Abstract
Background
Facial-predominant inflammatory dermatoses are diagnostically heterogeneous and may overlap with atopic dermatitis (AD), contact dermatitis, rosacea-like inflammation, and autoimmune mimics. Stapokibart, an IL-4Rα-targeted monoclonal antibody, has demonstrated efficacy in moderate-to-severe AD, but real-world experience in facial-predominant AD-like presentations remains limited.
Methods
We retrospectively reviewed five unpublished patients with facial-predominant inflammatory dermatoses treated with stapokibart in routine practice. Clinical phenotype, diagnostic work-up, prior and concomitant therapy, dosing, symptom scores, treatment course, recurrence, and adverse events were summarized descriptively. The cohort was not intended as a diagnostically uniform efficacy population, and no formal hypothesis testing was performed.
Results
Five women aged 28–75 years were included. Pruritus numerical rating scale changed from a median of 3 (range, 2–4) at baseline to 1 (range, 0–3) at first follow-up; four patients improved and one worsened. All three patients with a well-supported facial-predominant AD phenotype showed rapid improvement in facial lesions and pruritus after stapokibart. One of these patients developed an injection-site reaction that led to treatment discontinuation; no serious adverse events were observed. One patient initially treated for AD-like facial dermatitis was subsequently evaluated for possible early clinically amyopathic dermatomyositis after telangiectatic and mildly atrophic features became more apparent. Another patient with an incompletely characterized AD-like facial eruption worsened on day 2 after stapokibart.
Conclusion
In this small case series, rapid improvement was observed in all three patients with a well-supported facial-predominant AD phenotype, whereas atypical or incompletely characterized eruptions showed greater diagnostic complexity and variable outcomes. These preliminary observations support further investigation of stapokibart in facial-predominant AD while underscoring the need for careful phenotyping before IL-4Rα blockade.
Keywords: stapokibart, atopic dermatitis, facial dermatitis, IL-4Rα, dermatomyositis, dupilumab
Introduction
Facial inflammatory dermatoses are common in dermatologic practice and may substantially impair quality of life because of their visibility, recurrent course, pruritus, and potential psychosocial burden. However, facial erythema, edema, scaling, and pruritus are nonspecific manifestations shared by atopic dermatitis (AD), allergic contact dermatitis, irritant dermatitis, seborrheic dermatitis, rosacea-like dermatitis, photodermatitis, drug-related eruptions, infections, and connective tissue diseases. This overlap makes facial-predominant disease particularly difficult to classify in routine practice, especially when morphology evolves over time or diagnostic testing is incomplete. Accordingly, apparent treatment response should not be used by itself to confirm an AD diagnosis.
AD is a chronic inflammatory skin disease characterized by epidermal barrier dysfunction, immune dysregulation, and pruritus. Type 2 inflammation, particularly interleukin (IL)-4 and IL-13 signaling, contributes to barrier impairment, inflammatory recruitment, IgE production, and itch.1,2 Dupilumab established IL-4Rα blockade as an effective systemic strategy for moderate-to-severe AD.3,4 At the same time, facial and neck dermatitis during biologic therapy has highlighted the mechanistic and diagnostic heterogeneity of head-and-neck inflammation, including possible contributions from Malassezia-associated dermatitis, allergic contact dermatitis, rosacea-like inflammation, and mixed immune pathways.5
Stapokibart is a humanized monoclonal antibody targeting IL-4Rα and inhibiting IL-4 and IL-13 signaling. Phase 3 trials have demonstrated efficacy and safety in moderate-to-severe AD, including sustained responses through 52 weeks.6,7 More recently, an exploratory proteomic study in head-and-neck AD associated clinical response to stapokibart with suppression of the IL-36A axis.8 These data provide a rationale for studying stapokibart in facial and head-and-neck AD phenotypes, but they do not establish its role in diagnostically undifferentiated facial dermatitis.
