Monogenic ObesityObGeSemaNCT06380426
A Multicenter Pharmacoepidemiological Cohort on Real Life Use of Semaglutide in Adolescents or Adults With Monogenic Obesity
An observational study of Monogenic Obesity, run by Assistance Publique - Hôpitaux de Paris at 2 sites in France.
Trial summary
Rare genetic forms of obesity, so called monogenic obesity are linked to alteration in energy balance involving hypothalamic pathways. More than 60 genes encoding for proteins located in the hypothalamic leptin/melanocortin pathway have been described in the French National Protocol for Diagnostic and Care (PNDS). Read more about this study
- Who is it for?
- Ages 12 years and older
- Conditions the study is for
- Monogenic Obesity
- How many people
- 175 participants
- Where
- 2 sitesFrance
- Study dates
- 19 Sep 2024to 30 Nov 2027
- Phase
- Observational
- Are there results?
- Not yet: the study is under way
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 12 years and older
- All sexes
- No healthy volunteers
- Child, Adult, Older adult
Study population: Patients (≥12 years) with monogenic obesity due to any variant regardless of pathogenicity classification and already treated or with the physician's decision to initiate treatment with Semaglutide in the standard care. Patients under legal protection and State Medical Assistance (AME) will be included.
Who may be able to join
- Patients (≥12 years) having already initiated a treatment with SEMAGLUTIDE (regardless of the context: early access, routine care, self-financing, or exceptional reimbursement) or with a physician's decision to initiate treatment in the standard care. All patients having initiated treatment will be proposed to participate, including those having already stopped the treatment at the time of study initiation.
- Confirmation of monogenic obesity, as practiced in clinical routine, regardless of current classification (i.e., pathogenic, likely pathogenic, variant of uncertain significance [VUS], or benign) in a gene with leptin-melanocortin pathway described in PNDS (https://www.has-sante.fr/jcms/p_3280217/fr/generique-obesites-de-causes-rares). ) For patients with VUS or benign variants, inclusion is conditional on the availability of a polygenic risk score (PRS)
- Patients duly informed and not objecting to participate in the study. For patients ≥12 years <18 years Parents duly informed and not objecting that their child taking part in the study
- Patients affiliated to a social security scheme or State Medical Assistance (AME).
Who cannot join
- Pregnant and breastfeeding women
Trial locations and contacts
2 sites in 1 country. Contact the study team or a site near you to ask about taking part.
France2 sites, 2 recruiting
- Not yet recruiting
Centre de référence Syndrome de Prader-Willi et autres obésités avec troubles du comportement alimentaire (PRADORT). Service de Nutrition, GH Pitié-Salpêtrière, APHP
Paris, 75013
Emilie GUILLON, emilie.guillon-ext@aphp.fr
Sarra POCHON, +33(1)42167574, sarra.pochon@aphp.fr
- Recruiting
CHU Pitié Salpêtrière - APHP
Paris, 75013
Christine POITOU-BERNERT, MD, PhD, +33(0)142175771
Christine POITOU-BERNERT, MD,PhD
About this study
Rare genetic forms of obesity, so called monogenic obesity are linked to alteration in energy balance involving hypothalamic pathways.
More than 60 genes encoding for proteins located in the hypothalamic leptin/melanocortin pathway have been described in the French National Protocol for Diagnostic and Care (PNDS).
Read more
While pathogenic and likely pathogenic variants in these genes are well-established causes of monogenic obesity, current evidence supports a broader genetic architecture of obesity, better understood as a continuum ranging from rare high-impact variants to polygenic susceptibility.
Variants of uncertain significance (VUS) as well as variants currently classified as benign or likely benign are frequently identified in clinical practice, and their classification may evolve over time as genomic databases expand and functional data accumulate In addition, polygenic background may interact with rare variants and contribute to the severity of the phenotype, disease progression, and therapeutic response.
The natural history of monogenic obesity is characterized by an early onset in childhood, with a major increase in weight in adolescence and young adulthood. The worsening of obesity exposes these patients to severe complications.
Severe obesity and eating disorders have a major impact on the quality of life of the person but also of the family and caregivers. Clinical management is complex and requires comprehensive, specialized and multidisciplinary management. The usual lifestyle approaches have so far shown disappointing results, similarly to bariatric surgery which leads to a more frequent weight regain in the situation of monogenic obesity, justifying new approaches.
