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>Jane Osbourn
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About The Speaker

Jane Osbourn

ALCHEMAB THERAPEUTICS, CSO

Jane Osbourn

ALCHEMAB THERAPEUTICS, CSO

Jane is Chief Scientific Officer at Alchemab Therapeutics, which focusses on identifying self-protective antibodies as therapies for neurodegeneration and oncology. She was an early employee of Cambridge Antibody Technology, which became MedImmune, the biologics arm of AstraZeneca, where she contributed to the development of phage display technology, authored many key publications and patents, and contributed to the discovery and development of eight marketed drugs. She is passionate about the development of the biotechnology sector and served as Chair of the UK BioIndustry Association (BIA) from 2015-2019.

She is also the Chair of Mogrify, a Cambridge-based cell-therapy company, a founder of RQ Bio a UK-based infectious disease company, and has been a Director of Cambridge Enterprise, and of Babraham Research Campus. In 2019 she was awarded an OBE for services to drug discovery, development and biotechnology, and in the same year the Scrip Lifetime Achievement Award for contribution to the pharma industry.

In 2023 she was awarded the BIA life time achievement award, recognising her sustained contribution to biologics drug development.

Targeting FcRn for the therapy of autoimmune disease

The central role of FcRn in regulating immunoglobulin G (IgG) persistence and transport provides opportunities for targeting this receptor in multiple different diagnostic and therapeutic situations. The engineering of IgGs with higher affinity for FcRn can be used to produce antibodies with longer in vivo half-lives, but only if the low affinity of the IgG-FcRninteraction at near neutral pH is retained. Conversely, an engineered IgG or Fc fragmentwith increased affinity for FcRn at both acidic and near neutral pH acts as a potent inhibitor of FcRn. Consequently, such an antibody (‘Abdeg’, for antibody that enhancesIgG degradation) can lower the levels of endogenous IgG and has led to the FcRn antagonist, efgartigimod, that has been developed by argenx and recently approved for the treatment of myasthenia gravis. Our recent work has also resulted in the generation of engineered Fc-fusions that selectively clear antigen-specific antibodies (‘Seldegs’, for selective degradation). Developments related to the modulation of the dynamic behavior of IgG in the bodywill be presented.