PemphigusNCT06285435
Coagulation Activation in Patients With Pemphigus
An observational study of Pemphigus, run by Assiut University.
Trial summary
Aim of work: 1. To evaluate the plasma markers of coagulation activation: prothrombin F1+2 and d-dimer levels in pemphigus patients with active disease and compare them with age and sex-matched controls. 2. Read more about this study
- Who is it for?
- Ages 18 to 60 yearsHealthy volunteers can take part
- Conditions the study is for
- Pemphigus
- What is being tested?
- prothrombin fragment 1+2
- How many people
- 54 participants
- Where
- No sites listed yet
- Study dates
- 1 Mar 2024to Feb 2026
- 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 60 years
- All sexes
- Healthy volunteers accepted
- Adult
Study population: Patients with active pemphigus who are either in a relapse for less than a week or are newly diagnosed cases will be included. The active stage of PV is defined as the de novo development of blisters on a healthy (unaffected or healed) site of either the skin or the mucous membrane. Clinical assessment, histopathological analysis (acantholysis and intraepidermal splitting) will be used to confirm the diagnosis of each patient. Control group: Healthy age and sex-matched subjects, who are free of chronic systemic diseases or dermatological conditions, will be enrolled as control.
Who may be able to join
- pemphigus vulgaris patients at active stage of the disease.
- patients between the ages of 18 and 60.
Who cannot join
- Patients with other autoimmune bullous diseases.
- Patients with other skin diseases.
- Patients with chronic liver, renal or haematological diseases.
- Patients with malignant tumors.
Trial locations and contacts
No sites are listed yet.
About this study
Official title: Activation of Coagulation as an Indicator of a Pro-thrombotic State in Patients With Pemphigus: A Case-control Study
Aim of work:
- To evaluate the plasma markers of coagulation activation: prothrombin F1+2 and d-dimer levels in pemphigus patients with active disease and compare them with age and sex-matched controls.
- To evaluate the correlation of these markers with disease severity score by using Pemphigus Disease Area Index (PDAI) and with disease activity by measurement of anti-desmoglein 1 and 3 antibody titers.
Read the detailed description
Pemphigus encompasses a group of autoimmune bullous diseases characterized clinically by the presence of flaccid blisters and erosions of the mucous membranes and/or skin. It is characterized by autoantibodies directed against the desmosomal desmogleins; Desmoglein 1 (Dsg1) and Desmoglein 3 (Dsg3) on keratinocyte cell surfaces resulting in acantholysis, which is the mechanism underlying pemphigus.
Pemphigus diseases can be classified into 4 main forms based on clinical and immunopathological features: pemphigus vulgaris, in about 70-80% of patients; pemphigus foliaceus, in about 20%; paraneoplastic pemphigus, in about 5%; and IgA pemphigus, in 1-3%.
The global incidence of PV ranges from 0.7 to 5 cases per million per year. PV predominantly affects adults in the 4th-6th decade of life. PV often begins with painful, non-healing erosions in oral mucosa, and develops into blisters in the skin.
The diagnosis of pemphigus is based on triad of history taking, clinical examination and immunologic investigations. ELISA using recombinant Dsgs enables detection of circulating autoantibodies in pemphigus. The sensitivity and specificity of anti-Dsg ELISA are 96% to 100% .The autoantibody titers often fluctuate in parallel with disease activity and decline with clinical improvement; therefore, these titers are useful not only for diagnosis but also for monitoring of disease activity and a decrease in the ELISA index value can be a useful guide for steroid tapering in the lesion-free phase.
Growing evidence has suggested that several autoimmune disorders are significantly associated with an increased risk of venous thromboembolism (VTE). However, the primary contribution of pemphigus to VTE development is unclear.
A retrospective cohort study demonstrated a 5% venous thromboembolism rate in patients with pemphigus within the first year after diagnosis.
A large-scale population-based longitudinal cohort study concluded that pemphigus is associated with an increased risk of pulmonary embolism (PE), particularly during the 1st year of the disease.
The mechanism underlying the increased VTE risk in pemphigus had not been clearly defined. However, there is evidence that systemic inflammation, which exists in pemphigus as well as in other autoimmune diseases, may promote thrombosis through upregulation of pro-coagulation systems, anticoagulant suppression, and antifibrinolytic effects. Elevated levels of tumor necrosis alpha (TNF-α) and interleukin (IL)-1, IL-6 and IL-8 released into systemic circulation have been found to promote coagulation.
Additional possible risk factors for VTE development in patients with pemphigus are hospitalization, immobility and high prevalence of infections. Corticosteroid therapy, the mainstay of pemphigus treatment, increases the risk of VTE by increasing the levels of fibrinogen and clotting factors.
