Asthma; EosinophilicPhase 4BREATHNCT06288516
BenRalizumab Effect on Airway Remodeling in Severe asTHma
A Phase 4 study testing Benralizumab 30 mg/ml in people with Asthma; Eosinophilic and Airway Remodeling, run by Aristotle University Of Thessaloniki at 1 site in Greece.
Trial summary
Response to biologic therapies in severe asthma is variable, with patients being either non-responders, responders or super-responders. There is currently no explanation for this broad variation in response. Read more about this study
- Who is it for?
- Ages 18 to 85 years
- Conditions the study is for
- Asthma; Eosinophilic, Airway Remodeling
- What is being tested?
- Benralizumab 30 mg/ml
- Type of treatment
- Injection or infusion
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 36 participants
- Where
- 1 siteGreece
- Study dates
- 1 Mar 2024to 27 Oct 2026
- Phase
- Phase 4
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 85 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- Written informed consent must be obtained at screening visit, before any assessment will be performed. Subjects should be able to provide informed written consent (study participation informed consent form): Able to give written informed consent prior to participation in the study, which will include the ability to comply with the requirements and restrictions listed in the consent form. Subjects must be able to read, comprehend, and write at a level sufficient to complete study related materials.
- Confirmed severe asthma diagnosis and treatment requirements according to American Thoracic Society(ATS)/European Respiratory Society (ERS) guidelines and Global Initiative for Asthma (GINA) 2023.
- Blood eosinophils ≥150cells/ul at screening visit or ≥300cells/ul the last 12 months.
- Patients with history ≥ 1 exacerbation the previous year under the treatment of high dose of inhaled corticosteroid(ICS)+LABA±LAMA or receiving oral/systemic corticosteroids at least 3 days. For subjects on maintenance oral corticosteroids, an exacerbation requiring oral corticosteroids was defined as the use of oral/systemic corticosteroids at least double the existing dose for at least 3 days.
- Meet requirements for biologic therapy with Benralizumab.
Who cannot join
- Asthma exacerbation, within 6 weeks prior to screening that required hospitalization or emergency room visit.
- Prior use of other biologics that has potential to interfere/ affect disease progression.
- Pregnant or nursing women, or women of child-bearing potential.
- History of malignancy of any organ system or any other serious co-morbidities defined by the treating physician.
- Patients with a history of conditions other than asthma that could result in elevated eosinophils (e.g. hypereosinophilic syndromes, Churg-Strauss Syndrome, eosinophilic esophagitis).
Trial locations and contacts
1 site in 1 country.
Greece1 site
Pulmonary Clinic, Aristotle University of Thessaloniki, George Papanikolaou Hospital
Thessaloniki, Thessaloniki, 57010
About this study
Official title: BenRalizumab Effect on Airway Remodeling in Severe Eosinophilic asTHmatics
Response to biologic therapies in severe asthma is variable, with patients being either non-responders, responders or super-responders. There is currently no explanation for this broad variation in response. It is important to examine whether these patients have distinct characteristics that could help the treating physician in making the correct diagnosis in clinical practice.
Aim of this clinical study is to evaluate the efficacy of benralizumab, a humanized an anti-interleukin 5 receptor α monoclonal antibody in patients with severe eosinophilic asthma and to evaluate airway remodeling before and after benralizumab treatment.
Read more
Hypothesis Identification of pathological and clinical characteristics in patients with severe eosinophilic asthma after benralizumab treatment regarding the airway remodeling, inflammatory cells, and other biomarkers on a long-term basis.
Research questions Is there any improvement in airway remodeling? Are there any biomarkers to predict response to benralizumab treatment in severe eosinophilic asthmatic patients?
Read the detailed description
Interleukin (IL)-5 is the main cytokine responsible for the activation of eosinophils, hence therapeutic strategies have been investigated and developed for clinical use. Biologics targeting IL-5 and its receptor have been recently approved and used as add-on therapy for severe eosinophilic asthma resulting in a reduction in the circulating eosinophil count, improvement in lung function and exacerbation reduction in patients with severe asthma.
