Arrhythmogenic CardiomyopathyPhase 2TaRGETNCT06174220
Targeted Therapy With Glycogen Synthase Kinase-3 Inhibition for Arrhythmogenic Cardiomyopathy
A Phase 2 study testing Tideglusib in people with Arrhythmogenic Cardiomyopathy and Arrhythmogenic Right Ventricular Cardiomyopathy, run by Hamilton Health Sciences Corporation at 17 sites in Canada.
Trial summary
The TaRGET study is a multi-centre, prospective, randomized, double-blind, placebo-controlled trial designed to evaluate the potential therapeutic efficacy of tideglusib, a glycogen synthase kinase-3 β inhibitor, in genotype positive arrhythmogenic cardiomyopathy. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Arrhythmogenic Cardiomyopathy, Arrhythmogenic Right Ventricular Cardiomyopathy
- What is being tested?
- Tideglusib
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 120 participants
- Where
- 17 sitesCanada
- Study dates
- 21 Mar 2025to 1 Jul 2027
- Phase
- Phase 2
- Are there results?
- Not yet: the study is under way
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 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- A pathogenic or likely pathogenic desmosomal (PKP2, DSG2, DSC2, DSP, or JUP*) rare variant OR the TMEM43-p.S358L variant
- JUP carriers must be homozygous or compound heterozygous
- Mean ≥ 500 PVCs per 24 hours on a baseline screening 7-day Holter monitor
- Clinical ACM diagnosis or recognition of genetic carrier status for ≥ 6 months prior to screening
Who cannot join
- NYHA class IV heart failure
- Ventricular scar secondary to coronary artery disease
- Initiation, cessation, or dose change of a Class I or III anti-arrhythmic drug in the 3 months prior to screening
- Any potentially harmful chronic liver disease
- ALT value > 2X the upper limit of the normal reference range at Screening
- Total bilirubin value greater than the upper limit of the normal reference range at Screening, unless documented Gilbert's syndrome. For individuals with Gilbert's syndrome, total bilirubin value greater than 2-fold the upper limit of the normal reference range at Screening.
Show all 14Show fewer
- A history of alcohol or illicit substance use disorders
- Regular and long-term use of strong CYP3A4 inhibitors, including clarithromycin, telithromycin, ketoconazole, itraconazole, posaconazole, nefazodone, idinavir and ritonavir
- Serum creatinine > 150 micromole/L or creatinine clearance ≤ 60 mL/min (according to Cockcroft-Gault formula) at Screening
- Pregnant at time of enrollment and women of childbearing age who do not use a highly effective form of contraception
- Males, engaged in sexual relations with a female of child-bearing potential, not using an acceptable contraceptive method if not surgically sterile
- Patients unwilling to provide informed consent or comply with follow-up
- Hypersensitivity to tideglusib or any components of its formulation, including allergy to strawberry
- Concurrent use of drugs metabolized by CYP3A4 with a narrow therapeutic window e.g. warfarin and digoxin
Trial locations and contacts
17 sites in 1 country. Contact the study team or a site near you to ask about taking part.