D-Dimer is a biomarker of fibrin formation and degradation. So far, the guidelines for the diagnosis and treatment of PE have clearly stated that only D-dimer tests are used in laboratory tests for diagnosis to date.
Although D-dimer is considered a sensitive biomarker for thromboembolic events, it does not show as much specificity. Other conditions can also raise D-dimer level, such as pregnancy, renal failure and sepsis. An elevated D-dimer value is not sufficient to establish the diagnosis of pulmonary thromboembolism.
The most important marker of coagulation activation is the prothrombin fragment 1 + 2 (F1 + 2), which is a small peptide released when prothrombin is converted to thrombin by the prothrombinase complex on negatively charged phospholipids expressed on membranes of activated platelets. Consequently, an increased rate of conversion of prothrombin to thrombin, as it may occur in prothrombotic states, should result in an increase of F1 + 2 concentration in plasma. Owing to its relatively short half-life (approximately 90 minutes), the plasma levels of F1 + 2 are considered as reliable estimates of thrombin formation in vivo at the time of blood sampling.
- Conditions
- Pemphigus
- Being tested
- prothrombin fragment 1+2
- Medical subject headings
- Pemphigus
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
prothrombin fragment 1+2Diagnostic test
Also called D-dimer
Blood sample
| Study group | Role | What they receive |
|---|---|---|
| pemphigus vulgaris patients | Not described Receives: Diagnostic Test: prothrombin fragment 1+2 | |
| control group | Not described Receives: Diagnostic Test: prothrombin fragment 1+2 |
What is being measured
The primary outcome is the main question the study is designed to answer.
Comparison of coagulation activation markers in pemphigus patients with controls
Evaluate the plasma markers of coagulation activation: prothrombin F1+2 and d-dimer levels in pemphigus patients with active disease and compare them with age and sex-matched controls.
Measured: Baseline
Secondary outcomes (1)
Correlation of markers with disease severity
Evaluate correlation of these markers with disease severity score by using Pemphigus Disease Area Index (PDAI) and with disease activity by measurement of anti-desmoglein 1 and 3 antibody titers.
Measured: Baseline
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted29 Feb 2024
- Study start1 Mar 2024 (estimated)
- Primary completionOct 2025 (estimated)
- Study completionFeb 2026 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (13)Papers the sponsor has linked to this study.
- Other trials for PemphigusStudies of the same condition, open and under way.
- More trials run by Assiut UniversityThe sponsor's other registered studies.
- 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
- Case-control
- Time perspective
- Prospective
- Enrolment
- 54 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Assiut University
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Youstina Zaghloul, Assiut University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06285435
- Sponsor's protocol ID
- coagulation activation in PV
- Status last verified
- Feb 2024
- First submitted
- 22 Feb 2024
- Last updated
- 29 Feb 2024
- Results posted
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
Gregoriou S, Efthymiou O, Stefanaki C, Rigopoulos D. Management of pemphigus vulgaris: challenges and solutions. Clin Cosmet Investig Dermatol. 2015 Oct 21;8:521-7. doi: 10.2147/CCID.S75908. eCollection 2015.
PubMed 26543381Jiang C, Adjei S, Santiago S, Lu J, Duran M, Tyring S. Novel use of dupilumab in pemphigus vulgaris and pemphigus foliaceus. JAAD Case Rep. 2023 Sep 30;42:12-15. doi: 10.1016/j.jdcr.2023.09.018. eCollection 2023 Dec. No abstract available.
PubMed 37965194Beek NV, Zillikens D, Schmidt E. Bullous Autoimmune Dermatoses-Clinical Features, Diagnostic Evaluation, and Treatment Options. Dtsch Arztebl Int. 2021 Jun 18;118(24):413-420. doi: 10.3238/arztebl.m2021.0136.
PubMed 34369370Yuan Q, Yang W, Zhang X. Immune cells in pemphigus vulgaris and bullous Pemphigoid: From pathogenic roles to targeting therapies. Int Immunopharmacol. 2023 Oct;123:110694. doi: 10.1016/j.intimp.2023.110694. Epub 2023 Jul 29.
PubMed 37523970Kridin K, Kridin M, Amber KT, Shalom G, Comaneshter D, Batat E, Cohen AD. The Risk of Pulmonary Embolism in Patients With Pemphigus: A Population-Based Large-Scale Longitudinal Study. Front Immunol. 2019 Jul 24;10:1559. doi: 10.3389/fimmu.2019.01559. eCollection 2019.
