Rheumatoid ArthritisSOARNCT05112120
Exploiting Leading Edge 7T MRI Brain Imaging to Decipher Olumiant's Mode of Analgesic Action in Rheumatoid Arthritis
An observational study of Rheumatoid Arthritis, run by NHS Greater Glasgow and Clyde at 1 site in United Kingdom.
Trial summary
The revolution in treatments for rheumatoid arthritis (RA) has transformed patient outcomes, but many patients continue to experience life disabling pain. Even those who achieve full disease remission with state-of-the-art treatments report substantially higher levels of pain when compared to the general population. Read more about this study
- Who is it for?
- Ages 18 to 74 years
- Conditions the study is for
- Rheumatoid Arthritis
- What is being tested?
- Olumiant
- How many people
- 13 participants
- Where
- 1 siteUnited Kingdom
- Study dates
- 21 Jul 2021to 3 Aug 2023
- 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 74 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Patients with active RA attending clinics in NHS Greater Glasgow and Clyde who are scheduled to begin Olumiant as part of their standard NHS clinical care will be asked to contribute to this study by their point of care team.
Who may be able to join
- Adults ≥ 18 years < 75 years.
- Clinical diagnosis of RA
- Selected to start Olumiant by their usual rheumatology clinical team in line with local guidance (previous failure of at least 2 DMARDs and moderate to severe disease active disease)
- Right-handed (to reduce neuroimaging heterogeneity)
Who cannot join
- Inability to provide written informed consent.
- Severe physical impairment (e.g. blindness, deafness, paraplegia).
- Pregnant or breast feeding.
- Contraindications to MRI (e.g. severe claustrophobia).
- Major confounding neurological disease including Multiple Sclerosis, Stroke, Traumatic Brain Injury, Parkinson's Disease, Alzheimer's Disease
- Previous targeted synthetic (e.g. Oluminant, tofacitinib) DMARD exposure.
Show all 9Show fewer
- Co-morbid medical conditions that may significantly impair physical functional status
- Medical or psychiatric conditions that in the judgment of study personnel would preclude participation in this study (e.g., malignancy, psychosis, suicidal ideation)
- BMI > 40 or unable to lie comfortably in MRI
Trial locations and contacts
1 site in 1 country.
About this study
The revolution in treatments for rheumatoid arthritis (RA) has transformed patient outcomes, but many patients continue to experience life disabling pain. Even those who achieve full disease remission with state-of-the-art treatments report substantially higher levels of pain when compared to the general population. Researchers believe this disconnect is due to the existence of pain sources that are in addition to those present in the joints. In particular, the central nervous system (CNS) may have an important role in determining RA pain.
According to a recent study, RA patients who received treatment with Olumiant (a Janus Kinase (JAK) inhibitor that works by interfering with the inflammatory processes that lead to the symptoms of RA) reported better and quicker pain improvements compared to those receiving other types of therapy. However, this could not be explained by levels of peripheral inflammation alone and remains to be fully understood. Investigators think this improvement may be related to the role of the JAK pathway in the brain and that inhibition of this pathway with Olumiant could normalise brain connectivity in respect to pain processing.
Advanced brain scanning methods have already helped to identify specific regions of the brain that are thought to be important in pain processing and peripheral inflammation; a) enhanced functional connectivity between the Default Mode Network (DMN) and insula and b) enhanced functional connectivity between the Dorsal Attention Network (DAN) and the left inferior parietal lobule (LIPL). This study aims to elucidate the mechanisms of analgesic action of Olumiant by examining changes in functional connectivity and glutamate levels within the CNS and exploring the relationship between MRI markers, pain, clinical phenotype and peripheral immune markers.
Read the detailed description
Investigators believe that RA is a mixed pain state i.e. pain pathways exist in addition to established peripheral inflammatory nociceptive mechanisms. In particular, the central nervous system (CNS) may have an important role in determining RA pain. Recently this group were the first to delineate distinct neurobiological pain signatures in the brains of RA patients by employing 3T functional connectivity magnetic resonance imaging (fcMRI) - a recent adaptation of functional MRI data that examines the synchrony of neural activity which modulates the efficiency and extent of neuronal transmission between brain regions. Specifically, researchers identified and replicated two distinct pain signatures: a) enhanced functional connectivity between the Default Mode Network (DMN) and insula which was unrelated to levels of peripheral inflammation but, intriguingly, is an established neurobiological marker of fibromyalgia (an archetypal CNS determined chronic pain disorder) and b) enhanced functional connectivity between the Dorsal Attention Network (DAN) and the left inferior parietal lobule (LIPL)6 which was related to levels of peripheral inflammation.
