For the treatment of moderate to severe hidradenitis suppurativa (HS) in patients 12 years of age and older

TREATING HS IS POSSIBLE

Proven and clinically meaningful efficacy data

At week 12,

Many moderate to severe HS patients achieved HiSCR.^1-3
HiSCR requires:

HiSCR requires no increase in abscess count relative to baseline at week 12

HiSCR requires no increase in draining fistula count relative to baseline at week 12

See efficacy data

Learn more about HiSCR

See flare data

Transcript

HS & the Moderate to Severe HS Patient

Dermatologist Dr. Cather discusses the chronic, progressive, inflammatory nature of HS disease, who it typically affects, and the importance of timely diagnosis and treatment.

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DR. CATHER:

Hi, I’m Dr. Jennifer Cather and I’d like to talk to you about hidradenitis suppurativa, or HS. The goal of this video is to help you understand the chronic, progressive, immune-mediated nature of HS; learn more about the people who have it; and highlight the importance of diagnosing and treating it early.

So, what exactly is HS? HS is a chronic, inflammatory skin disease that affects skin containing apocrine glands. It’s characterized by nodules, abscesses and draining fistulas. HS can have a devastating effect on patients. As it progresses, nodules and abscesses can become more difficult to manage, increasing the impact HS has on a person’s life.

The exact cause of HS is unknown. But what we do know is, elevated levels of cytokines like IL-1ß, IL-10 and TNF-α play a key role in fueling HS inflammation. One study showed that HS lesions expressed five times more TNF-α than normal skin.

In HS patients, hair follicles become plugged and rupture, and an inflammatory response fueled by an overproduction of proinflammatory cytokines follows, causing an inflammatory nodule or abscess to form. Then, these lesions may heal, but the process becomes chronic. This can lead to sinus tracts and scarring. These wounds may become infected, but it’s important to note, HS is not a primary skin infection.

Let’s take a look at who the HS patient is. Approximately 200,000 people in the US suffer from moderate to severe HS, affecting more women than men. The age of onset is typically between a patient’s early 20s to 50s. Studies suggest tobacco use and obesity could potentially exacerbate HS. For women, the most commonly affected areas are under the breasts and in the groin. Men, however, are more commonly affected on the buttocks and in the perianal area.

So, as you can see, HS affects areas that are difficult to examine, and patients can find it embarrassing to show and discuss all aspects of the disease. Because of this, they often minimize the impact their disease has on their lives; it’s hard for them to ask for help. Sometimes it’s necessary for the physician to ask.

As HS progresses it causes the destruction of cutaneous architecture making it more challenging to treat. This could result in a number of debilitating medical and psychosocial sequelae. First, lesions can spontaneously rupture or coalesce to form painful abscesses. These often exude a purulent discharge.

Patients may also experience limited limb mobility or even loss of limb function, caused by excessive scarring and fibrosis produced by the lesions. And, patients may develop draining sinuses that may produce a foul discharge.

Between the drainage, the odor that comes from it, and the scarring, there’s a significant amount of burden for patients that accompanies HS. Especially with the odor. I’ve seen so many patients who always think they smell. Many of them have resorted to taping maxi pads underneath their arms to stop the dripping. I’ve heard patients say they’re embarrassed when friends and coworkers notice the nodules and abscesses in their armpits. I’ve also heard patients sat that even sitting down is uncomfortable when they have numerous lesions around their inner thighs and buttocks.

Hearing from patients what they go through and what they’ve missed out on is heartbreaking. When physicians understand the impact that moderate to severe HS can have on a patient, they would prioritize this disease. It is crucial to treat patients’ symptoms and manage the underlying inflammation as soon as possible.

Transcript

Identifying & Treating Moderate to Severe HS

Dr. Cather discusses the appearance of HS, its frequency in underarms, groin and other areas, nodules, abscesses and how to differentiate it from other skin conditions, the Hurley Staging System, and common, non-FDA-approved, HS treatments.

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DR. CATHER:

Hi, I’m Dr. Jennifer Cather and I’d like to talk to you about how to identify and treat moderate to severe hidradenitis suppurativa, or HS, and how to differentiate it from other skin conditions. We’ll also take a look at some common, but non-FDA-approved, treatment options.

