BIMEKIZUMAB delivered sustained, high-level skin clearance in patients with psoriasis for up to four years, with new molecular data suggesting the drug acted by normalising pathogenic immune cells that drive long-term disease persistence.
Psoriasis is a chronic inflammatory skin condition affecting around 2–3% of adults worldwide and is characterised by immune-driven epidermal hyperproliferation and recurrent plaques. Although biologic therapies targeting interleukin (IL)-17 pathways have transformed short-term disease control, long-term durability and mechanisms underlying sustained remission have remained key clinical questions.
Bimekizumab Durability in Psoriasis Remission
New pooled analyses from multiple Phase III trials and their long-term extension showed that bimekizumab durability remained high among patients who achieved early complete skin clearance. Of those who reached complete clearance after 16 weeks and continued treatment, 73.0% maintained this response at Year 4. These findings were drawn from three 1-year Phase 3 feeder studies, alongside the 3-year open-label extension.
Bimekizumab is a monoclonal antibody that selectively inhibits both IL-17A and IL-17F, two key cytokines implicated in psoriasis pathogenesis. By targeting both, the therapy aimed to achieve deeper and more durable immune modulation than agents that inhibit IL-17A alone.
To explore the biological basis of this sustained response, researchers performed bulk and single-cell transcriptomic analyses on lesional skin samples. They identified a distinct population of tissue-resident memory T (TRM) cells expressing IL-17A and/or IL-17F that were largely absent from healthy skin. These pathogenic TRM cells also expressed pro-survival factors believed to prolong their persistence within psoriatic lesions.
Treatment with bimekizumab reversed the expression of these pro-survival genes and normalised a broader TRM cell gene signature within eight weeks. This molecular normalisation suggested that long-term efficacy may be linked to reducing the survival and pathogenic activity of IL-17–producing TRM cells, rather than simply suppressing inflammation transiently.
Implications for Long-Term Psoriasis Management
The findings provided mechanistic support for the durable clinical responses seen with bimekizumab and highlighted the importance of targeting tissue-resident immune memory in chronic inflammatory disease. While limitations included reliance on patients who achieved early clearance and continued therapy, the results strengthened evidence for long-term disease modification.
For clinicians, these data reinforced the potential of bimekizumab to deliver sustained remission in moderate-to-severe psoriasis, with implications for long-term treatment planning and patient expectations. Additional studies will be needed investigate other cell types that express IL-17A and IL-17F, and to confirm whether these durable responses translate broadly across diverse clinical populations.
Reference
Krueger JG et al. Bimekizumab long-term response in psoriasis: mechanistic insights into efficacy level and durability. J Allergy Clin Immunol. 2026; DOI:10.1016/j.jaci.2025.12.1013.