In this context, evaluating the response to treatment in the particular condition of monogenic obesity is crucial to propose therapeutic options as early as possible to limit weight evolution and its complications.
GLP-1 (glucagon-like peptide 1) based innovative therapies have recently emerged as a promising option for treatment of obesity and its complications. This is the case for Semaglutide marketed as OZEMPIC® and WEGOVY®, developed by Novo Nordisk. However, there is a lack of data to confirm that semaglutide could be also effective in monogenic obesity.
The aim of the ObGeSema project is to set up a cohort composed of patients (1) having already initiated a treatment and (2) newly treated by Semaglutide in 21 pediatric and adult Specialized Obesity Centres (CSOs) and describe their evolution over a 4 years follow-up.
Read the detailed description
Rare genetic forms of obesity, so called monogenic obesity are linked to alteration in energy balance involving hypothalamic pathways. More than 60 genes encoding for proteins located in the hypothalamic leptin/melanocortin pathway have been described in the French National Protocol for Diagnostic and Care (PNDS) https://www.has-sante.fr/jcms/p_3280217/fr/generique-obesites-de-causes-rares).
While pathogenic and likely pathogenic variants in these genes are well-established causes of monogenic obesity, current evidence supports a broader genetic architecture of obesity, better understood as a continuum ranging from rare high-impact variants to polygenic susceptibility.
Variants of uncertain significance (VUS) as well as variants currently classified as benign or likely benign are frequently identified in clinical practice, and their classification may evolve over time as genomic databases expand and functional data accumulate In addition, polygenic background may interact with rare variants and contribute to the severity of the phenotype, disease progression, and therapeutic response.
The natural history of monogenic obesity is characterized by an early onset in childhood, with a major increase in weight in adolescence and young adulthood. The worsening of obesity exposes these patients to severe complications. Severe obesity and eating disorders have a major impact on the quality of life of the person but also of the family and caregivers. Clinical management is complex and requires comprehensive, specialized and multidisciplinary management. The usual lifestyle approaches have so far shown disappointing results, similarly to bariatric surgery which leads to a more frequent weight regain in the situation of monogenic obesity, justifying new approaches.
In this context, evaluating the response to treatment in the particular condition of monogenic obesity is crucial to propose therapeutic options as early as possible to limit weight evolution and its complications.
GLP-1 based innovative therapies have recently emerged as a promising option for treatment of obesity and its complications. This is the case for Semaglutide marketed as OZEMPIC® and WEGOVY®, developed by Novo Nordisk. However, there is a lack of data to confirm that semaglutide could be also effective in monogenic obesity, particularly across the full spectrum of genetic variants involved in the leptin-melanocortin pathway.
In France, semaglutide is currently accessible through several regulatory frameworks:
OZEMPIC® (up to 2 mg/week) is reimbursed by the French Social Security for the treatment of type 2 diabetes in adult patients.
WEGOVY® (up to 2.4 mg/week) was available through an Early Access Programme from May 2022 to September 2024 for adults with BMI >40 kg/m² and at least one comorbidity. Treatment initiated in this framework can be continued until December 2025.
Since November 2024, WEGOVY® (up to 2.4 mg/week) has had marketing authorization for the treatment of adolescents and adults ≥12 years with BMI ≥30 kg/m². However, the drug is not yet reimbursed, except in rare cases through individual exceptional reimbursement for rare and complex diseases.
Given this evolving regulatory landscape, it is essential to assess the real-life efficacy and safety of semaglutide in individuals with including both adolescents and adults carrying variants across the continuum of genetic susceptibility.
The aim of the ObGeSema project is to set up a cohort composed of patients (1) having already initiated a treatment and (2) newly treated by Semaglutide in 21 pediatric and adult Specialized Obesity Centres (CSOs) and describe their evolution over a 4 years follow-up.
- Conditions
- Monogenic Obesity
- Keywords
- Monogenic obesity, Semaglutide, WEGOVY
What is being measured
The primary outcome is the main question the study is designed to answer.
