The science

Go to the roots.See what connects.

Aging is a major risk factor for many chronic diseases. Gerotherapeutics target biological processes that can contribute to dysfunction across tissues.

Shared biology

Different branches.Common roots.

Cellular stress, inflammation, and changes in tissue repair can influence several diseases at once. Understanding these connections creates opportunities to intervene upstream.

We apply this perspective to oncology, fibrosis, neurodegeneration, and healthy aging.

Illustration of a tree rooted in aging, with branches leading to age-related diseases including cancer, dementia, diabetes, heart disease, and arthritis.
Diagram of the hallmarks of aging arranged around a central sphere, with cellular senescence highlighted.
Hallmarks of aging

Cellular senescence is one of the best-characterized hallmarks of aging, and one of the most tractable for small-molecule medicines.

Current focus

Cellular senescence

Senescent cells stop dividing and can accumulate with age, stress, or injury. Their signals can promote inflammation and alter surrounding tissues.

We discover senotherapeutics designed to selectively remove harmful senescent cells or modulate their activity.

A shared target

Across tissues.
Across disease areas.

One biological process can create opportunities in oncology, fibrosis, neurodegeneration, and healthy aging.

Where we focus

Why thesediseases.

We prioritize settings where senescent cells are abundant, where their contribution to disease is well supported, and where patients need better options.

  • Oncology

    Chemotherapy and radiation induce senescence in tumor and surrounding cells. Persisting senescent cells can promote inflammation, recurrence, and treatment resistance, which makes them a target alongside standard therapy.

  • Fibrosis

    Senescent cells accumulate in fibrotic liver, lung, and kidney, where their secretions keep pro-fibrotic programs switched on long after the original injury.

  • Neurodegeneration

    Senescent glial cells build up in the aging brain and are associated with neuroinflammation and decline in models of neurodegenerative disease.