Quizartinib (AC220): A Breakthrough FLT3 Inhibitor for AML

Discover the potent therapeutic potential of Quizartinib in targeting FLT3 mutations for Acute Myeloid Leukemia.

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Product Advantages

High Selectivity and Potency

Quizartinib exhibits a significantly higher selectivity for FLT3 over other kinases, demonstrating potent IC50 values in cellular assays, making it a precise tool for FLT3-targeted therapy.

Effective Against FLT3 Mutations

Its efficacy is particularly noted in AML patients with FLT3 internal tandem duplication (ITD) mutations, a common driver in aggressive forms of the disease, offering a targeted approach to treatment.

Induces Apoptosis and Cell Death

The compound effectively induces apoptosis in tumor cells, a critical mechanism for eliminating cancer cells and a key factor in its antitumor properties observed in vivo.

Key Applications

Acute Myeloid Leukemia (AML) Treatment

Primary application is in the treatment of AML, particularly for patients with FLT3-ITD positive mutations, as part of combination therapy.

Oncology Research

Used in research settings to study FLT3 signaling pathways, drug resistance mechanisms, and to develop new anti-cancer strategies.

Pharmaceutical Intermediate

Serves as a critical pharmaceutical intermediate in the synthesis of advanced therapeutic agents for various oncological applications.

Targeted Therapy Development

A key compound in the development of targeted therapies, offering a model for selective kinase inhibition in cancer treatment.