MelanomaPhase 2NCT01942993
The Effects of Treatment With Vemurafenib on the Immune System in Advanced Melanoma
A Phase 2 study testing Vemurafenib in people with Melanoma, run by Philip Friedlander at 1 site in United States.
Trial summary
Approximately 40-60 % of cutaneous melanomas select for a mutation in a protein called BRAF which is part of a signaling pathway called the Mitogen Activated Protein Kinase (MAPK) pathway. When BRAF is mutated the MAPK pathway remains active allowing for melanoma to grow. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Melanoma
- What is being tested?
- Vemurafenib
- Type of treatment
- Pill or oral medicine
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 3 participants
- Where
- 1 siteUnited States
- Study dates
- Sep 2013to Nov 2015
- Phase
- Phase 2
- Are there results?
- Yes, posted in the registrySummary in the doctors' view
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
- Histologically confirmed stage IV or unresectable stage III melanoma with documented BRAF V600 mutation
- Age > 18 years
- ECOG Performance Status 0,1, or 2
- Measurable disease by RECIST v1.1
- Adequate organ function: Hemoglobin > 9 g/dl, ANC> 1.5 x 109/L, platelets > 100 x 109/L, AST and ALT < 2.5 x upper limit of normal, bilirubin < 1.5 x upper limit normal, Cr < 1.5 x upper limit normal
- Adequate recovery from prior systemic or local melanoma therapy. No systemic anticancer therapy in the 4 weeks and no ipilimumab in the 6 weeks from planned vemurafenib administration. No radiation therapy in 2 weeks prior to date plan to initiate vemurafenib treatment and no surgery in 3 weeks prior to date of planned vemurafenib administration.
Show all 9Show fewer
- Agreement for females of childbearing potential use 2 acceptable methods contraception. Men with female partners of childbearing potential must agree to use of latex condom and advise female partner to use additional method contraception during the study and 6 months after discontinuation of vemurafenib
- Negative serum or urine pregnancy test within 7 days prior to and including the morning of day -7 (first potential day of research blood draw and tumor biopsy)
- Agreement not to donate blood or blood products or to donate sperm during the study and for at least 6 months after discontinuation of vemurafenib.
Who cannot join
- Prior vemurafenib treatment
- Use of oral or intravenous corticosteroids or other immunosuppressive medications such as cyclosporine or azathioprine. Subjects must not have received any systemic immunosuppressive drug such as corticosteroids for at least 2 weeks prior to study entry. Maintenance inhaled corticosteroids for controlled asthma or COPD or maintenance systemic steroids to correct autoimmune endocrinopathy due to prior ipilimumab treatment is allowed as is the use of topical steroids and anti-inflammatory eye drops.
- Symptomatic CNS metastases requiring steroid use.
- No active second malignancy
- Pregnant or breast feeding
- Mean QTc interval > 450 (triplicate ECGs) or history congenital prolonged QT interval
Show all 14Show fewer
- Any of the following within 3 months prior to study drug administration: myocardial infarction, unstable angina, symptomatic congestive heart failure, cerebrovascular accident or transient ischemic attack, or pulmonary embolism
- Inability to swallow pills
- Ongoing cardiac dysrhythmia >2 (per NCI CTCAE, v4.0)
- Unwillingness to practice birth control
- Inability to comply with requirements of the protocol
- Uncontrolled medical illness such as infection requiring intravenous antibiotics.
- Known allergy to treatment medication (vemurafenib)
- Known active or chronic infection with HIV.
Trial locations and contacts
1 site in 1 country.
United States1 site
Icahn School of Medicine at Mount Sinai
New York, New York, 11103
About this study
Official title: The Effect of BRAF Inhibition With Vemurafenib On The Innate and Adaptive Immune Systems in Patients With Unresectable Stage III or Stage IV Melanoma Expressing a V600 BRAF Mutation
Approximately 40-60 % of cutaneous melanomas select for a mutation in a protein called BRAF which is part of a signaling pathway called the Mitogen Activated Protein Kinase (MAPK) pathway. When BRAF is mutated the MAPK pathway remains active allowing for melanoma to grow. Vemurafenib is an oral treatment which blocks the activity of BRAF which leads to decreasing the activity of the MAPK pathway. When patients with melanoma expressing specific mutation in BRAF are treated with vemurafenib approximately 50% will develop a response to treatment with shrinkage of tumor. When compared to a standard chemotherapy called dacarbazine used to treat melanoma, treatment with vemurafenib leads to a statistically significant overall survival or living longer benefit. Because of this survival benefit vemurafenib was Food and Drug Administration (FDA) approved for the treatment of metastatic melanoma expressing a BRAF mutation called V600E BRAF. There is increasing evidence that the immune system can also be important in affecting melanoma growth and survival and there are immune treatments FDA approved for the treatment of metastatic melanoma. There is some limited evidence that blocking BRAF with vemurafenib may affect the activity of components of the immune system. It is important to better characterize and understand the effects of vemurafenib treatment on various components of the immune system. The purpose of this study is to systematically evaluate the effects of vemurafenib treatment (at FDA approved dosing regimen) on parts of the immune systems called the innate and adaptive immune systems. The hypothesis is that vemurafenib treatment will affect the immune system.