Change in weight and Body Mass Index (BMI)
Percentage of subjects with a change in weight and Body Mass Index (BMI).Weight will be measured at initiation and at 12 months of the Semaglutide treatment
Measured: From baseline (T0) to T12
Secondary outcomes (18)
Change in weight and Body Mass Index (BMI)
Percentage of subjects with a change in weight and Body Mass Index (BMI). Weight will be measured at initiation of the Semaglutide treatment and at each visit
Measured: From baseline (T0) to 6 and/or 24 and/or 36 and/or 48 and/or 60 months
Reduction of body weight equal to or above 5%
Percentage of subjects achieving a reduction of body weight equal to or above 5%(number of subjects with a % of body weight changes > -5%)X100/ number of the total subject
Measured: From baseline (T0) to 6 and/or 12 and/or 24 and/or 36 and/or 48 and/or 60 months
Change in Hunger score
Number and percentage of subjects with change in Hunger score
Measured: From baseline (T0) to 12 and/or 24 and/or 36 and/or 48 and/or 60 months
Change in eating behaviour measured by Food Craving questionnaire
Number and percentage of subjects with change in Food Craving scale
Measured: From baseline (T0) to 12 months
Change in eating behaviour measured by the Binge Eating Scale (BES)
Number and percentage of subjects with change in Binge Eating Scale (BES)
Measured: From baseline (T0) to 12 months
Change in eating behaviour measured by the Dutch Eating Behaviour Questionnaire (DEBQ)
Number and percentage of subjects with change in Dutch Eating Behaviour Questionnaire (DEBQ)
Measured: From baseline (T0) to 12 months
Change in eating behaviour measured by the Dykens questionnaire for ≥18 years patients
Number and percentage of subjects with change in Hyperphagia score with the Dykens questionnaire for intellectual disability
Measured: From baseline (T0) to 12 months
Change in eating behaviour measured by the Child Eating Behaviour Questionnaire (CEBQ)
Number and percentage of subjects with change in the Child Eating Behaviour Questionnaire (CEBQ) for intellectual disability for ≥18 years patients
Measured: From baseline (T0) to 12 months
Change in the International physical activity questionnaire (IPAQ - short form) for ≥18 years patients
Number and percentage of subjects with change of the International physical activity
Measured: From baseline (T0) to 12 months
Change in Digestive disorders (GIQLI ) for ≥18 years patients
Number and percentage of subjects with change in Digestive disorders (GIQLI ). Digestive disorders are measured by the Gastrointestinal Quality of Life Index (GIQLI)
Measured: From baseline (T0) to 12 and/or 24 and/or 36 and/or 48 and/or 60 months
Change in score of quality of life scores (patient and parents) for ≥18 years patients
Number and percentage of subjects with change in score of quality of life scores .Quality of life is measured with the Impact of Weight on Quality of Life-Lite scale (IWQOL-Lite)
Measured: From baseline (T0) to 12 months
Change in sleep disorder (MCTQ score) for ≥18 years patients
Number and percentage of subjects with Change in sleep disorder. Sleep disorder is measured with the Micro Munich Chronotype Questionnaire (MCTQ)
Measured: From baseline (T0) to 12 months
Change in anxiety and depression score for ≥18 years patients
Number and percent of subjects with change in anxiety and depression score. Anxiety and depression is measured with the Hospital Anxiety and Depression scale (HAD)
Measured: From baseline (T0) to 12 and/or 24 and/or 36 and/or 48 and/or 60 months
● Change in Body Mass Index : BMI Z-score for 12 to <18 years
Weight will be measured at initiation of the Semaglutide treatment and at each visit
Measured: From baseline (T0) to 6 and/or 12 and/or 24 and/or 36 and/or 48 and/or 60 months
Change in eating behaviour scores CEBQ ( Child Eating Behaviour Questionnaire) or Hyperphagia score with the Dykens questionnaire and for intellectual disability. For 12 to <18 years patients
Number and percentage of subjects with change
Measured: From baseline (T0) to 12 months
Change in score of IWQOL Impact of Weight on Quality of Life (patient and parents). For 12 to <18 years patients
Number and percentage of subjects with change in score Impact of Weight on Quality of Life
Measured: From baseline (T0) to 12 months
Change in Digestive disorders GIQLI score (Gastrointestinal Quality of Life Index). For 12 to <18 years patients
Number and percentage of subjects with change
Measured: From baseline (T0) to 12 and/or 24 and/or 36 and/or 48 and/or 60 months
Treatment-emergent adverse events (TEAEs) and serious adverse events (SAEs)
Number of treatment-emergent adverse events (TEAEs) and serious adverse events (SAEs)
Measured: From baseline (T0) to 6 and/or 12 and/or 24 and/or 36 and/or 48 and/or 60 months
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted23 Apr 2024
- Study start19 Sep 2024
- Primary completion30 Apr 2027 (estimated)
- Study completion30 Nov 2027 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for Monogenic ObesityStudies of the same condition, open and under way.
