Targeting the metabolic pathways that drive disease

Metabolism governs how every cell in the body senses energy, generates fuel, and responds to stress. When key metabolic pathways, AMPK and mTOR, are dysregulated by aging or chronic nutrient excess, the consequences are broad. Cambrian is developing therapeutics that restore these critical functions.

Metabolic decline underlies some of the world's most prevalent chronic diseases

Metabolism governs how every cell in the body senses energy, generates fuel, and responds to stress. When key metabolic pathways (AMPK and mTOR) decline with age, or are accelerated by obesity, the consequences are broad: excess fat accumulation, declining muscle function, impaired glucose regulation, and an accelerating slide toward cardiometabolic disease.

The two pathways that govern metabolism

Two interconnected signaling systems sit at the center of this decline: the AMPK network and mTOR. Together they govern whether a cell burns fuel or stores it, grows or maintains itself. When this balance breaks, with age or chronic nutrient excess, the consequences manifest as some of the most prevalent diseases in the world.

The AMPK network

AMPK is the master regulator of cellular energy balance. When energy demand rises, AMPK activates its signaling network, driving glucose and fatty acid uptake into the cell.

When the AMPK activity declines with age and chronic nutrient excess, cells lose the ability to adapt to shifts in energy demand, accelerating fat accumulation, insulin resistance, and metabolic disease.

Therapeutic Goal

Restore AMPK network activation to re-engage the cell's energy-sensing capacity and reverse downstream metabolic dysfunction.

mTOR regulation

mTOR is a central regulator of cellular growth and nutrient sensing, functioning through two distinct complexes: mTORC1, which promotes anabolic, pro-growth processes, and mTORC2, which supports metabolic homeostasis and immune function.

Chronic activation of mTORC1 drives sustained pro-growth signaling while suppressing essential cellular maintenance processes such as autophagy, which is responsible for clearing damaged proteins and organelles. This imbalance between growth and repair contributes to the accumulation of cellular damage the development of age-related disease.

Therapeutic Goal

Selectively inhibit mTORC1 while preserving mTORC2 activity, restoring the pulsatile balance that healthy cells maintain.

Accessibility Icon