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VYNE Reports Positive Preclinical Data for Lead BET Inhibitor, VYN201, in Human Skin Model of Vitiligo
VYN201 0.1% and 1% resulted in statistically significant improvement in reducing both melanocyte loss and key inflammatory biomarkers involved in the
About this update from Vyne Therapeutics Inc.
[{"type":"text","content":"VYN201 0.1% and 1% resulted in statistically significant improvement in reducing both melanocyte loss and key inflammatory biomarkers involved in the pathogenesis of vitiligo, an immune-modulated skin disorder.VYN201 0.1% and 1% demonstrated upregulaton of the WNT signalling pathway, recognized as an important indicator of melanocyte regeneration.VYN201 0.1% and 1% were numerically superior to the active control ruxolitinib cream, 1.5%. BRIDGEWATER, N.J., March 07, 2022 (GLOBE NEWSWIRE) -- VYNE Therapeutics Inc. (Nasdaq: VYNE) (“VYNE” or the “Company”), a biopharmaceutical company focused on developing proprietary, innovative, and differentiated therapies for the treatment of immuno-inflammatory conditions, today announced positive preclinical data in an ex vivo skin model of vitiligo. In the preclinical model, pan-bromodomain and extra-terminal (“BET”) inhibitor VYN201 reduced the expression of key pro-inflammatory biomarkers relevant to the pathogenesis of vitiligo, and demonstrated marked reduction in melanocyte loss. Vitiligo is a chronic autoimmune depigmenting disorder of the skin. There are currently no FDA approved drug therapies for the treatment of vitiligo. It is the most common depigmenting skin condition, with a prevalence estimated at 0.5-2% of the world population.1 Vitiligo is characterized by increased MMP-9 secretion and soluble E-cadherin2, resulting in a loss of pigment in the skin. Reconstituted Human Epithelial Skin Model of Vitiligo The objectives of this study were to evaluate the potential of VYN201 to (i) reduce Matrix Metalloproteinase-9 (“MMP-9”) secretion (reducing the secretion of MMP-9 allows for melanocyte stabilization and limits loss of melanocytes/depigmentation in vitiligo); (ii) reduce soluble adhesion molecule, E-cadherin (soluble E-cadherin is a biomarker of melanocyte loss due to degradation of matrix-bound E-cadherin by MMP-92); (iii) minimize the loss of melanocytes by assessing melanin pigment content and (iv) affect the expression of genes commonly associated with melanogenesis (melanin synthesis, melanosome maturation and transport). In the study, reconstituted human epithelial skin cultures were stimulated with Tumor Necrosis Factor alpha (TNF-α) and Interferon gamma (IFN-ɣ) cytokines to induce a vitiligo phenotype (loss of melanin, increased MMP-9 secretion and increased soluble E-c...