- More trials run by Assistance Publique - Hôpitaux de ParisThe 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
- Cohort
- Time perspective
- Other
- Enrolment
- 175 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Assistance Publique - Hôpitaux de Paris
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Christine POITOU-BERNERT, MD,PhD, Principal investigator, Assistance Publique - Hôpitaux de ParisBéatrice DUBERN, MD,PhD, Study director, Assistance Publique - Hôpitaux de Paris
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06380426
- Sponsor's protocol ID
- APHP230441
- Other IDs
- IDRCB : 2023-A02003-42
- Acronym
- ObGeSema
- Status last verified
- Jun 2026
- First submitted
- 11 Apr 2024
- Last updated
- 24 Jun 2026
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Yes: Data are available upon reasonable request. The procedures carried out with the French data privacy authority (CNIL, Commission nationale de l'informatique et des libertés) do not provide for the transmission of the database, nor do the information and consent documents signed by the patients. Consultation by the editorial board or interested researchers of individual participant data that underlie the results reported in the article after deidentification may nevertheless be considered, subject to prior determination of the terms and conditions of such consultation and in respect for compliance with the applicable regulations.
Study at a glance
From the registry record, last updated by the sponsor on 24 Jun 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- A Multicenter Pharmacoepidemiological Cohort on Real Life Use of Semaglutide in Adolescents or Adults With Monogenic Obesity
- ClinicalTrials.gov ID
- NCT06380426
- Acronym / sponsor ID
- ObGeSema / APHP230441
- Conditions
- Monogenic Obesity
- Keywords
- Monogenic obesity, Semaglutide, WEGOVY
- Study type
- Observational
- Recruitment status
- Recruiting
- Enrolment
- 175 participants (estimated)
- Lead sponsor
- Assistance Publique - Hôpitaux de ParisUniversity, hospital or other
- Study start
- 19 Sep 2024 (actual)
- Primary completion
- 30 Apr 2027 (estimated)
- Study completion
- 30 Nov 2027 (estimated)
- First posted
- 23 Apr 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.
Rare genetic forms of obesity, so called monogenic obesity are linked to alteration in energy balance involving hypothalamic pathways.
More than 60 genes encoding for proteins located in the hypothalamic leptin/melanocortin pathway have been described in the French National Protocol for Diagnostic and Care (PNDS).
While pathogenic and likely pathogenic variants in these genes are well-established causes of monogenic obesity, current evidence supports a broader genetic architecture of obesity, better understood as a continuum ranging from rare high-impact variants to polygenic susceptibility.
Variants of uncertain significance (VUS) as well as variants currently classified as benign or likely benign are frequently identified in clinical practice, and their classification may evolve over time as genomic databases expand and functional data accumulate In addition, polygenic background may interact with rare variants and contribute to the severity of the phenotype, disease progression, and therapeutic response.
The natural history of monogenic obesity is characterized by an early onset in childhood, with a major increase in weight in adolescence and young adulthood. The worsening of obesity exposes these patients to severe complications.
Severe obesity and eating disorders have a major impact on the quality of life of the person but also of the family and caregivers. Clinical management is complex and requires comprehensive, specialized and multidisciplinary management. The usual lifestyle approaches have so far shown disappointing results, similarly to bariatric surgery which leads to a more frequent weight regain in the situation of monogenic obesity, justifying new approaches.
In this context, evaluating the response to treatment in the particular condition of monogenic obesity is crucial to propose therapeutic options as early as possible to limit weight evolution and its complications.
GLP-1 (glucagon-like peptide 1) based innovative therapies have recently emerged as a promising option for treatment of obesity and its complications. This is the case for Semaglutide marketed as OZEMPIC® and WEGOVY®, developed by Novo Nordisk. However, there is a lack of data to confirm that semaglutide could be also effective in monogenic obesity.
The aim of the ObGeSema project is to set up a cohort composed of patients (1) having already initiated a treatment and (2) newly treated by Semaglutide in 21 pediatric and adult Specialized Obesity Centres (CSOs) and describe their evolution over a 4 years follow-up.
