Peer reviewed – experimental study - animals
An experimental cancer drug could stop osteoporosis and help women stay slim after the menopause – according to new research from the University of East Anglia.
A study published today reveals that a compound originally designed to fight cancer may not only protect against osteoporosis - but could also reduce body fat and reverse some of the metabolic changes linked to menopause.
The drug, known as CADD522, was developed to block a protein which helps drive the growth and spread of several cancers.
But scientists found the treatment appeared to strengthen bones in post-menopausal mice while also helping them stay leaner.
Lead researcher Dr Darrell Green, from UEA's Norwich Medical School, said: "Osteoporosis affects around one in three women over the age of 50, leaving sufferers vulnerable to painful fractures that can seriously impact quality of life.
"Current treatments exist, but many are plagued by side effects, safety concerns or inconvenient dosing schedules that make long-term use difficult.
"We have uncovered an entirely new way of tackling the disease.
"We found that a drug originally developed to stop cancer could help millions of women facing the twin challenge of fragile bones and midlife weight gain.
"We hope our work could lead to a new generation of osteoporosis treatments that tackle bone loss while also addressing some of the wider metabolic consequences of menopause."
How the research happened
Researchers used mice that had undergone surgery to mimic the hormonal changes seen after menopause.
Animals treated with CADD522 for eight weeks showed significant improvements in bone health. Scans revealed increased bone volume and better preservation of the delicate honeycomb-like structures inside bones that are crucial for strength and resilience.
Blood tests suggested the drug stimulated new bone growth, while not interfering with the body's normal process of breaking down and rebuilding bone.
Dr Green said: "This is particularly important because many existing osteoporosis drugs work by suppressing bone loss, which can sometimes lead to complications when used for long periods.
"But the biggest surprise came when we looked beyond bone health.
"The mice receiving CADD522 weighed less than their untreated counterparts despite eating the same amount of food.
"They also had less body fat and fewer fat deposits accumulating inside their bone marrow - a process that is commonly seen after menopause and is linked to declining bone health."
The team also examined brain tissue and found the drug appeared to reverse several menopause-related changes in fatty acids.
Levels of beneficial omega-3 fats, including DHA, remained largely intact, while a number of other lipid abnormalities shifted back towards healthier patterns.
Dr Green said: "We didn't directly test for memory or thinking ability, but our work raises questions about whether this drug could one day help address wider menopause-related health problems."
The treatment's prospects as a future medicine also received a boost from safety testing.
Experiments in mice, rats and dogs found CADD522 could be taken orally and was well tolerated.
The team also found the drug appeared to be metabolised more slowly in human tissue than in rodents, potentially improving its performance in people.
"This is still in the early stages and has so far only been tested in animals but we hope that the benefits will translate to humans to ultimately reduce fracture rates," added Dr Green.
This research was led by UEA in collaboration with the University of Maryland (US), the Scintillon Research Institute in San Diego (US) and the University of Stirling (Scotland).
Safety testing was funded by The Sir William Coxen Trust as part of CADD522's development as a childhood cancer treatment.
'RUNX2 inhibitor CADD522 improves bone microarchitecture and lipid metabolism in post-menopausal bone loss' is published in the journal npj Drug Discovery.
