Type I DiabetesPhase 1GABANCT02002130
The Use of Glutamic Acid Decarboxylase (GAD) and Gamma-Amino Butyric Acid (GABA) in the Treatment of Type I Diabetes
A Phase 1 study testing Active Oral GABA and Active GAD-alum injection in people with Type I Diabetes, run by University of Alabama at Birmingham at 1 site in United States.
Trial summary
Type I Diabetes is an auto immune disease in which the body's immune system attacks and destroys the insulin-producing beta cells of the pancreas. Therefore, children affected by this condition present with high blood sugars. Read more about this study
- Who is it for?
- Ages 4 to 18 years
- Conditions the study is for
- Type I Diabetes
- What is being tested?
- Active Oral GABA and Active GAD-alum injection
- Type of treatment
- Vaccines, Pill or oral medicine, Injection or infusion
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 101 participants
- Where
- 1 siteUnited States
- Study dates
- Jan 2015to 15 Apr 2022
- Phase
- Phase 1
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 4 to 18 years
- All sexes
- No healthy volunteers
- Child, Adult
Who may be able to join
- Patients must be positive for GAD-65 antibody.
- They must meet ADA criteria for diabetes: classic symptoms, plus blood sugar > 200mg/dL or fasting blood sugar > 126 mg/dL.
- Must be enrolled with 5 weeks of diagnosis
- Females who are post-menarchal must use 2 forms of contraception if not abstinent. The types of contraception deemed acceptable would be oral contraceptives, intrauterine devices, and barrier methods.
- Signed informed consent form.
Who cannot join
- Chronic systemic steroid use, including inhaled compounds, or any medication which can alter glucose metabolism
- Obesity, defined as BMI > 95% or BMI > 27 in adolescents with acanthosis score between 1-1.5.
- Pregnant and/or breast feeding
- History of seizure disorder
- Patients on medications that may disturb GABA action, such as Baclofen, Valium, Acamprosate, Neurontin, or Lyrica
- history of any alcoholism or substance abuse.
- Chronic Disease (such as liver, cancer, cystic fibrosis, or renal failure)
- Chromosome abnormality (such as Trisomy 21, Turner Syndrome, etc.)
Trial locations and contacts
1 site in 1 country.
About this study
Official title: The Use of Glutamic Acid Decarboxylase (GAD)and Gamma-Amino Butyric Acid(GABA)in the Treatment of Type I Diabetes.
Type I Diabetes is an auto immune disease in which the body's immune system attacks and destroys the insulin-producing beta cells of the pancreas. Therefore, children affected by this condition present with high blood sugars. This condition affects 1:400/500 persons worldwide.Type I Diabetes, previously known as Juvenile Diabetes,usually strikes in childhood, adolescence, or young adulthood, but lasts for a lifetime. To date, there has been no treatments that can arrest, or reverse the ongoing beta cell destruction. We hypothesize that GABA, a naturally occurring substance, has the potential to reduce the inflammation and protect the pancreatic beta cells from autoimmune destruction. GAD-alum may contribute to the preservation of residual insulin secretion in patients with recent onset, Type I Diabetes.
Read the detailed description
The primary defect in autoimmune Type I Diabetes Mellitus (T1DM) involves the infiltration of the pancreatic islet cells by T-lymphocytes, macrophages, and other immune cells, and consequent loss of beta cells. At the onset of T1DM more than 70% of the beta cells are destroyed, whereas the residual beta cells most likely represent the only reservoir for the potential regeneration of the islet beta cell mass. A series of immunological abnormalities have been reported in those with T1DM including, but not limited to, the production of autoantibodies (i.e., glutamic acid decarboxylase (GAD-65), tyrosine phosphatase-related islet antigen 2 (IA2), Zinc Transporter 8 (ZnT8A), or insulin (IAA) as well as alterations in the capacity of regulatory T cells (Treg) to suppress the action of effector T cells (Teff); the latter population thought as playing a key role in the immune destructive process. Therefore, a vast majority of studies attempting to prevent or reverse the disease have focused on immune suppression. While some of these studies have shown limited promise, many has side effects which were significant enough that one must question the value of short term benefits associated with utilizing these drugs.
