Alpha 1-Antitrypsin DeficiencyAATD_EpiNCT02691611
Epigenetic Regulation of Immunity in Alpha-1 Anti-trypsin Deficiency
An observational study of Alpha 1-Antitrypsin Deficiency, run by National Jewish Health at 1 site in United States.
Trial summary
The investigators hypothesize that environmentally influenced histone modifications regulate AM mediated inflammation, contributing to a variable clinical course of AATD, and may also influence or be influenced by the activity of AAT augmentation therapy. Read more about this study
- Who is it for?
- Ages 18 to 85 yearsHealthy volunteers can take part
- Conditions the study is for
- Alpha 1-Antitrypsin Deficiency
- How many people
- 39 participants
- Where
- 1 siteUnited States
- Study dates
- Dec 2015to Jul 2020
- 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 85 years
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Study population: * AATD from clinic * Healthy controls from community
Who may be able to join
- AATD
- Age between the ages of 18 and 85
- Have a diagnosis of AATD PiZZ or PiMZ established by AAT blood levels and Pi genotyping
- Are not and have not been on AAT augmentation therapy for the past 6 months
- Able to tolerate and willing to undergo study procedures
- Provide signed informed consent.
Who cannot join
- AATD
- History of comorbid condition severe enough to significantly increase risks based on investigator discretion
- Diagnosis of unstable cardiovascular disease including myocardial infarction in the past 6 weeks, uncontrolled congestive heart failure, or uncontrolled arrhythmia
- Partial Pressure of Oxygen (PaO2) on room air at rest <50 mmHg or Oxygen saturation (SaO2) on room air at rest <85%
- Post bronchodilator Forced expiratory volume in one second (FEV1)<30% predicted
- Use of anticoagulation (patients on warfarin or clopidogrel will be excluded; patients on aspirin alone can be studied even with concurrent use)
Show all 34Show fewer
- Dementia or other cognitive dysfunction which in the opinion of the investigator would prevent the participant from consenting to the study or completing study procedures
- Active pulmonary infection with tuberculosis
- History of pulmonary embolism in the past 2 years
- Non-Chronic Obstructive Pulmonary Disease (COPD) obstructive disease (various bronchiolitides, sarcoid, lymphangioleiomyomatosis (LAM), histiocytosis X) or parenchymal lung disease, pulmonary vascular disease, pleural disease, severe kyphoscoliosis, neuromuscular weakness, or other cardiovascular and pulmonary disease, that, in the opinion of the investigator, limit the interpretability of the pulmonary function measures
- Prior significant difficulties with pulmonary function testing
- Hypersensitivity to or intolerance of albuterol sulfate or ipratropium bromide or propellants or excipients of the inhalers
- Hypersensitivity to or intolerance of all drugs required for sedation during conscious sedation bronchoscopy.
- History of Lung volume reduction surgery, lung resection or bronchoscopic lung volume reduction in any form
- History of lung or other organ transplant
- History of large thoracic metal implants (e.g., Implantable cardioverter-defibrillator (AICD) and/or pacemaker) that in the opinion of the investigator limit the interpretability of CT scans
- Currently taking >=10mg a day/20mg every other day of prednisone or equivalent systemic corticosteroid
- Currently taking any immunosuppressive agent excepting systemic corticosteroids
- History of lung cancer or any cancer that spread to multiple locations in the body
- Current illicit substance abuse, excluding marijuana
- Known HIV/AIDS infection
- History of or current exposure to chemotherapy or radiation treatments that, in the opinion of the investigator, limits the interpretability of the pulmonary function measures.
- Has a BMI > 40 kg/m2 at baseline exam
- Current or planned pregnancy within the study course.
- Currently institutionalized (e.g., prisons, long-term care facilities)
- Have a genotype of PiMZ and ever received intravenous or inhaled alpha-1 augmentation therapy (Alpha-1 Proteinase Inhibitor, A1PI)
- Conditional Exclusions
- Participants who present with an upper respiratory infection or pulmonary exacerbation, either solely participant-identified or that has been clinically treated, in the last six weeks can be rescreened for the study once the six-week window has passed.
