FKBP12 PROTAC FM4 

FKBP12 PROTAC FM4 is a PROTAC degrader of FKBP12, with a DC50 value of 0.09-0.22 nM. FKBP12 PROTAC FM4 inhibits global protein synthesis, induces apoptosis, and selectively reduces the viability of cervical cancer cells expressing MTH1-E6 and FKBP12^F36V-tagged SARS1. FKBP12 PROTAC FM4 is applicable to research related to HPV-positive cervical cancer^[1]. (Pink: FKBP12 ligand (HY-129363); Blue: MTH1 ligand (HY-134724); Black: linker (HY-W190962)).

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.

1336.52

C₇₃H₈₉N₇O₁₇

3115268-06-6

Solid

Light yellow to green yellow

CC[C@@H](C1=CC(OC)=C(C(OC)=C1)OC)C(N2CCCC[C@H]2C(O[C@@H](C3=CC=CC(OCCNC(COCCOCCOCCOCCOCCNC(C4=CC=C(C=N4)C5=CC=C6N=CC(C(NC)=O)=C(C6=C5)NC7=CC=CC=C7)=O)=O)=C3)CCC8=CC(OC)=C(C=C8)OC)=O)=O

Room temperature in continental US; may vary elsewhere.

-20°C, sealed storage, away from moisture and light

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

• [1]. Mangano K, et al. VIPER-TACs leverage viral E3 ligases for disease-specific targeted protein degradation. Cell Chem Biol. 2025;32(3):423-433.e9.  [Content Brief]