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Clinical-trials landscape

TL;DR — The asthma pipeline has shifted from proving bronchodilation and broad anti-inflammatory efficacy toward upstream alarmins, longer-interval biologics, remission, airway remodeling, attack interception, obesity-associated disease and implementation. The key design change is equally important: future trials must distinguish symptom improvement from severe-attack prevention, oral-steroid sparing, disease modification and equitable delivery. As of a live ClinicalTrials.gov API v2 re-query on 2026-08-30 (statuses rechecked 2026-10-29), active examples include phase 3 dupilumab remission testing ([NCT07309614](https://clinicaltrials.gov/study/NCT07309614){target="_blank" rel="noopener"}), phase 2 high-risk-asthma lunsekimig ([NCT06676319](https://clinicaltrials.gov/study/NCT06676319){target="_blank" rel="noopener"}), emergency-department tezepelumab ([NCT06705764](https://clinicaltrials.gov/study/NCT06705764){target="_blank" rel="noopener"}) and a 2,000-person SMART implementation study ([NCT07241117](https://clinicaltrials.gov/study/NCT07241117){target="_blank" rel="noopener"}). Registry status is provisional, not evidence of efficacy.

How this landscape was assembled

ClinicalTrials.gov API v2 was queried live on 2026-08-29 for six asthma domains: biologics, alarmins, remission/disease modification, digital monitoring, prevention/preschool wheeze and non-eosinophilic/type-2-low disease. The search returned 482 unique registry records. Every tracked identifier was re-fetched individually on 2026-08-30, and focused searches for biologic comparison, withdrawal, pregnancy, type-2-low disease and prevention were repeated. The table below is a purposive horizon scan, not a complete trial registry export.

On 2026-10-15 the periodic sweep re-fetched all 19 tracked records. Two changed status (NCT06818019 and NCT07746921, both now recruiting), and none had posted results. ISRCTN was queried for non-US asthma registrations. Cochrane CENTRAL could not be searched (HTTP 403), so the scan cannot claim completeness for trials registered only outside ClinicalTrials.gov and ISRCTN.

PubMed was queried separately for completed trials and systematic evidence. Every PMID and every NCT identifier on this page was resolved live in this session.

Interpret registry fields cautiously:

  • “recruiting” can lag site-level reality;
  • estimated enrollment and completion can change;
  • a posted primary outcome may be amended;
  • registration does not imply peer review, regulatory endorsement or positive results;
  • completed registry status does not mean results are publicly available.

On 2026-10-22 all 22 currently cited ClinicalTrials.gov records were re-fetched. No recruitment-status change or newly posted results was found versus the 2026-10-15 snapshots; NIMBLE and PERFORM already had results posted. The paediatric digital-management record (NCT06902766), updated 2026-10-16, now estimates primary completion in July 2027 rather than January 2027; it remains recruiting without posted results. The WRAPT ISRCTN API record still lists recruitment beginning 2026-11-09. These are registry observations, not efficacy findings.

On 2026-10-29 the same 22 records plus CHRONICLE ([NCT03373045](https://clinicaltrials.gov/study/NCT03373045){target="_blank" rel="noopener"}) were re-fetched. No recruitment-status change and no newly posted results were found versus 22 October. The anti-TSLP dose-finding record ([NCT06748053](https://clinicaltrials.gov/study/NCT06748053){target="_blank" rel="noopener"}) was updated 2026-10-26; it remains active, not recruiting, with primary completion still 2026-07-14 and no results posted. GATA-3 ([NCT05254314](https://clinicaltrials.gov/study/NCT05254314){target="_blank" rel="noopener"}) still has no results after its 2026-09-28 primary completion date. WRAPT (ISRCTN91904759) still lists recruitment 2026-11-09 to 2027-10-31 (record last updated 2026-10-09).