GABA is a naturally occurring substance in physiology and has the potential to locally reduce inflammation and protect pancreatic beta cells from auto-immune destruction. GABA, synthesized from glutamate by GAD, is a well known neurotransmitter in the CNS and acts mainly through the GABAA receptor (GABAAR). GABA is locally produced by the pancreatic beta cells. GABAARs are also expressed in various immune cells, including T-cells, peripheral blood mononuclear cells, and are known to exert immune-inhibitory effects. BABA appears to play multiple roles in the pancreas. GABA promotes beta-cell growth and survival, and GABA can also act on the GABA(A) receptors in the pancreatic alpha cells, in so doing suppressing glucagon secretion, and GABA suppresses inflammation and increases regulatory T-cell numbers. Based on the aforementioned information, we envisage that administering GABA to those with new onset T1DM may preserve or increase residual insulin production, suppress glucagon release, and decrease inflammation surrounding the pancreas. With this, GABA may prolong the beta-cell life after diagnosis. Combining with GAD-alum injections, which aim to halt the autoimmune attack by inducing tolerance thereby saving residual insulin production, may improve glycemic control even more and significantly decrease the risk of hypoglycemia and long-term complications in the future.
- Conditions
- Type I Diabetes
- Being tested
- Placebo GABA and Placebo GAD-alum, GABA and Placebo GAD-alum, Active Oral GABA and Active GAD-alum injection
- Keywords
- Diabetes
- Medical subject headings
- Diabetes Mellitus, Type 1, Diabetes Mellitus
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Placebo GABA and Placebo GAD-alumDrug
Also called Placebo for Gamma-Amino Butyric Acid
Maltodextrin as a placebo formulation for GABA Placebo GAD-alum injection
GABA and Placebo GAD-alumDrug
Oral Active GABA with Placebo GAD-alum
Active Oral GABA and Active GAD-alum injectionDrug
Active Oral GABA and Active GAD-alum injection
| Study group | Role | What they receive |
|---|---|---|
| Placebo GABA and Placebo GAD-alum | Placebo comparator | Placebo formulation, Maltodextrin, for Gamma-Amino Butyric Acid (GABA) capsule-identical in appearance and taste, but no active medication will be taken with meals.Number of pills based on body surface area.
Placebo GAD-alum(Glutamic Acid Decarboxylase in alum) injection- identical in appearance but no active medication will be received at baseline and 1 month. Receives: Drug: Placebo GABA and Placebo GAD-alum |
| GABA and placebo GAD-alum | Active comparator | Patients will receive the Active GABA (Gamma-Amino Butyric Acid) capsules. Each capsule 250mg. Dosage will be calculated according to body surface area of the child and divided between 2 meals/day. Larger dose taken with larger meal.
Patients will receive the GAD-alum( Glutamic Acid Decarboxylase in alum) placebo at baseline and 1 month. Receives: Drug: GABA and Placebo GAD-alum |
| Active Oral GABA and Active GAD-alum Injection | Active comparator | Patients will receive Oral GABA(Gamma-Amino Butyric Acid) 250mg capsules. Dosage (# of capsules) based on body surface area and divided between 2 meals/day.
Patients will receive a primary (at baseline)injection of recombinant human GAD(Glutamic Acid Decarboxylase) in a standard vaccine formulation with alum, and a booster injection of the same at 1 month after baseline. Receives: Drug: Active Oral GABA and Active GAD-alum injection |
What is being measured
The primary outcome is the main question the study is designed to answer.
Compare the effect of oral GABA or oral GABA/GAD combination administration on pancreatic beta cell function by quantitative C-peptide secretion
This will be assessed by meal stimulated c-peptide secretion in treatment cohorts compared to age matched placebo controls before and after 1 year of treatment.
Measured: 12 months after baseline
Secondary outcomes (4)
Compare the effect of oral GABA or GABA/GAD administration on fasting and meal stimulated glucagon and pro-insulin levels.
