New antidote for cobra bites discovered


By Dr. Tim Sandle
July 22, 2024
DIGITAL JOURNAL

By Kamalnv CC BY 3.0

Scientists working at the University of Sydney and Liverpool School of Tropical Medicine have discovered that the commonly used blood thinner, heparin, can be repurposed as an inexpensive antidote for cobra venom.

Cobras kill thousands of people a year worldwide (around 138,000 people a year, based on current data). In addition, hundreds of thousands more people are seriously maimed by necrosis (the death of body tissue and cells) caused by the venom. Sometimes this can lead to amputation.

The World Health Organization has identified snakebite as a priority in its program for tackling neglected tropical diseases. It has announced an ambitious goal of reducing the global burden of snakebite in half by 2030.

Current antivenom treatment is expensive, especially in lower-income countries, and such treatments do not effectively treat the necrosis of the flesh at the site where the bite occurs. In particular, antivenoms are largely ineffective against severe local envenoming, which involves painful progressive swelling, blistering and/or tissue necrosis around the bite site. Envenomation is the process by which venom is injected by the bite or sting of a venomous animal.

“Our discovery could drastically reduce the terrible injuries from necrosis caused by cobra bites – and it might also slow the venom, which could improve survival rates,” observes Professor Greg Neely (from the Charles Perkins Centre and Faculty of Science at the University of Sydney).

By deploying clustered regularly interspaced short palindromic repeats (CRISPR) gene-editing technology to identify ways to block cobra venom, the research group successfully repurposed heparin and related drugs and showed they can stop the necrosis caused by cobra bites.

This approach was earlier used to identify an antidote to box jellyfish venom.

In the application for snake venom, CRISPR was used to find the human genes that cobra venom needs to cause necrosis that kills the flesh around the bite. One of the required venom targets are enzymes needed to produce the related molecules heparan and heparin, which many human and animal cells produce. Heparan is on the cell surface and heparin is released during an immune response.

The similar structure means the venom can bind to both. The team used this knowledge to make an antidote that can stop necrosis in human cells and mice.

In terms of biological function, the heparinoid drugs act as a ‘decoy’ antidote. By flooding the bite site with ‘decoy’ heparin sulphate or related heparinoid molecules, the antidote can bind to and neutralise the toxins within the venom that cause tissue damage.

The research has been published in the journal Science Translational Medicine. The research paper is titled “Molecular dissection of cobra venom highlights heparinoids as an antidote for spitting cobra envenoming.”