AI Article Synopsis
- FLT3 mutations are found in around 30% of acute myeloid leukemia (AML) cases, making FLT3 a promising target for new treatments.
- Early FLT3 inhibitors were effective but had high toxicity due to off-target effects, while new selective inhibitors have been developed to target specific mutations more safely.
- The review discusses the progression of FLT3 inhibitors, their varied chemical structures, effectiveness against different types of FLT3 mutations, and highlights compounds that are nearing market release or advanced clinical stages.
Article Abstract
Fms-like tyrosine kinase-3 (FLT3) mutations occur in approximately 30% of acute myeloid leukemia (AML) cases, suggesting FLT3 as an attractive target for AML treatment. Early FLT3 inhibitors enhance antileukemia efficacy by inhibiting multiple targets, and thus had stronger off-target activity, increasing their toxicity. Recently, a number of potent and selective FLT3 inhibitors have been developed, many of which are effective against multiple mutations. This review outlines the evolution of AML-targeting FLT3 inhibitors by focusing on their chemotypes, selectivity and activity over FLT3 wild-type and FLT3 mutations as well as new techniques related to FLT3. Compounds that currently enter the late clinical stage or have entered the market are also briefly reported.
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| http://dx.doi.org/10.4155/fmc-2019-0365 | DOI Listing |
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