Our Progress: Congenital Long QT Syndrome & Drug-Induced Long QT
We have rapidly advanced our portfolio of SGK1 inhibitors to investigate their use as precision therapeutics in various genetic arrhythmias. So far, our progress includes:
Repeated positive in vitro effects on APD90 (a surrogate for QT interval) using our lead SGK1 inhibitor in cardiomyocytes derived from LQTS patient stem cells of all three major Long QT subtypes (type 1, 2, and 3).
Repeated positive in vitro effects of our lead SGK1 inhibitor in a dofetilide model of drug-induced Long QT using stem cell derived cardiomyocytes and in the langendorff-perfused guinea pig model.
Completion of all pre-clinical animal toxicology studies necessary for initiation of clinical studies in humans.
Completion of the Phase 1 healthy volunteer study, showing:
LQT-1213 was well tolerated with good bioavailability and predictable pharmacokinetics.
Mild concentration dependent reductions in QTcF were seen with a single dose of LQT-1213.
Data from our WAVE I Part 1 clinical proof of efficacy study: LQT-1213 Rapidly and Meaningfully Reduces QT Interval in Individuals with Prolonged QT Induced by Dofetilide. Read More.
Initiation of our WAVE I: Part 2 study to evaluate the safety, tolerability, and pharmacokinetics of our compound in patients diagnosed with congenital Long QT Syndrome Types 1, 2 & 3. Learn More.
Initiation of our Non-Interventional "My QT Wave" study where we hope to change the lives of people with Long QT Syndrome Type 2 and Type 3 expected to start in 2025.
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Long QT Syndrome (LQTS) is a rare genetic condition that causes an elongation between the Q and T waves during a heartbeat. The lengthening of the interval can lead to unexpected and life-threatening arrhythmias called torsades de pointes. These arrhythmias are generally in response to exercise and stress.
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A prolonged QT interval can be caused by any number of environmental factors including acute and chronic use of certain prescription medications. These therapeutics are prescribed despite the risks of QT prolongation as the risk of a developing an arrhythmia is outweighed by the benefit of the intervention where limited options are available. This risk is obviously more severe in patients with underlying risk factors including cLQTS.
Our Progress: Atrial Fibrillation & Heart Failure
Demonstration of preventive effect of a SGK1 inhibitor in an animal model of high-fat diet induced-atrial fibrillation.
IND/CTA-enabling preclinical studies are completed.
Healthy volunteer Phase 1 study commenced in Q2 2024.
Two, independent, two-hit animal models heart failure with preserved ejection fraction (HFpEF) to evaluate the effect of SGK1 inhibition commenced in Q4 2023 with data expected in H1 2024.
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Atrial Fibrillation is a type of arrhythmia (irregular heart rhythm) which may present as a rapid, slow, or abnormal heart rate. These arrhythmias reduce the ability of the heart to efficiently to pump blood and may lead to blood clots localized in the heart which can dislodge and increase the risk of stroke, heart failure and other heart-related complications.