Kratom Leaf & Mitragynine

Looking for the 60-second version? What the Hell Is 7-OH? covers the basics in plain language.

TL;DR

• Kratom is the dried leaf of a Southeast Asian tree (Mitragyna speciosa) that contains dozens of related compounds called alkaloids.
• Mitragynine is the main one, about 1–2% of the dry leaf, and it’s a weak, partial activator of the same receptor (mu-opioid) that opioid painkillers act on.
• 7-OH (7-hydroxymitragynine) is a very minor alkaloid in the leaf, typically under 0.04%, but it binds that receptor far more tightly and is more efficacious than mitragynine. The body also makes a small amount of 7-OH from mitragynine in the liver.
• The concentrated “7-OH” tablets, shots, and gummies sold in the US deliver 7-OH at roughly 100× to 1,000× the concentration found in natural leaf, a level that peer-reviewed analytical chemistry says can only be achieved by semi-synthetic conversion or adding exogenous 7-OH, not by extracting leaf.
• “Kratom” and “7-OH product” are therefore not interchangeable terms, even though the marketing often blurs them. This site is about quitting the concentrated 7-OH products.

Kratom basics (start here)

Kratom is a leaf from a tree (Mitragyna speciosa) native to Thailand, Malaysia, Indonesia, and other parts of Southeast Asia. The tree is in the same botanical family as coffee. In its countries of origin, people have chewed fresh leaves, brewed them as tea, or ground dried leaf into powder for centuries.

Why people take it. At lower amounts, users describe stimulant-like effects, alertness, mild stimulation, similar in feel to strong coffee. At higher amounts, the effects shift toward sedation and pain relief, more in line with what a mild opioid does. Both effects come from the same plant; what differs is the dose. (Throughout this page, “users describe” or “reported” is the framing used for subjective effects, because the receptor pharmacology that produces them is documented separately below.)

How it’s sold in the US today. Plain dried-leaf forms, powder, capsules, brewed teas, are still common. So are “extracts” of varying concentration. In the last several years a separate, much more potent product category has taken over the US market: tablets, gummies, drink mixes, and shots built around a specific alkaloid called 7-hydroxymitragynine (7-OH). These last products are what most of this site is about. Whether they should be called “kratom” at all is part of what the rest of this page explains.

A level deeper: the leaf itself

Mitragyna speciosa is a tree in the Rubiaceae family (the coffee family), traditionally cultivated and harvested in southern Thailand, peninsular Malaysia, and parts of Indonesia. Its use is documented in ethnobotany literature going back over a century, traditionally as a mild stimulant for manual labor, a folk treatment for diarrhea and chronic pain, and a substitute for opium during periods when opium was harder to obtain. Most published Western pharmacology research on the plant is much more recent: roughly the last fifteen years.

Forms sold in the US.

• Plain dried-leaf powder and capsules. Bulk leaf material, varying in colour and country of origin.
• Standard liquid or solid extracts. Concentrated forms with higher mitragynine per gram, typically labeled with a percentage or a ratio.
• Concentrated 7-OH products. Tablets, shots, gummies, and drink mixes specifically engineered to deliver 7-OH at concentrations that don’t naturally occur in leaf, categorically different from the first two and the focus of the rest of this site.

Leaf composition

Dried Mitragyna speciosa leaf contains dozens of alkaloids, a chemistry term for naturally-occurring nitrogen-containing plant compounds. The major ones, by concentration:

• Mitragynine: the dominant alkaloid, accounting for the largest share of opioid-receptor activity in leaf preparations.
• Paynantheine, speciogynine, speciociliatine: minor diastereomers (slightly different 3D arrangements of the same atoms) with their own receptor activity, especially at serotonin and adrenergic receptors. Background context lives on the Kratom’s Minor Alkaloids page.
• 7-Hydroxymitragynine: the alkaloid this site is named around. Present in very small amounts in fresh leaf; somewhat more in dried/aged leaf because mitragynine oxidizes to 7-OH over time.
• Mitraphylline, rhynchophylline, and others, trace alkaloids with limited or non-opioid activity.
• Mitragynine pseudoindoxyl: not typically present in fresh leaf in meaningful amounts but produced as a degradation product and now appears as a synthetic in some designer-drug products.

The key numbers, by dry weight of leaf

• Mitragynine: roughly 0.5–2.7% across published analyses; most authenticated leaf samples cluster around 1–2%. Concentration varies with region, cultivar, leaf maturity, and harvest season (Leksungnoen et al., PeerJ 2022; Murayama et al., J AOAC Int 2025; Tanna et al., Molecules 2024).
• 7-Hydroxymitragynine: roughly 0.003–0.04% in authenticated leaf, two orders of magnitude lower than mitragynine. Drying, storage, heat, and oxygen exposure increase 7-OH content as mitragynine oxidizes (Murayama 2025; Tanna 2024; Smith et al., Addiction 2025).

