Cushing SyndromeMYOSECRETNCT03229395
Alterations of Muscle Secretome Associated With Muscle Atrophy Caused by Glucocorticoids
An observational study of Cushing Syndrome, run by Cliniques universitaires Saint-Luc- Université Catholique de Louvain at 1 site in Belgium.
Trial summary
Several studies have shown that lean mass, in particular muscle mass, is an excellent predictive survival factor in many diseases. A better knowledge of the mechanisms responsible for muscle atrophy and the identification of atrophic process markers are deeply needed for the development of new anti-atrophic therapies. Read more about this study
- Who is it for?
- Ages 18 years and olderHealthy volunteers can take part
- Conditions the study is for
- Cushing Syndrome
- How many people
- 35 participants
- Where
- 1 siteBelgium
- Study dates
- 2 Jan 2014to 18 Jul 2017
- 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 years and older
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Study population: Patients with Cushing's syndrome are caracterised by elevated circulating glucocorticoid levels generally due to a pitiutary or adrenal adenoma. These patients were compared to heathly control patients who are matched for age and sex.
Who may be able to join
- Pituitary or adrenal endogenous Cushing's syndrome formally demonstrated by the standard endocrinological assessment
- New diagnosis or recurrence or persistent Cushing's syndrome after pituitary surgery
Who cannot join
- Pseudo Cushing's syndrome
- Paraneoplasic Cushing's syndrome
- Cyclic Cushing's syndrome
- Adrenocortical carcinoma
- Pituitary irradiation during the last six months
Trial locations and contacts
1 site in 1 country.
About this study
Several studies have shown that lean mass, in particular muscle mass, is an excellent predictive survival factor in many diseases. A better knowledge of the mechanisms responsible for muscle atrophy and the identification of atrophic process markers are deeply needed for the development of new anti-atrophic therapies. Either as drugs used to treat several medical conditions or as endocrine hormones released in response to many stress situations (e.g., sepsis, cancer, insulinopenia…), glucocorticoids (GC) are recognized to play a major role in skeletal muscle atrophy. Indeed, the inhibition of GC action by a receptor antagonist (RU486) or by muscle-specific invalidation of the GC receptor inhibits the muscle atrophy in these stress situations. Therefore, all these data clearly indicate that GC play a major role in skeletal muscle atrophy observed in several conditions. Emerging evidence has revealed that the skeletal muscle has a secretory function. Human skeletal muscle secretome was first estimated at about 300 proteins by computational analysis and proteomic analysis have recently confirmed these results. Some of these secreted proteins, conceptualized as myokines, can act locally on muscle cells through autocrine/paracrine loops and on surrounding tissues such as muscle blood vessels or can be released into the blood stream to produce systemic effects. One prominent example is interleukin (IL)-6 which is released into circulation by contracting skeletal muscle and can regulate metabolic and inflammatory processes. As IL-6, several other potential myokines have been identified including IL-8, IL-15, insulin-growth factor I (IGF-I), follistatin-like 1 (FSTL1) or fibroblast-growth factor (FGF)-21. Moreover, secreted proteins may also reflected metabolic changes which take place in muscle cells. Indeed, myoblast differentiation is accompanied by dramatic changes in the secreted proteins profile as increased expression of Semaphorins, IGF-I, matrix metalloproteinase (MMP)-2 or Collagens. Thereby, the investigators hypothesized that skeletal muscle atrophy induced by GC is associated with specific alterations of the muscle secretome. The aim of this project is to identify the GC-induced changes in the secretome of human skeletal muscle cells in culture (in vitro approach) and to determine how these changes translate into the circulation of subjects exposed to high concentrations of GC (Cushing's syndrome) (in vivo approach). Characterization of these changes in human subjects should allow to better understand the cellular mechanisms involved in muscle atrophy and might lead to identify circulating biomarkers associated with skeletal muscle atrophy, as telopeptides are for bone tissue.
- Conditions
- Cushing Syndrome
- Keywords
- skeletal muscle, muscle mass, glucocorticoids, biomarkers
- Medical subject headings
- Cushing Syndrome
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| patients with Cushing's syndrome | Patients were selected by the PI at the diagnosis. | |
| control patients | Selected patients are matched for age and sex. |
What is being measured
The primary outcome is the main question the study is designed to answer.
