Office
CN · China
Patent Type
Applications(China)
Current Assignee / Owner
Filing Date
2026-04-15
Publication Date
2026-06-05
Estimated Expiration
2046-04-15

AI Technical Summary

Technical Problem

The efficacy of existing FLT3 inhibitors in treating FLT3-mutant acute myeloid leukemia is easily limited by secondary TKD mutations, and they also have toxic side effects and pharmacokinetic limitations, making it difficult to effectively overcome drug resistance mutations.

Method used

Develop a selective, ATP-competitive oral drug, SGI-7079, which inhibits FLT3 and its downstream signaling pathways by stably binding to FLT3, induces apoptosis, and directly targets and binds to the FLT3-ITD protein to overcome FLT3-TKD resistance mutations.

Benefits of technology

SGI-7079 significantly inhibits the proliferation of FLT3-mutant leukemia cells and prolongs survival, outperforming existing FLT3 inhibitors. It also shows a strong inhibitory effect on secondary TKD resistance mutations, improving histopathological features and prolonging survival.

✦ Generated by Eureka AI based on patent content.
Patent Text Reader

Abstract

The invention discloses an application of SGI-7079 in treatment of FLT3 mutant type acute myelogenous leukemia (FLT3). Researches show that SGI-7079 can be stably combined with FLT3, the phosphorylation level of FLT3 and downstream STAT5, AKT and ERK of FLT3 is inhibited, and G1 phase retardation and cell apoptosis are induced. In vitro, the SGI-7079 has a strong inhibition effect on both the FLT3-ITD and the drug-resistant mutant cells; in an FLT3-ITD mouse model, the leukemia load can be remarkably reduced, the lifetime can be prolonged, and the curative effect on drug-resistant mutation such as F691L and D835Y is superior to that of an existing drug. Meanwhile, the SGI-7079 also has a remarkable inhibition effect in primary cells of FLT3-ITD positive patients. Therefore, the SGI-7079 can be used as a new drug candidate for treating FLT3 mutation and drug-resistant AML, and a new direction is provided for optimizing a targeted therapy strategy.
Need to check novelty before this filing date? Find Prior Art