Acute Coronary SyndromePhase 2IR-TREATNCT03700424
Inflammation Reduction by TREhalose AdminisTration
A Phase 2 study testing Trehalose and Normal saline in people with Acute Coronary Syndrome, run by Mashhad University of Medical Sciences at 1 site in Iran.
Trial summary
Arterial wall inflammation has been consistently suggested to serve a causal role in promoting atherosclerosis and predisposing to hard cardiovascular outcomes. Therefore, there is a global trend in the pharmaceutical industry to develop safe and effective anti-inflammatory agents that could lessen arterial wall… Read more about this study
- Who is it for?
- Ages 18 to 55 years
- Conditions the study is for
- Acute Coronary Syndrome
- What is being tested?
- Trehalose and Normal saline
- Type of treatment
- Injection or infusion
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 15 participants
- Where
- 1 siteIran
- Study dates
- 20 Aug 2020to Aug 2022
- Phase
- Phase 2
- 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 55 years
- All sexes
- No healthy volunteers
- Adult
Who may be able to join
- Men and women aged between 18-55 years
- Having a history of acute coronary syndrome
- Having a baseline high-sensitivity C-reactive protein (hs-CRP) of ≥ 2mg/L
- Willingness to participate in the trials.
Who cannot join
- Lactation or breastfeeding
- Diabetes mellitus
- Nephrotic syndrome or Estimated Glomerular Filtration Rate (eGFR) < 30/mL/min/1.73m2
- Active or recurrent hepatic disease or/and alanine aminotransferase (ALT)/aspartate aminotransferase (AST) (ALT/AST) of > 3 times upper normal limit or total bilirubin of > 2 times upper normal limit
- Active infectious or febrile disease
- Any type of malignancy
- History of transplantation
- Consumption of immunosuppressive drugs.
Trial locations and contacts
1 site in 1 country.
Iran1 site, 1 recruiting
- Recruiting
Ghaem Educational, Research and Treatment Center
Mashhad, Razavi Khorasan Province, 9919991766
Amirhossein Sahebkar, PharmD, PhD, +989151221496, sahebkara@mums.ac.ir
About this study
Official title: The Use of Intravenous Trehalose to Reduce Vascular Inflammation in Acute Coronary Syndrome
Arterial wall inflammation has been consistently suggested to serve a causal role in promoting atherosclerosis and predisposing to hard cardiovascular outcomes. Therefore, there is a global trend in the pharmaceutical industry to develop safe and effective anti-inflammatory agents that could lessen arterial wall inflammation and prevent its detrimental impact on atheroma growth and instability. To this end, autophagy has emerged as a key regulator of inflammation and dysfunctional autophagy machinery has been consistently reported as a contributing factor to atherosclerosis and inflammation. Trehalose, a natural disaccharide sugar found extensively among miscellaneous organisms, by preventing protein denaturation plays various protective roles against stress conditions. Numerous studies indicated trehalose's ability to induce macrophage autophagy-lysosomal biogenesis and reduce inflammation. Also, intravenous (IV) administration of trehalose showed beneficial effects in the reversal of atherosclerosis in atherosclerotic animals. Therefore, in this study, the investigators will explore the potential efficacy of IV trehalose administration on arterial inflammation by employing an positron emission tomography (PET) with 18F-labeled fluoro-2-deoxyglucose (18F-FDG) and computed tomography (18F-FDG PET/CT) technique which noninvasively characterizes vascular inflammation and atherosclerosis.
- Conditions
- Acute Coronary Syndrome
- Being tested
- Trehalose, Normal saline
- Keywords
- Acute Coronary Syndrome, Trehalose, Arterial inflammation, Autophagy
- Medical subject headings
- Acute Coronary Syndrome, Arteritis
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
TrehaloseDrug
Also called Mycose
Trehalose is a natural disaccharide sugar found extensively among miscellaneous organisms including bacteria, plants, insects, yeast, fungi, and invertebrates. By preventing protein denaturation, it plays various protective roles against stress conditions such as heat, freeze, oxidation, desiccation and dehydration. Owing to this capacity, trehalose is an FDA-approved pharmaceutical excipient that is used as a stabilizer in numerous medicines including parenteral products.
