The primary mechanism of action for low-dose rapamycin in longevity is inhibiting mTOR. Reduced inflammation is an important side effect, but mTOR inhibition is the goal. It mimicks fasting, causing cells to ramp up autophagy—a natural process by which organisms recycle half-functioning cells (senescent cells) and use the proteins to build new cells that function properly and don’t produce toxic byproducts.

mTOR inhibition is not the only pathway in cellular metabolism that triggers autophagy, but it’s a major one with a measurable effect.

In simpler terms, inhibiting mTOR by fasting (or by mimicking fasting with intermittent low-dose rapamycin), signals that times are tough and pushes organisms to hunker down for survival. This is good, because it promotes better overall health at a cellular level. The reduction of toxic byproducts from senescent cells is likely a driver of the reduced inflammation that has been observed.

That said, “anti-aging” is a cringey buzzword that hurts the credibility of the field.

Rapamycin has the most promise of any longevity intervention, with over 20 years of research and results that have been reproduced by the NIH.

It’s difficult to fund a clinical trial in humans for this particular use of rapamycin, however, because there is no profit motive for pharmaceutical companies. FDA approval for new uses of an off-patent drug won’t make pharma companies rich. The same problem exists for research on many traditional medicines.