ADPKDNCT03717883
ADPKD Alterations in Hepatic Transporter Function
An observational study of ADPKD and Autosomal Dominant Polycystic Kidney Disease, run by University of North Carolina, Chapel Hill at 1 site in United States.
Trial summary
This is a single center, comparative cohort study to investigate alterations in hepatic transporter function in subjects with autosomal dominant polycystic kidney disease (ADPKD) compared to healthy subjects and subjects with non-ADPKD renal disease. Read more about this study
- Who is it for?
- Ages 18 to 65 yearsHealthy volunteers can take part
- Conditions the study is for
- ADPKD, Autosomal Dominant Polycystic Kidney Disease, Renal Disease
- How many people
- 24 participants
- Where
- 1 siteUnited States
- Study dates
- 17 Sep 2018to 29 Jan 2020
- Phase
- Observational
- 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 18 to 65 years
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Study population: Healthy vs. ADPKD vs. non-ADPKD renal disease subjects
Who may be able to join
- Provide signed and dated informed consent
- Willing to comply with all study procedures and be available for the duration of the study
- Male or female, aged 18 to 65
- Negative quantitative human chorionic gonadotropin (hCG) blood test (for women of child-bearing age only)
- For healthy subjects:
- Normal liver functions tests (LFTs) as defined by the University of North Carolina (UNC) hospital laboratory reference range [aspartate aminotransferase (AST)14-38 U/L, alanine aminotransferase (ALT) 15-48 U/L, alkaline phosphatase 38-126 U/L]
Show all 11Show fewer
- Normal clinical laboratory results including kidney function (serum creatinine) and lipid panel as reviewed by the study physician
- For subjects with ADPKD:
- Man or woman between the ages of 18 and 65 with documented ADPKD
- For subjects with non-ADPKD renal disease:
- Man or woman between the ages of 18 and 65 with documented non-ADPKD renal disease as determined by the study physician
Who cannot join
- All Participants:
- Donation of blood within the last 30 days
- Diagnosis of human immunodeficiency virus (HIV) and/or untreated hepatitis C virus (HCV)
- History of significant alcohol abuse and/or illicit drug use
- More than 1 glass of wine or 2 beers (or equivalent in % alcohol) per day during the 48 hours prior to study and/or screening visit
- Inability to fast for 8 hours prior to study and screening sample collection
Show all 25Show fewer
- Women who are pregnant, trying to become pregnant, or breastfeeding
- Current or recent (within 30 days) use of bile acid sequestrants, bile acid derivatives (i.e. ursodiol) or fibric acid derivatives
- History of diabetes or taking blood glucose lowering treatments
- Radiologic imaging consistent with cirrhosis and portal hypertension
- Evidence of decompensated liver disease defined as any of the following: serum albumin <3.2 g/dL, total bilirubin > 1.5 mg/dL, or prothrombin time (PT)/international normalized ratio (INR) > 1.3 times normal at screening, or history or presence of ascites, encephalopathy, or bleeding from esophageal varices
- Estimated glomerular filtration rate (GFR)< 15 mL/min per 1.73 m2, or on dialysis, at screening
- Subjects with a condition requiring systemic treatment with either corticosteroids (> 10 mg daily prednisone equivalent) or other immunosuppressive medications (including inhaled) within 14 days of study visit. Corticosteroids with minimal systemic absorption (for example topical) and adrenal replacement steroid doses ≤ 10 mg daily prednisone equivalent, are permitted in the absence of active autoimmune disease provided the dose has been stable for ≥4 weeks and is not expected to change during the course of the study.
