The LEV Foundation initiates RMR2, applying eight damage‐repair interventions to midlife mice with rapamycin baseline and exercise to assess lifespan and healthspan improvements.
Key points
- RMR2 begins mid-life (18–20 months) in C57BL/6J mice with rapamycin baseline and voluntary exercise to assess rejuvenation capacity.
- Eight interventions—including D-PUFAs, recombinant serum albumin, MSCs, partial reprogramming, IL-11 blockade, CASIN, LC-FACS inhibition, and oxytocin—target molecular and cellular aging mechanisms.
- Twenty treatment combinations across male and female cohorts (50 mice each, 2000 total) evaluate lifespan, morbidity, and functional decline metrics.
Why it matters: By testing combined molecular repair interventions in aged mice, RMR2 may reveal synergistic anti‐aging therapies to revolutionize longevity medicine.
Q&A
- Why include rapamycin across all groups?
- What are deuterated polyunsaturated fatty acids (D-PUFAs)?
- How does partial cellular reprogramming rejuvenate tissues?
- What is LC-FACS-based selective senolysis?