Response to biologic therapies in severe asthma is variable, with patients being either non-responders, responders or super-responders. There is currently no explanation for this broad variation in response. It is important to examine whether these patients have distinct characteristics that could help the treating physician in making the correct diagnosis in clinical practice.
Aim of this clinical study is to evaluate the efficacy of benralizumab, a humanized an anti-interleukin 5 receptor α monoclonal antibody in patients with severe eosinophilic asthma and to evaluate airway remodeling before and after benralizumab treatment. Every patient will be a control to himself by comparing baseline's biomarker measurements of each patient to the following timepoint's measurements. However, we have added 10 severe asthmatics with no intervention, receiving standard of care as control groups to make more comparisons.
Several methods are used to investigate airway inflammation: direct measurements (like bronchial biopsies or bronchoalveolar lavages) and indirect methods (like symptom assessment, blood sample analysis and lung function tests). The direct techniques have the advantage of reliably assessing the airway inflammation, but they are invasive and not feasible at large scale because of patient discomfort and the risk incurred. As for the indirect methods, they poorly correlate with the direct assessment of airway inflammation.
In this study, among patients' clinical characteristics spirometry, biomarkers of inflammation such as blood eosinophils, Fractional Exhaled Nitric Oxide (FeNO), immunoglobulin E (IgE) levels), and airway remodeling via bronchoscopy will be evaluated. The precise effects of increased airway smooth muscle area on airway narrowing are not known and may vary with disease severity. In addition, biomarkers of inflammation will also be evaluated before and after 52-week of benralizumab treatment in biological fluids (serum and bronchial samples). Biomarkers of inflammation are very important to identify treatment response.
Besides, asthmatic disease is characterized by a chronic mucosal inflammatory process, which results in irreversible changes of the bronchial wall, known today as "bronchial remodeling". Glandular and smooth muscle fibers hyperplasia and/or hypertrophy, goblet cells hyperplasia, and variable thickening of basement membrane (BM) present under the respiratory epithelium are part of these morphological changes. the changes generated at the epithelium-connective interface account for an "adaptive response" to inflammatory stress and sporadic bronchoconstriction. However, current data on BM reactivity in asthmatic patient are still incomplete for an accurate assessment of its involvement in pathogenesis and specifically in bronchial wall remodeling, mainly as collagen deposits in lamina reticularis are not correlated to the degree of disease severity.
Moreover, it is increasingly evident that severe asthma is not a single disease, as evidenced by the variety of clinical presentations, physiologic characteristics, and outcomes seen in patients with asthma. To better understand this heterogeneity, the concept of asthma phenotyping and endotyping has emerged. Phenotyping integrates both biological and clinical features, from molecular, cellular, morphologic, and functional to patient-oriented characteristics with the goal to improve therapy. Ultimately, these phenotypes evolve into asthma "endotypes," which combine clinical characteristics with identifiable mechanistic pathways. Biomarkers, defined as characteristics that can be objectively measured and serve as an indicator of underlying biological processes or pathogenesis, are crucial in defining phenotypes and endotypes. In asthma, genetic polymorphisms, measures of airway physiology, and levels of inflammatory mediators in urine, blood, sputum, tissue, exhaled gas, and breath condensate have all been studied as potential markers to improve and objectify asthma diagnosis and management. Developing such tools will allow us to phenotype and endotype the various clinical patterns described in asthma, with the ultimate goal of tailoring therapy based on a specific biomarker profile. Biomarkers can then be used to help better understand the pharmacologic response to an intervention and adjust therapy accordingly.
Biomarkers have been critical for studies of disease pathogenesis and the development of new therapies in severe asthma. In particular, biomarkers of type 2 inflammation have proven valuable for endotyping and targeting new biological agents. Because of these successes in understanding and marking type 2 inflammation, lack of knowledge regarding non-type 2 inflammatory mechanisms in asthma will soon be the major obstacle to the development of new treatments and management strategies in severe asthma. Other potential biomarkers include innate lymphoid cells, IL-33 or thymic stromal lymphopoietin.