- Primary, secondary or extra-hepatic malignancy
- BMI > 35 kg/m2 at screening
- Inability or unwillingness to give informed consent or abide by the study protocol
- History or other evidence of illness, any gastrointestinal surgery (e.g., gall bladder removal), or any other conditions or drug therapies that would make the patient, in the opinion of the investigator, unsuitable for the study (such as poorly controlled psychiatric disease, coronary artery disease, gall bladder disease, active gastrointestinal conditions or taking drugs known to interfere with bile acid synthesis or metabolism or the metabolism/transport of other drugs)
- Healthy Subjects:
- Taking concomitant medications, both prescription and non-prescription (including herbal products and over-the-counter medications), other than oral contraceptives and multivitamins (women stabilized on hormonal methods of birth control will be allowed to participate)
- History or other evidence of liver, gall bladder, or intestinal disease in the opinion of the study investigators
- BMI > 35 kg/m2 at screening.
- Subjects with non-ADPKD renal disease:
- ADPKD
- Proteinuria of ≥3 grams per day of protein into the urine; or on a single spot urine collection, the presence of ≥2 grams of protein per gram of urine creatinine (i.e., excluding patients with nephrotic-range proteinuria)
- Diabetic nephropathy patients
Trial locations and contacts
1 site in 1 country.
United States1 site
University of North Carolina
Chapel Hill, North Carolina, 27713
About this study
Official title: Endogenous Molecule Profiling in Subjects With Autosomal Dominant Polycystic Kidney Disease (ADPKD)
This is a single center, comparative cohort study to investigate alterations in hepatic transporter function in subjects with autosomal dominant polycystic kidney disease (ADPKD) compared to healthy subjects and subjects with non-ADPKD renal disease. Eligible subjects will be 18-65 years of age and of any race/ethnicity and gender.
Read the detailed description
ADPKD is a relatively common genetic disease affecting about 1 out of every 1000 people worldwide. Progression of ADPKD is characterized by the proliferation of fluid-filled kidney cysts. Development of these cysts is progressive and can lead to end-stage renal disease and ultimately, renal failure in many patients. The most common extra-renal complication of ADPKD is the formation of liver cysts, which can vary from minor to extensive. Hepatic cysts can develop from medium-sized bile ducts and complications (i.e., cyst rupture, infection, obstruction of bile ducts, and compromised portal venous flow) can arise from increasing cystic burden. Previous studies have shown that elevated levels of endogenous molecules such as bile acids in ADPKD may indicate altered transporter function. Other endogenous molecules such as coproporphyrin (CP) I and III may be used as probes to assess hepatic transporter function.
The objective of this study is to investigate and quantify ADPKD-associated alterations in endogenous molecule profiles (e.g., bile acids, CP) relative to subjects with non-ADPKD renal disease and healthy individuals, and to investigate specific hepatic transporter polymorphisms that may be related to the alterations. This is important because subjects with ADPKD may be predisposed to adverse reactions associated with some medications that require hepatic transporters for excretion.
Potential study participants will be pre-screened over the phone and then scheduled for a 2-hour study visit. All urine samples within the 2-hour interval will be collected from all participants along with clinical, physical and questionnaire data. Fasting blood samples will be collected at time 0 and 120 min.
- Keywords
- hepatic transporters
- Medical subject headings
- Polycystic Kidney, Autosomal Dominant, Kidney Diseases
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| Healthy subjects | Not described | |
| Subjects with ADPKD | Not described |
What is being measured
The primary outcome is the main question the study is designed to answer.
Difference in serum coproporphyrin I and III concentrations
nmol
Measured: 2 hours
Secondary outcomes (2)
Difference in serum and urine bile acid profiles
nmol
Measured: 2 hours
Difference in renal clearance of coproporphyrin I and III
mL/min
Measured: 2 hours
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted24 Oct 2018
- Study start17 Sep 2018
- Primary completion29 Jan 2020
- Study completion29 Jan 2020
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (19)Papers the sponsor has linked to this study.
- Other trials for ADPKDStudies of the same condition, open and under way.