In this study, all injections will be conducted by a trained nurse in the presence of a specialist physician at a duration of 45-90 minutes.
Normal salineDrug
Also called Physiological saline, Isotonic saline
A solution of 0.90% w/v of sodium chloride (NaCl) in water
| Study group | Role | What they receive |
|---|---|---|
| Trehalose | Experimental | Participants will be received intravenous trehalose infusion weekly (15 g/week) for a period of 12 weeks Receives: Drug: Trehalose |
| Placebo | Placebo comparator | Participants will be received equal volume of normal saline weekly for a period of 12 weeks Receives: Drug: Normal saline |
What is being measured
The primary outcome is the main question the study is designed to answer.
Arterial wall inflammation in the aorta and carotid arteries
This will be assessed using the 18F-FDG PET/CT imaging technique
Measured: At the beginning and end of the intervention trial (Day 0 and week 12)
Secondary outcomes (11)
Carotid intima-media thickness (cIMT)
This will be assessed using doppler sonography
Measured: At the beginning and end of the intervention trial (Day 0 and week 12)
Measuring beclin-1 to assess autophagy activation
Measured: At the beginning and end of the intervention trial (Day 0 and week 12)
Measuring high-sensitivity C-reactive protein (hs-CRP) to assess systemic inflammation
Measured: At the beginning and end of the intervention trial (Day 0 and week 12)
Measuring complete blood count (CBC) (Safety)
Measured: At the beginning and end of the intervention trial (Day 0 and week 12)
Assessing lipid profile (Safety)
Including triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C)
Measured: At the beginning and end of the intervention trial (Day 0 and week 12)
Assessing glucose (Safety)
Fasting blood glucose (FBS)
Measured: At the beginning and end of the intervention trial (Day 0 and week 12)
Measuring thyroid-stimulating hormone (TSH) to assess thyroid function (Safety)
Measured: At the beginning and end of the intervention trial (Day 0 and week 12)
Measuring alanine aminotransferase (ALT), aspartate aminotransferase (AST) and bilirubin (Bil) to assess liver function (Safety)
Measured: At the beginning and end of the intervention trial (Day 0 and week 12)
Measuring creatinine (Cr), urine (Ur) and blood urea nitrogen (BUN) to assess renal function (Safety)
Measured: At the beginning and end of the intervention trial (Day 0 and week 12)
Evaluating electrocardiogram (ECG) and heart rhythm to assess heart function (Safety)
Measured: At the beginning and end of the intervention trial (Day 0 and week 12)
Measuring creatinine phosphokinase (CPK) to detect muscle damage (Safety)
Measured: At the beginning and end of the intervention trial (Day 0 and week 12)
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted9 Oct 2018
- Study start20 Aug 2020
- Primary completion20 May 2022 (estimated)
- Study completionAug 2022 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (14)Papers the sponsor has linked to this study.
- Other trials for Acute Coronary SyndromeStudies 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
- Interventional
- Phase
- Phase 2
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Quadruple blind
- Who is masked
- Participant, Care provider, Investigator, Outcomes assessor
- Enrolment
- 15 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Mashhad University of Medical Sciences
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Amirhossein Sahebkar, Mashhad University of Medical Sciences
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT03700424
- Sponsor's protocol ID
- 964334
- Acronym
- IR-TREAT
- Status last verified
- Sep 2020
- First submitted
- 3 Oct 2018
- Last updated
- 21 Sep 2020
- Results posted
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Libby P. Inflammation in atherosclerosis. Arterioscler Thromb Vasc Biol. 2012 Sep;32(9):2045-51. doi: 10.1161/ATVBAHA.108.179705.