Maha Mushtaha contact
17 sites in 1 country
Canada17 sites, 17 recruiting
- Recruiting
University of Calgary
Calgary, Alberta, T2N 2T9
Erkan Ilhan, 403-210-6047, erkan.ilhan@ucalgary.ca
Erkan Ilhan, MD
- Recruiting
Nova Scotia Health
Halifax, Nova Scotia, B3H 2Y9
Victoria Newman, 902-473-5341, victoria.newman@nshealth.ca
David Lee, MD
- Recruiting
Hamilton General Hospital
Hamilton, Ontario, L8L 2X2
Jeff Healey, 905-527-0271 ext. 40312, jeff.healey@phri.ca
Jeff S Healey, MD
- Not yet recruiting
Kingston General Hospital
Kingston, Ontario, K7L 2V7
Chris Simpson, MD
Amar Thakrar, MD
- Recruiting
London Health Sciences Centre
London, Ontario, N6A 5A5
Sara El-Richani, 519-685-8500 ext. 36808, lhrp.research@lhsc.on.ca
Habib R Khan, MD
- Recruiting
Montreal Heart Institute
Montreal, Quebec, H1T 1C8
Jeremie Cortial, 514-376-3330 ext. 2293, jeremie.cortial@icm-mhi.org
Julia Cadrin-Tourigny, MD PhD
- Not yet recruiting
McGill University Health Centre
Montreal, Quebec, H4A 3J1
Jacqueline Joza, MD
Michael Chetrit, MD
- Not yet recruiting
Hopital du Sacré-Coeur de Montréal
Montreal, Quebec, H4J 1C5
Leila Laroussi, MD
Alexios Hadjis, MD
- Not yet recruiting
Newmarket Electrophysiologist Research Group 'NERG'
Newmarket, Ontario, L3Y 2P9
Mouhannad Sadek, MD
Molly Thangaroopan, MD
- Not yet recruiting
University of Ottawa Heart Institute
Ottawa, Ontario, K1Y 4W7
Simon Hansom, MD
Martin Green, MD
- Recruiting
University Institute of Cardiology and Pneumology of Quebec
Québec, Quebec, G1V 4G5
Dr. Christian Steinberg, 418-656-8711, christian.steinberg@criucpq.ulaval.ca
Christian Steinberg, MD
- Recruiting
Heart Health Institute Research Inc
Scarborough Village, Ontario, M1E 4B9
Emily Magimaidoss, 416-281-9499 ext. 3015, emagimaidoss@hearthealthinstitute.net
Bhavanesh Makanjee, MD
- Recruiting
NL Health Services
St. John's, Newfoundland and Labrador, A1B 3V6
Stephen Duffett, 709-752-4636, stephen.duffett@easternhealth.ca
Stephen Duffett, MD
- Not yet recruiting
Sunnybrook Health Sciences Centre
Toronto, Ontario, M4N 3M5
Christopher Cheung, MD
Idan Roifman, MD
- Not yet recruiting
St. Michael's Hospital
Toronto, Ontario, M5B 1W8
Paul Angaran, MD
Geraldine Ong, MD
- Recruiting
University of British Columbia
Vancouver, British Columbia, V6Z 1Y6
Thomas Roston, 604-682-2344 ext. 66863, rostonm@alumni.ubc.ca
Thomas M Roston, MD PhD
- Recruiting
Victoria Cardiac Arrhythmia Trials Inc.
Victoria, British Columbia, V8Z 0B9
May Woodburn, 250-595-0400, mwoodburn@catrials.org
Martin van Zyl, MD
About this study
The TaRGET study is a multi-centre, prospective, randomized, double-blind, placebo-controlled trial designed to evaluate the potential therapeutic efficacy of tideglusib, a glycogen synthase kinase-3 β inhibitor, in genotype positive arrhythmogenic cardiomyopathy.
Read the detailed description
Arrhythmogenic cardiomyopathy (ACM) is a heritable form of structural heart disease characterized by myocardial fibrosis that confers vulnerability to malignant ventricular arrhythmias and sudden cardiac death (SCD). A subgroup of cases preferentially involves the right ventricle and is termed arrhythmogenic right ventricular cardiomyopathy (ARVC). Although an increasingly diverse set of genes have been implicated in ACM, its most prominent genetic culprits are constituents of the desmosome, a specialized cellular structure within the intercalated disc that mediates intercellular adhesion. An additional ACM genetic subtype develops secondary to the TMEM43-p.S358L variant and is associated with an aggressive clinical phenotype, particularly among males.
Despite dramatic progress in unravelling the genetic underpinnings of ACM, insight into its pathophysiology remains modest. A lack of understanding of its operative biological pathways has rendered development of tailored treatments challenging, leading to approaches to medical therapy being largely adopted from those utilized for more common forms of cardiomyopathy. An implantable cardioverter defibrillator (ICD) is recommended for prevention of SCD for all ACM patients considered high risk for malignant ventricular arrhythmias, however does not address its underlying pathophysiology. Subsequent prevention of painful ICD shocks for ventricular tachycardia often requires interventions that may carry modest efficacy and significant risks for adverse events, including anti-arrhythmic drugs and invasive combined endo- and epicardial catheter ablation procedures.
In 2014, a high-throughput screen of a library of bioactive compounds against a zebrafish model of ACM identified a small molecule classified as a glycogen synthase kinase-3 (GSK3) inhibitor that successfully prevented and rescued the phenotype, findings that have subsequently been reproduced in a series of ACM murine models. GSK3 is an enzyme that modulates the activity of a broad spectrum of intracellular signaling pathways, including the canonical Wnt/β-catenin pathway, whose suppression has been suggested to exert an important role in ACM pathogenesis.
