Neoplasms

Symptoms and General Pathology

All Conditions

Nutritional and Metabolic Diseases

Musculoskeletal Diseases

Rare Diseases

Neoplasm Metastasis

Obesity

Craniopharyngioma

Adamantinoma

Ameloblastoma

Overweight

Overnutrition

Nutrition Disorders

Body Weight

Neuroectodermal Tumors

Neuroectodermal Tumors, Primitive

Neoplasms, Germ Cell and Embryonal

Neoplasms by Histologic Type

Neoplasms, Nerve Tissue

Bone Neoplasms

Bone Diseases

Hypothalamic Obesity

Neuroepithelioma

Hypoglycemic Agents

All Drugs and Chemicals

Antihypertensive Agents

Vasodilator Agents

Insulin

Insulin, Globin Zinc

Metformin

Diazoxide

Diazoxide will be initiated at half the dose (100 mg per day) for 2 weeks to allow the insulin sensitizing action of metformin to take effect. Dosage will be increased to 200mg daily, divided twice daily with meals for 6 months.

Metformin will be initiated at 500 mg twice daily and increased to 1000 mg twice daily over a one week period to minimize gastrointestinal side effects. the 2000mg is to be taken with meals for 6 months.

Jill Hamilton, MD

To study the effect of combined diazoxide-metformin therapy on body weight in youth with hypothalamic obesity following treatment for craniopharyngioma. A secondary objective is to evaluate changes in insulin resistance (IR), beta-cell function, features of the metabolic syndrome, muscle metabolism and intramyocellular lipid.

Hypothesis: Treatment with diazoxide and metformin will result in weight loss or slowed weight gain and improved metabolic profile, compared to pretreatment levels.

46 children under the age of 22 years have been treated surgically for craniopharyngioma tumor and are currently followed at the Hospital for Sick Children, Toronto. Approximately 50% are obese (BMI ≥ 95th percentile for age and gender assessed from the updated Centre for Disease Control growth charts), all of whom have panhypopituitarism requiring hormone replacement therapy. These children are assessed regularly in Endocrine Clinic and also are invited to attend a comprehensive care clinic for evaluation by an endocrinologist (Principal Investigator), neurosurgical clinical nurse practitioner, dietitian, exercise physiologist, psychologist and social worker to provide multi-disciplinary dietary and exercise consultation and psychological counseling for weight related concerns. This clinic will provide the infrastructure for recruitment and follow-up of study patients. Recruitment of eight subjects for this pilot study will occur over 6 months from patients attending the comprehensive clinic. This number was chosen as it is equivalent to the number chosen in the pilot study of octreotide by Lustig which showed beneficial changes in body mass index with treatment.

This study evaluates a novel combination therapy in children with hypothalamic obesity at very high risk for complications. Evaluation of insulin resistance and metabolic changes on therapy will allow a better understanding of how insulin secretion relates to weight gain in this population. Successful therapy in a pilot setting will provide necessary data for a larger randomized trial in individuals with hypothalamic obesity including children with craniopharyngioma and others with damage to the hypothalamus secondary to other tumors, surgery or cranial irradiation.

Hypothalamic Obesity Following Craniopharyngioma Surgery: A Pilot Trial of Combined Metformin and Diazoxide Therapy

Combined Diazoxide and Metformin Therapy in Children With Hypothalamic Obesity Secondary to Craniopharyngioma: A Pilot Study

The Hospital for Sick Children

Staff Endocrinologist

Central Nervous System Depressants

Gastrointestinal Agents

Other Dietary Supplements

Glucagon-Like Peptide 1

Liraglutide

Benzocaine

Glucagon

Glucagon-Like Peptide-1 Receptor Agonists

Incretins

Hormones

Hormone Antagonists

Tannic Acid

Patients will receive subcutaneous injections of Saxenda 18 mg/3 mL Pen (liraglutide_obesity) starting at 0.6 mg qd. Increase by 0.6 mg qd at weekly intervals to 1.2 mg qd in week 2, 1.8 mg qd in week 3, 2.4 mg qd in week 4, 3.0 mg qd in week 5, and maintain for 8 weeks at a maximally tolerated dose within 3.0 mg starting in week 5. If the subject's response to treatment does not allow for escalation to the planned dose, subjects will inject an adaptive maximally tolerated dose within the planned dose at each cycle. Total duration of Saxenda treatment is 12 weeks.

