About This Program
This program aims to develop anti-GITRL therapeutic fusion protein for immuno-oncology.
Chimeric fusion proteins, with their ability to extend plasma half-life and prolong therapeutic activity, offer exciting benefits over antibody-based therapeutics. Companies are intensely investigating into fusion protein therapeutics as a promising alternative to antibodies.
GITRL, a member of the tumor necrosis factor (TNF) family of ligands, functions to activate the co-stimulatory receptor GITR to enhance T-cell-modulated immune responses. Many studies have shown that GITRL-FP (fusion protein) binds to its co-stimulatory surface receptor GITR expressed on T lymphocytes and activates T lymphocytes, causing T-lymphocyte proliferation and suppression of the regulatory T cells (Treg) activity. This promotes cytotoxic T-lymphocyte (CTL)-mediated killing of tumor cells, highlighting a clear rationale for GITRL-FP-based cancer immunotherapy.
GITRL
GITRL (TNFSF18) is mainly expressed in immature and mature DCs, B cells, endothelial cells, macrophages, and microglia. The GITRL/GITR system has been implicated in various processes, including CD4+CD25+ Tregs suppression, antiviral and antitumoral responses, leukocyte extravasation, RA development, and chronic lung inflammation.
Full Article: Next-IO™ Anti-GITRL Therapeutic Fusion Protein Program
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