Bimekizumab for Hidradenitis Suppurativa (BE-HEARD I/II, BJD 2026)

30-second key takeaways

Key Points

Source: a 2026 British Journal of Dermatology critically appraised topic (McCarthy & Ring) appraising the two phase III trials of bimekizumab for moderate-to-severe hidradenitis suppurativa, BE-HEARD I and II (original trials: Kimball et al., Lancet 2024). The trials were funded by UCB Pharma, which the appraisers note may introduce bias.
Disease and mechanism: HS causes recurrent abscesses, tunnels (sinus tracts), and scars in flexural sites (armpits, groin, buttocks); it is painful and severely impairs quality of life. IL-17 is a key driver — HS tunnels highly express IL-17 family cytokines. Approved HS biologics: adalimumab (anti-TNF-α), secukinumab (anti-IL-17A), and bimekizumab (anti-IL-17A and IL-17F).
Trial design: BE-HEARD I and II were two identically designed, randomized, double-blind, placebo-controlled, multicentre phase III trials. They enrolled adults ≥18 with moderate-to-severe HS (≥5 inflammatory lesions across ≥2 areas, at least one Hurley II or III) and inadequate response to systemic antibiotics. Randomization was 2:2:2:1 to four arms. The primary endpoint was HiSCR 50 at week 16 (≥50% reduction in total abscess/inflammatory-nodule count).
Primary efficacy: at week 16, the bimekizumab 320 mg every-2-weeks arm reached HiSCR 50 in 48% (BE-HEARD I) and 52% (II), clearly better than placebo's 29% and 32% (both statistically significant). The every-4-weeks arm reached significance only in BE-HEARD II.
Secondary efficacy: the stricter HiSCR 75, quality of life (DLQI), and worst skin pain also improved versus placebo; but flare showed no significant between-group difference in BE-HEARD II. Overall efficacy appears broadly comparable to existing data on adalimumab and secukinumab.
Safety: generally tolerable. Of 995 treated patients, 64 had a serious treatment-emergent adverse event and 67 discontinued. The most common adverse events were candida infections (23% and 25%) and hypersensitivity reactions (21% and 27%); inflammatory bowel disease (IBD) occurred in 7 patients total. Week-16 completion was 89–91%, but fell to 66–76% by week 48.
Appraisal limitations: a high placebo response (31% met the primary endpoint); no comparator beyond week 16; a predominantly White, female cohort (only 15% Black or Asian); exclusion of the most severe phenotype (>20 draining tunnels); no reported efficacy in biologic-experienced patients; antibiotics for flares were permitted, possibly confounding efficacy. The authors conclude bimekizumab is effective and safe but more real-world data and head-to-head studies are needed.
Taiwan context: in Taiwan, adalimumab (Humira®) and secukinumab are the HS biologics more commonly discussed (see our HS overview for details). Bimekizumab is newer; whether it has a Taiwan HS indication and NHI coverage should follow the TFDA label and NHIA announcements — this article is not individual treatment advice.

A quick primer on hidradenitis suppurativa (HS)

Hidradenitis suppurativa (HS, also called acne inversa) is a chronic, relapsing inflammatory skin disease. Typically, painful red nodules and abscesses recur in skin folds — armpits, groin, buttocks, under the breasts, perineum — discharging pus when they rupture and, over time, forming interconnected tunnels (sinus tracts) under the skin with rope-like scarring. It is not caused by poor hygiene and is not contagious; it results from follicular occlusion plus dysregulated immune inflammation.

Severity is often described with Hurley staging: stage I is single or multiple abscesses without tunnels or scarring; stage II is recurrent abscesses with tunnels and scarring but separated lesions; stage III is extensive interconnected tunnels and abscesses. In moderate-to-severe disease (often Hurley II–III, or enough inflammatory lesions), topicals and oral antibiotics frequently fail to control it, so systemic therapy — including biologics — is considered. For HS staging, daily care, and other treatments overall, see our separate article; this one focuses on the trial evidence for bimekizumab.

Why IL-17? How bimekizumab differs from other biologics

Studying HS pathophysiology, researchers found that interleukin-17 (IL-17), a family of inflammatory signaling molecules, plays a major role — especially in HS tunnel tissue, where IL-17 family cytokines are highly expressed. Among the family, IL-17A and IL-17F are the two of greatest therapeutic interest. Blocking these inflammatory signals is the design logic behind HS biologics.

