RJS308 TFA is a selective Cyclophilin A ( CypA) PROTAC degrader. RJS308 TFA induces ubiquitin-dependent CypA degradation by recruiting the VHL E3 ligase complex, and forms a ternary complex with CypA and VHL/elongin C/elongin B. RJS308 TFA exhibits anti- HIV-1 and anti- HCV activities. RJS308 TFA can be used in studies related to viral infections [1]. (Pink: Cyclophilin A ligand; Blue: VHL ligand; Black: linker ).
In Vitro, RJS308 TFA binds to recombinant full-length human CypA in SPR binding assays with a KD value of 108 nM, and also binds to N-terminally truncated human CypB with a KD value of 320 nM[1]. RJS308 TFA (0.01-10 μM; 0-6 days) degrades CypA in Jurkat cells[1]. RJS308 TFA (1-5 μM; 48 h) exhibits anti-HIV-1 activity in primary activated human CD4+ T cells, and this activity depends on VHL-mediated CypA degradation[1]. RJS308 TFA (1-5 μM; 48 h) exhibits anti-HCV activity in Huh7 human hepatocellular carcinoma cells, and this activity depends on VHL-mediated CypA degradation[1].
References:
[1]. Newton LS, et al., Macrocycle-based PROTACs selectively degrade cyclophilin A and inhibit HIV-1 and HCV. Nat Commun. 2025 Feb 10;16(1):1484.
In Vitro, RJS308 TFA binds to recombinant full-length human CypA in SPR binding assays with a KD value of 108 nM, and also binds to N-terminally truncated human CypB with a KD value of 320 nM[1]. RJS308 TFA (0.01-10 μM; 0-6 days) degrades CypA in Jurkat cells[1]. RJS308 TFA (1-5 μM; 48 h) exhibits anti-HIV-1 activity in primary activated human CD4+ T cells, and this activity depends on VHL-mediated CypA degradation[1]. RJS308 TFA (1-5 μM; 48 h) exhibits anti-HCV activity in Huh7 human hepatocellular carcinoma cells, and this activity depends on VHL-mediated CypA degradation[1].
References:
[1]. Newton LS, et al., Macrocycle-based PROTACs selectively degrade cyclophilin A and inhibit HIV-1 and HCV. Nat Commun. 2025 Feb 10;16(1):1484.