- 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
- 24 participants (actual)
Sponsor and investigators
- Lead sponsor
- University of North Carolina, Chapel Hill
- Sponsor type
- University, hospital or other
- Collaborators
- National Institute of General Medical Sciences (NIGMS)
- Responsible party
- Sponsor
- Investigators
- Vimal Derebail, MD, MPH, Principal investigator, University of North Carolina, Chapel HillKim Brouwer, PharmD, PhD, Study director, University of North Carolina, Chapel Hill
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT03717883
- Sponsor's protocol ID
- 16-2984
- Other IDs
- 5R35GM122576-02
- Status last verified
- Mar 2020
- First submitted
- 22 Oct 2018
- Last updated
- 25 Mar 2020
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
Igarashi P, Somlo S. Genetics and pathogenesis of polycystic kidney disease. J Am Soc Nephrol. 2002 Sep;13(9):2384-98. doi: 10.1097/01.asn.0000028643.17901.42. No abstract available.
PubMed 12191984Boucher C, Sandford R. Autosomal dominant polycystic kidney disease (ADPKD, MIM 173900, PKD1 and PKD2 genes, protein products known as polycystin-1 and polycystin-2). Eur J Hum Genet. 2004 May;12(5):347-54. doi: 10.1038/sj.ejhg.5201162.
PubMed 14872199Cnossen WR, Drenth JP. Polycystic liver disease: an overview of pathogenesis, clinical manifestations and management. Orphanet J Rare Dis. 2014 May 1;9:69. doi: 10.1186/1750-1172-9-69.
PubMed 24886261Salam M, Keeffe EB. Liver cysts associated with polycystic kidney disease: role of Tc-99m hepatobiliary imaging. Clin Nucl Med. 1989 Nov;14(11):803-7. doi: 10.1097/00003072-198911000-00003.
PubMed 2598550Hofmann AF. The continuing importance of bile acids in liver and intestinal disease. Arch Intern Med. 1999 Dec 13-27;159(22):2647-58. doi: 10.1001/archinte.159.22.2647.
PubMed 10597755Zollner G, Fickert P, Silbert D, Fuchsbichler A, Marschall HU, Zatloukal K, Denk H, Trauner M. Adaptive changes in hepatobiliary transporter expression in primary biliary cirrhosis. J Hepatol. 2003 Jun;38(6):717-27. doi: 10.1016/s0168-8278(03)00096-5.
PubMed 12763363Kullak-Ublick GA, Stieger B, Meier PJ. Enterohepatic bile salt transporters in normal physiology and liver disease. Gastroenterology. 2004 Jan;126(1):322-42. doi: 10.1053/j.gastro.2003.06.005.
PubMed 14699511Munoz-Garrido P, Marin JJ, Perugorria MJ, Urribarri AD, Erice O, Saez E, Uriz M, Sarvide S, Portu A, Concepcion AR, Romero MR, Monte MJ, Santos-Laso A, Hijona E, Jimenez-Aguero R, Marzioni M, Beuers U, Masyuk TV, LaRusso NF, Prieto J, Bujanda L, Drenth JP, Banales JM. Ursodeoxycholic acid inhibits hepatic cystogenesis in experimental models of polycystic liver disease. J Hepatol. 2015 Oct;63(4):952-61. doi: 10.1016/j.jhep.2015.05.023. Epub 2015 Jun 1.
PubMed 26044126Shen H, Dai J, Liu T, Cheng Y, Chen W, Freeden C, Zhang Y, Humphreys WG, Marathe P, Lai Y. Coproporphyrins I and III as Functional Markers of OATP1B Activity: In Vitro and In Vivo Evaluation in Preclinical Species. J Pharmacol Exp Ther. 2016 May;357(2):382-93. doi: 10.1124/jpet.116.232066. Epub 2016 Feb 23.
PubMed 26907622Gilibili RR, Chatterjee S, Bagul P, Mosure KW, Murali BV, Mariappan TT, Mandlekar S, Lai Y. Coproporphyrin-I: A Fluorescent, Endogenous Optimal Probe Substrate for ABCC2 (MRP2) Suitable for Vesicle-Based MRP2 Inhibition Assay. Drug Metab Dispos. 2017 Jun;45(6):604-611. doi: 10.1124/dmd.116.074740. Epub 2017 Mar 21.