The three biologics currently approved for HS act on different targets:

adalimumab: inhibits tumour necrosis factor-α (TNF-α); the first biologic approved for HS, with the most accumulated experience.
secukinumab: inhibits IL-17A only.
bimekizumab: inhibits both IL-17A and IL-17F — its key difference from secukinumab. In theory, blocking two inflammatory signals may be more complete than blocking one; but more complete in theory does not guarantee better in practice, and direct head-to-head comparisons are still lacking.

Figure 1. The three approved HS biologics act on different targets. adalimumab blocks TNF-α; secukinumab blocks IL-17A only; bimekizumab blocks both IL-17A and IL-17F. Blocking one extra signal is bimekizumab's design rationale, but whether that translates into better clinical outcomes still needs direct comparative studies.

How the BE-HEARD I and II trials were run

BE-HEARD I and II were two identically designed, randomized, double-blind, placebo-controlled, multicentre phase III trials — running two identical trials lets each verify whether the result is reproducible. Eligibility:

Adults ≥18 with moderate-to-severe HS: at least 5 inflammatory lesions across at least 2 body areas, with at least one site at Hurley stage II or III.
Inadequate response to systemic (oral) antibiotics — i.e. this is for people who have already tried basic treatment without enough effect.

Participants were randomized 2:2:2:1 to four arms: (1) bimekizumab 320 mg subcutaneously every 2 weeks; (2) every 2 weeks for 16 weeks, then every 4 weeks; (3) every 4 weeks; (4) placebo to week 16, then bimekizumab every 2 weeks. After week 16, everyone (including the placebo group) switched to bimekizumab through week 48. The primary endpoint was HiSCR 50 at week 16.

Jargon: HiSCR

HiSCR (Hidradenitis Suppurativa Clinical Response) is the most common efficacy measure in HS trials. HiSCR 50 means a ≥50% reduction in total abscess and inflammatory-nodule count from baseline, with no increase in abscesses or draining tunnels. HiSCR 75 is the stricter ≥75% reduction. It captures reduction of inflammatory lesions but reflects established tunnels and scars poorly — one limitation the appraisal raises.

Efficacy: about half reached HiSCR 50 at week 16

The two trials enrolled 1014 participants (57% female, 63% under 40, 80% White). The main result: in both BE-HEARD trials, the every-2-weeks bimekizumab arm met the primary endpoint; the every-4-weeks arm reached significance only in BE-HEARD II. The week-16 HiSCR 50 figures:

Figure 2. Week-16 HiSCR 50 in BE-HEARD I and II. The every-2-weeks arm (dark green) clearly beat placebo (grey) in both trials; the every-4-weeks arm (light green) also did well in BE-HEARD II but did not reach significance in BE-HEARD I. Note the placebo arm reached 29–32% — this fairly high placebo response is a key appraisal point. Source: Kimball et al., Lancet 2024 (as summarized by McCarthy & Ring 2026).

Beyond the primary endpoint, the stricter HiSCR 75, quality of life (DLQI), and worst skin pain all improved versus placebo. Comparing the every-2-weeks arm with placebo:

Week-16 outcome	I: bime q2w	I: placebo	II: bime q2w	II: placebo
HiSCR 50 (≥50% lesion reduction)	48%	29%	52%	32%
HiSCR 75 (≥75% lesion reduction)	33%	18%	36%	16%
DLQI quality of life (change from baseline)	−5.0	−2.7	−4.5	−3.1
Worst skin pain (change from baseline)	−1.9	−1.1	−1.9	−0.4

(Every-4-weeks HiSCR 50: 45% [I] / 54% [II]. DLQI and pain are mean changes; negative means improvement, more negative is better. The q2w-vs-placebo differences for HiSCR 50/75, DLQI, and pain were mostly statistically significant; only flare in BE-HEARD II showed no significant between-group difference. Data from Table 1 of Kimball et al., Lancet 2024, as reported by McCarthy & Ring 2026.)

How to read this? On the positive side, about half of these moderate-to-severe, antibiotic-refractory patients had their inflammatory lesions halved after 16 weeks of bimekizumab, with parallel gains in quality of life and pain — meaningful progress for a notoriously stubborn, life-disrupting disease. The appraisers also note this overall efficacy is broadly comparable to existing adalimumab and secukinumab data — i.e. bimekizumab is one more effective option, but there is no evidence it is clearly stronger than the others, because direct comparisons are lacking.

