Age-Related Macular DegenerationNCT02762188
Genetic Biomarkers for the Response to Anti-VEGF (Vascular Endothelial Growth Factor).Treatment in Wet Age-related Macular Degeneration (Wet ARMD)
A study testing Genotype analysis in people with Age-Related Macular Degeneration, run by Brugmann University Hospital at 1 site in Belgium.
Trial summary
Age-Related Macular Degeneration (ARMD) is the most common cause of blindness in the adult population of the Western World. It affects the macula - the region of the retina most rich in photoreceptors and responsible for central vision. The ethiology of ARMD remains poorly understood. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Age-Related Macular Degeneration
- What is being tested?
- Genotype analysis
- Type of treatment
- Injection or infusion, Medical device
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 501 participants
- Where
- 1 siteBelgium
- Study dates
- 1 Aug 2013to 18 Jan 2018
- Phase
- Interventional
- 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
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- Patients with the wet form of ARMD who receive or have received in the past anti VEGF intra vitreal injections
Who cannot join
- Patients whi had received treatments other than anti VEGF, before the use of anti-VEGF
- Patients without follow-up
- Patients receiving anti-VEGF because of another pathology than ARMD
Trial locations and contacts
1 site in 1 country.
About this study
Age-Related Macular Degeneration (ARMD) is the most common cause of blindness in the adult population of the Western World. It affects the macula - the region of the retina most rich in photoreceptors and responsible for central vision. The ethiology of ARMD remains poorly understood. Population-based studies have demonstrated a complex ethiology, with contributions from a combination of genetic and environmental factors.
Two major forms of ARMD are clinically distinguishable: the dry and wet form. The latter represents the more aggressive clinical subgroup, and is characterized by the abnormal growth of new blood vessels (neovascularization) under the macula, thus leading to the accumulation of fluid under the retina, bleeding, progression to fibrosis, and finally loss of central vision.
Read more
The pathogenesis of this neovascularization is not fully understood, although the VEGF pathway is well known to be involved in angiogenesis and was implicated in the development of the new vessels under the macula. The VEGFs are the most specific and potent stimulators of the angiogenesis.
Molecules that bind and inactivate the VEGF have been developed for the treatment of ARMD and they are applied in ARMD clinic through intra vitreal injections.The difference seen in response to anti VEGF treatment for ARMD between the patients is suggestive for the presence of factors influencing the effect of the drug. Some of these could be genetic variants within genes involved in ARMD pathogenesis or VEGF pathway. Few associations with markers within genes previously found to be related with the pathogenesis of ARMD have been found. It remains unknown whether variants involved in the anti VEGF treatment response could influence the therapeutic outcome.
The purpose of this trial is to evaluate the association between a panel of selected polymorphic markers in the VEGF pathway and the response to therapy with anti VEGF antibody for ARMD. The hypothesis is that the individual genotype influences the response to the anti VEGF. This can lead to identification of genetic biomarkers allowing treatment individualization and optimization of the visual outcomes.
Read the detailed description
Age-Related Macular Degeneration (ARMD) is the most common cause of blindness in the adult population of the Western World. It affects the macula - the region of the retina most rich in photoreceptors and responsible for central vision.
Despite this manifest importance, the ethiology of ARMD remains poorly understood. Population-based studies have demonstrated a complex ethiology, with contributions from a combination of genetic and environmental factors. Genome-wide association studies revealed the presence of loci associated with susceptibility in a wide range of genes, including genes involved in the complement system, cholesterol homeostasis, growth factor diffusion and angiogenesis. Smoking has been identified as a major environmental factor.
Two major forms of ARMD are clinically distinguishable: the dry and wet form. The latter represents the more aggressive clinical subgroup, and is characterized by the abnormal growth of new blood vessels (neovascularization) under the macula, thus leading to the accumulation of fluid under the retina, bleeding, progression to fibrosis, and finally loss of central vision.
