Dual cancer immunotherapy has entered clinical medical trials
Recently, Lycera announced the launch of a clinical 1/2a trial to test the efficacy of the company's cancer immunotherapy LYC-55716 in patients with advanced, recurrent, or refractory solid tumors. Lycera is a biopharmaceutical company dedicated to the development of breakthrough immunomodulatory drugs. LYC-55716 is a RORγ agonist developed by the company, which can produce a “dual effect†on T lymphocytes, which weakens the immunosuppressive mechanism while activating T lymphocyte function, thereby making the anti-cancer function of T lymphocytes stronger.
Cancer immunotherapy is one of the hot spots of cancer therapy, but most cancer immunotherapy is based on blocking the immunosuppressive pathway. For example, the mechanism of action of inhibitors targeting PD-1, PD-L1 and other immunological checkpoint proteins blocks the immunosuppressive pathway, allowing T lymphocytes to attack tumors. But not all cancer patients respond to immunological checkpoint therapy. For some patients, it is also important to activate their immune response to the tumor.
Lycela's LYC-55716 is unique in that it simultaneously activates the immune system and weakens the immunosuppressive pathway. LYC-55716 is an oral ROR gamma agonist. RORγ is an important transcription factor that regulates the development and function of CD4-positive Th17 and CD8-positive Tc17 lymphocytes. Approximately 15% of tumor infiltrating lymphocytes express RORγ. Lycera's preclinical studies of RORγ agonists have shown that RORγ agonists enhance the levels of interleukin-17 and other cytokines secreted by lymphocytes, thereby increasing lymphocyte cytotoxicity. These agonists also improve the survival of Th17 and Tc17 lymphocytes. At the same time, RORγ agonists are able to inhibit the production of regulatory T cells, which inhibit immune responses, so agonists can push the balance of immune responses to the direction of activation.
â–²The mechanism of action of LYC-55716 (Source: Lycera official website)
RORγ agonists can also promote the expression of a series of costimulatory molecules (Co-Stimulatory Molecule) such as CD226, CD27 and 4-1BB (CD137), and inhibit co-suppressor molecules such as PD-1, TIGIT, TIM3, CD73 and LAG3 ( Expression of Co-Inhibitory Molecule) to promote T cell activation. In a variety of Syngeneic Tumor Models, oral ROR gamma agonists are capable of inhibiting tumor growth and prolonging the survival of animals by an immune response. The results of this study have been published in the journal OncoImmunology.
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