What established the present platform

Development Landmark signal What remained unanswered
Early ICS in mild disease Budesonide reduced severe events, HR 0.56 (95% CI 0.45–0.71) (Pauwels 2003, PMID 12672309) Prevention versus suppression; minimum exposure
Anti-inflammatory reliever As-needed budesonide–formoterol reduced severe attacks versus SABA alone, rate ratio 0.36 (0.27–0.49) (O'Byrne 2018, PMID 29768149) Pediatric formulations, implementation and long-term trajectories
Anti-IgE Omalizumab established targeted therapy for allergic severe asthma (Hanania 2011, PMID 21536936) Reliable individual response prediction
Anti-IL-5 Mepolizumab cut attacks in selected eosinophilic disease (Pavord 2012, PMID 22901886) Remission, withdrawal and residual non-eosinophilic attacks
Anti-IL-4Rα Dupilumab linked response to eosinophil/FeNO biology (Castro 2018, PMID 29782217) Comparative selection and long-term modification
Anti-TSLP Tezepelumab reduced attacks across broad biomarker strata (Menzies-Gow 2021, PMID 33979488) Which low-marker patients derive clinically meaningful absolute benefit
Macrolide strategy AMAZES reduced exacerbations in persistent uncontrolled adult asthma (Gibson 2017, PMID 28687413) Resistance ecology and responder definition

These successes define the new comparator problem: placebo on top of optimized care, active biologic comparison, and implementation against real access barriers are more informative than another short symptom-only study.

Active horizon scan

Status and registry details below are as posted on 2026-08-30.

Upstream and next-generation biologics

Trial Registry status; design Population/enrollment Primary question
Lunsekimig high-risk asthma [NCT06676319](https://clinicaltrials.gov/study/NCT06676319){target="_blank" rel="noopener"}; active, not recruiting; phase 2 Adults 18–80; actual n=556 Annualized exacerbation rate through 52 weeks
Verekitug VALOUR [NCT06966479](https://clinicaltrials.gov/study/NCT06966479){target="_blank" rel="noopener"}; active, not recruiting; phase 2 Severe adult asthma; actual n=396 Long-term adverse and serious adverse events to week 64
GSK5784283 dose finding [NCT06748053](https://clinicaltrials.gov/study/NCT06748053){target="_blank" rel="noopener"}; active, not recruiting; phase 2 Uncontrolled asthma age 18–75; actual n=307 FeNO change across doses through week 26
CDX-622 first asthma cohort [NCT07330778](https://clinicaltrials.gov/study/NCT07330778){target="_blank" rel="noopener"}; recruiting; phase 1 Mild-to-moderate adult asthma; estimated n=12 Safety/tolerability through day 85
Depemokimab age 6–11 [NCT07671001](https://clinicaltrials.gov/study/NCT07671001){target="_blank" rel="noopener"}; recruiting; phase 3 Children 6–11; estimated n=34 Plasma concentration through week 52

Lunsekimig is positioned in high-risk disease and uses attacks as the principal endpoint. GSK5784283 instead uses FeNO change as a phase 2 primary endpoint, a pharmacodynamic decision signal rather than direct proof of patient benefit. CDX-622 is an early safety study whose sample is intentionally too small to establish efficacy.

Longer-interval depemokimab development tests whether dosing convenience can preserve biologic effect. The pediatric study’s primary pharmacokinetic endpoint is appropriate for bridging but does not independently establish comparative clinical benefit.

Attack interception

TERAA tests a single tezepelumab strategy in adults presenting with emergency-room asthma, with moderate/severe exacerbations through 90 days as primary outcome; it is phase 4, recruiting, estimated n=100 ([NCT06705764](https://clinicaltrials.gov/study/NCT06705764){target="_blank" rel="noopener"}).

This changes timing from chronic prevention to event-linked intervention. Key interpretation issues will include standard acute therapy, phenotype at presentation, discharge adherence and whether benefit extends beyond suppressing one post-attack high-risk window.

Biomarker-defined hospitalized attacks are heterogeneous and can shift at recurrence, supporting prospective sampling rather than assuming every attack reproduces the stable-state phenotype (Ghanizada 2024, PMID 39169832).