PubMed 28325716Devuyst O, Chapman AB, Gansevoort RT, Higashihara E, Perrone RD, Torres VE, Blais JD, Zhou W, Ouyang J, Czerwiec FS. Urine Osmolality, Response to Tolvaptan, and Outcome in Autosomal Dominant Polycystic Kidney Disease: Results from the TEMPO 3:4 Trial. J Am Soc Nephrol. 2017 May;28(5):1592-1602. doi: 10.1681/ASN.2016040448. Epub 2016 Dec 5.
PubMed 27920153Watkins PB, Lewis JH, Kaplowitz N, Alpers DH, Blais JD, Smotzer DM, Krasa H, Ouyang J, Torres VE, Czerwiec FS, Zimmer CA. Clinical Pattern of Tolvaptan-Associated Liver Injury in Subjects with Autosomal Dominant Polycystic Kidney Disease: Analysis of Clinical Trials Database. Drug Saf. 2015 Nov;38(11):1103-13. doi: 10.1007/s40264-015-0327-3.
PubMed 26188764Lai Y, Mandlekar S, Shen H, Holenarsipur VK, Langish R, Rajanna P, Murugesan S, Gaud N, Selvam S, Date O, Cheng Y, Shipkova P, Dai J, Humphreys WG, Marathe P. Coproporphyrins in Plasma and Urine Can Be Appropriate Clinical Biomarkers to Recapitulate Drug-Drug Interactions Mediated by Organic Anion Transporting Polypeptide Inhibition. J Pharmacol Exp Ther. 2016 Sep;358(3):397-404. doi: 10.1124/jpet.116.234914. Epub 2016 Jun 17.
PubMed 27317801Brock WJ, Beaudoin JJ, Slizgi JR, Su M, Jia W, Roth SE, Brouwer KLR. Bile Acids as Potential Biomarkers to Assess Liver Impairment in Polycystic Kidney Disease. Int J Toxicol. 2018 Mar/Apr;37(2):144-154. doi: 10.1177/1091581818760746.
PubMed 29587557Ferslew BC, Xie G, Johnston CK, Su M, Stewart PW, Jia W, Brouwer KL, Barritt AS 4th. Altered Bile Acid Metabolome in Patients with Nonalcoholic Steatohepatitis. Dig Dis Sci. 2015 Nov;60(11):3318-28. doi: 10.1007/s10620-015-3776-8. Epub 2015 Jul 3.
PubMed 26138654
Study at a glance
From the registry record, last updated by the sponsor on 25 Mar 2020. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Endogenous Molecule Profiling in Subjects With Autosomal Dominant Polycystic Kidney Disease (ADPKD)
- ClinicalTrials.gov ID
- NCT03717883
- Acronym / sponsor ID
- 16-2984
- Keywords
- hepatic transporters
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 24 participants (actual)
- Lead sponsor
- University of North Carolina, Chapel HillUniversity, hospital or other
- Collaborators
- National Institute of General Medical Sciences (NIGMS)
- Study start
- 17 Sep 2018 (actual)
- Primary completion
- 29 Jan 2020 (actual)
- Study completion
- 29 Jan 2020 (actual)
- First posted
- 24 Oct 2018 (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.
This is a single center, comparative cohort study to investigate alterations in hepatic transporter function in subjects with autosomal dominant polycystic kidney disease (ADPKD) compared to healthy subjects and subjects with non-ADPKD renal disease. Eligible subjects will be 18-65 years of age and of any race/ethnicity and gender.
Detailed description
ADPKD is a relatively common genetic disease affecting about 1 out of every 1000 people worldwide. Progression of ADPKD is characterized by the proliferation of fluid-filled kidney cysts. Development of these cysts is progressive and can lead to end-stage renal disease and ultimately, renal failure in many patients. The most common extra-renal complication of ADPKD is the formation of liver cysts, which can vary from minor to extensive. Hepatic cysts can develop from medium-sized bile ducts and complications (i.e., cyst rupture, infection, obstruction of bile ducts, and compromised portal venous flow) can arise from increasing cystic burden. Previous studies have shown that elevated levels of endogenous molecules such as bile acids in ADPKD may indicate altered transporter function. Other endogenous molecules such as coproporphyrin (CP) I and III may be used as probes to assess hepatic transporter function.
