FKBP12 PROTAC FM4

FKBP12 PROTAC FM4 (0.001-100 nM; 24 h) potently and selectively degrades BRD4-FKBP12 in transiently transfected HEK293T cells via a VHL- or CRBN-dependent proteasomal pathway, with DC₅₀ values of 0.09-0.22 nM and 90% or 81% maximum degradation at 24 h, respectively, and no cytotoxicity at up to 100 nM^[1].
FKBP12 PROTAC FM4 (0.001-100 nM; 24 h) degrades MST2-FKBP12 in transiently transfected HEK293T cells via a CRBN-dependent proteasomal pathway, with 80% maximum degradation at 24 h, while VHL-MTH1 shows minimal activity against this target^[1].
FKBP12 PROTAC FM4 (0.001-100 nM; 24 h) degrades KRAS-FKBP12 in transiently transfected HEK293T cells via VHL- or CRBN-dependent proteasomal pathways, with 59% maximum degradation at 24 h for VHL-MTH1, and degradation is dependent on proximity of the dimerization tags^[1].
FKBP12 PROTAC FM4 (0.001-100 nM; 24 h) induces dose-dependent degradation of BRD4 and MST2 in transiently transfected HEK293T cells via multiple viral E3 ligases, with maximum degradation ranging from 50% to 89% at 24 h, and degradation is proteasome-dependent^[1].
FKBP12 PROTAC FM4 (0.001-100 nM; 24 h) degrades multiple pan-essential proteins in transiently transfected HEK293T cells via MTH1-E6, with SARS1 and eIF2S1 showing over 60% maximum degradation at 24 h, and degradation is dependent on E6 interaction with E6AP^[1].
FKBP12 PROTAC FM4 (0.0001-100 nM; 6, 48 h) selectively induces proteasome-dependent degradation of SARS1, inhibits protein synthesis, triggers apoptosis, and reduces cell viability with an EC₅₀ of 0.2 nM in C33A^SARS1-FH:E6 cervical carcinoma cells, while having no effect on parental cells, demonstrating disease-specific targeted protein degradation^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.