ABS241002

ABS241002 binds to PDL1 and prevents its interaction with PD-1, thus disrupting the immune checkpoint mechanism that typically suppresses the immune response. By inhibiting this interaction, ABS241002 can potentially restore T cell function and promote an anti-cancer immune response, making it a promising candidate for cancer immunotherapy. This mechanism positions ABS241002 as a strong contender for therapeutic applications aimed at enhancing immune activity against cancer cells.

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Programmed death-ligand 1 (PDL1) is a protein that plays a key role in immune system regulation, particularly in the context of cancer. PDL1 is expressed on the surface of various cells, including tumor cells, where it interacts with its receptor, PD-1, found on T cells. This interaction suppresses the immune response by inhibiting T cell activation, allowing cancer cells to evade detection and destruction by the immune system. By blocking the PD-1/PDL1 interaction, therapies can restore T cell activity, enhancing the body’s ability to recognize and attack cancer cells. This mechanism is central to many immunotherapies designed to treat cancers by promoting anti-tumor immune responses.

We have designed a molecule, ABS241002, that functions as a binder specifically targeting PDL1. ABS241002 binds to PDL1 and prevents its interaction with PD-1, thus disrupting the immune checkpoint mechanism that typically suppresses the immune response. By inhibiting this interaction, ABS241002 can potentially restore T cell function and promote an anti-cancer immune response, making it a promising candidate for cancer immunotherapy. This mechanism positions ABS241002 as a strong contender for therapeutic applications aimed at enhancing immune activity against cancer cells.

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