Martina J. Porter, MD, is a dermatologist at Beth Israel Deaconess Medical Center.

Martina Porter, MD

Povorcitinib met the primary endpoint in both trials at Week 12.

About 40% of patients on either dose achieved HiSCR50, versus roughly 30% on placebo.

Serious adverse events stayed low through week 12, rising modestly to 5%-6% by Week 54.

Acne was the most common side effect, and no new safety signals emerged.

 remains 1 of the most challenging inflammatory skin conditions to manage, with limited options for treatment and a significant impact on patients' quality of life.

 Q&A, Martina Porter, MD, known for her work with Beth Israel Deaconess Medical Center and Harvard Medical School, speaks on why HS has historically lagged behind other dermatologic conditions in treatment development, and what makes the recently published 

 a notable shift for patients and clinicians alike.

Porter walks through the mechanism behind povorcitinib, an oral therapy under investigation for HS, and explains how it may offer a meaningfully different option for patients who haven't responded to existing treatments. She also unpacks the trials' efficacy and safety findings. The full conversation highlights Porter's complete take on where povorcitinib may fit into the evolving HS treatment landscape:

 For readers who may not be familiar, can you explain what hidradenitis suppurativa is and why it's often described as a difficult condition to treat?

I think anyone who's ever treated an HS patient knows that it's much more difficult to treat HS than a lot of our other inflammatory skin disorders. Some of this, I think, is related to the availability of treatments. It's a newer disease state, essentially, that we've started to investigate from a research perspective to find more treatments, and we still haven't quite hit the bar that we want to for efficacy. If you compare it to psoriasis or even atopic dermatitis, the disease for patients is extremely difficult to have and has a really profound impact on their quality of life.

This is a disease that has very high rates of depression, anxiety, and even suicidality. Even for milder patients, living with the condition and not knowing when it's going to flare up, or not knowing when they're going to be able to walk, or get dressed, or have relationships with other people, really impacts every aspect of their living.

What made the STOP-HS1 and STOP-HS2 trials significant? Why does it matter that this is the first phase 3 publication for an oral therapy in HS?

As you've alluded to, we do have a couple of other medications now that are FDA-approved and also approved in the EU for use for HS. They're all for the moderate to severe population. But all of them, so far, are biologics. So we have adalimumab, which is a TNF-alpha inhibitor, and then secukinumab, which is an IL-17 inhibitor, and bimekizumab, which is an IL-17A and F inhibitor. There are even a couple of other drugs like sonelokimab and iscalimab that are also IL-17 inhibitors and have finished phase 3.

But the STOP-HS1 and STOP-HS2 trials are the very first medication that's oral…Povarcitinib is a selective JAK-1 inhibitor, and we have other JAK inhibitors in dermatology, but we actually don't have povarcitinib approved for any other disease indication now. So, we have a new drug, but not a new mechanism. But for HS specifically, we have a new drug, a new mechanism, and an oral option. For a lot of patients, especially younger patients, the idea of getting injections is off-putting. To just have another option, I think, is very good for them from that perspective as well.

Many speak about needle-phobia as being a factor when determining whether or not to pursue an oral drug for treating skin diseases. Is that your experience?

 I would say that there are quite a few patients for whom the idea of taking a medicine that affects their whole body is very scary for them, and then to find out that it comes as an injection is another layer of difficulty, I think, in sort of accepting that they're taking a whole new lifestyle change for this. There is a little bit less needle-phobia, in general because of GLP-1s. People have sort of gotten used to the idea that they need to take injectable medications. But I definitely think for younger patients and those who do not really feel comfortable with medications in general, having a pill option is really helpful.

Also, the idea that they can start and stop it is also helpful too when we go through the counseling and the shared decision making process of getting patients to take therapies because unlike some of our other inflammatory disorders, when we look at HS patients, there's a willingness from dermatologists and APPs to want to prescribe some of these medications for patients. But there's much more hesitancy in the moderate to severe HS population than there is in a moderate to severe psoriasis population or a moderate to severe atopic dermatitis population. Some may be related to baseline demographics that they share or don't share.