Read the detailed description
Approximately 40-60 % of cutaneous melanomas select for a mutation in the BRAF protein which is part of a signaling pathway called the Mitogen Activated Protein Kinase (MAPK) pathway. Over 90% of mutations in BRAF occur at position V600 with the most common being a V600E mutation. Mutation at position V600 of BRAF activates the MAPK pathway which facilitates melanoma proliferation and growth. The response rate to treatment with vemurafenib in patients with stage IV melanoma expressing a V600E BRAF mutation is approximately 50%. A phase III study comparing first line treatment with vemurafenib compared to standard dacarbazine chemotherapy demonstrated a statistically significant overall survival benefit in this patient population. Based on this survival benefit vemurafenib was FDA approved for treatment of stage IV melanoma expressing a V600E BRAF mutation. Vemurafenib is administered at a dose of 960 milligrams orally twice daily.
While targeting BRAF can lead to survival benefits in patients with melanoma expressing BRAF mutation it is becoming increasingly apparent that the immune system is important in modulating the growth of melanoma. As such there are immune therapies FDA approved for the treatment of stage IV melanoma including ipilimumab which confers an overall survival benefit by activating the immune system through inhibition of the CTLA-4 protein expressed on certain T-cells. Little is known about how the exposure of different classes of immune cells to vemurafenib modulates the activity of the immune system. We do know that many melanomas express differentiation antigens which could potentially be recognized by the immune system. This recognition could potentially be utilized in the development of novel immunotherapeutic treatment approaches. The pharmacologic inhibition of the MAPK pathway does lead to increased expression of various melanoma differentiation antigens along with improved recognition by antigen-specific T-lymphocytes. Evaluation of a limited number of tumor biopsy specimens suggest that the infiltration of melanomas by CD4+ and CD8+ T-lymphocytes markedly increases following treatment with a BRAF inhibitor. Furthermore the viability and function (determined using assays for cytokine release assays and cytotoxic activity) of T-lymphocytes was not negatively affected by exposure to vemurafenib at concentrations known to cause anti-tumor effects.
The MAPK pathway is a pathway utilized by many cell types including immune cells and cells in the tumor microenvironment. As such vemurafenib could potentially modulate the activity of the MAPK pathway in the melanoma cells, immune cells, and components of the tumor microenvironment. Effects of vemurafenib on tumor cells may directly lead to changes in antigen presentation and effects on the innate and adaptive immune systems could potentially alter recognition of tumor cells and modulate positively or negatively immune recognition and antitumor activity. Therefore, a better understanding of immune modulation induced by anti-BRAF therapy should provide data to model and develop in a more rational fashion therapies which combine BRAF targeted and immune modulatory agents potentially using such agents as ipilimumab or anti-PD1 or anti-PDL1 antibodies.
- Conditions
- Melanoma
- Being tested
- Vemurafenib
- Keywords
- melanoma, unresectable, mutation, BRAF protein
- Medical subject headings
- Melanoma, Hereditary Sensory and Autonomic Neuropathies
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
VemurafenibDrug
Vemurafenib will be administered at the FDA approved dose of 960 mg approximately 12 hours apart with or without a meal. Vemurafenib is provided at 240-mg film-coated tablets packed in bottles for oral administration. Vemurafenib should be swallowed whole with a glass of water and the medication should not be chewed or crushed. Management of symptomatic adverse events may require dose reductions, treatment interruptions, or treatment discontinuation. Dose reductions below 480 mg twice daily are not recommended.
| Study group | Role | What they receive |
|---|---|---|
| Vemurafenib | Experimental | 960 mg (four tablets of 240 mg each) of vemurafenib PO BID Receives: Drug: Vemurafenib |
What is being measured
The primary outcome is the main question the study is designed to answer.