Pre-clinical experiments have not only implicated the JAK- signal transducer and activator of transcription (STAT) pathway with peripheral immune system functioning but also the brain. In the CNS, this pathway promotes gene expression associated with inflammation which in turn generates pro-nociceptive cytokines such as TNFα. However, there is now also emerging evidence to support the pathway's direct role in synaptic transmission and neurotransmitter receptor modulation. Specifically, the JAK-STAT pathway appears important in N-methyl-d-aspartate (NMDA) related synaptic plasticity - a ubiquitous glutamate receptor of the human brain. Their induction is selectively blocked by JAK inhibitors and JAK2 knockdown abolishes NMDA functioning. Increases in glutamate and subsequent binding to NMDA receptors cause chaotic and incoherent neuronal functional activity. In human studies of fibromyalgia, we have consistently evidenced both elevated glutamate levels within the insula and dysfunctional neural connectivity. Moreover, this group have shown that fibromyalgia pharmacotherapy (pregablin), considered to reduce neural glutamate, rectifies both insular glutamate and pro-nociceptive brain functional connectivity (DMN-insula). JAK inhibition (JAKi) may facilitate the reduction of glutamate-NMDA binding and ultimately pain alleviation by normalising the functional activity of these same neural connections.
There are clear practical constraints of sampling fresh human brain tissue in order to interrogate these possible mechanisms. Instead, neurobiological surrogate imaging measures may be employed. Glasgow benefits from the only clinical based ultra-high resolution 7T MRI scanner in the UK. Unlike lesser resolutions, 7T can distinguish the resonance of glutamate from other metabolites and so more precisely quantify the chemical of interest. Further, the superior spatial resolution of 7T enhances capacity to indirectly measure neuronal functional connectivity.
Investigators hypothesise that Olumiant's mechanism of analgesic action is determined by at least two factors. The first is related to those pathways seen in fibromyalgia, mediated via DMN-insula connectivity and insular glutamate. The second is related to peripheral inflammation, mediated via DAN-LIPL.
The study objectives include: 1) To evaluate the effects of Olumiant on DMN-Insula connectivity and insular glutamate levels in RA (neurobiological markers of fibromyalgia). 2) To evaluate the effects of Olumiant on DAN-LIPL connectivity in RA (neurobiological marker of peripheral inflammation). 3) To explore the relationship between pain, clinical phenotype, peripheral immune markers and their change with MRI markers indicative of CNS pathway function. The study will involve participants aged over 18 years with RA who are scheduled to start outpatient Olumiant as part of standard clinical practice, and who meet the inclusion criteria and none of the exclusion criteria.
- Conditions
- Rheumatoid Arthritis
- Being tested
- Olumiant
- Medical subject headings
- Arthritis, Rheumatoid
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
OlumiantDrug
Also called Baricitinib
Olumiant (4mg) will be administered in line with standard of care guidance.
| Study group | Role | What they receive |
|---|---|---|
| Single centre single arm observational cohort | Olumiant (4mg) will be administered in line with standard of care guidance. This is the standard dose in line with license for use in active moderate to severe RA. A dose adjustment from 4mg to 2mg is permitted during the study depending on side-effects Receives: Drug: Olumiant |
What is being measured
The primary outcome is the main question the study is designed to answer.
To evaluate the effects of Olumiant on DMN-Insula connectivity
To measure brain functional connectivity DMN- insula and DNA- LIPL as measured by 7T MRS
Measured: 12 weeks
To evaluate the effects of Oluminant treatment on insular glutamate levels in RA (neurobiological markers of fibromyalgia).