- Conditions
- Asthma; Eosinophilic, Airway Remodeling
- Being tested
- Benralizumab 30 mg/ml
- Keywords
- severe asthma, airway remodeling, eosinophilic, biomarkers, bronchoscopy
- Medical subject headings
- Pulmonary Eosinophilia, Airway Remodeling, Asthma
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Benralizumab 30 mg/mlDrug
Also called biological
Benralizumab administered subcutaneously every 4 weeks for the first 3 dose and then every 8 weeks
| Study group | Role | What they receive |
|---|---|---|
| Benralizumab Arm A | Experimental | Benralizumab (30mg) administered subcutaneously every 4 weeks for the first 3 dose and then every 8 weeks. Receives: Drug: Benralizumab 30 mg/ml |
| No intervention Arm B | No intervention | No intervention. Standard of care as treatment. |
What is being measured
The primary outcome is the main question the study is designed to answer.
Change in sub-basement membrane thickness
The identification of clinical characteristics of non-responders and super-responders. Any improvement in this parameter will be measured as change from baseline compared to measurement after 1 year of treatment.
Measured: through study completion, 52 weeks
Change in airway smooth muscle area
The identification of clinical characteristics of non-responders and super-responders. Any improvement in this parameter will be measured as change from baseline compared to measurement after 1 year of treatment.
Measured: through study completion, 52 weeks
Change in airway smooth muscle layer thickness
The identification of clinical characteristics of non-responders and super-responders. Any improvement in this parameter will be measured as change from baseline compared to measurement after 1 year of treatment.
Measured: through study completion, 52 weeks
Change in submucosal eosinophil number
The identification of clinical characteristics of non-responders and super-responders. Any improvement in this parameter will be measured as change from baseline compared to measurement after 1 year of treatment.
Measured: through study completion, 52 weeks
Change in epithelial integrity
The identification of clinical characteristics of non-responders and super-responders. Any improvement in this parameter will be measured as change from baseline compared to measurement after 1 year of treatment.
Measured: through study completion, 52 weeks
Change in collagen thickness
The identification of clinical characteristics of non-responders and super-responders. Any improvement in this parameter will be measured as change from baseline compared to measurement after 1 year of treatment, measured by electron microscopy.
Measured: through study completion, 52 weeks
Secondary outcomes (4)
Change of cytokine and protein levels
To identify any possible biomarkers of response of non-responders versus super-responders in different biological fluids as peripheral blood and bronchial washing. The identification of clinical characteristics of non-responders and super-responders.
Change from baseline compared to measurements after 6 months and after 1 year of benralizumab treatment.
Measured: through study completion, 52 weeks
Change in exacerbation rate
Measurement of the change in exacerbation rate in each severe eosinophilic asthmatic patient under benralizumab treatment for 52 weeks of treatment.
Measured: through study completion, 52 weeks
Change in blood eosinophil levels
Measurement of the change in blood eosinophil levels in each severe eosinophilic asthmatic patient under benralizumab treatment for 52 weeks of treatment.
Measured: through study completion, 52 weeks
dentification of clinical characteristics of response, change in Forced Expiratory Volume (FEV1)
The identification of clinical characteristics of non-responders and super-responders. FEV1 change from baseline, before treatment initiation, compared to measurements every 3 months until 1 year of treatment. FEV1 is the maximal amount of air you can forcefully exhale in one second measured by spirometry.
Measured: through study completion, 52 weeks
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted1 Mar 2024
- Study start1 Mar 2024
- Primary completion31 Aug 2026
- Study completion27 Oct 2026
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (6)Papers the sponsor has linked to this study.
- Other trials for Asthma; EosinophilicStudies of the same condition, open and under way.
- More trials run by Aristotle University Of ThessalonikiThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 4
- Primary purpose
- Treatment
- Allocation
- Non-randomised
- Intervention model
- Parallel groups
- Model description
- Benralizumab (30mg) administered subcutaneously every 4 weeks for the first 3 dose and then every 8 weeks
- Masking
- None (open label)
- Enrolment
- 36 participants (actual)
Sponsor and investigators
- Lead sponsor
- Aristotle University Of Thessaloniki
- Sponsor type
- University, hospital or other
- Collaborators
- Pulmonary Clinic, University of Ioannina, Pulmonary Clinic, Democritus University of Thrace, National and Kapodistrian University of Athens, University Hospital of Crete, University Hospital of Patras
- Responsible party
- Principal investigator, Kalliopi Domvri, Aristotle University Of Thessaloniki
- Investigators
- Kalliopi Domvri, Dr, Principal investigator, Aristotle University Of Thessaloniki
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06288516
- Sponsor's protocol ID
- 7484
- Acronym
- BREATH
- Status last verified
- Oct 2026
- First submitted
- 25 Feb 2024
- Last updated
- 28 Oct 2026
- Results posted
- No
- Data monitoring committee
- Yes
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Yes: A reference of the published article will be shared here.
