CHMFL-48 is a potent BCR-ABL kinase inhibitor that effectively targets both wild-type and imatinib-resistant mutants. With IC50 values of 1 nM for ABL wild-type and 0.8 nM for the ABL T315I mutant, CHMFL-48 inhibits autophosphorylation of BCR-ABL, disrupting downstream signaling pathways involving STAT5 and CRKL. This mechanism results in cell cycle arrest and the induction of apoptosis, making CHMFL-48 a valuable tool for research focused on chronic myeloid leukemia (CML).
CHMFL-48 is a potent BCR-ABL kinase inhibitor that effectively targets both wild-type and imatinib-resistant mutants. With IC50 values of 1 nM for ABL wild-type and 0.8 nM for the ABL T315I mutant, CHMFL-48 inhibits autophosphorylation of BCR-ABL, disrupting downstream signaling pathways involving STAT5 and CRKL. This mechanism results in cell cycle arrest and the induction of apoptosis, making CHMFL-48 a valuable tool for research focused on chronic myeloid leukemia (CML).
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