PubMed 22895665Libby P, Hansson GK. Taming Immune and Inflammatory Responses to Treat Atherosclerosis. J Am Coll Cardiol. 2018 Jan 16;71(2):173-176. doi: 10.1016/j.jacc.2017.10.081. No abstract available.
PubMed 29325641Liao X, Sluimer JC, Wang Y, Subramanian M, Brown K, Pattison JS, Robbins J, Martinez J, Tabas I. Macrophage autophagy plays a protective role in advanced atherosclerosis. Cell Metab. 2012 Apr 4;15(4):545-53. doi: 10.1016/j.cmet.2012.01.022. Epub 2012 Mar 22.
PubMed 22445600Maiuri MC, Grassia G, Platt AM, Carnuccio R, Ialenti A, Maffia P. Macrophage autophagy in atherosclerosis. Mediators Inflamm. 2013;2013:584715. doi: 10.1155/2013/584715. Epub 2013 Jan 21.
PubMed 23401644Shao BZ, Han BZ, Zeng YX, Su DF, Liu C. The roles of macrophage autophagy in atherosclerosis. Acta Pharmacol Sin. 2016 Feb;37(2):150-6. doi: 10.1038/aps.2015.87. Epub 2016 Jan 11.
PubMed 26750103Iwatsuka R, Matsue Y, Yonetsu T, O'uchi T, Matsumura A, Hashimoto Y, Hirao K. Arterial inflammation measured by 18F-FDG-PET-CT to predict coronary events in older subjects. Atherosclerosis. 2018 Jan;268:49-54. doi: 10.1016/j.atherosclerosis.2017.11.016. Epub 2017 Nov 21.
PubMed 29175654Chrapko BE, Chrapko M, Nocun A, Stefaniak B, Zubilewicz T, Drop A. Role of 18F-FDG PET/CT in the diagnosis of inflammatory and infectious vascular disease. Nucl Med Rev Cent East Eur. 2016;19(1):28-36. doi: 10.5603/NMR.2016.0006.
PubMed 26841377Menezes LJ, Kotze CW, Hutton BF, Endozo R, Dickson JC, Cullum I, Yusuf SW, Ell PJ, Groves AM. Vascular inflammation imaging with 18F-FDG PET/CT: when to image? J Nucl Med. 2009 Jun;50(6):854-7. doi: 10.2967/jnumed.108.061432. Epub 2009 May 14.
PubMed 19443587Chen Q, Haddad GG. Role of trehalose phosphate synthase and trehalose during hypoxia: from flies to mammals. J Exp Biol. 2004 Aug;207(Pt 18):3125-9. doi: 10.1242/jeb.01133.
PubMed 15299033Castillo K, Nassif M, Valenzuela V, Rojas F, Matus S, Mercado G, Court FA, van Zundert B, Hetz C. Trehalose delays the progression of amyotrophic lateral sclerosis by enhancing autophagy in motoneurons. Autophagy. 2013 Sep;9(9):1308-20. doi: 10.4161/auto.25188. Epub 2013 Jun 6.
PubMed 23851366Mardones P, Rubinsztein DC, Hetz C. Mystery solved: Trehalose kickstarts autophagy by blocking glucose transport. Sci Signal. 2016 Feb 23;9(416):fs2. doi: 10.1126/scisignal.aaf1937.
PubMed 26905424Sergin I, Evans TD, Zhang X, Bhattacharya S, Stokes CJ, Song E, Ali S, Dehestani B, Holloway KB, Micevych PS, Javaheri A, Crowley JR, Ballabio A, Schilling JD, Epelman S, Weihl CC, Diwan A, Fan D, Zayed MA, Razani B. Exploiting macrophage autophagy-lysosomal biogenesis as a therapy for atherosclerosis. Nat Commun. 2017 Jun 7;8:15750. doi: 10.1038/ncomms15750.
