In Morocco there grows a cactus-like plant that’s so hot, I have to insist that the next few sentences aren’t hyperbole. On the Scoville Scale of hotness, its active ingredient, resiniferatoxin, clocks in at 16 billion units. That’s 10,000 times hotter than the Carolina reaper, the world’s hottest pepper, and 45,000 times hotter than the hottest of habaneros, and 4.5 million times hotter than a piddling little jalapeno. Euphorbia resinifera, aka the resin spurge, is not to be eaten. Just to be safe, you probably shouldn’t even look at it.

But while that toxicity will lay up any mammal dumb enough to chew on the resin spurge, resiniferatoxin has also emerged as a promising painkiller. Inject RTX, as it’s known, into an aching joint, and it’ll actually destroy the nerve endings that signal pain. Which means medicine could soon get a new tool to help free us from the grasp of opioids.

The human body is loaded with different kinds of sensory neurons. Some flavors respond to light touch, others signal joint position, yet others respond only to stimuli like tissue injury and burns. RTX isn’t going to destroy the endings of all these neurons willy-nilly. Instead, it binds to a major molecule in specifically pain-sensing nerve endings, called TRPV1 (pronounced TRIP-vee one).

SIGN UP TODAY Sign up for the Daily newsletter and never miss the best of WIRED.

This TRPV1 receptor normally responds to temperature. But it also responds to a family of molecules called pungents, which includes capsaicin, the active ingredient in hot pepper. “So when you put hot pepper on your tongue and it feels like it's burning, it's not because your tongue is on fire,” says Tony Yaksh, a professor in the anesthesiology and pharmacology department at UC San Diego who’s studied RTX. “It's simply activating the same sensory axons that would have been activated if your tongue had been on fire.”

RTX is a capsaicin analog, only it’s between 500 and 1,000 times more potent. When RTX binds to TRPV1, it props open the nerve cell’s ion channel, letting a whole lot of calcium in. That’s toxic, leading to the inactivation of the pain-sensing nerve endings.

This leaves other varieties of sensory neurons unaffected, because RTX is highly specific to TRPV1. “So you gain selectivity because it only acts on TRPV1, which is only on a certain class of fibers, which only transmit pain,” says Yaksh. “Therefore you can selectively knock out pain without knocking out, say, light touch or your ability to walk.”

So if you wanted to treat knee pain, you could directly inject RTX into the knee tissue. You’d anesthetize the patient first, of course, since the resulting pain would be intense. But after a few hours, that pain wears off, and you end up with a knee that’s desensitized to pain.

Researchers have already done this with dogs. “It is profoundly effective there, and lasts much, much longer than I might have expected, maybe a median of 5 months before the owners of the dogs asked for reinjection,” says Michael Iadarola, who’s studying RTX at the National Institutes of Health. “The animals went from basically limping to running around.” One dog even went 18 months before its owners noticed the pain had returned.

That’s a very targeted application, but what about more widespread pain? Cancer patients, for instance, can live in agony through their end-of-life care. Here, too, RTX might work as a powerful painkiller. In fact, the NIH is in the midst of trials with bone cancer patients.

“We use the same technique for administering this as we would a spinal anesthetic,” says NIH anesthesiologist Andrew Mannes. “The whole idea is you're not injecting into the spinal column itself, you're injecting it into the fluid that surrounds the spinal column.” Injecting straight into the cord would damage it. Patients are anesthetized for all of this, and treated with short-term painkillers when they wake. “That seems to get them over the worst of it, and then over the next few hours it subsides until the point where they don't feel the pain any longer.”