AsthmaNCT05078021
Phenotyping Disease Severity in Asthma
An observational study of Asthma, run by University of Calgary at 1 site in Canada.
Trial summary
The purpose of this study is to characterize and compare the molecular gene expression profile in endobronchial biopsies and cells recovered in bronchial washings from study subjects who have asthma of varying disease severity and who are on maintenance inhaled corticosteroid (ICS) treatment, with that for healthy… Read more about this study
- Who is it for?
- Ages 18 to 60 years
- Conditions the study is for
- Asthma
- What is being tested?
- Bronchoscopy
- How many people
- 60 participants
- Where
- 1 siteCanada
- Study dates
- 21 Apr 2022to Sep 2024
- Phase
- Observational
- 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 60 years
- All sexes
- Adult
Study population: For the asthma cohort, the asthma diagnosis will be defined by objective evidence of ≥12% post-bronchodilator reversibility or PC20 methacholine <16mg/ml within the past 36 months. Asthma severity will be defined by the requirement of low, medium, or high dose of ICS to achieve symptom control, with the correlating ICS doses being the daily equivalent of budesonide 200-400mcg, 400-800mcg, or >800mcg respectively Control subjects will be those without a diagnosis of asthma.
Who may be able to join
- Age 18-60
- Confirmed diagnosis of asthma by CTS criteria
- No contraindication to bronchoscopy
- No treatment with azithromycin
- No oral corticosteroid in the 4 weeks prior
- No participation in another drug study in the 4 weeks prior
- On stable doses of asthma inhaled therapies for 12 weeks prior to bronchoscopy
- FEV1 >80%
Who cannot join
- Current smokers (within past year)
- Subjects with ≥10 pack-year lifetime smoking history
- History of asthma exacerbation (requiring oral prednisone) in the 4 weeks prior to study entry
Trial locations and contacts
1 site in 1 country.
Richard Leigh contact
Canada1 site, 1 recruiting
- Recruiting
University of Calgary
Calgary, Alberta, T2N 4Z6
Curtis Dumonceaux, 403-220-2123
About this study
Official title: Phenotyping Disease Severity in Asthma: Molecular Investigations of Corticosteroid
The purpose of this study is to characterize and compare the molecular gene expression profile in endobronchial biopsies and cells recovered in bronchial washings from study subjects who have asthma of varying disease severity and who are on maintenance inhaled corticosteroid (ICS) treatment, with that for healthy control subjects. These studies will produce transcriptomic profiles of gene expression associated with asthma disease severity. The investigators will also culture epithelial cells from study participant endobronchial brushings, including those with asthma of varying disease severity and healthy control subjects, to examine differences in the response to corticosteroids (CS) in vitro. These studies will test whether intrinsic differences exist between the responses to ICS in each group.
60 participants will be recruited with 15 of each mild, moderate and severe asthma as defined by the Global Initiative for Asthma (GINA) guidelines, as well as 15 healthy controls. Participants will undergo an initial visit to obtain informed consent, bloodwork and to assess asthma control using the Asthma Control Questionnaire (ACQ); if >1.5, ICS dose will be increased, as per GINA strategy, for a 2 week 'stabilization' phase. Repeat ACQ, spirometry and sputum induction will be performed at visit 2. Bronchoscopy will be performed at visit 3, 2-4 weeks after visit 2. Mucosal biopsies, bronchial brushings and bronchial washings will be performed and processed as per our prior methods. Mucosal biopsies will be homogenized and processed for RNA, or fixed for later sectioning and histological examination. Biopsy RNA will be assessed for quality and subjected to RNA-sequencing of all human genes (mRNA-seq). Bronchial washing cells will be collected for differential cell counting and mRNA-seq analysis. Bronchial epithelial cells (BECs) from the brushings will be cultured. BECs treated with CS and inflammatory cytokines will allow comparative assessment of BEC responses.
