dtagv1 tfa

dTAGV-1 TFA is a highly efficient, highly selective VHL-dependent PROTAC-mediated protein degrader that specifically targets and degrades mutant FKBP12 fusion proteins. dTAGV-1 TFA efficiently induces the degradation of FKBP12 fusion proteins at both the cellular and in vivo levels.

Degrader targeting mutant FKBP12F36V fusion proteins. Comprises a ligand selective for F36V single-point mutated FKBP12, a linker and a von Hippel-Lindau (VHL)-binding ligand. Induces potent and selective degradation of FKBP12F36V fusion proteins in vitro and in vivo. Selectively degrades FKBP12F36V-EWS/FLI fusion proteins and inhibits cell proliferation in FKBP12F36V-EWS/FLI-expressing Ewing sarcoma cells. Hydrochloride salt (Cat.No. 7374) available; suitable for in vivo use. Negative control dTAGV-1-NEG (Cat. No. 6915) also available. FKBP12F36V can be expressed as a fusion with a target protein of interest using genome engineering techniques, via transgene expression or CRISPR-mediated locus-specific knock-in. Custom knock-in cell lines for the dTAG and aTAG platforms are available from our sister brand R&D Systems. Email TPD@bio-techne.com to enquire. Plasmid vectors for the lentiviral expression and CRISPR-mediated knock-in of FKBP12F36V are available from Addgene.

dTAGV-1 hydrochloride is a PROTAC-based bifunctional degrader that utilizes the VHL E3 ligase recruitment mechanism to efficiently and selectively induce the in vivo and in vitro degradation of FKBP12F36V-tagged proteins, while having no effect on wild-type FKBP12 protein.