https://www.selleckchem.com/products/ted-347.html T cell-redirecting bispecific antibodies (BsAbs) are emerging as a potent cancer therapy that crosslinks tumor cells and T cells by simultaneously binding to tumor-associated antigen and CD3ε. However, immune inhibitory molecules can be remarkably upregulated after BsAbs treatment, leading to a suppressive tumor microenvironment and treatment resistance. This can be partially reversed by combination with immune checkpoint inhibitors. In our previous work, we successfully constructed the recombinant protein iRGD-antiCD3 and demonstrated that it promoted antitumor efficacy of transferred T cells by promoting T cell activation and infiltration. We detected the levels of both PD-1 and PD-L1 as resistance to iRGD-antiCD3 treatment. Using cord blood-derived T cells, we assessed the activation and effects of iRGD-antiCD3 combined with PD-1 as evidenced by activation markers, Th1/Th2-cytokines, and killing capability against tumor cells in vitro. Moreover, to better mimic the physiological characteristics of in vRGD-antiCD3 with PD-1 blockade could further improve antitumor efficacy of T cells, and this strategy holds great potential for the treatment of solid malignancies. These results demonstrated that combining iRGD-antiCD3 with PD-1 blockade could further improve antitumor efficacy of T cells, and this strategy holds great potential for the treatment of solid malignancies. Ovarian cancer is one of the most common gynecological cancers worldwide. While, therapies against ovarian cancer have not been completely effective, sinomenine has been proved to have anti-tumor activity in various cancer cells. However, study of its anti-ovarian cancer effect is still rare, and the underlying mechanism has not been elucidated. Therefore, we aim to explore the mechanism of sinomenine anti-ovarian cancer. The effect of anti-ovarian cancer HeyA8 cells was analyzed by CCK8 and colony formation assay. The mechanism of sinomenine anti-ova