Abstract
Despite decades of effort, there is a pressing need for better in vitro cardiac and cardiotoxicity
models. Cardiovascular diseases (CVD) remain the leading global cause of death and cardiotoxicity is
responsible for a third of all pre-clinical pharmaceutical regulatory failures. While traditional models
(ex vivo and in vivo animal models, primary human tissue and immortalised cell lines) have provided
valuable insights, there remains a translational gap between the “bench and bedside” due to issues
with human-relevance, alongside well-characterized challenges with availability, throughput and
cost.
Researchers have therefore been turning to human iPSC-derived cardiomyocytes for their
potential to provide a limitless source of consistent, human-relevant cardiac cells. By taking donor
cells, reprogramming them to an iPSC state and then differentiating them into cardiomyocytes,
researchers can mimic human physiology in a scalable format, using these cells to power advanced
in vitro cardiac disease and cardiotoxicity models.
However, standard differentiation protocols can lead to less mature cardiomyocyte phenotypes,
impairing functional performance and therefore the utility of human iPSC-based models. Key
measures of immature phenotype include the following parameters: poor sarcomere alignment, low
cardiac maturity marker expression, greater levels of spontaneous beating, longer field potential
duration (FPD) and slower conduction velocity (CV).
Axol Bioscience, in collaboration with partner organizations, have been exploring a new
metabolic maturation media to enhance the maturity of human iPSC-derived cardiomyocytes,
enabling better models for cardiac research, disease and cardiotoxicity. This media is referred to as
‘cardiac maturation media’ in this poster.