Remission and remodeling

Trial Design Endpoint concept
Dupilumab remission trial [NCT07309614](https://clinicaltrials.gov/study/NCT07309614){target="_blank" rel="noopener"}; recruiting phase 3; adults; estimated n=150 Win ratio based on remission criteria through week 56
ReNORM [NCT07174713](https://clinicaltrials.gov/study/NCT07174713){target="_blank" rel="noopener"}; not yet recruiting; observational/interventional biologic cohort; n=200 Imaging, spirometric and symptom remission at years 1–2
Depemokimab imaging/bronchoscopy substudy [NCT06979323](https://clinicaltrials.gov/study/NCT06979323){target="_blank" rel="noopener"}; recruiting phase 3; n=150 Change in total mucus-plug volume at week 26
Dupilumab withdrawal [NCT06818019](https://clinicaltrials.gov/study/NCT06818019){target="_blank" rel="noopener"}; recruiting phase 4 (was not yet recruiting on 2026-08-30); estimated n=205 Strategy failure over 24 months after stopping dupilumab

“Remission” is not yet a single endpoint. Candidate domains include no severe attacks, no systemic corticosteroids, controlled symptoms, stable/normal lung function, suppressed inflammation and absence of treatment toxicity. Trials must state whether remission is on treatment or after withdrawal.

Mucus-plug imaging creates an intermediate structural endpoint. A treatment can reduce plugs without proving durable modification; conversely, attacks can fall without complete imaging resolution.

Systematic review of severe-asthma biologic cohorts found variable remission definitions and attainment, limiting cross-study comparison (Shackleford 2025, PMID 39549709). A core outcome set is needed before “remission-inducing” becomes a marketing label.

Two 2026 publications move this forward without settling it. A modified Delphi process proposed paired definitions of remission and a less stringent minimal clinical disease activity state in severe asthma, spanning exacerbations, steroid use, lung function and quality of life. Its authors state the definitions still need real-world validation (Couillard 2026, PMID 42463041; abstract-level). The open-label pragmatic PERFORM trial (n=1,236; [NCT06372496](https://clinicaltrials.gov/study/NCT06372496){target="_blank" rel="noopener"}) used remission as a prespecified secondary outcome at week 52. It reached 29.7% (184/619) with single-inhaler fluticasone furoate/umeclidinium/vilanterol versus 17.0% (105/617) with usual-care ICS/LABA (adjusted OR 2.13, 95% CI 1.54–2.94), and results were consistent across alternative definitions (Noorduyn 2026, PMID 42474701; figures checked against the open full text). Remission is therefore now an inhaled-therapy endpoint too, not only a biologic one.

The withdrawal registration corrects a previously stale evidence-gap formulation: as of 2026-08-30, a prospective stopping strategy is registered, but recruitment has not started and no outcome result is available. The unresolved question is therefore not whether a withdrawal study exists, but whether its strategy can identify durable off-treatment control without excess failure.

Pregnancy-safety evidence generation

Asthma pregnancy evidence remains observational rather than pivotal-RCT evidence, but it is not an empty registry landscape. A completed North American post-authorization study enrolled 581 dupilumab-exposed or comparator pregnancies and included asthma among eligible conditions ([NCT04173442](https://clinicaltrials.gov/study/NCT04173442){target="_blank" rel="noopener"}); the historical omalizumab EXPECT registry completed with 309 participants ([NCT00373061](https://clinicaltrials.gov/study/NCT00373061){target="_blank" rel="noopener"}). A benralizumab exposure study terminated after enrolling 299 participants ([NCT03794999](https://clinicaltrials.gov/study/NCT03794999){target="_blank" rel="noopener"}). Registry completion or enrollment does not establish comparative safety; posted results, disease-severity adjustment and infant follow-up determine what can be inferred.

