7-hydroxymitragynine (7-OH) is the opioid-active compound that explains kratom’s effects. Concentrated 7-OH products only began appearing widely in U.S. retail markets in 2024, but the biology is not new: the human body converts mitragynine (from kratom) into 7-OH.
Claims that “7-OH is dangerous but kratom is safe” misstate basic pharmacology. Kratom’s psychoactive and addictive effects depend on the formation of 7-OH in vivo. New 7-OH products remove this biological constraint by delivering the active opioid compound directly.
7-OH is the opioid-active driver. Kratom’s pharmacologic effects depend on metabolic conversion of mitragynine into 7-hydroxymitragynine (7-OH), a potent μ-opioid receptor agonist.
New products, same biology. Concentrated 7-OH tablets, gummies, and shots entered U.S. retail markets broadly in 2024, bypassing metabolism and delivering the active opioid compound directly.
False separation narrative. Claims that “7-OH causes harm but kratom does not” ignore that kratom’s effects require in-body formation of 7-OH. The distinction is commercial, not pharmacologic.
Regulatory implications. Both kratom and 7-OH products raise the same public-health concerns: dependence, withdrawal, overdose risk, youth access, and unapproved drug distribution.
Some trade groups argue that concentrated 7-OH products are dangerous but that kratom leaf or powder is fundamentally different. This framing is misleading and inconsistent with established pharmacology.
Scientific reality. Mitragynine itself has limited opioid activity. Its clinical effects depend on conversion to 7-OH after ingestion.
What changed in 2024. Manufacturers began isolating and concentrating 7-OH into tablets and shots, removing the body’s natural metabolic limits.
Why this matters. The distinction affects enforcement strategy, not biological risk. Both pathways deliver the same opioid-active compound.
The images below document how 7-OH appears in kratom-derived products sold in U.S. retail settings. Packaging and placement mirror consumer supplements, energy products, and candy rather than controlled opioid-active substances.
These reports document how concentrated 7-OH products entered retail markets, why states began acting in 2024, and what clinicians are observing in emergency departments and addiction treatment settings.
Acute effects. Sedation, respiratory depression, impaired cognition, nausea, and loss of consciousness—especially at higher doses or with other depressants.
Dependence and withdrawal. Regular exposure produces tolerance and withdrawal syndromes clinically indistinguishable from opioid withdrawal.
Emergency care utilization. Poison control data and hospital reports describe increasing calls and ED visits associated with kratom and 7-OH use.
Vulnerable populations. Adolescents, pregnant individuals, and persons with prior substance-use disorders face disproportionate risk.
Traditional kratom products require metabolic conversion of mitragynine to 7-OH, introducing limits on dose and speed of onset. Concentrated 7-OH products remove these constraints.
Loss of metabolic buffer. Direct 7-OH delivery increases peak opioid exposure.
Faster onset. Tablets, gummies, and shots increase abuse liability.
Dosing uncertainty. Label variability amplifies overdose risk.
Regulatory significance. These features align with unapproved opioid drugs.