This will be assessed by meal stimulated glucagon and pro-insulin secretion in treatment cohorts compared with age matched placebo controls before and after 1 year of treatment.
Measured: 12 months after baseline
Compare the effect of oral GABA or GABA/GAD administration on total daily insulin usage by participants and corrected Hemoglobin A1C.
This will be assessed by measuring insulin usage and corrected Hemoglobin A1C linearly for each participant, in addition to comparison with age matched controls
Measured: 12 months after baseline
Compare the effect of oral GABA or oral GABA/GAD administration on indices of immune system function.
This will be assessed by measuring immunologic markers of inflammation linearly over the 12 month treatment course for each patient and comparing to age matched placebo controls.
Measured: 12 months after baseline
Compare the effect of oral GABA or oral GABA/GAD administration on diabetes related autoantibodies
This will be assessed by measuring GAD65, ICA512, and Zinc Transporter 8 antibodies throughout the treatment period.
Measured: 12 months after baseline
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted5 Dec 2013 (estimated)
- Study startJan 2015
- Primary completion15 Oct 2021
- Study completion15 Apr 2022
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (4)Papers the sponsor has linked to this study.
- Other trials for Type I DiabetesStudies of the same condition, open and under way.
- More trials run by University of Alabama at BirminghamThe 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
- Interventional
- Phase
- Phase 1
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Quadruple blind
- Who is masked
- Participant, Care provider, Investigator, Outcomes assessor
- Enrolment
- 101 participants (actual)
Sponsor and investigators
- Lead sponsor
- University of Alabama at Birmingham
- Sponsor type
- University, hospital or other
- Collaborators
- Diamyd Inc, NOW Foods, Janssen Pharmaceuticals, Juvenile Diabetes Research Foundation
- Responsible party
- Principal investigator, Kenneth McCormick, University of Alabama at Birmingham
- Investigators
- Kenneth McCormick, MD, Principal investigator, University of Alabama at BirminghamGail Mick, MD, Principal investigator, University of Alabama at Birmingham
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02002130
- Sponsor's protocol ID
- GABA-GAD
- Acronym
- GABA
- Status last verified
- May 2022
- First submitted
- 18 Nov 2013
- Last updated
- 6 May 2022
- Results posted
- No
- Data monitoring committee
- Yes
- FDA-regulated drug
- Yes
- FDA-regulated device
- No
Publications
Ludvigsson J, Faresjo M, Hjorth M, Axelsson S, Cheramy M, Pihl M, Vaarala O, Forsander G, Ivarsson S, Johansson C, Lindh A, Nilsson NO, Aman J, Ortqvist E, Zerhouni P, Casas R. GAD treatment and insulin secretion in recent-onset type 1 diabetes. N Engl J Med. 2008 Oct 30;359(18):1909-20. doi: 10.1056/NEJMoa0804328. Epub 2008 Oct 8.
PubMed 18843118Soltani N, Qiu H, Aleksic M, Glinka Y, Zhao F, Liu R, Li Y, Zhang N, Chakrabarti R, Ng T, Jin T, Zhang H, Lu WY, Feng ZP, Prud'homme GJ, Wang Q. GABA exerts protective and regenerative effects on islet beta cells and reverses diabetes. Proc Natl Acad Sci U S A. 2011 Jul 12;108(28):11692-7. doi: 10.1073/pnas.1102715108. Epub 2011 Jun 27.
PubMed 21709230Heath KE, Feduska JM, Taylor JP, Houp JA, Botta D, Lund FE, Mick GJ, McGwin G Jr, McCormick KL, Tse HM. GABA and Combined GABA with GAD65-Alum Treatment Alters Th1 Cytokine Responses of PBMCs from Children with Recent-Onset Type 1 Diabetes. Biomedicines. 2023 Jul 10;11(7):1948. doi: 10.3390/biomedicines11071948.
