By James Gamble via SWNS

The venom of one of the world’s deadliest spiders could provide life-saving treatment for victims of heart attacks.

A molecule in the venom of funnel-web spiders was found to prevent cells in the heart from dying due to lack of oxygen during heart attacks and strokes in preclinical tests.

The new drug candidate, called Hi1a, is also believed to be able to extend the lives of donor hearts used for organ transplants.

The Australian scientists behind the study, published in the European Heart Journal, say it works by stopping a ‘death signal’ sent from the heart in the wake of an attack and could soon be administered by first responders.

The researchers hope to test the drug in human trials in the coming years to provide the first-ever drug that prevents damage caused by heart attacks.

The research team, from the University of Queensland (UQ), identified a small protein in the venom of the Fraser Island (K’gari) funnel-web spider that was shown to protect cells from damage caused by heart attacks and strokes.

The arachnid species are amongst the deadliest spiders in the world – with its venomous bite able to kill a child in just 15 minutes.

The discovered venom molecule has recently undergone a series of preclinical tests designed to mimic real-life treatment scenarios and passed with flying colors.

Associate Professor Nathan Palpant, a lead author of the study from UQ’s Institute for Molecular Bioscience, said these tests were a ‘major step’ towards understanding how Hi1a could be used as a therapeutic, at what stage of a heart attack it should be used and the optimal dosage required.

“We established that Hi1a is as effective at protecting the heart as the only cardioprotective drug to reach Phase 3 clinical trials, a drug that was ultimately shelved due to side effects,” Dr Palpant said.

“Importantly, we found that Hi1a only interacts with cells in the injured zone of the heart during an attack and doesn’t bind to healthy regions of the heart – reducing the chance of side effects.”

After a heart attack, blood flow to the heart is reduced, meaning a lack of oxygen goes to the heart.

This lack of oxygen causes the cell environment to become acidic, which combines to send a message for heart cells to die.

Despite decades of research, scientists have thus far been unable to develop a drug that stops this death signal in heart cells, which is one of the reasons heart disease continues to be the leading cause of death in the world.

Dr. Pallant and his team tested the Hi1a protein using beating human heart cells exposed to heart attack stresses to observe whether the drug improved their survival.

The spider venom protein was found to block acid-sensing ion channels in the heart, meaning the death message is blocked and cell deaths are reduced.

Professor Glenn King, another UQ researcher who recently won the Prime Minister’s Prize for Innovation for developing the world’s first insecticides from spider venom, described the new drug candidate as ‘super exciting’.

“There is no drug at the moment to protect the heart during a heart attack,” he said.

“The possibility that we could develop the first-ever drug to minimize damage during a heart attack is super exciting.

“Hi1a could reduce damage to the heart and brain during heart attacks and strokes by preventing cell death caused by lack of oxygen.

“For heart attack victims, our vision for the future is that Hi1a could be administered by first responders in the ambulance, which would really change the health outcomes of heart disease.”

Infensa Bioscience, a company co-founded by the researchers, has already raised AU$23 million (£11m) to develop Hi1a for commercial purposes.

Professor Peter Macdonald, a senior cardiologist at the Victor Chang Cardiac Research Institute, added that the drug could also improve the number and quality of donor hearts.

“The survival of heart cells is vital in heart transplants,” he said.

“This will not only help the hundreds of thousands of people who have a heart attack every year around the world, it could also increase the number and quality of donor hearts, which will give hope to those waiting on the transplant list.

“Treating hearts with Hi1a and reducing cell death will increase how far the heart can be transported and improve the likelihood of a successful transplant.

“Usually, if the donor heart has stopped beating for more than 30 minutes before retrieval, the heart can’t be used – even if we can buy an extra 10 minutes, that could make the difference between someone having a heart and someone missing out.

“For people who are literally on death’s door, this could be life-changing.”

The researchers now aim to conduct human clinical trials for both stroke and heart disease within two to three years.