Tideglusib is an oral GSK3β inhibitor with an established safety profile in humans. Driven by promising findings observed for tideglusib in ACM mouse models, we now seek to evaluate its potential efficacy in a randomized clinical trial involving genotype positive ACM patients.
- Being tested
- Tideglusib, Placebo
- Keywords
- sudden cardiac death, ventricular cardiomyopathy, genetics, arrhythmia
- Medical subject headings
- Arrhythmogenic Right Ventricular Dysplasia, Death, Sudden, Cardiac, Arrhythmias, Cardiac
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
TideglusibDrug
Tideglusib 1g po daily
PlaceboDrug
Matching placebo 1g po daily
| Study group | Role | What they receive |
|---|---|---|
| Tideglusib | Active comparator | Randomization to Tideglusib 1g po daily or matching placebo Receives: Drug: Tideglusib |
| Placebo | Placebo comparator | Randomization to matching placebo 1g po daily Receives: Drug: Placebo |
What is being measured
The primary outcome is the main question the study is designed to answer.
PVC burden
Change in mean PVC count per 24 hours on 7-day Holter
Measured: Baseline and 6 months
Secondary outcomes (3)
Ventricular strain
Change in ventricular strain on echocardiography
Measured: Baseline and 6 months
Implantable cardioverter-defibrillator (ICD) therapies
Number of ICD therapies (shock or anti-tachycardia pacing)
Measured: Baseline and 6 months
Sustained ventricular tachycardia (VT) events
Number of sustained VT events (defined as symptomatic or duration > 30 seconds and > 100bpm)
Measured: Baseline and 6 months
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted18 Dec 2023
- Study start21 Mar 2025
- Primary completion1 Feb 2027 (estimated)
- Study completion1 Jul 2027 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (5)Papers the sponsor has linked to this study.
- Other trials for Arrhythmogenic CardiomyopathyStudies 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
- Interventional
- Phase
- Phase 2
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Model description
- Patients will be randomized in a 1:1 ratio using an automated central, web-based system within 30 days of completing their baseline Holter. Randomization will be stratified by TMEM43-p.S358L variant status.
- Masking
- Quadruple blind
- Who is masked
- Participant, Care provider, Investigator, Outcomes assessor
- Enrolment
- 120 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Hamilton Health Sciences Corporation
- Sponsor type
- University, hospital or other
- Collaborators
- Canadian Institutes of Health Research (CIHR), Canadian SADS, AMO Pharma Limited, Hearts in Rhythm Organization (HiRO), Population Health Research Institute
- Responsible party
- Sponsor
- Investigators
- Jason D Roberts, MD MAS, Principal investigator, McMaster University and Population Health Research Institute
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06174220
- Sponsor's protocol ID
- PHRI.TaRGET
- Acronym
- TaRGET
- Status last verified
- Apr 2025
- First submitted
- 1 Dec 2023
- Last updated
- 12 Mar 2026
- Results posted
- No
- Data monitoring committee
- Yes
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Krahn AD, Wilde AAM, Calkins H, La Gerche A, Cadrin-Tourigny J, Roberts JD, Han HC. Arrhythmogenic Right Ventricular Cardiomyopathy. JACC Clin Electrophysiol. 2022 Apr;8(4):533-553. doi: 10.1016/j.jacep.2021.12.002.
PubMed 35450611Asimaki A, Kapoor S, Plovie E, Karin Arndt A, Adams E, Liu Z, James CA, Judge DP, Calkins H, Churko J, Wu JC, MacRae CA, Kleber AG, Saffitz JE. Identification of a new modulator of the intercalated disc in a zebrafish model of arrhythmogenic cardiomyopathy. Sci Transl Med. 2014 Jun 11;6(240):240ra74. doi: 10.1126/scitranslmed.3008008.
PubMed 24920660Chelko SP, Asimaki A, Andersen P, Bedja D, Amat-Alarcon N, DeMazumder D, Jasti R, MacRae CA, Leber R, Kleber AG, Saffitz JE, Judge DP. Central role for GSK3beta in the pathogenesis of arrhythmogenic cardiomyopathy. JCI Insight. 2016 Apr 21;1(5):e85923. doi: 10.1172/jci.insight.85923.