Detailed description
Rare genetic forms of obesity, so called monogenic obesity are linked to alteration in energy balance involving hypothalamic pathways. More than 60 genes encoding for proteins located in the hypothalamic leptin/melanocortin pathway have been described in the French National Protocol for Diagnostic and Care (PNDS) https://www.has-sante.fr/jcms/p_3280217/fr/generique-obesites-de-causes-rares).
While pathogenic and likely pathogenic variants in these genes are well-established causes of monogenic obesity, current evidence supports a broader genetic architecture of obesity, better understood as a continuum ranging from rare high-impact variants to polygenic susceptibility.
Variants of uncertain significance (VUS) as well as variants currently classified as benign or likely benign are frequently identified in clinical practice, and their classification may evolve over time as genomic databases expand and functional data accumulate In addition, polygenic background may interact with rare variants and contribute to the severity of the phenotype, disease progression, and therapeutic response.
The natural history of monogenic obesity is characterized by an early onset in childhood, with a major increase in weight in adolescence and young adulthood. The worsening of obesity exposes these patients to severe complications. Severe obesity and eating disorders have a major impact on the quality of life of the person but also of the family and caregivers. Clinical management is complex and requires comprehensive, specialized and multidisciplinary management. The usual lifestyle approaches have so far shown disappointing results, similarly to bariatric surgery which leads to a more frequent weight regain in the situation of monogenic obesity, justifying new approaches.
In this context, evaluating the response to treatment in the particular condition of monogenic obesity is crucial to propose therapeutic options as early as possible to limit weight evolution and its complications.
GLP-1 based innovative therapies have recently emerged as a promising option for treatment of obesity and its complications. This is the case for Semaglutide marketed as OZEMPIC® and WEGOVY®, developed by Novo Nordisk. However, there is a lack of data to confirm that semaglutide could be also effective in monogenic obesity, particularly across the full spectrum of genetic variants involved in the leptin-melanocortin pathway.
In France, semaglutide is currently accessible through several regulatory frameworks:
OZEMPIC® (up to 2 mg/week) is reimbursed by the French Social Security for the treatment of type 2 diabetes in adult patients.
WEGOVY® (up to 2.4 mg/week) was available through an Early Access Programme from May 2022 to September 2024 for adults with BMI >40 kg/m² and at least one comorbidity. Treatment initiated in this framework can be continued until December 2025.
Since November 2024, WEGOVY® (up to 2.4 mg/week) has had marketing authorization for the treatment of adolescents and adults ≥12 years with BMI ≥30 kg/m². However, the drug is not yet reimbursed, except in rare cases through individual exceptional reimbursement for rare and complex diseases.
Given this evolving regulatory landscape, it is essential to assess the real-life efficacy and safety of semaglutide in individuals with including both adolescents and adults carrying variants across the continuum of genetic susceptibility.
The aim of the ObGeSema project is to set up a cohort composed of patients (1) having already initiated a treatment and (2) newly treated by Semaglutide in 21 pediatric and adult Specialized Obesity Centres (CSOs) and describe their evolution over a 4 years follow-up.
Study design
- Observational model
- Cohort
- Time perspective
- Other
Who may qualify
- Ages
- 12 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Child, Adult, Older adult
- Study population
- Patients (≥12 years) with monogenic obesity due to any variant regardless of pathogenicity classification and already treated or with the physician's decision to initiate treatment with Semaglutide in the standard care. Patients under legal protection and State Medical Assistance (AME) will be included.
Key inclusion criteria (4 listed)
- Patients (≥12 years) having already initiated a treatment with SEMAGLUTIDE (regardless of the context: early access, routine care, self-financing, or exceptional reimbursement) or with a physician's decision to initiate treatment in the standard care. All patients having initiated treatment will be proposed to participate, including those having already stopped the treatment at the time of study initiation.
- Confirmation of monogenic obesity, as practiced in clinical routine, regardless of current classification (i.e., pathogenic, likely pathogenic, variant of uncertain significance [VUS], or benign) in a gene with leptin-melanocortin pathway described in PNDS (https://www.has-sante.fr/jcms/p_3280217/fr/generique-obesites-de-causes-rares). ) For patients with VUS or benign variants, inclusion is conditional on the availability of a polygenic risk score (PRS)
- Patients duly informed and not objecting to participate in the study. For patients ≥12 years <18 years Parents duly informed and not objecting that their child taking part in the study
- Patients affiliated to a social security scheme or State Medical Assistance (AME).