- Participants who present with current use of acute antibiotics or steroids can be rescreened for the study ≥30 days after discontinuing acute antibiotics/steroids.
- This does not apply to participants who are on chronic prednisone therapy of <10 mg per day or <20 mg every other day.
- Participants who present with a myocardial infarction or eye, chest, or abdominal surgery within six weeks can be rescreened after the six week window has passed.
- Study coordinators should consult with the site principal investigator prior to rescreening these participants.
- Female participants who present <3 months after giving birth will be asked to reschedule their visit until three months have passed since the birth.
- Individuals who are PiZZ receiving alpha-1 augmentation therapy (Alpha-1 Proteinase Inhibitor, A1PI) must be off augmentation therapy for >6 months to qualify for stratified enrollment in the PiZZ group not receiving augmentation therapy.
Trial locations and contacts
1 site in 1 country.
About this study
Official title: Defining Epigenetic Regulation of Immunity in Alpha-1 Anti-trypsin Deficiency
The investigators hypothesize that environmentally influenced histone modifications regulate AM mediated inflammation, contributing to a variable clinical course of AATD, and may also influence or be influenced by the activity of AAT augmentation therapy.
Read the detailed description
The variable natural clinical course of alpha-1 anti-trypsin deficiency (AATD) disease and strong influence of environmental exposures such as smoking, implicate a major role for epigenetic mechanisms in modifying AATD disease penetrance. The goal of this study proposal is to investigate epigenetic regulation of alveolar macrophage (AM) inflammation and function in AATD homozygous alpha 1-protease inhibitor deficiency (PiZZ) (two Z genes) and homozygous alpha 1-protease inhibitor deficiency (PiMZ) (one M and one Z gene) patients. The investigators proposal focuses on epigenetic histone modifications and gene expression specifically in AM.
AAT augmentation therapy, which alters disease symptoms, may also modulate AM epigenetics. To identify epigenetic regulation of AM inflammation in AATD in the context of AAT therapy, the investigators will perform and computationally integrate chromatin immunoprecipitation sequencing (ChIP-seq) and RNA-seq data. This will help elucidate the immunomodulatory mechanisms regulating AATD and provide an epigenetic map for diagnosis and targeted treatment. The investigators will test the efficacy of FDA-approved histone modifying drugs, such as Suberoylanilide Hydroxamic Acid (SAHA) and more specific next-generation histone modifiers, such as GSK-J4, to modulate AM AATD-associated activity ex vivo.
The goal of this study is to enroll up to a total of 13 AATD cases and 6 healthy controls. All AATD patients will be asked to give a blood sample and/or undergo a bronchoscopy. AATD patients will also be asked to undergo a follow up bronchoscopy and/or blood draw after 6 months if treatment with alpha-1 antitrypsin augmentation therapy is initiated to study the changes in these markers after augmentation therapy.
- Conditions
- Alpha 1-Antitrypsin Deficiency
- Medical subject headings
- alpha 1-Antitrypsin Deficiency
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 |
|---|---|---|
| Alpha-1 Antitrypsin | All AATD patients who will start treatment with alpha-1 antitrypsin augmentation therapy | |
| Healthy Control | Healthy controls with no lung diseases |
What is being measured
The primary outcome is the main question the study is designed to answer.
Epigenetic signature of specific inflammation-associated histone modifications from CD14+ macrophages
Measured: Change from Baseline histones at 6 months
Secondary outcomes (2)
Epigenetically regulated genomic profile of AATD in AM
Measured: Change from Baseline polyA RNA at 6 months
Epigenetic mechanisms to regulate gene expression and cell function
Measured: Change from Baseline epigenetic modified cells at 6 months
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted25 Feb 2016 (estimated)
- Study startDec 2015
- Primary completionNov 2018
- Study completionJul 2020
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (33)Papers the sponsor has linked to this study.
