We develop therapeutics to directly target the heart, using an authentic human cardiac organoid discovery engine.
Heart failure affects 4% of the US population, yet treatment options are primarily symptomatic, including blood thinners, assistive devices and heart transplant. Patients today face a 50% 5-year survival rate upon diagnosis.
It’s time to change that.
Our approach is to engineer human cardiac organoids that function similarly to adult human heart tissue, enabling us to directly target therapeutics to the heart. We aim to address the root cause of heart failure and restore heart function.
We’ve developed HeartDyno, our cardiac organoid discovery engine, using scalable, authentic and predictive cardiac organoids that reflect adult heart phenotype, toxicology, and physiological function. HeartDyno combines these with a deep multi-omics data approach, uncovering novel therapeutic targets and candidates that offer better efficacy and safety profiles in humans.
Engineered from stem cells at scale
Mature phenotype and physiology
Translates to clinical observation
March, 2021
QIMR Berghofer researchers in collaboration with Dynomics and Resverlogix have discovered some of the ways COVID-19 damages the heart, and identified a class of drugs that could potentially protect or reverse this cardiac injury.
April, 2020
Structural and functional changes following infarction in a human heart can be modeled with human cardiac organoids set in hypoxic gradient and stimulated with the neurotransmitter noradrenaline.
March, 2019
When it comes to determining whether new drugs will be effective, our team looked to mini beating human hearts. Thousands of them.
September, 2017
“A switch in a newborn’s metabolism means this ability to regenerate heart tissue disappears, usually within a week. Now we have identified the process that causes this to occur, we believe there could be an opportunity to reactivate regeneration in adult hearts.”
March, 2017
Using stem cells we bioengineer a beating human heart muscle, as well as heart tissue that is able to repair itself.
Mills, R. J. et al. Bromodomain and Extraterminal Inhibition Blocks Inflammation-Induced Cardiac Dysfunction and SARS-CoV-2 Infection (Pre-Clinical). bioRxiv 2020.08.23.258574 (2021)
Mills, R. J. et al. Drug Screening in Human PSC-Cardiac Organoids Identifies Pro-proliferative Compounds Acting via the Mevalonate Pathway. Cell Stem Cell 24, 895-907.e6 (2019).
Mills, R. J. & Hudson, J. E. Bioengineering adult human heart tissue: How close are we? APL Bioengineering 3, 010901 (2019).
Voges, H. K. et al. Development of a human cardiac organoid injury model reveals innate regenerative potential. Development 144, 1118–1127 (2017).
Mills, R. J. et al. Functional screening in human cardiac organoids reveals a metabolic mechanism for cardiomyocyte cell cycle arrest. PNAS 114, E8372–E8381 (2017).
Quaife-Ryan, G. A. et al. β-Catenin drives distinct transcriptional networks in proliferative and nonproliferative cardiomyocytes. Development 147, (2020).
Quaife-Ryan G. A. et al. Multicellular Transcriptional Analysis of Mammalian Heart Regeneration. Circulation 136, 1123–1139 (2017).
Porrello, E. R. et al. Transient Regenerative Potential of the Neonatal Mouse Heart. Science 331, 1078–1080 (2011).
Molecules to restore heart function.