PubMed 37509587Freese J, Al-Rawi R, Choat H, Martin A, Lunsford A, Tse H, Mick G, McCormick K. Proinsulin to C-Peptide Ratio in the First Year After Diagnosis of Type 1 Diabetes. J Clin Endocrinol Metab. 2021 Oct 21;106(11):e4318-e4326. doi: 10.1210/clinem/dgab463.
PubMed 34228132
Study at a glance
From the registry record, last updated by the sponsor on 6 May 2022. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- The Use of Glutamic Acid Decarboxylase (GAD)and Gamma-Amino Butyric Acid(GABA)in the Treatment of Type I Diabetes.
- ClinicalTrials.gov ID
- NCT02002130
- Acronym / sponsor ID
- GABA / GABA-GAD
- Conditions
- Type I Diabetes
- Keywords
- Diabetes
- Phase
- Phase 1
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 101 participants (actual)
- Lead sponsor
- University of Alabama at BirminghamUniversity, hospital or other
- Collaborators
- Diamyd Inc, NOW Foods, Janssen Pharmaceuticals, Juvenile Diabetes Research Foundation
- Study start
- Jan 2015 (actual)
- Primary completion
- 15 Oct 2021 (actual)
- Study completion
- 15 Apr 2022 (actual)
- First posted
- 5 Dec 2013 (estimated)
- 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.
Type I Diabetes is an auto immune disease in which the body's immune system attacks and destroys the insulin-producing beta cells of the pancreas. Therefore, children affected by this condition present with high blood sugars. This condition affects 1:400/500 persons worldwide.Type I Diabetes, previously known as Juvenile Diabetes,usually strikes in childhood, adolescence, or young adulthood, but lasts for a lifetime. To date, there has been no treatments that can arrest, or reverse the ongoing beta cell destruction. We hypothesize that GABA, a naturally occurring substance, has the potential to reduce the inflammation and protect the pancreatic beta cells from autoimmune destruction. GAD-alum may contribute to the preservation of residual insulin secretion in patients with recent onset, Type I Diabetes.
Detailed description
The primary defect in autoimmune Type I Diabetes Mellitus (T1DM) involves the infiltration of the pancreatic islet cells by T-lymphocytes, macrophages, and other immune cells, and consequent loss of beta cells. At the onset of T1DM more than 70% of the beta cells are destroyed, whereas the residual beta cells most likely represent the only reservoir for the potential regeneration of the islet beta cell mass. A series of immunological abnormalities have been reported in those with T1DM including, but not limited to, the production of autoantibodies (i.e., glutamic acid decarboxylase (GAD-65), tyrosine phosphatase-related islet antigen 2 (IA2), Zinc Transporter 8 (ZnT8A), or insulin (IAA) as well as alterations in the capacity of regulatory T cells (Treg) to suppress the action of effector T cells (Teff); the latter population thought as playing a key role in the immune destructive process. Therefore, a vast majority of studies attempting to prevent or reverse the disease have focused on immune suppression. While some of these studies have shown limited promise, many has side effects which were significant enough that one must question the value of short term benefits associated with utilizing these drugs.