We previously reported a pregnancy-associated case of acute eczematous facial dermatitis with atopic features that showed rapid improvement after stapokibart therapy.9 To extend this clinical observation while explicitly examining diagnostic and response heterogeneity, we retrospectively analyzed five additional unpublished patients with facial-predominant inflammatory dermatoses treated with stapokibart in routine practice. The aim was descriptive: to summarize treatment trajectories, switching, recurrence, adverse events, diagnostic revision, and early worsening rather than to estimate treatment efficacy.
Materials and Methods
Study Design and Setting
This was a retrospective observational case series conducted at the Department of Dermatology, Shenzhen Nanshan People’s Hospital/Affiliated Nanshan Hospital of Shenzhen University, Shenzhen, China. The study was designed to describe real-world clinical trajectories in patients with facial-predominant inflammatory dermatoses who had already received stapokibart in routine clinical care. Treatment selection, diagnostic testing, and follow-up were determined by the treating dermatologists before and independently of this retrospective analysis; the study did not prospectively assign stapokibart or any comparator treatment.
Patient Selection
Patients were eligible if they had (1) a facial-predominant inflammatory eruption for which stapokibart had been prescribed in routine practice; (2) available baseline clinical information and at least one follow-up assessment; and (3) medical records documenting the working diagnosis, previous treatments, stapokibart regimen, clinical course, and safety outcomes. The series intentionally included heterogeneous real-world phenotypes rather than a diagnostically uniform efficacy cohort. Five unpublished patients met these criteria. One previously published pregnancy-associated case was cited only as an index case for contextual discussion; no previously published clinical images or detailed individual case material were reused.
Data Collection
Clinical data were collected retrospectively from outpatient medical records and follow-up communication. Extracted variables included age, sex, disease duration, facial distribution, working and revised diagnoses, atopic history, available diagnostic investigations, previous and concomitant therapy, stapokibart dose and injection dates, time to improvement or worsening, recurrence after discontinuation or switching, adverse events, and follow-up outcomes. Pruritus NRS was collected when available because it reflects patient-reported itch severity across different inflammatory dermatoses. IGA was summarized only in patients with a clinical diagnosis of AD and was not applied to suspected dermatomyositis or diagnostically undifferentiated facial dermatitis.
Diagnostic Classification
Diagnostic classification reflected the treating dermatologists’ working diagnosis at each clinical time point and was based on morphology, symptom pattern, atopic history, available laboratory data, and subsequent clinical evolution. Because this was a retrospective real-world series, investigations were individualized rather than protocolized and therefore were not uniform across patients. AD/AD-like classifications were based on an eczematous and pruritic phenotype together with supportive atopic features and/or a relapsing course when present; non-AD mimics were reconsidered when atypical morphology, laboratory findings, or an unexpected clinical course emerged. Treatment response itself was not used as a diagnostic criterion. Case 1 was subsequently considered possible early clinically amyopathic dermatomyositis after persistent telangiectatic and mildly atrophic changes became more apparent and autoimmune testing showed ANA and anti-Mi-2β positivity. Case 5 remained diagnostically undifferentiated because a definitive diagnostic work-up was not completed.
Outcome Assessment
The primary descriptive outcome was clinical change in facial lesions after stapokibart treatment, assessed from physician documentation, patient-reported symptom changes, and available clinical photographs. Secondary descriptive outcomes included time to improvement, recurrence after treatment discontinuation or switching, adverse events, and diagnostic revision. Pruritus NRS changes were summarized descriptively in the full cohort, whereas IGA changes were summarized only in the AD subgroup. Continuous variables were summarized as median and range and categorical variables as counts and percentages. Because of the small sample size, heterogeneous diagnoses, variable prior or concomitant therapies, and retrospective design, no formal hypothesis testing was performed and temporal associations were not interpreted as causal treatment effects.