Povorcitinib is described as a highly-selective JAK1 inhibitor. Can you explain, in simple terms, what that means and why it matters for HS patients?

The JAK-STAT pathways have gotten a lot of press, and there are different types of JAKs: JAK1, JAK2, and JAK3. The JAK2 and JAK3, they've always thought, are involved more in hematopoiesis, and so we see different side effects with each of the different JAKs. Actually, even a selective JAK1, for example, may still hit JAK2 or JAK3. So that's why we get into these terms like highly selective, where they're really hitting almost only Jak one and very little, if any, of JAK2 or JAK3. Then we ideally like to see from a safety profile those differences. But also, I think in terms of the pathogenesis, we still don't really understand what causes HS or what the main drivers are.

I personally think that HS is probably very heterogeneous in the sense that not every patient with HS is going to have the same things driving their disease. Therefore, not every treatment is going to work for probably every single patient. The JAK1 pathway in general is a little bit broader than what we expect for a TNF alpha inhibitor and definitely for an IL-17 inhibitor, and actually interesting. JAK1 has little impact on TNF and IL-17 overall, and so it's really nice in HS, especially for patients that have been on some of these biologics before, that this new mechanism is very different. Whereas TNF and IL-17 are very similar, so it may offer an opportunity for patients who have already tried some other medications to have another option that could work for them.

But also, in general, what I've seen with Jackson, my clinical practice in HS, is that they work quite well in patients who have actually early nodular disease and not a lot of drainage, and also patients that have really severe disease, as we see in Crohn's or cutaneous Crohn's, that have a lot of tunneling and drainage. So I think it'll be interesting over time to see where all these drugs fit.

 What were the key efficacy findings on povorcitinib from the STOP-HS1 and HS2 trials?

 For povorcitinib in the STOP-HS1 and 2 trials, they looked at Week 12 as the primary endpoint, and they used High Score 50, which is the same endpoint that we've historically used for other HS trials, and it loosely correlates to about 50% in disease improvement, and it's a binary outcome. So patients either achieve it or they don't. So they could be at 55% improvement or 90% improvement, and they would still fall into the high score of 50. But what they found is that at Week 12, about 40% of patients in the quovositinib arm, of which there were two doses, 45 and 75 milligrams, performed about the same. They achieved a high score of 50, so about 40% compared to 30% of the placebo.

That doesn't sound like a very large difference, but it's actually almost in line with what we've seen in some other trials; it's very similar to secukinumab and a little bit less than adalimumab and bemichizimab's data. But there are a lot of caveats in how we compare some of these numbers because the placebo rates are highly different from each trial. The adalimumab trial, for example, which was PIONEER I and II, was all bio-naïve patients, which we typically consider to be easier to treat than patients who are bio-experienced, and pulvarsitinib studies had about 30% of patients who had been exposed to a biologic before, so potentially a more treatment-refractory population at baseline. Then also, the time points of the endpoint.

So Week 12 might have been a little bit early because sometimes we do trials out to Week 16, and the vast majority of these drugs at 24 weeks and definitely a year out, we're seeing a lot more continued improvement. But we just cannot do a placebo-controlled trial for six months or 12 months in patients who have moderate to severe HS, so I think the good news is that we're in the same range, and this really will be an efficacious treatment for patients.

 Can you tell me what the safety findings showed?

 The most common safety findings were actually not dose-dependent. So, the 45 and 75 milligram groups had about the same number of AEs, and the most common adverse event was actually acne. It was about 17 to 20 percent of the population on the study drug, and then followed by nasopharyngitis, upper respiratory tract infection, which is not that uncommon, I would say, for a medication that acts on the immune system. The acne, I think, is notable, and one of the things to also think about is in HS trials, we tend to see a younger population, so the average age is in the 30s, and the vast majority of patients are women. And the acne in this trial was all deemed to be mild, essentially.

