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Transforming the treatment of Cardio-Kidney-Metabolic (CKM) diseases

Centaurus Therapeutics is developing first-in-class therapies that target ceramides, a validated driver of cardio-kidney-metabolic diseases, to unlock transformative outcomes for patients.

Ceramides:
A  balancing act

Historically, ceramides were thought to be inert molecules, but research in the mid 1990s demonstrated their powerful role. Ceramides make up just 1% of lipids in the body but have a significant influence on health and disease. Ceramides, like cholesterol, are a type of lipid used for cell signaling but in excess they cause damage to mitochondria, alter metabolic pathways and trigger stress responses in vital organs.

Centaurus Therapeutics is a clinical-stage biotechnology company developing novel therapies for ceramide-driven diseases

Centaurus Therapeutics is a clinical-stage
biotechnology company developing novel
therapies for ceramide-driven diseases

Centaurus’ first-in-class therapies have been designed to target de novo ceramide synthesis to successfully and safely inhibit excess production and restore lipid balance.

Supported by strong human genetics, clear mechanistic insights and validated biomarkers, ceramide biology represents a promising new therapeutic avenue.

Lead asset: CNT2130 currently in clinical trials

A once-daily, oral DES1 inhibitor with demonstrated therapeutic activity across kidney, cardiac, hepatic, and metabolic endpoints. Supported by extensive human genetic validation and IND-enabling safety data, CNT2130 has a clear path to clinical proof-of-concept in CKM diseases and beyond.

The Centaurus approach

Our work centers on the upstream biology that controls ceramide production, opening new possibilities for treating multiple CKM diseases.

Our small-molecule candidates target and inhibit DES1, the enzyme that catalyzes the final step of de novo ceramide synthesis (converting dihydroceramide to ceramide).  DES1 presents a precise therapeutic opportunity to check an uncontrolled production cycle and address hyperceramidemia at its source before it triggers organ decline.