3-Deazaadenosine (3-DZA) is an inhibitor of SAH (Sadenosylhomocysteine) hydrolase (Ki = 3.9 μM). It has antiinflammatory properties, inhibiting leukocyte adhesion and chemotaxis, lymphocyte-mediated cytolysis, phagocytosis, degranulation, and NF-κB signaling. 3-DZA also has anti-viral and anti-bacterial activities.
Possesses antiviral activity. It is an inhibitor of leukocyte adhesion to TNF-treated endothelial cells.
Possesses antiviral activity inhibitor of leukocyte adhesion to TNF-treated endothelial cells.
3-deazaadenosine showed inhibitory values against the ebo-z viruses, ebo, and marburg virus in various cell lines of primate (sw13, vero 76, frhl, llc-mk2, mrc-5, vero e6) and mouse (balb/3t3 clone a31) origin. 3-deazaadenosine at 2 μg/ml could reduce viral replication by 3 logs in a dose-dependent manner. however, there was no further inhibition even with a 100-fold increase in concentration [1].
in vehicle control group, adult balb/c mice lethally infected with mouse-adapted ebola virus die 5-7 days after infection. in contrast, 3-deazaadenosine treatment initiated on day 0 or 1 led to a dose-dependent protection, with mortality completely prevented at doses around 0.7 mg/kg every 8 h. moreover, there was significant protection when 3-deazaadenosine treatment was begun on day 2, at which time, the spleen had an average titer of 2 × 106 pfu/g and the liver had 3 × 105 pfu/g virus. treatment with 3-aeazaadenosine at 2.2 mg/kg initiated on day 3 resulted in 40% survival [1].
[1] huggins, z. x. zhang and m. bray. antiretroviral drug therapy of filovirus infections: s-adenosylhomocysteine hydrolase inhibitors inhibit ebola virus in vitro and in a lethal mouse model. journal of infectious diseases 179 (1), s240-s247 (1999).
