Aim:To investigate the anticancer activity of dihydroartemisinin (DHA),a deriva-tive of antimalaria drug artemisinin in a panel of human ovarian cancer cell lines.Methods:Cell growth was determined by the MTT viability assay.Apoptosis andcell cycle progression were evaluated by a DNA fragmentation gel electro-phoresis,flow cytometry assay,and TUNEL assay;protein and mRNA expression wereanalyzed by Western blotting and RT-PCR assay.Results:Artemisinin and itsderivatives,including artesunate,arteether,artemether,arteannuin,and DHA,exhibit anticancer growth activities in human ovarian cancer cells.Among them,DHA is the most effective in inhibiting cell growth.Ovarian cancer cell lines aremore sensitive (5-10-fold) to DHA treatment compared to normal ovarian celllines.DHA at micromolar dose levels exhibits a dose-and time-dependent cyto-toxicity in ovarian cancer cell lines.Furthermore,DHA induced apoptosis and G_2cell cycle arrest,accompanied by a decrease of Bcl-x_L and Bcl-2 and an increase ofBax and Bad.Conclusion:The promising results show for the first time that DHAinhibits the growth of human ovarian cancer cells.The selective inhibition ofovarian cancer cell growth,apoptosis induction,and G_2 arrest provide in vitroevidence for further studies of DHA as a possible anticancer drug in the clinicaltreatment of ovarian cancer. Aim: To investigate the anticancer activity of dihydroartemisinin (DHA), a deriva-tive of antimalaria drug artemisinin in a panel of human ovarian cancer cell lines. Methods: Cell growth was determined by the MTT viability assay. Apoptosis and cell cycle progression were evaluated by a DNA fragmentation gel electro-phoresis, flow cytometry assay, and TUNEL assay; protein and mRNA expression were analyzed by Western blotting and RT-PCR assay. Results: Artemisinin and its derivatives, including artesunate, arteether, artemether, arteannuin, and DHA, exhibit anticancer Growth activities in human ovarian cancer cells. Among them, DHA is the most effective in inhibiting cell growth. Ovarian cancer cell lines aremore sensitive (5-10-fold) to DHA treatment compared to normal ovarian cell lines. DHA at micromolar dose levels exhibits a dose-and time-dependent cyto-toxicity in ovarian cancer cell lines. Fultrther, DHA induced apoptosis and G_2 cell cycle arrest, accompanied by a decrease of Bcl-x_L and Bcl-2 and an incr ease of Bax and Bad. Conflusion: The promising results show for the first time that DHA inhibits the growth of human ovarian cancer cells. The selective inhibition ofovarian cancer cell growth, apoptosis induction, and G_2 arrest provide in vitro criteria for further studies of DHA as a possible anticancer drug in the clinical treatment of ovarian cancer.