Atopic DermatitisPhase 2NCT01806662
Pilot Study of Ustekinumab for Subjects With Chronic Atopic Dermatitis
A Phase 2 study testing Ustekinumab in people with Atopic Dermatitis, run by Rockefeller University at 1 site in United States.
Trial summary
Atopic dermatitis (AD) is a chronic disease associated with intense itching, which affects most aspects of everyday life in the majority of patients. Acute inflammation and extensor/facial involvement is common in infants, whereas chronic inflammation increases in prevalence with age, as do localization to flexures. Read more about this study
- Who is it for?
- Ages 18 to 75 years
- Conditions the study is for
- Atopic Dermatitis
- What is being tested?
- Ustekinumab
- Type of treatment
- Injection or infusion
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 32 participants
- Where
- 1 siteUnited States
- Study dates
- Mar 2013to Mar 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 to 75 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- Are male or female and ages 18-75.
- Have moderate to severe AD (as determined using the Objective SCORAD scale ≥15) and a history of therapeutic failure with at least two of the three different treatment categories as listed within the inclusion criteria.
- Patients must have tried and failed at least two of the three treatment categories of the following treatment modalities:
- Category 1 : Hydration plus topical steroids and/or antibiotics Category 2: Systemic Steroids and/or Phototherapy Category 3: Cyclosporine and/or Other Immunomodulators (Methotrexate, CellCept, Immuran, topical Calcineurin inhibitors)
- Patients who initially respond to cyclosporine but cannot sustain a response after the drug is discontinued will also be eligible.
- Patients that have contraindications to category 3 drugs will also be allowed to participate in the study.
Show all 16Show fewer
- A washout period prior to screening will be required for the following medications:
- Cyclosporine/Oral Steroids/Imuran/Mycophenolate Mofetil/Other systemic immunosuppressants: 4 weeks
- Phototherapy/Moderate to High Potency Topical Corticosteroids: 2 weeks
- Women of childbearing potential must test negative for pregnancy and be using adequate birth control measures (e.g., Abstinence, oral contraceptives, intrauterine device, barrier method with spermicide, or have had a tubal ligation or a hysterectomy) during the study and for 6 months after receiving the last treatment. Likewise, men capable of fathering children must also use appropriate methods of birth control (e.g., abstinence, barrier methods with spermicide, or have had surgical sterilization such as vasectomy).
- Patients must be in general good health in the opinion of the investigator.
- Patients with stable chronic asthma, treated with inhaled corticosteroids, will be eligible.
- The screening laboratory tests must meet the following criteria:
- Hemoglobin >9 g/dl WBC count >3.5 x 109 cells/L Neutrophils >1.5 x 109 cells/L Platelets >100 x 109 cells/L AST/SGOT and ALT/SGPT levels must be within 2 times the upper limit of normal for the laboratory conducting the test. Alkaline phosphatase levels must be within 2 times the upper limit of normal for the laboratory conducting the test.
- Are PPD negative at the time of screening.
- The patients will be allowed to use topical therapy during the washout period. These will include emollients, and mild steroids (class 6 or 7), except on one target area that will be the site for the skin biopsies.
Who cannot join
- Previous treatment with ustekinumab or other agent that specifically targets IL-12 or 23
- Have a history of latent or active granulomatous infection, including TB, histoplasmosis, or coccidioidomycosis, prior to screening, or are frequently in contact with individuals who carry active TB infection or a non-tubercular mycobacterial infection or an opportunistic infection
- Are HIV positive by history or POCT on the screening visit
- Have documented current active hepatitis B (surface antigen positive or asymptomatic chronic carriers) or hepatitis C infection (anti-HCV positive), by history and/or screening test
- Have a history of substance abuse (drug or alcohol) within the past year before screening
- Have any serious concomitant illness that could require the use of systemic corticosteroids or otherwise interfere with the patient's participation in the trial
- Pregnant women or women that are breast-feeding or plan to breast feed. Women of childbearing age who plan to get pregnant within 15 weeks of stopping study agent
Trial locations and contacts
1 site in 1 country.
