Cell therapy based on fibroblasts has shown promise in the treatment of psoriasis due to immune modulation capability and strong expansion when cultured. Work at Fibrobiologics Inc. has focused on the impact of culture format and donors of human dermal fibroblasts (HDFs) on the therapeutic efficacy and immune responses in murine models of psoriasis.
Recludix Pharma Inc. recently presented data on their new STAT1/3 inhibitors REX-6553 and REX-6547 for treating dermatological inflammatory skin diseases.
Genescience Pharmaceutical Co. Ltd. has presented data on a new STAT6 PROTAC degrader – GenSciP166 – which selectively targets STAT6 for proteasomal degradation. GenSciP166 was assayed in vitro as well as in vivo in the MC903 atopic dermatitis murine model.
Netherton syndrome is a rare disease caused by loss of activity of the lympho-epithelial Kazal-type-related inhibitor (LEKTI) protein, which in turn is caused by mutations in its encoding gene, SPINK5. This deficiency leads to the triggering of the kallikrein (KLK) signaling cascade resulting in skin barrier dysfunction, inflammation and atopy. At the recent Society for Investigative Dermatology meeting, Biocryst Pharmaceuticals Inc. presented early data on BCX-17725, a KLK5/KLK14 inhibitor fusion protein developed to restore LEKTI functioning in patients with Netherton syndrome.
Researchers from Recludix Pharma Inc. reported preclinical efficacy data on REX-8756 (SAR-448755), a first-in-class orthosteric STAT6 inhibitor in models of atopic dermatitis (AD). Targeting STAT6, the key downstream mediator, offers a more selective strategy that could reproduce biologic efficacy while reducing off-target effects.
