J. Wiegand

PROTAC-mediated dual degradation of BCL-xL and BCL-2 is a highly effective therapeutic strategy in small-cell lung cancer

This paper evaluates a dual BCL-xL/BCL-2 degrader, 753b, showing it effectively reduces tumor viability and growth in SCLC models while avoiding platelet toxicity seen with navitoclax.

Co-targeting BCL-XL and MCL-1 with DT2216 and AZD8055 synergistically inhibits small-cell lung cancer growth without causing on-target toxicities in mice