PubMed 28589926van der Valk FM, Bekkering S, Kroon J, Yeang C, Van den Bossche J, van Buul JD, Ravandi A, Nederveen AJ, Verberne HJ, Scipione C, Nieuwdorp M, Joosten LA, Netea MG, Koschinsky ML, Witztum JL, Tsimikas S, Riksen NP, Stroes ES. Oxidized Phospholipids on Lipoprotein(a) Elicit Arterial Wall Inflammation and an Inflammatory Monocyte Response in Humans. Circulation. 2016 Aug 23;134(8):611-24. doi: 10.1161/CIRCULATIONAHA.116.020838. Epub 2016 Aug 5.
PubMed 27496857van der Valk FM, Verweij SL, Zwinderman KA, Strang AC, Kaiser Y, Marquering HA, Nederveen AJ, Stroes ES, Verberne HJ, Rudd JH. Thresholds for Arterial Wall Inflammation Quantified by 18F-FDG PET Imaging: Implications for Vascular Interventional Studies. JACC Cardiovasc Imaging. 2016 Oct;9(10):1198-1207. doi: 10.1016/j.jcmg.2016.04.007. Epub 2016 Sep 14.
PubMed 27639759
Study at a glance
From the registry record, last updated by the sponsor on 21 Sep 2020. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- The Use of Intravenous Trehalose to Reduce Vascular Inflammation in Acute Coronary Syndrome
- ClinicalTrials.gov ID
- NCT03700424
- Acronym / sponsor ID
- IR-TREAT / 964334
- Conditions
- Acute Coronary Syndrome
- Keywords
- Acute Coronary Syndrome, Trehalose, Arterial inflammation, Autophagy
- Phase
- Phase 2
- Study type
- Interventional
- Recruitment status
- Unknown status
- Enrolment
- 15 participants (estimated)
- Lead sponsor
- Mashhad University of Medical SciencesUniversity, hospital or other
- Study start
- 20 Aug 2020 (actual)
- Primary completion
- 20 May 2022 (estimated)
- Study completion
- Aug 2022 (estimated)
- First posted
- 9 Oct 2018 (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.
Arterial wall inflammation has been consistently suggested to serve a causal role in promoting atherosclerosis and predisposing to hard cardiovascular outcomes. Therefore, there is a global trend in the pharmaceutical industry to develop safe and effective anti-inflammatory agents that could lessen arterial wall inflammation and prevent its detrimental impact on atheroma growth and instability. To this end, autophagy has emerged as a key regulator of inflammation and dysfunctional autophagy machinery has been consistently reported as a contributing factor to atherosclerosis and inflammation. Trehalose, a natural disaccharide sugar found extensively among miscellaneous organisms, by preventing protein denaturation plays various protective roles against stress conditions. Numerous studies indicated trehalose's ability to induce macrophage autophagy-lysosomal biogenesis and reduce inflammation. Also, intravenous (IV) administration of trehalose showed beneficial effects in the reversal of atherosclerosis in atherosclerotic animals. Therefore, in this study, the investigators will explore the potential efficacy of IV trehalose administration on arterial inflammation by employing an positron emission tomography (PET) with 18F-labeled fluoro-2-deoxyglucose (18F-FDG) and computed tomography (18F-FDG PET/CT) technique which noninvasively characterizes vascular inflammation and atherosclerosis.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Quadruple blind (participant, care provider, investigator, outcomes assessor)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Trehalose | Experimental | Drug: TrehaloseParticipants will be received intravenous trehalose infusion weekly (15 g/week) for a period of 12 weeks |
| Placebo | Placebo comparator | Drug: Normal salineParticipants will be received equal volume of normal saline weekly for a period of 12 weeks |
Who may qualify
- Ages
- 18 to 55 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult
Key inclusion criteria (4 listed)
- Men and women aged between 18-55 years
- Having a history of acute coronary syndrome
- Having a baseline high-sensitivity C-reactive protein (hs-CRP) of ≥ 2mg/L
- Willingness to participate in the trials.
