Cardiol Therapeutics Inc. announced that study results demonstrate the active pharmaceutical ingredient ("API") in CardiolRxTM inhibits and also promotes the reversal of mechanisms known to play a role in the occurrence and development of fibrotic CVD. The data were presented by its research collaborators from Houston Methodist DeBakey Heart & Vascular Center at The Annual Scientific Meeting of the Heart Failure Society of America ("HFSA2022"). The poster entitled "Cannabidiol Inhibits Endothelial-to-Mesenchymal Transition and also Promotes the Reverse Process in vitro" was presented within the "Basic and Translational Science" category of the HFSA2022 Scientific Programme.

The authors concluded that the API in CardiolRxTM protects cardiac function and exhibits an anti-fibrotic effect, possibly mediated by endothelial-to-mesenchymal transition.EndoMT is a complex biological process whereby an endothelial cell, the main cell type found in the inside lining of blood vessels, undergoes a series of molecular events that alter its characteristics towards a mesenchymal cell, such as a myofibroblast. Myofibroblast cells are the primary cells during wound healing and fibrosis. Mounting evidence indicates EndoMT is involved in adult CVD, and the mechanism has been described to contribute to myocardial fibrosis, an important part of heart remodelling that can lead to heart failure.

In the study, EndoMT was induced in HUVEC cells, a model system for studying human endothelial cell function, using a combination of agents (L-NAME and angiotensin-II). EndoMT was characterized through immunofluorescence ("IF") for endothelial (CD31) and mesenchymal (Vimentin) markers. CardiolRxTM was added during the EndoMT induction process, and on Day 4 following induction IF studies were performed.

CardiolRxTM was shown to reduce the expression of the mesenchymal marker Vimentin in a dose dependent manner. Separately, CardiolRxTM was added to EndoMT transitioned cells (after Day 4 of EndoMT), and IF studies were performed on Day 8. In this experiment CardiolRxTM was shown to reduce Vimentin expression, suggesting reversal of EndoMT in vitro. This provides evidence that the cardioprotective properties of CardiolRxTM are due, in part, to the modulation of EndoMT.