Because of the way the trial is designed, the treatments that we usually use for acne, like topical antibiotics, topical retinoids, oral antibiotics, isotretinoin- a lot of them overlap with HS therapies, and so they're actually prohibited because they're not. They could potentially impact the efficacy of HS. So it's kind of hard to say how these patients would do overall with their acne if they had, in regular practice, been allowed to get a bunch of other therapies. I think the other key safety findings are related to what we think of the JAK stat profile so far. We know that there's a black box warning on the other JAK inhibitors for the MACE events, [or] the major adverse cardiac events. Then also for thromboembolic events and malignancy. The good news is that these were actually very, very low in this population.

There were, I think, about three thromboembolic events, maybe four in the whole trial up to the one-year mark. This is in a patient population that already has an increased background risk due to their background demographics. Half the patients in this study are smokers. Their average BMI is about 35. So again, higher risk profile, but actually not a very high number of adverse events for those. There was one death of undetermined etiology that the investigator at that site deemed unrelated to treatment. I think for a JAK inhibitor, the safety profile is quite clean, but it still sort of fits in line with JAK inhibitors overall.

Are there any other points you want clinicians to be aware of regarding povorcitinib?

Yeah, I briefly mentioned this when I talked about the primary endpoint, but the article actually has out to the Week 54 data. If we look at some of the patients who, for example, achieve high score of 50 at Week 12, three quarters of them essentially maintain that response at Week 24 and even out to week 54, so I think that is the information that we really like to see too in these trials: how do they do in the first early months, [and] really how is it going down the line? A lot of the patients, actually, saw efficacy rates improve over time.

There are more patients achieving a high score of 50 at the six-month mark and at the one-year mark. I think this is really important because when we're using other biologics in psoriasis and atopic dermatitis, usually at the three-month mark, we expect them to essentially be at their best, almost or very close to being clear. But for HS, we're really waiting six months or longer, and the three-month assessment is just to make sure that they're on track. I think it is really important to think about both the short-term and the long-term gains.

One of the other very nice things about this medication is they actually started looking at some of the effects of the medication in terms of the efficacy endpoints and the patient-reported outcomes at Week 3. And there was actually a difference even at that time point between patients who got the study drug and patients who were on placebo. So we can see some rapid improvement in symptoms. But again, they're just really not at their peak until further down the line.

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.

Porter ML, Martorell A, Zouboulis CC, et al. Povorcitinib for hidradenitis suppurativa: the randomized, double-blind, placebo-controlled STOP-HS1 and STOP-HS2 phase 3 trials. Nat Med. 2026 Jul 23. doi: 10.1038/s41591-026-04534-z. Epub ahead of print. PMID: 42493571.

Porter M. Why Povorcitinib's JAK1 Mechanism Matters for HS, With Martina Porter, MD. HCPLive. August 3, 2026. 

https://www.hcplive.com/view/why-povorcitinib-jak1-mechanism-matters-for-hs-with-martina-porter-md

Articles

Hidradenitis suppurativa remains therapeutically underserved versus psoriasis and atopic dermatitis, with profound quality-of-life burden and high psychiatric comorbidity. Phase 3 STOP-HS1/STOP-HS2 introduce povorcitinib, a highly selective oral JAK1 inhibitor, expanding HS options beyond injectable biologics and offering a mechanistically distinct alternative after TNF-α or IL-17 failure. At Week 12, HiSCR50 responses were ~40% on povorcitinib versus ~30% placebo, with durability and incremental gains through Week 54 and early symptom separation by Week 3.  

STOP-HS1 and STOP-HS2 data show povorcitinib nearly doubled treatment response rates versus placebo in moderate to severe HS.

Q&A: How STOP-HS Povorcitinib Data Impact Hidradenitis Suppurativa

New phase 3 data from the STOP-HS1 and STOP-HS2 trials show povorcitinib produced meaningful improvement in 

, with efficacy and safety findings that compare favorably to existing biologic therapies.

These data were described by Martina Porter, MD, of Beth Israel Deaconess Medical Center and Harvard Medical School, who spoke in 

 editorial team. Porter described the significance of the trials in a recent interview and went in depth regarding the data during this new segment of her interview.

STOP-HS: Povorcitinib Shows Durable Response in HS at Week 54

How Effective Was Povorcitinib in the STOP-HS Trials?

