Treatment Trials

20 Clinical Trials for Various Conditions

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RECRUITING
RZ358 Treatment for Congenital Hyperinsulinism
Description

The Phase 3 pivotal study is designed to evaluate the efficacy and safety of RZ358 for the treatment of congenital hyperinsulinism (HI) as add-on to standard-of-care (SOC) therapy compared to SOC alone over 24 weeks and to evaluate the longer-term safety and efficacy of RZ358 during a subsequent open-label extension (OLE) period.

RECRUITING
HM15136 Treatment for 8 Weeks in Subjects Aged ≥2 Years With Congenital Hyperinsulinism (CHI)
Description

This study is designed to evaluate the safety, tolerability, pharmacokinetics (PK), and efficacy of HM15136 when used as add-on therapy in subjects with CHI with persistent hypoglycemia while on standard of care treatment (SoC). HM15136 will be administered once weekly in multiple doses to subjects in multiple age including pediatric to find appropriate exposure-response data.

COMPLETED
An Open-Label Multiple Dose Study of RZ358 in Patients With Congenital Hyperinsulinism
Description

The objective of this trial is to evaluate the safety, tolerability and glucose-raising effects of RZ358 in patients with Congenital Hyperinsulinism (HI).

RECRUITING
18FluoroLDOPA PET Imaging for the Detection and Localization of Focal Congenital Hyperinsulinism
Description

The goal of this project is to determine the role of FDOPA/PET as a pre-operative diagnostic imaging procedure for differentiating focal and diffuse forms of congenital hyperinsulinism and locating focal lesions in the pancreas to guide surgical resection.

COMPLETED
Trial Evaluating Efficacy and Safety of Dasiglucagon in Children With Congenital Hyperinsulinism
Description

The objective of the trial is to evaluate the efficacy of dasiglucagon in reducing glucose requirements in children with persistent congenital hyperinsulinism (CHI) requiring continuous intravenous (IV) glucose administration to prevent/manage hypoglycemia.

ACTIVE_NOT_RECRUITING
Extension Trial Evaluating the Long-term Safety and Efficacy of Dasiglucagon in Children With Congenital Hyperinsulinism
Description

This is an open-label, multinational, multicenter, long-term safety and efficacy extension trial in patients with Congenital Hyperinsulinism (CHI) who completed either ZP4207-17103 or ZP4207-17109 (defined as lead-in trials). The primary objective is to evaluate the long-term safety of dasiglucagon administered as subcutaneous (SC) infusion in children with CHI.

COMPLETED
A Two-Period Open-label Trial Evaluating Efficacy and Safety of Dasiglucagon in Children With Congenital Hyperinsulinism
Description

The objective of the trial is to evaluate the efficacy and safety of dasiglucagon administered as a subcutaneous (SC) infusion in reducing hypoglycemia in children with CHI.

COMPLETED
CSI-Glucagon for Prevention of Hypoglycemia in Children With Congenital Hyperinsulinism
Description

This is a Phase 2, multi-center, randomized, placebo-controlled, double-blind trial with open-label follow-up designed to assess the efficacy of Xeris Glucagon delivered as a continuous subcutaneous infusion to prevent hypoglycemia with lower intravenous glucose infusion rates in children \< 1 year of age with congenital hyperinsulinism.

COMPLETED
A Single-Dose Open-Label Study of XOMA 358 in Subjects With Congenital Hyperinsulinism
Description

The purpose of this study is to evaluate the safety and clinical pharmacology of a single dose pharmacokinetics and pharmacodynamics of XOMA 358 in subjects with hypoglycemia associated with congenital hyperinsulinism.

RECRUITING
Fluorodopa F 18 in Congenital Hyperinsulinism and Insulinoma
Description

Low blood sugars are known to cause brain damage in newborn babies. One of the most common causes of low blood sugars persisting beyond the new born period is a condition called congenital hyperinsulinism (HI). This is a disease whereby the pancreas secretes too much insulin and causes low blood sugars. Twenty to forty percent of these babies will have brain damage. There are two forms of this disease. In one form only a small part of the pancreas makes too much insulin (focal HI) and in the other, the whole pancreas make too much insulin (diffuse HI). Another very similar disease is insulinoma which occurs after birth, but also causes hyperinsulinism. If a surgeon could know which part of the pancreas has the focal lesion he could remove it and cure the patient. The purpose of this study is to investigate whether a new investigational drug called Fluorodopa F 18, when used with a PET scan, can find the focal lesion and guide the surgeon to remove it, thus curing the patient and preventing further brain damage.

