On September 11, 2024 ImmuneOnco Biopharma 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, SEP 11, 2024, View Source [SID1234655703]).

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Reference is made to the announcements of the Company dated August 1, 2024 and August 22, 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") and the upfront payment received under the License and Collaboration Agreement.

The board (the "Board") of directors ("Directors", and each a "Director") of the Company is pleased to announce that the Company has received a near-term payment of US$5 million from SynBioTx in line with the License and Collaboration Agreement. As of the date of this announcement, the Company has received an upfront and near-term payment in aggregate of US$15 million under the License and Collaboration Agreement. Pursuant to the License and Collaboration Agreement, the Company expects to receive the remaining potential nearterm payments of up to US$35 million in the future.

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.