Inflammaging

Inflammaging is the chronic, low-grade, sterile inflammation that accompanies aging. It is not caused by infection. It is driven by the accumulation of senescent cells, mitochondrial dysfunction, and a lifetime of immune activation — and it is one of the strongest predictors of age-related disease.

Why it matters

Elevated circulating IL-6, TNF, and CRP in older adults predict frailty, sarcopenia, cardiovascular events, cognitive decline, and all-cause mortality. Inflammaging is not a cosmetic problem of aging — it is a driver of the diseases that define old age.

• Senescent cells stop dividing but do not die. They secrete a cocktail of inflammatory mediators — the senescence-associated secretory phenotype, or SASP.
• Chronic SASP exposure reprograms neighboring cells, spreads senescence, and degrades tissue function.
• The immune system itself ages: T-cell repertoire narrows, myeloid cells skew inflammatory, and resolution capacity declines.

The therapeutic opportunity

Senolytics — drugs that selectively clear senescent cells — have shown promise in early trials for frailty and osteoarthritis. But clearing senescent cells is only half the problem: the inflammatory environment they leave behind must also be resolved. We are developing therapies that combine senescent-cell targeting with active resolution signaling, aiming to reset the tissue environment rather than simply deplete one cell type.

Our approach

Our inflammaging program is preclinical. It pairs a senescent-cell-directed antibody with a pro-resolving mediator, and is being developed first for a well-defined geriatric indication with measurable inflammatory biomarkers.