Read the detailed description
Background:
While inhaled corticosteroids (ICS), either as monotherapy or in combination with long-acting β2 agonists (LABA), provide effective control in mild to moderate asthma, they are less effective in severe asthma. Following a guideline-based stepwise approach of treatment escalation often results in extended periods during which both the underlying airway inflammation and the asthma symptoms remain uncontrolled in these patients with severe asthma. This can lead to permanent damage, often termed airway remodeling, which results in fixed airflow obstruction that is no longer amenable to pharmacological therapy. The ability to identify molecular phenotypes associated with severe asthma should enable a more direct transition to appropriate therapies.
The respiratory epithelium drives airway inflammation and represents a primary target for ICS, which act through the glucocorticoid receptor (GR) to inhibit inflammatory gene expression. In an effort to predict therapeutic responses, considerable work has gone into investigating the clinical and molecular phenotyping of asthmatic individuals. This has produced a focus on gene-expression profiles (in blood) of asthmatics that associates with Th2 inflammatory phenotypes. However, there remains a paucity of studies investigating transcriptomic differences in the airways of mild and severe asthmatics.
The investigators now submit that characterization of inflammatory gene expression that escapes repression by CS or, alternatively, induces further inflammation, even in the setting of increasing ICS exposure, is crucial to understanding the mechanisms underpinning severe asthma.
Hypothesis:
Rather than being merely an amplified version of mild asthma, the investigators hypothesize that severe asthma shows a distinct inflammatory gene expression profile, with specific genes escaping repression, or being enhanced in expression by CS. Such effects, as apparent in cell-based models, could contribute to a molecular phenotype that is inherently resistant to the anti-inflammatory effects of ICS.
- Conditions
- Asthma
- Being tested
- Bronchoscopy
- Medical subject headings
- Asthma
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
BronchoscopyDiagnostic test
Bronchoscopy will be performed in all groups with endobronchial biopsies, brushings and bronchial washing performed.
| Study group | Role | What they receive |
|---|---|---|
| Normal control | Healthy, non-asthmatic control subjects Receives: Diagnostic Test: Bronchoscopy | |
| Mild asthma | Requiring low dose inhaled corticosteroid (ICS) plus as needed short acting beta-agonist (SABA) or as needed ICS-Formoterol. Receives: Diagnostic Test: Bronchoscopy | |
| Moderate asthma | Low dose ICS-Long acting beta-agonist (LABA) maintenance + ICS-LABA reliever or SABA reliever Receives: Diagnostic Test: Bronchoscopy | |
| Severe asthma | Medium to high dose ICS-LABA maintenance + as needed SABA or ICS-formoterol Receives: Diagnostic Test: Bronchoscopy |
What is being measured
The primary outcome is the main question the study is designed to answer.
Molecular gene expression profile
From endobronchial biopsies and cells recovered in bronchial washings
Measured: Sept 2021-Sept 2024
To test whether intrinsic differences exist between the responses to ICS
From cultured epithelial cells
Measured: Sept 2021-Sept 2024
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted14 Oct 2021
- Study start21 Apr 2022
- Primary completionSep 2024 (estimated)
- Study completionSep 2024 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (20)Papers the sponsor has linked to this study.
- Other trials for AsthmaStudies of the same condition, open and under way.
- More trials run by University of CalgaryThe 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
- Observational
- Observational model
- Case-control
- Time perspective
- Cross-sectional
- Enrolment
- 60 participants (estimated)
Sponsor and investigators
- Lead sponsor
- University of Calgary
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05078021
- Sponsor's protocol ID
- 20-2123
- Status last verified
- Nov 2023
- First submitted
- 22 Sep 2021
- Last updated
- 30 Nov 2023
- Results posted
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Lougheed MD, Leniere C, Ducharme FM, Licskai C, Dell SD, Rowe BH, FitzGerald M, Leigh R, Watson W, Boulet LP; Canadian Thoracic Society Asthma Clinical Assemby. Canadian Thoracic Society 2012 guideline update: Diagnosis and management of asthma in preschoolers, children and adults: executive summary. Can Respir J. 2012 Nov-Dec;19(6):e81-8. doi: 10.1155/2012/214129.