Saxenda

Sumin Lee

GLP-1 analogs are used as agents in the existing treatment of obesity. However, there are lack of previous reports on the effectiveness and role of GLP-1 analogs in the development of obesity traits in patients with functionally impaired hypothalamus. With this preliminary study, the investigators would explore the role of GLP-1 analogues to identify eating behavioral pathology subtype differences in the therapeutic efficacy of GLP-1 analogues in hypothalamic obesity patients. This will allow us to identify the role of specific nuclei which could be the pathogenesis of hypothalamic obesity.

Our hypotheses: GLP-1 analogs will effectively induce weight loss in patients with hypothalamic obesity, and different subtypes of hypothalamic obesity will respond differently to GLP-1 analogs.

Study Overview

* Collecting baseline clinical information, comorbidities, pituitary hormone status assessment, and treatment options, including supplemental therapies and surgery.
* Assessment of factors associated with obesity through physical measurements, questionnaires, and cognitive-behavioral tasks, and division of patients by eating behavior subtypes for further analysis.
* Collecting patients' meal records and meal times by self-reporting.
* Collecting data on patients' activity and sleep patterns through wearable devices.
* Patients will receive subcutaneous injections of Saxenda 18 mg/3 mL Pen (liraglutide_obesity) starting at 0.6 mg qd. Increase by 0.6 mg qd at weekly intervals to 1.2 mg qd in week 2, 1.8 mg qd in week 3, 2.4 mg qd in week 4, 3.0 mg qd in week 5, and maintain for 8 weeks at a maximally tolerated dose within 3.0 mg starting in week 5. If the subject's response to treatment does not allow for escalation to the planned dose, subjects will inject an adaptive maximally tolerated dose within the planned dose at each cycle. Total duration of Saxenda treatment is 12 weeks.

Eating behavior assessment questionnaires and cognitive behavioral tasks will be completed before the first dose, before the end of the dose escalation period, and after the final dose to explore treatment response.

Study Eligibility

- Patients aged 19 years and older who were diagnosed with a hypothalamic tumor and surgically treated at Seoul National University Hospital, and who met the inclusion and exclusion criteria after receiving a full explanation of the study and voluntary consent.

The Effect of GLP-1 Agonist in Patients With Hypothalamic Obesity: Prospective, Pilot Study

Seoul National University Hospital

associate professor

Nervous System Diseases

Weight Loss

Brain Neoplasms

Anti-Obesity Agents

Exenatide

All patients received exenatide 10mcg BID x 50 weeks

Treatment with exenatide 5 mcg twice daily for 4 weeks, then 10 mcg twice daily for 46 weeks.

Ashley Shoemaker, M.D.

The purpose of this study is to determine whether exenatide can cause weight loss in patients with a history of craniopharyngioma or other brain lesion.

Hypothalamic obesity occurs in up to 60% of patients with tumors in the hypothalamic region, most commonly craniopharyngiomas. Hypothalamic dysfunction can be due to tumor infiltration and as a consequence of surgery or radiation therapy. Survivors who develop obesity have greater morbidity and mortality than normal weight survivors. Prevention and treatment of obesity in this population is vital in order to decrease the morbidity and mortality from diabetes, stroke and myocardial infarction.

Exenatide (Byetta®) is a GLP-1 homologue that was FDA approved for treatment of type 2 diabetes in 2005. It also decreases the rate of gastric emptying and increases satiety and has been shown to cause weight loss in some people. Exenatide may improve insulin sensitivity and satiety in patients with hypothalamic obesity but without the risks of bariatric surgery. The investigators hypothesize that treatment with exenatide will lead to weight loss in patients with hypothalamic obesity.