Obesity-associated asthma

A phase 3 trial plans metformin versus placebo in children aged 10–17 with obesity-associated asthma, estimated n=182, with 26-week ACT change as primary outcome ([NCT07622290](https://clinicaltrials.gov/study/NCT07622290){target="_blank" rel="noopener"}).

The trial targets metabolic biology rather than escalating airway immunosuppression. Its symptom-score endpoint should be interpreted alongside attacks, lung function, weight/metabolic change and adverse effects. Obesity-related breathlessness can improve without changing airway inflammation, and vice versa.

Incretin therapy is now under placebo-controlled test. GATA-3, a single-centre US phase 2 trial of semaglutide versus placebo (estimated n=100; ACQ-7 and serum periostin primary), reached primary completion on 2026-09-28 with no results posted ([NCT05254314](https://clinicaltrials.gov/study/NCT05254314){target="_blank" rel="noopener"}). A UK phase 2 trial, WRAPT (ISRCTN91904759, registered 2026-09-21), plans 138 adults with obesity and poorly controlled asthma (ACQ-7 >1.5) on at least moderate-dose MART. They will be randomized 1:1 to tirzepatide up-titrated to 15 mg weekly or an identical saline injection for 52 weeks, with counselling in both arms. ACQ-7 is the primary outcome and mechanisms are secondary. Recruitment is listed to start 2026-11-09. A 2026 systematic review found that observational GLP-1 receptor agonist data consistently associate with fewer exacerbations in people with obesity and/or type 2 diabetes, while airway-intrinsic effects remain largely preclinical (Saadat 2026, PMID 42167405; abstract-level). GATA-3 and WRAPT are the kind of randomized test that review calls for.

Weight-loss RCT review suggests clinically relevant control gains in some adults and mixed pediatric effects, but trials remain small and heterogeneous (Okoniewski 2019, PMID 30605347).

Type-2-low and provocation biology

A phase 1 nasal endotoxin-challenge study plans single-cell RNA sequencing of neutrophil heterogeneity in adults with asthma, estimated n=60 ([NCT06270576](https://clinicaltrials.gov/study/NCT06270576){target="_blank" rel="noopener"}). Its registry status is “not yet recruiting” despite an estimated April 2024 start, an internal inconsistency that requires direct site confirmation.

Challenge studies can establish pathway engagement with small samples but may not reproduce spontaneous infection/pollution-driven attacks. The major type-2-low gap remains a validated marker-treatment pair with attack reduction.

Macrolide meta-analysis and AMAZES support efficacy in some uncontrolled asthma, but antimicrobial resistance, cardiac/hearing risk and unclear mechanistic selection prevent indiscriminate use (Gibson 2017, PMID 28687413; Ohnishi 2024, PMID 38296770).

A 2026 GRADE meta-analysis of 19 RCTs (n=1,825), done for forthcoming AAAAI/ACAAI severe-asthma practice parameters, found high-certainty improvement in ACQ-6 (mean difference −0.23, 95% CI −0.32 to −0.13) and moderate-certainty reduction in severe exacerbations (IRR 0.75, 0.57–0.98; 0.26 fewer events per patient-year), with little to no effect on serious adverse events or mortality. Relative effects were similar in type-2-high and type-2-low asthma (Ologundudu 2026, PMID 41654262; abstract-level). That last finding weakens the use of macrolides as a type-2-low-specific option, and the abstract does not report antimicrobial-resistance outcomes.

Digital monitoring and implementation

Trial Population/enrollment Intervention and main outcome
CHEST SMART implementation [NCT07241117](https://clinicaltrials.gov/study/NCT07241117){target="_blank" rel="noopener"}; recruiting phase 4; age ≥12; n=2,000 Community-health-center implementation bundle; patient effectiveness, clinician adoption and clinic prescribing
Pediatric digital management [NCT06902766](https://clinicaltrials.gov/study/NCT06902766){target="_blank" rel="noopener"}; recruiting; age 4–12; n=50 Active digital-inhaler telemonitoring; change in composite severity index at 8 months
Smart inhaler in intellectual/developmental disability [NCT07746921](https://clinicaltrials.gov/study/NCT07746921){target="_blank" rel="noopener"}; recruiting (was not yet recruiting on 2026-08-30); age 10–17; n=34 Active versus passive remote system; feasibility, acceptability and usability

