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BCR-ABL ProgramChronic Myelogeous Leukemia (CML) program DCC-2036 DCC-2036 inhibits BCR-ABL kinase, an oncogenic fusion protein kinase resulting from chromosomal translocation (Philadelphia + chromosome). BCR-ABL is causative of myeloproliferative diseases, including chronic myelogenous leukemia (CML). Late-stage preclinical development
In preclinical studies, DCC-2036 has demonstrated potent enzymatic and cellular inhibition of BCR-ABL, the T315I gatekeeper mutant, and other clinically relevant P-loop & Activation loop mutants. DCC-2036 is highly efficacious in animal models of human T315I CML. DCC-2036 is being developed as an orally administered treatment for CML. DCC-2157 DCC-2157 inhibits BCR-ABL kinase, an oncogenic fusion protein kinase resulting from chromosomal translocation (Philadelphia + chromosome). BCR-ABL is causative of myeloproliferative diseases, including chronic myelogenous leukemia (CML). CML candidate- preclinical development
In preclinical studies, DCC-2157 has demonstrated potent enzymatic and cellular inhibition of BCR-ABL, the T315I gatekeeper mutant, and other clinically relevant P-loop & Activation loop mutants. DCC-2157 is highly efficacious in animal models of human T315I CML. DCC-2157 is being developed as an orally administered treatment for CML. |
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