the converse applies for human influenza viruses . Species such as pigs that contain both ��2,3 and ��2,6 linked receptors allow 1624602-30-7 coinfection with both human and avian influenza viruses . Genome reassortment of coinfecting influenza viruses may result in a new influenza virus strain containing different subtypes of HA or NA previously unseen in humans. Humans may not have preexisting immunity to a new strain of influenza virus, so pandemics can result from genome reassortment . Human cases of H5N1 have occurred sporadically since 1997 and in 2013 human cases of H7N9 have been reported . Both H5N1 and H7N9 are highly pathogenic in humans and are currently circulating in avian reservoirs . The potential of H5N1 or H7N9 viruses to jump to humans emphasize the need for broad spectrum influenza inhibitors since vaccine development would require months. Considering the possibility of increased resistance to neuraminidase inhibitors , and the threat of avian viruses to gain transmissibility among humans, new influenza inhibitors are urgently needed. Fusion inhibitors have been successfully used in the treatment of HIV . For instance, enfuvirtide is a peptide derived from gp41 that blocks refolding of gp41, effectively arresting fusion of HIV to the cell membrane . A peptide based inhibitor with a cholesterol moiety attached has successfully targeted influenza virus fusion in vitro . LJ001, a small molecule able to inhibit fusion of many pseudotyped enveloped viruses, proves that small molecules can block the fusion pathway of viruses . If the influenza virus fusion pathway could be targeted effectively by small molecule inhibitors, these inhibitors could become an important new class of inhibitors for controlling influenza virus. A potent inhibitor of influenza virus, -3- -5- – 3- pentyl)furan-2-yl)-methylene)-2-thioxothiazolidin-4-one, was developed recently , but the mechanism of inhibition by 136 was not clearly defined. Here we report that 136 1532533-67-7 citations interferes with the fusion process of influenza virus, likely by disrupting the structure of the viral envelope necessary for fusion to cellular membranes. MDCK-2 cells were cultured in EMEM supplemented with 5 FBS and pen