A separate, already-published single-centre pilot RCT in 28 adolescents with intellectual and developmental disabilities found an audiovisual-feedback smart inhaler feasible and acceptable. Observer-rated inhaler proficiency improved by 1.5 points (95% CI 0.4–2.6) versus education alone, with no difference in lung function (Park 2026, PMID 42413691; abstract-level).

CHEST treats uptake as a co-primary scientific problem, which is appropriate when efficacy already exceeds routine adoption. It should report reach, fidelity and disparities as well as prescribing.

The disability-focused smart-inhaler trial addresses a population commonly excluded from digital research. Feasibility is an appropriate first endpoint, but later trials must measure caregiver workload, accessibility, control, attacks and privacy harms.

Digital interventions improved adherence more reliably than attacks in a 40-RCT Cochrane review (Chan 2022, PMID 35691614). An electronic-monitor meta-analysis found adherence SMD 0.41 (95% CI 0.22–0.60) but uncertain ACT improvement, SMD 0.47 (−0.14 to 1.08) (Garin 2023, PMID 36986513).

Prevention and environmental modification

A cluster-style kindergarten rewilding study is recruiting 320 children aged 1–5, comparing biodiversity intervention with playground equipment; its primary endpoint is skin Gammaproteobacteria through three years ([NCT06390878](https://clinicaltrials.gov/study/NCT06390878){target="_blank" rel="noopener"}).

This is a mechanistic prevention study, not yet a test that rewilding prevents asthma. Microbial endpoints need linkage to clinical allergic/wheeze outcomes and assessment of exposures, geography and unintended harms.

Early ICS in high-risk preschool children improved disease during treatment but did not change the post-withdrawal course (Guilbert 2006, PMID 16687711). Prevention trials therefore need off-treatment clinical endpoints and long follow-up.

Pipeline by biological layer

Layer Established targets Current frontier Main failure mode
Bronchoconstriction β2-agonist, antimuscarinic Combined anti-inflammatory rescue Symptom relief without risk reduction
Adaptive type-2 IgE, IL-5/5R, IL-4Rα Better selection, switching, withdrawal Biomarker overlap and no direct comparisons
Epithelial alarm TSLP IL-33/ST2 and multi-alarmin approaches Biology may not translate to incremental benefit
Mucus/remodeling Indirect biologic effects Plug imaging, structural and vascular reversal Surrogate change without durable outcomes
Non-type-2 Macrolide in selected adults Neutrophil/protease/metabolic targets Unstable phenotype and infection confounding
Delivery/system Action plans, adherence support SMART implementation, accessible monitoring Digital divide and surveillance burden
Prevention Exposure reduction, sensitization research Microbiome/biodiversity, early risk modification Long latency and phenotype dilution

Trial-design priorities

Choose endpoints that patients feel

Domain Preferred measure
Attacks Annualized severe attacks plus proportion attack-free
Steroid harm Cumulative systemic dose, maintenance dose and toxicity
Symptoms Validated control score with minimal important difference
Function Pre/post-bronchodilator FEV1, activity and work/school participation
Quality of life Validated patient-reported instrument
Safety Serious events plus mechanism-specific surveillance
Equity Enrollment, retention and benefit by access-relevant strata

Composite remission endpoints should not allow a large biomarker change to compensate for continued attacks. Hierarchical win-ratio approaches need transparent ordering and component results.

Improve comparators

  • biologic head-to-head trials in overlapping eligibility;
  • optimized usual care with documented technique/adherence;
  • active reliever comparators rather than obsolete SABA-only care where inappropriate;
  • pragmatic formulary and access comparisons;
  • withdrawal studies after sustained response;
  • mechanism-specific add-on designs for residual attacks.

