Release Date: 23-Jan-2025
Rilvegostomig, previously known as AZD2936, is an innovative bispecific antibody currently under development by Compugen and AstraZeneca. It is derived from Compugen’s COM902 program and specifically targets two immune checkpoint receptors, PD-1 and TIGIT. This bispecific molecule is designed to simultaneously block both receptors, aiming to enhance the body’s immune response against tumors. The molecule’s dual inhibition of PD-1 and TIGIT has the potential to significantly improve antitumor immunity by promoting T-cell activation and inhibiting immune suppression mechanisms that tumors often exploit to evade detection by the immune system.
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As a humanized IgG1 antibody, Rilvegostomig has a high affinity for both PD-1 and TIGIT, which allows it to bind to these receptors cooperatively. The binding to PD-1 helps to prevent its inhibitory effects on immune cells, while the blockade of TIGIT further enhances T-cell function, which is crucial for targeting and destroying tumor cells. The unique design of Rilvegostomig aims to synergistically activate the immune system and overcome the resistance mechanisms that tumors often deploy.
A distinctive feature of Rilvegostomig is its engineered triple-mutant Fc domain. This modification reduces the antibody’s ability to induce antibody-dependent cell-mediated cytotoxicity (ADCC) or antibody-dependent cellular phagocytosis (ADCP), two immune processes that can lead to the unwanted depletion of immune cells. By minimizing these effects, Rilvegostomig enhances its therapeutic potential while limiting potential side effects associated with Fc-mediated immune responses.
Currently, Rilvegostomig is being evaluated in a Phase 3 clinical trial for its efficacy and safety in the treatment of biliary tract cancer, a difficult-to-treat malignancy with limited treatment options. The development of this bispecific antibody represents a promising approach in cancer immunotherapy, aiming to improve outcomes for patients suffering from cancers that do not respond well to existing therapies.