A Prospective, Interventional, Exploratory Study Evaluating the Efficacy of Small-Molecule Compound XJH05 Ointment in the Treatment of Plaque Psoriasis

Psoriasis is a chronic, recurrent, inflammatory, and systemic disease mediated by immunity, induced by a combination of genetic and environmental factors. Its typical clinical manifestations are scaly erythema or plaques, which may be localized or widespread. It is non-contagious, difficult to treat, and often lifelong. The etiology of psoriasis involves multiple factors, including genetics, immunity, and environment. Through an immune response primarily mediated by T lymphocytes and jointly participated in by various immune cells, it causes hyperproliferation of keratinocytes or inflammation in joint synovial cells and chondrocytes. Psoriasis is an incurable disease; however, numerous therapeutic drugs and methods are currently available. Treatment regimens should be determined based on patient symptoms: mild psoriasis is mainly treated with topical therapies, while moderate-to-severe cases can be managed with systemic therapies. Targeted biologics may be appropriately selected for patients who show an inadequate response to traditional systemic therapies. The goals of psoriasis treatment focus on controlling symptoms and improving patients' quality of life. Psoriasis is classified into different subtypes, among which plaque psoriasis is the most common subtype (accounting for approximately 90%). Among these, about 80% of psoriasis patients have mild disease, with topical drug therapy being the preferred first-line treatment. Currently, commonly used topical agents include vitamin D3 derivatives, glucocorticoids, retinoids, and topical combination preparations. Recent studies have revealed that the interaction between lipocalin-2 (LCN2) and its receptor SLC22A17 plays a key role in the pathogenesis and progression of psoriasis: the LCN2/SLC22A17 axis induces abnormal cholesterol metabolism in keratinocytes by activating the SREBP2 pathway, and acts synergistically with the NLRC4 inflammasome to trigger the release of inflammatory mediators such as IL-1$\\beta$ and