CORRECTION: This story was updated on April 25, 2016, with the correct structure of indomethacin.

The sting of a scorpion can be deadly without the right anti-venom handy—each year, some 3,000 people die from encounters with these poisonous arthropods. Now, a research team in Brazil has discovered a potentially simple strategy to treat scorpion-sting victims: give them common anti-inflammatory drugs, such as indomethacin and celecoxib (Nat. Comm. 2016, DOI: 10.1038/ncomms10760).

The researchers, led by Lucia H. Faccioli of the University of São Paulo, showed that mice treated with these drugs after being given deadly doses of scorpion venom were able to recover. If the work in mice translates to humans, first aid professionals could turn to these common drugs when treating patients in remote, hot, or poor regions that may not have consistent supplies of antibody-based anti-venoms, Faccioli says.

Anti-venoms such as these require cold storage, are expensive, and work only as antidotes for the venom of specific species, comments Noah Palm, an immunologist at Yale University who has studied the effects of venom. For example, he says, it’s not practical for scientists studying poisonous animals in the field to carry anti-venoms designed to counteract every dangerous species they come across. “The possibility for a generic treatment is exciting,” Palm adds. He’d like to see whether Faccioli’s results in scorpions could be extended to snakes and other venomous creatures.

Faccioli and her team found that mice stung by scorpions experienced a severe immune reaction. This type of overreaction can be worse than the direct effects of the venom’s poison: The immune system’s frenzy causes life-threatening lung edema—filling of the lungs with fluid—w hich puts individuals at risk for death by suffocation.

Sign up for C&EN's must-read weekly newsletter Email Address * Subscribe » Contact us to opt out anytime

Working with mice, Faccioli’s team teased out the immune signaling pathways activated by the venom of the Brazilian yellow scorpion, Tityus serrulatus. She and her colleagues found that levels of the lipid signaling molecule prostaglandin E 2 skyrocketed, correlating with severe inflammation and lung edema in the animals. The role of prostaglandin E 2 in the deadly reaction made Faccioli suspect that common nonsteroidal anti-inflammatory drugs (NSAIDs)—which reduce overall prostaglandin levels in the body—could control the inflammation caused by the scorpion venom.