Psoriasis is a chronic inflammatory skin disease driven by dysregulated innate and adaptive immunity, with the IL-23/Th17 axis playing a central role in sustaining disease activity. In an imiquimod-induced psoriasis mouse model, both HDF spheroids and single-cell HDF preparations reduced disease severity; however, spheroids provided a more favorable systemic safety profile by avoiding the innate immune activation observed with single-cell delivery, an important distinction for a cell-based therapy intended for systemic administration.

In a chronic-relapsing psoriasis model, booster dosing of HDF spheroids sustained therapeutic efficacy and prevented splenomegaly, a marker of systemic immune burden. Additionally, CYPS317 demonstrated significant reductions in PASI scores, normalization of monocyte-to-lymphocyte ratios, and reduced splenic immune cell accumulation. Histological analyses confirmed that spheroid-treated animals were protected against epidermal thickening and immune cell infiltration, two hallmarks of active psoriatic disease. Cytokine profiling across disease stages demonstrated that single and multiple doses of HDF spheroids differentially regulated key inflammatory mediators, consistent with targeted immunomodulation rather than broad immune suppression.

"Our preclinical data reinforce the significant potential of a cell-based therapeutic for psoriasis and the importance of targeted immune modulation," said Hamid Khoja, Ph.D., Chief Scientific Officer of FibroBiologics. "Our fibroblast spheroid-based therapeutics have demonstrated durable immunomodulation across several chronic disease models. We believe these findings meaningfully strengthen the foundation for CYPS317 as a differentiated therapeutic approach for patients living with psoriasis."