Cynthia Kenyon, Cindy Bayley, and Leonard Guarente, cofounders of Elixir Pharmaceuticals, have developed roundworms that reproduce vigorously and are remarkably good-looking, given that they live two to six times longer than unaltered worms--the human equivalent of 170 years. "It is miraculous," says Dr. Kenyon.

This is not supermarket tabloid fodder; the scientists' research on extending the life spans of worms, fruit flies, yeast, and mice has appeared in the journals Cell and Nature. Elixir, based in Cambridge, Massachusetts, in April recruited its CEO, Ed Cannon, from Dyax, a publicly held biotech company. In December, the venture capital firms Arch Venture Partners, Oxford Bioscience Partners, and Tredegar provided $8.5 million in funding; and Elixir is now looking to raise an additional $30 million.

Aging is not inevitable, the Elixir scientists assert, but is actually a process regulated by complex biochemical pathways that have persisted throughout evolution. By mutating single genes in these pathways, the scientists have extended the lives of laboratory animals. Elixir believes it can develop drug targets that will let humans remain young longer and will delay the onset of age-related disease. By 2005, Elixir hopes to be testing its drug targets on mice and signing partnerships with large pharmaceutical companies.

But some are skeptical. Tom Johnson, associate professor at the Institute for Behavioral Genetics in Boulder, Colorado, contends that while biochemical pathways in worms and fruit flies are the same as in mammals, the proteins don't necessarily behave the same way in humans. Dr. Johnson says developing antiaging drugs that work in humans will take years longer than Elixir hopes.

Another wrinkle: the October 19 issue of Cell features papers by Robert Weinberg; Dr. Guarente and his colleagues at the Massachusetts Institute of Technology's Whitehead Institute; and Wei Gu, along with his colleagues at Columbia University, that suggest a protein called SIR2, which Elixir manipulated to make worms and yeast live longer, regulates a cancer gene, P53. In mammals, a drug target that disturbs SIR2 could conceivably cause cancer cells to live when they would ordinarily die.

But Dr. Guarente denies that his paper contradicts Elixir's research. "The relationship between cell death and aging is not firmly established, but the link between SIR2 and P53 provides a clue that cell death may be a cause of aging," he says. "Aging on the one hand; cancer on the other hand--I don't think that there needs to be a trade-off. I think you could have a drug that would slow down aging and not promote cancer." Here's hoping youth doesn't have too high a price.