The pathogenesis of this neovascularization is not fully understood, although the VEGF pathway is well known to be involved in angiogenesis and was implicated in the development of the new vessels under the macula. The VEGFs are the most specific and potent stimulators of the angiogenesis. VEGF-A is a 45kD glycoprotein binding to transmembrane tyrosine kinase receptors, VEGFRs, which activates a cascade of downstream factors. VEGF-A has the strongest pro-angiogenic effect in the retina by promoting proliferation, sprouting and tubing of the endothelial cells. It can bind to at least two receptors -VEGFR1 and VEGFR2, although the most of the proangiogenic activity appears to be mediated through VEGFR2. Expression of a VEGFR2 isoform that lacks both the intracellular signaling domain and the transmembrane domain, represents a soluble form of the receptor, inactivating VEGF extracellularly.
Similarly, molecules that bind and inactivate the VEGF have been developed for the treatment of ARMD and they are applied in ARMD clinic through intra vitreal injections. These include antibodies, a recombinant receptor fusion protein and a synthetic aptamer. The anti-VEGFA antibodies - ranibizumab and bevacizumab, off-label, have been associated with limited side-effects and significant therapeutic improvement, and became the standard in the treatment of the wet form of ARMD. Indeed, for example in the first clinical trials for ranibizumab, monthly injections of ranibizumab demonstrated an average gain in visual acuity of 6.6 and 10.7 ETDRS letters after 24 months. However, currently most clinical centres apply modified treatment protocols. Commonly used is an initial loading dose of three consecutive monthly injections and subsequent follow-up and administration of additional injections depending on the evolution of visual acuity, optical coherence tomography and fluorescein angiography data . 25% of the ARMD patients show significant improvement of the visual acuity, 70% maintain or show slightly increased visual acuity, and the remaining 5 percent of the patients fail to respond to the treatment and continue to loose vision.
The difference seen in response to anti VEGF treatment for ARMD between the patients is suggestive for the presence of factors influencing the effect of the drug. Some of these could be genetic variants within genes involved in ARMD pathogenesis or VEGF pathway. Few associations with markers within genes previously found to be related with the pathogenesis of ARMD have been found. It remains unknown whether variants involved in the anti VEGF treatment response could influence the therapeutic outcome.
A study demonstrated that the single nucleotide polymorphism (SNP) in VEGFR1 rs7993418 (TAC codon) form is associated to resistance to the anti VEGF therapy in carcinoma patients. This specific genotype leads to an increased expression of the VEGFR1 without changing the amino acid content of the protein. The increased VEGFR1 protein is most likely due to higher efficiency of messenger ribonucleic acid (mRNA) translation.
The purpose of this trial is to evaluate the association between a panel of selected polymorphic markers in the VEGF pathway and the response to therapy with anti VEGF antibody for ARMD. The hypothesis is that the individual genotype influences the response to the anti VEGF. This can lead to identification of genetic biomarkers allowing treatment individualization and optimization of the visual outcomes.
- Conditions
- Age-Related Macular Degeneration
- Being tested
- Genotype analysis
- Keywords
- wet ARMD, VEGF, intra vitreal injections
- Medical subject headings
- Macular Degeneration
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Genotype analysisDevice
After signing informed consent, a blood sample is taken and DNA extracted according to standard procedures. The samples are genotyped with the Mass Array iPlex Gold. Processing of the data is done using the previously described protocol by Lambrechts and co.
Statistical analysis will be done to evaluate the association between the different genetic variants and the clinical outcomes collected during the standard of care follow-up for ARMD.
| Study group | Role | What they receive |
|---|---|---|
| wet ARMD patients | Experimental | Patients with the wet form of ARMD who receive or have received in the past anti VEGF intra vitreal injections. Diagnosis of wet ARMD is made based on clinical data-visual acuity, fundus presence of subretinal fluid and/or haemorrhage and/or hard exudates, fundus photographs -color and red free, optical coherence tomography (SD-OCT), fluorescein angiography and indocyanine green angiography showing the presence and activity of subretinal neovascularisation. Receives: Device: Genotype analysis |
What is being measured
The primary outcome is the main question the study is designed to answer.
Snellen visual acuity test result
The visual acuity test is used to determine the smallest letters you can read on a standardized chart (Snellen chart).
Measured: Baseline
Snellen visual acuity test result
The visual acuity test is used to determine the smallest letters you can read on a standardized chart (Snellen chart).
