Introduction
Hidradenitis suppurativa (HS), characterized by heterogeneity in clinical presentation, disease progression, and treatment response, remains one of the most challenging inflammatory dermatologic diseases to treat. At the 2026 American Academy of Dermatology (AAD) Annual Meeting, HS had a noticeably expanded presence compared with prior years, with numerous dedicated HS-focused sessions as well as integrated discussions within broader medical dermatology and general educational programming. Collectively, these sessions highlighted the rapidly evolving landscape of HS management, including the redefining of moderate disease severity, use of dual targeted therapy (DTT) for severe recalcitrant patients, therapeutic drug monitoring (TDM), metabolic treatment strategies, and emerging pipeline therapeutics. This commentary summarizes select clinically relevant HS updates presented at the meeting, highlights notable late-breaking abstracts, and discusses their potential implications for the management of HS. Sessions were selected for inclusion in this commentary on the basis of their focus on medical rather than surgical management of HS, clinical relevance, and representation of meaningful advances beyond already well-established treatment approaches, while abstracts were selected on the basis of their late-breaking designation at the meeting.
Redefining “Moderate” HS Disease
An important theme across multiple HS sessions was the evolving definition of “moderate” disease severity and the importance of identifying the therapeutic “window of opportunity” before irreversible disease progression occurs. Traditional clinical trial eligibility criteria for patients with moderate-to-severe HS, which commonly require ≥ 5 total abscesses and inflammatory nodule count and Hurley stage II/III disease [1], may not fully capture the heterogeneous morphologic presentation and clinical burden encountered in real-world practice. Existing established scoring systems also vary in their definition of moderate disease. For example, in the Hurley staging system, Hurley II, which is often equated to “moderate” HS disease, requires the presence of a scar or tunnel. On the other hand, the International Hidradenitis Suppurativa Severity Score System (IHS4) uses a weighted system that counts nodules, abscesses, and draining tunnels, and does not require a scar or tunnel to pass the threshold for moderate disease, but does not count inflamed non-draining tunnels as an active lesion type. Moreover, several speakers emphasized that patients with persistent symptoms despite conventional therapies, even with lower inflammatory lesion counts, may still have clinically significant disease warranting treatment escalation.
To address these gaps, proposed frameworks presented during the meeting characterized moderate HS more broadly, including patients with the presence of 3–4 or more inflammatory lesions, one inflamed tunnel (incorporating non-draining tunnels), or those with inadequate symptom control on conventional therapies. The potential inclusion of inflamed non-draining tunnels as an active HS lesion type was discussed, as these lesions may reflect ongoing inflammatory activity and be symptomatic despite the absence of drainage [2]. Collectively, these concepts reflect a shift toward earlier recognition of clinically meaningful disease and promote a more proactive initiation of targeted therapies during the “window of opportunity” before the development of irreversible structural damage.
Dual Targeted Therapy for Refractory Disease
DTT also emerged as an area of growing interest at this year’s meeting, particularly for patients with severe, treatment-refractory HS who continue to demonstrate active disease despite biologic monotherapy. This approach reflects the increasingly recognized immunologic complexity of HS, with concurrent activation of multiple inflammatory pathways, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1, IL-17, and IL-23, among others [3]. As a result, inhibition of a single pathway with a biologic or small molecule inhibitor may not provide adequate disease control in a subset of patients, particularly those with extensive inflammatory burden [4]. Potential combination strategies discussed during the meeting included pairing biologics or small molecule inhibitors across complementary pathways spanning TNF-α, IL-17, IL-12/23 or IL-23, and Janus kinase (JAK) inhibition. Although HS-specific evidence remains limited, currently published case reports have described clinical improvement with combinations including secukinumab plus baricitinib, adalimumab plus upadacitinib, and upadacitinib plus bimekizumab [5–7]. In the latter case, a patient with treatment-refractory HS experienced sustained improvement with acceptable tolerability over 18 months following combined JAK1 and IL-17A/F inhibition [7].