Publications
Kuo CW, Liao XM, Huang YC, Chang HY, Shieh CC. Bronchoscopy-guided bronchial epithelium sampling as a tool for selecting the optimal biologic treatment in a patient with severe asthma: a case report. Allergy Asthma Clin Immunol. 2019 Nov 27;15:76. doi: 10.1186/s13223-019-0378-6. eCollection 2019.
PubMed 31798645Bara I, Ozier A, Tunon de Lara JM, Marthan R, Berger P. Pathophysiology of bronchial smooth muscle remodelling in asthma. Eur Respir J. 2010 Nov;36(5):1174-84. doi: 10.1183/09031936.00019810.
PubMed 21037369Rasmussen F, Taylor DR, Flannery EM, Cowan JO, Greene JM, Herbison GP, Sears MR. Risk factors for airway remodeling in asthma manifested by a low postbronchodilator FEV1/vital capacity ratio: a longitudinal population study from childhood to adulthood. Am J Respir Crit Care Med. 2002 Jun 1;165(11):1480-8. doi: 10.1164/rccm.2108009.
PubMed 12045120Yancey SW, Keene ON, Albers FC, Ortega H, Bates S, Bleecker ER, Pavord I. Biomarkers for severe eosinophilic asthma. J Allergy Clin Immunol. 2017 Dec;140(6):1509-1518. doi: 10.1016/j.jaci.2017.10.005.
PubMed 29221581Siddiqui S, Bachert C, Bjermer L, Buchheit KM, Castro M, Qin Y, Rupani H, Sagara H, Howarth P, Taille C. Eosinophils and tissue remodeling: Relevance to airway disease. J Allergy Clin Immunol. 2023 Oct;152(4):841-857. doi: 10.1016/j.jaci.2023.06.005. Epub 2023 Jun 19.
PubMed 37343842Berair R, Hartley R, Mistry V, Sheshadri A, Gupta S, Singapuri A, Gonem S, Marshall RP, Sousa AR, Shikotra A, Kay R, Wardlaw A, Bradding P, Siddiqui S, Castro M, Brightling CE. Associations in asthma between quantitative computed tomography and bronchial biopsy-derived airway remodelling. Eur Respir J. 2017 May 1;49(5):1601507. doi: 10.1183/13993003.01507-2016. Print 2017 May.
PubMed 28461289
Study at a glance
From the registry record, last updated by the sponsor on 28 Oct 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- BenRalizumab Effect on Airway Remodeling in Severe Eosinophilic asTHmatics
- ClinicalTrials.gov ID
- NCT06288516
- Acronym / sponsor ID
- BREATH / 7484
- Conditions
- Asthma; Eosinophilic, Airway Remodeling
- Keywords
- severe asthma, airway remodeling, eosinophilic, biomarkers, bronchoscopy
- Phase
- Phase 4
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 36 participants (actual)
- Lead sponsor
- Aristotle University Of ThessalonikiUniversity, hospital or other
- Collaborators
- Pulmonary Clinic, University of Ioannina, Pulmonary Clinic, Democritus University of Thrace, National and Kapodistrian University of Athens, University Hospital of Crete, University Hospital of Patras
- Study start
- 1 Mar 2024 (actual)
- Primary completion
- 31 Aug 2026 (actual)
- Study completion
- 27 Oct 2026 (actual)
- First posted
- 1 Mar 2024 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Response to biologic therapies in severe asthma is variable, with patients being either non-responders, responders or super-responders. There is currently no explanation for this broad variation in response. It is important to examine whether these patients have distinct characteristics that could help the treating physician in making the correct diagnosis in clinical practice.
