DIBA-1

DIBA-1 (10 μM; 0-100 min) can displace zinc from recombinant HIV-1 NCp7 in vitro^[1].
DIBA-1 (5 μM; 24 h) inhibits the zinc-dependent binding of HIV-1 NCp7 to Ψ RNA^[1].
DIBA-1 (0-100 μM, administered 48 h after 24 h of TNF-α induction) potently reduces the release of virion-associated p24 in TNF-α-induced U1 cells, with an IC₅₀ of 7.5 μM, and causes no significant cytotoxicity even at concentrations as high as 100 μM^[2].
DIBA-1 (6.25-25 μM; 48 h following 24 h TNF-α induction) induces intermolecular disulfide bond cross-linking of Gag precursor molecules, blocks the normal processing of Pr55_gag in TNF-α-induced U1 cells, and causes accumulation of unprocessed Pr55_gag as well as absence of mature p7NC and p24^[2].
DIBA-1 (0.1-10 μM; 12 h) inhibits the release of Pr55gag-bearing pseudovirus particles from Gag-transfected COS cells, without altering the synthesis or myristoylation modification of Pr55gag^[2].
DIBA-1 (2-50 μM; 1 h at 37°C) induces disulfide bond-mediated intermolecular cross-linking of Pr55gag in structurally intact, tightly packed Pr55gag-loaded pseudovirus particles, but exhibits no such effect on solubilized Pr55gag monomers^[2].
DIBA-1 (25-50 μM; 1 h pre-incubation with pseudovirions, followed by 1 h incubation with protease) induces cross-linking of Pr55gag in intact pseudoviral particles, thereby inhibiting subsequent processing of Pr55gag by HIV-1 protease^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.