GABA is a naturally occurring substance in physiology and has the potential to locally reduce inflammation and protect pancreatic beta cells from auto-immune destruction. GABA, synthesized from glutamate by GAD, is a well known neurotransmitter in the CNS and acts mainly through the GABAA receptor (GABAAR). GABA is locally produced by the pancreatic beta cells. GABAARs are also expressed in various immune cells, including T-cells, peripheral blood mononuclear cells, and are known to exert immune-inhibitory effects. BABA appears to play multiple roles in the pancreas. GABA promotes beta-cell growth and survival, and GABA can also act on the GABA(A) receptors in the pancreatic alpha cells, in so doing suppressing glucagon secretion, and GABA suppresses inflammation and increases regulatory T-cell numbers. Based on the aforementioned information, we envisage that administering GABA to those with new onset T1DM may preserve or increase residual insulin production, suppress glucagon release, and decrease inflammation surrounding the pancreas. With this, GABA may prolong the beta-cell life after diagnosis. Combining with GAD-alum injections, which aim to halt the autoimmune attack by inducing tolerance thereby saving residual insulin production, may improve glycemic control even more and significantly decrease the risk of hypoglycemia and long-term complications in the future.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Quadruple blind (participant, care provider, investigator, outcomes assessor)
- Number of arms
- 3
| Arm | Type | Receives |
|---|---|---|
| Placebo GABA and Placebo GAD-alum | Placebo comparator | Drug: Placebo GABA and Placebo GAD-alumPlacebo formulation, Maltodextrin, for Gamma-Amino Butyric Acid (GABA) capsule-identical in appearance and taste, but no active medication will be taken with meals.Number of pills based on body surface area. Placebo GAD-alum(Glutamic Acid Decarboxylase in alum) injection- identical in appearance but no active medication will be received at baseline and 1 month. |
| GABA and placebo GAD-alum | Active comparator | Drug: GABA and Placebo GAD-alumPatients will receive the Active GABA (Gamma-Amino Butyric Acid) capsules. Each capsule 250mg. Dosage will be calculated according to body surface area of the child and divided between 2 meals/day. Larger dose taken with larger meal. Patients will receive the GAD-alum( Glutamic Acid Decarboxylase in alum) placebo at baseline and 1 month. |
| Active Oral GABA and Active GAD-alum Injection | Active comparator | Drug: Active Oral GABA and Active GAD-alum injectionPatients will receive Oral GABA(Gamma-Amino Butyric Acid) 250mg capsules. Dosage (# of capsules) based on body surface area and divided between 2 meals/day. Patients will receive a primary (at baseline)injection of recombinant human GAD(Glutamic Acid Decarboxylase) in a standard vaccine formulation with alum, and a booster injection of the same at 1 month after baseline. |
Who may qualify
- Ages
- 4 to 18 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Child, Adult
Key inclusion criteria (5 listed)
- Patients must be positive for GAD-65 antibody.
- They must meet ADA criteria for diabetes: classic symptoms, plus blood sugar > 200mg/dL or fasting blood sugar > 126 mg/dL.
- Must be enrolled with 5 weeks of diagnosis
- Females who are post-menarchal must use 2 forms of contraception if not abstinent. The types of contraception deemed acceptable would be oral contraceptives, intrauterine devices, and barrier methods.
- Signed informed consent form.
Key exclusion criteria (8 listed)
- Chronic systemic steroid use, including inhaled compounds, or any medication which can alter glucose metabolism
- Obesity, defined as BMI > 95% or BMI > 27 in adolescents with acanthosis score between 1-1.5.
- Pregnant and/or breast feeding
- History of seizure disorder
- Patients on medications that may disturb GABA action, such as Baclofen, Valium, Acamprosate, Neurontin, or Lyrica
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Placebo GABA and Placebo GAD-alumAlso: Placebo for Gamma-Amino Butyric AcidMaltodextrin as a placebo formulation for GABA Placebo GAD-alum injection | Drug | Placebo GABA and Placebo GAD-alum |
| GABA and Placebo GAD-alumOral Active GABA with Placebo GAD-alum | Drug | GABA and placebo GAD-alum |
| Active Oral GABA and Active GAD-alum injectionActive Oral GABA and Active GAD-alum injection | Drug | Active Oral GABA and Active GAD-alum Injection |
Primary outcome
Compare the effect of oral GABA or oral GABA/GAD combination administration on pancreatic beta cell function by quantitative C-peptide secretion
Time frame: 12 months after baseline
This will be assessed by meal stimulated c-peptide secretion in treatment cohorts compared to age matched placebo controls before and after 1 year of treatment.
4 secondary outcomes
Compare the effect of oral GABA or GABA/GAD administration on fasting and meal stimulated glucagon and pro-insulin levels.
Time frame: 12 months after baseline
Compare the effect of oral GABA or GABA/GAD administration on total daily insulin usage by participants and corrected Hemoglobin A1C.
Time frame: 12 months after baseline
Compare the effect of oral GABA or oral GABA/GAD administration on indices of immune system function.
