How does this anticancer drug differ from existing cancer treatments?

Unlike conventional chemotherapies, which also harm normal cells and cause horrific side effects, this drug is designed to target cancer's distinctive metabolism. In vitro, it harms cancer cells but not normal cells.

What cancers has this drug been shown to work against?

It has been shown to work against many different cancers, including breast and lung cancers, in independent testing by the National Cancer Institute (USA).

How might this drug slow aging?

The drug boosts IF1 protein, which slows metabolic rate. Species with more IF1 protein — and lower metabolic rates — age slower and live longer. In mice, increasing IF1 protein has been shown to slow aging by an established marker.

How can I support this cancer research?

You can donate directly to fund the research, or support it by buying IF1 skincare — the profits from which fund our cancer research.

Attacking Cancer’s Achilles’ Heel, Immortality, and Possibly Gifting Us All a Longer Life

New Anticancer Drug Selectively Harms Cancer and May Slow Aging

Why haven’t we cured cancer?

The problem is that present anticancer drugs also harm normal cells. Causing horrific side effects, which kill many and make many others abandon treatment. Millions die of cancer per year. The solution would be a drug that only harms cancer. Unlike normal cells, cancers are immortal. Cancer can kill its patient and live on forever if looked after. This difference is because of cancer’s distinctive metabolism. Our pioneering paper reports a drug designed to target this abnormal metabolism, which harms cancer cells but not normal cells in vitro.

Chemical structure of the anticancer drug candidate — a deuterated small molecule featuring imidazole, dichlorophenyl, cyanobenzoyl, and 4-chloroanilino groups — Chemical structure of the anticancer drug candidate.

To illustrate, Henrietta Lacks died of cancer a long time ago but her cancer is still alive today and is studied in laboratories worldwide. Demonstrating cancer’s immortality, a clear difference from normal cells, which this drug attacks. It turns cancer’s distinctive strength, immortality, into its weakness. Shown to work for many different cancers, such as breast and lung cancers, in independent testing by the National Cancer Institute (USA).

Bar chart showing percentage decrease in cancer growth across NCI-60 cell lines — breast, prostate, renal, ovarian, skin, CNS, colon, lung cancers, and leukemias — after treatment with the anticancer drug candidate — Independent National Cancer Institute (USA) testing across diverse human cancer cell lines.

Moreover, as designed and demonstrated in mice, this drug doesn’t simply leave normal cells unharmed. It helps them, making their metabolism more efficient, permitting a lower metabolic rate. Humans and other species with a lower metabolic rate live longer.

Indeed, this same paper reports that different mammal species have diverse life spans due to differing metabolic rates, where more IF1 protein confers a slower metabolic rate, thereby a slower aging rate. Explaining, for example, how a whale can live centuries longer than a mouse. The paper shows that increasing IF1 protein in mice slows aging, as measured by an established marker of aging.

A drug to slow aging is desperately wanted, and has been since the dawn of humanity. It would be a single drug for the many, varied diseases of aging, such as Alzheimer’s disease.

Most cancer research never gets to the point of a new anticancer drug, whereas we have. Please consider supporting our medical research by making a donation. And/or you can support by using our skincare. Thank you.

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