Measurement of BMI in kg/m^2
Measurement of weight in kilograms and height in meters to determine BMI as BMI=weight/height^2
Measured: 1 day (one assessment at diagnosis)
Evaluation of quality of life of Cushing's patients
The CushingQoL questionnaire was used to evaluate quality of life of Cushing's patients
Measured: 1 day (one assessment at diagnosis)
Measure of body lean mass of Cushing's and control patients
Bioelectrical Impedance Vector Analysis (BIA) was used for evaluation of lean and fat mass.
Measured: 1 day (one assessment at diagnosis)
Muscle strenght measurement of Cushing's and control patients
Evalutation by dynamometer "Jamar type"
Measured: 1 day (one assessment at diagnosis)
Measurement of Mid-arm muscle circumference (MAMC, cm)
Measurement of triceps skinfold thickness (TSF, in cm), and midarm circumference (MAC, in cm) to determine the MAMC according to the following formula: MAMC= MAC - (Pi x TSF).
MAMC is a bedside anthropometric measurement that estimates somatic protein reserve, an early indicator of nutritional depletion.
Measured: 1 day (one assessment at diagnosis)
Evaluation of daily energy expenditure (DEE) of Cushing's and control patients
Evaluation of DEE by completing the QAPSE questionnaire.
Measured: 1 day (one assessment at diagnosis)
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted25 Jul 2017
- Study start2 Jan 2014
- Primary completion13 Jul 2017
- Study completion18 Jul 2017
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (15)Papers the sponsor has linked to this study.
- Other trials for Cushing SyndromeStudies of the same condition, open and under way.
- More trials run by Cliniques universitaires Saint-Luc- Université Catholique de LouvainThe 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
- Other
- Time perspective
- Prospective
- Enrolment
- 35 participants (actual)
Sponsor and investigators
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Marie De Barsy, Nurse, Study chair, Cliniques Universitaires St Luc
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT03229395
- Sponsor's protocol ID
- UCL-MYOSECRET 2014-1
- Acronym
- MYOSECRET
- Status last verified
- Dec 2016
- First submitted
- 21 Dec 2016
- Last updated
- 25 Jul 2017
- Results posted
- No
- Data monitoring committee
- No
- Individual data sharing
- No
Publications
Pedersen BK. Muscle as a secretory organ. Compr Physiol. 2013 Jul;3(3):1337-62. doi: 10.1002/cphy.c120033.
PubMed 23897689Schakman O, Kalista S, Barbe C, Loumaye A, Thissen JP. Glucocorticoid-induced skeletal muscle atrophy. Int J Biochem Cell Biol. 2013 Oct;45(10):2163-72. doi: 10.1016/j.biocel.2013.05.036. Epub 2013 Jun 24.
PubMed 23806868Stastna M, Van Eyk JE. Secreted proteins as a fundamental source for biomarker discovery. Proteomics. 2012 Feb;12(4-5):722-35. doi: 10.1002/pmic.201100346. Epub 2012 Jan 19.
PubMed 22247067Baracos VE, Reiman T, Mourtzakis M, Gioulbasanis I, Antoun S. Body composition in patients with non-small cell lung cancer: a contemporary view of cancer cachexia with the use of computed tomography image analysis. Am J Clin Nutr. 2010 Apr;91(4):1133S-1137S. doi: 10.3945/ajcn.2010.28608C. Epub 2010 Feb 17.
PubMed 20164322Bortoluzzi S, Scannapieco P, Cestaro A, Danieli GA, Schiaffino S. Computational reconstruction of the human skeletal muscle secretome. Proteins. 2006 Mar 15;62(3):776-92. doi: 10.1002/prot.20803.
PubMed 16342272Braun TP, Grossberg AJ, Krasnow SM, Levasseur PR, Szumowski M, Zhu XX, Maxson JE, Knoll JG, Barnes AP, Marks DL. Cancer- and endotoxin-induced cachexia require intact glucocorticoid signaling in skeletal muscle. FASEB J. 2013 Sep;27(9):3572-82. doi: 10.1096/fj.13-230375. Epub 2013 Jun 3.
PubMed 23733748Gueugneau M, Coudy-Gandilhon C, Theron L, Meunier B, Barboiron C, Combaret L, Taillandier D, Polge C, Attaix D, Picard B, Verney J, Roche F, Feasson L, Barthelemy JC, Bechet D. Skeletal muscle lipid content and oxidative activity in relation to muscle fiber type in aging and metabolic syndrome. J Gerontol A Biol Sci Med Sci. 2015 May;70(5):566-76. doi: 10.1093/gerona/glu086. Epub 2014 Jun 17.