- Other trials for Alpha 1-Antitrypsin DeficiencyStudies of the same condition, open and under way.
- 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
- Prospective
- Enrolment
- 39 participants (actual)
Sponsor and investigators
- Lead sponsor
- National Jewish Health
- Sponsor type
- University, hospital or other
- Collaborators
- Medical University of South Carolina
- Responsible party
- Sponsor
- Investigators
- Brian P O'Connor, PhD, Principal investigator, National Jewish HealthNabeel Y Hamzeh, MD, Principal investigator, National Jewish HealthRobert Sandhaus, MD, PhD, Principal investigator, National Jewish Health
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02691611
- Sponsor's protocol ID
- HS-2939
- Acronym
- AATD_Epi
- Status last verified
- Mar 2019
- First submitted
- 12 Feb 2016
- Last updated
- 6 Jun 2025
- Results posted
- No
- Data monitoring committee
- Yes
- Individual data sharing
- No
Publications
Silverman EK, Sandhaus RA. Clinical practice. Alpha1-antitrypsin deficiency. N Engl J Med. 2009 Jun 25;360(26):2749-57. doi: 10.1056/NEJMcp0900449. No abstract available.
PubMed 19553648Kim WJ, Wood AM, Barker AF, Brantly ML, Campbell EJ, Eden E, McElvaney G, Rennard SI, Sandhaus RA, Stocks JM, Stoller JK, Strange C, Turino G, Silverman EK, Stockley RA, Demeo DL. Association of IREB2 and CHRNA3 polymorphisms with airflow obstruction in severe alpha-1 antitrypsin deficiency. Respir Res. 2012 Feb 22;13(1):16. doi: 10.1186/1465-9921-13-16.
PubMed 22356581Bouchecareilh M, Hutt DM, Szajner P, Flotte TR, Balch WE. Histone deacetylase inhibitor (HDACi) suberoylanilide hydroxamic acid (SAHA)-mediated correction of alpha1-antitrypsin deficiency. J Biol Chem. 2012 Nov 2;287(45):38265-78. doi: 10.1074/jbc.M112.404707. Epub 2012 Sep 20.
PubMed 22995909Breton CV, Byun HM, Wenten M, Pan F, Yang A, Gilliland FD. Prenatal tobacco smoke exposure affects global and gene-specific DNA methylation. Am J Respir Crit Care Med. 2009 Sep 1;180(5):462-7. doi: 10.1164/rccm.200901-0135OC. Epub 2009 Jun 4.
PubMed 19498054Sanders YY, Ambalavanan N, Halloran B, Zhang X, Liu H, Crossman DK, Bray M, Zhang K, Thannickal VJ, Hagood JS. Altered DNA methylation profile in idiopathic pulmonary fibrosis. Am J Respir Crit Care Med. 2012 Sep 15;186(6):525-35. doi: 10.1164/rccm.201201-0077OC. Epub 2012 Jun 14.
PubMed 22700861Jeffries MA, Dozmorov M, Tang Y, Merrill JT, Wren JD, Sawalha AH. Genome-wide DNA methylation patterns in CD4+ T cells from patients with systemic lupus erythematosus. Epigenetics. 2011 May;6(5):593-601. doi: 10.4161/epi.6.5.15374. Epub 2011 May 1.
PubMed 21436623Cortessis VK, Thomas DC, Levine AJ, Breton CV, Mack TM, Siegmund KD, Haile RW, Laird PW. Environmental epigenetics: prospects for studying epigenetic mediation of exposure-response relationships. Hum Genet. 2012 Oct;131(10):1565-89. doi: 10.1007/s00439-012-1189-8. Epub 2012 Jun 28.
PubMed 22740325Akimova T, Beier UH, Liu Y, Wang L, Hancock WW. Histone/protein deacetylases and T-cell immune responses. Blood. 2012 Mar 15;119(11):2443-51. doi: 10.1182/blood-2011-10-292003. Epub 2012 Jan 12.