Interest in DTT has additionally been informed by experience in other immune-mediated diseases such as rheumatoid arthritis, inflammatory bowel disease (IBD), and psoriatic arthritis, where combination therapy has demonstrated clinical benefit with generally acceptable short-term tolerability in select refractory populations [8]. However, DTT has not yet been evaluated in any HS clinical trial, current evidence remains limited primarily to case reports, case series, and extrapolation from other disease states, and long-term safety data of DTT in HS are lacking. Notably, caution with combining TNF-alpha and IL-1 inhibitors has been recommended given potential safety concerns [8], highlighting the need for careful patient selection and monitoring as combination strategies continue to be explored. Larger prospective studies are needed to better define optimal combination regimens, additive efficacy, and the long-term safety profile of DTT in HS.
Therapeutic Drug Monitoring
TDM data highlighted at the meeting demonstrated that higher adalimumab trough serum concentrations and lower drug clearance were each independently associated with improved clinical response, supporting the potential role of TDM in identifying patients who may benefit from dose escalation versus therapeutic switching. Proposed cutoffs of 10.7 µg/mL for adalimumab trough concentration and 0.5 L/day for drug clearance were identified as potential thresholds for clinical response [9]. For high responders, median adalimumab concentration was 24.6 µg/mL. Notably, the median adalimumab concentration among high responders in HS exceeds levels associated with optimal response in psoriasis and IBD [9], suggesting that HS may require higher drug exposure for adequate disease control. Importantly, however, HS-specific therapeutic thresholds remain investigational as current TDM data are limited to adalimumab and infliximab and are based on small sample sizes. Furthermore, clinical laboratory reference ranges for adalimumab are largely derived from IBD populations, underscoring the absence of standardized HS-specific guidelines for routine practice.
Glucagon-Like Peptide-1 Receptor Agonists as Adjunctive Therapy
Glucagon-like peptide-1 receptor agonists (GLP-1RAs) and dual GLP-1/glucose-dependent insulinotropic polypeptide (GIP) receptor agonists were also discussed as an emerging class of therapy for HS, particularly given the strong association between HS, obesity, and metabolic dysfunction [10]. Among patients receiving adjunctive GLP-1RA treatment in one retrospective cohort study, improvements in HS disease severity were observed, including reductions in HS-Physician Global Assessment (HS-PGA) and pain scores, along with decreases in leukocyte counts and erythrocyte sedimentation rate. Notably, these improvements occurred despite no significant change in body mass index, suggesting that the observed benefit may extend beyond weight reduction alone [11]. Potential mechanisms underlying these findings include modulation of nuclear factor-kappa B (NF-κB) signaling, downregulation of pro-inflammatory mediators including IL-17, IL-22, IL-23, and TNF-α, as well as reduction in insulin resistance and weight loss [12]. Additional research has found reduced rates of HS-related surgeries, hospitalizations, and future biologic initiation among patients prescribed GLP-1RAs, suggesting potential lower rates of healthcare utilization for these patients [13, 14]. A recent systematic review encompassing 19 studies mirrored these findings, reporting clinical improvement in Hurley stage and improvements in quality of life with GLP-1RAs in HS, while noting that current evidence remains limited and heterogeneous, with the relative contributions of weight-dependent versus weight-independent effects yet to be determined [15]. Collectively, these findings support GLP-1RAs and dual GLP-1/GIP receptor agonists as a promising, synergistic addition to the HS treatment armamentarium.
