Atopic dermatitis (AD) is a chronic and highly prevalent skin disorder with multifactorial pathogenesis that includes mast cell (MC) activation as one of the main players.
Several cancer types are treated with epidermal growth factor receptor (EGFR)-targeting agents (EGFR inhibitors), but this treatment is associated with dermal toxicity in up to 90% of cases, where 80% of cases have rash, among other issues. This skin toxicity is mainly driven by elevation of Staphylococcus aureus and the proinflammatory cytokine IL-36γ. Skin keratinocytes’ cutaneous immune defense is impaired by EGFR inhibitors.
South Korea’s Hanall Biopharma Co. Ltd., of Songpa-gu, Seoul, agreed to an exclusive licensing deal with San Francisco-based Turn Biotechnologies Inc. to develop novel ophthalmic and optic therapies using the latter’s mRNA-based technology.
Netherton syndrome (NS) is a rare genetic disease caused by loss of functional lympho-epithelial Kazal-type-related inhibitor (LEKTI, SPINK5). It was hypothesized that small-molecule inhibitors of KLK5 could replace deficient LEKTI in NS.
A little over two months after the granting of its very first patent which described computer-based systems for diagnosing psoriasis, Belletorus Corp. welcomed the publication of two continuation-in-part child filings on similar such systems for the diagnosis of eczema and determining the severity of skin diseases such as psoriasis, eczema and skin cancer.
Aryl hydrocarbon receptor (AhR) agonists have been reported in an Eli Lilly & Co. patent and described as potentially useful for the treatment of psoriasis, atopic dermatitis, ulcerative colitis, multiple sclerosis, Crohn’s disease, rheumatoid arthritis, graft-vs.-host disease and systemic lupus erythematosus.
Netherton syndrome (NS) is caused by mutations in the serine protease inhibitor Kazal type 5 gene (SPINK5), which encodes lympho-epithelial Kazal-type-related inhibitor (LEKTI).
JJP Biologics Sp. z o.o. has received clearance from the EMA to conduct a first-in-human study of its CD89 antagonist, JJP-1212, for IgA-mediated autoimmune and fibrotic diseases. A phase I study in healthy participants will be conducted in Poland.
It is known that transient receptor potential cation channel subfamily V member 3 (TRPV3) is crucial for the modulation of skin homeostasis by regulation of Ca2+.
Gaining full rights to a bispecific antibody to treat atopic dermatitis, Johnson & Johnson is paying $1.25 billion to acquire Yellow Jersey Therapeutics, a wholly owned subsidiary of Numab Therapeutics AG. The subsidiary houses all assets related to NM-26, which targets IL-4Ra (type I and II receptors) and IL-31, and was designed with Numab’s MATCH (Multispecific Antibody-based Therapeutics by Cognate Heterodimerization) technology platform. It is ready for phase II development for atopic dermatitis, although J&J intends to develop, manufacture and commercialize the drug globally for follow-on indications as well.
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