On 19 July, Novartis announced that it has entered into an exclusive license agreement with Galapagos NV, based in Belgium, and MorphoSys , based in Germany, to pursue the global development and marketing of MOR106 for the treatment of atopic dermatitis.
MOR106 is a monoclonal antibody (mAb) that inhibits interleukin (IL) 17C. Novartis will make an initial upfront payment of $110m, with subsequent further payments for reaching certain milestones of development up to $987m. MOR106 has had its efficacy demonstrated in a double-blinded, placebo-controlled Phase Ib study, is currently undergoing a Phase II trial as part of the IGUANA programme and is undergoing preclinical testing for psoriasis. Although moderate-to-severe atopic dermatitis patients already have access to mAb IL inhibitors, most notably Sanofi/Regeneron’s IL-4-targeting Dupixent (dupilumab), MOR106 has the potential to be the first to target IL-17C.
This IL is known to be proinflammatory, stimulating the release of other proinflammatory factors such as tumour necrosis factor alpha (TNFα) and IL-1β, and it specifically regulates Th17 cell development by binding to the IL-17RE expressed on CD4+ T cells. Since it is proinflammatory, IL-17C was suspected of being a viable target for treating chronic inflammatory conditions like atopic dermatitis when its role in mice inflammatory signalling was elucidated. Wild type (WT) mice and mice lacking IL-17C (Il17C-/-) were both induced with experimental autoimmune encephalomyelitis (EAE). WT mice were shown to have a 15 times greater amount of IL-17C in their central nervous system, and Il17C-/- mice had a great decrease in the severity of disease compared to the WT mice, although the time of disease onset was unchanged.
MOR106 is not the only new mAb treatment to be coming to the atopic dermatitis market in the near future; late-stage development treatments include Galderma ’s nemolizumab, an anti-IL-31 mAb that aims to tackle inflammation by targeting pruritus and relieve scratching of lesions, and LEO Pharma’s tralokinumab, an anti-IL-13 mAb that aims to prevent the underlying inflammation caused by the proliferation of proinflammatory cell types. Despite having different mechanisms of action, all of these pipeline therapies will have to work hard to dethrone Dupixent as the current standard of care in atopic dermatitis, as patients report high rates of satisfaction on the potentially blockbuster drug.