Porter explained that both trials used HiSCR50 at week 12 as the primary endpoint, a binary measure requiring at least 50% improvement in disease activity. Approximately 40% of patients receiving povorcitinib, at either the 45 mg or 75 mg dose, achieved this outcome compared with 30% on placebo.

Porter noted this margin is consistent with results seen in other HS trials, though cross-trial comparisons are complicated by differences in placebo response rates, patients' prior biologic exposure, and endpoint timing. She emphasized that no current HS therapy achieves complete clearance in all patients.

What Do Safety Findings Show for Povorcitinib?

According to Porter, adverse events were similar across both dose groups, with acne as the most common finding, affecting 17% - 20% of patients, followed by nasopharyngitis and upper respiratory tract infection. She noted that acne cases were mild and that standard acne therapies were prohibited during the trial due to overlap with HS treatments.

Regarding class-related safety concerns, Porter said rates of major adverse cardiac events, thromboembolic events, and malignancy remained low despite a patient population with elevated baseline cardiovascular risk factors, including high rates of smoking and obesity. One death of undetermined cause was reported and deemed unrelated to treatment.

How Durable Was the Response to Povorcitinib Over Time?

Porter highlighted Week 54 data showing that roughly three-quarters of patients who achieved HiSCR50 at Week 12 maintained that response through Week 24 and Week 54, with efficacy rates continuing to improve over the course of a year. She noted that some patients showed measurable improvement as early as Week 3, though peak treatment effects in HS typically emerge later than in conditions like psoriasis or atopic dermatitis.

Videos

New STOP-HS trial data show durable povorcitinib response through week 54, with a favorable safety profile in hidradenitis suppurativa.

The STOP-HS1 and STOP-HS2 trials mark the first phase 3 publication of an oral therapy for hidradenitis suppurativa.

Povorcitinib's JAK1-selective mechanism differs from existing biologic options like TNF-alpha and IL-17 inhibitors.

The oral option may benefit patients hesitant about injections or those who haven't responded to biologic therapy.

 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 

 interview about the treatment, about HS, and about the unique aspects of these new data.

Why Povorcitinib's JAK1 Mechanism Matters for HS (Hidradenitis Suppurativa), With Martina Porter, MD

Why Povorcitinib's JAK1 Mechanism Matters for HS, With Martina Porter, MD

Why Is Hidradenitis Suppurativa So Difficult to Treat?

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.

What Makes Povorcitinib and the STOP-HS Trials Significant?

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.

How Does Povorcitinib's Mechanism Differ From Existing HS Drugs?

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.

Porter M. Povorcitinib Delivers Deepening Responses Through 54 Weeks in Moderate-to-Severe HS, With Martina Porter, MD. HCPLive. April 1, 2026. Accessed August 3, 2026. 

https://www.hcplive.com/view/povorcitinib-delivers-deepening-responses-through-54-weeks-moderate-to-severe-hs-porter

Martina Porter, MD, discusses new STOP-HS trial data on povorcitinib, the first oral phase 3 therapy for hidradenitis suppurativa.

Contextualizing JAK Safety With Povorcitinib in HS, With Martina Porter, MD

The 54-week STOP-HS data for povorcitinib showed deepening inflammatory response, broad and sustained improvements across patient-reported outcomes in people with moderate-to-severe 

Povorcitinib is an investigational oral JAK1-selective inhibitor - the JAK inhibitor class carries FDA black box warnings for major adverse cardiovascular events (MACE) and thromboembolic events, and these labels that loom over any new agent in the class.

Martina L. Porter, MD, of Harvard Medical School and Beth Israel Deaconess Medical Center in Boston, presented the 54-week STOP-HS data at the 2026 American Academy of Dermatology (AAD) Annual Meeting, and sat down with 

to discuss povorcitnib’s safety and efficacy data in the context of JAK safety signals.

