BMS-378806 is a recently discovered small molecule HIV-1 inhibitor that blocks viral entrance to cells. The compound exhibits potent inhibitory activity against a panel of R5-(virus using the CCR5 coreceptor), X4-(virus using the CXCR4 coreceptor), and R5/X4 HIV-1 laboratory and clinical isolates of the B subtype (median EC50 of 0.04 microM) in culture assays. BMS-378806 is selective for HIV-1 and inactive against HIV-2, SIV and a panel of other viruses, and exhibits no significant cytotoxicity in the 14 cell types tested (concentration for 50% reduction of cell growth, >225 microM). BMS-378806 was proved to be specific for HIV-1, with no activity against HIV-2 or simian immunodeficiency virus. BMS-378806 is active against HIV-1 isolates irrespective of chemokine receptor preference. Mechanism of action studies demonstrated that BMS-378806 binds to gp120 and inhibits the interactions of the HIV-1 envelope protein to cellular CD4 receptors. BMS-378806 potently inhibited HIV-1 infection regardless of the particular chemokine receptor used.

BMS-345541 is a highly selective inhibitor of I kappa B kinase that binds at an allosteric site of the enzyme and blocks NF-kappa B-dependent transcription in mice. BMS-345541 was identified as a selective inhibitor of the catalytic subunits of IKK (IKK-2 IC(50) = 0.3 uM, IKK-1 IC(50) = 4 uM). A binding model is proposed in which BMS-345541 binds to similar allosteric sites on IKK-1 and IKK-2, which then affects the active sites of the subunits differently. BMS-345541 was shown to have excellent pharmacokinetics in mice, and peroral administration showed the compound to dose-dependently inhibit the production of serum tumor necrosis factor alpha following intraperitoneal challenge with lipopolysaccharide. BMS-345541 is effective against NF-kappa B activation in mice and represents an important tool for investigating the role of IKK in disease models. BMS-345541 blocks both joint inflammation and destruction in collagen-induced arthritis in mice.

BMS 265246 is a potent inhibitor of cyclin dependent kinase 1 and 2. It was under investigation with BristolMyers Squibb in the USA with potential in the treatment of cancer, however, BristolMyers Squibb no longer lists this product on its research and development pipelines which suggests that development of the programme has been discontinued.