Results
Overall Clinical Characteristics
Five female patients with facial-predominant inflammatory dermatoses were included. Their ages ranged from 28 to 75 years. Three patients (Cases 2–4) had a well-supported facial-predominant AD phenotype, and all three showed rapid improvement in facial lesions and pruritus after stapokibart. Case 1 had an initially AD-like eruption that improved before atypical residual features prompted evaluation for possible early clinically amyopathic dermatomyositis, whereas Case 5 had an incompletely characterized AD-like eruption with early worsening after stapokibart. Pruritus NRS was available for all five patients. The median baseline NRS was 3 (range, 2–4), and the median NRS at first follow-up was 1 (range, 0–3); four patients improved and one worsened. IGA was applicable in the three patients with AD and decreased from 3 at baseline to 1 at first follow-up in each patient. These findings are presented as preliminary descriptive observations. Baseline characteristics are summarized in Table 1, descriptive treatment outcomes in Table 2, and representative contrasting clinical photographs in Figure 1.
Table 1.
Baseline Characteristics of Patients with Facial-Predominant Inflammatory Dermatoses Treated with Stapokibart
| Variable | Overall Cohort (N = 5, 100%) |
|---|---|
| Age, years, median (range, mean) | 35 (28–75, 42.4) |
| Female sex, n (%) | 5 (100.0) |
| Clinical phenotype | |
| Facial-predominant AD, n (%) | 3 (60.0) |
| Possible early clinically amyopathic dermatomyositis considered, n (%) | 1 (20.0) |
| Undifferentiated AD-like facial dermatitis, n (%) | 1 (20.0) |
| Atopic background | |
| Known AD or allergic rhinitis, n (%) | 3 (60.0) |
| Allergic rhinitis, n (%) | 2 (40.0) |
| Prior treatment exposure | |
| Previous conventional treatment with inadequate response, n (%) | 4 (80.0) |
| Previous dupilumab exposure, n (%) | 1 (20.0) |
| Previous JAK inhibitor exposure, n (%) | 1 (20.0) |
| Stapokibart initial regimen | |
| 600 mg loading dose, n (%) | 4 (80.0) |
| 300 mg initial dose, n (%) | 1 (20.0) |
Notes: Clinical phenotypes represent working or revised diagnoses based on morphology, atopic history, available investigations, and subsequent clinical evolution; response to stapokibart was not used to establish diagnosis. IGA was applied only to the three patients with a clinical diagnosis of AD and was not used for suspected dermatomyositis or diagnostically undifferentiated facial dermatitis.
Abbreviations: AD, atopic dermatitis; IGA, Investigator’s Global Assessment; JAK, Janus kinase; NRS, numerical rating scale.
Table 2.
Descriptive Summary of Treatment Outcomes After Stapokibart
| Variable | Result |
|---|---|
| Pruritus NRS available, n/N | 5/5 |
| Baseline pruritus NRS, median (range) | 3 (2–4) |
| First-follow-up pruritus NRS, median (range) | 1 (0–3) |
| Pruritus improvement, n/N (%) | 4/5 (80.0%) |
| Pruritus worsening, n/N (%) | 1/5 (20.0%) |
| AD patients with applicable IGA, n | 3 |
| Baseline IGA in AD subgroup, median (range) | 3 (3–3) |
| First-follow-up IGA in AD subgroup, median (range) | 1 (1–1) |
| Early clinical worsening, n/N (%) | 1/5 (20.0%) |
| Injection-site reaction, n/N (%) | 1/5 (20.0%) |
| Recurrence after treatment switch/discontinuation, n/N (%) | 1/5 (20.0%) |
Notes: IGA was summarized only for the three patients with a clinical diagnosis of AD and was not applied to suspected dermatomyositis or diagnostically undifferentiated facial dermatitis.
Abbreviations: AD, atopic dermatitis; IGA, Investigator’s Global Assessment; NRS, numerical rating scale.
Figure 1.
Representative clinical photographs illustrating contrasting outcomes after stapokibart. (A and B) Case 1: before treatment on April 8, 2026, extensive erythema with fine scaling was present on the forehead and bilateral cheeks; at the 2-week follow-up after stapokibart 300 mg, diffuse erythema and scaling had markedly improved, making persistent telangiectatic changes more apparent. (C and D) Case 5: before stapokibart on June 5, 2026, facial erythema and inflammatory lesions involved the forehead, cheeks, perioral area, and perinasal region; on June 7, 2026, facial erythema and pruritus had worsened after stapokibart 600 mg. The figure is intended to show two representative contrasting trajectories rather than all five cases.