To begin, it’s important to understand that HS is a dynamic, progressive disease that varies considerably from patient to patient. That can make it challenging to figure out how to help patients navigate their therapeutic options.

So, what does HS look like? Some of the typical morphological features of HS include: inflamed nodules, as seen here, abscesses, sinus tracts, and hypertrophic fibrous, or “bridged,” scarring like this. Because several other skin conditions manifest in a similar fashion, it can be difficult to distinguish HS, especially in cases where only a single nodule appears. Because of this, diagnosis of HS is sometimes delayed for as long as 7 to 8 years.

A differential diagnosis of HS is extensive and includes these skin conditions: boils, acne, anogenital cutaneous Crohn’s disease, epidermoid or dermoid cyst, furuncle—which is caused by a staphylococcal infection, and carbuncle—a cluster of furuncles, pilonidal cyst, erysipelas, and sexually transmitted infections, including granuloma inguinale, lymphogranuloma venereum, and noduloulcerative syphilis.

As HS progresses, the diagnosis becomes more apparent, especially in cases where a patient is presenting with frequent recurrences, scarring, fistulas, sinus tracts, and incomplete healing. But by then, the damage may be permanent. Which is why it’s so important to diagnose moderate to severe HS early. Because HS is a progressive condition, severity increases over time and the therapeutic needs at each stage continue to change.

To determine HS severity, dermatologists rely on the Hurley Staging System, a widely used classification system. The system classifies patients into 3 groups based largely on the presence and extent of scarring and sinus tracts. Let’s take a closer look at the 3 stages. Stage I typically presents as single or multiple abscesses, without the presence of sinus tracts or scarring. By Stage II the disease typically presents as single or multiple, widely separated, recurrent abscesses with sinus tract formation and scarring. And finally, Stage III. At this point, the disease typically presents as diffuse or near-diffuse involvement with multiple interconnected sinus tracts and abscesses across the entire area.

Now, let’s take a look at some common treatment approaches to HS. In my clinical experience, when I started my own practice and began to see patients with HS return, I realized that the inflammatory lesions under the arms, breasts, and groin were part of a bigger inflammatory disease state. After I understood the chronic, recurrent, progressive nature of HS, I became more aggressive in my management of the disease, but there wasn’t much data regarding the type of efficacy I could expect for my patients with the available treatment options.

Many therapies have been used to manage symptoms, though none of these have been approved for HS treatment by the FDA. Although literature about specific HS treatment guidelines is limited, systemic antibiotics are frequently recommended as a first-line therapy. While the role of bacteria in HS is unclear, antibiotics, administered topically or systemically, are used to treat and prevent secondary infection in existing lesions. Corticosteroids are also used, both intralesionally and orally. Oral contraceptive agents that contain a high estrogen to progesterone ratio are used to address the possible hormonal etiology of HS. Another approach is incision and drainage. This helps by providing short-term relief for early, limited disease. And finally, surgery. When patients with HS progress beyond mild, surgery is used to excise the lesions, sinus tracts, or scarring.

While many of these treatment options manage symptoms, they do not target one of the key sources that contribute to inflammation.

Well-studied safety profile

The safety profile of HS was consistent with the safety profile of HUMIRA overall—no new safety signals in adults.^1,4,5

Safety data in HS

Dosing for adults and adolescents (≥12 yrs)

Once a week dosing schedule following initial doses for adults + adolescents ≥60 kg (132 lbs)¹
Every-other-week dosing schedule following initial dose for adolescents ≥30kg to <60 kg (66 lbs to <132 lbs)¹

Dosing in HS

HUMIRA Citrate-free

No citrate buffers. Thinner needle (29 gauge vs 27 gauge). Less pain immediately following injection when compared with the HUMIRA 40 mg/0.8 mL presentation.^6*†

Learn more about HUMIRA Citrate-free

^*HUMIRA Citrate-free is available to all indicated patients in the United States. HUMIRA Citrate-free features the same safety and efficacy profile of HUMIRA you've come to count on.^†Injection site pain immediately following injection as measured using a 0-10 cm Visual Analog Scale: HUMIRA 40 mg/0.4 mL vs HUMIRA 40 mg/0.8 mL.

