On August 22, 2024 ImmuneOnco Biopharmaceuticals reported on a voluntary basis to inform shareholders and potential investors of the Company about the latest business development of the Group (Press release, ImmuneOnco Biopharma, AUG 22, 2024, View Source [SID1234655702]).
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Reference is made to the announcement of the Company dated August 1, 2024, in relation to the entry into a license and collaboration agreement (the "License and Collaboration Agreement") dated August 1, 2024, between the Company and SynBioTx Inc.("SynBioTx").
The board (the "Board") of directors ("Directors", and each a "Director") of the Company is pleased to announce that the Company has received an upfront payment of US$10 million from SynBioTx in line with the License and Collaboration Agreement. Pursuant to the License and Collaboration Agreement, the Company expects to receive potential nearterm payments of up to US$40 million in the future, the earliest of which is expected to be received in September of 2024. Furthermore, the Company and SynBioTx have established a joint Clinical Development & Operations Committee and will actively advance the development of the IMM2510 and IMM27M.
ABOUT IMM2510
IMM2510, independently developed by the Group, is a bispecific molecule with a mAbTrap structure targeting vascular endothelial growth factor (VEGF) and programmed cell death ligand 1 (PD-L1). IMM2510 can inhibit angiogenesis, leading to tumor shrinkage, and sensitize tumor cells to immune responses, while activating T cells, NK cells, and macrophages via the blockade of PD-L1/programmed cell death protein 1 (PD-1) interaction and the induction of Fc-mediated antibody-dependent cellular cytotoxicity (ADCC)/antibody-dependent cellular phagocytosis (ADCP) activity.
ABOUT IMM27M
IMM27M is a new generation cytotoxic T-lymphocyte-associated protein 4 (CTLA-4)antibody with enhanced ADCC activity. It can induce potent immune responses targeting CTLA-4 overexpressed immune-suppressive Treg cells and promote Treg depletion from the tumor microenvironment (TME), thus enhancing T-cell antitumor response.