FKBP Degrader

FKBP12 PROTAC dTAG-13 (dTAG-13) is a FKBP12^F36V PROTAC degrader and a PXR partial agonist. FKBP12 PROTAC dTAG-13 induces ubiquitination and proteasomal degradation of proteins tagged with FKBP12^F36V, without degrading wild-type FKBP12 or un-fused PXR. It weakly promotes the recruitment of SRC-1, strongly inhibits the interaction between NCoR and PXR, and upregulates the expression of CYP3A4 and other drug metabolism-related genes. FKBP12 PROTAC dTAG-13 is applicable to research related to breast cancer and leukemia^[1].

dTAGV-1 TFA is a selective FKBP12^F36V PORTAC degrader. dTAGV-1 TFA induces rapid degradation of FKBP12^F36V-tagged oncogenic fusion proteins, triggering collapse of downstream cellular signaling pathways, reduced proliferative capacity of cancer cells, and decreased levels of target proteins. dTAGV-1 TFA is applicable to functional validation studies of cancer and undegradable oncoproteins.

dTAGV-1 hydrochloride is a selective FKBP12^F36V PORTAC degrader. dTAGV-1 hydrochloride induces rapid degradation of FKBP12^F36V-tagged oncogenic fusion proteins, triggering collapse of downstream cellular signaling pathways, reduced proliferative capacity of cancer cells, and decreased levels of target proteins. dTAGV-1 hydrochloride is applicable to functional validation studies of cancer and undegradable oncoproteins.

dTAG-47 is a heterobifunctional PROTAC degrader that specifically binds to the FKBP12^F36V domain and Cereblon (CRBN). By recruiting the CRBN E3 ubiquitin ligase, dTAG-47 induces ubiquitination and proteasomal degradation of FKBP12^F36V-fused Cas9 and tagged KDM5A. dTAG-47 can induce upregulated expression of some endogenous retrovirus (ERV) genes and is suitable for cancer research.

dTAGV-1 is a selective FKBP12^F36V PORTAC degrader. dTAGV-1 induces rapid degradation of FKBP12^F36V-tagged oncogenic fusion proteins, triggering collapse of downstream cellular signaling pathways, reduced proliferative capacity of cancer cells, and decreased levels of target proteins. dTAGV-1 is applicable to functional validation studies of cancer and undegradable oncoproteins.

22-SLF is a PROTAC degrader, that degrades FK506-binding protein 12 (FKBP12) with a DC₅₀ of 0.5 µM. 22-SLF interacts with C227 and C228 in FBXO22 to induce a ternary complex between FKBP12 and FBXO22, and degrades FKBP12 in a FBXO22-dependent manner. 22-SLF can be used for fundamental cancer research as a probe to study the FBXO22 degradation pathway.

SP3N hydrochloride is a specific degrader of the prolyl isomerase (FKBP12). The alkylamine of SP3N hydrochloride is metabolized to a reactive aldehyde (SP3CHO), which recruits the SCF^FBXO22 ligase for FKBP12 degradation. SP3N hydrochloride may be used in research for cancer.

SP3N is a specific degrader of the prolyl isomerase (FKBP12). The alkylamine of SP3N is metabolized to a reactive aldehyde (SP3CHO), which recruits the SCF^FBXO22 ligase for FKBP12 degradation. SP3N may be used in research for cancer.

BRD4/FKBP12 degrader-1(a1d) is a BRD4/FKBP12 degrader with anti-cancer activity (BRD4 ligand: HY-78695, FKBP12 ligand: HY-176501, linker: HY-140212).

10-SLF is a PROTAC FKBP12 degrader. 10-SLF induces a ternary complex between FKBP12 and FBXW7-R465C, and promotes FBXW7-R465C-dependent proteasomal degradation of FKBP12. 10-SLF selectively reduces FKBP12 levels in cells expressing FBXW7-R465C.

SelDeg51 is a selective FKBP51 PROTAC degrader with a K_d value of 18 nM and a D_max of 90%. SelDeg51 induces proteasomal degradation of FKBP51 via the FKBP51:SelDeg51:VCB ternary complex and reactivates the glucocorticoid receptor signaling pathway. SelDeg51 can be used for research on stress-related mental disorders, chronic pain, and obesity.

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.

BRD4/FKBP12 degrader-2 (a1dj) is a BRD4/FKBP12 degrader and shows anticancer activity (BRD4 ligand: HY-78695, FKBP12 ligand: HY-176502, linker: HY-140212).

MC-25B is a DCAF16-recruiting FKBP12 PROTAC degrader with a DC₅₀ of 0.35 μM. MC-25B promotes the formation of a ternary complex with DCAF16 and nuclear-localized FKBP12_NLS, thereby mediating DCAF16-dependent degradation of FKBP12_NLS via the proteasome and Cullin-RING ligase pathway.

RAFKBP12 is a FKBP12 CAP-TAC (proteinase complex cap-targeted chimera) degrader. RAFKBP12 demonstrates the feasibility of the CAP-TAC strategy, which enables proteasome-dependent degradation of FKBP12 that is independent of E3 ubiquitin ligases and protein ubiquitination.