PubMed 24939997Henningsen J, Rigbolt KT, Blagoev B, Pedersen BK, Kratchmarova I. Dynamics of the skeletal muscle secretome during myoblast differentiation. Mol Cell Proteomics. 2010 Nov;9(11):2482-96. doi: 10.1074/mcp.M110.002113. Epub 2010 Jul 14.
PubMed 20631206Hu Z, Wang H, Lee IH, Du J, Mitch WE. Endogenous glucocorticoids and impaired insulin signaling are both required to stimulate muscle wasting under pathophysiological conditions in mice. J Clin Invest. 2009 Oct;119(10):3059-69. doi: 10.1172/JCI38770. Epub 2009 Sep 14.
PubMed 19759515Le Bihan MC, Bigot A, Jensen SS, Dennis JL, Rogowska-Wrzesinska A, Laine J, Gache V, Furling D, Jensen ON, Voit T, Mouly V, Coulton GR, Butler-Browne G. In-depth analysis of the secretome identifies three major independent secretory pathways in differentiating human myoblasts. J Proteomics. 2012 Dec 21;77:344-56. doi: 10.1016/j.jprot.2012.09.008. Epub 2012 Sep 20.
PubMed 23000592Mourtzakis M, Prado CM, Lieffers JR, Reiman T, McCargar LJ, Baracos VE. A practical and precise approach to quantification of body composition in cancer patients using computed tomography images acquired during routine care. Appl Physiol Nutr Metab. 2008 Oct;33(5):997-1006. doi: 10.1139/H08-075.
PubMed 18923576Neves M Jr, Barreto G, Boobis L, Harris R, Roschel H, Tricoli V, Ugrinowitsch C, Negrao C, Gualano B. Incidence of adverse events associated with percutaneous muscular biopsy among healthy and diseased subjects. Scand J Med Sci Sports. 2012 Apr;22(2):175-8. doi: 10.1111/j.1600-0838.2010.01264.x. Epub 2011 Mar 10.
PubMed 21392121Piccoli A. Patterns of bioelectrical impedance vector analysis: learning from electrocardiography and forgetting electric circuit models. Nutrition. 2002 Jun;18(6):520-1. doi: 10.1016/s0899-9007(02)00771-2. No abstract available.
PubMed 12044826Schakman O, Dehoux M, Bouchuari S, Delaere S, Lause P, Decroly N, Shoelson SE, Thissen JP. Role of IGF-I and the TNFalpha/NF-kappaB pathway in the induction of muscle atrogenes by acute inflammation. Am J Physiol Endocrinol Metab. 2012 Sep 15;303(6):E729-39. doi: 10.1152/ajpendo.00060.2012. Epub 2012 Jun 26.
PubMed 22739109Webb SM, Badia X, Barahona MJ, Colao A, Strasburger CJ, Tabarin A, van Aken MO, Pivonello R, Stalla G, Lamberts SW, Glusman JE. Evaluation of health-related quality of life in patients with Cushing's syndrome with a new questionnaire. Eur J Endocrinol. 2008 May;158(5):623-30. doi: 10.1530/EJE-07-0762.
PubMed 18426820
Study at a glance
From the registry record, last updated by the sponsor on 25 Jul 2017. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Alterations of Muscle Secretome Associated With Muscle Atrophy Caused by Glucocorticoids
- ClinicalTrials.gov ID
- NCT03229395
- Acronym / sponsor ID
- MYOSECRET / UCL-MYOSECRET 2014-1
- Conditions
- Cushing Syndrome
- Keywords
- skeletal muscle, muscle mass, glucocorticoids, biomarkers
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 35 participants (actual)
- Lead sponsor
- Cliniques universitaires Saint-Luc- Université Catholique de LouvainUniversity, hospital or other
- Study start
- 2 Jan 2014 (actual)
- Primary completion
- 13 Jul 2017 (actual)
- Study completion
- 18 Jul 2017 (actual)
- First posted
- 25 Jul 2017 (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.