Weight Loss Study for Patients With Obesity Due to Craniopharyngioma or Other Brain Tumor

Effects of Exenatide on Body Weight in Patients With Hypothalamic Obesity

Change in body weight from baseline to end of study

Change in resting energy expenditure from baseline to 50 weeks

Change in visual analogue scales scores from baseline to 50 weeks. Higher score indicates greater satiety (minimum 0, maximum 100).

Change in insulin secretion from baseline

Change in the isotope excretion half life during a gastric emptying test at baseline and at 50 weeks

Vanderbilt University Medical Center

Assistant Professor of Pediatrics

Age, Categorical

Gender

Ethnicity (NIH/OMB)

Race (NIH/OMB)

United States

Region of Enrollment

Weight

Resting energy expenditure

Satiety

Insulin AUC

Gastric emptying half life

Ashley Shoemaker

Body Weight (kg)

8 patients completed the study but one patient did not have REE data available due to technical difficulties

Resting Energy Expenditure (Kcals Per Day)

Exenatide: Treatment with exenatide 5 mcg twice daily for 4 weeks, then 10 mcg twice daily for 46 weeks.

Visual Analogue Scales for Post-meal Satiety

Insulin Secretion (Area Under the Curve)

Gastric Emptying Rate (13C-octanoic Acid Isotope Excretion Half Life)

Overall Study

Hypothalamic Neoplasms

Injections of glucagon-like peptide (GLP)-1 agonist exenatide once weekly extended-release (Bydureon®) for 36 weeks in randomized intervention followed by 18 weeks open label exenatide once weekly extended-release.

Weekly injections of placebo for 36 weeks followed by 18 weeks open label exenatide once weekly extended-release.

placebo

Christian Roth, MD

The proposed multicenter study will test the effect of glucagon-like peptide (GLP)-1 agonist exenatide once weekly extended-release (ExQW, Bydureon®) on clinical outcomes and metabolic parameters in a double-blind, placebo-controlled 36 week randomized trial with an 18 week open label extension. Following baseline testing, 48 patients will be randomly assigned with equal allocation to ExQW or matching placebo injection for 36 weeks, followed by an 18 week open label extension during which all patients receive ExQW. Changes of weight status, body composition, free-living total daily energy expenditure (EE) by doubly labeled water (DLW), activity by acetimetry, energy intake (questionnaires and food diary), as well as glucose tolerance and hormonal parameters of energy homeostasis and insulin resistance will be assessed before treatment and at the end of the placebo-controlled phase (week 36). Activity, metabolic outcomes, energy intake will be also assessed at study week 18 (mid treatment of randomized study), as well as week 54 (end of open label treatment).

Excessive weight gain and its cardiometabolic sequela are frequent complications of hypothalamic tumors, a condition known as hypothalamic obesity (HO). Most tumors in this region are craniopharyngiomas (CP),1 which constitute 5-9% of childhood brain tumors. Patients with CP typically become obese and have more features of the metabolic syndrome compared to matched controls. Overall, a 3-19-fold higher cardiovascular mortality had been reported, and a recent nationwide population-based study in Sweden demonstrated increased rates for cerebral infarction (7-fold), death due to cerebrovascular diseases (5-fold), and type 2 diabetes mellitus (6-fold) in CP patients in comparison to the general population. Thus, early and effective management of obesity is vital for this population, which is more resistant to treatment than uncomplicated obesity. Recognized risk factors for severe obesity include large hypothalamic tumors or lesions affecting several medial and posterior hypothalamic nuclei that impact satiety signaling pathways. Structural damage in these nuclei often lead to uncontrolled appetite, rapid weight gain, central insulin and leptin resistance, decreased sympathetic activity, low energy expenditure (EE), and increased energy storage in adipose tissue. Recently, the investigators developed a semi-quantitative assessment of hypothalamic damage on brain magnetic resonance imaging (MRI) to predict the risk for HO development in CP.

