Figure 1
Addition of 1.2 nM or 1.2 µM ABL001 to ATP-competitive TKIs increases the degree of Bcr-Abl kinase inhibition achieved in vitro in CML mononuclear cells.Patient MNC were incubated for 2 h with (A) IM (B) NIL and (C) DAS + 1.2 nM (middle) or 1.2 µM (right) ABL001 and IC50 calculated by determining the concentration of TKI causing 50% reduction in p-CrkL. Solid dots represent diagnosis patients; open circles represent patients switching TKI for intolerance or resistance; Numbers are shown in parentheses; Black lines are means; error bars are SEM. The eight patients in (A) are shown in (D) paired with their response to 1.2 nM ABL001 (dotted line indicates the average IC50IM for 62 de novo CMLs in the TIDEL trial).

Addition of 1.2 nM or 1.2 µM ABL001 to ATP-competitive TKIs increases the degree of Bcr-Abl kinase inhibition achieved in vitro in CML mononuclear cells.Patient MNC were incubated for 2 h with (A) IM (B) NIL and (C) DAS + 1.2 nM (middle) or 1.2 µM (right) ABL001 and IC50 calculated by determining the concentration of TKI causing 50% reduction in p-CrkL. Solid dots represent diagnosis patients; open circles represent patients switching TKI for intolerance or resistance; Numbers are shown in parentheses; Black lines are means; error bars are SEM. The eight patients in (A) are shown in (D) paired with their response to 1.2 nM ABL001 (dotted line indicates the average IC50IM for 62 de novo CMLs in the TIDEL trial).

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