Several studies have shown that lean mass, in particular muscle mass, is an excellent predictive survival factor in many diseases. A better knowledge of the mechanisms responsible for muscle atrophy and the identification of atrophic process markers are deeply needed for the development of new anti-atrophic therapies. Either as drugs used to treat several medical conditions or as endocrine hormones released in response to many stress situations (e.g., sepsis, cancer, insulinopenia…), glucocorticoids (GC) are recognized to play a major role in skeletal muscle atrophy. Indeed, the inhibition of GC action by a receptor antagonist (RU486) or by muscle-specific invalidation of the GC receptor inhibits the muscle atrophy in these stress situations. Therefore, all these data clearly indicate that GC play a major role in skeletal muscle atrophy observed in several conditions. Emerging evidence has revealed that the skeletal muscle has a secretory function. Human skeletal muscle secretome was first estimated at about 300 proteins by computational analysis and proteomic analysis have recently confirmed these results. Some of these secreted proteins, conceptualized as myokines, can act locally on muscle cells through autocrine/paracrine loops and on surrounding tissues such as muscle blood vessels or can be released into the blood stream to produce systemic effects. One prominent example is interleukin (IL)-6 which is released into circulation by contracting skeletal muscle and can regulate metabolic and inflammatory processes. As IL-6, several other potential myokines have been identified including IL-8, IL-15, insulin-growth factor I (IGF-I), follistatin-like 1 (FSTL1) or fibroblast-growth factor (FGF)-21. Moreover, secreted proteins may also reflected metabolic changes which take place in muscle cells. Indeed, myoblast differentiation is accompanied by dramatic changes in the secreted proteins profile as increased expression of Semaphorins, IGF-I, matrix metalloproteinase (MMP)-2 or Collagens. Thereby, the investigators hypothesized that skeletal muscle atrophy induced by GC is associated with specific alterations of the muscle secretome. The aim of this project is to identify the GC-induced changes in the secretome of human skeletal muscle cells in culture (in vitro approach) and to determine how these changes translate into the circulation of subjects exposed to high concentrations of GC (Cushing's syndrome) (in vivo approach). Characterization of these changes in human subjects should allow to better understand the cellular mechanisms involved in muscle atrophy and might lead to identify circulating biomarkers associated with skeletal muscle atrophy, as telopeptides are for bone tissue.
Study design
- Observational model
- Other
- Time perspective
- Prospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| patients with Cushing's syndrome | – | –Patients were selected by the PI at the diagnosis. |
| control patients | – | –Selected patients are matched for age and sex. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
- Study population
- Patients with Cushing's syndrome are caracterised by elevated circulating glucocorticoid levels generally due to a pitiutary or adrenal adenoma. These patients were compared to heathly control patients who are matched for age and sex.
Key inclusion criteria (2 listed)
- Pituitary or adrenal endogenous Cushing's syndrome formally demonstrated by the standard endocrinological assessment
- New diagnosis or recurrence or persistent Cushing's syndrome after pituitary surgery
Key exclusion criteria (5 listed)
- Pseudo Cushing's syndrome
- Paraneoplasic Cushing's syndrome
- Cyclic Cushing's syndrome
- Adrenocortical carcinoma
- Pituitary irradiation during the last six months
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Measurement of BMI in kg/m^2
Time frame: 1 day (one assessment at diagnosis)
Measurement of weight in kilograms and height in meters to determine BMI as BMI=weight/height^2
Evaluation of quality of life of Cushing's patients
Time frame: 1 day (one assessment at diagnosis)
The CushingQoL questionnaire was used to evaluate quality of life of Cushing's patients
Measure of body lean mass of Cushing's and control patients
Time frame: 1 day (one assessment at diagnosis)
Bioelectrical Impedance Vector Analysis (BIA) was used for evaluation of lean and fat mass.
Muscle strenght measurement of Cushing's and control patients
Time frame: 1 day (one assessment at diagnosis)
Evalutation by dynamometer "Jamar type"
Measurement of Mid-arm muscle circumference (MAMC, cm)
Time frame: 1 day (one assessment at diagnosis)
Measurement of triceps skinfold thickness (TSF, in cm), and midarm circumference (MAC, in cm) to determine the MAMC according to the following formula: MAMC= MAC - (Pi x TSF). MAMC is a bedside anthropometric measurement that estimates somatic protein reserve, an early indicator of nutritional depletion.
Evaluation of daily energy expenditure (DEE) of Cushing's and control patients
Time frame: 1 day (one assessment at diagnosis)
Evaluation of DEE by completing the QAPSE questionnaire.
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 25 Jul 2017.
- Background: PubMed 23897689Pedersen BK. Muscle as a secretory organ. Compr Physiol. 2013 Jul;3(3):1337-62. doi: 10.1002/cphy.c120033.
- Background: PubMed 23806868Schakman O, Kalista S, Barbe C, Loumaye A, Thissen JP. Glucocorticoid-induced skeletal muscle atrophy. Int J Biochem Cell Biol. 2013 Oct;45(10):2163-72. doi: 10.1016/j.biocel.2013.05.036. Epub 2013 Jun 24.