Key exclusion criteria (1 listed)
- Pregnant and breastfeeding women
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Change in weight and Body Mass Index (BMI)
Time frame: From baseline (T0) to T12
Percentage of subjects with a change in weight and Body Mass Index (BMI).Weight will be measured at initiation and at 12 months of the Semaglutide treatment
18 secondary outcomes
Change in weight and Body Mass Index (BMI)
Time frame: From baseline (T0) to 6 and/or 24 and/or 36 and/or 48 and/or 60 months
Reduction of body weight equal to or above 5%
Time frame: From baseline (T0) to 6 and/or 12 and/or 24 and/or 36 and/or 48 and/or 60 months
Change in Hunger score
Time frame: From baseline (T0) to 12 and/or 24 and/or 36 and/or 48 and/or 60 months
Change in eating behaviour measured by Food Craving questionnaire
Time frame: From baseline (T0) to 12 months
Change in eating behaviour measured by the Binge Eating Scale (BES)
Time frame: From baseline (T0) to 12 months
Change in eating behaviour measured by the Dutch Eating Behaviour Questionnaire (DEBQ)
Time frame: From baseline (T0) to 12 months
Change in eating behaviour measured by the Dykens questionnaire for ≥18 years patients
Time frame: From baseline (T0) to 12 months
Change in eating behaviour measured by the Child Eating Behaviour Questionnaire (CEBQ)
Time frame: From baseline (T0) to 12 months
Change in the International physical activity questionnaire (IPAQ - short form) for ≥18 years patients
Time frame: From baseline (T0) to 12 months
Change in Digestive disorders (GIQLI ) for ≥18 years patients
Time frame: From baseline (T0) to 12 and/or 24 and/or 36 and/or 48 and/or 60 months
Change in score of quality of life scores (patient and parents) for ≥18 years patients
Time frame: From baseline (T0) to 12 months
Change in sleep disorder (MCTQ score) for ≥18 years patients
Time frame: From baseline (T0) to 12 months
Change in anxiety and depression score for ≥18 years patients
Time frame: From baseline (T0) to 12 and/or 24 and/or 36 and/or 48 and/or 60 months
● Change in Body Mass Index : BMI Z-score for 12 to <18 years
Time frame: From baseline (T0) to 6 and/or 12 and/or 24 and/or 36 and/or 48 and/or 60 months
Change in eating behaviour scores CEBQ ( Child Eating Behaviour Questionnaire) or Hyperphagia score with the Dykens questionnaire and for intellectual disability. For 12 to <18 years patients
Time frame: From baseline (T0) to 12 months
Change in score of IWQOL Impact of Weight on Quality of Life (patient and parents). For 12 to <18 years patients
Time frame: From baseline (T0) to 12 months
Change in Digestive disorders GIQLI score (Gastrointestinal Quality of Life Index). For 12 to <18 years patients
Time frame: From baseline (T0) to 12 and/or 24 and/or 36 and/or 48 and/or 60 months
Treatment-emergent adverse events (TEAEs) and serious adverse events (SAEs)
Time frame: From baseline (T0) to 6 and/or 12 and/or 24 and/or 36 and/or 48 and/or 60 months
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 24 Jun 2026.
- Individual participant dataSharing planned: Yes. Data are available upon reasonable request. The procedures carried out with the French data privacy authority (CNIL, Commission nationale de l'informatique et des libertés) do not provide for the transmission of the database, nor do the information and consent documents signed by the patients. Consultation by the editorial board or interested researchers of individual participant data that underlie the results reported in the article after deidentification may nevertheless be considered, subject to prior determination of the terms and conditions of such consultation and in respect for compliance with the applicable regulations.
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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.
Christine POITOU-BERNERT, MD,PhD principal investigator
Assistance Publique - Hôpitaux de Paris
Béatrice DUBERN, MD,PhD study director
Assistance Publique - Hôpitaux de Paris
2 sites in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Monogenic Obesity, run by Assistance Publique - Hôpitaux de Paris at 2 sites in France.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 4 inclusion and 1 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: looking for participants now, as of the sponsor's last update on 24 Jun 2026. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 2 sites in France. 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?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
Contact Christine POITOU-BERNERT, MD,PhD (+33(0)142175771, christine.poitou-bernert@aphp.fr), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Change in weight and Body Mass Index (BMI) (time frame: From baseline (T0) to T12). 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 24 Jun 2026.