June 8 (UPI) -- Preliminary tests of an experimental cancer drug appear to slow inflammation linked to heart disease, giving home for a new therapy, researchers said in a study released Thursday.
Details about the study, led by the New York University Grossman School of Medicine, are found in a report published in the journal Nature Cardiovascular Research.
The drug, saracatinib, already has been tested as a potential treatment for cancer, lung and Alzheimer's disease. Scientists say it may also have the potential of slowing the progression of atherosclerosis, which often leads to heart disease.
Grossman researchers explored the mechanisms behind atherosclerosis, in which fatty deposits build up in blood vessels. That buildup hardens into plaques and causes misplaced immune reactions or inflammation. The inflammation then blocks blood flow to cause heart attacks and strokes.
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In research, saracatinib appeared to reduce inflammation in more than 90% in human blood samples and diseased tissue samples.
"Our findings provide new insight into the inflammatory mechanisms in atherosclerosis and suggest for the first time that saracatinib may offer an effective therapy in cases where standard therapy, in the form of statins, fails to help," Letizia Amadori, a senior research scientist at NYU Langone Health and study's co-lead author, said in a news release.
In past research, scientists found that inflammation stubbornly persisted even when prescribing statins to reduce the harmful fats in the blood.
That persistence keeps patients at high risk for heart attacks and strokes. Equally, past anti-inflammatory treatments proved sometimes ineffective in addressing the issue in other studies.
In the study of saracatinib, researchers analyzed blood samples from 34 men and women with the condition specifically termed atherosclerotic cardiovascular disease, and all of whom were on statins, and compared them with samples from 24 healthy patients.
The authors looked at 4,823 genes, including 277 already known to play a role in inflammation and produce cytokines and other proteins that promote a chronic immune response.
Instead of trying to create a new drug, they looked at those already approved or being tested for other uses. They checked thousands of test results mapping the effects of various molecules, signaling proteins and genetic changes on human cells.
Since saracatinib had already been shown to target genes that lead to heart disease, it was chosen for further examination. The results showed that saracatinib blocks gene activity responsible for producing inflammatory proteins such as interleukin-1 beta and interleukin-6 that maintained atherosclerosis immune reactivity.
In rabbit testing, saracatinib reduced plaque-based inflammation by about 97% compared with untreated animals. In mice, the same therapy showed an 80% reduction in cells linked to inflammation in plaques and shrunk plaque deposits by up to 70% in some cases.
"Our reverse-engineering method of finding new uses for old drugs can in theory be harnessed to uncover therapies for practically any disease that involves inflammation," study senior author Chiara Giannarelli said.
"Since these chemicals have already been tested for safety, this technique offers a swift and cost-effective approach to pharmaceutical development."
