One part of longevity research is to screen as many as possible existing drugs on cells and lower animals to see what effect they have; it's a first step that may then lead on to finding epigenetic changes to replicate the effect, and then uncover the underlying mechanisms which may point towards novel longevity mutations. This is a long road - consider that researchers still don't fully understand calorie restriction, for example, never mind more recently discovered effects. Here is an open access paper that illustrates how this research process works. Note that the choice of compounds to check is steered by regulation rather than by scientific knowledge - not a good situation: "Screening a library of drugs with known safety profiles in humans yielded 30 drugs that reliably protected mammalian neurons against glucose toxicity. Subsequent screening demonstrated that 6 of these 30 drugs increase lifespan in C. elegans: caffeine, ciclopirox olamine, tannic acid, acetaminophen, bacitracin, and baicalein. Every drug significantly reduced the age-dependent acceleration of mortality rate. These protective effects were blocked by RNAi inhibition of cbp-1 in adults only, which also blocks protective effects of dietary restriction. Only 2 drugs, caffeine and tannic acid, exhibited a similar dependency on DAF-16. Caffeine, tannic acid, and bacitracin also reduced pathology in a transgenic model of proteotoxicity associated with Alzheimer's disease. These results further support a key role for glucose toxicity in driving age-related pathologies and for CBP-1 in protection against age-related pathologies. These results also provide novel lead compounds with known safety profiles in human for treatment of age-related diseases, including Alzheimer's disease and diabetic complications."