Preliminary research shows new cancer drug FY26 can shut down a cancer cell’s metabolism. Researchers are hopeful that in the future, the drug will have fewer risks and can be produced at a lower cost than current treatments for ovarian and bowel cancer.

Researchers at the University of Warwick say testing shows new cancer drug FY26 is 49 times more potent than Cisplatin, an intravenous chemotherapy drug used to treat a variety of cancers.

The new drug could also cause less harm to healthy cells than current treatments.

FY26 was developed using osmium, a rare precious metal. It could prove more effective in cancer cells that are resistant to platinum-based drugs.

The researchers believe it could also be produced at a lower cost.

The Wellcome Trust Sanger Institute carried out testing on 809 cancer cell lines. The National Cancer Institute USA tested 60 cell lines and came up with similar results. Details of the research are published in the journal PNAS.

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All cells need energy to survive. When cells are healthy, they use their mitochondria to generate that energy. Mitochondria act as mini power plants for healthy cells.

Cancer cells have defective mitochondria. They turn to metabolic activity in their cytoplasm for their energy supply. It’s a matter of survival.

The key to FY26’s success is that it forces cancer cells to go back to using mitochondria. Unable to get energy, the cancer cells die.

Professor Peter Sadler of the University of Warwick’s Department of Chemistry was the lead researcher. He explained that platinum-based drugs can’t distinguish between cancerous and noncancerous cells.

“This can lead to a wide range of side effects, from renal failure to neurotoxicity, ototoxicity, nausea, and vomiting,” he said.

Current drugs can also lose effectiveness after the first course.

“Our new osmium compound, with its different mechanism of action, remains active against cancer cells that have become resistant to drugs such as Cisplatin,” said Sadler.

This type of research could lead to improved survival rates for some forms of cancer.

According to co-researcher Isolda Romero-Canelón, Ph.D., one in two people will develop some kind of cancer during their lifetime.

“It is clear that a new generation of drugs is necessary to save more lives,” she said. “And our research points to a highly effective way of defeating cancerous cells.”

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While patients are understandably anxious for more effective treatments, the process can be lengthy. Sadler told Healthline that FY26 was discovered about five years ago.

“We wanted to advance towards the clinic more quickly, but FY26 is an unconventional drug with an unusual mechanism of action,” he said.

“FY26 is multi-targeted consensus, whereas in recent years there has been a widespread belief that new drugs need to have single targets,” Sadler added. “However, it has become apparent that cancer cells can readily become resistant to single-target drugs and that multi-targeted drugs might be more effective.”

Sandler believes progress with FY26 and related compounds will be speeding up. Despite his optimism, he told Healthline a lot of hurdles in the drug development pipeline remain. He’d like to be ready for clinical trials within three years.

“That might not sound as hopeful as people might like, but we are learning a lot as we progress,” he said. “Not least, that FY26 might be particularly effective against cancer cells which have mutations in their mitochondrial DNA.”

Down the road, doctors may be better able to tailor treatment to individual patients.

“We would hope that in the future, genetic screening of patients will aid decisions on the best drug for the patient to receive,” said Sadler.

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