The standard way to find a therapeutic antibody is to immunise a genetically engineered mouse and see what its immune system comes up with. Infinimmune’s argument is that human beings have already run that experiment, several billion times over.
On August 11 the Bay Area biotech closed a $75 million Series A co-led by Regeneron Ventures and Playground Global, with RA Capital Management, Forge Life Science Partners and Goldcrest Capital joining as newcomers and existing investor Merck returning. The money funds two lead antibodies into Phase 1 next year, both in atopic dermatitis: IFX-201, aimed at interleukin-13, and IFX-101, aimed at interleukin-22. Behind them sit earlier candidates against APRIL and interleukin-17F for IgA nephropathy and ulcerative colitis. In March, Merck signed a discovery pact with the company worth up to roughly $838 million.
Why the pairing is the whole point
An antibody is built from two chains, heavy and light, and the particular combination of the two decides what it grabs and how tightly. Antibodies raised in mice have to be humanised afterwards, which means swapping mouse sequence for human sequence, and that process can quietly wear down the thing that made the antibody good in the first place. Phage display, the other standard route, builds vast synthetic libraries in which heavy and light chains are shuffled together more or less at random. Enormous diversity, but pairings no immune system ever actually produced.
Infinimmune takes memory B cells directly out of people and sequences them one cell at a time, so the heavy chain and light chain that arrive together are the pair that evolved together, inside a human, against a real target. Nothing needs humanising because nothing was ever non-human. The approach only became practical once single-cell sequencing got cheap enough to run across millions of B cells at once.
Regeneron is funding its own competition
Dupixent, Regeneron’s inflammation blockbuster, blocks interleukin-4 and interleukin-13. IFX-201 targets interleukin-13. Regeneron Ventures co-led the round anyway, which reads as either confidence or hedging depending on how you look at it. Chief executive Wyatt McDonnell’s case is that eczema patients frequently stop responding to one drug and then respond to another hitting the same target, so a second molecule against a proven mechanism can work alongside the first one, not just imitate it. The second candidate, IFX-101, goes after interleukin-22, which McDonnell describes as an underestimated part of eczema biology with no approved biologic against it.
Why it matters
Mice became the default because they were convenient. A mouse immune system has never encountered human atopic dermatitis, and everything it produces has to be translated afterwards. Reading antibodies out of the people who actually have the disease is the more obvious idea, and it has been waiting on the cost of sequencing to fall, not on any conceptual breakthrough. Whether it yields better drugs is a question for 2027, when both lead candidates reach first-in-human studies.
Sources: Infinimmune Series A announcement (BioSpace); MedCity News.