Key exclusion criteria (8 listed)
- Lactation or breastfeeding
- Diabetes mellitus
- Nephrotic syndrome or Estimated Glomerular Filtration Rate (eGFR) < 30/mL/min/1.73m2
- Active or recurrent hepatic disease or/and alanine aminotransferase (ALT)/aspartate aminotransferase (AST) (ALT/AST) of > 3 times upper normal limit or total bilirubin of > 2 times upper normal limit
- Active infectious or febrile disease
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 |
|---|---|---|
| TrehaloseAlso: MycoseTrehalose is a natural disaccharide sugar found extensively among miscellaneous organisms including bacteria, plants, insects, yeast, fungi, and invertebrates. By preventing protein denaturation, it plays various protective roles against stress conditions such as heat, freeze, oxidation, desiccation and dehydration. Owing to this capacity, trehalose is an FDA-approved pharmaceutical excipient that is used as a stabilizer in numerous medicines including parenteral products. In this study, all injections will be conducted by a trained nurse in the presence of a specialist physician at a duration of 45-90 minutes. | Drug | Trehalose |
| Normal salineAlso: Physiological saline, Isotonic salineA solution of 0.90% w/v of sodium chloride (NaCl) in water | Drug | Placebo |
Primary outcome
Arterial wall inflammation in the aorta and carotid arteries
Time frame: At the beginning and end of the intervention trial (Day 0 and week 12)
This will be assessed using the 18F-FDG PET/CT imaging technique
11 secondary outcomes
Carotid intima-media thickness (cIMT)
Time frame: At the beginning and end of the intervention trial (Day 0 and week 12)
Measuring beclin-1 to assess autophagy activation
Time frame: At the beginning and end of the intervention trial (Day 0 and week 12)
Measuring high-sensitivity C-reactive protein (hs-CRP) to assess systemic inflammation
Time frame: At the beginning and end of the intervention trial (Day 0 and week 12)
Measuring complete blood count (CBC) (Safety)
Time frame: At the beginning and end of the intervention trial (Day 0 and week 12)
Assessing lipid profile (Safety)
Time frame: At the beginning and end of the intervention trial (Day 0 and week 12)
Assessing glucose (Safety)
Time frame: At the beginning and end of the intervention trial (Day 0 and week 12)
Measuring thyroid-stimulating hormone (TSH) to assess thyroid function (Safety)
Time frame: At the beginning and end of the intervention trial (Day 0 and week 12)
Measuring alanine aminotransferase (ALT), aspartate aminotransferase (AST) and bilirubin (Bil) to assess liver function (Safety)
Time frame: At the beginning and end of the intervention trial (Day 0 and week 12)
Measuring creatinine (Cr), urine (Ur) and blood urea nitrogen (BUN) to assess renal function (Safety)
Time frame: At the beginning and end of the intervention trial (Day 0 and week 12)
Evaluating electrocardiogram (ECG) and heart rhythm to assess heart function (Safety)
Time frame: At the beginning and end of the intervention trial (Day 0 and week 12)
Measuring creatinine phosphokinase (CPK) to detect muscle damage (Safety)
Time frame: At the beginning and end of the intervention trial (Day 0 and week 12)
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 21 Sep 2020.
- Background: PubMed 22895665Libby P. Inflammation in atherosclerosis. Arterioscler Thromb Vasc Biol. 2012 Sep;32(9):2045-51. doi: 10.1161/ATVBAHA.108.179705.
- Background: PubMed 29325641Libby P, Hansson GK. Taming Immune and Inflammatory Responses to Treat Atherosclerosis. J Am Coll Cardiol. 2018 Jan 16;71(2):173-176. doi: 10.1016/j.jacc.2017.10.081. No abstract available.
- Background: PubMed 22445600Liao X, Sluimer JC, Wang Y, Subramanian M, Brown K, Pattison JS, Robbins J, Martinez J, Tabas I. Macrophage autophagy plays a protective role in advanced atherosclerosis. Cell Metab. 2012 Apr 4;15(4):545-53. doi: 10.1016/j.cmet.2012.01.022. Epub 2012 Mar 22.