COMPLETED
Effect of Exendin-(9-39) on Glycemic Control in Subjects With Congenital Hyperinsulinism
Description

The purpose of this study is to determine if Exendin-(9-39), an antagonist of the glucagon-like peptide-1 (GLP-1) receptor with effects on the pancreatic beta cell, increases fasting blood glucose levels in subjects with congenital hyperinsulinism.

NO_LONGER_AVAILABLE
Compassionate Use of SOM230 for Hyperinsulinemic/Hypoglycemia
Description

Congenital hyperinsulinism is a rare condition that can cause life-threatening hypoglycemia. Current treatment for congenital hyperinsulinism is often suboptimal, and such individuals may respond to a new somatostatin analog, pasireotide. This is a compassionate use study of the effects of pasireotide on individuals with suboptimally treated congenital hyperinsulinism.

AVAILABLE
18F-L-Fluoro-DOPA PET/CT Scan Localization of Focal Pancreatic Lesions in Subjects With Hyperinsulinemic Hypoglycemia
Description

This purpose of this study is to determine the ability of an 18F-fluoro-L-dihydroxyphenylalanine (18F-DOPA) PET (Positron Emission Tomography) scan to detect a focal lesion of hyperinsulinism and determine the location in patients with congenital hyperinsulinism, Beckwith Wiedemann Syndrome and suspected insulinoma. Safety data will be collected.

COMPLETED
Phase II Safety and Efficacy Study of 18FDOPA PET-CT in Children With Hyperinsulinemic Hypoglycemia
Description

Children with congenital hyperinsulinism (CHI) have low blood sugar, and some of these children may require surgery to remove part or all of their pancreas. In this study, researchers will test how well a radioactive drug, 18-labeled L-fluorodeoxyphenylalanine (called F-DOPA) can detect a form of hyperinsulinism (focal HI) that may be cured by surgery. Eligible participants in this study will have positron emission tomography/computerized tomography (PET/CT) scans with F-DOPA prior to surgery.

COMPLETED
Effect of Exendin-(9-39) on Fasting Adaptation and Protein Sensitivity
Description

The purpose of this study is to examine the effects of exendin-(9-39) on fasting blood glucose and protein induced hypoglycemia on subjects with Congenital Hyperinsulinism. Funding Source - FDA Office of Orphan Products Development (OODP).

TERMINATED
Effect of Exendin (9-39) on Glucose Requirements to Maintain Euglycemia
Description

The primary aim of this study is to evaluate the effect of Exendin (9-39) on glucose requirements to maintain euglycemia in pediatric patients with congenital hyperinsulinism (CHI) who have failed medical therapy. The secondary aims are to determine the therapeutic plasma levels, plasma half-life and pharmacokinetics of Exendin (9-39) during a 9-hour intravenous infusion.

COMPLETED
Utility of [F-18] fluoroDOPA for Neonatal Hyperinsulinism
Description

Children with congenital hyperinsulinism (CHI) have low blood sugar, and some of these children may require surgery. In this study, researchers affiliated with the University of Pennsylvania will test how well a radioactive drug (called F-DOPA) can detect a form of hyperinsulinism that may be cured by surgery. Eligible participants in this study will have positron emission tomography (PET) scans with F-DOPA prior to surgery.

NO_LONGER_AVAILABLE
Study of the Use of [18F]-DOPA in Hyperinsulinemic Hypoglycemia
Description

The primary objective of this study is to evaluate the utility of \[18F\]-DOPA PET to provide improved presurgical planning and distinguish between focal and diffuse forms of HI. The investigators will perform descriptive analysis, relying on visual analysis to diagnose and localize a focal lesion. Our findings will be compared to surgical histopathology to determine sensitivity and specificity or this technique. The investigators will also track patient surgical outcomes, specifically whether the patient is surgically "cured" or still requires medical management to control residual hypoglycemia.

ENROLLING_BY_INVITATION
International Registry of Congenital Portosystemic Shunt (IRCPSS)
Description

Congenital Portosystemic Shunt (CPSS) is a rare condition important by the multiplicity and severity of associated complications. CPSS is venous anomaly in which blood coming from the intestines only partially passes through the liver. This leads to the accumulation of potentially toxic factors that cause systemic effects. Complications vary among the individuals, and currently, it is challenging to predict which individuals will develop severe complications. The IRCPSS registry is established with the aim of centralizing detailed clinical follow-up and biological information from participants around the world who suffer from Congenital Portosystemic Shunt (CPSS). A multidisciplinary consortium of experts is collaborating to enhance our understanding of the prevalence, natural history, individual risks, and physiopathology of the disease through the IRCPSS registry.