Previous results of treating HO with a glucagon-like-peptide-1 receptor agonist (GLP1RA) in rats and humans provide promising proof-of-principle data to support this current randomized clinical trial. The primary hypothesis of this study is that drugs causing weight loss via intact hindbrain signaling pathways offer a desperately needed option for treatment of HO, even in very obese HO subjects with severe hypothalamic damage. Induction of weight loss by GLP1RAs is believed to be related to multiple mechanisms involving the gastrointestinal tract, vagus nerve, and the brain leading to increased satiety. Peripheral administration of GLP-1 or GLP1RA reduces blood glucose and energy intake in humans and rodents, and long-term treatment results in loss of body weight. Critically, the investigators do not know whether GLP1RA treatment affects EE and activity, or whether the site and size of brain lesions affect responses to GLP1RA treatment.

The investigators' previous clinical studies of the GLP1RA exenatide in obese adolescents and adults have generated the critical safety and efficacy data needed to design a clinical trial. In a pilot study conducted at Children's Hospitals and Clinics of MN, pretreatment hyperphagia was associated with BMI reduction. Using these data, the investigators have designed a prospective, multicenter trial that will examine the effects of GLP1RA on BMI, cardiovascular disease (CVD) risk factors, energy homeostasis and other factors in subjects with HO secondary to CP.

Energy Balance & Weight Loss in Craniopharyngioma-related or Other Hypothalamic Tumors in Hypothalamic Obesity

Glucagon-Like Peptide-1 Agonist Effects on Energy Balance in Hypothalamic Obesity

Percent change of body mass index (BMI), as calculated by the formula: body weight in kg divided by height in meters², between baseline and the end of the 36-week randomized drug treatment phase.

Body composition change between baseline and the end of the 36-week randomized drug treatment phase assessed by dual energy x-ray absorptiometry (DEXA) and expressed as the change in adipose tissue mass.

Changes in fat and total calorie intake during free buffet meals assessed at baseline and after 36-weeks of study drug treatment.

The buffet meal is an objective measure of satiety as it assesses food intake and choice after a caloric preload. A standardized test meal preload provided 20% of estimated daily caloric requirements,based on the Schofield-HW equation. The purpose of the test meal is to ensure that study participants are in an equally fed state. Ninety minutes later, an ad libitum buffet meal was served consisting of a wide variety of food items and more than the child's estimated daily calorie requirements will be offered (5,000 kcal). Children had access to the buffet for 30 min, after which calorie intake and composition of consumed foods was measured by weighing back uneaten food.

Change in fasting blood glucose between baseline and the end of the 36-week randomized drug treatment phase.

Change in fasting HDL cholesterol and triglycerides between baseline and the end of the 36-week randomized drug treatment phase.

Change in C-reactive protein (CRP) between baseline and the end of the 36-week randomized drug treatment phase.

Changes of insulin resistance estimated by the homeostasis model assessment of insulin resistance (HOMA-IR) using the formula HOMA-IR = insulin \[mU/l\] x glucose \[mmol/l\]) / 22.5 where both insulin and glucose values are obtained from a fasting blood sample.

Change in circulating leptin between baseline and the end of the 36-week randomized drug treatment phase.

Total energy expenditure in the free-living environment was measured using doubly labeled water which estimates carbon dioxide production by measuring the elimination of the tracers deuterium (²H) and oxygen-18 (¹⁸O) from the body. These measures are used to determine the average daily rate of carbon dioxide production which is then used to calculate total energy expenditure using an equation from Weir and an assumed food quotient (0.85).

Self-reported daily energy intake was assessed by Automated Self-Administered 24-Hour Dietary Recall (ASA24-Kids, http://appliedresearch.cancer.gov/tools/instruments/asa24/), a web-based diet assessment tool that allows 24-hour diet recall using branded food items.

