INTRODUCTION
Psoriasis is a chronic, immune-mediated inflammatory skin disease affecting more than 125 million individuals worldwide.1-3 At the cellular level, aberrant activation of inflammatory pathways triggers keratinocyte hyperproliferation, resulting in the formation of thick, scaly plaques.3,4 Two cytokines central to this process, interleukin (IL)-23 and type I interferons (IFNs), signal through the intracellular enzyme tyrosine kinase 2 (TYK2).1,5,6 As a member of the Janus kinase (JAK) family, TYK2 plays an essential role in mediating inflammatory signaling cascades, and overactivation of this pathway contributes to psoriasis pathogenesis.4 This pivotal role has made TYK2 an attractive therapeutic target.1,5,6
First- and second-generation TYK2 inhibitors developed for immune-mediated diseases, including psoriasis, act by blocking the adenosine triphosphate (ATP) binding site on the TYK2 catalytic domain.7,8 Deucravacitinib represents a paradigm shift as a next-generation, oral, selective, allosteric TYK2 inhibitor that binds the regulatory domain rather than the catalytic domain.7 This unique mechanism confers greater receptor specificity and minimizes off-target inhibition of other JAK pathways, reducing the potential side effect burden.8,9 Deucravacitinib is the first FDA-approved oral medication in its class for moderate-to-severe plaque psoriasis and is administered at a dose of 6 mg once daily.10





