At CSHL, BioAge showed that suppressing NLRP3, the protein that drives chronic inflammation in aging, restored mobility, feeding behavior, and social contact in old mice to young-animal levels; a related compound is already in two Phase 2 human trials
At CSHL, BioAge showed that suppressing NLRP3, the protein that drives chronic inflammation in aging, restored mobility, feeding behavior, and social contact in old mice to young-animal levels; a related compound is already in two Phase 2 human trials
At the Cold Spring Harbor Laboratory conference "Mechanisms of Aging 2026" (September 22 to 26), biotech company BioAge Labs presented a poster on an experiment in 21-month-old mice: daily dosing with compound BAL-1901 brought their locomotion speed, time spent eating and drinking, and group behavior in line with younger mice of the same strain. BAL-1901 is an analog of BGE-102, the compound BioAge is testing in humans in two Phase 2 trials targeting cardiovascular risk and diabetic macular edema.
NLRP3 is a sensor of the innate immune system. With age, it triggers sterile inflammation, a response to the body's own damaged cells that accumulate over a lifetime. As early as 2013, the Pennington Biomedical Research Center showed that mice lacking the Nlrp3 gene have reduced baseline inflammation and that older animals show improved memory and motor coordination. In 2020, Spanish researchers found that these mice also live longer. These findings made NLRP3 a drug target.
For the poster, BioAge used mice aged 21 months (advanced old age for a strain that lives two to two and a half years) and dosed them daily with either plain vehicle or BAL-1901 at 20 mg/kg. A group of 12-month-old mice served as young controls. All animals were monitored around the clock by in-cage cameras and microphones, recording steps, speed, time at the feeder and water bottle, and distance between cagemates.
Untreated old mice moved more slowly and less overall, spent longer eating, drank less, and maintained different spacing from cagemates compared to the younger group. After the course of BAL-1901, the gap nearly disappeared: locomotion speed and distance approached the young group's levels, eating and drinking time normalized, and the former social spacing returned.
Acute infection triggers a similar set of responses: reduced movement, reduced feeding, reduced social contact. The body conserves resources for fighting the pathogen, and the threat is recognized by the same NLRP3 pathway. In old mice, the same program runs chronically and without any infection, simply because of accumulated damage. This is why a single inhibitor shifts all three measures at once.
The related molecule, BGE-102, completed Phase 1, in which the inflammatory marker hsCRP fell by 86%, and is now in two Phase 2 human trials: QUELL-CV for cardiovascular risk (enrollment closed, results pending) and QUELL-DME for diabetic macular edema (started September 8, 2026, approximately 180 participants).
BAL-1901 and BGE-102 are related but distinct molecules from the same BioAge pipeline: the poster validates the NLRP3 target itself, while both human trials use BGE-102. The company justifies the target with its own analyses linking NLRP3 activity to all-cause mortality in humans; a peer-reviewed publication has not yet appeared. The poster's authors are exclusively BioAge employees, including CEO Kristen Fortney.
In June 2026, researchers published in Science Advances a study of mice with a heterozygous Nlrp3 knockout, a model that more closely mirrors the effect of a drug than the earlier complete knockout. In these mice, by 16 months inflammation does not subside but accelerates: the body upregulates the related protein NLRP1, which together with the remaining NLRP3 amplifies the same inflammatory response. Suppressing both proteins worked better than suppressing NLRP3 alone. In humans, BGE-102 works the same way: it reduces NLRP3 activity without shutting it down completely.