dTAGV-1 TFA is a highly effective and specific compound that targets mutant FKBP12 F36V fusion proteins for degradation. It possesses potent activity in inducing the degradation of the FKBP12 F36V -Nluc protein in living organisms.

dTAGV-1 (0.1 nM-10 μM; 24 h) TFA induces potent degradation of FKBP12 F36V -Nluc with no effects on FKBP12 WT -Nluc in 293FT cells[1]. dTAGV-1 (125-2000 nM; 24 h) TFA co-treatment with THAL-SNS-032 leads to pronounced degradation of both LACZ-FKBP12 F36V and CDK9[1]. dTAGV-1 (500 nM; 1-24 h) TFA leads to rapid KRAS G12V and pERK1/2 degradation[1]. dTAGV-1 (50-5000 nM; 24 h) TFA enables EWS/FLI degradation in Ewing sarcoma[1].

dTAGV-1 (35 mg/kg; i.p. once daily for 4 days) TFA induces degradation of FKBP12 F36V -Nluc in mice[1]. dTAGV-1 (2-10 mg/kg; i.p.) TFA exhbits half-lives (T 1/2 =3.64 and 4.4 h), C max (595 and 2123 ng/mL) and great exposure (AUC inf =3136 and?18517 h?ng/mL) in mice[1]. dTAGV-1 (2 mg/kg; i.v.) TFA exhbits half-life (T 1/2 =3.02 h), C max (7780 ng/mL) and great exposure (AUC inf =3329 h?ng/mL) in mice[1]. Animal Model: 8-week-old immunocompromised female mice were transplanted with MV4;11 luc-FKBP12 F36V cells[1]Dosage: 35 mg/kg Administration: I.p. once daily for 4 days Result: Observed striking loss of bioluminescent signal 4?h after the first and three administrations. Degradation evident 28?h after the final administration.