A tyrosine kinase inhibitor (TKI) has nestled into the binding pocket of Bcr-Abl, preventing ATP from binding — and keeping Bcr from becoming activated.
Frame from an animation sequence (appears in latest promotional reel).
Bcr–Abl is the driving mutation in chronic myeloid leukemia (CML).
In chronic myeloid leukemia, TKIs target the abnormal BCR-ABL protein that causes uncontrolled CML cell growth and block its function, causing the CML cells to die.