Measured: 3 months after treatment
Snellen visual acuity test result
The visual acuity test is used to determine the smallest letters you can read on a standardized chart (Snellen chart).
Measured: 6 months after treatment
Snellen visual acuity test result
The visual acuity test is used to determine the smallest letters you can read on a standardized chart (Snellen chart).
Measured: 12 months after treatment
Number of injections received per year
Measured: 1 year
Central foveal thickness (µm)
Measured by optical coherence tomography (Heidelberg \& Zeiss)
Measured: Baseline
Central foveal thickness (µm)
Measured by optical coherence tomography (Heidelberg \& Zeiss)
Measured: 3 months after treatment
Central foveal thickness (µm)
Measured by optical coherence tomography (Heidelberg \& Zeiss)
Measured: 6 months after treatment
Central foveal thickness (µm)
Measured by optical coherence tomography (Heidelberg \& Zeiss)
Measured: 12 months after treatment
Presence of Intra Retinal Cysts (yes/no)
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Measured: Baseline
Presence of Intra Retinal Cysts (yes/no)
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Measured: 3 months after treatment
Presence of Intra Retinal Cysts (yes/no)
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Measured: 4 months after treatment
Presence of Subretinal Fluid (yes/no)
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Measured: Baseline
Presence of Subretinal Fluid (yes/no)
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Measured: 3 months after treatment
Presence of Subretinal Fluid (yes/no)
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Measured: 4 months after treatment
Presence of Pigment Epithelial Detachment (yes/no)
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Measured: Baseline
Presence of Pigment Epithelial Detachment (yes/no)
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Measured: 3 months after treatment
Presence of Pigment Epithelial Detachment (yes/no)
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Measured: 4 months after treatment
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted4 May 2016 (estimated)
- Study start1 Aug 2013
- Primary completion18 Jan 2018
- Study completion18 Jan 2018
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for Age-Related Macular DegenerationStudies 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 N/A
- Primary purpose
- Basic science
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Enrolment
- 501 participants (actual)
Sponsor and investigators
- Lead sponsor
- Brugmann University Hospital
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Laurence Postelmans, Brugmann University Hospital
- Investigators
- Laurence Postelmans, MD, Principal investigator, CHU Brugmann
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02762188
- Sponsor's protocol ID
- CHUB-SAMBA
- Status last verified
- Jan 2018
- First submitted
- 25 Apr 2016
- Last updated
- 23 Jan 2018
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Study at a glance
From the registry record, last updated by the sponsor on 23 Jan 2018. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Genetic Biomarkers for the Response to Anti-VEGF (Vascular Endothelial Growth Factor).Treatment in Wet Age-related Macular Degeneration (Wet ARMD)
- ClinicalTrials.gov ID
- NCT02762188
- Acronym / sponsor ID
- CHUB-SAMBA
- Conditions
- Age-Related Macular Degeneration
- Keywords
- wet ARMD, VEGF, intra vitreal injections
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 501 participants (actual)
- Lead sponsor
- Brugmann University HospitalUniversity, hospital or other
- Study start
- 1 Aug 2013 (actual)
- Primary completion
- 18 Jan 2018 (actual)
- Study completion
- 18 Jan 2018 (actual)
- First posted
- 4 May 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.
Age-Related Macular Degeneration (ARMD) is the most common cause of blindness in the adult population of the Western World. It affects the macula - the region of the retina most rich in photoreceptors and responsible for central vision. The ethiology of ARMD remains poorly understood. Population-based studies have demonstrated a complex ethiology, with contributions from a combination of genetic and environmental factors.
Two major forms of ARMD are clinically distinguishable: the dry and wet form. The latter represents the more aggressive clinical subgroup, and is characterized by the abnormal growth of new blood vessels (neovascularization) under the macula, thus leading to the accumulation of fluid under the retina, bleeding, progression to fibrosis, and finally loss of central vision.
The pathogenesis of this neovascularization is not fully understood, although the VEGF pathway is well known to be involved in angiogenesis and was implicated in the development of the new vessels under the macula. The VEGFs are the most specific and potent stimulators of the angiogenesis.