The STOP-HS1 (NCT05620823) and STOP-HS2 (NCT05620836) phase 3 trials enrolled a combined 1,227 adults with moderate-to-severe HS, randomized 1:1:1 to povorcitinib 75 mg once daily, 45 mg once daily, or placebo for 12 weeks, followed by a 42-week blinded extension through week 54. The HS population enrolled in these trials shares several features with patients historically associated with elevated cardiovascular and thromboembolic risk in other JAK inhibitor programs: high rates of obesity, significant smoking history, and elevated systemic inflammatory burden. These are the same comorbidity factors implicated in the cardiovascular safety signals that emerged from JAK inhibitor trials in older rheumatoid arthritis populations and contributed to the class-wide black box labeling. Porter acknowledged this concern directly, noting it was among the most frequent questions she fielded at the meeting.

The STOP-HS safety data through 54 weeks did not reveal a pattern consistent with amplified risk in this higher-comorbidity population. Across both studies, thromboembolic events were infrequent, and MACE occurred in 1 patient (0.3%) in STOP-HS2. Porter noted that this MACE event — an ischemic cerebrovascular event — was also counted within the thromboembolic event category per the study's classification scheme, meaning that the total cardiovascular and thromboembolic event count is partially overlapping rather than additive. Serious treatment-emergent adverse events (AEs) occurred in 3.7% to 6.4% of patients across arms, and laboratory abnormalities were relatively uncommon — a finding Porter suggested may reflect the relative JAK1 selectivity of povorcitinib compared with less selective agents in the class, since hematologic abnormalities in particular tend to be mediated through JAK2 rather than JAK1 signaling.

She also noted that the absence of a dose-dependent safety signal across the 45 mg and 75 mg arms was specifically reassuring. JAK inhibitor AEs typically track with degree of JAK pathway inhibition, and a flat safety profile across doses is consistent with a compound that achieves meaningful JAK1 engagement without proportional off-target JAK2 or JAK3 effects. The most common treatment-emergent AE was acne, occurring in 16.4% to 21.1% of patients — a rate Porter contextualized as likely reflecting 2 overlapping factors: the known acne association with JAK inhibitor use as a class, and the demographic profile of the STOP-HS population, which skews toward younger women who may be on oral contraceptives as a trial requirement, some formulations of which have known acne-promoting effects independent of JAK inhibition. The acne observed was predominantly mild in severity and did not drive meaningful discontinuation.

At the primary efficacy endpoint of HiSCR50 at week 12, both doses achieved statistical significance versus placebo in both studies — 40.2% (45 mg) and 40.6% (75 mg) versus 29.7% for placebo in STOP-HS1 (

 <.025), and 42.3% for both doses versus 28.6% for placebo in STOP-HS2 (

 <.01) — with responses deepening through week 54 to HiSCR50 rates of 60.2% to 67.5% across studies and doses on continuous povorcitinib. Up to 29.0% of patients achieved HiSCR100 at week 54. Porter's overall assessment of the safety profile was that it is consistent with the established JAK class picture but without the amplification in cardiovascular or thromboembolic events that the comorbidity burden of the HS population might have been expected to produce — a finding she characterized as meaningful precisely because it was not the obvious outcome given the patient profile.

“[I thought the safety data] looked quite good for a HS clinical population. And I say this because HS clinical trials and Hs patients tend to have a lot more adverse events that occur. And we see this even in the beginning of the trial, when it's placebo controlled, that the patients on placebo have very high rates of adverse events, and it's probably related to their comorbidity burden,” Porter said.

Relevant disclosures for Porter include Abbvie, Bristol Myers Squibb, Janssen, Eli Lilly, Novartis, Pfizer, UCB, Trifecta Clinical, Incyte, and Anaptys Bio.

Porter ML, et al. Povorcitinib in moderate-to-severe hidradenitis suppurativa: 54-week results from the phase 3 STOP-HS1 and STOP-HS2 trials. Presented at: AAD Annual Meeting; Denver, Colorado; March 27-31, 2026.

Porter ML, et al. Povorcitinib efficacy in biologic-experienced patients with moderate-to-severe hidradenitis suppurativa: subgroup analysis from STOP-HS1 and STOP-HS2. Presented at: AAD Annual Meeting; Denver, Colorado; March 27-31, 2026.

54-week STOP-HS safety data for the JAK1-selective inhibitor povorcitinib showed no dose-dependent safety signal and few laboratory abnormalities.