Changes in the Immune Cellular Signature in the Blood Circulation
Immuno-fluorescence and flow cytometry will be performed on blood specimens obtained to determine changes in the immune cell signature in the blood on day 8 and day 57 after initiation of vemurafenib treatment as compared to baseline
Measured: baseline, day 8, and day 57
Secondary outcomes (13)
Changes in the Immune Cellular Signature in the Tumor
Immuno-fluorescence and flow cytometry will be performed on tumor specimens obtained to determine changes in the immune cell signature in the tumor on day 8-10 and day 57 after initiation of vemurafenib treatment as compared to baseline
Measured: baseline, day 8-10, and day 57
Changes in Transcriptional Profile in the Blood
Global changes in the blood transcriptome in response to vemurafenib therapy will be performed using gene expression arrays. Change in the blood transcriptosome on day 8 and day 57 as compared to baseline.
Measured: baseline, day 8, and day 57
Change in Transcriptional Profile in Tumor
Global changes in the transcriptosome of tumor associated immune cells in response to therapy will be performed using gene expression arrays. The transcriptosome in tumor will be compared on purified tumor immune cells obtained from a pretreatment tumor biopsy performed at baseline and a second biopsy obtained after starting treatment and obtained between days 8-10.
Measured: baseline and day 8-10
Changes in Dendritic Cell Function in Blood
change in dendritic cell function at day 8 and day 57 as compared to baseline
Measured: baseline day 8, and day 57
Changes in Dendritic Cell Function in Tumor
Changes in dendritic cell function in tumor on day 8-10 as compared to baseline
Measured: baseline and day 8-10
Changes in Macrophage Function in Blood
Changes in macrophage function in blood at day 8 and day 57 as compared to baseline
Measured: baseline, day 8, and day 57
Changes in Macrophage Function in Tumor
changes in macrophage function in tumor on day 8-10 as compared to baseline
Measured: baseline and day 8-10
Changes in Global T Cell Function in Blood
changes in global T cell function in blood on day 8 and day 57 as compared to baseline
Measured: baseline, day 8, and day 57
Changes in Global T Cell Function in Tumor
Changes in Global T cell function in Tumor on day 8 as compared to baseline
Measured: baseline and day 8-10
Changes in Tumor Antigen Specific T Cell Function in Blood
Changes in Tumor Antigen Specific T cell Function using CD154 induction assay on day 8, day 15 and day 126 as compared to baseline
Measured: baseline, day 8, day 15 and day 126
Changes in Histocytometry of Tumor
Changes in Histocytometry of tumor on day 8-10 as compared to baseline. Histocytometry is a novel microscopic analytical method (Gerner et al. 2012) which combines the advantages of flow cytometry and Microscopic techniques. This techniques allows for the visualization and quantification of phenotypically complex cellular subsets and provides spatial and cell-cell interactions.
Measured: baseline and day 8-10
Response to Vemurafenib Treatment
Response to vemurafenib treatment based on changes in tumor burden using CT or MRI imaging studies. Response are categorized as complete response (CR), partial response (PR), progressive disease (PD), and stable disease (SD),
Measured: up to 57 days
Number of Participants Who Developed of Cutaneous Squamous Cell Carcinomas
Number of participants who developed cutaneous squamous cell carcinomas while on the study
Measured: up to 5 months
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted16 Sep 2013 (estimated)
- Study startSep 2013
- Primary completionNov 2015
- Study completionNov 2015
Why it stopped: standard of care has changed
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Posted resultsParticipant flow, outcome measures and adverse events reported by the sponsor.
- Other trials for MelanomaStudies 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
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Enrolment
- 3 participants (actual)
Sponsor and investigators
- Lead sponsor
- Philip Friedlander
- Sponsor type
- University, hospital or other
- Collaborators
- Genentech, Inc.
- Responsible party
- Sponsor-investigator, Philip Friedlander, Icahn School of Medicine at Mount Sinai
- Investigators
- Philip Friedlander, MD, PhD, Principal investigator, Icahn School of Medicine at Mount Sinai
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01942993
- Sponsor's protocol ID
- GCO 13-0427
- Status last verified
- Sep 2020
- First submitted
- 11 Sep 2013
- Last updated
- 30 Sep 2020
- Results posted
- Yes, on ClinicalTrials.gov
- Data monitoring committee
- Yes
Study at a glance
From the registry record, last updated by the sponsor on 30 Sep 2020. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- The Effect of BRAF Inhibition With Vemurafenib On The Innate and Adaptive Immune Systems in Patients With Unresectable Stage III or Stage IV Melanoma Expressing a V600 BRAF Mutation
- ClinicalTrials.gov ID
- NCT01942993
- Acronym / sponsor ID
- GCO 13-0427
- Conditions
- Melanoma
- Keywords
- melanoma, unresectable, mutation, BRAF protein
- Phase
- Phase 2
- Study type
- Interventional
- Recruitment status
- TerminatedReason stopped: standard of care has changed
- Enrolment
- 3 participants (actual)
- Lead sponsor
- Philip FriedlanderUniversity, hospital or other
- Collaborators
- Genentech, Inc.