Time frame: 12 months after baseline
Compare the effect of oral GABA or oral GABA/GAD administration on diabetes related autoantibodies
Time frame: 12 months after baseline
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 6 May 2022.
- Background: PubMed 18843118Ludvigsson J, Faresjo M, Hjorth M, Axelsson S, Cheramy M, Pihl M, Vaarala O, Forsander G, Ivarsson S, Johansson C, Lindh A, Nilsson NO, Aman J, Ortqvist E, Zerhouni P, Casas R. GAD treatment and insulin secretion in recent-onset type 1 diabetes. N Engl J Med. 2008 Oct 30;359(18):1909-20. doi: 10.1056/NEJMoa0804328. Epub 2008 Oct 8.
- Background: PubMed 21709230Soltani N, Qiu H, Aleksic M, Glinka Y, Zhao F, Liu R, Li Y, Zhang N, Chakrabarti R, Ng T, Jin T, Zhang H, Lu WY, Feng ZP, Prud'homme GJ, Wang Q. GABA exerts protective and regenerative effects on islet beta cells and reverses diabetes. Proc Natl Acad Sci U S A. 2011 Jul 12;108(28):11692-7. doi: 10.1073/pnas.1102715108. Epub 2011 Jun 27.
- Derived from this study: PubMed 37509587Heath KE, Feduska JM, Taylor JP, Houp JA, Botta D, Lund FE, Mick GJ, McGwin G Jr, McCormick KL, Tse HM. GABA and Combined GABA with GAD65-Alum Treatment Alters Th1 Cytokine Responses of PBMCs from Children with Recent-Onset Type 1 Diabetes. Biomedicines. 2023 Jul 10;11(7):1948. doi: 10.3390/biomedicines11071948.
- Derived from this study: PubMed 34228132Freese J, Al-Rawi R, Choat H, Martin A, Lunsford A, Tse H, Mick G, McCormick K. Proinsulin to C-Peptide Ratio in the First Year After Diagnosis of Type 1 Diabetes. J Clin Endocrinol Metab. 2021 Oct 21;106(11):e4318-e4326. doi: 10.1210/clinem/dgab463.
Related trials for Type I Diabetes
RecruitingPhase 1
Pharmacokinetics, Safety, and Immunogenicity Comparison of Bmab1700 and Opdivo® as Adjuvant Monotherapy in Participants With Melanoma
Melanoma
Active, not recruitingPhase 2
A Study of Botensilimab and Balstilimab for the Treatment of Colorectal Cancer
Metastatic Colorectal Cancer
Not yet recruiting
Inter-Arm Differences in Continuous Glucose Monitor Readings in Adults With Diabetes
Continuous Glucose Monitoring, Type 1 Diabetes
RecruitingObservational study
Estimated Risk of Preeclampsia in the First Trimester and Its Association With Subclinical Atherosclerosis and Cardiovascular Risk in Women With Type 1 Diabetes
Type 1 Diabetes, Preeclampsia
Not yet recruiting
A Novel Miniature Equine-Assisted Diabetes Education Program for Youth: Evaluating the Diabetes Equine Empowerment Program (DEEP).
Diabetes (Insulin-requiring, Type 1 or Type 2), Pediatric Diabetes
Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Kenneth McCormick, MD principal investigator
University of Alabama at Birmingham
Gail Mick, MD principal investigator
University of Alabama at Birmingham
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 1 study testing Active Oral GABA and Active GAD-alum injection in people with Type I Diabetes, run by University of Alabama at Birmingham at 1 site in United States.
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 5 inclusion and 8 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: finished, as of the sponsor's last update on 6 May 2022. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. 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. Some participants in this study may receive a placebo. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 1 studies test a treatment in a small group of people for the first time or in a new way, mainly to check safety and find the right dose.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Compare the effect of oral GABA or oral GABA/GAD combination administration on pancreatic beta cell function by quantitative C-peptide secretion (time frame: 12 months after baseline). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT02002130, which also lists 4 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 6 May 2022.