PubMed 23248807Global Initiative for Asthma. Global Strategy for Asthma Management and Prevention, 2019. Available from: www.ginasthma.org
Hossny E, Caraballo L, Casale T, El-Gamal Y, Rosenwasser L. Severe asthma and quality of life. World Allergy Organ J. 2017 Aug 21;10(1):28. doi: 10.1186/s40413-017-0159-y. eCollection 2017.
PubMed 28855973FitzGerald J.M., Lemiere C, Lougheed M.D., Ducharme F, Dell S. Recognition and management of severe asthma: A Canadian Thoracic Society position statement. Canadian Journal of Respiratory, Critical Care, and Sleep Medicine. 2017; 1 (4), 199-221. https://doi.org/10.1080/24745332.2017.1395250
Bergeron C, Tulic MK, Hamid Q. Airway remodelling in asthma: from benchside to clinical practice. Can Respir J. 2010 Jul-Aug;17(4):e85-93. doi: 10.1155/2010/318029.
PubMed 20808979Fehrenbach H, Wagner C, Wegmann M. Airway remodeling in asthma: what really matters. Cell Tissue Res. 2017 Mar;367(3):551-569. doi: 10.1007/s00441-016-2566-8. Epub 2017 Feb 11.
PubMed 28190087Lambrecht BN, Hammad H. The airway epithelium in asthma. Nat Med. 2012 May 4;18(5):684-92. doi: 10.1038/nm.2737.
PubMed 22561832Klassen C, Karabinskaya A, Dejager L, Vettorazzi S, Van Moorleghem J, Luhder F, Meijsing SH, Tuckermann JP, Bohnenberger H, Libert C, Reichardt HM. Airway Epithelial Cells Are Crucial Targets of Glucocorticoids in a Mouse Model of Allergic Asthma. J Immunol. 2017 Jul 1;199(1):48-61. doi: 10.4049/jimmunol.1601691. Epub 2017 May 17.
PubMed 28515280Wenzel SE. Asthma phenotypes: the evolution from clinical to molecular approaches. Nat Med. 2012 May 4;18(5):716-25. doi: 10.1038/nm.2678.
PubMed 22561835Woodruff PG, Modrek B, Choy DF, Jia G, Abbas AR, Ellwanger A, Koth LL, Arron JR, Fahy JV. T-helper type 2-driven inflammation defines major subphenotypes of asthma. Am J Respir Crit Care Med. 2009 Sep 1;180(5):388-95. doi: 10.1164/rccm.200903-0392OC. Epub 2009 May 29.
PubMed 19483109Singh P, Sharma A, Jha R, Arora S, Ahmad R, Rahmani AH, Almatroodi SA, Dohare R, Syed MA. Transcriptomic analysis delineates potential signature genes and miRNAs associated with the pathogenesis of asthma. Sci Rep. 2020 Aug 7;10(1):13354. doi: 10.1038/s41598-020-70368-5.
PubMed 32770056Wang M, Bu X, Luan G, Lin L, Wang Y, Jin J, Zhang L, Wang C. Distinct type 2-high inflammation associated molecular signatures of chronic rhinosinusitis with nasal polyps with comorbid asthma. Clin Transl Allergy. 2020 Jul 3;10:26. doi: 10.1186/s13601-020-00332-z. eCollection 2020.
PubMed 32637070Leigh R, Mostafa MM, King EM, Rider CF, Shah S, Dumonceaux C, Traves SL, McWhae A, Kolisnik T, Kooi C, Slater DM, Kelly MM, Bieda M, Miller-Larsson A, Newton R. An inhaled dose of budesonide induces genes involved in transcription and signaling in the human airways: enhancement of anti- and proinflammatory effector genes. Pharmacol Res Perspect. 2016 Jul 12;4(4):e00243. doi: 10.1002/prp2.243. eCollection 2016 Aug.
