Treatment Trials

10 Clinical Trials for Various Conditions

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RECRUITING
Autologous Mobilized Peripheral Blood CD34+ Hematopoietic Stem and Progenitor Cells (HSPC) Transduced With the Elongation Factor Alpha Short Promoter (EFS) - Adenosine Deaminase (ADA) Gene (EFS-ADA) Lentiviral Vector for Adenosine Deaminase Severe Combined Immune Deficiency (ADA SCID)
Description

The aim of this study is to assess the safety and efficacy of autologous transplantation of hematopoietic stem cells (CD34+ cells) from mobilized peripheral blood (mPB) of ADA-deficient SCID infants and children following human ADA gene transfer by the EFS-ADA lentiviral vector. The level of gene transfer in blood cells and immune function will be measured as endpoints.

COMPLETED
Registry Study of Revcovi Treatment in Patients With ADA-SCID
Description

This registry study is being conducted in patients with adenosine deaminase severe combined immune deficiency (ADA-SCID) who require enzyme replacement therapy (ERT) treatment with Revcovi. Data on safety and on measures of efficacy are collected.

COMPLETED
Gene Transfer Therapy for Severe Combined Immunodeficieny Disease (SCID) Due to Adenosine Deaminase (ADA) Deficiency
Description

This study will evaluate a new method for delivering gene transfer therapy to patients with severe combined immunodeficiency disease (SCID) due to a defective adenosine deaminase (ADA) gene. This gene codes for the adenosine deaminase enzyme, which is essential for the proper growth and function of infection-fighting white blood cells called T and B lymphocytes. Patients who lack this enzyme are vulnerable to frequent and severe infections. Some patients with this disease receive enzyme replacement therapy with weekly injections of the drug PEG-ADA (ADAGEN). This drug may increase the number of immune cells and reduce infections, but it is not a cure. Gene transfer therapy, in which a normal ADA gene is inserted into the patient s cells, attempts to correct the underlying cause of disease. This therapy has been tried in a small number of patients with varying degrees of success. In this study, the gene will be inserted into the patient s stem cells (cells produced by the bone marrow that mature into the different blood components white cells, red cells and platelets). Patients with ADA deficiency and SCID who are taking PEG-ADA and are not candidates for HLA-identical sibling donor bone marrow transplantation may be eligible for this study. Participants will be admitted to the NIH Clinical Center for 2 to 3 days. Stem cells will be collected either from cord blood (in newborn patients) or from the bone marrow. The bone marrow procedure is done under light sedation or general anesthesia. It involves drawing a small amount of marrow through a needle inserted into the hip bone. The stem cells in the marrow will be grown in the laboratory and a normal human ADA gene will be transferred into them through a special type of disabled mouse virus. A few days later, the patient will receive the ADA-corrected cells through an infusion in the vein that will last from 10 minutes to 2 hours. Patients will be evaluated periodically for immune function with blood tests, skin tests, and reactions to tetanus, diphtheria, H. influenza B and S. pneumoniae vaccinations. The survival of ADA-corrected cells will be monitored through blood tests. The number and amount of blood tests will depend on the patient s age, weight and health, but is expected that blood will not be drawn more than twice a month. Patients will also undergo bone marrow biopsy aspirate (as described above) twice a year. Patients will be followed once a year indefinitely to evaluate the long-term effects of therapy.

COMPLETED
Total-Body Irradiation Followed By Cyclosporine and Mycophenolate Mofetil in Treating Patients With Severe Combined Immunodeficiency Undergoing Donor Bone Marrow Transplant
Description

This pilot clinical trial studies total-body irradiation followed by cyclosporine and mycophenolate mofetil in treating patients with severe combined immunodeficiency (SCID) undergoing donor bone marrow transplant. Giving total-body irradiation (TBI) before a donor bone marrow transplant using stem cells that closely match the patient's stem cells, helps stop the growth of abnormal cells. It may also stop the patient's immune system from rejecting the donor's stem cells. The donated stem cells may mix with the patient's immune cells and help destroy any remaining abnormal cells. Sometimes the transplanted cells from a donor can also make an immune response against the body's normal cells. Giving cyclosporine and mycophenolate mofetil after the transplant may stop this from happening.

