https://www.selleckchem.com/pr....oducts/Dihydroartemi
While the potentiation of CHK1i-mediated effects by BETi was BET-BRD4-dependent, MYC expression was BET-BRD4-independent. In MYC-RAD21+ pediatric OS xenografts, BETi + CHK1i significantly decreased tumor growth, increased survival, and was well tolerated. Therefore, targeting replication stress is a promising strategy to pursue as a therapeutic option for this devastating disease.Memristive systems can provide a novel strategy to conquer the von Neumann bottleneck by evaluating information where data are located in situ.
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