PubMed 28116096Donnelly LE, Barnes PJ. Expression of heme oxygenase in human airway epithelial cells. Am J Respir Cell Mol Biol. 2001 Mar;24(3):295-303. doi: 10.1165/ajrcmb.24.3.4001.
PubMed 11245628Dougherty RH, Sidhu SS, Raman K, Solon M, Solberg OD, Caughey GH, Woodruff PG, Fahy JV. Accumulation of intraepithelial mast cells with a unique protease phenotype in T(H)2-high asthma. J Allergy Clin Immunol. 2010 May;125(5):1046-1053.e8. doi: 10.1016/j.jaci.2010.03.003.
PubMed 20451039
Study at a glance
From the registry record, last updated by the sponsor on 30 Nov 2023. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Phenotyping Disease Severity in Asthma: Molecular Investigations of Corticosteroid
- ClinicalTrials.gov ID
- NCT05078021
- Acronym / sponsor ID
- 20-2123
- Conditions
- Asthma
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 60 participants (estimated)
- Lead sponsor
- University of CalgaryUniversity, hospital or other
- Study start
- 21 Apr 2022 (actual)
- Primary completion
- Sep 2024 (estimated)
- Study completion
- Sep 2024 (estimated)
- First posted
- 14 Oct 2021 (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.
The purpose of this study is to characterize and compare the molecular gene expression profile in endobronchial biopsies and cells recovered in bronchial washings from study subjects who have asthma of varying disease severity and who are on maintenance inhaled corticosteroid (ICS) treatment, with that for healthy control subjects. These studies will produce transcriptomic profiles of gene expression associated with asthma disease severity. The investigators will also culture epithelial cells from study participant endobronchial brushings, including those with asthma of varying disease severity and healthy control subjects, to examine differences in the response to corticosteroids (CS) in vitro. These studies will test whether intrinsic differences exist between the responses to ICS in each group.
60 participants will be recruited with 15 of each mild, moderate and severe asthma as defined by the Global Initiative for Asthma (GINA) guidelines, as well as 15 healthy controls. Participants will undergo an initial visit to obtain informed consent, bloodwork and to assess asthma control using the Asthma Control Questionnaire (ACQ); if >1.5, ICS dose will be increased, as per GINA strategy, for a 2 week 'stabilization' phase. Repeat ACQ, spirometry and sputum induction will be performed at visit 2. Bronchoscopy will be performed at visit 3, 2-4 weeks after visit 2. Mucosal biopsies, bronchial brushings and bronchial washings will be performed and processed as per our prior methods. Mucosal biopsies will be homogenized and processed for RNA, or fixed for later sectioning and histological examination. Biopsy RNA will be assessed for quality and subjected to RNA-sequencing of all human genes (mRNA-seq). Bronchial washing cells will be collected for differential cell counting and mRNA-seq analysis. Bronchial epithelial cells (BECs) from the brushings will be cultured. BECs treated with CS and inflammatory cytokines will allow comparative assessment of BEC responses.
Detailed description
Background:
While inhaled corticosteroids (ICS), either as monotherapy or in combination with long-acting β2 agonists (LABA), provide effective control in mild to moderate asthma, they are less effective in severe asthma. Following a guideline-based stepwise approach of treatment escalation often results in extended periods during which both the underlying airway inflammation and the asthma symptoms remain uncontrolled in these patients with severe asthma. This can lead to permanent damage, often termed airway remodeling, which results in fixed airflow obstruction that is no longer amenable to pharmacological therapy. The ability to identify molecular phenotypes associated with severe asthma should enable a more direct transition to appropriate therapies.