To examine changes in the insular glutamate signal as measured by the 7T MRS
Measured: 12 weeks
Secondary outcomes (18)
Changes in clinical phenotype as measured by the EULAR Disease Activity Score (DAS28)
Changes in clinical phenotype as measured by the EULAR Disease Activity Score (DAS28) from week 0 to week 12
Measured: 12 weeks
Changes in clinical phenotype as measured by the CDAI
Changes in clinical phenotype as measured by the Clinical Disease Activity Index from week 0 to week 12
Measured: 12 weeks
Changes in clinical phenotype as measured by the SDAI
Changes in clinical phenotype as measured by the Simple Disease Activity Index from week 0 to week 12
Measured: 12 weeks
Changes in sickness behaviour as measured by the 7-Day Symptom Diary (Number Rating Scale)
Changes in sickness behaviours as measured by the 7-Day Symptom Diary (Number Rating Scale) from week 0 to week 12
Measured: 12 weeks
Changes in sickness behaviour as measured by the American College of Rheumatology Fibromyalgia Scale
Changes in fibromyalgia as measured by the American College of Rheumatology Fibromyalgia Scale from week 0 to week 12
Measured: 12 weeks
Changes in sickness behaviour as measured by the McGill Pain Questionnaire
Changes in pain as measured by the McGill Pain Questionnaire from week 0 to week 12
Measured: 12 weeks
Changes in sickness behaviour as measured by the Michigan Body Map Regional Pain
Changes in pain as measured by the Michigan Body Map Regional Pain from week 0 to week 12
Measured: 12 weeks
Changes in sickness behaviour as measured by the PROMIS-Depression
Changes in depression as measured by the PROMIS-Depression from week 0 to week 12
Measured: 12 weeks
Changes in sickness behaviour as measured by the PROMIS-Anxiety
Changes in anxiety as measured by the PROMIS-Anxiety from week 0 to week 12
Measured: 12 weeks
Changes in sickness behaviour as measured by the PROMIS-Fatigue
Changes in fatigue as measured by the PROMIS-Fatigue from week 0 to week 12
Measured: 12 weeks
Changes in sickness behaviour as measured by the PROMIS-Sleep related impairment
Changes in sleep as measured by the PROMIS-Sleep related impairment from week 0 to week 12
Measured: 12 weeks
Changes in sickness behaviour as measured by the PROMIS-Physical functioning short form
Changes in physical functioning as measured by the PROMIS-Physical functioning short form from week 0 to week 12
Measured: 12 weeks
Changes in sickness behaviour as measured by the PROMIS-Pain inference
Changes in pain interference as measured by the PROMIS-Pain inference from week 0 to week 12
Measured: 12 weeks
Changes in sickness behaviour as measured by the Cognitive Failures Questionnaire
Changes in cognitive function as measured by the Cognitive Failures Questionnaire from week 0 to week 12
Measured: 12 weeks
Changes in sickness behaviour as measured by the Sickness Questionnaire
Changes in sickness behaviours as measured by the Sickness Questionnaire from week 0 to week 12
Measured: 12 weeks
Changes in joint inflammation as measured by the Synovitis score
Changes in joint inflammation as measured by the Synovitis score (from joint ultrasound) from week 0 to week 12
Measured: 12 weeks
Changes in pain as measured by the Pain sensitivity variables
Changes in pain as measured by the Pain sensitivity variables (from Quantitative Sensory Testing measures) from week 0 to week 12
Measured: 12 weeks
Changes in inflammation as measured by the Changes in inflammatory cytokines/chemokines
Changes in peripheral inflammation as measured by the changes in inflammatory cytokines/chemokines from week 0 to week 12
Measured: 12 weeks
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted8 Nov 2021
- Study start21 Jul 2021
- Primary completion3 Aug 2023
- Study completion3 Aug 2023
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for Rheumatoid ArthritisStudies 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
- Cohort
- Time perspective
- Prospective
- Enrolment
- 13 participants (actual)
Sponsor and investigators
- Lead sponsor
- NHS Greater Glasgow and Clyde
- Sponsor type
- University, hospital or other
- Collaborators
- University of Michigan
- Responsible party
- Sponsor
- Investigators
- Neil Basu, M.D Ph.D, Principal investigator, University of Glasgow
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05112120
- Sponsor's protocol ID
- GN19RH319
- Acronym
- SOAR
- Status last verified
- Oct 2023
- First submitted
- 1 Oct 2021
- Last updated
- 31 Oct 2023
- Results posted
- No
- Individual data sharing
- Undecided
Study at a glance
From the registry record, last updated by the sponsor on 31 Oct 2023. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Exploiting Leading Edge 7T MRI Brain Imaging to Decipher Olumiant's Mode of Analgesic Action in Rheumatoid Arthritis
- ClinicalTrials.gov ID
- NCT05112120
- Acronym / sponsor ID
- SOAR / GN19RH319
- Conditions
- Rheumatoid Arthritis
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 13 participants (actual)
- Lead sponsor
- NHS Greater Glasgow and ClydeUniversity, hospital or other
- Collaborators
- University of Michigan
- Study start
- 21 Jul 2021 (actual)
- Primary completion
- 3 Aug 2023 (actual)
- Study completion
- 3 Aug 2023 (actual)
- First posted
- 8 Nov 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 revolution in treatments for rheumatoid arthritis (RA) has transformed patient outcomes, but many patients continue to experience life disabling pain. Even those who achieve full disease remission with state-of-the-art treatments report substantially higher levels of pain when compared to the general population. Researchers believe this disconnect is due to the existence of pain sources that are in addition to those present in the joints. In particular, the central nervous system (CNS) may have an important role in determining RA pain.
