snake venom
Scientists used molecules in the Tropidolaemus wagleri snake's venom to design antiplatelet drugs. gbohne/Wiki Creative commons

Snake venom could form the basis of new, safer antiplatelet drugs, scientists have announced.

Antiplatelet drugs prevent blood cells called platelets from aggregating together and forming blood clots – thereby reducing the risk of heart attack.

However, these medications can also have serious side effects, including excessive bleeding after an injury. Scientists are thus attempting to develop safer antiplatelet drugs with limited bleeding side effects.

In a study now published in the journal Arteriosclerosis, Thrombosis and Vascular Biology, researchers describe a drug based on molecules which are found in snake venom.

They have designed it to interact with the protein glycoprotein VI (also known as GPVI), which is found on the surface of platelets.

Tropidolaemus wagleri snake

In recent years, a number of studies has showed that platelets that are missing GPVI on their surface do not form blood clots. Furthermore the risk of severe bleeding is reduced.

This led researchers to think that blocking GPVI could prevent blood clotting while avoiding the bleeding side effects of common antiplatelet drugs.

The authors of the new study, from the National Taiwan University, had previously published a paper showing thattrowaglerix, a protein in the venom of the Tropidolaemus wagleri snake - also known as the Wagler's pit viper - could bind to GPVI proteins and block their activity.

This is the commonest type of pit viper in South-east Asia and although they are venomous, they are not considered to be aggressive.

The new antiplatelet drug the scientists now describe contains a molecule based on the structure of trowaglerix. When mixed with blood, it appeared to prevent platelets from clotting.

Heart health
Antiplatelet drugs are given to limit the risk of heart attack. iStock

The scientists then tested the new drug in mice. They found that the animals who received it had slower blood clot formation compared to untreated mice. Furthermore, the treated mice did not bleed longer than untreated mice, suggesting that the worse side effect of antiplatelet drugs was avoided with this medication.

More research will now be needed to see if the drug is safe and effective in humans. Efforts to improve the drug's design and increase the duration of its effects in the body are also underway.

"In general, this type of molecule design does not last long in the body, so we'll have to improve formulation or delivery system to extend the exposure time in the human body," said co-author Jane Tseng. "The design must also be optimised to ensure that the molecule only interacts with GPVI and not other proteins which can cause unintended reactions."