The Expanding Therapeutic Pipeline
The robust and rapidly expanding HS therapeutic pipeline was another central topic highlighted at the meeting, reflecting the need for additional targeted therapies beyond currently approved biologics [16]. Agents under phase II and III investigation span multiple mechanistic classes, including JAK, IL-17, IL-1, Bruton’s tyrosine kinase (BTK), and IL-36 inhibition, and there are also emerging bispecific immune-targeting approaches as summarized in Table 1. Among JAK inhibitors, oral povorcitinib, a selective JAK1 inhibitor, has completed phase III trials [17, 18], while oral upadacitinib, another selective JAK1 inhibitor, is currently recruiting for a phase III study [19]. Topical ruxolitinib, a JAK1/2 inhibitor, is also being evaluated in phase III studies [20, 21]. Also discussed were sonelokimab, a nanobody IL-17A/F inhibitor with data reported from their phase III trials [22, 23], spesolimab, an IL-36 receptor inhibitor that completed phase IIb/III evaluation [24], remibrutinib, an oral BTK inhibitor in a phase III trial [25], and lutikizumab, a monoclonal antibody targeting IL-1α and IL-1β also in a phase III trial [26]. Emerging bispecific therapies were also discussed, such as brivekimig, which simultaneously targets TNF-α and OX40 ligand (OX40L) and is now in a phase II trial [27], and tibulizumab, an IL-17A and B cell-activating factor (BAFF) inhibitor now in a phase II trial [28]. Collectively, these therapies reflect the ongoing strong interest in HS therapeutics.
Table 1.
Phase III HS therapeutic pipeline discussed at the 2026 AAD annual meeting
| Agent | Mechanism/target | Route of administration | Trial phase and status* | ClinicalTrials.gov identifier |
|---|---|---|---|---|
| Lutikizumab | IL-1α/IL-1β inhibitor | Subcutaneous | Phase III (recruiting) | NCT06468228 |
| Povorcitinib | Selective JAK1 inhibitor | Oral | Phase III (completed) | |
| Remibrutinib | BTK inhibitor | Oral | Phase III (ongoing) | NCT06840392 |
| Ruxolitinib | JAK1/2 inhibitor | Topical | Phase III (recruiting) | |
| Sonelokimab | IL-17A/F inhibitor | Subcutaneous | Phase III (completed) | |
| Spesolimab | IL-36 receptor inhibitor | Intravenous and subcutaneous | Phase IIb/III (completed) | NCT05819398 |
| Upadacitinib | Selective JAK1 inhibitor | Oral | Phase III (recruiting) | NCT05889182 |
*Status reported as of June 2026
BAFF B-cell activating factor, BTK Bruton’s tyrosine kinase, IL interleukin, JAK Janus kinase, OX40L OX40 ligand, TNF-α tumor necrosis factor-alpha
Late-Breaking Abstracts
Finally, there were also notable late-breaking HS abstracts presented at the meeting. Integrative transcriptomic profiling studies identified macrophage-derived IL-1β/NLRP3 inflammasome signaling as a potentially dominant inflammatory axis in HS pathogenesis, further supporting IL-1β/NLRP3-directed therapeutic strategies [29]. Updated phase III data from the povorcitinib phase III STOP-HS1 and STOP-HS2 studies (NCT05620823, NCT05620836) demonstrated sustained clinical improvement with povorcitinib through week 54, including continued Hidradenitis Suppurativa Clinical Response (HiSCR), reductions in inflammatory lesion counts, and improvements in patient-reported outcomes [30]. Lastly, long-term phase III results for sonelokimab demonstrated continued improvement in HiSCR responses and lesion count reduction through week 40, with maintained improvements across pain and quality-of-life measures [31].
Contextualizing Updates within Current HS Management Guidelines
The most recent comprehensive North American guidelines for HS management were published in 2019, when adalimumab remained the only Food and Drug Administration (FDA)-approved biologic, and an updated guideline incorporating the subsequent approvals of secukinumab and bimekizumab is anticipated [32]. Thus, the medical management updates discussed in this commentary are not reflected in these outdated guidelines. However, concepts of DTT [8, 33], TDM [9], and GLP-1RAs [15] are gaining traction in the literature. In the interim, an expert updated practical management algorithm was proposed that does incorporate the updated principles that are discussed in this commentary [34].
