One less rival for Immunovant, as Alexion abandons FcRn inhibitor
Less than one year after Alexion parted with $25 million upfront to secure access to a second anti-FcRn asset, it is abandoning the experimental drug. The discontinuation, disclosed at the SVB Leerink Global Healthcare Conference in New York during a fireside chat, bodes well for rival Immunovant.
The drug (ABY-039), partnered for development with Sweden’s Affibody, was forsaken on the basis of early-stage data that was not viewed favorably, Baird and SVB Leerink analysts noted.
“We believe that this finding could have been due to a negative safety signal, as Alexion also acknowledged that they knew the program was high-risk, due to the fact that prior bacterial sequences had suggested an increased likelihood of immunogenicity,” Baird’s Brian Skorney said.
“Given this context, we do not believe this discontinuation should raise questions regarding the potential benefits and mechanistic properties involved with FcRn inhibition since Alexion dialogue may infer the decision was safety-based.”
Immunovant’s rival drug, IMVT-1401, is in multiple ongoing Phase II trials. SVB Leerink’s Thomas Smith has modeled peak sales of ~$2.7 billion for the company’s three identified lead indications: myasthenia gravis, thyroid eye disease and warm autoimmune hemolytic anemia.
“(T)he discontinuation of ABY-039 reads through as an incremental positive for Immunovant. Moving forward, we continue to believe that IMVT-1401 possesses best-in-class potential as a rapidly administered and highly efficacious FcRn inhibitor,” Skorney said.
With the discontinuation of ABY-039, there is one less FcRn antibody in clinical development. However, Alexion has another anti-FcRn asset it will hold on to — ALXN1830 — which it scored in a 2018 buyout deal of Syntimmune ($400 million upfront, with a potential $800 million in milestones). There are also other companies in the space, including argenx, Harbour BioMed and Momenta.
The neonatal Fc receptor (FcRn) is an immunoglobulin G (IgG) and albumin binding protein expressed on the cell surface of most hematopoietic, endothelial, and epithelial cells.
FcRn recycles IgG antibodies by shuttling them away from lysosomal degradation, thereby preserving pathogenic antibody levels in IgG-mediated diseases such as myasthenia gravis (a long-term neuromuscular condition). Drugs designed to inhibit FcRn, therefore, are designed to decrease total IgG — crucially pathogenic IgG — to treat patients.
Social image: Alexion