Despite major advances in medicine, cardiometabolic and fibrosis-driven diseases such as heart failure, chronic kidney disease, and myelofibrosis remain among the leading causes of morbidity and mortality worldwide. These conditions share underlying mechanisms of inflammation, cellular injury, and maladaptive tissue remodeling that lead to progressive organ failure. Yet, disease-modifying treatments remain limited or entirely absent.

At SEQUANTRIX, we are driving the next generation of disease-modifying therapies through AI, deep molecular understanding and translational models that mirror human biology. Cross-organ chronic diseases, fibrosis, regeneration and inflammation are central pathogenic features, and our platform enable the discovery of therapeutic interventions that restore tissue integrity and function.

Kidney Disease

CKD affects roughly one in ten adults worldwide, progressing silently toward renal failure. Existing interventions slow, but rarely halt, disease progression. New approaches are urgently needed to target key mechanisms such as tubular regeneration, glomerular injury leading to proteinuria, inflammation, fibrosis, and cyst formation in disorders like ADPKD.

Chronic kidney disease affects around 10% of the global population and remains a major unmet medical need. SEQUANTRIX develops advanced 2D and 3D organoid and tubuloid models to uncover and validate novel targets for tubular regeneration, anti-inflammation, and anti-fibrosis. Our research extends to glomerular pathologies—addressing proteinuria and disease mechanisms in rare diseases such as adult polycystic kidney disease (ADPKD).

Through one of the world’s largest multimodal single-cell and spatial genomic datasets from patients, animal models and complex organoid models, we select and validate preclinical models that closely reflect human renal disease. Our organoid and tubuloid models allow modeling tubule-interstitial injury, immune cell recruitment, glomerular and podocyte damage and cyst formation.

Heart Failure

Heart failure affects more than 60 million people globally and is the final common pathway of many cardiovascular conditions. Current therapies mainly provide symptomatic relief but do not reverse cardiomyocyte loss, fibrosis, or the chronic inflammation that drives disease progression. There is a pressing need for treatments that restore heart structure and function at a cellular level.

Heart failure, a leading cause of death worldwide, arises from complex interactions among cardiomyocytes, fibroblasts, vascular, and immune cells. SEQUANTRIX focuses on uncovering mechanisms driving fibrosis, inflammation, metabolic dysfunction, and cardiomyocyte loss. Using integrated cardiac organoid systems, spatial and single-cell atlases, and refined mouse models, we accelerate the discovery of therapeutic strategies that restore cardiac structure and function.

Myelofibrosis

Myelofibrosis is a severe myeloproliferative neoplasm with limited curative options. Current therapies primarily target the malignant hematopoietic clone, leaving the diseased stromal microenvironment unaddressed. The critical crosstalk between malignant and stromal cells drives fibrosis and marrow failure—representing a missed therapeutic opportunity that urgently needs to be addressed.

Myelofibrosis is a debilitating bone marrow disorder where current therapies largely target the malignant hematopoietic clone, overlooking the critical role of the stromal niche. SEQUANTRIX brings a new perspective by focusing on the interactions between malignant clones and the bone marrow stroma—particularly stromal cell heterogeneity, activation, and expansion. Our multimodal single-cell and spatial platforms, combined with advanced bone marrow models, enable a deeper understanding of fibrosis and the cellular crosstalk driving disease progression.

Fibrotic Diseases

Across organ systems, fibrosis represents a convergent endpoint of chronic injury and inflammation, affecting the heart, kidney, liver, lung, and bone marrow. Anti-fibrotic strategies have lagged behind other therapeutic areas, and there remains a broad, unmet need for interventions that directly modulate fibrotic remodeling, restore normal tissue architecture, and prevent organ failure.