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Science & Medicine· Explainer

The Feds Are Scheduling Three New Drugs at Once. The Chemists Are Already on a Fourth.

7-OH kratom, tianeptine, and medetomidine are three different chemicals with one thing in common: each showed up at a gas station or a drug supply near you before anyone in a lab coat had a name for what it does to a body.

ByThe Rize NewsroomAugust 28, 20266 min readNovel & Emerging Psychoactives

Behind the counter at a lot of gas stations, next to the energy shots and the synthetic-cannabinoid vapes, sit little bottles with names like “ZaZa Red” and “Tianna Red.” They’re marketed as mood boosters, hangover cures, energy supplements — legal, over the counter, no ID required in most states. What’s actually in them is tianeptine, a molecule that was sold in France and a handful of other countries for decades as a mild antidepressant before anyone worked out what it does at high doses in the human brain. It took roughly ten years after approval abroad for researchers to trace tianeptine’s real mechanism back to the same receptors that opioids hit. By then it had a nickname: gas station heroin.

The federal government is racing to schedule three unrelated chemicals at once, and the chemistry keeps outrunning the paperwork.

Tianeptine is one of three novel substances reshaping the fringe of the drug supply right now, alongside concentrated kratom extracts and a veterinary sedative called medetomidine. None of the three is fentanyl. None of the three is what most people picture when they picture “the drug crisis.” All three are moving faster than the agencies built to respond to them, and each one illustrates a different way the enforcement model breaks down when the compound gets to the shelf, or the supply, before the science does.

The kratom fight nobody agrees on, including the people fighting it

On August 5, a DEA emergency order took effect placing 7-hydroxymitragynine — a concentrated, chemically altered kratom extract known as 7-OH — into Schedule I, alongside three related synthetic and concentrated kratom alkaloids, for any product exceeding a 0.05% dry-weight threshold. FDA and HHS backed the move in a joint statement citing opioid-receptor activity, documented overdose deaths, and no accepted medical use. The order deliberately carves out whole-leaf kratom below that threshold — the traditional Southeast Asian leaf product millions of Americans already use, often to manage pain or opioid withdrawal on their own.

That carve-out is also where the fight lives. Mac Haddow, a lobbyist for the American Kratom Association, supports cracking down on concentrated 7-OH extracts but warns the ban’s language could sweep in ordinary leaf products too, because it also restricts mitragynine pseudoindoxyl — a compound that occurs naturally in raw kratom leaf at tiny, currently unmeasurable concentrations. If a lab can’t reliably tell a legal leaf product from a technically-scheduled one, Haddow argues, the rule criminalizes a market nobody intended to touch. North Dakota Governor Kelly Armstrong, backing the crackdown itself, called the unregulated 7-OH concentrate market “the Wild West” — two people who agree the current market is dangerous, unable to agree on where the fence should go.

What tianeptine actually does, in plain terms, and why it took so long to find out

Here’s the part that matters more than the scheduling fight: tianeptine’s danger isn’t really about being “a supplement gone wrong.” It’s about a drug maker’s basic tool for treating depression turning out, at high doses, to work on the same on-switch inside the brain that opioids use. A systematic review published this year in Drug and Alcohol Dependence, screening 53 studies, confirmed that tianeptine acts as an agonist at the mu- and delta-opioid receptors — the same receptor family targeted by heroin, oxycodone, and fentanyl, just reached by a completely different-looking molecule that spent a decade wearing an antidepressant’s paperwork.

That mechanism produces what the review’s authors describe as a hybrid withdrawal: on top of standard antidepressant discontinuation symptoms, someone dependent on high-dose tianeptine goes through something that looks and feels like opioid withdrawal, because pharmacologically, it is one. Tolerance builds fast. The product is sold at a convenience-store counter, not a pharmacy, so there’s no pharmacist checking doses, no prescriber tracking escalation, and — this is the part that should worry every case manager reading this — routine toxicology panels at most treatment intake desks don’t screen for it. Someone can walk into an assessment dependent on an opioid-receptor agonist and test clean, because the test was built for a different decade’s drugs.

Someone can walk into an assessment dependent on an opioid-receptor agonist and test clean, because the test was built for a different decade’s drugs.

If you’ve ever had a doctor or a treatment intake form miss what was actually happening in your body, you already know what it costs to be measured by the wrong yardstick. That’s not a hypothetical for tianeptine. It’s the default.

Medetomidine: the tranquilizer that made the last tranquilizer look manageable

The third substance is medetomidine, a veterinary sedative that has displaced xylazine — itself a veterinary sedative — as the dominant non-opioid adulterant in street fentanyl in multiple U.S. cities. In Philadelphia, the share of street-fentanyl samples testing positive for medetomidine rose from 29% to 90% between May 2024 and March 2026, while xylazine-positive samples fell from 97% to 28% over the same stretch — one veterinary tranquilizer swapping out for another, more potent one, in under two years.

The reason that swap matters clinically is mechanism, not just potency. Medetomidine works on alpha-2 adrenergic receptors — a different lock, with a different key, than the opioid receptors naloxone was built to block. Naloxone can restore someone’s breathing after a medetomidine-involved overdose, because it still reverses the fentanyl. It does nothing for the medetomidine itself: not the deep sedation, and not the withdrawal, which researchers studying the drug describe as rapidly progressive, severe, and often resistant to the therapies that work for standard opioid withdrawal. North Carolina’s state drug-checking lab has already logged the practical harm-reduction consequence: medetomidine test strips cost roughly six times what fentanyl test strips cost, which means the people most likely to encounter it are also the least likely to be able to afford to check for it.

This is the same trick the drug supply has run for forty years

None of this is new as a pattern, even though every molecule in it is new. In the early 1980s, underground chemists started producing “China White” — fentanyl analogs synthesized specifically because they weren’t yet named in federal drug schedules, which at the time listed substances one molecule at a time. Congress couldn’t schedule new analogs fast enough to keep up, so in 1986 it passed the Federal Analogue Act, which tried to ban entire chemical families sharing a core structure and effect, rather than chasing one formula after another. It was an attempt to stop playing whack-a-mole by widening the mallet. Xylazine’s federal scheduling push and medetomidine’s rise is that same forty-year-old story with new names: a study in the International Journal of Drug Policy, analyzing forensic lab data from 1999 through 2025, found that states which scheduled xylazine saw no drop in xylazine detections at all — only roughly 1,536 additional medetomidine detections per 100,000 forensic reports. A straight substitution, exactly like the Analogue Act was built to prevent, still happening forty years later, one veterinary tranquilizer at a time.

Scheduling a chemical doesn’t remove the demand it was filling — for a stimulant boost, a cheap opioid effect, a sedative strong enough to cut fentanyl without cutting the profit margin. It just changes which unregulated molecule shows up next, usually with less research behind it and less clinical familiarity than the one it replaced. Every clinician screening for these compounds is, right now, working from a shorter list than the drug supply is.

None of that makes any of these three substances safe, and none of it is an argument against scheduling — 7-OH concentrates, at minimum, genuinely warrant restriction. But naloxone still works on the opioid piece of a tianeptine or fentanyl-medetomidine exposure, tonight, regardless of what any agency schedules next month. That’s not nothing. It’s the one part of this story that doesn’t have to wait for the DEA, the Federal Register, or the next chemist to find the next loophole.

Filed Under

biologypsychologytrendsKratomTianeptineMedetomidineDEADrug SchedulingResearch Chemicals

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