PubMed 22246031Jirtle RL, Skinner MK. Environmental epigenomics and disease susceptibility. Nat Rev Genet. 2007 Apr;8(4):253-62. doi: 10.1038/nrg2045.
PubMed 17363974Feinberg AP. Epigenetics at the epicenter of modern medicine. JAMA. 2008 Mar 19;299(11):1345-50. doi: 10.1001/jama.299.11.1345.
PubMed 18349095Fraga MF, Ballestar E, Paz MF, Ropero S, Setien F, Ballestar ML, Heine-Suner D, Cigudosa JC, Urioste M, Benitez J, Boix-Chornet M, Sanchez-Aguilera A, Ling C, Carlsson E, Poulsen P, Vaag A, Stephan Z, Spector TD, Wu YZ, Plass C, Esteller M. Epigenetic differences arise during the lifetime of monozygotic twins. Proc Natl Acad Sci U S A. 2005 Jul 26;102(30):10604-9. doi: 10.1073/pnas.0500398102. Epub 2005 Jul 11.
PubMed 16009939Miller RL, Ho SM. Environmental epigenetics and asthma: current concepts and call for studies. Am J Respir Crit Care Med. 2008 Mar 15;177(6):567-73. doi: 10.1164/rccm.200710-1511PP. Epub 2008 Jan 10.
PubMed 18187692Yang IV, Schwartz DA. Epigenetic control of gene expression in the lung. Am J Respir Crit Care Med. 2011 May 15;183(10):1295-301. doi: 10.1164/rccm.201010-1579PP.
PubMed 21596832Hutt DM, Herman D, Rodrigues AP, Noel S, Pilewski JM, Matteson J, Hoch B, Kellner W, Kelly JW, Schmidt A, Thomas PJ, Matsumura Y, Skach WR, Gentzsch M, Riordan JR, Sorscher EJ, Okiyoneda T, Yates JR 3rd, Lukacs GL, Frizzell RA, Manning G, Gottesfeld JM, Balch WE. Reduced histone deacetylase 7 activity restores function to misfolded CFTR in cystic fibrosis. Nat Chem Biol. 2010 Jan;6(1):25-33. doi: 10.1038/nchembio.275. Epub 2009 Dec 6.
PubMed 19966789Mizuno S, Yasuo M, Bogaard HJ, Kraskauskas D, Natarajan R, Voelkel NF. Inhibition of histone deacetylase causes emphysema. Am J Physiol Lung Cell Mol Physiol. 2011 Mar;300(3):L402-13. doi: 10.1152/ajplung.00207.2010. Epub 2010 Dec 17.
PubMed 21224215
Study at a glance
From the registry record, last updated by the sponsor on 6 Jun 2025. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Defining Epigenetic Regulation of Immunity in Alpha-1 Anti-trypsin Deficiency
- ClinicalTrials.gov ID
- NCT02691611
- Acronym / sponsor ID
- AATD_Epi / HS-2939
- Conditions
- Alpha 1-Antitrypsin Deficiency
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 39 participants (actual)
- Lead sponsor
- National Jewish HealthUniversity, hospital or other
- Collaborators
- Medical University of South Carolina
- Study start
- Dec 2015
- Primary completion
- Nov 2018 (actual)
- Study completion
- Jul 2020 (actual)
- First posted
- 25 Feb 2016 (estimated)
- 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 investigators hypothesize that environmentally influenced histone modifications regulate AM mediated inflammation, contributing to a variable clinical course of AATD, and may also influence or be influenced by the activity of AAT augmentation therapy.
Detailed description
The variable natural clinical course of alpha-1 anti-trypsin deficiency (AATD) disease and strong influence of environmental exposures such as smoking, implicate a major role for epigenetic mechanisms in modifying AATD disease penetrance. The goal of this study proposal is to investigate epigenetic regulation of alveolar macrophage (AM) inflammation and function in AATD homozygous alpha 1-protease inhibitor deficiency (PiZZ) (two Z genes) and homozygous alpha 1-protease inhibitor deficiency (PiMZ) (one M and one Z gene) patients. The investigators proposal focuses on epigenetic histone modifications and gene expression specifically in AM.
