Alexion has paid Affibody $25 million (€22 million) to co-develop a treatment for rare IgG-mediated autoimmune diseases. The deal gives Alexion rights to an anti-FcRn drug designed to have a longer half-life than rival assets in development at Argenx, UCB and other companies.
Rare disease specialist Alexion bought its way into the race to bring an anti-FcRn antibody to market last year when it paid $400 million to acquire Syntimmune. That deal gave Alexion control of STNT001, a midphase asset jostling with Argenx’s efgartigimod and UCB’s rozanolixizumab toward the front of the FcRn race.
Now, Alexion has picked up rights to an earlier-phase asset designed to improve on the frontrunners, Affibody’s ABY-039. While other anti-FcRn drugs are monoclonal antibodies or antibody fragments, ABY-039 is an antibody mimetic. Such drugs specifically bind antigens, like antibodies do, but have a different structure than the better-known modality. Notably, ABY-039 is far smaller than a typical antibody, coming in at 18 kDa. IgG antibodies have molecular weights of around 150 kDa.
In the case of ABY-039, Alexion thinks the antibody mimetic modality has resulted in a drug that has a longer half life than antibodies directed at FcRn and can be delivered via low-volume subcutaneous administration. Those features could give ABY-039 an edge over other anti-FcRn drugs, including Alexion’s STNT001, now known as ALXN1830.
Alexion has neutralized the threat posed by ABY-039 by paying $25 million upfront and committing to up to $625 million in development and sales-based milestones. The deal will see Alexion lead joint clinical development and commercialization. Affibody has retained an option to co-promote the drug in the U.S. and lead clinical development in an undisclosed location.
Affibody moved ABY-039 into a phase 1 study in healthy volunteers last year to assess its safety, tolerability and pharmacokinetics. The trial is evaluating intravenous and subcutaneous formulations of ABY-039.
Beyond that, a range of opportunities for further development could open up. FcRn extends the half-life of IgG antibodies, including molecules that promote autoimmune disease. Disrupting interactions between FcRn and IgG could therefore accelerate the clearance of these disease-causing autoantibodies, thereby improving outcomes in a range of autoimmune diseases.
ALXN1830 is in development in indications including pemphigus and warm autoimmune hemolytic anemia, while Argenx and UCB are testing their drugs in myasthenia gravis.