Change in blood glucose measures 120 minutes post-glucose bolus during an oral glucose tolerance test between baseline and the end of the 36-week randomized drug treatment phase.

Children's Hospitals and Clinics of Minnesota

Vanderbilt University

Seattle Children's Hospital

Professor

Injections of glucagon-like peptide (GLP)-1 agonist exenatide once weekly extended-release (Bydureon®) for 36 weeks in randomized intervention

Exenatide: Weekly injections of active drug.

Double-Blind Exenatide Once Weekly Extended-release

Weekly injections of placebo for 36 weeks in randomized intervention

placebo: Weekly placebo injections

Double-Blind Placebo

18 weeks open label exenatide once weekly extended-release (Bydureon®) arm.

Exenatide: Weekly injections of active drug.

Open Label Exenatide Once Weekly Extended-release

Injections of glucagon-like peptide (GLP)-1 agonist exenatide once weekly extended-release (Bydureon®) for 36 weeks in randomized intervention followed by 18 weeks open label exenatide once weekly extended-release.

Exenatide: Weekly injections of active drug.

Exenatide Once Weekly Extended-release

Weekly injections of placebo for 36 weeks followed by 18 weeks open label exenatide once weekly extended-release.

placebo: Weekly placebo injections

Matching Placebo

Total

One participant withdrawn in placebo group

Age, Continuous

Sex: Female, Male

Calculated by the formula: body weight in kg divided by height in meters².

Body Mass Index

Christian L. Roth, MD

Analyses include all participants randomized to a study drug and received at least one drug treatment administration. Missing data was imputed using a last observation carry-forward approach.

Percent Change of Body Mass Index (BMI) as Calculated by the Formula: Body Weight in kg Divided by Height in Meters².

Of the 41 enrolled participants, 20 out of 23 participants randomized to exenatide once weekly extended-release and 15 out of 18 participants randomized to placebo completed both pre- and post-treatment assessments and are included in this analysis.

Changes in Body Composition as Assessed by Body Fat Mass Using Dual Energy X-ray Absorptiometry (DEXA)

Fat Intake

Total Calorie Intake

Of the 41 enrolled participants, 18 out of 23 participants randomized to exenatide once weekly extended-release and 15 out of 18 participants randomized to placebo completed both pre- and post-treatment assessments and are included in this analysis.

Changes in Fat and Total Calorie Intake Assessed by Free Buffet Meal Analysis.

Changes in Fasting Glucose

HDL Cholesterol

Triglycerides

Changes in HDL Cholesterol and Triglycerides Assessed by Fasting Lipids

Changes in Inflammation Assessed by C-reactive Protein (CRP)

Changes of Insulin Resistance Assessed by Homeostasis Model Assessment of Insulin Resistance (HOMA-IR)

Changes of Circulating Leptin Levels

Of the 41 enrolled participants, 19 out of 23 participants randomized to exenatide once weekly extended-release and 14 out of 18 participants randomized to placebo completed both pre- and post-treatment assessments and are included in this analysis.

Changes of Energy Expenditure Assessed by Doubly Labeled Water Analysis

Of the 41 enrolled participants, 14 out of 23 participants randomized to exenatide once weekly extended-release and 9 out of 18 participants randomized to placebo completed both pre- and post-treatment assessments and are included in this analysis.

Changes of Energy Intake Assessed by Automated Self-Administered 24-Hour Dietary Recall (ASA24-Kids)

Changes in Glucose 120 Minutes Following an Oral Glucose Tolerance Test

Randomization

36-week Randomized Trial

18-week Open Label Extension

Syndrome

Metabolic Syndrome

Insulin Resistance

Hyperinsulinism

Metabolic Diseases

Glucose Metabolism Disorders

Open-label lateral hypothalamic DBS stimulation for 1 year.