Aim of this clinical study is to evaluate the efficacy of benralizumab, a humanized an anti-interleukin 5 receptor α monoclonal antibody in patients with severe eosinophilic asthma and to evaluate airway remodeling before and after benralizumab treatment.
Hypothesis Identification of pathological and clinical characteristics in patients with severe eosinophilic asthma after benralizumab treatment regarding the airway remodeling, inflammatory cells, and other biomarkers on a long-term basis.
Research questions Is there any improvement in airway remodeling? Are there any biomarkers to predict response to benralizumab treatment in severe eosinophilic asthmatic patients?
Detailed description
Interleukin (IL)-5 is the main cytokine responsible for the activation of eosinophils, hence therapeutic strategies have been investigated and developed for clinical use. Biologics targeting IL-5 and its receptor have been recently approved and used as add-on therapy for severe eosinophilic asthma resulting in a reduction in the circulating eosinophil count, improvement in lung function and exacerbation reduction in patients with severe asthma.
Response to biologic therapies in severe asthma is variable, with patients being either non-responders, responders or super-responders. There is currently no explanation for this broad variation in response. It is important to examine whether these patients have distinct characteristics that could help the treating physician in making the correct diagnosis in clinical practice.
Aim of this clinical study is to evaluate the efficacy of benralizumab, a humanized an anti-interleukin 5 receptor α monoclonal antibody in patients with severe eosinophilic asthma and to evaluate airway remodeling before and after benralizumab treatment. Every patient will be a control to himself by comparing baseline's biomarker measurements of each patient to the following timepoint's measurements. However, we have added 10 severe asthmatics with no intervention, receiving standard of care as control groups to make more comparisons.
Several methods are used to investigate airway inflammation: direct measurements (like bronchial biopsies or bronchoalveolar lavages) and indirect methods (like symptom assessment, blood sample analysis and lung function tests). The direct techniques have the advantage of reliably assessing the airway inflammation, but they are invasive and not feasible at large scale because of patient discomfort and the risk incurred. As for the indirect methods, they poorly correlate with the direct assessment of airway inflammation.
In this study, among patients' clinical characteristics spirometry, biomarkers of inflammation such as blood eosinophils, Fractional Exhaled Nitric Oxide (FeNO), immunoglobulin E (IgE) levels), and airway remodeling via bronchoscopy will be evaluated. The precise effects of increased airway smooth muscle area on airway narrowing are not known and may vary with disease severity. In addition, biomarkers of inflammation will also be evaluated before and after 52-week of benralizumab treatment in biological fluids (serum and bronchial samples). Biomarkers of inflammation are very important to identify treatment response.
Besides, asthmatic disease is characterized by a chronic mucosal inflammatory process, which results in irreversible changes of the bronchial wall, known today as "bronchial remodeling". Glandular and smooth muscle fibers hyperplasia and/or hypertrophy, goblet cells hyperplasia, and variable thickening of basement membrane (BM) present under the respiratory epithelium are part of these morphological changes. the changes generated at the epithelium-connective interface account for an "adaptive response" to inflammatory stress and sporadic bronchoconstriction. However, current data on BM reactivity in asthmatic patient are still incomplete for an accurate assessment of its involvement in pathogenesis and specifically in bronchial wall remodeling, mainly as collagen deposits in lamina reticularis are not correlated to the degree of disease severity.
Moreover, it is increasingly evident that severe asthma is not a single disease, as evidenced by the variety of clinical presentations, physiologic characteristics, and outcomes seen in patients with asthma. To better understand this heterogeneity, the concept of asthma phenotyping and endotyping has emerged. Phenotyping integrates both biological and clinical features, from molecular, cellular, morphologic, and functional to patient-oriented characteristics with the goal to improve therapy. Ultimately, these phenotypes evolve into asthma "endotypes," which combine clinical characteristics with identifiable mechanistic pathways. Biomarkers, defined as characteristics that can be objectively measured and serve as an indicator of underlying biological processes or pathogenesis, are crucial in defining phenotypes and endotypes. In asthma, genetic polymorphisms, measures of airway physiology, and levels of inflammatory mediators in urine, blood, sputum, tissue, exhaled gas, and breath condensate have all been studied as potential markers to improve and objectify asthma diagnosis and management. Developing such tools will allow us to phenotype and endotype the various clinical patterns described in asthma, with the ultimate goal of tailoring therapy based on a specific biomarker profile. Biomarkers can then be used to help better understand the pharmacologic response to an intervention and adjust therapy accordingly.
