Cyclotriazadisulfonamide

Cyclotriazadisulfonamide (CADA) is a specific CD4-targeted HIV entry inhibitors. Cyclotriazadisulfonamide (CADA) inhibits the co-translational translocation of human CD4 (huCD4) into the ER lumen in a signal peptide (SP)-dependent way[1][2].

Signaling Pathways >> Anti-infection >> HIV

Research Areas >> Infection

Research Areas >> Inflammation/Immunology

Cyclotriazadisulfonamide (CADA) significantly decreases the amount of cell surface CD4 -the main receptor for HIV -without altering the expression of any other cellular receptor examined so far[1]. Cyclotriazadisulfonamide (CADA) exhibits an EC50 of 0.4 μg/mL for CD4 in MO-DC cells. Treatment of MO-DC with 10 μg/mL of CADA results in 83% downregulation of cell surface CD4, an effect that is similar to that observed for CADA treatment of CD4+ T cells[1]. CADA prevents MT-4 cells from HIV-1 and SIV infection (EC50 are 0.7 and 1.2 g/ml, respectively)[1]. Western Blot Analysis[1] Cell Line: MO-DCs. Concentration: 0.4 μg/mL. Incubation Time: 24 h. Result: A 50% reduction in CD4 expression was obtained.

[1]. Kurt Vermeire, et al. CADA, a potential anti-HIV microbicide that specifically targets the cellular CD4 receptor. Curr HIV Res. 2008 May;6(3):246-56.

[2]. Victor Van Puyenbroeck, et al. Preprotein signature for full susceptibility to the co-translational translocation inhibitor cyclotriazadisulfonamide. Traffic. 2020 Feb;21(2):250-264.