- Study start
- Sep 2013
- Primary completion
- Nov 2015 (actual)
- Study completion
- Nov 2015 (actual)
- First posted
- 16 Sep 2013 (estimated)
- Results
- Posted 30 Sep 2020
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Approximately 40-60 % of cutaneous melanomas select for a mutation in a protein called BRAF which is part of a signaling pathway called the Mitogen Activated Protein Kinase (MAPK) pathway. When BRAF is mutated the MAPK pathway remains active allowing for melanoma to grow. Vemurafenib is an oral treatment which blocks the activity of BRAF which leads to decreasing the activity of the MAPK pathway. When patients with melanoma expressing specific mutation in BRAF are treated with vemurafenib approximately 50% will develop a response to treatment with shrinkage of tumor. When compared to a standard chemotherapy called dacarbazine used to treat melanoma, treatment with vemurafenib leads to a statistically significant overall survival or living longer benefit. Because of this survival benefit vemurafenib was Food and Drug Administration (FDA) approved for the treatment of metastatic melanoma expressing a BRAF mutation called V600E BRAF. There is increasing evidence that the immune system can also be important in affecting melanoma growth and survival and there are immune treatments FDA approved for the treatment of metastatic melanoma. There is some limited evidence that blocking BRAF with vemurafenib may affect the activity of components of the immune system. It is important to better characterize and understand the effects of vemurafenib treatment on various components of the immune system. The purpose of this study is to systematically evaluate the effects of vemurafenib treatment (at FDA approved dosing regimen) on parts of the immune systems called the innate and adaptive immune systems. The hypothesis is that vemurafenib treatment will affect the immune system.
Detailed description
Approximately 40-60 % of cutaneous melanomas select for a mutation in the BRAF protein which is part of a signaling pathway called the Mitogen Activated Protein Kinase (MAPK) pathway. Over 90% of mutations in BRAF occur at position V600 with the most common being a V600E mutation. Mutation at position V600 of BRAF activates the MAPK pathway which facilitates melanoma proliferation and growth. The response rate to treatment with vemurafenib in patients with stage IV melanoma expressing a V600E BRAF mutation is approximately 50%. A phase III study comparing first line treatment with vemurafenib compared to standard dacarbazine chemotherapy demonstrated a statistically significant overall survival benefit in this patient population. Based on this survival benefit vemurafenib was FDA approved for treatment of stage IV melanoma expressing a V600E BRAF mutation. Vemurafenib is administered at a dose of 960 milligrams orally twice daily.
While targeting BRAF can lead to survival benefits in patients with melanoma expressing BRAF mutation it is becoming increasingly apparent that the immune system is important in modulating the growth of melanoma. As such there are immune therapies FDA approved for the treatment of stage IV melanoma including ipilimumab which confers an overall survival benefit by activating the immune system through inhibition of the CTLA-4 protein expressed on certain T-cells. Little is known about how the exposure of different classes of immune cells to vemurafenib modulates the activity of the immune system. We do know that many melanomas express differentiation antigens which could potentially be recognized by the immune system. This recognition could potentially be utilized in the development of novel immunotherapeutic treatment approaches. The pharmacologic inhibition of the MAPK pathway does lead to increased expression of various melanoma differentiation antigens along with improved recognition by antigen-specific T-lymphocytes. Evaluation of a limited number of tumor biopsy specimens suggest that the infiltration of melanomas by CD4+ and CD8+ T-lymphocytes markedly increases following treatment with a BRAF inhibitor. Furthermore the viability and function (determined using assays for cytokine release assays and cytotoxic activity) of T-lymphocytes was not negatively affected by exposure to vemurafenib at concentrations known to cause anti-tumor effects.