Molecules that bind and inactivate the VEGF have been developed for the treatment of ARMD and they are applied in ARMD clinic through intra vitreal injections.The difference seen in response to anti VEGF treatment for ARMD between the patients is suggestive for the presence of factors influencing the effect of the drug. Some of these could be genetic variants within genes involved in ARMD pathogenesis or VEGF pathway. Few associations with markers within genes previously found to be related with the pathogenesis of ARMD have been found. It remains unknown whether variants involved in the anti VEGF treatment response could influence the therapeutic outcome.
The purpose of this trial is to evaluate the association between a panel of selected polymorphic markers in the VEGF pathway and the response to therapy with anti VEGF antibody for ARMD. The hypothesis is that the individual genotype influences the response to the anti VEGF. This can lead to identification of genetic biomarkers allowing treatment individualization and optimization of the visual outcomes.
Detailed description
Age-Related Macular Degeneration (ARMD) is the most common cause of blindness in the adult population of the Western World. It affects the macula - the region of the retina most rich in photoreceptors and responsible for central vision.
Despite this manifest importance, the ethiology of ARMD remains poorly understood. Population-based studies have demonstrated a complex ethiology, with contributions from a combination of genetic and environmental factors. Genome-wide association studies revealed the presence of loci associated with susceptibility in a wide range of genes, including genes involved in the complement system, cholesterol homeostasis, growth factor diffusion and angiogenesis. Smoking has been identified as a major environmental factor.
Two major forms of ARMD are clinically distinguishable: the dry and wet form. The latter represents the more aggressive clinical subgroup, and is characterized by the abnormal growth of new blood vessels (neovascularization) under the macula, thus leading to the accumulation of fluid under the retina, bleeding, progression to fibrosis, and finally loss of central vision.
The pathogenesis of this neovascularization is not fully understood, although the VEGF pathway is well known to be involved in angiogenesis and was implicated in the development of the new vessels under the macula. The VEGFs are the most specific and potent stimulators of the angiogenesis. VEGF-A is a 45kD glycoprotein binding to transmembrane tyrosine kinase receptors, VEGFRs, which activates a cascade of downstream factors. VEGF-A has the strongest pro-angiogenic effect in the retina by promoting proliferation, sprouting and tubing of the endothelial cells. It can bind to at least two receptors -VEGFR1 and VEGFR2, although the most of the proangiogenic activity appears to be mediated through VEGFR2. Expression of a VEGFR2 isoform that lacks both the intracellular signaling domain and the transmembrane domain, represents a soluble form of the receptor, inactivating VEGF extracellularly.
Similarly, molecules that bind and inactivate the VEGF have been developed for the treatment of ARMD and they are applied in ARMD clinic through intra vitreal injections. These include antibodies, a recombinant receptor fusion protein and a synthetic aptamer. The anti-VEGFA antibodies - ranibizumab and bevacizumab, off-label, have been associated with limited side-effects and significant therapeutic improvement, and became the standard in the treatment of the wet form of ARMD. Indeed, for example in the first clinical trials for ranibizumab, monthly injections of ranibizumab demonstrated an average gain in visual acuity of 6.6 and 10.7 ETDRS letters after 24 months. However, currently most clinical centres apply modified treatment protocols. Commonly used is an initial loading dose of three consecutive monthly injections and subsequent follow-up and administration of additional injections depending on the evolution of visual acuity, optical coherence tomography and fluorescein angiography data . 25% of the ARMD patients show significant improvement of the visual acuity, 70% maintain or show slightly increased visual acuity, and the remaining 5 percent of the patients fail to respond to the treatment and continue to loose vision.
The difference seen in response to anti VEGF treatment for ARMD between the patients is suggestive for the presence of factors influencing the effect of the drug. Some of these could be genetic variants within genes involved in ARMD pathogenesis or VEGF pathway. Few associations with markers within genes previously found to be related with the pathogenesis of ARMD have been found. It remains unknown whether variants involved in the anti VEGF treatment response could influence the therapeutic outcome.
A study demonstrated that the single nucleotide polymorphism (SNP) in VEGFR1 rs7993418 (TAC codon) form is associated to resistance to the anti VEGF therapy in carcinoma patients. This specific genotype leads to an increased expression of the VEGFR1 without changing the amino acid content of the protein. The increased VEGFR1 protein is most likely due to higher efficiency of messenger ribonucleic acid (mRNA) translation.
