MK-8722 AMPK activator extended lifespan in C. elegans and improved metabolic measures in aged mice
In this abstract, the AMPK activator MK-8722 extended lifespan in C. elegans in an AMPK-dependent way and, given to mice from 18 to 24 months, reduced body fat and blocked some age-related metabolic declines. These are preclinical findings, not evidence of human lifespan benefit. [1]
Automatic summary · not editorially reviewed
The key findings
MK-8722 is described as a specific, potent pharmacologic AMPK activator tested for lifespan in C. elegans and healthspan in aged mice. [1]
Treatment from adulthood extended lifespan in an AMPK-dependent manner in wildtype and csb-1 mutant C. elegans without impairing motility or reproduction. [1]
Mice treated from 18 to 24 months of age showed reduced body fat, blocked age-associated declines in fasting blood glucose and enhanced circadian rhythmicity in respiratory quotient. [1]
The source at a glance
- Study type / format
- Preclinical experimental study (abstract)
- Population / context
- C. elegans (wildtype and csb-1 mutants) and mice aged 18 to 24 months
- Summary based on
- Study abstract
- Publication status
- Preprint · peer-review status not confirmed
- Original publication
- April 23, 2026
MK-8722 tested in worms and aged mice
The abstract describes testing a specific, potent pharmacologic AMPK activator, MK-8722, for lifespan in C. elegans and healthspan in aged mice. AMPK is described as a conserved master regulator of energy metabolism, and dysregulated energy metabolism as a hallmark of aging. The authors note that direct genetic AMPK activation extends lifespan in multiple species, which frames the pharmacologic approach.
Supporting source [1]
Worm lifespan and mouse metabolic outcomes
Treatment from adulthood significantly extended lifespan in an AMPK-dependent manner in both wildtype and Cockayne syndrome model csb-1 mutant C. elegans, without impairing motility or reproductive capacity. Mice treated from 18 until 24 months of age had significantly reduced body fat accumulation, blocked age-associated declines in fasting blood glucose and enhanced circadian rhythmicity in respiratory quotient. Liver RNA sequencing showed fewer inflammation-related and more sterol metabolic pathways, consistent with increased sterol-derived metabolites including lithocholic acid, described as a proposed mediator of caloric restriction benefits.
Supporting source [1]
Preclinical scope of the MK-8722 findings
The results are presented as support for pharmacologic AMPK activation as a promising gerotherapeutic strategy. Lifespan was measured in worms, while the mouse work addressed metabolic and liver measures over 18 to 24 months of age, not mouse lifespan. The abstract does not report human data, and the full text was not reviewed.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Lifespan was measured in C. elegans, while mouse outcomes were metabolic and liver measures, not mouse lifespan. No human data are reported.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Altintas Ö, Knufinke M, Mann CG, Langston PK, Rabinowitz JD, Murphy CT, Ewald CY, Mitchell SJ, MacArthur MR. · europepmc.org · April 23, 2026