Individual Clinical Courses
Case 1
A 75-year-old woman presented with a 2-month history of extensive erythema and desquamation involving both cheeks and the forehead, accompanied by pruritus. She had no muscle weakness, myalgia, dysphagia, cough, dyspnea, or other pulmonary symptoms. Physical examination showed confluent erythematous patches over the bilateral cheeks and forehead with fine scaling and visible telangiectatic changes. She had previously received topical desonide and oral levocetirizine solution without meaningful improvement. At that time, the eczematous morphology, pruritus, and lack of response to conventional therapy were considered compatible with an AD-like facial dermatitis.
On April 8, 2026, she received her first subcutaneous injection of stapokibart 300 mg. The treatment was selected in routine clinical care on the basis of the working AD-like diagnosis, our department’s prior clinical experience with stapokibart in facial AD-like disease, and established clinical evidence supporting stapokibart in moderate-to-severe AD, after discussion of potential benefits and uncertainties with the patient. Baseline pruritus NRS was 3. Facial eruption and pruritus began to improve within 3 days. At the 2-week follow-up on April 22, pruritus had resolved (NRS 0), facial erythema and scaling had markedly regressed on clinical photographs (Figure 1A and B), and stapokibart 300 mg was administered again. No additional systemic or topical therapy was used after stapokibart.
At the 2-week follow-up, reduction of the diffuse inflammatory erythema and scaling made persistent telangiectatic and mildly atrophic changes more apparent, prompting reconsideration of the initial AD-like diagnosis and further evaluation for connective tissue disease. Complete blood count showed leukopenia, with a white blood cell count of 2.0 × 109/L, neutrophil count of 1.25 × 109/L, and lymphocyte count of 0.59 × 109/L. Antinuclear antibody testing was positive at 1:320, and myositis-specific antibody testing revealed anti-Mi-2β positivity; anti-dsDNA and other tested myositis-associated antibodies were negative. Muscle-related enzymes were largely within normal limits, including AST 21 U/L, CK 144 U/L, and LDH 202 U/L, with only mild HBDH elevation to 150 U/L.
Based on the evolving cutaneous morphology, telangiectatic and mildly atrophic changes, positive ANA, anti-Mi-2β positivity, absence of muscle symptoms, and normal CK, possible early clinically amyopathic dermatomyositis with facial-predominant cutaneous involvement was considered. The observed improvement after stapokibart should not be interpreted as evidence that stapokibart treats dermatomyositis or controls systemic disease. Continued surveillance for muscle involvement, interstitial lung disease, and malignancy was recommended.
Case 2
A 28-year-old woman with a history of AD had previously received dupilumab for approximately 1 year with generally good disease control. Because her symptoms were adequately controlled, dupilumab was discontinued by the patient. Approximately 3 months later, she developed a new flare concentrated on the head and face, whereas previous lesions had mainly involved the trunk. The flare presented with diffuse facial erythema, mild swelling, and pruritus; baseline NRS and IGA were both 3. No topical therapy or antihistamine was used for the current flare before stapokibart. Because the recurrence was now facial-predominant, the treating team selected stapokibart rather than immediately reintroducing dupilumab, based on accumulated clinical experience with stapokibart in facial AD-like disease and emerging head-and-neck evidence. This was an individualized routine-care choice and was not intended to imply that stapokibart is superior to dupilumab.
On June 5, 2026, she received subcutaneous stapokibart 600 mg. At follow-up on June 12, 2026, the facial eruption had almost completely resolved, with NRS decreasing to 1 and IGA decreasing to 1. No obvious adverse event was reported, and maintenance stapokibart 300 mg was planned. This temporal response is reported descriptively and does not establish comparative efficacy over reintroduction of dupilumab.
