Mesoblast - Model CHF - Revascor

CHF is characterized by an enlarged heart and insufficient blood flow to the organs and extremities of the body. The condition, which affects 2% of the adult population of the United States, is progressive and can be caused by many factors that put an excess demand on the heart muscle such as high blood pressure, faulty valves, infections or congenital heart problems. CHF prevalence is expected to grow 46% by 2030, affecting more than 8 million Americans¹.

CHF is classified in relation to the severity of the symptoms experienced by the patient. The most commonly used classification system was established by the New York Heart Association (NYHA) and ranges from Class I (mild) to Class IV or end stage (severe).

Patients with advanced or Class II/III heart failure disease continue to represent the greatest unmet medical need despite recent advances in new therapies.

Revascor consists of 150 million mesenchymal precursor cells (MPCs) administered by direct injection into the heart muscle in patients suffering from CHF and progressive loss of heart function.

MPCs release a range of factors when triggered by specific receptor-ligand interactions within damaged tissue. Based on preclinical data, it is believed that these factors induce functional cardiac recovery by simultaneous activation of multiple pathways, including induction of endogenous vascular network formation, reduction in harmful inflammation, reduction in cardiac scarring and fibrosis, and regeneration of heart muscle through activation of tissue precursors.

In July 2019, Circulation Research published a Special Article, titled ‘Phase 3 DREAM-HF Trial of Mesenchymal Precursor Cells in Chronic Heart Failure; A Review of Biological Plausibility and Implementation of Flexible Clinical Trial Design’, highlighting the important potential clinical benefits of MPCs as immunotherapy in patients with advanced chronic heart failure. The Special Article highlighted that cardiac inflammation drives heart failure progression, and concluded that based on preclinical and Phase 2 clinical data there is a biologic rationale for the use of MPCs in targeting this inflammatory process in order to improve heart failure outcomes.