PubMed 31396203Shaheen MS, Silverberg JI. Association of inflammatory skin diseases with venous thromboembolism in US adults. Arch Dermatol Res. 2021 May;313(4):281-289. doi: 10.1007/s00403-020-02099-6. Epub 2020 Jul 8.
PubMed 32642810Yang P, Li H, Zhang J, Xu X. Research progress on biomarkers of pulmonary embolism. Clin Respir J. 2021 Oct;15(10):1046-1055. doi: 10.1111/crj.13414. Epub 2021 Aug 3.
PubMed 34214256Marin M, Orso D, Federici N, Vetrugno L, Bove T. D-dimer specificity and clinical context: an old unlearned story. Crit Care. 2021 Mar 10;25(1):101. doi: 10.1186/s13054-021-03532-6. No abstract available.
PubMed 33691711Capecchi M, Scalambrino E, Griffini S, Grovetti E, Clerici M, Merati G, Chantarangkul V, Cugno M, Peyvandi F, Tripodi A. Relationship between thrombin generation parameters and prothrombin fragment 1 + 2 plasma levels. Int J Lab Hematol. 2021 Oct;43(5):e248-e251. doi: 10.1111/ijlh.13462. Epub 2021 Jan 12. No abstract available.
PubMed 33433957Lee SH, Hong WJ, Kim SC. Analysis of Serum Cytokine Profile in Pemphigus. Ann Dermatol. 2017 Aug;29(4):438-445. doi: 10.5021/ad.2017.29.4.438. Epub 2017 Jun 21.
PubMed 28761292Rosenbach M, Murrell DF, Bystryn JC, Dulay S, Dick S, Fakharzadeh S, Hall R, Korman NJ, Lin J, Okawa J, Pandya AG, Payne AS, Rose M, Rubenstein D, Woodley D, Vittorio C, Werth BB, Williams EA, Taylor L, Troxel AB, Werth VP. Reliability and convergent validity of two outcome instruments for pemphigus. J Invest Dermatol. 2009 Oct;129(10):2404-10. doi: 10.1038/jid.2009.72. Epub 2009 Apr 9.
PubMed 19357707Leshem YA, Atzmony L, Dudkiewicz I, Hodak E, Mimouni D. Venous thromboembolism in patients with pemphigus: A cohort study. J Am Acad Dermatol. 2017 Aug;77(2):256-260. doi: 10.1016/j.jaad.2017.01.059. Epub 2017 May 9.
PubMed 28495498Egami S, Yamagami J, Amagai M. Autoimmune bullous skin diseases, pemphigus and pemphigoid. J Allergy Clin Immunol. 2020 Apr;145(4):1031-1047. doi: 10.1016/j.jaci.2020.02.013.
PubMed 32272980
Study at a glance
From the registry record, last updated by the sponsor on 29 Feb 2024. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Activation of Coagulation as an Indicator of a Pro-thrombotic State in Patients With Pemphigus: A Case-control Study
- ClinicalTrials.gov ID
- NCT06285435
- Acronym / sponsor ID
- coagulation activation in PV
- Conditions
- Pemphigus
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 54 participants (estimated)
- Lead sponsor
- Assiut UniversityUniversity, hospital or other
- Study start
- 1 Mar 2024 (estimated)
- Primary completion
- Oct 2025 (estimated)
- Study completion
- Feb 2026 (estimated)
- First posted
- 29 Feb 2024 (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.
Aim of work:
- To evaluate the plasma markers of coagulation activation: prothrombin F1+2 and d-dimer levels in pemphigus patients with active disease and compare them with age and sex-matched controls.
- To evaluate the correlation of these markers with disease severity score by using Pemphigus Disease Area Index (PDAI) and with disease activity by measurement of anti-desmoglein 1 and 3 antibody titers.
Detailed description
Pemphigus encompasses a group of autoimmune bullous diseases characterized clinically by the presence of flaccid blisters and erosions of the mucous membranes and/or skin. It is characterized by autoantibodies directed against the desmosomal desmogleins; Desmoglein 1 (Dsg1) and Desmoglein 3 (Dsg3) on keratinocyte cell surfaces resulting in acantholysis, which is the mechanism underlying pemphigus.
Pemphigus diseases can be classified into 4 main forms based on clinical and immunopathological features: pemphigus vulgaris, in about 70-80% of patients; pemphigus foliaceus, in about 20%; paraneoplastic pemphigus, in about 5%; and IgA pemphigus, in 1-3%.
The global incidence of PV ranges from 0.7 to 5 cases per million per year. PV predominantly affects adults in the 4th-6th decade of life. PV often begins with painful, non-healing erosions in oral mucosa, and develops into blisters in the skin.
