Z-Asp-CH2-DCB is an irreversible broad spectrum caspase inhibitor. Z-Asp-CH2-DCB also inhibits proteases with caspase-like activity. Z-D-CH2-DCB blocks the production of IL-1β, TNF-α, IL-6, and IFN-γ in staphylococcal enterotoxin B (SEB)-stimulated peripheral blood mononuclear cells (PBMC), and reduces SEB-1-stimulated T-cell proliferation in a dose-dependent manner. Z-Asp-CH2-DCB prevents SU5416-induced septal cell apoptosis and emphysema development^[1][2][3]. In Vitro: Z-Asp-CH2-DCB (10-100 μM) blocks the production of IL-1β, TNF-α, IL-6, and IFN-γ in SEB-stimulated (200 ng; 16 hours) PBMC in a dose-dependent manner. The production of the chemokines MCP-1, MIP-1α, and MIP-1β was also suppresses. The inhibitory effect of Z-Asp-CH2-DCB on TSST-1-activated PBMC is similar, reducing IL-1β, IL-6, TNF-α, IFN-γ, MCP-1, MIP-1α, and MIP-1β to 10, 36, 25, 10, 11, 25, and 30%, respectively, of levels in untreated cells^[1].
Z-Asp-CH2-DCB (10-100 μM; 48 hours) inhibits T-cell proliferation in PBMC stimulated with 200 ng of SEB/ml ^[1]. In Vivo: Z-Asp-CH2-DCB (1 mg; i.p.; every day for 3 weeks) prevents SU5416-induced septal cell apoptosis^[1].