Bempikibart may incite hair regrowth after treatment cessation in severe alopecia areata
Key takeaways:
- Patients with severe to very severe alopecia areata saw hair regrowth with bempikibart treatment within 24 weeks.
- Hair regrowth seemed to persist after treatment cessation to week 36.
ORLANDO — Bempikibart demonstrated positive, durable responses among patients with severe to very severe alopecia areata, according to a late-breaking presentation at the American Academy of Dermatology Annual Meeting.
Bempikibart is a bifunctional interleukin-7 receptor alpha antagonist antibody that also blocks thymic stromal lymphopoietin signaling, which is responsible for a type 2 immune response implicated in allergic diseases.
According to Brett King, MD, PhD, associate professor of dermatology at Yale University School of Medicine, bempikibart has an ideal mechanism of action for the treatment of alopecia areata (AA).
“There is very longstanding scientific literature suggesting a role for IL-7 in modulation of T-cell responses underlying inflammatory disease and autoimmune disease and it is thought that IL-7 blockade can lead to a sort of renewed T-cell homeostasis,” King, who is also a member of Healio Dermatology’s Peer Perspective Board, said during the late-breaking session. “Very interestingly, there is, in the C3H mouse model of alopecia areata, demonstration that blockade of IL-7 can reverse alopecia areata.”
King presented results from the SIGNAL-AA study, a randomized, placebo-controlled phase 2a study evaluating the efficacy and safety of bempikibart in patients with severe to very severe AA, which is defined as having a Severity of Alopecia Tool (SALT) score of 50 to 100, or 50% to 100% hair loss.
In the per-protocol population, 27 patients were randomly assigned to receive either bempikibart 200 mg (n = 23), administered subcutaneously, or placebo (n = 4) once every 2 weeks for 24 weeks.
According to the presentation, the study met the primary endpoint of a proportion of patients achieving a percentage change from baseline in SALT score at week 24, with the bempikibart group experiencing a 16% reduction in their SALT score vs. a 2% reduction among the placebo group.
By week 24, 9% of all patients (SALT 50-100) treated with bempikibart reached a SALT score of 20 or less, as did 13.3% of those who only had severe disease (SALT 50-95; n = 15). In contrast, none of the patients in the placebo group achieved the same.
During a post-treatment follow-up period of 12 weeks after the initial 24 weeks of treatment, the investigators found that patients who had since stopped bempikibart treatment continued to experience a reduction of AA severity. Among patients with severe AA, 26.7% reached a SALT score of 30 by week 24, but 53.8% reached the same score by week 36.
“This is kind of provocative, right?” King said about the data. “This suggests a continued effect after dosing cessation.”
Safety data were derived from the modified intention-to-treat group, comprised of 33 bempikibart-treated patients and eight placebo-treated patients. According to King, bempikibart had a favorable safety profile, with no patients experiencing grade 3 or higher events related to the study drug. Treatment-emergent adverse events occurred in 70% of the bempikibart group vs. 38% of the placebo group. Most events were mild to moderate in severity.