The respiratory epithelium drives airway inflammation and represents a primary target for ICS, which act through the glucocorticoid receptor (GR) to inhibit inflammatory gene expression. In an effort to predict therapeutic responses, considerable work has gone into investigating the clinical and molecular phenotyping of asthmatic individuals. This has produced a focus on gene-expression profiles (in blood) of asthmatics that associates with Th2 inflammatory phenotypes. However, there remains a paucity of studies investigating transcriptomic differences in the airways of mild and severe asthmatics.
The investigators now submit that characterization of inflammatory gene expression that escapes repression by CS or, alternatively, induces further inflammation, even in the setting of increasing ICS exposure, is crucial to understanding the mechanisms underpinning severe asthma.
Hypothesis:
Rather than being merely an amplified version of mild asthma, the investigators hypothesize that severe asthma shows a distinct inflammatory gene expression profile, with specific genes escaping repression, or being enhanced in expression by CS. Such effects, as apparent in cell-based models, could contribute to a molecular phenotype that is inherently resistant to the anti-inflammatory effects of ICS.
Study design
- Observational model
- Case-control
- Time perspective
- Cross-sectional
- Number of arms
- 4
| Arm | Type | Receives |
|---|---|---|
| Normal control | – | Diagnostic Test: BronchoscopyHealthy, non-asthmatic control subjects |
| Mild asthma | – | Diagnostic Test: BronchoscopyRequiring low dose inhaled corticosteroid (ICS) plus as needed short acting beta-agonist (SABA) or as needed ICS-Formoterol. |
| Moderate asthma | – | Diagnostic Test: BronchoscopyLow dose ICS-Long acting beta-agonist (LABA) maintenance + ICS-LABA reliever or SABA reliever |
| Severe asthma | – | Diagnostic Test: BronchoscopyMedium to high dose ICS-LABA maintenance + as needed SABA or ICS-formoterol |
Who may qualify
- Ages
- 18 to 60 years
- Sex
- All
- Age groups
- Adult
- Study population
- For the asthma cohort, the asthma diagnosis will be defined by objective evidence of ≥12% post-bronchodilator reversibility or PC20 methacholine <16mg/ml within the past 36 months. Asthma severity will be defined by the requirement of low, medium, or high dose of ICS to achieve symptom control, with the correlating ICS doses being the daily equivalent of budesonide 200-400mcg, 400-800mcg, or >800mcg respectively Control subjects will be those without a diagnosis of asthma.
Key inclusion criteria (8 listed)
- Age 18-60
- Confirmed diagnosis of asthma by CTS criteria
- No contraindication to bronchoscopy
- No treatment with azithromycin
- No oral corticosteroid in the 4 weeks prior
Key exclusion criteria (3 listed)
- Current smokers (within past year)
- Subjects with ≥10 pack-year lifetime smoking history
- History of asthma exacerbation (requiring oral prednisone) in the 4 weeks prior to study entry
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 |
|---|---|---|
| BronchoscopyBronchoscopy will be performed in all groups with endobronchial biopsies, brushings and bronchial washing performed. | Diagnostic test | Mild asthma, Moderate asthma, Normal control, Severe asthma |
Primary outcome
Molecular gene expression profile
Time frame: Sept 2021-Sept 2024
From endobronchial biopsies and cells recovered in bronchial washings
To test whether intrinsic differences exist between the responses to ICS
Time frame: Sept 2021-Sept 2024
From cultured epithelial cells
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 30 Nov 2023.
- Background: PubMed 23248807Lougheed MD, Leniere C, Ducharme FM, Licskai C, Dell SD, Rowe BH, FitzGerald M, Leigh R, Watson W, Boulet LP; Canadian Thoracic Society Asthma Clinical Assemby. Canadian Thoracic Society 2012 guideline update: Diagnosis and management of asthma in preschoolers, children and adults: executive summary. Can Respir J. 2012 Nov-Dec;19(6):e81-8. doi: 10.1155/2012/214129.
