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The trophoblast cell line HTR\u20108 (H8) was treated with cobalt chloride (CoCl<jats:sub>2<\/jats:sub>) with or without a 1\u2010hr edaravone pretreatment, followed by assessment of intracellular reactive oxygen species (ROS) levels, cell proliferation, apoptosis, migration, and invasion. Metrics of apoptosis included measurement of cysteine\u2010aspartic acid protease 3 (CASP3) activity as well as BAX and BCL2 expression. Migration and invasion phenotypes were complemented with expression analysis of matrix metalloproteinase 2 (<jats:italic>MMP2<\/jats:italic>) and tissue inhibitor of metalloproteinase 2 (<jats:italic>TIMP2<\/jats:italic>) at the transcript and protein levels. CoCl<jats:sub>2<\/jats:sub> inhibited the proliferation of H8 cells, promoted apoptosis, and up\u2010regulated CASP3 activation and BAX expression while inhibiting BCL2 expression. CoCl<jats:sub>2<\/jats:sub> treatment also reduced the invasiveness of H8 cells by inhibiting MMP2 activity. Edaravone significantly increased H8 cell proliferation; inhibited apoptosis by down\u2010regulating CASP3 activation and BAX production while promoting BCL2 stability; and ameliorated the migration and invasion phenotypes associated with CoCl<jats:sub>2<\/jats:sub> treatment. These results suggest that edaravone may rescue hypoxia\u2010induced abnormalities in H8 cell proliferation, apoptosis, and invasion, thereby protecting the trophoblast lineage against hypoxia. <jats:italic>Mol. Reprod. 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