What this Trial Is About

Vitiligo affects approximately 1 to 2% of the global population and significantly impacts people's quality of life. Achieving the best treatment outcomes for vitiligo involves addressing the autoimmune inflammatory response to stop the depigmentation process and promoting the differentiation of melanocyte stem cells to induce repigmentation. The loss of melanocytes in vitiligo is a result of an autoimmune process. While the IFN gamma pathway plays a crucial role in the adaptive immune response in vitiligo, there is increasing evidence highlighting the importance of the innate immune response. Deucravacitinib, an allosteric TYK2 inhibitor, has shown effectiveness and safety in treating psoriasis. It inhibits the responses of IFN alpha (IFNα), IFN beta (IFNβ), and IL12, and may also have an impact on the Th1 response. The hypothesis is that by targeting the IFN type I response and IL12, deucravacitinib could effectively halt the depigmentation process and facilitate repigmentation of vitiligo lesions. When combined with NB-UVB, the process of repigmentation should be significantly enhanced. The primary objective is to compare the proportion of patients treated with deucravacitinib versus placebo achieving VITIL-IA 50 at week 24. Interventions Following central randomization, patients will be assigned to receive either deucravacitinib 12mg daily (QD) or a placebo daily (QD) for a duration of 24 weeks. At the end of this period, patients will be re-randomized to receive either deucravacitinib 12mg QD alone or deucravacitinib 12mg QD + twice weekly narrowband UVB treatment twice weekly for an additional 24 weeks. Throughout the study, there will be a total of six visits conducted: selection, inclusion, Week 12, Week 24, Week 36, and Week 48. In patients who volunteer, a skin biopsy will be performed on both the lesional and peri-lesional areas at baseline, Week 12 and Week 36. Serum and plasma samples will be collected at the screening visit, Week 12, Week 24, Week 36, and Week 48.

Vitiligo Treatment by Targeting TYK2 Mediated Responses