A study published in the journal Science Translational Medicine, claims the development of a new drug that prevents the formation of blood clots without increasing the risk of bleeding— a side effect attributed to most of the antiplatelet medications currently available.
The researchers, in the study, detailed the drug and its mechanism of delivery and also demonstrated that the drug is a functional treatment for heart attacks in animal models. Xiaoping Du, author of the study, said, "Unfortunately, current antiplatelet medications prevent the blood clotting that causes heart attack and stroke but also disrupt platelets' ability to stop bleeding if a blood vessel is torn."
"The magic of this new drug is it prevents clots but does not make people prone to bleeding, which other drugs have failed to do," added Du.
Targetting Signaling Mechanism
In a previous study, the research team identified a signaling mechanism that is important in the blood clotting process but not required for platelets' ability to adhere to a wound and prevent bleeding. Based on this finding, the researchers derived a peptide to target the signaling mechanism and designed a nanoparticle that successfully delivered the peptide into platelets.
The peptide-derived nanoparticle drug -- called M3mP6 high-loading peptide nanoparticle, of HLPN -- was then tested in mice as a possible treatment for heart attacks. Du said a heart attack can cause heart failure and death in two different ways. One, from the initial damage caused by the clot, which blocks blood flow and reduces oxygen supply.
Drug Reduces Damage The Heart
This typically is treated by a procedure called angioplasty and a stent to open the artery, combined with antiplatelet drugs to prevent it from clotting again. However, fresh blood flowing into the damaged heart tissue following the reopening of the artery can trigger inflammation, causing leaks and clots in small blood vessels and further damage to the heart, the researchers said.
"This is called reperfusion injury and this is the second way a heart attack can lead to heart failure or death," Du said. In the study, among mice that received the treatment, administered as an injection, there was reduced damage to the heart, reduced clotting, and reduced inflammation. There also was improved heart function and improved survival.
"It is very exciting to see such promising results in the lab and we hope to one day test this in humans," Du said. "We were hopeful that this new drug, which does not cause blood vessel leaks, would help limit reperfusion injury and reduce the chance of heart failure and death," the study authors wrote.
(With inputs from agencies)