Limitations
The selection of sessions and abstracts for inclusion in this commentary was based on the authors’ expert opinion on which topics represented a meaningful update to current treatment approaches and does not capture every topic discussed at the meeting. Additionally, several of the areas discussed are supported primarily by early-phase trials, retrospective studies, or case-level evidence, and require confirmation in larger prospective and controlled studies before broad clinical adoption.
Conclusions
Collectively, the HS-focused sessions and late-breaking presentations at the 2026 AAD Annual Meeting highlighted the remarkable progress that has occurred in HS over the past several years, spanning advances in immunopathogenesis, disease classification, therapeutic monitoring, and targeted drug development. Numerous additional HS-related topics were also discussed throughout the meeting beyond those highlighted in this commentary, underscoring the increasing interest and research efforts within the field. Nevertheless, many patients continue to experience delayed diagnosis and treatment initiation, refractory disease, and incomplete treatment responses, emphasizing that substantial unmet needs in HS remain. Despite these ongoing challenges, the expanding therapeutic pipeline, increasing interest in combination treatment strategies, and continued emergence of mechanistic insights into HS’s biology all contribute to growing optimism for the future management of this disease.
Acknowledgments
Medical Writing/Editorial Assistance
ChatGPT (OpenAI) was used to check grammar during manuscript preparation. No other medical writing or editorial assistance was used.
Author Contributions
Kenan Kherallah: conceptualization (lead); literature review (lead); formal analysis (lead); writing—original draft (lead); writing—review and editing (lead). Claire S. Chung: conceptualization (supporting); literature review (supporting); writing—original draft (supporting); writing—review and editing (supporting). Katrina H. Lee: conceptualization (supporting); writing—review and editing (supporting). Vivian Y. Shi: conceptualization (supporting); writing—review and editing (supporting). Jennifer L. Hsiao: conceptualization (lead); formal analysis (supporting); writing—review and editing (lead); supervision (lead).
Funding
No funding or sponsorship was received for this study or publication of this article.
Data Availability
Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.
Declarations
Conflict of Interest
Katrina H. Lee has served as an investigator or advisory board member for Novartis, Incyte. Vivian Y. Shi is an Editorial Board member of Dermatology and Therapy. Vivian Y. Shi was not involved in the selection of peer reviewers for the manuscript nor any of the subsequent editorial decisions. Vivian Y. Shi is on the board of directors for the Hidradenitis Suppurativa Foundation (HSF), an advisor for the National Eczema Association, is a stock shareholder of Learn Health and has served as an advisory board member, investigator, speaker, and/or received research funding from Sanofi Genzyme, Regeneron, AbbVie, Genentech, Eli Lilly, Novartis, SUN Pharma, LEO Pharma, Pfizer, Incyte, Dermavant, Apogee, MoonLake, Navigator Medicine, Boehringer Ingelheim, Almirall, Alumis, Aristea Therapeutics, Menlo Therapeutics, Dermira, Burt’s Bees, Oruka, Takeda, Galderma, Kiniksa, UCB, Ceraclere, Bain Capital, Target-PharmaSolutions, Castle Bioscience, Altus Lab/cQuell, MYOR, Polyfins Technology, GpSkin, and Skin Actives Scientific. Jennifer L. Hsiao is an Editor-in-Chief of Dermatology and Therapy. Jennifer L. Hsiao was not involved in the selection of peer reviewers for the manuscript nor any of the subsequent editorial decisions. Jennifer L. Hsiao is on the board of directors for the HS Foundation, and has served as an advisor, investigator, and/or speaker for AbbVie, Amgen, Aclaris, AstraZeneca, Boehringer Ingelheim, Galderma, Incyte, Insmed, Moonlake, Navigator Medicines, Novartis, Oruka Therapeutics, Pfizer, Sanofi, Regeneron, and UCB. The other authors, Kenan Kherallah and Claire S. Chung, have no other conflicts to disclose.
Ethical Approval
This article is based on previously conducted studies and does not contain any new studies with human participants or animals performed by any of the authors.
Footnotes
Publisher’s Note
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.