- Background: PubMed 23401644Maiuri MC, Grassia G, Platt AM, Carnuccio R, Ialenti A, Maffia P. Macrophage autophagy in atherosclerosis. Mediators Inflamm. 2013;2013:584715. doi: 10.1155/2013/584715. Epub 2013 Jan 21.
- Background: PubMed 26750103Shao BZ, Han BZ, Zeng YX, Su DF, Liu C. The roles of macrophage autophagy in atherosclerosis. Acta Pharmacol Sin. 2016 Feb;37(2):150-6. doi: 10.1038/aps.2015.87. Epub 2016 Jan 11.
- Background: PubMed 29175654Iwatsuka R, Matsue Y, Yonetsu T, O'uchi T, Matsumura A, Hashimoto Y, Hirao K. Arterial inflammation measured by 18F-FDG-PET-CT to predict coronary events in older subjects. Atherosclerosis. 2018 Jan;268:49-54. doi: 10.1016/j.atherosclerosis.2017.11.016. Epub 2017 Nov 21.
- Background: PubMed 26841377Chrapko BE, Chrapko M, Nocun A, Stefaniak B, Zubilewicz T, Drop A. Role of 18F-FDG PET/CT in the diagnosis of inflammatory and infectious vascular disease. Nucl Med Rev Cent East Eur. 2016;19(1):28-36. doi: 10.5603/NMR.2016.0006.
- Background: PubMed 19443587Menezes LJ, Kotze CW, Hutton BF, Endozo R, Dickson JC, Cullum I, Yusuf SW, Ell PJ, Groves AM. Vascular inflammation imaging with 18F-FDG PET/CT: when to image? J Nucl Med. 2009 Jun;50(6):854-7. doi: 10.2967/jnumed.108.061432. Epub 2009 May 14.
- Background: PubMed 15299033Chen Q, Haddad GG. Role of trehalose phosphate synthase and trehalose during hypoxia: from flies to mammals. J Exp Biol. 2004 Aug;207(Pt 18):3125-9. doi: 10.1242/jeb.01133.
- Background: PubMed 23851366Castillo K, Nassif M, Valenzuela V, Rojas F, Matus S, Mercado G, Court FA, van Zundert B, Hetz C. Trehalose delays the progression of amyotrophic lateral sclerosis by enhancing autophagy in motoneurons. Autophagy. 2013 Sep;9(9):1308-20. doi: 10.4161/auto.25188. Epub 2013 Jun 6.
- Background: PubMed 26905424Mardones P, Rubinsztein DC, Hetz C. Mystery solved: Trehalose kickstarts autophagy by blocking glucose transport. Sci Signal. 2016 Feb 23;9(416):fs2. doi: 10.1126/scisignal.aaf1937.
- Background: PubMed 28589926Sergin I, Evans TD, Zhang X, Bhattacharya S, Stokes CJ, Song E, Ali S, Dehestani B, Holloway KB, Micevych PS, Javaheri A, Crowley JR, Ballabio A, Schilling JD, Epelman S, Weihl CC, Diwan A, Fan D, Zayed MA, Razani B. Exploiting macrophage autophagy-lysosomal biogenesis as a therapy for atherosclerosis. Nat Commun. 2017 Jun 7;8:15750. doi: 10.1038/ncomms15750.
- 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.
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 2 study testing Trehalose and Normal saline in people with Acute Coronary Syndrome, run by Mashhad University of Medical Sciences at 1 site in Iran.
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 4 inclusion and 8 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 21 Sep 2020. 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 Iran. 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. Some participants in this study may receive a placebo. 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 2 studies give the treatment to a larger group to see whether it has the intended effect and to keep checking safety.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
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 Amirhossien Sahebkar, PharmD, PhD (+985138002299, SahebkarA@mums.ac.ir), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Arterial wall inflammation in the aorta and carotid arteries (time frame: At the beginning and end of the intervention trial (Day 0 and week 12)). 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 NCT03700424, which also lists 14 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 21 Sep 2020.