The diagnosis of pemphigus is based on triad of history taking, clinical examination and immunologic investigations. ELISA using recombinant Dsgs enables detection of circulating autoantibodies in pemphigus. The sensitivity and specificity of anti-Dsg ELISA are 96% to 100% .The autoantibody titers often fluctuate in parallel with disease activity and decline with clinical improvement; therefore, these titers are useful not only for diagnosis but also for monitoring of disease activity and a decrease in the ELISA index value can be a useful guide for steroid tapering in the lesion-free phase.
Growing evidence has suggested that several autoimmune disorders are significantly associated with an increased risk of venous thromboembolism (VTE). However, the primary contribution of pemphigus to VTE development is unclear.
A retrospective cohort study demonstrated a 5% venous thromboembolism rate in patients with pemphigus within the first year after diagnosis.
A large-scale population-based longitudinal cohort study concluded that pemphigus is associated with an increased risk of pulmonary embolism (PE), particularly during the 1st year of the disease.
The mechanism underlying the increased VTE risk in pemphigus had not been clearly defined. However, there is evidence that systemic inflammation, which exists in pemphigus as well as in other autoimmune diseases, may promote thrombosis through upregulation of pro-coagulation systems, anticoagulant suppression, and antifibrinolytic effects. Elevated levels of tumor necrosis alpha (TNF-α) and interleukin (IL)-1, IL-6 and IL-8 released into systemic circulation have been found to promote coagulation.
Additional possible risk factors for VTE development in patients with pemphigus are hospitalization, immobility and high prevalence of infections. Corticosteroid therapy, the mainstay of pemphigus treatment, increases the risk of VTE by increasing the levels of fibrinogen and clotting factors.
D-Dimer is a biomarker of fibrin formation and degradation. So far, the guidelines for the diagnosis and treatment of PE have clearly stated that only D-dimer tests are used in laboratory tests for diagnosis to date.
Although D-dimer is considered a sensitive biomarker for thromboembolic events, it does not show as much specificity. Other conditions can also raise D-dimer level, such as pregnancy, renal failure and sepsis. An elevated D-dimer value is not sufficient to establish the diagnosis of pulmonary thromboembolism.
The most important marker of coagulation activation is the prothrombin fragment 1 + 2 (F1 + 2), which is a small peptide released when prothrombin is converted to thrombin by the prothrombinase complex on negatively charged phospholipids expressed on membranes of activated platelets. Consequently, an increased rate of conversion of prothrombin to thrombin, as it may occur in prothrombotic states, should result in an increase of F1 + 2 concentration in plasma. Owing to its relatively short half-life (approximately 90 minutes), the plasma levels of F1 + 2 are considered as reliable estimates of thrombin formation in vivo at the time of blood sampling.
Study design
- Observational model
- Case-control
- Time perspective
- Prospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| pemphigus vulgaris patients | – | Diagnostic Test: prothrombin fragment 1+2 |
| control group | – | Diagnostic Test: prothrombin fragment 1+2 |
Who may qualify
- Ages
- 18 to 60 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult
- Study population
- Patients with active pemphigus who are either in a relapse for less than a week or are newly diagnosed cases will be included. The active stage of PV is defined as the de novo development of blisters on a healthy (unaffected or healed) site of either the skin or the mucous membrane. Clinical assessment, histopathological analysis (acantholysis and intraepidermal splitting) will be used to confirm the diagnosis of each patient. Control group: Healthy age and sex-matched subjects, who are free of chronic systemic diseases or dermatological conditions, will be enrolled as control.
Key inclusion criteria (2 listed)
- pemphigus vulgaris patients at active stage of the disease.
- patients between the ages of 18 and 60.
Key exclusion criteria (4 listed)
- Patients with other autoimmune bullous diseases.
- Patients with other skin diseases.
- Patients with chronic liver, renal or haematological diseases.
- Patients with malignant tumors.
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 |
|---|---|---|
| prothrombin fragment 1+2Also: D-dimerBlood sample | Diagnostic test | control group, pemphigus vulgaris patients |
Primary outcome
Comparison of coagulation activation markers in pemphigus patients with controls
Time frame: Baseline
Evaluate the plasma markers of coagulation activation: prothrombin F1+2 and d-dimer levels in pemphigus patients with active disease and compare them with age and sex-matched controls.
1 secondary outcome
Correlation of markers with disease severity
Time frame: Baseline
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 29 Feb 2024.
- Results publication: PubMed 26543381Gregoriou S, Efthymiou O, Stefanaki C, Rigopoulos D. Management of pemphigus vulgaris: challenges and solutions. Clin Cosmet Investig Dermatol. 2015 Oct 21;8:521-7. doi: 10.2147/CCID.S75908. eCollection 2015.