Case 3
A 28-year-old woman first presented on May 17, 2025, with a 5-day history of facial erythema and pruritus. She was initially diagnosed with facial dermatitis and treated with oral prednisone acetate 10 mg three times daily, recombinant human epidermal growth factor gel, and oral levocetirizine solution. On May 27, 2025, she returned with recurrent and aggravated facial erythema. Detailed history revealed recurrent facial erythema and pruritus for more than 2 years and a history of allergic rhinitis. Serum IgE was 125 IU/mL. Based on the chronic relapsing course, pruritus, atopic background, and facial-predominant eczema-like lesions, AD was diagnosed.
She was treated with abrocitinib 100 mg once daily for 14 days, topical pimecrolimus cream, and a 7-mg intramuscular injection of compound betamethasone. At follow-up on June 19, 2025, facial erythema had improved during abrocitinib therapy, but recurrence occurred after treatment discontinuation. Long-term maintenance with abrocitinib 100 mg once daily was therefore resumed. However, at follow-up visits on July 30 and August 22, 2025, she continued to report recurrent facial erythema despite abrocitinib maintenance.
On February 3, 2026, she developed newly aggravated facial erythema and swelling and was treated with oral prednisone acetate 10 mg three times daily and moxifloxacin 0.4 g once daily. On March 5, 2026, her facial eruption worsened again, with NRS 4 and IGA 3. Because long-term abrocitinib had not provided adequate control of recurrent facial lesions, abrocitinib was discontinued and replaced by stapokibart; no concomitant abrocitinib was administered. Stapokibart was initiated at a loading dose of 600 mg subcutaneously. At follow-up on March 20, 2026, facial erythema had nearly cleared, with NRS decreasing to 1 and IGA decreasing to 1, and stapokibart 300 mg was administered as consolidation therapy.
After the second injection, during which an autoinjector device was used, she developed a localized injection-site reaction on the lateral aspect of the left upper arm, characterized by painful erythematous swelling and induration approximately 3 cm in radius. The reaction lasted more than 1 week and resolved slowly despite cold compresses and topical desonide. On April 8, 2026, stapokibart 300 mg was continued as maintenance therapy with the autoinjector device, and the facial dermatitis remained well controlled, although local injection-site reaction persisted. On April 22, 2026, because of concern regarding recurrent injection-site reactions, treatment was switched to dupilumab 300 mg for maintenance. Dupilumab 300 mg was continued on May 6 and June 5, 2026. However, on June 10, 2026, facial erythema recurred, with NRS 2 and IGA 2. She was temporarily treated with oral levocetirizine solution, recombinant human epidermal growth factor gel, and tofacitinib citrate 5 mg twice daily. Retreatment with stapokibart 300 mg was planned but was not included in the present analysis.
This sequence raises the possibility of an individual preferential response to stapokibart in this patient’s facial-predominant AD, given the inadequate control during long-term abrocitinib, near-clearance after switching to stapokibart, and recurrence during subsequent dupilumab maintenance. However, this single non-randomized treatment sequence cannot establish comparative superiority and should be considered hypothesis-generating.
Case 4
A 35-year-old woman had a more than 10-year history of recurrent facial erythema and pruritus and a history of allergic rhinitis. On January 23, 2026, physical examination showed diffuse erythema on the face and neck with scattered acneiform lesions. She had received acrivastine capsules, compound glycyrrhizin tablets, topical fluticasone propionate, and other conventional treatments, but the response was poor. Serum IgE was 119 IU/mL. Based on the longstanding relapsing course, prominent pruritus, eczematous morphology, allergic rhinitis, and elevated IgE, the clinical diagnosis of facial-predominant AD was made.
On February 6, 2026, she returned with increased facial erythema. Baseline NRS and IGA were both 3. Considering facial-predominant AD with inadequate response to conventional therapy, subcutaneous stapokibart 600 mg was administered. At follow-up on February 25, the lesions had markedly improved, with NRS decreasing to 0 and IGA decreasing to 1, and stapokibart 300 mg was given as maintenance therapy. Maintenance therapy continued on March 14, March 31, April 15, April 30, May 15, and May 29, 2026. No facial recurrence or adverse event was observed during follow-up. This case represented a typical responder with a well-supported facial-predominant AD phenotype and supported the potential role of stapokibart in appropriately selected patients.