Biomarkers have been critical for studies of disease pathogenesis and the development of new therapies in severe asthma. In particular, biomarkers of type 2 inflammation have proven valuable for endotyping and targeting new biological agents. Because of these successes in understanding and marking type 2 inflammation, lack of knowledge regarding non-type 2 inflammatory mechanisms in asthma will soon be the major obstacle to the development of new treatments and management strategies in severe asthma. Other potential biomarkers include innate lymphoid cells, IL-33 or thymic stromal lymphopoietin.
Study design
- Primary purpose
- Treatment
- Allocation
- Non-randomised
- Intervention model
- Parallel groups
- Masking
- None (open label)
- Number of arms
- 2
- Model description
- Benralizumab (30mg) administered subcutaneously every 4 weeks for the first 3 dose and then every 8 weeks
| Arm | Type | Receives |
|---|---|---|
| Benralizumab Arm A | Experimental | Drug: Benralizumab 30 mg/mlBenralizumab (30mg) administered subcutaneously every 4 weeks for the first 3 dose and then every 8 weeks. |
| No intervention Arm B | No intervention | –No intervention. Standard of care as treatment. |
Who may qualify
- Ages
- 18 to 85 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (5 listed)
- Written informed consent must be obtained at screening visit, before any assessment will be performed. Subjects should be able to provide informed written consent (study participation informed consent form): Able to give written informed consent prior to participation in the study, which will include the ability to comply with the requirements and restrictions listed in the consent form. Subjects must be able to read, comprehend, and write at a level sufficient to complete study related materials.
- Confirmed severe asthma diagnosis and treatment requirements according to American Thoracic Society(ATS)/European Respiratory Society (ERS) guidelines and Global Initiative for Asthma (GINA) 2023.
- Blood eosinophils ≥150cells/ul at screening visit or ≥300cells/ul the last 12 months.
- Patients with history ≥ 1 exacerbation the previous year under the treatment of high dose of inhaled corticosteroid(ICS)+LABA±LAMA or receiving oral/systemic corticosteroids at least 3 days. For subjects on maintenance oral corticosteroids, an exacerbation requiring oral corticosteroids was defined as the use of oral/systemic corticosteroids at least double the existing dose for at least 3 days.
- Meet requirements for biologic therapy with Benralizumab.
Key exclusion criteria (5 listed)
- Asthma exacerbation, within 6 weeks prior to screening that required hospitalization or emergency room visit.
- Prior use of other biologics that has potential to interfere/ affect disease progression.
- Pregnant or nursing women, or women of child-bearing potential.
- History of malignancy of any organ system or any other serious co-morbidities defined by the treating physician.
- Patients with a history of conditions other than asthma that could result in elevated eosinophils (e.g. hypereosinophilic syndromes, Churg-Strauss Syndrome, eosinophilic esophagitis).
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Benralizumab 30 mg/mlAlso: biologicalBenralizumab administered subcutaneously every 4 weeks for the first 3 dose and then every 8 weeks | Drug | Benralizumab Arm A |
Primary outcome
Change in sub-basement membrane thickness
Time frame: through study completion, 52 weeks
The identification of clinical characteristics of non-responders and super-responders. Any improvement in this parameter will be measured as change from baseline compared to measurement after 1 year of treatment.
Change in airway smooth muscle area
Time frame: through study completion, 52 weeks
The identification of clinical characteristics of non-responders and super-responders. Any improvement in this parameter will be measured as change from baseline compared to measurement after 1 year of treatment.
Change in airway smooth muscle layer thickness
Time frame: through study completion, 52 weeks
The identification of clinical characteristics of non-responders and super-responders. Any improvement in this parameter will be measured as change from baseline compared to measurement after 1 year of treatment.