The MAPK pathway is a pathway utilized by many cell types including immune cells and cells in the tumor microenvironment. As such vemurafenib could potentially modulate the activity of the MAPK pathway in the melanoma cells, immune cells, and components of the tumor microenvironment. Effects of vemurafenib on tumor cells may directly lead to changes in antigen presentation and effects on the innate and adaptive immune systems could potentially alter recognition of tumor cells and modulate positively or negatively immune recognition and antitumor activity. Therefore, a better understanding of immune modulation induced by anti-BRAF therapy should provide data to model and develop in a more rational fashion therapies which combine BRAF targeted and immune modulatory agents potentially using such agents as ipilimumab or anti-PD1 or anti-PDL1 antibodies.
Study design
- Primary purpose
- Treatment
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| Vemurafenib | Experimental | Drug: Vemurafenib960 mg (four tablets of 240 mg each) of vemurafenib PO BID |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (9 listed)
- Histologically confirmed stage IV or unresectable stage III melanoma with documented BRAF V600 mutation
- Age > 18 years
- ECOG Performance Status 0,1, or 2
- Measurable disease by RECIST v1.1
- Adequate organ function: Hemoglobin > 9 g/dl, ANC> 1.5 x 109/L, platelets > 100 x 109/L, AST and ALT < 2.5 x upper limit of normal, bilirubin < 1.5 x upper limit normal, Cr < 1.5 x upper limit normal
Key exclusion criteria (14 listed)
- Prior vemurafenib treatment
- Use of oral or intravenous corticosteroids or other immunosuppressive medications such as cyclosporine or azathioprine. Subjects must not have received any systemic immunosuppressive drug such as corticosteroids for at least 2 weeks prior to study entry. Maintenance inhaled corticosteroids for controlled asthma or COPD or maintenance systemic steroids to correct autoimmune endocrinopathy due to prior ipilimumab treatment is allowed as is the use of topical steroids and anti-inflammatory eye drops.
- Symptomatic CNS metastases requiring steroid use.
- No active second malignancy
- Pregnant or breast feeding
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 |
|---|---|---|
| VemurafenibVemurafenib will be administered at the FDA approved dose of 960 mg approximately 12 hours apart with or without a meal. Vemurafenib is provided at 240-mg film-coated tablets packed in bottles for oral administration. Vemurafenib should be swallowed whole with a glass of water and the medication should not be chewed or crushed. Management of symptomatic adverse events may require dose reductions, treatment interruptions, or treatment discontinuation. Dose reductions below 480 mg twice daily are not recommended. | Drug | Vemurafenib |
Primary outcome
Changes in the Immune Cellular Signature in the Blood Circulation
Time frame: baseline, day 8, and day 57
Immuno-fluorescence and flow cytometry will be performed on blood specimens obtained to determine changes in the immune cell signature in the blood on day 8 and day 57 after initiation of vemurafenib treatment as compared to baseline
13 secondary outcomes
Changes in the Immune Cellular Signature in the Tumor
Time frame: baseline, day 8-10, and day 57
Changes in Transcriptional Profile in the Blood
Time frame: baseline, day 8, and day 57
Change in Transcriptional Profile in Tumor
Time frame: baseline and day 8-10
Changes in Dendritic Cell Function in Blood
Time frame: baseline day 8, and day 57
Changes in Dendritic Cell Function in Tumor
Time frame: baseline and day 8-10
Changes in Macrophage Function in Blood
Time frame: baseline, day 8, and day 57
Changes in Macrophage Function in Tumor
Time frame: baseline and day 8-10
Changes in Global T Cell Function in Blood
Time frame: baseline, day 8, and day 57
Changes in Global T Cell Function in Tumor
Time frame: baseline and day 8-10
Changes in Tumor Antigen Specific T Cell Function in Blood
Time frame: baseline, day 8, day 15 and day 126
Changes in Histocytometry of Tumor
Time frame: baseline and day 8-10
Response to Vemurafenib Treatment
Time frame: up to 57 days
Number of Participants Who Developed of Cutaneous Squamous Cell Carcinomas
Time frame: up to 5 months
Results and safety
Loading the posted results from ClinicalTrials.gov…
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 30 Sep 2020.
- Posted resultsParticipant flow, baseline, all outcome measures and adverse events.
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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.
Philip Friedlander, MD, PhD principal investigator
Icahn School of Medicine at Mount Sinai
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 Vemurafenib in people with Melanoma, run by Philip Friedlander 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 9 inclusion and 14 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: stopped early, as of the sponsor's last update on 30 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 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.
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?
Yes. Results are posted in the registry (first posted 30 Sep 2020). A summary is in the For doctors view, and the full results are on ClinicalTrials.gov.
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?
Changes in the Immune Cellular Signature in the Blood Circulation (time frame: baseline, day 8, and day 57). 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 30 Sep 2020.