- Results publication: PubMed 37965194Jiang C, Adjei S, Santiago S, Lu J, Duran M, Tyring S. Novel use of dupilumab in pemphigus vulgaris and pemphigus foliaceus. JAAD Case Rep. 2023 Sep 30;42:12-15. doi: 10.1016/j.jdcr.2023.09.018. eCollection 2023 Dec. No abstract available.
- Results publication: PubMed 34369370Beek NV, Zillikens D, Schmidt E. Bullous Autoimmune Dermatoses-Clinical Features, Diagnostic Evaluation, and Treatment Options. Dtsch Arztebl Int. 2021 Jun 18;118(24):413-420. doi: 10.3238/arztebl.m2021.0136.
- Results publication: PubMed 37523970Yuan Q, Yang W, Zhang X. Immune cells in pemphigus vulgaris and bullous Pemphigoid: From pathogenic roles to targeting therapies. Int Immunopharmacol. 2023 Oct;123:110694. doi: 10.1016/j.intimp.2023.110694. Epub 2023 Jul 29.
- Results publication: PubMed 31396203Kridin K, Kridin M, Amber KT, Shalom G, Comaneshter D, Batat E, Cohen AD. The Risk of Pulmonary Embolism in Patients With Pemphigus: A Population-Based Large-Scale Longitudinal Study. Front Immunol. 2019 Jul 24;10:1559. doi: 10.3389/fimmu.2019.01559. eCollection 2019.
- Results publication: PubMed 32642810Shaheen MS, Silverberg JI. Association of inflammatory skin diseases with venous thromboembolism in US adults. Arch Dermatol Res. 2021 May;313(4):281-289. doi: 10.1007/s00403-020-02099-6. Epub 2020 Jul 8.
- Results publication: PubMed 34214256Yang P, Li H, Zhang J, Xu X. Research progress on biomarkers of pulmonary embolism. Clin Respir J. 2021 Oct;15(10):1046-1055. doi: 10.1111/crj.13414. Epub 2021 Aug 3.
- Results publication: PubMed 33691711Marin M, Orso D, Federici N, Vetrugno L, Bove T. D-dimer specificity and clinical context: an old unlearned story. Crit Care. 2021 Mar 10;25(1):101. doi: 10.1186/s13054-021-03532-6. No abstract available.
- Results publication: PubMed 33433957Capecchi M, Scalambrino E, Griffini S, Grovetti E, Clerici M, Merati G, Chantarangkul V, Cugno M, Peyvandi F, Tripodi A. Relationship between thrombin generation parameters and prothrombin fragment 1 + 2 plasma levels. Int J Lab Hematol. 2021 Oct;43(5):e248-e251. doi: 10.1111/ijlh.13462. Epub 2021 Jan 12. No abstract available.
- Results publication: PubMed 28761292Lee SH, Hong WJ, Kim SC. Analysis of Serum Cytokine Profile in Pemphigus. Ann Dermatol. 2017 Aug;29(4):438-445. doi: 10.5021/ad.2017.29.4.438. Epub 2017 Jun 21.
- Results publication: PubMed 19357707Rosenbach M, Murrell DF, Bystryn JC, Dulay S, Dick S, Fakharzadeh S, Hall R, Korman NJ, Lin J, Okawa J, Pandya AG, Payne AS, Rose M, Rubenstein D, Woodley D, Vittorio C, Werth BB, Williams EA, Taylor L, Troxel AB, Werth VP. Reliability and convergent validity of two outcome instruments for pemphigus. J Invest Dermatol. 2009 Oct;129(10):2404-10. doi: 10.1038/jid.2009.72. Epub 2009 Apr 9.
- Results publication: PubMed 28495498Leshem YA, Atzmony L, Dudkiewicz I, Hodak E, Mimouni D. Venous thromboembolism in patients with pemphigus: A cohort study. J Am Acad Dermatol. 2017 Aug;77(2):256-260. doi: 10.1016/j.jaad.2017.01.059. Epub 2017 May 9.
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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.
Questions about this trial
What is this clinical trial studying?
An observational study of Pemphigus, run by Assiut University.
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 2 inclusion and 4 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 29 Feb 2024. Status can change between updates, so confirm with the study contact before making plans.
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?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Youstina Zaghloul (01002142707, yostina.zaghloul@gmail.com), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Comparison of coagulation activation markers in pemphigus patients with controls (time frame: Baseline). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT06285435, which also lists 13 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 29 Feb 2024.