According to a recent study, RA patients who received treatment with Olumiant (a Janus Kinase (JAK) inhibitor that works by interfering with the inflammatory processes that lead to the symptoms of RA) reported better and quicker pain improvements compared to those receiving other types of therapy. However, this could not be explained by levels of peripheral inflammation alone and remains to be fully understood. Investigators think this improvement may be related to the role of the JAK pathway in the brain and that inhibition of this pathway with Olumiant could normalise brain connectivity in respect to pain processing.
Advanced brain scanning methods have already helped to identify specific regions of the brain that are thought to be important in pain processing and peripheral inflammation; a) enhanced functional connectivity between the Default Mode Network (DMN) and insula and b) enhanced functional connectivity between the Dorsal Attention Network (DAN) and the left inferior parietal lobule (LIPL). This study aims to elucidate the mechanisms of analgesic action of Olumiant by examining changes in functional connectivity and glutamate levels within the CNS and exploring the relationship between MRI markers, pain, clinical phenotype and peripheral immune markers.
Detailed description
Investigators believe that RA is a mixed pain state i.e. pain pathways exist in addition to established peripheral inflammatory nociceptive mechanisms. In particular, the central nervous system (CNS) may have an important role in determining RA pain. Recently this group were the first to delineate distinct neurobiological pain signatures in the brains of RA patients by employing 3T functional connectivity magnetic resonance imaging (fcMRI) - a recent adaptation of functional MRI data that examines the synchrony of neural activity which modulates the efficiency and extent of neuronal transmission between brain regions. Specifically, researchers identified and replicated two distinct pain signatures: a) enhanced functional connectivity between the Default Mode Network (DMN) and insula which was unrelated to levels of peripheral inflammation but, intriguingly, is an established neurobiological marker of fibromyalgia (an archetypal CNS determined chronic pain disorder) and b) enhanced functional connectivity between the Dorsal Attention Network (DAN) and the left inferior parietal lobule (LIPL)6 which was related to levels of peripheral inflammation.
Pre-clinical experiments have not only implicated the JAK- signal transducer and activator of transcription (STAT) pathway with peripheral immune system functioning but also the brain. In the CNS, this pathway promotes gene expression associated with inflammation which in turn generates pro-nociceptive cytokines such as TNFα. However, there is now also emerging evidence to support the pathway's direct role in synaptic transmission and neurotransmitter receptor modulation. Specifically, the JAK-STAT pathway appears important in N-methyl-d-aspartate (NMDA) related synaptic plasticity - a ubiquitous glutamate receptor of the human brain. Their induction is selectively blocked by JAK inhibitors and JAK2 knockdown abolishes NMDA functioning. Increases in glutamate and subsequent binding to NMDA receptors cause chaotic and incoherent neuronal functional activity. In human studies of fibromyalgia, we have consistently evidenced both elevated glutamate levels within the insula and dysfunctional neural connectivity. Moreover, this group have shown that fibromyalgia pharmacotherapy (pregablin), considered to reduce neural glutamate, rectifies both insular glutamate and pro-nociceptive brain functional connectivity (DMN-insula). JAK inhibition (JAKi) may facilitate the reduction of glutamate-NMDA binding and ultimately pain alleviation by normalising the functional activity of these same neural connections.
There are clear practical constraints of sampling fresh human brain tissue in order to interrogate these possible mechanisms. Instead, neurobiological surrogate imaging measures may be employed. Glasgow benefits from the only clinical based ultra-high resolution 7T MRI scanner in the UK. Unlike lesser resolutions, 7T can distinguish the resonance of glutamate from other metabolites and so more precisely quantify the chemical of interest. Further, the superior spatial resolution of 7T enhances capacity to indirectly measure neuronal functional connectivity.
Investigators hypothesise that Olumiant's mechanism of analgesic action is determined by at least two factors. The first is related to those pathways seen in fibromyalgia, mediated via DMN-insula connectivity and insular glutamate. The second is related to peripheral inflammation, mediated via DAN-LIPL.
