The most potent inhibitor in the series efficiently blocked the binding of <i>h</i>Gal-1 to the surface of MDA-MB-231 tumor cells, reduced their viability, and completely suppressed <i>h</i>Gal-1-induced phosphatidylserine exposure in Jurkat cells, a process previously described as preaparesis rather than classical apoptosis. Here, LGALS1 is linked to neoplasm.