Abstract::Psoriasis is a relapsing, chronic, and inflammatory disease of the skin. However, its
impact goes beyond just pathophysiology and takes a toll on the physical and psychological aspects
of the health of the afflicted, lowering the quality of life significantly. It is also a mechanistically
complex disease with a substantial immune component. Therefore, ongoing treatment
strategies focus on targeting at least one immune component associated with the disease development
and progression by employing biological agents like IL-1 inhibitors, IL-23 inhibitors,
IL-36 inhibitors, and TNF-α inhibitors. Psoriasis-induced disruptions in cellular signalling
pathways have drawn significant attention as novel drug targets. Numerous novel synthetic
agents, such as JAK/STAT inhibitors [ruxolitinib, peficitinib], TYK2 inhibitors [zasocitinib,
ropsacitinib], RORꝩT inhibitors [cedirogant], A3AR agonists [piclodenoson], and CXCR2 antagonists
[vimnerixin] are undergoing extensive clinical trials and have demonstrated beneficial
outcomes in multiple phases of these trials. Deucravacitinib, an orally administered TYK2 inhibitor,
has recently received FDA approval for the treatment of moderate to severe plaque psoriasis.
These synthetic agents hold promise to change the outlook of psoriasis management by
modulating specific molecular targets associated with the dysregulated immune response observed
in psoriasis. Moreover, these pathways can be exploited to personalize anti-psoriatic
therapy, minimize side effects, and maximize therapeutic outcomes. Altogether, the integration
of biological agents and synthetic agents can overcome the challenges associated with the management
of the repertoire of psoriatic pathophysiology and symptoms.