The objective of this study is to investigate and quantify ADPKD-associated alterations in endogenous molecule profiles (e.g., bile acids, CP) relative to subjects with non-ADPKD renal disease and healthy individuals, and to investigate specific hepatic transporter polymorphisms that may be related to the alterations. This is important because subjects with ADPKD may be predisposed to adverse reactions associated with some medications that require hepatic transporters for excretion.
Potential study participants will be pre-screened over the phone and then scheduled for a 2-hour study visit. All urine samples within the 2-hour interval will be collected from all participants along with clinical, physical and questionnaire data. Fasting blood samples will be collected at time 0 and 120 min.
Study design
- Observational model
- Cohort
- Time perspective
- Other
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Healthy subjects | – | – |
| Subjects with ADPKD | – | – |
Who may qualify
- Ages
- 18 to 65 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
- Study population
- Healthy vs. ADPKD vs. non-ADPKD renal disease subjects
Key inclusion criteria (11 listed)
- Provide signed and dated informed consent
- Willing to comply with all study procedures and be available for the duration of the study
- Male or female, aged 18 to 65
- Negative quantitative human chorionic gonadotropin (hCG) blood test (for women of child-bearing age only)
- Normal liver functions tests (LFTs) as defined by the University of North Carolina (UNC) hospital laboratory reference range [aspartate aminotransferase (AST)14-38 U/L, alanine aminotransferase (ALT) 15-48 U/L, alkaline phosphatase 38-126 U/L]
Key exclusion criteria (25 listed)
- Donation of blood within the last 30 days
- Diagnosis of human immunodeficiency virus (HIV) and/or untreated hepatitis C virus (HCV)
- History of significant alcohol abuse and/or illicit drug use
- More than 1 glass of wine or 2 beers (or equivalent in % alcohol) per day during the 48 hours prior to study and/or screening visit
- Inability to fast for 8 hours prior to study and screening sample collection
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
Difference in serum coproporphyrin I and III concentrations
Time frame: 2 hours
nmol
2 secondary outcomes
Difference in serum and urine bile acid profiles
Time frame: 2 hours
Difference in renal clearance of coproporphyrin I and III
Time frame: 2 hours
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 25 Mar 2020.
- Background: PubMed 12191984Igarashi P, Somlo S. Genetics and pathogenesis of polycystic kidney disease. J Am Soc Nephrol. 2002 Sep;13(9):2384-98. doi: 10.1097/01.asn.0000028643.17901.42. No abstract available.
- Background: PubMed 14872199Boucher C, Sandford R. Autosomal dominant polycystic kidney disease (ADPKD, MIM 173900, PKD1 and PKD2 genes, protein products known as polycystin-1 and polycystin-2). Eur J Hum Genet. 2004 May;12(5):347-54. doi: 10.1038/sj.ejhg.5201162.
- Background: PubMed 24886261Cnossen WR, Drenth JP. Polycystic liver disease: an overview of pathogenesis, clinical manifestations and management. Orphanet J Rare Dis. 2014 May 1;9:69. doi: 10.1186/1750-1172-9-69.
- Background: PubMed 2598550Salam M, Keeffe EB. Liver cysts associated with polycystic kidney disease: role of Tc-99m hepatobiliary imaging. Clin Nucl Med. 1989 Nov;14(11):803-7. doi: 10.1097/00003072-198911000-00003.
- Background: PubMed 10597755Hofmann AF. The continuing importance of bile acids in liver and intestinal disease. Arch Intern Med. 1999 Dec 13-27;159(22):2647-58. doi: 10.1001/archinte.159.22.2647.
