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

Cyclotriazadisulfonamide (CADA) markedly reduces CD4 expression, the primary HIV receptor, without affecting other cellular receptors examined[1]. In MO-DC cells, CADA has an EC50 of 0.4 μg/mL and at 10 μg/mL, it downregulates cell surface CD4 by 83%, a similar effect observed in CD4+ T cells[1]. CADA inhibits HIV-1 and SIV infection in MT-4 cells with EC50 values of 0.7 and 1.2 μg/mL, respectively[1]. Western Blot Analysis in MO-DCs showed a 50% reduction in CD4 expression at 0.4 μg/mL after 24 hours.