INDICATION(S) and IMPORTANT SAFETY INFORMATION FOR HUMIRA (adalimumab)¹

INDICATION(S)¹

Plaque Psoriasis: HUMIRA is indicated for the treatment of adult patients with moderate to severe chronic plaque psoriasis who are candidates for systemic therapy or phototherapy, and when other systemic therapies are medically less appropriate. HUMIRA should only be administered to patients who will be closely monitored and have regular follow-up visits with a physician.

Psoriatic Arthritis: HUMIRA is indicated, alone or in combination with non-biologic DMARDs, for reducing signs and symptoms, inhibiting the progression of structural damage, and improving physical function in adult patients with active psoriatic arthritis.

Hidradenitis Suppurativa: HUMIRA is indicated for the treatment of moderate to severe hidradenitis suppurativa in patients 12 years of age and older.

IMPORTANT SAFETY INFORMATION¹

SERIOUS INFECTIONS

Patients treated with HUMIRA are at increased risk for developing serious infections that may lead to hospitalization or death. Most patients who developed these infections were taking concomitant immunosuppressants such as methotrexate or corticosteroids.

Discontinue HUMIRA if a patient develops a serious infection or sepsis.

Reported infections include:

Active tuberculosis (TB), including reactivation of latent TB. Patients with TB have frequently presented with disseminated or extrapulmonary disease. Test patients for latent TB before HUMIRA use and during therapy. Initiate treatment for latent TB prior to HUMIRA use.
Invasive fungal infections, including histoplasmosis, coccidioidomycosis, candidiasis, aspergillosis, blastomycosis, and pneumocystosis. Patients with histoplasmosis or other invasive fungal infections may present with disseminated, rather than localized, disease. Antigen and antibody testing for histoplasmosis may be negative in some patients with active infection. Consider empiric anti-fungal therapy in patients at risk for invasive fungal infections who develop severe systemic illness.
Bacterial, viral, and other infections due to opportunistic pathogens, including Legionella and Listeria.

Carefully consider the risks and benefits of treatment with HUMIRA prior to initiating therapy in patients: 1. with chronic or recurrent infection, 2. who have been exposed to TB, 3. with a history of opportunistic infection, 4. who resided in or traveled in regions where mycoses are endemic, 5. with underlying conditions that may predispose them to infection. Monitor patients closely for the development of signs and symptoms of infection during and after treatment with HUMIRA, including the possible development of TB in patients who tested negative for latent TB infection prior to initiating therapy.

Do not start HUMIRA during an active infection, including localized infections.
Patients older than 65 years, patients with co-morbid conditions, and/or patients taking concomitant immunosuppressants may be at greater risk of infection.
If an infection develops, monitor carefully and initiate appropriate therapy.
Drug interactions with biologic products: A higher rate of serious infections has been observed in RA patients treated with rituximab who received subsequent treatment with a TNF blocker. An increased risk of serious infections has been seen with the combination of TNF blockers with anakinra or abatacept, with no demonstrated added benefit in patients with RA. Concomitant administration of HUMIRA with other biologic DMARDs (e.g., anakinra or abatacept) or other TNF blockers is not recommended based on the possible increased risk for infections and other potential pharmacological interactions.

MALIGNANCY

Lymphoma and other malignancies, some fatal, have been reported in children and adolescent patients treated with TNF blockers, including HUMIRA. Postmarketing cases of hepatosplenic T-cell lymphoma (HSTCL), a rare type of T-cell lymphoma, have been reported in patients treated with TNF blockers, including HUMIRA. These cases have had a very aggressive disease course and have been fatal. The majority of reported TNF blocker cases have occurred in patients with Crohn’s disease or ulcerative colitis and the majority were in adolescent and young adult males. Almost all of these patients had received treatment with azathioprine or 6-mercaptopurine concomitantly with a TNF blocker at or prior to diagnosis. It is uncertain whether the occurrence of HSTCL is related to use of a TNF blocker or a TNF blocker in combination with these other immunosuppressants.

