Johnson & Johnson has announced the completion of its acquisition of Yellow Jersey Therapeutics, a subsidiary of Numab Therapeutics, in a transaction valued at approximately $1.25 billion. This acquisition secures global rights to NM26, a promising investigational bispecific antibody ready for Phase 2 trials in atopic dermatitis (AD).
NM26 targets two clinically proven pathways, the IL-4R alpha subunit (IL-4Rα) and IL-31, which are responsible for Th2-mediated skin inflammation and itching, respectively. David Lee, Global Immunology Therapeutic Area Head at Johnson & Johnson Innovative Medicine, emphasized the significance of NM26, stating, "NM26 is designed to help different subpopulations of patients by targeting two disease-driving pathways, which is key when treating a heterogeneous disease like AD." This development is seen as a potential game-changer in the standard of care for AD and other inflammatory skin diseases involving Th2 inflammation and itch.
Atopic dermatitis is the most common inflammatory skin disease, characterized by itching and inflammation exacerbated by scratching. The condition can lead to severe skin infections, pain, sleep disturbances, anxiety, stress, depression, and even an increased risk of suicide. According to Candice Long, Worldwide Vice President, Immunology at Johnson & Johnson, "Nearly three-quarters of people with AD are not achieving remission with currently available treatments. The unmet need is high, and we must do better for patients."
Johnson & Johnson's investment in NM26 underscores its commitment to addressing the high unmet needs in AD treatment. The company aims to achieve durable, symptom-free remission for all patients living with immune-mediated diseases. As Long highlights, "Our investment in NM26, and other bispecific antibodies, is another important step towards our mission."
In a separate study published in Nature, researchers examined the H5N1 avian influenza virus in U.S. dairy cattle. The findings revealed that viruses derived from lactating dairy cattle induced severe disease in mice and ferrets when administered via intranasal inoculation. Although the virus bound to both avian and human-type cellular receptors, it did not efficiently transmit among ferrets exposed via respiratory droplets.