Cyclotriazadisulfonamide (CADA) is a specific inhibitor of HIV entry that targets CD4. It functions by preventing the co-translational translocation of human CD4 (huCD4) into the endoplasmic reticulum (ER) lumen through a mechanism dependent on the signal peptide (SP).

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 EC 50 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 (EC 50 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.