Safety: candida infections, hypersensitivity, IBD, and long-term retention

Overall, bimekizumab was generally tolerable in the trials, but several safety signals are worth knowing:

Candida infections were most common: 23% and 25% across the two trials. This is an expected class effect of IL-17 inhibitors — IL-17 normally helps defend against fungi (especially candida), so blocking it raises the chance of oral or skin candidiasis (e.g. thrush, candidal dermatitis). Whether blocking both IL-17A and F raises candida risk further is worth watching; most cases are treatable.
Hypersensitivity reactions were frequent: 21% and 27%. One was a serious hypersensitivity reaction leading to discontinuation. Injection-site and allergy-related reactions are common with biologics and are mostly manageable.
Inflammatory bowel disease (IBD): a total of 7 bimekizumab patients across the trials developed IBD. The IL-17-inhibitor / IBD association has been discussed in psoriasis too; although numbers are small, clinicians pay special attention in people with bowel symptoms or a relevant history.
Serious events and discontinuation: of 995 treated patients, 64 had a serious treatment-emergent adverse event and 67 discontinued bimekizumab.
Long-term retention fell: at week 16, 89% and 91% completed; but by week 48, completion dropped to 66% and 76%. Withdrawals were mainly due to consent withdrawal, adverse events, or lack of efficacy. The appraisers note this raises a question about long-term tolerability — though dropout rates were comparable to prior large HS trials.

Critical appraisal: strengths and limits the CAT raised

The value of this paper is not just collating numbers but that it is a critically appraised topic — it asks, with a methodological eye: is this result trustworthy, and does it apply to my patients? Here is the appraisers' assessment.

Strengths: the study quality is solid

High internal validity: randomized, double-blind, placebo-controlled; intention-to-treat analyses (counting dropouts too) reduce completer bias; the sample size had appropriate power calculations allowing for 10% dropout in the first 16 weeks.
Two identical trials cross-validate: BE-HEARD I and II share a design and point the same way, raising confidence over a single trial. Reporting met all items of the CONSORT trial-reporting checklist.

Where to discount it: limitations

Industry funding: the original trials were funded by UCB Pharma, the maker of bimekizumab; the appraisers explicitly flag this as a potential source of bias (not an allegation of fabrication, but a reason for cautious interpretation).
High placebo response: 31% of the placebo group (45 of 146) also met the primary endpoint. This means the drug's true added effect must be read after subtracting that 31%; it also reflects limitations of HiSCR or the pathogenic complexity of HS itself.
No comparator after week 16: the primary endpoint was at week 16, after which everyone (including the placebo group) switched to bimekizumab, so the later long-term efficacy is uncontrolled single-arm data and should be read cautiously.
No efficacy reported for biologic-experienced patients: about 19% had previously received a biologic, but the authors did not report this subgroup separately — so whether switchers can expect the same efficacy remains unknown.
Antibiotics for flares were permitted: systemic antibiotics could be used for flares during the trial, which may confound the read on bimekizumab's own efficacy; and antibiotic use was higher in the bimekizumab arm of BE-HEARD II but the reverse in BE-HEARD I — inconsistent directions.
The most severe phenotype was excluded: people with more than 20 draining tunnels were excluded, so bimekizumab's effect in the most extensive, hardest-to-treat patients remains unevaluated.
Possible unblinding: because injection schedules differed by dosing frequency, investigators or participants might guess the allocation, raising an unblinding concern. Also, the every-4-weeks arm in BE-HEARD I had a higher average weight, which may partly explain its lower response.

A point that matters especially for Taiwan / Asian readers:80% of participants were White and 57% female; only 15% were Black or Asian. So these favorable numbers come mainly from a White, female population. HS may differ across ethnic groups in presentation, severity, and treatment response, so applying these results directly to Taiwanese / Asian patients warrants some uncertainty — one reason the appraisers stress the need for more real-world data.

The Taiwan context

Taiwan context · key points

When discussing systemic / biologic therapy for HS in Taiwan, the biologics more commonly referenced are adalimumab (Humira®, anti-TNF-α) and secukinumab (anti-IL-17A). Our HS overview covers their role, NHI coverage conditions, and monitoring more fully.

Bimekizumab (Bimzelx®) is a newer dual IL-17A/F inhibitor. Whether it has obtained a hidradenitis suppurativa indication in Taiwan, and whether NHI reimburses it for HS, should follow the TFDA-approved label and the latest NHIA announcements — this article cannot and should not replace official information. Whether you can actually use it, out-of-pocket vs covered, and the cost, must be confirmed in person with your dermatologist.