- BackgroundGlobal Initiative for Asthma. Global Strategy for Asthma Management and Prevention, 2019. Available from: www.ginasthma.org
- Background: PubMed 28855973Hossny E, Caraballo L, Casale T, El-Gamal Y, Rosenwasser L. Severe asthma and quality of life. World Allergy Organ J. 2017 Aug 21;10(1):28. doi: 10.1186/s40413-017-0159-y. eCollection 2017.
- BackgroundFitzGerald J.M., Lemiere C, Lougheed M.D., Ducharme F, Dell S. Recognition and management of severe asthma: A Canadian Thoracic Society position statement. Canadian Journal of Respiratory, Critical Care, and Sleep Medicine. 2017; 1 (4), 199-221. https://doi.org/10.1080/24745332.2017.1395250
- Background: PubMed 20808979Bergeron C, Tulic MK, Hamid Q. Airway remodelling in asthma: from benchside to clinical practice. Can Respir J. 2010 Jul-Aug;17(4):e85-93. doi: 10.1155/2010/318029.
- Background: PubMed 28190087Fehrenbach H, Wagner C, Wegmann M. Airway remodeling in asthma: what really matters. Cell Tissue Res. 2017 Mar;367(3):551-569. doi: 10.1007/s00441-016-2566-8. Epub 2017 Feb 11.
- Background: PubMed 22561832Lambrecht BN, Hammad H. The airway epithelium in asthma. Nat Med. 2012 May 4;18(5):684-92. doi: 10.1038/nm.2737.
- Background: PubMed 28515280Klassen C, Karabinskaya A, Dejager L, Vettorazzi S, Van Moorleghem J, Luhder F, Meijsing SH, Tuckermann JP, Bohnenberger H, Libert C, Reichardt HM. Airway Epithelial Cells Are Crucial Targets of Glucocorticoids in a Mouse Model of Allergic Asthma. J Immunol. 2017 Jul 1;199(1):48-61. doi: 10.4049/jimmunol.1601691. Epub 2017 May 17.
- Background: PubMed 22561835Wenzel SE. Asthma phenotypes: the evolution from clinical to molecular approaches. Nat Med. 2012 May 4;18(5):716-25. doi: 10.1038/nm.2678.
- Background: PubMed 19483109Woodruff PG, Modrek B, Choy DF, Jia G, Abbas AR, Ellwanger A, Koth LL, Arron JR, Fahy JV. T-helper type 2-driven inflammation defines major subphenotypes of asthma. Am J Respir Crit Care Med. 2009 Sep 1;180(5):388-95. doi: 10.1164/rccm.200903-0392OC. Epub 2009 May 29.
- Background: PubMed 32770056Singh P, Sharma A, Jha R, Arora S, Ahmad R, Rahmani AH, Almatroodi SA, Dohare R, Syed MA. Transcriptomic analysis delineates potential signature genes and miRNAs associated with the pathogenesis of asthma. Sci Rep. 2020 Aug 7;10(1):13354. doi: 10.1038/s41598-020-70368-5.
- Background: PubMed 32637070Wang M, Bu X, Luan G, Lin L, Wang Y, Jin J, Zhang L, Wang C. Distinct type 2-high inflammation associated molecular signatures of chronic rhinosinusitis with nasal polyps with comorbid asthma. Clin Transl Allergy. 2020 Jul 3;10:26. doi: 10.1186/s13601-020-00332-z. eCollection 2020.
- Individual participant dataSharing planned: No
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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.
Richard Leigh contact
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Asthma, run by University of Calgary at 1 site in Canada.
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 8 inclusion and 3 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: status not confirmed, as of the sponsor's last update on 30 Nov 2023. 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 Canada. 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.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Brianne S Philipenko, MD (3063806777, brianne.philipenko@gmail.com), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Molecular gene expression profile (time frame: Sept 2021-Sept 2024). The study lists 2 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 NCT05078021, which also lists 20 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 30 Nov 2023.