Case 5
A 46-year-old woman presented on May 19, 2026, with an 8-day history of erythema involving the cheeks, perioral area, and perinasal region, accompanied by desquamation and pruritus. Baseline pruritus NRS was 2. She received topical desonide cream, oral acrivastine, and compound glycyrrhizin tablets, but the lesions did not improve and new lesions continued to appear. At follow-up on June 5, 2026, the eruption remained diagnostically undifferentiated although its morphology was AD-like. Considering persistent AD-like facial dermatitis despite initial conventional therapy and the patient’s preference for active treatment after discussion of the potential benefits, uncertainties, and risks, subcutaneous stapokibart 600 mg was administered. This treatment decision was made in routine clinical care and was not directed by the retrospective study.
On June 7, 2026, the second day after injection, facial erythema and pruritus worsened markedly, with increased inflammatory lesions compared with pre-treatment photographs (Figure 1C and D); pruritus NRS increased to 3. Treatment was changed to topical mometasone furoate cream, tofacitinib 5 mg twice daily, and prednisone 10 mg three times daily, after which the acute inflammatory symptoms gradually improved. No biopsy, patch testing, fungal examination, Demodex evaluation, ANA testing, or other definitive diagnostic work-up had been performed before stapokibart. This rapid aggravation was interpreted cautiously as a clinically important nonresponse or paradoxical worsening. Natural disease progression, diagnostic mismatch, contact dermatitis, rosacea-like dermatitis, infection, irritant exposure, or another non-type 2 inflammatory process could not be excluded. This case emphasizes that biologic therapy should not be used blindly in undifferentiated facial dermatitis and that careful phenotyping is essential before IL-4Rα blockade.
Previously Published Index Case
In addition to the five unpublished patients, our previously published pregnancy-associated case of acute eczematous facial dermatitis was referenced only as an index case for contextual discussion.9 That patient experienced rapid short-term improvement after stapokibart therapy during pregnancy. No previously published clinical images or detailed individual case data were reused in the present study.
Discussion
In this five-patient retrospective real-world case series, all three patients with a well-supported facial-predominant AD phenotype (Cases 2–4) showed rapid improvement in facial lesions and pruritus after stapokibart, whereas the atypical or incompletely characterized eruptions in Cases 1 and 5 followed more diagnostically complex and variable courses. Overall tolerability was acceptable: no serious adverse events were observed, although one injection-site reaction led to treatment discontinuation. These findings are preliminary descriptive observations rather than formal efficacy estimates, but they suggest potential clinical value for stapokibart in appropriately selected patients with facial-predominant AD.
This clinical signal is concordant with the established role of IL-4Rα blockade in moderate-to-severe AD,3,4 phase 3 and longer-term evidence for stapokibart,6,7 and emerging head-and-neck-specific data linking clinical response to suppression of the IL-36A axis.8 Our previously published pregnancy-associated facial dermatitis case provides additional clinical context.9 Together, these observations support further study of stapokibart in facial-predominant AD, while the distinct differential diagnosis of facial inflammation means that they should not be extrapolated to diagnostically undifferentiated eruptions.
Cases 2 and 3 also illustrate individualized treatment sequencing. In Case 2, stapokibart was selected after a facial-predominant relapse following discontinuation of previously effective dupilumab. In Case 3, stapokibart replaced long-term abrocitinib and was not used concomitantly with it. The inadequate control during long-term abrocitinib, near-clearance after switching to stapokibart, and recurrence during subsequent dupilumab maintenance raise the possibility of an individual preferential response to stapokibart in this patient’s facial-predominant AD. However, this single non-randomized treatment sequence cannot establish comparative superiority and should be considered hypothesis-generating. A recent real-world study supports the feasibility of switching from dupilumab to stapokibart in AD,10 but comparative effectiveness between IL-4Rα antibodies or versus JAK inhibition remains undetermined.
