Eluciderm Inc. has identified compounds acting as inhibitors of Wnt signaling and/or poly(ADP-ribose) polymerase tankyrase-2 (TNKS2; PARP5B) and/or poly(ADP-ribose) polymerase 1 (PARP-1; ARTD1) and/or PARP-2 (ARTD2) reported to be useful for the treatment of cancer, acne, rosacea, psoriasis and scleroderma.
In a new publication in Molecular Therapy, researchers from Paracelsus Medical University, Salzburg, Austria, and collaborators present a promising prime editing strategy for junctional epidermolysis bullosa (JEB) treatment.
In atopic dermatitis (AD), the itch-scratch cycle is tied to skin inflammation exacerbation that accelerates the progression of the disease, thus impacting the patient’s quality of life, where IL-31 is crucial to induce skin itching. Helixon Ltd. has developed a bispecific antibody targeting both IL-31 and OX40L, HXN-1022, for the treatment of AD.
Genescience Pharmaceuticals Co. Ltd. has discovered new tyrosinase (TYR) inhibitors acting as melanin inhibitors potentially useful for the treatment of skin hyperpigmentation.
Janssen Pharmaceutica NV has identified interleukin-17A (IL-17A)/IL-17 receptor A (IL-17RA) interaction inhibitors reported to be useful for the treatment of psoriasis, rheumatoid arthritis, radiographic axial spondyloarthritis (ankylosing spondylitis), multiple sclerosis, asthma, chronic obstructive pulmonary disease, atopic dermatitis and systemic lupus erythematosus, among others.
Researchers at the Keck School of Medicine at the University of Southern California explored whether CC-90009 can promote readthrough in the two types of epidermolysis bullosa.
Haisco Pharmaceutical Group Co. Ltd. has identified compounds acting as TNF-α/TNF receptor superfamily member 1A (TNFR1) interaction inhibitors reported to be useful for the treatment of psoriasis and rheumatoid arthritis.
Arcus Biosciences Inc. has announced five new research programs for autoimmune and inflammatory diseases, and is targeting initiation of the first clinical studies next year.
Recent evidence in atopic dermatitis (AD) points to the involvement of additional pro-inflammatory pathways besides core Th2 responses. Current therapeutic approaches that work target mostly the IL-4/IL-13 pathway, but the duration of response and depth could be improved.
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