Change in submucosal eosinophil number
Time frame: through study completion, 52 weeks
The identification of clinical characteristics of non-responders and super-responders. Any improvement in this parameter will be measured as change from baseline compared to measurement after 1 year of treatment.
Change in epithelial integrity
Time frame: through study completion, 52 weeks
The identification of clinical characteristics of non-responders and super-responders. Any improvement in this parameter will be measured as change from baseline compared to measurement after 1 year of treatment.
Change in collagen thickness
Time frame: through study completion, 52 weeks
The identification of clinical characteristics of non-responders and super-responders. Any improvement in this parameter will be measured as change from baseline compared to measurement after 1 year of treatment, measured by electron microscopy.
4 secondary outcomes
Change of cytokine and protein levels
Time frame: through study completion, 52 weeks
Change in exacerbation rate
Time frame: through study completion, 52 weeks
Change in blood eosinophil levels
Time frame: through study completion, 52 weeks
dentification of clinical characteristics of response, change in Forced Expiratory Volume (FEV1)
Time frame: through study completion, 52 weeks
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 28 Oct 2026.
- Results publication: PubMed 31798645Kuo CW, Liao XM, Huang YC, Chang HY, Shieh CC. Bronchoscopy-guided bronchial epithelium sampling as a tool for selecting the optimal biologic treatment in a patient with severe asthma: a case report. Allergy Asthma Clin Immunol. 2019 Nov 27;15:76. doi: 10.1186/s13223-019-0378-6. eCollection 2019.
- Results publication: PubMed 21037369Bara I, Ozier A, Tunon de Lara JM, Marthan R, Berger P. Pathophysiology of bronchial smooth muscle remodelling in asthma. Eur Respir J. 2010 Nov;36(5):1174-84. doi: 10.1183/09031936.00019810.
- Results publication: PubMed 12045120Rasmussen F, Taylor DR, Flannery EM, Cowan JO, Greene JM, Herbison GP, Sears MR. Risk factors for airway remodeling in asthma manifested by a low postbronchodilator FEV1/vital capacity ratio: a longitudinal population study from childhood to adulthood. Am J Respir Crit Care Med. 2002 Jun 1;165(11):1480-8. doi: 10.1164/rccm.2108009.
- Results publication: PubMed 29221581Yancey SW, Keene ON, Albers FC, Ortega H, Bates S, Bleecker ER, Pavord I. Biomarkers for severe eosinophilic asthma. J Allergy Clin Immunol. 2017 Dec;140(6):1509-1518. doi: 10.1016/j.jaci.2017.10.005.
- Results publication: PubMed 37343842Siddiqui S, Bachert C, Bjermer L, Buchheit KM, Castro M, Qin Y, Rupani H, Sagara H, Howarth P, Taille C. Eosinophils and tissue remodeling: Relevance to airway disease. J Allergy Clin Immunol. 2023 Oct;152(4):841-857. doi: 10.1016/j.jaci.2023.06.005. Epub 2023 Jun 19.
- Results publication: PubMed 28461289Berair R, Hartley R, Mistry V, Sheshadri A, Gupta S, Singapuri A, Gonem S, Marshall RP, Sousa AR, Shikotra A, Kay R, Wardlaw A, Bradding P, Siddiqui S, Castro M, Brightling CE. Associations in asthma between quantitative computed tomography and bronchial biopsy-derived airway remodelling. Eur Respir J. 2017 May 1;49(5):1601507. doi: 10.1183/13993003.01507-2016. Print 2017 May.
- Individual participant dataSharing planned: Yes. A reference of the published article will be shared here.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Kalliopi Domvri, Dr principal investigator
Aristotle University Of Thessaloniki
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 4 study testing Benralizumab 30 mg/ml in people with Asthma; Eosinophilic and Airway Remodeling, run by Aristotle University Of Thessaloniki at 1 site in Greece.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 5 inclusion and 5 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 28 Oct 2026. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Greece. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 4 studies take place after a treatment is approved, to learn more about its long-term benefits and risks in everyday use.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Change in sub-basement membrane thickness (time frame: through study completion, 52 weeks). The study lists 6 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT06288516, which also lists 6 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 28 Oct 2026.