About this study
Official title: Randomized Pilot Study of Ustekinumab for Subjects With Chronic Atopic Dermatitis Who Have Sub-optimal Response to Prior Therapy
Atopic dermatitis (AD) is a chronic disease associated with intense itching, which affects most aspects of everyday life in the majority of patients. Acute inflammation and extensor/facial involvement is common in infants, whereas chronic inflammation increases in prevalence with age, as do localization to flexures. AD has a complex background characterized by immune activation, increased epidermal thickness in chronic diseased skin, and defective barrier function. In normal, healthy skin, the outer layer of the epidermis, the stratum corneum is made up flattened dead cells called corneocytes held together by a mixture of lipids and proteins. The stratum corneum and, in particular, the lipid layer are vital in providing a natural barrier function that locks water inside the skin and keeps allergens and irritants out. In people with AD, the barrier function is defective, which leads to dry skin. As the skin dries out, it cracks allowing allergens and irritants to penetrate.
Mild AD can be controlled with emollients and topical medications. However, moderate to severe AD is extremely difficult to control and requires systemic treatment that is often unsatisfactory due to impracticality and lack of effectiveness. Only three therapeutic options exist for moderate to severe AD, including: 1) oral steroids 2) cyclosporine A (CsA), that is not widely used in the US as it is not FDA approved for AD and 3) ultraviolet phototherapy. Oral steroids and CsA treatments have major side effects and UV radiation therapy is highly inconvenient for patients. Several biologic medications, such as TNF-alpha inhibitors, are effective, convenient, and relatively safe therapies for psoriasis, but have thus far not shown efficacy in AD. Ustekinumab is a unique biologic medication that may specifically target AD.
The investigators study will determine whether there is a reversal of the skin thickness and the immune pathways involved in the disease during treatment with Ustekinumab and what specific immune cells are involved. The investigators are also interested to understand how the clinical reversal of the disease will correlate with tissue reversal of the disease.
Read the detailed description
In psoriasis, epidermal hyperplasia is driven by underlying immune activation, whether as a direct response to IL-20 family cytokines that induces hyperplasia and inhibits keratinocyte terminal differentiation or as an indirect response to immune-mediated injury to keratinocytes. The epidermal reaction in psoriasis is largely restored to normal with selective immune suppression. Hence, one might hypothesize that similar epidermal responses should occur in the presence of "generalized" cellular immune activation, in diseases with similar inflammatory infiltrate and epidermal hyperplasia, such as AD. In fact, psoriasis and AD share features of dense T-cells and dendritic cell infiltrates, as well as over-expression of IL-22 in skin lesions. These diseases also share similar epidermal hyperplasia in their chronic phases.
Work from the investigators group showed that IL-22 is a key cytokine in the pathogenesis of both AD and psoriasis. The investigators have demonstrated that in psoriasis, ustekinumab suppresses the production of IL-12, IL-23, and IL-22. Additionally, by RT-PCR the investigators demonstrated that the mRNA expression of p40 cytokine and the IL23R is up-regulated in AD as compared to both normal skin and psoriasis. The investigators therefore hypothesize that ustekinumab will suppress IL-22 and possibly also p40 production in AD lesions and reverse both the epidermal growth/differentiation defects and the underlying immune activation, and hence will suppress disease activity. Interestingly, p40 was also found to be significantly up-regulated in non-lesional AD skin as compared with normal skin.
Although AD is thought to be predominately a disease of Th2-type cells, in the chronic stage, there is large Th1 component. To date, the precise mechanism by which sequential activation of Th2 and Th1 cells in AD is achieved remains unknown. IL-12 induces the differentiation and maturation of human Th cells into Th1-type cells. Recent circumstantial evidence suggests that in AD patients IL-12 may facilitate a change from the Th2-type to a Th1 cytokine profile. IL-12 was recently shown to be highly elevated in pediatric AD and its levels were strongly associated with disease severity.
Expression of IL-12 p40 mRNA is significantly enhanced in lesional skin from AD, suggesting that the enhanced local production of IL-12 in dendritic cells and macrophages may be responsible for the increased production of IFN-γ in chronic lesions potentially suggesting that IL-12 may have a pivotal role in promoting inflammation in atopic dermatitis. Topical steroids which constitute a mainstay of therapy in AD are known to strongly down-regulate IL-12 expression, possibly also indicating that targeted anti IL-12 therapy might important role in treating AD.
Recently, the Th1/Th2 paradigm in autoimmunity and allergy has been revisited to include a role for a new population of IL-17-producing Th cells known as Th17. Th17 cells are characterized by the production of inflammatory cytokines such as IL-17A, IL-17F, IL-22, and IL-26. One of the key factors involved in naive Th-cell commitment to a Th17 phenotype is IL-23.
