AI Article Synopsis
- A new compound, identified as FLT3/CHK1 dual inhibitor (numbered 30), shows strong effectiveness in stopping the growth of MV4-11 cancer cells.
- It selectively targets the FLT3 kinase with minimal impact on the c-Kit enzyme and demonstrates low risk of affecting heart cells (hERG).
- Compound 30 is also effective against resistant cell lines with specific FLT3 mutations and has good oral bioavailability, suggesting its potential for future drug development.
Article Abstract
Here, we discover an FLT3/CHK1 dual inhibitor (30) that exhibits excellent kinase potency and antiproliferative activity against MV4-11 cells. Simultaneously, 30 possesses high selectivity over c-Kit enzyme and low hERG inhibitory ability. Compound 30, meanwhile, overcomes varied resistance in BaF3 cell lines carrying FLT3-TKD and FLT3-ITD mutations. Moreover, 30 demonstrates favorable oral PK properties and kinase selectivity. These conclusions support that compound 30 may be a promising potential FLT3/CHK1 dual agent for further development.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10880922 | PMC |
| http://dx.doi.org/10.1039/d3md00597f | DOI Listing |
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Article Synopsis
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- Compound 30 is also effective against resistant cell lines with specific FLT3 mutations and has good oral bioavailability, suggesting its potential for future drug development.
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