A reminder: biologics are prescription drugs. Before starting, infection screening (e.g. tuberculosis, hepatitis B) is usually done, and infections and other adverse effects are monitored during treatment — all dermatologist-led. For general biologic monitoring principles, see our article on psoriasis biologic monitoring (different disease, but shared monitoring concepts).

Frequently asked questions

Q1. What is bimekizumab, and how is it different?

Bimekizumab is a biologic that uniquely inhibits both IL-17A and IL-17F inflammatory signals. By contrast, secukinumab inhibits IL-17A only, and adalimumab inhibits a different pathway, TNF-α. It is given by subcutaneous injection.

Q2. Does it work for HS, and how well?

In the BE-HEARD I/II phase III trials, the every-2-weeks arm reached HiSCR 50 (lesions halved) in about 48–52% at week 16, versus 29–32% on placebo; quality of life and pain also improved. So for moderate-to-severe, antibiotic-refractory patients it is a meaningful but not magical option — remember about a third of the placebo group also responded.

Q3. Is it better than adalimumab or secukinumab?

Not as things stand. The appraisal notes bimekizumab's overall efficacy is broadly comparable to existing adalimumab and secukinumab data, and there is no head-to-head trial pitting it directly against the others. Blocking the extra IL-17F is a theoretical advantage, but proving clinical superiority needs direct comparative studies.

Q4. How long until it works? Do I have to keep injecting?

The trials' primary assessment was at week 16, so expect effects on a scale of weeks to months, not a single shot. HS is chronic, and biologics are usually about ongoing treatment to maintain control, not a course that cures. The actual regimen and frequency (every 2 or 4 weeks) are adjusted by your doctor based on response.

Q5. What are the side effects? What's with the candida infections?

The most common in the trials were candida infections (~23–25%) and hypersensitivity reactions (~21–27%). Candida infection is an expected effect of IL-17 inhibitors — IL-17 normally helps defend against fungi, so blocking it raises the chance of oral/skin candidiasis, which is mostly treatable. A few IBD cases were also seen. So your doctor assesses infection risk and bowel symptoms before and during treatment.

Q6. I'm Asian — do these data apply to me?

With some uncertainty. 80% of participants were White and 57% female; only 15% were Black or Asian, so the numbers mainly reflect a White, female population. HS may differ across groups, so for Taiwanese / Asian patients efficacy and safety may not be identical — more real-world data are needed.

Q7. Is it available in Taiwan? Is it NHI-covered?

Whether bimekizumab has an HS indication in Taiwan and whether NHI covers it for HS should follow the TFDA label and the latest NHIA announcements; this article does not replace official information. The HS biologics more commonly used in Taiwan are adalimumab and secukinumab. Confirm actual availability and cost in person with your dermatologist.

Q8. What preparation is needed before starting a biologic?

Typically the doctor reviews history and infection risk, does infection screening (e.g. tuberculosis, hepatitis B/C), checks vaccination status, and counsels on infection warning signs and injection technique. Efficacy and adverse effects are monitored during treatment. This is a specialist-led process, not something to self-decide or self-purchase.

Common myths

Myth	Reality
"A biologic cures hidradenitis suppurativa."	HS is chronic; the goal is control and improvement, not a one-time cure, and stopping may lead to relapse. Established tunnels and scars are hard for any drug to fully erase.
"Bimekizumab blocks an extra IL-17F, so it must be stronger."	A theoretical edge is not clinical superiority. The appraisal notes overall efficacy is broadly comparable to adalimumab and secukinumab, with no head-to-head comparison.
"It worked in the trial, so it works for every HS patient."	The trial excluded the most severe phenotype (>20 tunnels), did not report efficacy in biologic-experienced patients, and was mostly White and female — extrapolation to other groups and severe disease needs caution.
"Placebo did nothing, so the drug's number is its true effect."	The placebo group still reached the primary endpoint in 31%. The drug's true added effect is seen only after subtracting the placebo response.
"IL-17 inhibitors are very safe, with no side effects."	Candida infections are fairly common (about a quarter), with a few IBD and serious hypersensitivity cases. Specialist assessment and monitoring are needed.