Network meta-analyses can compare biologics indirectly but inherit cross-trial differences in eligibility, biomarkers, OCS use and endpoints (Edris 2019, PMID 31395084). They do not replace randomized head-to-head trials.

A CHRONICLE self-controlled case-series (480 adults with a severe exacerbation, 85 US sites; [NCT03373045](https://clinicaltrials.gov/study/NCT03373045){target="_blank" rel="noopener"}) found biologics associated with fewer severe exacerbations in exposed versus unexposed periods (IRR 0.43, 95% CI 0.39–0.48), close to a pooled rate ratio of 0.53 (0.47–0.60) from six pivotal RCTs of FDA-approved biologics. Four RCT-style eligibility cuts modified that real-world association (ratio of IRRs, exclusion as reference): smoking ≥10 pack-years 0.50 (0.38–0.66), ≥2 versus 1 prior-year exacerbation 0.49 (0.36–0.65), FeNO ≥50 ppb 0.63 (0.42–0.92), and blood eosinophils ≥300/µL 0.65 (0.51–0.82). COPD, bronchiectasis, FEV1 % predicted, FEV1/FVC and bronchodilator reversibility did not (Boakye-Dankwa 2026, PMID 42242757; full text, Table 2). The authors note residual time-varying confounding, pooled-biologic analysis, and that many participants already on a biologic at enrolment were excluded. Spirometry-based exclusions therefore look less informative for trial success than type-2 biomarkers, smoking history and exacerbation frequency.

Represent the population

Pregnant people, older adults, smokers, people with multimorbidity, low-resource populations and those with cognitive/disability-related support needs are underrepresented. Pediatric bridging must account for dose, device, development and natural history, not only body weight.

Severe-asthma registries show substantial geographic and treatment heterogeneity, making external validity a design requirement (Wang 2020, PMID 31785254).

Reading a new trial result

  1. Was asthma objectively confirmed?
  2. Was background therapy optimized and actual adherence measured?
  3. Was the population enriched by attack history and a plausible target?
  4. Is the outcome a patient benefit, surrogate or implementation measure?
  5. Report both relative and absolute effects with confidence intervals.
  6. Examine every component of composites.
  7. Check missing data, estimand, multiplicity and early stopping.
  8. Compare harms, burden and cost with realistic alternatives.
  9. Ask whether sites and participants resemble intended practice.
  10. Confirm registry-specified outcomes against the publication.

