Tissue Dynamics and Galmed Pharmaceuticals have announced a collaboration to develop a novel human chronic cardiac fibrosis model designed to accelerate the discovery and development of new Aramchol-based therapeutic approaches for complex fibrotic heart diseases. Cardiac fibrosis is a major driver of chronic heart failure, including long-term remodeling after Myocardial Infarction (MI) and heart failure with preserved ejection fraction, or HFpEF.

Cardiovascular disease remains the leading cause of death globally, responsible for an estimated 20.5 million deaths in 2025. Despite this burden, there are no approved therapies that directly and durably reverse cardiac fibrosis. The disease is increasingly understood as a failure of tissue repair rooted in metabolic dysfunction: disturbed lipid uptake, oxidation, storage, and signaling can drive lipotoxicity, mitochondrial dysfunction, inflammation, fibroblast activation, and impaired regenerative remodeling.

SCD1, a key enzyme controlling monounsaturated fatty-acid synthesis and membrane-lipid composition, sits at the center of this biology. Studies have shown SCD1 upregulation in experimental heart failure and linked cardiac SCD activity to lipid overload, collagen gene expression, hypertrophy, and cardiac dysfunction, while SCD also influences angiogenesis and energy metabolism in the hypoxic myocardium after myocardial infarction.

A central obstacle in cardiac fibrosis has been the lack of models capable of reproducing chronic, multicellular, mechanically active, metabolically dynamic human disease. Animal models and short-term in vitro assays often fail to capture the long-term transition from injury response to persistent fibrosis, particularly in diseases such as MI and HFpEF where human metabolism, vascular function, inflammation, and tissue mechanics interact over time.

Regulators are now explicitly encouraging more human-relevant approaches. The US Food and Drug Administration (FDA) has described a 'transformative shift' toward advanced human-relevant methods, including AI-powered models and human organ-on-chip systems, and has stated that New Approach Methodologies (NAMs) can improve predictivity, identify mechanisms of action, and support safer clinical development. The FDA has also announced plans to promote human organoids and organ-on-chip systems that mimic human organs, including heart models, while the EMA supports regulatory acceptance of scientifically sound NAMs and provides interaction routes for developers through its Innovation Task Force.

Tissue Dynamics and Galmed are collaborating on the development of the new platform as a high-throughput, human-centered model of chronic cardiac fibrosis, with an initial focus on the long-term effects of MI and the fibrotic-metabolic remodeling associated with HFpEF. The platform will combine Tissue Dynamics' highly physiological vascularised, multichambered cardiac organoids with embedded metabolic sensors, massive automation, and continuous real-time monitoring. Tissue Dynamics' DynamiX platform is designed to test more than 20,000 human organoids in parallel, capturing real-time functional kinetics through embedded metabolic sensors and generating longitudinal human-relevant data across metabolism, fibrosis, electrical conduction, inflammatory signaling, lipid handling, and stress pathways.

The collaboration comes at a pivotal moment for Aramchol's drug development. In the new cardiac fibrosis program, the companies intend to apply Galmed's expertise in SCD1 biology and metabolic-pathway modulation to human cardiac disease settings where lipid imbalance may impair vascular repair, cardiomyocyte function, fibroblast behavior, and extracellular-matrix remodeling. By monitoring thousands of organoids over time and applying AI-driven analysis to functional, metabolic, structural, and molecular endpoints, the model is expected to support rapid evaluation of Aramchol-based candidates, combinations, dosing strategies, and disease-stage-specific interventions.

Galmed aims to use this platform to develop and investigate new Aramchol-based therapies for chronic cardiac fibrotic disease.

Dr Avner Ehrlich, CEO, Tissue Dynamics, said, "We believe that combining Tissue Dynamics' human cardiac organoid technology, embedded sensors, automation, and AI with Galmed's expertise in modulating fibrotic pathways gives us a unique opportunity to change how cardiac fibrosis therapies are developed. The ability to model chronic human fibrosis in real time and at scale could allow us to investigate interventions that do more than delay disease progression. If we can identify approaches that improve tissue repair and help resolve fibrosis by correcting the underlying metabolic dysfunction, this has the potential to be a game changer for patients and for drug development in this field."