Commit Biologics raises additional €5.5m seed financing

According to Commit Biologics A/S, the proceeds will be used to advance the BiCE platform and work towards drug candidate selection. Commit Biologic‘s Bispecific Complement Engaging (BiCE™) platform uses single domain antibodies that bind to the complement protein C1q to activate and direct the complement system. BiCE is a modular system that can arm antibodies to direct the complement system in a highly targeted way to selectively kill tumour cells or cells implicated in autoimmune disease.

To drive the plan forward, Commit has appointed Chief Scientific Officer Mikkel Wandahl Pedersen as Interim CEO. Pedersen brings in two decades of experience in immuno-oncology and autoimmune disease drug discovery and development. Welcoming Eva Van Overmeire, Senior Investment Manager at Korys, to the Board of Directors, Pedersen highlighted that the investment would secure the start-up’s financial runway through late 2026.

Spun out of Aarhus University, and building on more than three decades of research, Commit’s Bispecific Complement Engaging (BiCE™) platform can supercharge a conventional monoclonal antibody to activate the complement system more effectively. This is achieved by combining single domain antibodies that engage C1q, the starting point for the complement activation cascade, with an antibody that binds to a cellular target. The modular approach of the BiCE™ technology can be used to develop therapeutics across multiple tumour-associated antigens and immune cell targets.

Complement is a largely untapped aspect of the body’s natural immune system that leverages both the direct cytolytic activity of complement along with its ability to bridge recruitment and activation of both innate and adaptive immune cells – a new approach to killing cells which can be used in combination or on a standalone basis. Current monoclonal antibodies developed for therapeutic purposes have structural restraints that hinder effective engagement to C1q, thus limiting complement mediated cytotoxicity and other complement mediated effector functions.