A groundbreaking study conducted on animals has revealed that a drug commonly used to treat multiple sclerosis could potentially aid in the recovery process of heart attack victims.
Dr. Rachel Sarig, a leading research scientist and the study’s head, explained that this widely prescribed drug works by suppressing inflammation in the body.
Given the essential role played by the immune system in heart repair, Dr. Sarig thought it would be worth investigating whether Copaxone (glatiramer acetate) could have a positive impact on the healing process. Much to her surprise, the drug was found to significantly enhance blood flow, a crucial element in the recovery of heart attack patients.
“While we expected a favorable outcome, we were taken aback by the robust effect of the drug,” Dr. Sarig expressed.
The researchers emphasized that this discovery holds immense significance, particularly because heart attack victims do not always seek immediate medical attention.
Through their experiments on mice, the team observed a considerable reduction in scar tissue in the heart muscles of those treated with Copaxone. The treated mice exhibited only small, insignificant scars, whereas the control group, which received no treatment, had large scars covering 30% or more of their left ventricles. Scar tissue hampers the heart’s ability to contract effectively and pump blood.
Given the high cost and slow production pace associated with developing new drugs, repurposing existing medications is an attractive alternative, the researchers explained.
In a separate experiment conducted during the study, rats remained untreated for an extended period after experiencing heart attacks. One group received treatment nearly one month after the event, by which time they had developed chronic heart failure, while the control group received no treatment at all.
Following a two-month treatment with glatiramer acetate, the rats showed a remarkable 30% improvement in blood-pumping rate per beat and a nearly 60% increase in the ventricles’ ability to contract. The strength with which the heart contracts indicates its capacity to pump blood efficiently throughout the body.
“The mice and rats used in these studies did not die, but they did suffer from impaired heart functions,” Dr. Sarig clarified.
Explaining the mechanism behind Copaxone’s efficacy, Dr. Sarig stated that the drug helps existing cells survive and contract effectively, stimulates the production of blood vessels that supply the cells, and delays scar tissue formation.
Despite the availability of generic versions of Copaxone on the market, securing further research support from pharmaceutical companies has proven challenging for the team.
Dr. Sarig, however, remains determined to develop and market this repurposed medication.
“The approval process for repurposed drugs is also faster and simpler compared to the development of new drugs,” Dr. Sarig pointed out, citing recent approvals like Colchicine for reducing cardiovascular events in patients with established cardiovascular disease. “We will seek funding from potential donors and explore options for slightly modifying the composition of glatiramer acetate or developing a combined treatment that can be patented. However, the quicker approach would be to utilize the existing approved substance.”
The study received support from the Sagol Institute for Longevity Research, the Helen and Martin Kimmel Institute for Stem Cell Research, and the Gabriella Schmidt Research Fellow Chair. The authors of the study declared no conflicts of interest.
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