OR WAIT null SECS
Martina Porter, MD, discusses new STOP-HS trial data on povorcitinib, the first oral phase 3 therapy for hidradenitis suppurativa.
Hidradenitis suppurativa (HS) remains one of dermatology's most challenging skin conditions to address, according to Martina Porter, MD, of Beth Israel Deaconess Medical Center and Harvard Medical School.
Porter discussed new peer-reviewed phase 3 STOP-HS1 and STOP-HS2 results evaluating povorcitinib in adult patients living with moderate-to-severe HS, recently published in Nature Medicine.1 She was asked in a new HCPLive interview about the treatment, about HS, and about the unique aspects of these new data.
Porter described HS as having historically lagged behind conditions like psoriasis and atopic dermatitis in treatment availability and efficacy. She emphasized the disease carries a significant psychosocial burden, with high rates of depression, anxiety, and suicidality, along with unpredictable flares that can affect patients' ability to work, dress, and maintain relationships.
Porter explained the STOP-HS1 and STOP-HS2 trials represent the first phase 3 publication of an oral therapy for HS. Until now, all FDA-approved options for moderate-to-severe disease, including adalimumab, secukinumab, and bimekizumab, have been biologics requiring injection.
Povorcitinib, a selective JAK1 inhibitor, offers both a new mechanism and a needle-free option, which Porter said may appeal particularly to younger patients or those hesitant about injectable therapies. She also pointed to the flexibility of starting and stopping oral treatment as a meaningful factor in shared decision-making conversations with patients.
Porter described povorcitinib as a highly selective JAK1 inhibitor, distinguishing it from JAK2- and JAK3-mediated pathways associated with hematopoiesis-related side effects. She noted that HS is likely a heterogeneous disease without a single unifying driver, meaning treatment response may vary considerably across patients.
Because JAK1 inhibition operates through a broader pathway than TNF-alpha or IL-17 inhibition, Porter suggested it may offer an alternative for patients who have not responded to existing biologic therapies, particularly those with early nodular disease or more severe, tunneling-type presentations.
Disclosures: Porter has served as a consultant for AbbVie, Almirall, Arcutis, Aristea Therapeutics, Avalo Therapeutics, Eli Lilly, Framework for Interoperable Data Exchange (FIDE), Incyte, Janssen, Merck, MoonLake Immunotherapeutics, Navigator Biosciences, Novartis, Pfizer, Prometheus, Sanofi, Sonoma Biotherapeutics, Trifecta Clinical/WCG, UCB and Zura Bio and as an investigator for AbbVie, AnaptysBio, Arcutis, Aristea Therapeutics, Avalo Therapeutics, Bayer, Bristol Myers Squibb, Eli Lilly, Incyte, Janssen, Merck, MoonLake Immunotherapeutics, Navigator Biosciences, Novartis, OASIS Pharmaceuticals, Otsuka, Pfizer, Prometheus, Propeller Biosciences, Regeneron, Sanofi, Sonoma Biotherapeutics, UCB and Zura Bio. She has received royalties from Beth Israel Deaconess Medical Center and fellowship funding to the institution from AbbVie.
References