Open questions

References

  1. ClinicalTrials.gov API v2. Live asthma landscape re-query, 2026-08-30. NCT07309614; NCT07671001; NCT06676319; NCT06966479; NCT06748053.
  2. ClinicalTrials.gov API v2. Live asthma landscape re-query, 2026-08-30. NCT06705764; NCT07330778; NCT07622290; NCT07746921; NCT07241117.
  3. ClinicalTrials.gov API v2. Live asthma landscape re-query, 2026-08-30. NCT06902766; NCT06390878; NCT06270576; NCT07174713; NCT06979323; NCT06818019.
  4. ClinicalTrials.gov API v2. Live pregnancy-safety re-query, 2026-08-30. NCT04173442; NCT00373061; NCT03794999.
  5. Pauwels RA, et al. Early intervention with budesonide in mild persistent asthma. Lancet. 2003. PMID 12672309
  6. O'Byrne PM, et al. As-needed budesonide–formoterol in mild asthma. N Engl J Med. 2018. PMID 29768149
  7. Hanania NA, et al. Omalizumab in severe allergic asthma inadequately controlled with standard therapy. Ann Intern Med. 2011. PMID 21536936
  8. Pavord ID, et al. Mepolizumab for severe eosinophilic asthma: DREAM. Lancet. 2012. PMID 22901886
  9. Castro M, et al. Dupilumab efficacy and safety in uncontrolled asthma. N Engl J Med. 2018. PMID 29782217
  10. Menzies-Gow A, et al. Tezepelumab in severe uncontrolled asthma. N Engl J Med. 2021. PMID 33979488
  11. Gibson PG, et al. Azithromycin in persistent uncontrolled asthma: AMAZES. Lancet. 2017. PMID 28687413
  12. Ghanizada M, et al. Biomarker-defined infective and inflammatory hospitalized-attack phenotypes. J Asthma. 2024;61(12):1715-1726. PMID 39169832
  13. Shackleford TK, et al. Severe-asthma biologic remission: systematic review and meta-analysis. Lancet Respir Med. 2025;13(1):23-34. PMID 39549709
  14. Okoniewski W, et al. Weight loss in obesity and asthma: systematic review. Ann Am Thorac Soc. 2019. PMID 30605347
  15. Ohnishi H, et al. Macrolides in adult asthma: systematic review and meta-analysis. Allergol Int. 2024;73(3):382-389. PMID 38296770
  16. Chan A, et al. Digital interventions to improve asthma maintenance adherence. Cochrane Database Syst Rev. 2022. PMID 35691614
  17. Garin N, et al. Electronic inhaler monitoring: systematic review and meta-analysis. Pharmaceuticals. 2023. PMID 36986513
  18. Guilbert TW, et al. Long-term ICS in preschool children at high asthma risk. N Engl J Med. 2006. PMID 16687711
  19. Edris A, et al. Monoclonal antibodies in type-2 asthma: systematic review and network meta-analysis. Respir Res. 2019. PMID 31395084
  20. Wang E, et al. Characterization of severe asthma worldwide: ISAR. Chest. 2020. PMID 31785254
  21. ClinicalTrials.gov API v2. Periodic-sweep re-fetch of all 19 tracked records, 2026-10-15; PERFORM record NCT06372496 and GATA-3 record NCT05254314 fetched the same day.
  22. ISRCTN registry. WRAPT: Weight Reduction in Asthma Programme with Tirzepatide. ISRCTN91904759, record retrieved 2026-10-15.
  23. Ologundudu LM, et al. Macrolides for asthma: a systematic review and meta-analysis of randomized trials. J Allergy Clin Immunol. 2026;158(4):970-981. PMID 41654262
  24. Couillard S, et al. Defining minimal clinical disease activity and remission in severe asthma: a modified Delphi consensus. J Allergy Clin Immunol Pract. 2026;14(10):2262-2275.e3. PMID 42463041
  25. Noorduyn SG, et al. Clinical remission with FF/UMEC/VI versus ICS/LABA in uncontrolled asthma: the PERFORM pragmatic randomized controlled trial. Adv Ther. 2026;43(10):4730-4748. PMID 42474701
  26. Saadat S, et al. Glucagon-like peptide-1 receptor agonists in asthma and obesity-associated asthma: a systematic review of clinical outcomes and translational mechanisms. J Allergy Clin Immunol Pract. 2026;14(9):2070-2082.e10. PMID 42167405
  27. Park S, et al. Smart inhaler randomized controlled trial for improving inhaler technique in adolescents with intellectual and developmental disabilities and asthma. Acad Pediatr. 2026;26(7):103387. PMID 42413691
  28. ClinicalTrials.gov API v2. All 22 cited records re-fetched 2026-10-22; digital-management NCT06902766 updated 2026-10-16. ISRCTN API: ISRCTN91904759 re-fetched 2026-10-22 (record last updated 2026-10-09).
  29. Boakye-Dankwa E, et al. Clinical trial eligibility criteria and biologic-associated reductions in severe asthma exacerbations: CHRONICLE self-controlled case series. Eur Respir J. 2026;68(4). PMID 42242757
  30. ClinicalTrials.gov API v2. All 22 previously cited records plus NCT03373045 re-fetched 2026-10-29; NCT06748053 last updated 2026-10-26. ISRCTN API: ISRCTN91904759 re-fetched 2026-10-29 (recruitment 2026-11-09 to 2027-10-31; record last updated 2026-10-09).