The study objectives include: 1) To evaluate the effects of Olumiant on DMN-Insula connectivity and insular glutamate levels in RA (neurobiological markers of fibromyalgia). 2) To evaluate the effects of Olumiant on DAN-LIPL connectivity in RA (neurobiological marker of peripheral inflammation). 3) To explore the relationship between pain, clinical phenotype, peripheral immune markers and their change with MRI markers indicative of CNS pathway function. The study will involve participants aged over 18 years with RA who are scheduled to start outpatient Olumiant as part of standard clinical practice, and who meet the inclusion criteria and none of the exclusion criteria.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| Single centre single arm observational cohort | – | Drug: OlumiantOlumiant (4mg) will be administered in line with standard of care guidance. This is the standard dose in line with license for use in active moderate to severe RA. A dose adjustment from 4mg to 2mg is permitted during the study depending on side-effects |
Who may qualify
- Ages
- 18 to 74 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Patients with active RA attending clinics in NHS Greater Glasgow and Clyde who are scheduled to begin Olumiant as part of their standard NHS clinical care will be asked to contribute to this study by their point of care team.
Key inclusion criteria (4 listed)
- Adults ≥ 18 years < 75 years.
- Clinical diagnosis of RA
- Selected to start Olumiant by their usual rheumatology clinical team in line with local guidance (previous failure of at least 2 DMARDs and moderate to severe disease active disease)
- Right-handed (to reduce neuroimaging heterogeneity)
Key exclusion criteria (9 listed)
- Inability to provide written informed consent.
- Severe physical impairment (e.g. blindness, deafness, paraplegia).
- Pregnant or breast feeding.
- Contraindications to MRI (e.g. severe claustrophobia).
- Major confounding neurological disease including Multiple Sclerosis, Stroke, Traumatic Brain Injury, Parkinson's Disease, Alzheimer's 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 |
|---|---|---|
| OlumiantAlso: BaricitinibOlumiant (4mg) will be administered in line with standard of care guidance. | Drug | Single centre single arm observational cohort |
Primary outcome
To evaluate the effects of Olumiant on DMN-Insula connectivity
Time frame: 12 weeks
To measure brain functional connectivity DMN- insula and DNA- LIPL as measured by 7T MRS
To evaluate the effects of Oluminant treatment on insular glutamate levels in RA (neurobiological markers of fibromyalgia).
Time frame: 12 weeks
To examine changes in the insular glutamate signal as measured by the 7T MRS
18 secondary outcomes
Changes in clinical phenotype as measured by the EULAR Disease Activity Score (DAS28)
Time frame: 12 weeks
Changes in clinical phenotype as measured by the CDAI
Time frame: 12 weeks
Changes in clinical phenotype as measured by the SDAI
Time frame: 12 weeks
Changes in sickness behaviour as measured by the 7-Day Symptom Diary (Number Rating Scale)
Time frame: 12 weeks
Changes in sickness behaviour as measured by the American College of Rheumatology Fibromyalgia Scale
Time frame: 12 weeks
Changes in sickness behaviour as measured by the McGill Pain Questionnaire
Time frame: 12 weeks
Changes in sickness behaviour as measured by the Michigan Body Map Regional Pain
Time frame: 12 weeks
Changes in sickness behaviour as measured by the PROMIS-Depression
Time frame: 12 weeks
Changes in sickness behaviour as measured by the PROMIS-Anxiety
Time frame: 12 weeks
Changes in sickness behaviour as measured by the PROMIS-Fatigue
Time frame: 12 weeks
Changes in sickness behaviour as measured by the PROMIS-Sleep related impairment
Time frame: 12 weeks
Changes in sickness behaviour as measured by the PROMIS-Physical functioning short form
Time frame: 12 weeks
Changes in sickness behaviour as measured by the PROMIS-Pain inference
Time frame: 12 weeks
Changes in sickness behaviour as measured by the Cognitive Failures Questionnaire
Time frame: 12 weeks
Changes in sickness behaviour as measured by the Sickness Questionnaire
Time frame: 12 weeks
Changes in joint inflammation as measured by the Synovitis score
Time frame: 12 weeks
Changes in pain as measured by the Pain sensitivity variables
Time frame: 12 weeks
Changes in inflammation as measured by the Changes in inflammatory cytokines/chemokines
Time frame: 12 weeks
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 31 Oct 2023.
- Individual participant dataSharing planned: Undecided
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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.
Neil Basu, M.D Ph.D principal investigator
University of Glasgow
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 Rheumatoid Arthritis, run by NHS Greater Glasgow and Clyde at 1 site in United Kingdom.
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 9 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 31 Oct 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 United Kingdom. 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?
To evaluate the effects of Olumiant on DMN-Insula connectivity (time frame: 12 weeks). 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?
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 31 Oct 2023.