Patients with acute AD were found to have increased Th17 T-cells in peripheral blood by flow cytometry and intracellular cytokine staining 26 as well as by immunohistochemistry (IHC) in lesions. Since IL-23 is the major inducer of Th17 T-cells, as well as "T22" T-cells, neutralization of IL-23 could potentially result in both decreased Th17 signal in acute AD as well as decreased "T22/IL22" signal. Therefore the investigators postulate that ustekinumab in AD will act both inhibiting the IL-12-dependent Th1 shift in chronic AD stage as well as the pathogenic IL-22/"T22" axis in this disease.
- Conditions
- Atopic Dermatitis
- Being tested
- Ustekinumab, Placebo
- Keywords
- Atopic Dermatitis, Eczema
- Medical subject headings
- Dermatitis, Atopic, Eczema
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
UstekinumabDrug
Also called Stelara
Injection of monoclonal antibody against the p40 subunit of IL-12/23
PlaceboOther
Injection of placebo
| Study group | Role | What they receive |
|---|---|---|
| Treatment Arm (Ustekinumab first, Then Placebo) | Experimental | Since there is a crossover design, each patient will be in the treatment arm for 16 weeks of the study. Receives: Drug: Ustekinumab; Other: Placebo |
| Placebo Arm (Placebo first, Then Ustekinumab) | Placebo comparator | Since there is a crossover design, each patient will be in the placebo arm for 16 weeks of the study. If a patient begins in the placebo arm, they will switch over to the treatment arm at week 16. Receives: Drug: Ustekinumab; Other: Placebo |
What is being measured
The primary outcome is the main question the study is designed to answer.
Proportion of SCORAD-50 Response at Week 16.
Greater improvement from their baseline objective SCORAD (SCORing Atopic Dermatitis) at Week 16. The efficacy variable for each randomized group is the proportion of subjects who achieve an improvement of 50% or greater from their baseline objective SCORAD at Week 16 (at crossover). SCORAD-50 is the percentage of decrease in baseline SCOARD at Week 16.
SCORAD is a clinical tool used to assess the extent and severity of eczema. Calculation is based on extent of involvement (skin involvement) and subjective symptoms of itching and loss of sleep. The SCORAD scale ranges from 0 (minimum, lowest possible score, Mild severity) to 103 (maximum, highest possible score, Severe severity) [last observation carry forward].
Measured: Week 16
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted7 Mar 2013 (estimated)
- Study startMar 2013
- Primary completionMar 2015
- Study completionMar 2015
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 Atopic DermatitisStudies 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
- Crossover
- Masking
- Double blind
- Who is masked
- Participant, Investigator
- Enrolment
- 32 participants (actual)
Sponsor and investigators
- Lead sponsor
- Rockefeller University
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- James Krueger, MD PhD, Principal investigator, Rockefeller University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01806662
- Sponsor's protocol ID
- JKR-0737
- Status last verified
- Feb 2018
- First submitted
- 28 Feb 2013
- Last updated
- 14 Mar 2018
- Results posted
- Yes, on ClinicalTrials.gov
- Data monitoring committee
- No
- Individual data sharing
- Undecided
Study at a glance
From the registry record, last updated by the sponsor on 14 Mar 2018. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Randomized Pilot Study of Ustekinumab for Subjects With Chronic Atopic Dermatitis Who Have Sub-optimal Response to Prior Therapy
- ClinicalTrials.gov ID
- NCT01806662
- Acronym / sponsor ID
- JKR-0737
- Conditions
- Atopic Dermatitis
- Keywords
- Atopic Dermatitis, Eczema
- Phase
- Phase 2
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 32 participants (actual)
- Lead sponsor
- Rockefeller UniversityUniversity, hospital or other
- Study start
- Mar 2013
- Primary completion
- Mar 2015 (actual)
- Study completion
- Mar 2015 (actual)
- First posted
- 7 Mar 2013 (estimated)
- Results
- Posted 19 Dec 2017
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Atopic dermatitis (AD) is a chronic disease associated with intense itching, which affects most aspects of everyday life in the majority of patients. Acute inflammation and extensor/facial involvement is common in infants, whereas chronic inflammation increases in prevalence with age, as do localization to flexures. AD has a complex background characterized by immune activation, increased epidermal thickness in chronic diseased skin, and defective barrier function. In normal, healthy skin, the outer layer of the epidermis, the stratum corneum is made up flattened dead cells called corneocytes held together by a mixture of lipids and proteins. The stratum corneum and, in particular, the lipid layer are vital in providing a natural barrier function that locks water inside the skin and keeps allergens and irritants out. In people with AD, the barrier function is defective, which leads to dry skin. As the skin dries out, it cracks allowing allergens and irritants to penetrate.
