The mechanism of action and efficacy of Teclistamab-cqyv

Teritusumab (Teclistamab-cqyv) is a novel bispecificT cell engager (BiTE) that has shown important medical value in the treatment of relapsed or refractory multiple myeloma (MM). Its unique mechanism of action is to exert immune effects by simultaneously combining two targets, CD3 and BCMA (B cell maturation antigen). CD3 is an important receptor on the surface of T cells, and BCMA is widely expressed on the surface of myeloma cells. Teritusumab uses this mechanism to "guide" the patient's own T cells around myeloma cells, thereby activating the killing effect of T cells and achieving precise elimination of tumor cells.

The advantage of this bispecific mechanism is that it does not require the antigen presentation process of T cells. Instead, it directly prompts T cells to release cytokines and perforate tumor cells and induce apoptosis. In addition, because BCMA is a molecule expressed almost exclusively on plasma cells and their malignantly transformed myeloma cells, teritusumab has a high degree of targeting and a low off-target risk. Compared with traditional chemotherapy or monoclonal antibody drugs, it provides a new strategy that does not depend on the mutation status of tumor antigens, which is of great significance for multiple myeloma, a highly heterogeneous disease.

In countries such as Europe and the United States, teritolumab has been approved for the treatment of myeloma patients who have failed multiple lines of therapy. Although its treatment may cause immune-related side effects such as cytokine release syndrome (CRS) or neurotoxicity, these adverse reactions are gradually being better managed with the accumulation of clinical experience. Therefore, teritusumab is considered a major breakthrough in the field of immunotherapy for multiple myeloma. Its biotechnology has broad prospects, and it also provides a reference template for the future development of targeted drugs with similar mechanisms.

Reference materials:https://www.tecvayli.com/