Mechanistic analysis of the bioactivity of the JMN3-003 compound class through characterization of exposed cells and time-of-addition experiments revealed two distinct phenotypes, a temporary cell cycle arrest in the G 1 /S phase and an arrest in the myxovirus life cycle at a post-entry step. Current libraries of chemical analogs of JMN3-003 do not yet permit a definitive conclusion as to whether both activities adhere to discrete structure-activity relationships or are causally linked, but a bulk of experimental data demonstrate that host cell cycle arrest per se has no inhibitory effect on replication of paramyxoviruses such as MeV. Not only does the virus itself induce a G 1 /S-phase arrest in infected T lymphocytes [29, 30] , we also found that exposure of infected cells to alsterpaullone, a potent blocker of G 1 /S-phase cell cycle progression through nanomolar inhibition of cellular cyclindependent kinases [28] , did not affect the extent of virus replication even at concentrations exceeding reported alsterpaullone EC 50 values by more than 1,000-fold. Likewise consistent with the notion that the antiviral activity of JMN3-003 is not based on cell cycle arrest itself, virus inhibition was not restricted to the context of immortalized, rapidly dividing tissue culture cell lines but extended with equal potency to primary human PBMCs.