Mild AD can be controlled with emollients and topical medications. However, moderate to severe AD is extremely difficult to control and requires systemic treatment that is often unsatisfactory due to impracticality and lack of effectiveness. Only three therapeutic options exist for moderate to severe AD, including: 1) oral steroids 2) cyclosporine A (CsA), that is not widely used in the US as it is not FDA approved for AD and 3) ultraviolet phototherapy. Oral steroids and CsA treatments have major side effects and UV radiation therapy is highly inconvenient for patients. Several biologic medications, such as TNF-alpha inhibitors, are effective, convenient, and relatively safe therapies for psoriasis, but have thus far not shown efficacy in AD. Ustekinumab is a unique biologic medication that may specifically target AD.
The investigators study will determine whether there is a reversal of the skin thickness and the immune pathways involved in the disease during treatment with Ustekinumab and what specific immune cells are involved. The investigators are also interested to understand how the clinical reversal of the disease will correlate with tissue reversal of the disease.
Detailed description
In psoriasis, epidermal hyperplasia is driven by underlying immune activation, whether as a direct response to IL-20 family cytokines that induces hyperplasia and inhibits keratinocyte terminal differentiation or as an indirect response to immune-mediated injury to keratinocytes. The epidermal reaction in psoriasis is largely restored to normal with selective immune suppression. Hence, one might hypothesize that similar epidermal responses should occur in the presence of "generalized" cellular immune activation, in diseases with similar inflammatory infiltrate and epidermal hyperplasia, such as AD. In fact, psoriasis and AD share features of dense T-cells and dendritic cell infiltrates, as well as over-expression of IL-22 in skin lesions. These diseases also share similar epidermal hyperplasia in their chronic phases.
Work from the investigators group showed that IL-22 is a key cytokine in the pathogenesis of both AD and psoriasis. The investigators have demonstrated that in psoriasis, ustekinumab suppresses the production of IL-12, IL-23, and IL-22. Additionally, by RT-PCR the investigators demonstrated that the mRNA expression of p40 cytokine and the IL23R is up-regulated in AD as compared to both normal skin and psoriasis. The investigators therefore hypothesize that ustekinumab will suppress IL-22 and possibly also p40 production in AD lesions and reverse both the epidermal growth/differentiation defects and the underlying immune activation, and hence will suppress disease activity. Interestingly, p40 was also found to be significantly up-regulated in non-lesional AD skin as compared with normal skin.
Although AD is thought to be predominately a disease of Th2-type cells, in the chronic stage, there is large Th1 component. To date, the precise mechanism by which sequential activation of Th2 and Th1 cells in AD is achieved remains unknown. IL-12 induces the differentiation and maturation of human Th cells into Th1-type cells. Recent circumstantial evidence suggests that in AD patients IL-12 may facilitate a change from the Th2-type to a Th1 cytokine profile. IL-12 was recently shown to be highly elevated in pediatric AD and its levels were strongly associated with disease severity.
Expression of IL-12 p40 mRNA is significantly enhanced in lesional skin from AD, suggesting that the enhanced local production of IL-12 in dendritic cells and macrophages may be responsible for the increased production of IFN-γ in chronic lesions potentially suggesting that IL-12 may have a pivotal role in promoting inflammation in atopic dermatitis. Topical steroids which constitute a mainstay of therapy in AD are known to strongly down-regulate IL-12 expression, possibly also indicating that targeted anti IL-12 therapy might important role in treating AD.
Recently, the Th1/Th2 paradigm in autoimmunity and allergy has been revisited to include a role for a new population of IL-17-producing Th cells known as Th17. Th17 cells are characterized by the production of inflammatory cytokines such as IL-17A, IL-17F, IL-22, and IL-26. One of the key factors involved in naive Th-cell commitment to a Th17 phenotype is IL-23.
Patients with acute AD were found to have increased Th17 T-cells in peripheral blood by flow cytometry and intracellular cytokine staining 26 as well as by immunohistochemistry (IHC) in lesions. Since IL-23 is the major inducer of Th17 T-cells, as well as "T22" T-cells, neutralization of IL-23 could potentially result in both decreased Th17 signal in acute AD as well as decreased "T22/IL22" signal. Therefore the investigators postulate that ustekinumab in AD will act both inhibiting the IL-12-dependent Th1 shift in chronic AD stage as well as the pathogenic IL-22/"T22" axis in this disease.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Double blind (participant, investigator)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Treatment Arm (Ustekinumab first, Then Placebo) | Experimental | Drug: Ustekinumab, Other: PlaceboSince there is a crossover design, each patient will be in the treatment arm for 16 weeks of the study. |
| Placebo Arm (Placebo first, Then Ustekinumab) | Placebo comparator | Drug: Ustekinumab, Other: PlaceboSince there is a crossover design, each patient will be in the placebo arm for 16 weeks of the study. If a patient begins in the placebo arm, they will switch over to the treatment arm at week 16. |
Who may qualify
- Ages
- 18 to 75 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (16 listed)
- Are male or female and ages 18-75.