PubMed 27170944Roberts JD, Murphy NP, Hamilton RM, Lubbers ER, James CA, Kline CF, Gollob MH, Krahn AD, Sturm AC, Musa H, El-Refaey M, Koenig S, Aneq MA, Hoorntje ET, Graw SL, Davies RW, Rafiq MA, Koopmann TT, Aafaqi S, Fatah M, Chiasson DA, Taylor MR, Simmons SL, Han M, van Opbergen CJ, Wold LE, Sinagra G, Mittal K, Tichnell C, Murray B, Codima A, Nazer B, Nguyen DT, Marcus FI, Sobriera N, Lodder EM, van den Berg MP, Spears DA, Robinson JF, Ursell PC, Green AK, Skanes AC, Tang AS, Gardner MJ, Hegele RA, van Veen TA, Wilde AA, Healey JS, Janssen PM, Mestroni L, van Tintelen JP, Calkins H, Judge DP, Hund TJ, Scheinman MM, Mohler PJ. Ankyrin-B dysfunction predisposes to arrhythmogenic cardiomyopathy and is amenable to therapy. J Clin Invest. 2019 Jul 2;129(8):3171-3184. doi: 10.1172/JCI125538. eCollection 2019 Jul 2.
PubMed 31264976Padron-Barthe L, Villalba-Orero M, Gomez-Salinero JM, Dominguez F, Roman M, Larrasa-Alonso J, Ortiz-Sanchez P, Martinez F, Lopez-Olaneta M, Bonzon-Kulichenko E, Vazquez J, Marti-Gomez C, Santiago DJ, Prados B, Giovinazzo G, Gomez-Gaviro MV, Priori S, Garcia-Pavia P, Lara-Pezzi E. Severe Cardiac Dysfunction and Death Caused by Arrhythmogenic Right Ventricular Cardiomyopathy Type 5 Are Improved by Inhibition of Glycogen Synthase Kinase-3beta. Circulation. 2019 Oct;140(14):1188-1204. doi: 10.1161/CIRCULATIONAHA.119.040366. Epub 2019 Sep 5.
PubMed 31567019
Study at a glance
From the registry record, last updated by the sponsor on 12 Mar 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Targeted Therapy With Glycogen Synthase Kinase-3 Inhibition for Arrhythmogenic Cardiomyopathy
- ClinicalTrials.gov ID
- NCT06174220
- Acronym / sponsor ID
- TaRGET / PHRI.TaRGET
- Keywords
- sudden cardiac death, ventricular cardiomyopathy, genetics, arrhythmia
- Phase
- Phase 2
- Study type
- Interventional
- Recruitment status
- Recruiting
- Enrolment
- 120 participants (estimated)
- Lead sponsor
- Hamilton Health Sciences CorporationUniversity, hospital or other
- Collaborators
- Canadian Institutes of Health Research (CIHR), Canadian SADS, AMO Pharma Limited, Hearts in Rhythm Organization (HiRO), Population Health Research Institute
- Study start
- 21 Mar 2025 (actual)
- Primary completion
- 1 Feb 2027 (estimated)
- Study completion
- 1 Jul 2027 (estimated)
- First posted
- 18 Dec 2023 (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.
The TaRGET study is a multi-centre, prospective, randomized, double-blind, placebo-controlled trial designed to evaluate the potential therapeutic efficacy of tideglusib, a glycogen synthase kinase-3 β inhibitor, in genotype positive arrhythmogenic cardiomyopathy.
Detailed description
Arrhythmogenic cardiomyopathy (ACM) is a heritable form of structural heart disease characterized by myocardial fibrosis that confers vulnerability to malignant ventricular arrhythmias and sudden cardiac death (SCD). A subgroup of cases preferentially involves the right ventricle and is termed arrhythmogenic right ventricular cardiomyopathy (ARVC). Although an increasingly diverse set of genes have been implicated in ACM, its most prominent genetic culprits are constituents of the desmosome, a specialized cellular structure within the intercalated disc that mediates intercellular adhesion. An additional ACM genetic subtype develops secondary to the TMEM43-p.S358L variant and is associated with an aggressive clinical phenotype, particularly among males.