- Background: PubMed 22247067Stastna M, Van Eyk JE. Secreted proteins as a fundamental source for biomarker discovery. Proteomics. 2012 Feb;12(4-5):722-35. doi: 10.1002/pmic.201100346. Epub 2012 Jan 19.
- Results publication: PubMed 20164322Baracos VE, Reiman T, Mourtzakis M, Gioulbasanis I, Antoun S. Body composition in patients with non-small cell lung cancer: a contemporary view of cancer cachexia with the use of computed tomography image analysis. Am J Clin Nutr. 2010 Apr;91(4):1133S-1137S. doi: 10.3945/ajcn.2010.28608C. Epub 2010 Feb 17.
- Results publication: PubMed 16342272Bortoluzzi S, Scannapieco P, Cestaro A, Danieli GA, Schiaffino S. Computational reconstruction of the human skeletal muscle secretome. Proteins. 2006 Mar 15;62(3):776-92. doi: 10.1002/prot.20803.
- Results publication: PubMed 23733748Braun TP, Grossberg AJ, Krasnow SM, Levasseur PR, Szumowski M, Zhu XX, Maxson JE, Knoll JG, Barnes AP, Marks DL. Cancer- and endotoxin-induced cachexia require intact glucocorticoid signaling in skeletal muscle. FASEB J. 2013 Sep;27(9):3572-82. doi: 10.1096/fj.13-230375. Epub 2013 Jun 3.
- Results publication: PubMed 24939997Gueugneau M, Coudy-Gandilhon C, Theron L, Meunier B, Barboiron C, Combaret L, Taillandier D, Polge C, Attaix D, Picard B, Verney J, Roche F, Feasson L, Barthelemy JC, Bechet D. Skeletal muscle lipid content and oxidative activity in relation to muscle fiber type in aging and metabolic syndrome. J Gerontol A Biol Sci Med Sci. 2015 May;70(5):566-76. doi: 10.1093/gerona/glu086. Epub 2014 Jun 17.
- Results publication: PubMed 20631206Henningsen J, Rigbolt KT, Blagoev B, Pedersen BK, Kratchmarova I. Dynamics of the skeletal muscle secretome during myoblast differentiation. Mol Cell Proteomics. 2010 Nov;9(11):2482-96. doi: 10.1074/mcp.M110.002113. Epub 2010 Jul 14.
- Results publication: PubMed 19759515Hu Z, Wang H, Lee IH, Du J, Mitch WE. Endogenous glucocorticoids and impaired insulin signaling are both required to stimulate muscle wasting under pathophysiological conditions in mice. J Clin Invest. 2009 Oct;119(10):3059-69. doi: 10.1172/JCI38770. Epub 2009 Sep 14.
- Results publication: PubMed 23000592Le Bihan MC, Bigot A, Jensen SS, Dennis JL, Rogowska-Wrzesinska A, Laine J, Gache V, Furling D, Jensen ON, Voit T, Mouly V, Coulton GR, Butler-Browne G. In-depth analysis of the secretome identifies three major independent secretory pathways in differentiating human myoblasts. J Proteomics. 2012 Dec 21;77:344-56. doi: 10.1016/j.jprot.2012.09.008. Epub 2012 Sep 20.
- Results publication: PubMed 18923576Mourtzakis M, Prado CM, Lieffers JR, Reiman T, McCargar LJ, Baracos VE. A practical and precise approach to quantification of body composition in cancer patients using computed tomography images acquired during routine care. Appl Physiol Nutr Metab. 2008 Oct;33(5):997-1006. doi: 10.1139/H08-075.
- Results publication: PubMed 21392121Neves M Jr, Barreto G, Boobis L, Harris R, Roschel H, Tricoli V, Ugrinowitsch C, Negrao C, Gualano B. Incidence of adverse events associated with percutaneous muscular biopsy among healthy and diseased subjects. Scand J Med Sci Sports. 2012 Apr;22(2):175-8. doi: 10.1111/j.1600-0838.2010.01264.x. Epub 2011 Mar 10.
- 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.
Marie De Barsy, Nurse study chair
Cliniques Universitaires St Luc
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 Cushing Syndrome, run by Cliniques universitaires Saint-Luc- Université Catholique de Louvain at 1 site in Belgium.
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 2 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 25 Jul 2017. 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 Belgium. 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?
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?
Measurement of BMI in kg/m^2 (time frame: 1 day (one assessment at diagnosis)). 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 NCT03229395, which also lists 15 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 25 Jul 2017.