Consider the risks and benefits of HUMIRA treatment prior to initiating or continuing therapy in a patient with known malignancy.
In clinical trials, more cases of malignancies were observed among HUMIRA-treated patients compared to control patients.
Non-melanoma skin cancer (NMSC) was reported during clinical trials for HUMIRA-treated patients. Examine all patients, particularly those with a history of prolonged immunosuppressant or PUVA therapy, for the presence of NMSC prior to and during treatment with HUMIRA.
In HUMIRA clinical trials, there was an approximate 3-fold higher rate of lymphoma than expected in the general U.S. population. Patients with chronic inflammatory diseases, particularly those with highly active disease and/or chronic exposure to immunosuppressant therapies, may be at higher risk of lymphoma than the general population, even in the absence of TNF blockers.
Postmarketing cases of acute and chronic leukemia were reported with TNF blocker use. Approximately half of the postmarketing cases of malignancies in children, adolescents, and young adults receiving TNF blockers were lymphomas; other cases included rare malignancies associated with immunosuppression and malignancies not usually observed in children and adolescents.

HYPERSENSITIVITY

Anaphylaxis and angioneurotic edema have been reported following HUMIRA administration. If a serious allergic reaction occurs, stop HUMIRA and institute appropriate therapy.

HEPATITIS B VIRUS REACTIVATION

Use of TNF blockers, including HUMIRA, may increase the risk of reactivation of hepatitis B virus (HBV) in patients who are chronic carriers. Some cases have been fatal.
Evaluate patients at risk for HBV infection for prior evidence of HBV infection before initiating TNF blocker therapy.
Exercise caution in patients who are carriers of HBV and monitor them during and after HUMIRA treatment.
Discontinue HUMIRA and begin antiviral therapy in patients who develop HBV reactivation. Exercise caution when resuming HUMIRA after HBV treatment.

NEUROLOGIC REACTIONS

TNF blockers, including HUMIRA, have been associated with rare cases of new onset or exacerbation of central nervous system and peripheral demyelinating diseases, including multiple sclerosis, optic neuritis, and Guillain-Barré syndrome.
Exercise caution when considering HUMIRA for patients with these disorders; discontinuation of HUMIRA should be considered if any of these disorders develop.
There is a known association between intermediate uveitis and central demyelinating disorders.

HEMATOLOGIC REACTIONS

Rare reports of pancytopenia, including aplastic anemia, have been reported with TNF blockers. Medically significant cytopenia has been infrequently reported with HUMIRA.
Consider stopping HUMIRA if significant hematologic abnormalities occur.

CONGESTIVE HEART FAILURE

Worsening and new onset congestive heart failure (CHF) has been reported with TNF blockers. Cases of worsening CHF have been observed with HUMIRA; exercise caution and monitor carefully.

AUTOIMMUNITY

Treatment with HUMIRA may result in the formation of autoantibodies and, rarely, in development of a lupus-like syndrome. Discontinue treatment if symptoms of a lupus-like syndrome develop.

IMMUNIZATIONS

Patients on HUMIRA should not receive live vaccines.
Pediatric patients, if possible, should be brought up to date with all immunizations before initiating HUMIRA therapy.
Adalimumab is actively transferred across the placenta during the third trimester of pregnancy and may affect immune response in the in utero exposed infant. The safety of administering live or live-attenuated vaccines in infants exposed to HUMIRA in utero is unknown. Risks and benefits should be considered prior to vaccinating (live or live-attenuated) exposed infants.

ADVERSE REACTIONS

The most common adverse reactions in HUMIRA clinical trials (>10%) were: infections (e.g., upper respiratory, sinusitis), injection site reactions, headache, and rash.