One-year continuous hypothalamic deep brain stimulation

Hypothalamic Deep Brain Stimulation

The balance between hunger and satiety is imperative for an individual's survival and overall health.). Without this balance, individuals can become morbidly obese or lack adequate nutrition for survival. Craniopharyngioma (CP) is a benign tumour that occurs at the base of the brain in children. Unfortunately, pediatric neurosurgeons sometimes inadvertently destroy a child's satiety centre during CP tumour removal surgery. This leaves the child with a post-operative complication: an insatiable appetite. This form of obesity is called "hypothalamic obesity". This study is designed to investigate Deep Brain Stimulation for hypothalamic obesity in n=6 young adults who have stabilized tumours.

For young adults with destroyed satiety centres due to childhood CP surgery, we believe directly re-balancing the brain's control of hunger and satiety is necessary for sustained and long-term therapy. n=6 patients will be recruited in this Phase 1 DBS trial. The proposed research will hope to improve personal health among the young adults involved in this study by improving quality of life and avoiding long-term cardiovascular morbidities. Furthermore, this study will elucidate what brain regions drive excessive hunger and develop a treatment that attempts to reverse these abnormalities.

Neuromodulation for Hypothalamic Obesity

Deep Brain Stimulation for Hypothalamic Obesity: A Surgical & Neuroimaging Study

Measuring BMI(kg/m\^2) following 12 months of constant stimulation

University of British Columbia

Professor & Neurosurgeon

Reproductive Control Agents

Oxytocin

Week 0 to Week 7: Intranasal oxytocin, administered 3 times per day (at mealtimes) for 8 weeks (dosage based on weight: 16 IU to 24 IU; dose escalation, if appropriate, occurs at 2 weeks)

Week 8 to Week 11: Washout

Week 12 to Week 20: Intranasal placebo, administered 3 times per day (at mealtimes) for 8 weeks (dosage based on weight: 16 IU to 24 IU; dose escalation, if appropriate, occurs at 2 weeks)

\*Dose Escalation, as appropriate, at 2 Weeks

Week 0 to Week 7: Intranasal placebo, administered 3 times per day (at mealtimes) for 8 weeks (dosage based on weight: 16 IU to 24 IU; dose escalation, if appropriate, occurs at 2 weeks)

Week 8 to Week 11: Washout

Week 12 to Week 20: Intranasal oxytocin, administered 3 times per day (at mealtimes) for 8 weeks (dosage based on weight: 16 IU to 24 IU; dose escalation, if appropriate, occurs at 2 weeks)

The active substance of Syntocinon is a synthetic nonapeptide identical to the posterior pituitary hormone oxytocin.

Syntocinon

The placebo is identical to the Syntocinon formulation with the exception of the active compound, i.e., without oxytocin.

Placebo (for Syntocinon)

Shana E McCormack, MD

This research study will test if oxytocin, delivered by nasal spray, will promote weight loss in children, adolescents, and adults with Hypothalamic Obesity as compared to a placebo. The study is divided into two parts. During the first part, subjects will receive either oxytocin or placebo. In the second part, subjects will "cross-over" to receive the other treatment - either oxytocin or placebo. During study visits participants will do blood tests, physical exams, metabolic testing, a MRI scan, and some surveys and questionnaires.

Intranasal Oxytocin in Hypothalamic Obesity

Intranasal Oxytocin to Promote Weight Loss in Children, Adolescents, and Adults With Brain Tumors and Hypothalamic Obesity Syndrome

Cognitive Restraint at Test Meal Attributable to Oxytocin vs Placebo measured using stop-signal task, stop signal reaction time (SSRT).

For this exploratory outcome, in order to minimize participant burden, each participant had the assessment at one time point with either the low or high dose of oxytocin. And at one point during the placebo block for comparison.

Within Participant Difference in Calories Consumed Attributable to Oxytocin vs Placebo Dose 1 (Week 0 \& Week 12). Total number of calories consumed during the standardized test meal.

Within Participant Difference in Calories Consumed Attributable to Oxytocin vs Placebo Dose 2 (Week 2 \& Week 14). Total number of calories consumed during the standardized test meal.