ENROLLING_BY_INVITATION
Early Check: Expanded Screening in Newborns
Description

Early Check provides voluntary screening of newborns for a selected panel of conditions. The study has three main objectives: 1) develop and implement an approach to identify affected infants, 2) address the impact on infants and families who screen positive, and 3) evaluate the Early Check program. The Early Check screening will lead to earlier identification of newborns with rare health conditions in addition to providing important data on the implementation of this model program. Early diagnosis may result in health and development benefits for the newborns. Infants who have newborn screening in North Carolina will be eligible to participate, equating to over 120,000 eligible infants a year. Over 95% of participants are expected to screen negative. Newborns who screen positive and their parents are invited to additional research activities and services. Parents can enroll eligible newborns on the Early Check electronic Research Portal. Screening tests are conducted on residual blood from existing newborn screening dried blood spots. Confirmatory testing is provided free-of-charge for infants who screen positive, and carrier testing is provided to mothers of infants with fragile X. Affected newborns have a physical and developmental evaluation. Their parents have genetic counseling and are invited to participate in surveys and interviews. Ongoing evaluation of the program includes additional parent interviews.

Conditions
Spinal Muscular AtrophyFragile X SyndromeFragile X - PremutationDuchenne Muscular DystrophyHyperinsulinemic Hypoglycemia, Familial 1Diabetes MellitusAdrenoleukodystrophy, NeonatalMedium-chain Acyl-CoA Dehydrogenase DeficiencyVery Long Chain Acyl Coa Dehydrogenase DeficiencyBeta-ketothiolase DeficiencySevere Combined Immunodeficiency Due to Adenosine Deaminase DeficiencyPrimary Hyperoxaluria Type 1Congenital Bile Acid Synthesis Defect Type 2Pyridoxine-Dependent EpilepsyHereditary Fructose IntoleranceHypophosphatasiaHyperargininemiaMucopolysaccharidosis Type 6Argininosuccinic AciduriaCitrullinemia, Type IWilson DiseaseMaple Syrup Urine Disease, Type 1AMaple Syrup Urine Disease, Type 1BBiotinidase DeficiencyNeonatal Severe Primary HyperparathyroidismIntrinsic Factor DeficiencyUsher Syndrome Type 1D/F Digenic (Diagnosis)Cystic FibrosisStickler Syndrome Type 2Stickler Syndrome Type 1Alport Syndrome, Autosomal RecessiveAlport Syndrome, X-LinkedCarbamoyl Phosphate Synthetase I Deficiency DiseaseCarnitine Palmitoyl Transferase 1A DeficiencyCarnitine Palmitoyltransferase II DeficiencyCystinosisChronic Granulomatous DiseaseCerebrotendinous XanthomatosesMaple Syrup Urine Disease, Type 2Severe Combined Immunodeficiency Due to DCLRE1C DeficiencyThyroid Dyshormonogenesis 6Thyroid Dyshormonogenesis 5Supravalvar Aortic StenosisFactor X DeficiencyHemophilia AHemophilia BTyrosinemia, Type IFructose 1,6 Bisphosphatase DeficiencyGlycogen Storage Disease Type IG6PD DeficiencyGlycogen Storage Disease IIGalactokinase DeficiencyMucopolysaccharidosis Type IV AGalactosemiasGuanidinoacetate Methyltransferase DeficiencyAgat DeficiencyGlutaryl-CoA Dehydrogenase DeficiencyGtp Cyclohydrolase I DeficiencyHyperinsulinism-Hyperammonemia SyndromePrimary Hyperoxaluria Type 23-Hydroxyacyl-CoA Dehydrogenase DeficiencyLong-chain 3-hydroxyacyl-CoA Dehydrogenase DeficiencyMitochondrial Trifunctional Protein DeficiencySickle Cell DiseaseBeta-ThalassemiaHolocarboxylase Synthetase Deficiency3-Hydroxy-3-Methylglutaric AciduriaPrimary Hyperoxaluria Type 3Hermansky-Pudlak Syndrome 1Hermansky-Pudlak