Case 1 and Case 5 define important diagnostic boundaries. In Case 1, reduction of diffuse erythema and scaling made persistent telangiectatic and mildly atrophic changes more apparent, prompting autoimmune evaluation and consideration of possible early clinically amyopathic dermatomyositis. Clinically amyopathic dermatomyositis requires longitudinal assessment,11 and the limited, mixed literature on IL-4Rα blockade in dermatomyositis does not support interpreting this improvement as evidence of an effect on dermatomyositis or systemic disease.12,13 In Case 5, the AD-like eruption was incompletely characterized and worsened shortly after treatment. Natural progression, diagnostic mismatch, contact dermatitis, rosacea-like dermatitis, infection, irritant exposure, or another non-type 2 process could not be excluded. This contrasting course reinforces that biologic therapy should not be used blindly in undifferentiated facial dermatitis and that unexpected worsening should prompt diagnostic reassessment.
This series has several limitations. The sample size is very small, all patients were treated at a single center, and the full cohort is diagnostically heterogeneous. Diagnostic investigations were individualized rather than standardized, and complete histories of remote prior treatments could not be reconstructed for all patients with long-standing disease. Follow-up duration varied, validated outcome measures were not uniformly applicable across diagnoses, and previous, concomitant, or rescue therapies may confound temporal associations. Patch testing, skin biopsy, fungal examination, Demodex evaluation, dermoscopy, and laboratory investigation were not performed uniformly. In Case 1, pulmonary and malignancy screening had not been completed at manuscript preparation. No causal treatment effect or direct comparison among stapokibart, dupilumab, JAK inhibitors, and conventional therapy can be inferred.
Conclusion
Stapokibart was associated with rapid clinical improvement in the three patients with well-supported facial-predominant AD, suggesting potential clinical value in appropriately selected patients. The contrasting courses in atypical or incompletely characterized facial eruptions underscore that adequate diagnosis and phenotyping should precede IL-4Rα blockade. These preliminary observations warrant further prospective investigation of stapokibart in facial-predominant AD while defining important diagnostic and treatment boundaries.
Funding Statement
This work was supported by the Sanming Project of Medicine in Shenzhen (No. SZSM202103014).
Generative Artificial Intelligence Statement
During preparation of this manuscript, OpenAI ChatGPT (GPT-5.6 Sol) was used only for language editing and structural drafting. All clinical data, diagnostic interpretation, scientific claims, references, and final wording were reviewed and verified by the authors, who take full responsibility for the content.
Abbreviations
AD, atopic dermatitis; ANA, antinuclear antibody; CK, creatine kinase; DLQI, Dermatology Life Quality Index; EASI, Eczema Area and Severity Index; HBDH, alpha-hydroxybutyrate dehydrogenase; IGA, Investigator’s Global Assessment; IL, interleukin; JAK, Janus kinase; NRS, numerical rating scale.
Data Sharing Statement
The data supporting the findings of this study are available from the corresponding author upon reasonable request.
Ethics Approval and Informed Consent
This study was conducted in accordance with the Declaration of Helsinki and was approved by the Scientific Research Ethics Committee of Shenzhen Nanshan People’s Hospital, Shenzhen, China (Approval No. ky-2026-061801). Shenzhen Nanshan People’s Hospital is also known as the Affiliated Nanshan Hospital of Shenzhen University. Written informed consent was obtained from all patients for participation in this study and for publication of their clinical information and images.
Consent for Publication
All patients provided written informed consent for publication of the case details. Patients whose clinical images are included provided written informed consent for publication of the accompanying clinical photographs.
Author Contributions
All authors made a significant contribution to the work reported, whether in study conception, study design, execution, acquisition of data, analysis and interpretation, or all these areas; took part in drafting, revising, or critically reviewing the article; gave final approval of the version to be published; agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.
Disclosure
The authors report no conflicts of interest in this work.