AAT augmentation therapy, which alters disease symptoms, may also modulate AM epigenetics. To identify epigenetic regulation of AM inflammation in AATD in the context of AAT therapy, the investigators will perform and computationally integrate chromatin immunoprecipitation sequencing (ChIP-seq) and RNA-seq data. This will help elucidate the immunomodulatory mechanisms regulating AATD and provide an epigenetic map for diagnosis and targeted treatment. The investigators will test the efficacy of FDA-approved histone modifying drugs, such as Suberoylanilide Hydroxamic Acid (SAHA) and more specific next-generation histone modifiers, such as GSK-J4, to modulate AM AATD-associated activity ex vivo.
The goal of this study is to enroll up to a total of 13 AATD cases and 6 healthy controls. All AATD patients will be asked to give a blood sample and/or undergo a bronchoscopy. AATD patients will also be asked to undergo a follow up bronchoscopy and/or blood draw after 6 months if treatment with alpha-1 antitrypsin augmentation therapy is initiated to study the changes in these markers after augmentation therapy.
Study design
- Observational model
- Case-control
- Time perspective
- Prospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Alpha-1 Antitrypsin | – | –All AATD patients who will start treatment with alpha-1 antitrypsin augmentation therapy |
| Healthy Control | – | –Healthy controls with no lung diseases |
Who may qualify
- Ages
- 18 to 85 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
- Study population
- * AATD from clinic * Healthy controls from community
Key inclusion criteria (6 listed)
- AATD
- Age between the ages of 18 and 85
- Have a diagnosis of AATD PiZZ or PiMZ established by AAT blood levels and Pi genotyping
- Are not and have not been on AAT augmentation therapy for the past 6 months
- Able to tolerate and willing to undergo study procedures
Key exclusion criteria (34 listed)
- AATD
- History of comorbid condition severe enough to significantly increase risks based on investigator discretion
- Diagnosis of unstable cardiovascular disease including myocardial infarction in the past 6 weeks, uncontrolled congestive heart failure, or uncontrolled arrhythmia
- Partial Pressure of Oxygen (PaO2) on room air at rest <50 mmHg or Oxygen saturation (SaO2) on room air at rest <85%
- Post bronchodilator Forced expiratory volume in one second (FEV1)<30% predicted
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
Epigenetic signature of specific inflammation-associated histone modifications from CD14+ macrophages
Time frame: Change from Baseline histones at 6 months
2 secondary outcomes
Epigenetically regulated genomic profile of AATD in AM
Time frame: Change from Baseline polyA RNA at 6 months
Epigenetic mechanisms to regulate gene expression and cell function
Time frame: Change from Baseline epigenetic modified cells at 6 months
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 6 Jun 2025.
- Background: PubMed 19553648Silverman EK, Sandhaus RA. Clinical practice. Alpha1-antitrypsin deficiency. N Engl J Med. 2009 Jun 25;360(26):2749-57. doi: 10.1056/NEJMcp0900449. No abstract available.
- Background: PubMed 22356581Kim WJ, Wood AM, Barker AF, Brantly ML, Campbell EJ, Eden E, McElvaney G, Rennard SI, Sandhaus RA, Stocks JM, Stoller JK, Strange C, Turino G, Silverman EK, Stockley RA, Demeo DL. Association of IREB2 and CHRNA3 polymorphisms with airflow obstruction in severe alpha-1 antitrypsin deficiency. Respir Res. 2012 Feb 22;13(1):16. doi: 10.1186/1465-9921-13-16.
- Background: PubMed 22995909Bouchecareilh M, Hutt DM, Szajner P, Flotte TR, Balch WE. Histone deacetylase inhibitor (HDACi) suberoylanilide hydroxamic acid (SAHA)-mediated correction of alpha1-antitrypsin deficiency. J Biol Chem. 2012 Nov 2;287(45):38265-78. doi: 10.1074/jbc.M112.404707. Epub 2012 Sep 20.
