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 (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.
Here are some published data about GITRL fusion protein as a potential combination target for cancer immunotherapy.
GITR expression in tumor-infiltrating lymphocytes has been found to be associated with cancer progression in patients suffering from esophageal adenocarcinomas. Deletion of GITR is associated with increased risk for neoplasia, including neuroblastoma, prostate cancer, lung cancer, melanoma and non-Hodgkin lymphomas. Recent studies of chronic lymphocytic leukemia (CLL) have shown that GITRL and GITR receptors are expressed at significantly higher levels in NK cells of CLL patients compared to healthy controls.
Based on the published data, we have decided to develop multiple fusion protein programs that apply to different indications (not limited to one specific tumor type), of which GITR is highly expressed.
Currently, several studies of GITRL ligand fusion proteins are undergoing early clinical trials for the treatment of various solid malignancies. An increasing number of GITRL fusion proteins have been confirmed to stimulate T cells and shown great promise in cancer treatment. However, further studies are needed to identify the efficacy, safety, and combination strategies of GITRL ligand fusion protein.
Therefore, GITRL fusion protein is a compelling target for novel drug development. Based on our state-of-art chimeric fusion protein platform, Creative Biolabs is planning to develop the following programs (including but not limited to):
Creative Biolabs has established the novel chimeric fusion protein platform for Agonist Redirected Checkpoint (ARC) program development. We have extensive knowledge of end-to-end program development. For each program, we are committed to delivering the final complete program to our clients within 1.5 years prior to entering the IND stage.
Fig.1 The timeline of Next-IOᵀᴹ programs.
Creative Biolabs is looking for potential partners (include but not limit to major pharma or biotech firms) to develop anti-GITRL therapeutic fusion protein program together. Our scientists are dedicated to bringing together years of valuable experience to our partner and achieve a meaningful partnership. By doing so, we wish to help both parties to proceed with IND and many stages of clinical trials beyond.
If you are interested, please feel free to contact us so that we can discuss the program and other possible opportunities for cooperation. Look forward to working with you in the near future.For Research Use Only | Not For Clinical Use
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