Nona Biosciences announced a research collaboration with the Medical University of Vienna, granting the inter-university Ignaz Semmelweis Institute access to Nona’s proprietary H2L2 Harbour Mice transgenic mouse technology platform to support antibody research for infectious diseases. The H2L2 Harbour Mice platform uses genetically modified mice that produce antibodies with fully human structures following immunization.
Under the agreement, MedUni Vienna is granted rights to use Nona’s technology for antibody generation and to further develop resulting antibodies for research, diagnostic, and therapeutic applications, while the platform and its associated intellectual property remain owned by Nona Biosciences. Nona, a wholly owned subsidiary of HBM Holding Limited, supports drug discovery programs through its I to I framework spanning target validation through early clinical development, and its Harbour Mice platform also includes a heavy chain-only antibody format that the company describes as the world’s first fully human HCAb transgenic mouse platform with clinical validation.
KEY QUOTES:
“We are delighted to partner with the Medical University of Vienna. This collaboration underscores the power of our H2L2 Harbour Mice platform to accelerate the discovery of fully human antibodies against clinically relevant targets. By combining our technology with the scientific expertise of Prof. Krammer and his team at the Ignaz Semmelweis Institute, we aim to make meaningful contributions to antiviral therapeutic development and pandemic preparedness.”
Dr. Di Hong, Chief Executive Officer, Nona Biosciences
“Access to this technology expands our capabilities to generate and characterise human antibodies against relevant biological targets, particularly viral spike proteins. This provides us with an additional foundation for the development of antiviral therapies, particularly with a view to future pandemics.”
Florian Krammer, Professor of Infectious Diseases, Medical University of Vienna and Director, Ignaz Semmelweis Institute