The purpose of this trial is to evaluate the association between a panel of selected polymorphic markers in the VEGF pathway and the response to therapy with anti VEGF antibody for ARMD. The hypothesis is that the individual genotype influences the response to the anti VEGF. This can lead to identification of genetic biomarkers allowing treatment individualization and optimization of the visual outcomes.
Study design
- Primary purpose
- Basic science
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| wet ARMD patients | Experimental | Device: Genotype analysisPatients with the wet form of ARMD who receive or have received in the past anti VEGF intra vitreal injections. Diagnosis of wet ARMD is made based on clinical data-visual acuity, fundus presence of subretinal fluid and/or haemorrhage and/or hard exudates, fundus photographs -color and red free, optical coherence tomography (SD-OCT), fluorescein angiography and indocyanine green angiography showing the presence and activity of subretinal neovascularisation. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (1 listed)
- Patients with the wet form of ARMD who receive or have received in the past anti VEGF intra vitreal injections
Key exclusion criteria (3 listed)
- Patients whi had received treatments other than anti VEGF, before the use of anti-VEGF
- Patients without follow-up
- Patients receiving anti-VEGF because of another pathology than ARMD
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 |
|---|---|---|
| Genotype analysisAfter signing informed consent, a blood sample is taken and DNA extracted according to standard procedures. The samples are genotyped with the Mass Array iPlex Gold. Processing of the data is done using the previously described protocol by Lambrechts and co. Statistical analysis will be done to evaluate the association between the different genetic variants and the clinical outcomes collected during the standard of care follow-up for ARMD. | Device | wet ARMD patients |
Primary outcome
Snellen visual acuity test result
Time frame: Baseline
The visual acuity test is used to determine the smallest letters you can read on a standardized chart (Snellen chart).
Snellen visual acuity test result
Time frame: 3 months after treatment
The visual acuity test is used to determine the smallest letters you can read on a standardized chart (Snellen chart).
Snellen visual acuity test result
Time frame: 6 months after treatment
The visual acuity test is used to determine the smallest letters you can read on a standardized chart (Snellen chart).
Snellen visual acuity test result
Time frame: 12 months after treatment
The visual acuity test is used to determine the smallest letters you can read on a standardized chart (Snellen chart).
Number of injections received per year
Time frame: 1 year
Central foveal thickness (µm)
Time frame: Baseline
Measured by optical coherence tomography (Heidelberg \& Zeiss)
Central foveal thickness (µm)
Time frame: 3 months after treatment
Measured by optical coherence tomography (Heidelberg \& Zeiss)
Central foveal thickness (µm)
Time frame: 6 months after treatment
Measured by optical coherence tomography (Heidelberg \& Zeiss)
Central foveal thickness (µm)
Time frame: 12 months after treatment
Measured by optical coherence tomography (Heidelberg \& Zeiss)
Presence of Intra Retinal Cysts (yes/no)
Time frame: Baseline
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Presence of Intra Retinal Cysts (yes/no)
Time frame: 3 months after treatment
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Presence of Intra Retinal Cysts (yes/no)
Time frame: 4 months after treatment
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Presence of Subretinal Fluid (yes/no)
Time frame: Baseline
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Presence of Subretinal Fluid (yes/no)
Time frame: 3 months after treatment
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Presence of Subretinal Fluid (yes/no)
Time frame: 4 months after treatment
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Presence of Pigment Epithelial Detachment (yes/no)
Time frame: Baseline
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Presence of Pigment Epithelial Detachment (yes/no)
Time frame: 3 months after treatment
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Presence of Pigment Epithelial Detachment (yes/no)
Time frame: 4 months after treatment
Tested by optical coherence tomography (Heidelberg \& Zeiss)
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 23 Jan 2018.
- 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.
Laurence Postelmans, MD principal investigator
CHU Brugmann
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Genotype analysis in people with Age-Related Macular Degeneration, run by Brugmann University Hospital 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 1 inclusion and 3 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 23 Jan 2018. 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?
Snellen visual acuity test result (time frame: Baseline). The study lists 18 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 23 Jan 2018; AzTrials last refreshed its copy on 8 Nov 2026.