3-Deazaadenosine, an inhibitor of S-adenosylhomocysteine hydrolase with a Ki of 3.9 μM, exhibits anti-inflammatory, anti-proliferative, and anti-HIV activity.

S-adenosylhomocysteine hydrolase:（ki）3.9 μM, HIV-1 (A018 isolate):0.20 μM, HIV-1 (A012 isolate):0.15

3-Deazaadenosine, an inhibitor of S-adenosylhomocysteine hydrolase (Ki = 3.9 μM), demonstrates anti-HIV activity by inhibiting p24 antigen in peripheral blood mononuclear (PBMCs) cells infected with HIV-1 isolates (A012 and A018) with IC50s of 0.15 and 0.20 μM, respectively[1]. At 100 μM, it enhances NF-κB nuclear translocation while blocking LPS-induced NF-κB transcriptional activity, an effect augmented by homocysteine[2]. At 50 μM, it suppresses vascular smooth muscle cell (VSMC) proliferation by interfering with Ras signaling[3]. Additionally, 3-Deazaadenosine (50, 100 μM) dose-dependently inhibits the phosphorylation of Raf and ERK, protein-dependent kinase 1, protein kinase B (Akt), and FoxO1a. Concentrations ranging from 1-100 μM inhibit LPS-induced TNF-α mRNA expression, increase NF-κB DNA binding activity, and cause proteolytic degradation of IκBα but not IκBβ in RAW 264.7 cells.