INDICATIONS¹

Rheumatoid Arthritis: HUMIRA is indicated, alone or in combination with methotrexate or other non-biologic DMARDs, for reducing signs and symptoms, inducing major clinical response, inhibiting the progression of structural damage, and improving physical function in adult patients with moderately to severely active rheumatoid arthritis.
Juvenile Idiopathic Arthritis: HUMIRA is indicated, alone or in combination with methotrexate, for reducing signs and symptoms of moderately to severely active polyarticular juvenile idiopathic arthritis in patients 2 years of age and older.
Psoriatic Arthritis: HUMIRA is indicated, alone or in combination with non-biologic DMARDs, for reducing signs and symptoms, inhibiting the progression of structural damage, and improving physical function in adult patients with active psoriatic arthritis.
Ankylosing Spondylitis: HUMIRA is indicated for reducing signs and symptoms in adult patients with active ankylosing spondylitis.
Adult Crohn’s Disease: HUMIRA is indicated for reducing signs and symptoms and inducing and maintaining clinical remission in adult patients with moderately to severely active Crohn’s disease who have had an inadequate response to conventional therapy, and reducing signs and symptoms and inducing clinical remission in these patients if they have also lost response to or are intolerant to infliximab.
Pediatric Crohn’s Disease: HUMIRA is indicated for reducing signs and symptoms and inducing and maintaining clinical remission in pediatric patients 6 years of age and older with moderately to severely active Crohn’s disease who have had an inadequate response to corticosteroids or immunomodulators such as azathioprine, 6-mercaptopurine, or methotrexate.
Ulcerative Colitis: HUMIRA is indicated for inducing and sustaining clinical remission in adult patients with moderately to severely active ulcerative colitis who have had an inadequate response to immunosuppressants such as corticosteroids, azathioprine, or 6-mercaptopurine. The effectiveness of HUMIRA has not been established in patients who have lost response to or were intolerant to anti-TNF agents.
Plaque Psoriasis: HUMIRA is indicated for the treatment of adult patients with moderate to severe chronic plaque psoriasis who are candidates for systemic therapy or phototherapy, and when other systemic therapies are medically less appropriate. HUMIRA should only be administered to patients who will be closely monitored and have regular follow-up visits with a physician.
Hidradenitis Suppurativa: HUMIRA is indicated for the treatment of moderate to severe hidradenitis suppurativa in patients 12 years of age and older.
Uveitis: HUMIRA is indicated for the treatment of non-infectious intermediate, posterior, and panuveitis in adults and pediatric patients 2 years of age and older.

Please see Full Prescribing Information.

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References: 1. HUMIRA Injection [package insert]. North Chicago, IL: AbbVie Inc. 2. Kimball AB, Okun MM, Williams DA, et al. Two phase 3 trials of adalimumab for hidradenitis suppurativa. N Engl J Med. 2016;375(5):422-434. 3. Kimball AB, Jemec GB, Yang M, et al. Assessing the validity, responsiveness and meaningfulness of the Hidradenitis Suppurativa Clinical Response (HiSCR) as the clinical endpoint for hidradenitis suppurative treatment. Br J Dermatol. 2014;171(6):1434-1442. 4. Zouboulis CC, Okun MM, Prens EP, et al. Long-term adalimumab efficacy in patients with moderate-to-severe hidradenitis suppurativa acne inversa: 3-year results of a phase 3 open-label extension study. J Am Acad Dermatol. 2019;80(1):60-69.e2. 5. Burmester GR, Panaccione R, Gordon KB, et al. Long-term safety of adalimumab (HUMIRA) in adult patients from global clinical trials across multiple indications: an updated analysis in 29,987 patients representing 56,951 patient-years. Poster presented at: the American College of Rheumatology Annual Meeting; November 3-8, 2017; San Diego, CA. 6. Nash P, Johan V, Hall S, et al. Randomized crossover comparison of injection site pain with 40mg/0.4 or 0.8 ml formulations of adalimumab in patients with rheumatoid arthritis. Rheumatol Ther. 2016(3):257-270.

REVEAL STUDY DESIGN^1,2,8

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REVEAL was a randomized, double-blind, placebo-controlled study of 1212 patients with chronic plaque psoriasis and ≥10% BSA involvement, PASI score ≥12, and PGA of at least moderate disease severity. Patients had a clinical diagnosis of psoriasis for at least 6 months and stable disease for at least 2 months before screening. Evaluations were performed over 3 treatment periods totaling 52 weeks. For the first 16 weeks (Period A), patients received either HUMIRA (n=814), at an initial dose of 80 mg SC at week 0 followed by 40 mg EOW SC starting at week 1, or placebo (n=398).

In Period B, patients who achieved at least a PASI 75 response at week 16 received open-label HUMIRA 40 mg EOW for 17 weeks. In Period C, patients who maintained at least a PASI 75 response at week 33 and were originally randomized to HUMIRA in Period A were re-randomized to receive HUMIRA 40 mg EOW or placebo for an additional 19 weeks. Primary efficacy endpoints at week 16 were proportion of patients achieving a PASI 75 response relative to baseline and proportion of patients achieving a PGA score of clear or minimal disease.

CHAMPION STUDY DESIGN^1,3

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Eligible adult patients had moderate to severe plaque psoriasis (defined as ≥10% BSA and PASI ≥10).

