A Hopeful Snakebite Treatment Ready for the Spotlight Takes an Unexpected Turn

In the dense jungles of Central America and northern South America, a silent killer lurks – the terciopelo snake, responsible for hundreds of fatalities each year due to its venomous bite.

A Hopeful Snakebite Treatment Ready for the Spotlight Takes an Unexpected Turn

Despite years of research and hopes pinned on a potential breakthrough, a recent setback has emerged: a once-promising antibody, designed to counteract the snake's venom, has failed in animal trials.


The antibody, meticulously developed by Christoffer Sørensen and his advisor Andreas Laustsen-Kiel at the Technical University of Denmark, aimed to neutralize a muscle-destroying toxin called myotoxin II found in the snake's venom. Initial laboratory and animal tests painted a rosy picture,


showing the antibody's efficacy in preventing damage to cells and mouse muscles. Excitement reached its peak in 2022 when a patent was filed for the antibody, and a scientific paper was in the works to share this groundbreaking discovery.


However, just days before the completion of Sørensen's dissertation, a shocking revelation halted the celebration. Collaborators at the University of Costa Rica found that, instead of protecting mice from muscle damage caused by the venom, the antibody exacerbated the harm, ultimately leading to the death of the mice. This unforeseen twist in the outcome is known as antibody-dependent enhancement.


Bruno Lomonte, a toxinologist at UCR, expressed his astonishment, calling it an unprecedented finding in toxinology. Sørensen, now a postdoctoral researcher, and the team scrambled to understand the anomaly. They explored modifications made to the antibody, undoing them in an attempt to rectify the issue.


Although the antibody became less lethal, it still failed to provide protection. Further experiments, including removing the antibody's core, resulted in even stranger outcomes, with one in five mice inexplicably succumbing to the treatment.


The researchers suspect that the myotoxin II might be hitchhiking on the antibodies, gaining increased access to the mice's cells. This phenomenon is not entirely unheard of; some pathogens, like the Dengue virus, use antibodies as a gateway into immune cells.

While the immediate results are disappointing, the findings could potentially guide future research on antibody drugs for snakebites.



Current treatments, relying on antivenoms derived from animal blood, pose logistical challenges and can induce severe allergic reactions. With snakebites remaining a significant threat, especially in rural areas, advancements in treatment options are critical.


Although the road ahead is uncertain, Sørensen hopes that the insights gained from this unexpected outcome will prompt researchers to incorporate rescue assays earlier in drug development. This precautionary step could prevent years of dedicated work from being derailed just before reaching the crucial next phase.


In the challenging battle against venomous snakebites, every lesson learned brings us one step closer to a safer and more effective solution.


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