Syndrome 4Apparent Mineralocorticoid ExcessHSDBCBAS1Mucopolysaccharidosis Type 2Mucopolysaccharidosis Type 1Severe Combined Immunodeficiency, X LinkedSevere Combined Immunodeficiency Due to IL-7Ralpha DeficiencyDiabetes Mellitus, Permanent NeonatalIsovaleric AcidemiaSevere Combined Immunodeficiency T-Cell Negative B-Cell Positive Due to Janus Kinase-3 Deficiency (Disorder)Jervell and Lange-Nielsen Syndrome 2Hyperinsulinemic Hypoglycemia, Familial, 2Diabetes Mellitus, Permanent Neonatal, With Neurologic FeaturesJervell and Lange-Nielsen Syndrome 1Lysosomal Acid Lipase DeficiencyCblF3-Methylcrotonyl CoA Carboxylase 1 Deficiency3-Methylcrotonyl CoA Carboxylase 2 DeficiencyWaardenburg Syndrome Type 2AMethylmalonic Aciduria cblA TypeMethylmalonic Aciduria cblB TypeMethylmalonic Aciduria and Homocystinuria Type cblCMAHCDMethylmalonic Aciduria Due to Methylmalonyl-CoA Mutase DeficiencyCongenital Disorder of Glycosylation Type 1BMthfr DeficiencyMethylcobalamin Deficiency Type Cbl G (Disorder)Methylcobalamin Deficiency Type cblEUsher Syndrome, Type 1BN-acetylglutamate Synthase DeficiencyOrnithine Transcarbamylase DeficiencyPhenylketonuriasWaardenburg Syndrome Type 1Congenital HypothyroidismPropionic AcidemiaUsher Syndrome, Type 1FPancreatic Agenesis 1Hereditary Hypophosphatemic RicketsGlycogen Storage Disease IXBGlycogen Storage Disease IXCMOWSEpilepsy, Early-Onset, Vitamin B6-DependentPyridoxal Phosphate-Responsive SeizuresPituitary Hormone Deficiency, Combined, 1PtsdDihydropteridine Reductase DeficiencySevere Combined Immunodeficiency Due to RAG1 DeficiencySevere Combined Immunodeficiency Due to RAG2 DeficiencyRetinoblastomaMultiple Endocrine Neoplasia Type 2BPseudohypoaldosteronism, Type ILiddle SyndromeBiotin-Responsive Basal Ganglia DiseaseSCDDIAR1GSD1CAcrodermatitis EnteropathicaThyroid Dyshormonogenesis 1Riboflavin Transporter DeficiencyWaardenburg Syndrome, Type 2ESRDCongenital Lipoid Adrenal Hyperplasia Due to STAR DeficiencyBarth SyndromeAdrenocorticotropic Hormone DeficiencyTranscobalamin II DeficiencyThyroid Dyshormonogenesis 3Segawa Syndrome, Autosomal RecessiveAutosomal Recessive Nonsyndromic Hearing LossThyroid Dyshormonogenesis 2ACongenital Isolated Thyroid Stimulating Hormone DeficiencyHypothyroidism Due to TSH Receptor MutationsUsher Syndrome Type 1CUsher Syndrome Type 1G (Diagnosis)Von Willebrand Disease, Type 3Combined Immunodeficiency Due to ZAP70 DeficiencyAdenine Phosphoribosyltransferase DeficiencyMetachromatic LeukodystrophyCanavan DiseaseMenkes DiseaseCarbonic Anhydrase VA DeficiencyDevelopmental and Epileptic Encephalopathy 217 Alpha-Hydroxylase DeficiencySmith-Lemli-Opitz SyndromeKrabbe DiseaseGlutathione Synthetase DeficiencyMucopolysaccharidosis Type 7Rett SyndromeMolybdenum Cofactor Deficiency, Type ANiemann-Pick Disease, Type C1Niemann-Pick Disease Type C2Ornithine Aminotransferase Deficiency3-Phosphoglycerate Dehydrogenase DeficiencyLeber Congenital Amaurosis 2Dravet SyndromeMucopolysaccharidosis Type 3 AOrnithine Translocase DeficiencyCarnitine-acylcarnitine Translocase DeficiencyGlucose Transporter Type 1 Deficiency SyndromeCreatine Transporter DeficiencyNiemann-Pick Disease Type APitt Hopkins SyndromeTuberous Sclerosis 1Tuberous Sclerosis 2Ataxia With Isolated Vitamin E DeficiencyAngelman SyndromePrader-Willi SyndromeHomocystinuriaPermanent Neonatal Diabetes MellitusTransient Neonatal Diabetes MellitusFactor VII DeficiencyGlycogen Storage Disease Type IXA1Glycogen Storage Disease, Type IXA2Glycogen Storage Disease ICGlycogen Storage Disease Type IBCentral Hypoventilation Syndrome With or Without Hirschsprung Disease