Within Participant Difference After Oxytocin vs After Placebo in Resting Energy Expenditure (kcal/kg lean body mass/day). Resting Energy Expenditure (REE) with output of kcal/kg lean body mass/day measured using indirect calorimetry.

Within Participant Difference After Oxytocin vs Placebo in Respiratory Quotient (RQ) measured using indirect calorimetry.

Total % Body Fat measured using dual energy x-ray absorptiometry (DXA).

Measured using MRI-based post-exercise Creatine Chemical Exchange Saturation Transfer (CrCEST) decline exponential time constant.

Measured using the Dykens Hyperphagia Questionnaire.

The Dykens Hyperphagia Questionnaire is a 11-item questionnaire with responses on a scale of 1 to 5. 1 = Not a Problem, 5 = Severe or Frequent Problem. The scale includes three domains: hyperphagic behavior, hyperphagic drive, and hyperphagic severity. There is also a total or overall score which is calculated by combining the scores from each domain. Maximum Possible Score: 55, Minimum Possible Score: 11. Higher scores indicated more severe and/or frequent Hyperphagia.

Within Participant Change in Disinhibition of Eating Attributable to Oxytocin vs Placebo. Measured using the Eating Inventory questionnaire.

The Eating Inventory consists of 36 statements where participants respond true or false, 14 questions where participants select a response from 1 (least severe: rarely or not at all) to 4 (most severe: always or very much), one final question askes participants to rate their level of restraint in eating from 1 (no restraint) to 6 (constantly limiting food). The scores are assessed in 3 dimensions: Dietary Restraint (Max Score: 21), Disinhibition (Max Score: 16), and Hunger (Max Score: 14).

Within Participant Change in Scores from the Disinhibition of Eating dimension are reported.

Study title	NCT ID	Conditions	Interventions	Eligibility	Organization
Hypothalamic Obesity Following Craniopharyngioma Surgery: A Pilot Trial of Combined Metformin and Diazoxide Therapy	NCT00892073	Hypothalamic Ob...	Diazoxide Metformin	9 Years - 22 Years	The Hospital for Sick Children
The Effect of GLP-1 Agonist in Patients With Hypothalamic Obesity: Prospective, Pilot Study	NCT06217848	Panhypopituitar... Craniopharyngio... Hypothalamic Ob...	Saxenda	19 Years -	Seoul National University Hospital
Weight Loss Study for Patients With Obesity Due to Craniopharyngioma or Other Brain Tumor	NCT01484873	Obesity Overweight Craniopharyngio...	Exenatide	18 Years - 40 Years	Vanderbilt University Medical Center
Energy Balance & Weight Loss in Craniopharyngioma-related or Other Hypothalamic Tumors in Hypothalamic Obesity	NCT02664441	Hypothalamic Ob...	Exenatide placebo	10 Years - 25 Years	Seattle Children's Hospital
The Effect of GLP-1 Agonist in Patients With Hypothalamic Obesity: Prospective, Pilot Study	NCT06217848	Panhypopituitar... Craniopharyngio... Hypothalamic Ob...	Saxenda	19 Years -	Seoul National University Hospital
Neuromodulation for Hypothalamic Obesity	NCT03708913	Craniopharyngio... Hypothalamic Ob... Metabolic Syndr...	Hypothalamic De...	18 Years - 30 Years	University of British Columbia
Intranasal Oxytocin in Hypothalamic Obesity	NCT02849743	Craniopharyngio... Hypothalamic Ob...	Syntocinon Placebo (for Sy...	10 Years - 35 Years	Children's Hospital of Philadelphia
Efficacy and Safety of Exenatide in the Treatment of Hypothalamic Obesity After Craniopharyngioma Therapy	NCT02860923	Craniopharyngio... Hypothalamic Ob...	Exenatide Placebo	18 Years - 75 Years	University Hospital, Bordeaux

Spots Global Cancer Trial Database for hypothalamic obesity