Despite dramatic progress in unravelling the genetic underpinnings of ACM, insight into its pathophysiology remains modest. A lack of understanding of its operative biological pathways has rendered development of tailored treatments challenging, leading to approaches to medical therapy being largely adopted from those utilized for more common forms of cardiomyopathy. An implantable cardioverter defibrillator (ICD) is recommended for prevention of SCD for all ACM patients considered high risk for malignant ventricular arrhythmias, however does not address its underlying pathophysiology. Subsequent prevention of painful ICD shocks for ventricular tachycardia often requires interventions that may carry modest efficacy and significant risks for adverse events, including anti-arrhythmic drugs and invasive combined endo- and epicardial catheter ablation procedures.
In 2014, a high-throughput screen of a library of bioactive compounds against a zebrafish model of ACM identified a small molecule classified as a glycogen synthase kinase-3 (GSK3) inhibitor that successfully prevented and rescued the phenotype, findings that have subsequently been reproduced in a series of ACM murine models. GSK3 is an enzyme that modulates the activity of a broad spectrum of intracellular signaling pathways, including the canonical Wnt/β-catenin pathway, whose suppression has been suggested to exert an important role in ACM pathogenesis.
Tideglusib is an oral GSK3β inhibitor with an established safety profile in humans. Driven by promising findings observed for tideglusib in ACM mouse models, we now seek to evaluate its potential efficacy in a randomized clinical trial involving genotype positive ACM patients.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Quadruple blind (participant, care provider, investigator, outcomes assessor)
- Number of arms
- 2
- Model description
- Patients will be randomized in a 1:1 ratio using an automated central, web-based system within 30 days of completing their baseline Holter. Randomization will be stratified by TMEM43-p.S358L variant status.
| Arm | Type | Receives |
|---|---|---|
| Tideglusib | Active comparator | Drug: TideglusibRandomization to Tideglusib 1g po daily or matching placebo |
| Placebo | Placebo comparator | Drug: PlaceboRandomization to matching placebo 1g po daily |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (4 listed)
- A pathogenic or likely pathogenic desmosomal (PKP2, DSG2, DSC2, DSP, or JUP*) rare variant OR the TMEM43-p.S358L variant
- JUP carriers must be homozygous or compound heterozygous
- Mean ≥ 500 PVCs per 24 hours on a baseline screening 7-day Holter monitor
- Clinical ACM diagnosis or recognition of genetic carrier status for ≥ 6 months prior to screening
Key exclusion criteria (14 listed)
- NYHA class IV heart failure
- Ventricular scar secondary to coronary artery disease
- Initiation, cessation, or dose change of a Class I or III anti-arrhythmic drug in the 3 months prior to screening
- Any potentially harmful chronic liver disease
- ALT value > 2X the upper limit of the normal reference range at Screening
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 |
|---|---|---|
| TideglusibTideglusib 1g po daily | Drug | Tideglusib |
| PlaceboMatching placebo 1g po daily | Drug | Placebo |
Primary outcome
PVC burden
Time frame: Baseline and 6 months
Change in mean PVC count per 24 hours on 7-day Holter
3 secondary outcomes
Ventricular strain
Time frame: Baseline and 6 months
Implantable cardioverter-defibrillator (ICD) therapies
Time frame: Baseline and 6 months
Sustained ventricular tachycardia (VT) events
Time frame: Baseline and 6 months
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 12 Mar 2026.
- Background: PubMed 35450611Krahn AD, Wilde AAM, Calkins H, La Gerche A, Cadrin-Tourigny J, Roberts JD, Han HC. Arrhythmogenic Right Ventricular Cardiomyopathy. JACC Clin Electrophysiol. 2022 Apr;8(4):533-553. doi: 10.1016/j.jacep.2021.12.002.
- Background: PubMed 24920660Asimaki A, Kapoor S, Plovie E, Karin Arndt A, Adams E, Liu Z, James CA, Judge DP, Calkins H, Churko J, Wu JC, MacRae CA, Kleber AG, Saffitz JE. Identification of a new modulator of the intercalated disc in a zebrafish model of arrhythmogenic cardiomyopathy. Sci Transl Med. 2014 Jun 11;6(240):240ra74. doi: 10.1126/scitranslmed.3008008.