- Background: PubMed 19498054Breton CV, Byun HM, Wenten M, Pan F, Yang A, Gilliland FD. Prenatal tobacco smoke exposure affects global and gene-specific DNA methylation. Am J Respir Crit Care Med. 2009 Sep 1;180(5):462-7. doi: 10.1164/rccm.200901-0135OC. Epub 2009 Jun 4.
- Background: PubMed 22700861Sanders YY, Ambalavanan N, Halloran B, Zhang X, Liu H, Crossman DK, Bray M, Zhang K, Thannickal VJ, Hagood JS. Altered DNA methylation profile in idiopathic pulmonary fibrosis. Am J Respir Crit Care Med. 2012 Sep 15;186(6):525-35. doi: 10.1164/rccm.201201-0077OC. Epub 2012 Jun 14.
- Background: PubMed 21436623Jeffries MA, Dozmorov M, Tang Y, Merrill JT, Wren JD, Sawalha AH. Genome-wide DNA methylation patterns in CD4+ T cells from patients with systemic lupus erythematosus. Epigenetics. 2011 May;6(5):593-601. doi: 10.4161/epi.6.5.15374. Epub 2011 May 1.
- Background: PubMed 22740325Cortessis VK, Thomas DC, Levine AJ, Breton CV, Mack TM, Siegmund KD, Haile RW, Laird PW. Environmental epigenetics: prospects for studying epigenetic mediation of exposure-response relationships. Hum Genet. 2012 Oct;131(10):1565-89. doi: 10.1007/s00439-012-1189-8. Epub 2012 Jun 28.
- Background: PubMed 22246031Akimova T, Beier UH, Liu Y, Wang L, Hancock WW. Histone/protein deacetylases and T-cell immune responses. Blood. 2012 Mar 15;119(11):2443-51. doi: 10.1182/blood-2011-10-292003. Epub 2012 Jan 12.
- Background: PubMed 17363974Jirtle RL, Skinner MK. Environmental epigenomics and disease susceptibility. Nat Rev Genet. 2007 Apr;8(4):253-62. doi: 10.1038/nrg2045.
- Background: PubMed 18349095Feinberg AP. Epigenetics at the epicenter of modern medicine. JAMA. 2008 Mar 19;299(11):1345-50. doi: 10.1001/jama.299.11.1345.
- Background: PubMed 16009939Fraga MF, Ballestar E, Paz MF, Ropero S, Setien F, Ballestar ML, Heine-Suner D, Cigudosa JC, Urioste M, Benitez J, Boix-Chornet M, Sanchez-Aguilera A, Ling C, Carlsson E, Poulsen P, Vaag A, Stephan Z, Spector TD, Wu YZ, Plass C, Esteller M. Epigenetic differences arise during the lifetime of monozygotic twins. Proc Natl Acad Sci U S A. 2005 Jul 26;102(30):10604-9. doi: 10.1073/pnas.0500398102. Epub 2005 Jul 11.
- Background: PubMed 18187692Miller RL, Ho SM. Environmental epigenetics and asthma: current concepts and call for studies. Am J Respir Crit Care Med. 2008 Mar 15;177(6):567-73. doi: 10.1164/rccm.200710-1511PP. Epub 2008 Jan 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.
Brian P O'Connor, PhD principal investigator
National Jewish Health
Nabeel Y Hamzeh, MD principal investigator
National Jewish Health
Robert Sandhaus, MD, PhD principal investigator
National Jewish Health
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 Alpha 1-Antitrypsin Deficiency, run by National Jewish Health at 1 site in United States.
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 6 inclusion and 34 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 6 Jun 2025. 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 United States. 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?
Epigenetic signature of specific inflammation-associated histone modifications from CD14+ macrophages (time frame: Change from Baseline histones at 6 months). 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 NCT02691611, which also lists 33 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 6 Jun 2025.