- Background: PubMed 12763363Zollner G, Fickert P, Silbert D, Fuchsbichler A, Marschall HU, Zatloukal K, Denk H, Trauner M. Adaptive changes in hepatobiliary transporter expression in primary biliary cirrhosis. J Hepatol. 2003 Jun;38(6):717-27. doi: 10.1016/s0168-8278(03)00096-5.
- Background: PubMed 14699511Kullak-Ublick GA, Stieger B, Meier PJ. Enterohepatic bile salt transporters in normal physiology and liver disease. Gastroenterology. 2004 Jan;126(1):322-42. doi: 10.1053/j.gastro.2003.06.005.
- Background: PubMed 26044126Munoz-Garrido P, Marin JJ, Perugorria MJ, Urribarri AD, Erice O, Saez E, Uriz M, Sarvide S, Portu A, Concepcion AR, Romero MR, Monte MJ, Santos-Laso A, Hijona E, Jimenez-Aguero R, Marzioni M, Beuers U, Masyuk TV, LaRusso NF, Prieto J, Bujanda L, Drenth JP, Banales JM. Ursodeoxycholic acid inhibits hepatic cystogenesis in experimental models of polycystic liver disease. J Hepatol. 2015 Oct;63(4):952-61. doi: 10.1016/j.jhep.2015.05.023. Epub 2015 Jun 1.
- Background: PubMed 26907622Shen H, Dai J, Liu T, Cheng Y, Chen W, Freeden C, Zhang Y, Humphreys WG, Marathe P, Lai Y. Coproporphyrins I and III as Functional Markers of OATP1B Activity: In Vitro and In Vivo Evaluation in Preclinical Species. J Pharmacol Exp Ther. 2016 May;357(2):382-93. doi: 10.1124/jpet.116.232066. Epub 2016 Feb 23.
- Background: PubMed 28325716Gilibili RR, Chatterjee S, Bagul P, Mosure KW, Murali BV, Mariappan TT, Mandlekar S, Lai Y. Coproporphyrin-I: A Fluorescent, Endogenous Optimal Probe Substrate for ABCC2 (MRP2) Suitable for Vesicle-Based MRP2 Inhibition Assay. Drug Metab Dispos. 2017 Jun;45(6):604-611. doi: 10.1124/dmd.116.074740. Epub 2017 Mar 21.
- Background: PubMed 27920153Devuyst O, Chapman AB, Gansevoort RT, Higashihara E, Perrone RD, Torres VE, Blais JD, Zhou W, Ouyang J, Czerwiec FS. Urine Osmolality, Response to Tolvaptan, and Outcome in Autosomal Dominant Polycystic Kidney Disease: Results from the TEMPO 3:4 Trial. J Am Soc Nephrol. 2017 May;28(5):1592-1602. doi: 10.1681/ASN.2016040448. Epub 2016 Dec 5.
- Background: PubMed 26188764Watkins PB, Lewis JH, Kaplowitz N, Alpers DH, Blais JD, Smotzer DM, Krasa H, Ouyang J, Torres VE, Czerwiec FS, Zimmer CA. Clinical Pattern of Tolvaptan-Associated Liver Injury in Subjects with Autosomal Dominant Polycystic Kidney Disease: Analysis of Clinical Trials Database. Drug Saf. 2015 Nov;38(11):1103-13. doi: 10.1007/s40264-015-0327-3.
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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. This study is not recruiting at the moment.
Vimal Derebail, MD, MPH principal investigator
University of North Carolina, Chapel Hill
Kim Brouwer, PharmD, PhD study director
University of North Carolina, Chapel Hill
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of ADPKD and Autosomal Dominant Polycystic Kidney Disease, run by University of North Carolina, Chapel Hill 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 11 inclusion and 25 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 25 Mar 2020. 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. 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?
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?
Difference in serum coproporphyrin I and III concentrations (time frame: 2 hours). 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 NCT03717883, which also lists 19 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 25 Mar 2020.