Alkaloid profile varies significantly between batches, regions, and processing methods. No single number above is universal, the ranges are what’s published.

Mitragynine pharmacology

Mu-opioid receptor activity. Mitragynine binds the human mu-opioid receptor (the same receptor that morphine and other classical opioids act on) as a partial agonist, meaning it activates the receptor incompletely. Binding affinity (Ki) is roughly 160–240 nM in radioligand assays (Obeng et al., J Med Chem 2020; Kruegel et al., JACS 2016; Frontiers in Pharmacology 2026), about 100–160× weaker than morphine (~1.5 nM at the same receptor in the same reference). Functionally, it’s a low-to-moderate-efficacy partial agonist with reduced β-arrestin recruitment relative to classical opioids, a signaling profile some researchers think contributes to its lower respiratory-depression risk at equivalent mu-receptor occupancy.

Other targets. Mitragynine has weak kappa-opioid activity and essentially no delta-opioid activity (Frontiers 2026). It binds α-1 and α-2 adrenergic receptors weakly (Kᵢ low-micromolar; Obeng et al., J Med Chem 2020 reports α-1A 1.34 µM, α-1B 4.77 µM, α-1D 5.48 µM, α-2A 4.72 µM, α-2B 9.29 µM, α-2C 2.32 µM) and acts as a low-efficacy α-2A agonist in vivo in rats, the same receptor that clonidine acts on. The minor alkaloids paynantheine and speciogynine bind serotonin (5-HT₁ₐ) receptors at low-nanomolar affinity (León et al., J Med Chem 2021).

Pharmacokinetics in humans. Oral bioavailability is poor (rat absolute bioavailability ≈ 3%; human studies model from this). Half-life in healthy users is roughly 23–61 hours depending on the study and dose form (Trakulsrichai et al., DDDT 2015; Tanna 2024). Primary metabolism is by hepatic CYP3A4 (an enzyme in the liver that processes many drugs), with secondary contributions from CYP2D6 and CYP2C9 (Kamble et al., DMD 2020 and follow-on PK studies). That same CYP3A4 pathway is what produces 7-OH from mitragynine inside the body, the central pharmacological link between leaf and 7-OH, discussed in detail below.

7-OH pharmacology

7-OH has its own dedicated page; the short version that matters here:

• Receptor activity: binds the mu-opioid receptor at roughly 7–15 nM, about 10–30× tighter than mitragynine, and acts as a near-full agonist (Obeng 2020; Frontiers 2026). In mice, equipotent to or more potent than morphine for antinociception (Berthold Br J Pharmacol 2022).
• Reinforcement: preclinical self-administration consistently shows 7-OH, not mitragynine, is the alkaloid that drives it. Rats self-administer 7-OH and substitute it for morphine; mitragynine alone is not self-administered above vehicle (Hemby Addiction Biol 2019).
• Half-life in humans: limited direct data. The only published numbers come from measuring 7-OH as a metabolite during mitragynine dosing, roughly 4–9 hours (Tanna 2024). No published human PK study has dosed isolated 7-OH as a single agent, a real evidence gap.

From leaf to 7-OH: three pathways

This is the section that matters most for understanding the discourse around these products. There are three distinct ways 7-OH ends up in a human body, and conflating them is where most of the confusion lives.

1. In the plant

A small amount of 7-OH forms naturally in the living leaf and in the process of drying and storing it. Mitragynine oxidizes to 7-OH on exposure to air, heat, and time, the longer and warmer the storage, the more 7-OH a batch of dried leaf will contain (Murayama 2025). Even so, the amounts stay in the range cited above, under 0.04% of dry weight in authenticated material.

2. In the body (in vivo conversion)

When mitragynine is consumed, a fraction is metabolized to 7-OH in the liver via CYP3A4. How much, and how much of leaf’s effect this explains, is contested in the literature.

• Kruegel et al., ACS Cent Sci 2019 argues from mouse data that brain 7-OH levels after mitragynine dosing are “sufficient to explain most or all of the opioid- receptor-mediated activity,” consistent with mitragynine acting largely through its conversion to 7-OH (a prodrug-like picture, though Kruegel doesn’t use that term).
• A direct rebuttal in mice (Maxwell et al., DMD 2022) reports brain 7-OH from mitragynine dosing is 4-fold lower than needed for equivalent effects from direct 7-OH, concluding mitragynine itself does most of the work in mice, while flagging that humans may convert more.
• The best human data (Tanna 2024) show plasma 7-OH at roughly 20–30% of mitragynine exposure (Cmax and AUC) after oral dried leaf, higher than the mouse ratios, but not yet linked to a specific share of subjective effect.