Clinical pearls for colleagues

For Clinicians

Efficacy placement: two identical phase III trials (BE-HEARD I/II); q2w met the primary endpoint in both (HiSCR 50 48%/52% vs placebo 29%/32%), q4w significant only in BE-HEARD II; the q4w arm in BE-HEARD I had higher average weight, possibly diluting response — hinting at a dose/weight relationship.
Internal validity: ITT + multiple imputation, power calculation allowing 10% dropout, full CONSORT compliance; but post-week-16 single-arm crossover (all on bimekizumab) removes the long-term comparator, and differing injection frequencies raise an unblinding concern.
Placebo response 31%: high, reflecting HiSCR's limitations as an endpoint or HS pathogenic heterogeneity; correct for placebo when interpreting absolute efficacy.
Safety class effect: candida 23–25% (IL-17's antifungal role), hypersensitivity 21–27%, 7 IBD cases total; pre-treatment infection screening (TB/HBV), watch bowel symptoms; whether dual A/F inhibition raises candida risk warrants follow-up.
Evidence gaps: no biologic-experienced subgroup (19%), exclusion of >20-tunnel severe disease, week-48 retention down to 66–76%, antibiotics-for-flares as a confounder, no head-to-head; limited extrapolation to Taiwan/Asian populations (80% White, only 15% Black/Asian).
Practical placement: bimekizumab is one more effective systemic option for moderate-to-severe, antibiotic-refractory HS, alongside adalimumab/secukinumab; drug choice remains individualized (comorbidity, infection risk, coverage, injection-frequency preference) and dermatologist-led.

Takeaway

HS is a painful, recurrent, stubborn, life-disrupting chronic inflammatory disease. Bimekizumab is a newer biologic inhibiting both IL-17A and IL-17F; the BE-HEARD I/II phase III trials show that with every-2-weeks dosing, about half of patients reached HiSCR 50 at week 16, with gains in quality of life and pain, and overall efficacy broadly comparable to adalimumab and secukinumab. The 2026 BJD critical appraisal sharpens the picture: a 31% placebo response, industry funding, no comparator beyond week 16 and no head-to-head, common candida infections, falling long-term retention, plus a predominantly White and female cohort and exclusion of the most severe phenotype — all of which mean the effective and safe conclusion warrants caution and more real-world data. For patients, bimekizumab is one more option for HS; whether it suits you and whether it is available in Taiwan should be decided by a dermatologist based on your situation, comorbidities, and coverage rules.

This article is educational and a research summary based on McCarthy & Ring (2026 BJD critical appraisal) and its cited references (including the Kimball et al. Lancet 2024 BE-HEARD I/II original trials); it cannot replace in-person medical care. Diagnosis of HS, the use and monitoring of biologics (including bimekizumab, adalimumab, secukinumab), and NHI/self-pay choices must be discussed with a board-certified dermatologist and decided per your situation. Bimekizumab's Taiwan indication and coverage follow the TFDA label and the latest NHIA announcements. This site does not run medical advertising, does not recommend specific clinics/hospitals/drugs/procedures, and accepts no sponsorship or paid promotion.

References

McCarthy R, Ring HC. Two phase III trials of bimekizumab for the treatment of moderate-to-severe hidradenitis suppurativa: a critically appraised research paper. Br J Dermatol. 2026;194(6):1064-1066. doi:10.1093/bjd/ljag051. https://doi.org/10.1093/bjd/ljag051
Kimball AB, Jemec GBE, Sayed CJ, et al. Efficacy and safety of bimekizumab in patients with moderate-to-severe hidradenitis suppurativa (BE HEARD I and BE HEARD II): two 48-week, randomised, double-blind, placebo-controlled, multicentre phase 3 trials. Lancet. 2024;403(10443):2504-2519.
Matusiak Ł. Profound consequences of hidradenitis suppurativa: a review. Br J Dermatol. 2020;183(6):e171-e177.
Matusiak Ł, Szczęch J, Bieniek A, et al. Increased interleukin (IL)-17 serum levels in patients with hidradenitis suppurativa: implications for treatment with anti-IL-17 agents. J Am Acad Dermatol. 2017;76(4):670-675.
Navrazhina K, Frew JW, Gilleaudeau P, et al. Epithelialized tunnels are a source of inflammation in hidradenitis suppurativa. J Allergy Clin Immunol. 2021;147(6):2213-2224.
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.
Kimball AB, Jemec GBE, Alavi A, et al. Secukinumab in moderate-to-severe hidradenitis suppurativa (SUNSHINE and SUNRISE): week 16 and week 52 results of two identical, multicentre, randomised, placebo-controlled, double-blind phase 3 trials. Lancet. 2023;401(10378):747-761.

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