Patients were to have plaque psoriasis for at least 1 year and stable plaque psoriasis for at least 2 months
Patients were candidates for systemic therapy or phototherapy
All patients were naïve to anti-TNF therapy and MTX
Concomitant psoriasis therapies were not permitted during the study, with the exception of shampoos free of corticosteroids, bland emollients, and low-potency topical corticosteroids for the palms, soles, face, inframammary areas, and groin only, provided they were not used within 24 hours of a study visit

^aPatients were randomized to receive HUMIRA (80 mg followed by 40 mg EOW beginning 1 week later) or placebo in a 2:1 ratio.

Co-primary efficacy endpoints were proportion of patients achieving PASI 75 relative to baseline and proportion of patients achieving a PGA of clear or minimal by week 16.

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PIONEER I and II STUDY DESIGNS^1,12,14,15

The first and only completed Phase 3 trials in HS

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HUMIRA PIONEER I and PIONEER II study designs

HUMIRA
40 mg EW
HUMIRA
40 mg EOW
Control

Enrolled patients had a total abscess and inflammatory nodule (AN) count of ≥3 with lesions in ≥2 anatomic areas, one of which was Hurley Stage II or III.

Primary efficacy endpoint was Hidradenitis Suppurativa Clinical Response (HiSCR) at week 12.
Period B explored the safety and efficacy of different maintenance regimens (continuous HUMIRA EW, reduction to HUMIRA EOW, or treatment withdrawal) over 24 weeks.

At or after week 16, patients were instructed to discontinue from Period B and enter the OLE phase if they achieved HiSCR in Period A and subsequently had a loss of response,^† or if they did not achieve HiSCR and experienced worsening or absence of improvement.^‡

Throughout the OLE, all patients received HUMIRA 40 mg weekly.

PIONEER I control=placebo PIONEER II control=placebo +/- antibiotic

^aStratified by baseline Hurley Stage II vs III (PIONEER I & II) and baseline concomitant antibiotic use (PIONEER II).

^b160 mg week 0; 80 mg week 2; 40 mg from week 4.

^cRe-randomization at entry to Period B, stratified by week 12 HiSCR status and baseline Hurley Stage II vs III.

^d160 mg week 12; 80 mg week 14; 40 mg weekly from week 16.

^*Weeks of efficacy and patient-reported outcomes analysis.

^†Loss of response=defined as a loss of ≥50% in improvement in AN count achieved from baseline to week 12.

^‡Worsening or absence of improvement=an AN count ≥ the baseline AN count at 2 consecutive visits (excluding week 12) occurring at least 14 days apart.

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HUMIRA demonstrated significant improvements from baseline in ACR components of disease activity (P<0.001)¹

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	HUMIRA^a 40 mg EOW (n=151)		Placebo EOW (n=162)
Parameter: median	Baseline	24 Weeks	Baseline	24 Weeks
Number of tender joints^b	20.0	5.0	23.0	17.0
Number of swollen joints^c	11.0	3.0	11.0	9.0
Physician global assessment^d	55.0	16.0	53.0	49.0
Patient global assessment^d	48.0	20.0	49.5	49.0
Pain^d	54.0	20.0	49.0	49.0
Disability index (HAQ)^e	1.0	0.4	1.0	0.9
CRP (mg/dL)^f	0.8	0.2	0.8	0.7

^aP<0.001 for HUMIRA vs placebo; comparisons based on mean changes.
^bScale 0-78.
^cScale 0-76.
^dVisual analog scale; 0=best, 100=worst.

^eDisability Index of the Health Assessment Questionnaire (HAQ-DI); 0=best, 3=worst; measures the patient’s ability to perform the following: dress/groom, arise, eat, walk, reach, grip, maintain hygiene, and maintain daily activity.
^fNormal range: 0-0.287 mg/dL.

