Objective：This study aims to prepare anti-tyrosine-kinase-like orphan receptor 1 （ROR1） IgG1（ROR1-IgG1）and the fusion protein of anti-ROR1 and Buthus martensii Karsch recombinant analgesic anti-tumor polypeptide（IgG1-AGAP），and compare their effect on ovarian cancer cells. Methods：ROR1Fab vectors screened and preserved in our laboratory was used as template to construct ROR1-IgG1 and IgG1-AGAP eukaryotic expression vectors；supernatant of CHO-S cells after transfected by ROR1- IgG1 and IgG1-AGAP plasmids was collected and purified，respectively. Their immunological activity was identified and detected by ELISA，Biacore X100，fluorescence-activated cell sorting（FACS）and immunofluorescence. Cell counting kit-8（CCK-8），wound healing，Transwell invasion assays were used to analyze the effects of two antibodies on the ovarian cancer cell HO8910. The expression of relevant markers of epithelial mesenchymal transition（EMT） was detected by Western blot to evaluate the effects of ROR1-IgG1 and IgG1-AGAP on the migration and invasion of ovarian cancer cells. Results：ROR1-IgG1 and IgG1-AGAP were successfully prepared，the binding efficiency of IgG1-AGAP were similarly as ROR1-IgG1. Both IgG1-AGAP and ROR1-IgG1 inhibited proliferation，migration and invasion of ROR1-positive ovarian cancer cell HO8910. Compared with ROR1-IgG1，IgG1-AGAP can significantly inhibit the proliferation and migration of tumor cells（P < 0.05），and these effects were not observed in ROR1-negative cells IOSE386. Western blot results showed that the expression levels of Snail in ROR1-IgG1 group and IgG1-AGAP group decreased compared with the blank control group，while E-cadherin showed the opposite， suggesting that ROR1-IgG1 and IgG1-AGAP can regulate Snail and E-cadherin and inhibit EMT in ovarian cancer cell HO8910，thereby inhibiting their migration and invasion. Conclusion：Our findings demonstrate that IgG1-AGAP can target ROR1 expressing ovarian cancer cells effectively and have obvious antitumor activity. IgG1-AGAP could be as an appropriate and promising therapeutic strategy for ROR1-positive human cancers.