COMPLETED
Gene Transfer Therapy for Severe Combined Immunodeficieny Disease (SCID) Due to Adenosine Deaminase (ADA) Deficiency: A Natural History Study
Description

This study will monitor the long-term effects of gene therapy in patients with severe combined immunodeficiency disease (SCID) due to a deficiency in an enzyme called adenosine deaminase (ADA). It will also follow the course of disease in children who are not receiving gene therapy, but may have received enzyme replacement therapy with the drug PEG-ADA. ADA is essential for the growth and proper functioning of infection-fighting white blood cells called T and B lymphocytes. Patients who lack this enzyme are, therefore, immune deficient and vulnerable to frequent infections. Injections of PEG-ADA may increase the number of immune cells and reduce infections, but this enzyme replacement therapy is not a definitive cure. In addition, patients may become resistant or allergic to the drug. Gene therapy, in which a normal ADA gene is inserted into the patient's cells, attempts to correcting the underlying cause of disease. Patients with SCID due to ADA deficiency may be eligible for this study. Patients may or may not have received enzyme replacement therapy or gene transfer therapy, or both. Participants will have follow-up visits at the National Institutes of Health in Bethesda, Maryland, at least once a year for a physical examination, blood tests, and possibly the following additional procedures to evaluate immune function: 1. Bone marrow sampling - A small amount of marrow from the hip bone is drawn (aspirated) through a needle. The procedure can be done under local anesthesia or light sedation. 2. Injection of small amounts of fluids into the arm to study if the patient's lymphocytes respond normally. 3. Administration of vaccination shots. 4. Collection of white blood cells through apheresis - Whole blood is collected through a needle placed in an arm vein. The blood circulates through a machine that separates it into its components. The white cells are then removed, and the red cells, platelets and plasma are returned to the body, either through the same needle used to draw the blood or through a second needle placed in the other arm. 5. Blood drawings to obtain and study the patient's lymphocytes.

COMPLETED
MND-ADA Transduction of CD34+ Cells From Children With ADA-SCID
Description

Severe combined immune deficiency (SCID) may result from inherited deficiency of the enzyme adenosine deaminase (ADA). Children with ADA-deficient SCID often die from infections in infancy, unless treated with either a bone marrow transplant or with ongoing injections of PEG-ADA (Adagen) enzyme replacement therapy. Successful BMT requires the availability of a matched sibling donor for greatest success, and treatment using bone marrow from a less-well matched donor may have a higher rate of complications. PEG-ADA may restore and sustain immunity for many years, but is very expensive and requires injections 1-2 times per week on an ongoing basis. This clinical trial is evaluating the efficacy and safety of an alternative approach, by adding a normal copy of the human ADA gene into stem cells from the bone marrow of patients with ADA-deficient SCID. Eligible patients with ADA-deficient SCID, lacking a matched sibling donor, will be eligible if they meet entry criteria for adequate organ function and absence of active infections and following the informed consent process. Bone marrow will be collected from the back of the pelvis from the patients and processed in the laboratory to isolate the stem cells and add the human ADA gene using a retroviral vector. The patients will receive a moderate dosage of busulfan, a chemotherapy agent that eliminates some of the bone marrow stem cells in the patient, to "make space" for the gene-corrected stem cells to grow once they are given back by IV. Patients will be followed for two years to assess the potentially beneficial effects of the procedure on the function of their immune system and to assess possible side-effects. This gene transfer approach may provide a better and safer alternative for treatment of patients with ADA-deficient SCID.

ENROLLING_BY_INVITATION
An Observational LTFU Study for Patients Previously Treated With Autologous ex Vivo Gene Therapy for ADA-SCID
Description

This observational long-term follow-up study is designed to collect safety and efficacy data from ADA-SCID patients previously treated with autologous ex vivo gene therapy products based on the EFS-ADA LV encoding for human adenosine deaminase (ADA) gene (EFS-ADA LV), as part of the OTL-101 clinical development program. No investigational medicinal product will be administered to these patients as part of the OTL-101-6 study.

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
COMPLETED
EZN-2279 in Patients With ADA-SCID
Description

The purpose of this study is to evaluate the safety, efficacy, and pharmacokinetics of EZN-2279 in patients with ADA-deficient combined immunodeficiency currently being treated with Adagen.

COMPLETED
The Role of Bacteria and Genetic Variations in Cystic Fibrosis
Description

This study will examine 1) the role of hereditary factors in cystic fibrosis; i.e., the relationship of the disease to specific gene variations, and 2) the role of bacterial products involved in lung infections substances produced by bacteria may worsen the disease. Patients with cystic fibrosis who are being followed by the Medical College of Wisconsin or the University of Wisconsin-Madison are eligible for this study. Participants will have blood tests, pulmonary function tests, a sputum culture, and buccal swabbing (cotton swabbing of the inside of the cheek to collect cells for DNA study). In addition, their medical records will be reviewed for a history of lung infections and the results of various tests, including pulmonary function studies, chest X-rays and bacterial cultures. Blood samples collected previously at the Medical College of Wisconsin or the University of Wisconsin-Madison will also be analyzed for antibodies to bacteria. Although this is a one-time study, participants may be asked to return for repeated tests. ...