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HUMIRA demonstrated significant improvements from baseline in every ACR component (P<0.001)¹

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	HUMIRA 40 mg EOW (n=151)		Placebo EOW (n=162)
Parameter: median	Baseline	24 Weeks	Baseline	24 Weeks
Number of tender joints	20.0	5.0	23.0	17.0
Number of swollen joints	11.0	3.0	11.0	9.0
Physician global assessment	55.0	16.0	53.0	49.0
Patient global assessment	48.0	20.0	49.5	49.0
Pain	54.0	20.0	49.0	49.0
Disability index (HAQ)	1.0	0.4	1.0	0.9
CRP (mg/dL)	0.8	0.2	0.8	0.7

^aP<0.001 for HUMIRA vs placebo; comparisons based on mean changes.
^bScale 0-78.
^cScale 0-76.
^dVisual analog scale; 0=best, 100=worst.

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PIONEER I and II STUDY DESIGNS—88 PATIENTS STUDIED IN OLE^1-4

88 patients who were studied in OLE received continuous HUMIRA weekly throughout the trial period (periods A and B) and throughout the OLE.

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HUMIRA
40 mg EW
HUMIRA
40 mg EOW
Control

Enrolled patients had a total abscess and inflammatory nodule (AN) count of ≥3 with lesions in ≥2 anatomic areas, one of which was Hurley Stage II or III.

Primary efficacy endpoint was Hidradenitis Suppurativa Clinical Response (HiSCR) at week 12.
Period B explored the safety and efficacy of different maintenance regimens (continuous HUMIRA EW, reduction to HUMIRA EOW, or treatment withdrawal) over 24 weeks.

At or after week 16, patients were instructed to discontinue from Period B and enter the OLE phase if they achieved HiSCR in Period A and subsequently had a loss of response,^† or if they did not achieve HiSCR and experienced worsening or absence of improvement.^‡

Throughout the OLE, all patients received HUMIRA 40 mg weekly.

PIONEER I control=placebo PIONEER II control=placebo +/- antibiotic

^aStratified by baseline Hurley Stage II vs III (PIONEER I & II) and baseline concomitant antibiotic use (PIONEER II).

^b160 mg week 0; 80 mg week 2; 40 mg from week 4.

^cRe-randomization at entry to Period B, stratified by week 12 HiSCR status and baseline Hurley Stage II vs III.

^d160 mg week 12; 80 mg week 14; 40 mg weekly from week 16.

^*Weeks of efficacy and patient-reported outcomes analysis.

^†Loss of response=defined as a loss of ≥ 50% in improvement in AN count achieved from baseline to week 12.

^‡Worsening or absence of improvement=an AN count ≥ the baseline AN count at 2 consecutive visits (excluding week 12) occurring at least 14 days apart.

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PIONEER I and II STUDY DESIGNS—88 PATIENTS STUDIED IN OLE^1,2,13,15

88 patients who were studied in OLE received continuous HUMIRA weekly throughout the trial period (periods A and B) and throughout the OLE.

Touch & Drag Image

HUMIRA
40 mg EW
HUMIRA
40 mg EOW
Control

Enrolled patients had a total abscess and inflammatory nodule (AN) count of ≥3 with lesions in ≥2 anatomic areas, one of which was Hurley Stage II or III.

Primary efficacy endpoint was Hidradenitis Suppurativa Clinical Response (HiSCR) at week 12.
Period B explored the safety and efficacy of different maintenance regimens (continuous HUMIRA EW, reduction to HUMIRA EOW, or treatment withdrawal) over 24 weeks.

At or after week 16, patients were instructed to discontinue from Period B and enter the OLE phase if they achieved HiSCR in Period A and subsequently had a loss of response,^† or if they did not achieve HiSCR and experienced worsening or absence of improvement.^†

Throughout the OLE, all patients received HUMIRA 40 mg weekly.

PIONEER I control=placebo PIONEER II control=placebo +/- antibiotic

Stratified by baseline Hurley Stage II vs III (PIONEER I & II) and baseline concomitant antibiotic use (PIONEER II).

160 mg week 0; 80 mg week 2; 40 mg from week 4.
Re-randomization at entry to Period B, stratified by week 12 HiSCR status and baseline Hurley Stage II vs III.
160 mg week 12; 80 mg week 14; 40 mg weekly from week 16.
Weeks of efficacy and patient-reported outcomes analysis.
^†Loss of response=defined as a loss of ≥ 50% in improvement in AN count achieved from baseline to week 12.
^‡Worsening or absence of improvement=an AN count ≥ the baseline AN count at 2 consecutive visits (excluding week 12) occurring at least 14 days apart.

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