References
- 1.Weidinger S, Novak N. Atopic dermatitis. Lancet. 2016;387:1109–10. doi: 10.1016/S0140-6736(15)00149-X [DOI] [PubMed] [Google Scholar]
- 2.Guttman-Yassky E, Waldman A, Ahluwalia J, Ong PY, Eichenfield LF. Atopic dermatitis: pathogenesis. Semin Cutan Med Surg. 2017;36:100–103. doi: 10.12788/j.sder.2017.036 [DOI] [PubMed] [Google Scholar]
- 3.Beck LA, Thaçi D, Hamilton JD, et al. Dupilumab treatment in adults with moderate-to-severe atopic dermatitis. N Engl J Med. 2014;371:130–139. doi: 10.1056/NEJMoa1314768 [DOI] [PubMed] [Google Scholar]
- 4.Simpson EL, Bieber T, Guttman-Yassky E, et al. Two phase 3 trials of dupilumab versus placebo in atopic dermatitis. N Engl J Med. 2016;375:2335–2348. doi: 10.1056/NEJMoa1610020 [DOI] [PubMed] [Google Scholar]
- 5.Jo CE, Finstad A, Georgakopoulos JR, et al. Facial and neck erythema associated with dupilumab treatment: a systematic review. J Am Acad Dermatol. 2021;84:1339–1347. doi: 10.1016/j.jaad.2021.01.012 [DOI] [PubMed] [Google Scholar]
- 6.Zhao Y, Zhang L, Zhang J; CM310AD005 Study Investigators. Efficacy and safety of stapokibart (CM310) in adults with moderate-to-severe atopic dermatitis: a multicenter, randomized, double-blind, placebo-controlled phase 3 trial. J Am Acad Dermatol. 2024;91:984–986. doi: 10.1016/j.jaad.2024.07.1447 [DOI] [PubMed] [Google Scholar]
- 7.Zhao Y, Zhang L, Wu L, et al. Long-term efficacy and safety of stapokibart for moderate-to-severe atopic dermatitis: 52-week results from a phase 3 trial. Allergy. 2025;80:1348–1357. doi: 10.1111/all.16368 [DOI] [PubMed] [Google Scholar]
- 8.Yang Y, Xu B, Zhang K, et al. IL-36A axis suppression associates with clinical response to stapokibart in head and neck atopic dermatitis-an exploratory proteomic study. J Am Acad Dermatol. 2026:95 2 518–520. doi: 10.1016/j.jaad.2026.04.018 [DOI] [PubMed] [Google Scholar]
- 9.Zhu Y, Chen J, Wang P. Rapid improvement of acute eczematous facial dermatitis during pregnancy following stapokibart therapy: a case report. Clin Cosmet Investig Dermatol. 2026;19:616321. doi: 10.2147/CCID.S616321 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10.Hou L, Li L, Lin M, et al. Real-world Chinese study of the effectiveness and safety of switching from dupilumab to stapokibart in patients with moderate-to-severe atopic dermatitis. Dermatitis. 2026:17103568261429235. doi: 10.1177/17103568261429235 [DOI] [PubMed] [Google Scholar]
- 11.Gerami P, Schope JM, McDonald L, Walling HW, Sontheimer RD. A systematic review of adult-onset clinically amyopathic dermatomyositis (dermatomyositis siné myositis): a missing link within the spectrum of the idiopathic inflammatory myopathies. J Am Acad Dermatol. 2006;54:597–613. doi: 10.1016/j.jaad.2005.10.041 [DOI] [PubMed] [Google Scholar]
- 12.O’Brien MA, Hsu S, Shevchenko A, Quartey A. Dupilumab failure in treating dermatomyositis-associated pruritus. Cureus. 2022;14:e28270. doi: 10.7759/cureus.28270 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 13.Wilson C, Castillo S, Ndoricimpa Y, Malone JC, Strickley J. Dupilumab therapy facilitates the histopathologic diagnosis of dermatomyositis in a patient with intercurrent severe atopic dermatitis and dermatomyositis. JAAD Case Rep. 2026;71:14–16. doi: 10.1016/j.jdcr.2026.02.045 [DOI] [PMC free article] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The data supporting the findings of this study are available from the corresponding author upon reasonable request.