- Have moderate to severe AD (as determined using the Objective SCORAD scale ≥15) and a history of therapeutic failure with at least two of the three different treatment categories as listed within the inclusion criteria.
- Patients must have tried and failed at least two of the three treatment categories of the following treatment modalities:
- Category 1 : Hydration plus topical steroids and/or antibiotics Category 2: Systemic Steroids and/or Phototherapy Category 3: Cyclosporine and/or Other Immunomodulators (Methotrexate, CellCept, Immuran, topical Calcineurin inhibitors)
- Patients who initially respond to cyclosporine but cannot sustain a response after the drug is discontinued will also be eligible.
Key exclusion criteria (7 listed)
- Previous treatment with ustekinumab or other agent that specifically targets IL-12 or 23
- Have a history of latent or active granulomatous infection, including TB, histoplasmosis, or coccidioidomycosis, prior to screening, or are frequently in contact with individuals who carry active TB infection or a non-tubercular mycobacterial infection or an opportunistic infection
- Are HIV positive by history or POCT on the screening visit
- Have documented current active hepatitis B (surface antigen positive or asymptomatic chronic carriers) or hepatitis C infection (anti-HCV positive), by history and/or screening test
- Have a history of substance abuse (drug or alcohol) within the past year before screening
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 |
|---|---|---|
| UstekinumabAlso: StelaraInjection of monoclonal antibody against the p40 subunit of IL-12/23 | Drug | Placebo Arm (Placebo first, Then Ustekinumab), Treatment Arm (Ustekinumab first, Then Placebo) |
| PlaceboInjection of placebo | Other | Placebo Arm (Placebo first, Then Ustekinumab), Treatment Arm (Ustekinumab first, Then Placebo) |
Primary outcome
Proportion of SCORAD-50 Response at Week 16.
Time frame: Week 16
Greater improvement from their baseline objective SCORAD (SCORing Atopic Dermatitis) at Week 16. The efficacy variable for each randomized group is the proportion of subjects who achieve an improvement of 50% or greater from their baseline objective SCORAD at Week 16 (at crossover). SCORAD-50 is the percentage of decrease in baseline SCOARD at Week 16. SCORAD is a clinical tool used to assess the extent and severity of eczema. Calculation is based on extent of involvement (skin involvement) and subjective symptoms of itching and loss of sleep. The SCORAD scale ranges from 0 (minimum, lowest possible score, Mild severity) to 103 (maximum, highest possible score, Severe severity) [last observation carry forward].
Results and safety
Loading the posted results from ClinicalTrials.gov…
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 14 Mar 2018.
- Posted resultsParticipant flow, baseline, all outcome measures and adverse events.
- Individual participant dataSharing planned: Undecided
Related trials for Atopic Dermatitis
Not yet recruitingPhase 1
A Phase I Study of GLR2053 Tablets in Chinese Healthy Adult Participants
Atopic Dermatitis
RecruitingObservational study
Blood, Urine, and Tissue Collection for Cutaneous Lymphoma, Eczema, and Atopic Dermatitis Research
Cutaneous T-cell Lymphoma, Sezary Syndrome
RecruitingPhase 1
First-in-Human Trial to Assess REGN20423 in Healthy Adult Participants and Adult Participants With Atopic Dermatitis
Healthy Volunteer, Atopic Dermatitis
Not yet recruitingPhase 1
A Study of HSK60002 Tablets in Participants With Moderate-to-Severe Atopic Dermatitis
Dermatitis Atopic
RecruitingPhase 3
A Study to Learn About the Study Medicine Called Tilrekimig in People With Moderate-to Severe Eczema
Atopic Dermatitis
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.
James Krueger, MD PhD principal investigator
Rockefeller University
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 Ustekinumab in people with Atopic Dermatitis, run by Rockefeller University 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 16 inclusion and 7 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 14 Mar 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 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. 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?
Yes. Results are posted in the registry (first posted 19 Dec 2017). 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?
Proportion of SCORAD-50 Response at Week 16. (time frame: Week 16). 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 14 Mar 2018.