- Background: PubMed 27170944Chelko SP, Asimaki A, Andersen P, Bedja D, Amat-Alarcon N, DeMazumder D, Jasti R, MacRae CA, Leber R, Kleber AG, Saffitz JE, Judge DP. Central role for GSK3beta in the pathogenesis of arrhythmogenic cardiomyopathy. JCI Insight. 2016 Apr 21;1(5):e85923. doi: 10.1172/jci.insight.85923.
- Background: PubMed 31264976Roberts JD, Murphy NP, Hamilton RM, Lubbers ER, James CA, Kline CF, Gollob MH, Krahn AD, Sturm AC, Musa H, El-Refaey M, Koenig S, Aneq MA, Hoorntje ET, Graw SL, Davies RW, Rafiq MA, Koopmann TT, Aafaqi S, Fatah M, Chiasson DA, Taylor MR, Simmons SL, Han M, van Opbergen CJ, Wold LE, Sinagra G, Mittal K, Tichnell C, Murray B, Codima A, Nazer B, Nguyen DT, Marcus FI, Sobriera N, Lodder EM, van den Berg MP, Spears DA, Robinson JF, Ursell PC, Green AK, Skanes AC, Tang AS, Gardner MJ, Hegele RA, van Veen TA, Wilde AA, Healey JS, Janssen PM, Mestroni L, van Tintelen JP, Calkins H, Judge DP, Hund TJ, Scheinman MM, Mohler PJ. Ankyrin-B dysfunction predisposes to arrhythmogenic cardiomyopathy and is amenable to therapy. J Clin Invest. 2019 Jul 2;129(8):3171-3184. doi: 10.1172/JCI125538. eCollection 2019 Jul 2.
- Background: PubMed 31567019Padron-Barthe L, Villalba-Orero M, Gomez-Salinero JM, Dominguez F, Roman M, Larrasa-Alonso J, Ortiz-Sanchez P, Martinez F, Lopez-Olaneta M, Bonzon-Kulichenko E, Vazquez J, Marti-Gomez C, Santiago DJ, Prados B, Giovinazzo G, Gomez-Gaviro MV, Priori S, Garcia-Pavia P, Lara-Pezzi E. Severe Cardiac Dysfunction and Death Caused by Arrhythmogenic Right Ventricular Cardiomyopathy Type 5 Are Improved by Inhibition of Glycogen Synthase Kinase-3beta. Circulation. 2019 Oct;140(14):1188-1204. doi: 10.1161/CIRCULATIONAHA.119.040366. Epub 2019 Sep 5.
- Individual participant dataSharing planned: No
Related trials for Arrhythmogenic Cardiomyopathy
RecruitingPhase 2
Statin Effect on Arrhythmogenic Cardiomyopathy Disease Progression (SEARCH)
Arrhythmogenic Cardiomyopathy
RecruitingObservational study
PKP2-ACM Natural History Study
Cardiomyopathies, Heart Diseases
RecruitingObservational study
Subcutaneous Implantable Cardioverter-defibrillator (S-ICD) Eligibility Over Time in Arrhythmogenic Cardiomyopathy
Arrhythmogenic Cardiomyopathy
RecruitingObservational study
Cardiomyopathies and Heart Muscle Diseases: Cardiac Imaging in the Evaluation of Myocardial Fibrosis Transition
Heart Failure With Preserved Ejection Fraction, Hypertrophic Cardiomyopathy
RecruitingObservational study
Cardiovascular Multimodality Imaging Study
Non-ischemic Cardiomyopathy, Cardiomyopathies
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.
Maha Mushtaha contact
Jason D Roberts, MD MAS principal investigator
McMaster University and Population Health Research Institute
17 sites in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 2 study testing Tideglusib in people with Arrhythmogenic Cardiomyopathy and Arrhythmogenic Right Ventricular Cardiomyopathy, run by Hamilton Health Sciences Corporation at 17 sites in Canada.
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 4 inclusion and 14 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: looking for participants now, as of the sponsor's last update on 12 Mar 2026. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 17 sites in Canada. 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 2 studies give the treatment to a larger group to see whether it has the intended effect and to keep checking safety.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
Contact Jason Roberts, MD MAS (905-521-2100 ext. 40354, jason.roberts@phri.ca), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
PVC burden (time frame: Baseline and 6 months). 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 NCT06174220, which also lists 5 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 12 Mar 2026.