Settled: the conversion happens and produces measurable circulating 7-OH. Not settled: how much of leaf’s opioid-like effect is mitragynine itself vs. converted 7-OH, and whether “prodrug” framing applies in humans. One other thing: in mice, mitragynine’s respiratory-depression effect plateaus at higher doses because conversion to 7-OH saturates, while direct 7-OH dosing is dose-linear (Berthold 2022). That’s a mechanistic argument for why oral leaf has a self-limiting opioid effect that purified 7-OH does not.

3. In manufacturing

Concentrated 7-OH products on the US market, tablets, gummies, shots, drink mixes, contain 7-OH at roughly 22–75 mg per gram of product (2.2–7.5% by weight), with some preparations reportedly up to 98% purity (Murayama 2025; Smith et al., Addiction 2025). That is roughly 100–1,000× the concentration of 7-OH in natural leaf.

Peer-reviewed analytical chemistry is explicit that these levels cannot be obtained by extracting leaf: Murayama’s J AOAC Int paper concludes the elevated 7-OH content of market products “would have to be synthetically created … or [from] the addition of exogenous 7-HMG” and that the process “creates additional, unidentified compounds also not native to kratom leaf.” FDA documentation has treated these products as a distinct, concentrated category from kratom leaf in its enforcement actions (FDA July 15, 2025 warning letters; FDA July 29, 2025 scheduling recommendation; FDA December 2, 2025 seizure).

The specific synthetic routes individual vendors use are not publicly disclosed and are not documented in the analytical literature beyond the observation that the products’ 7-OH content cannot have come from the leaf itself.

Where leaf fits in tapering off concentrated 7-OH

Some people in this community use plain dried-leaf preparations as a step-down tool when coming off concentrated 7-OH products. The pharmacological rationale: mitragynine is a much weaker, partial agonist at the same primary receptor that 7-OH activates more strongly. Substituting leaf for concentrate reduces overall mu-opioid stimulation while avoiding the abrupt receptor-occupancy drop that drives acute withdrawal.

This is not a recommendation, it’s a description of an approach that exists. Known caveats:

• Leaf itself is addictive and produces its own withdrawal.
• Dose calibration is hard. Alkaloid content varies between batches, strains, and vendors, so the “switch” is moving from a precisely-dosed product to one whose effective dose is unknown.
• Switching dependencies is not resolving dependency. Leaf tapering shifts what you depend on; it doesn’t, on its own, get you to abstinence.
• Clinician engagement varies a lot here. The leaf taper plan itself is mostly community ground, many clinicians have never encountered these compounds and won’t have a substantive taper conversation. The narrow asks where a prescriber helps are adjunct meds (clonidine, gabapentin) and lab work. The Telehealth Providers comparison flags options with specific kratom/7-OH experience if you want adjunct support alongside a leaf taper.

If you’re considering this approach in detail, the Quit 7-OH with Kratom Leaf page covers the practical structure and limitations the community has documented. The closely related approach of using a concentrated mitragynine extract product instead of plain leaf is covered on Quit 7-OH with Concentrated Mitragynine, along with the product-contamination concerns specific to that route.

Regulatory status (as of 2026-07-03)

• Kratom (mitragynine, leaf): not federally scheduled. FDA considers kratom-containing dietary supplements adulterated and maintains Import Alert 54-15 on bulk M. speciosa material (FDA on kratom).
• 7-OH: not yet federally scheduled, but the clock is running. On July 1, 2026, DEA filed a notice of intent to temporarily place 7-OH above a 0.05% / 1 mg threshold in Schedule I; the earliest the order can take effect is August 5, 2026. Leaf below the threshold is explicitly outside the action. Dates, scope, and process: The Federal 7-OH Ban.
• State actions: Louisiana placed mitragynine and 7-OH in state Schedule I effective Aug 1, 2025. Ohio enacted an emergency rule Dec 12, 2025 banning kratom-related products except pure-mitragynine vegetation, pending permanent rulemaking (governor’s office). Several other states have enacted narrower 7-OH restrictions (CRS summary).

The legal landscape changes frequently. Verify against current FDA and DEA primary sources before relying on anything specific.

Reminder. This is a pharmacology reference, not medical advice. If you’re trying to come off concentrated 7-OH products, the Withdrawal Help page is where to go for what to do right now, including the three real paths out (Suboxone, SR-17, or toughing it out with helper meds). For finding a prescriber for Suboxone or helper meds, see Telehealth Providers. SR-17 is off-prescription; community ground.