Kratom is a plant for which good public information is especially hard to find. Most of what circulates online is either vendor copy or forum folklore. This post is neither. It describes the plant and its chemistry for people who want to understand what the substance is before they form an opinion about it.
It contains no dosing guidance and no recommendation to use kratom. Where the evidence is thin, we say so.
The plant
Mitragyna speciosa Korth. is a tropical evergreen tree in the Rubiaceae, the coffee family. That relationship matters. It is why kratomâs alkaloids belong to a broadly familiar structural class, the indole alkaloids, and why the tree behaves agronomically like other understorey Rubiaceae.
Its native range runs through mainland and maritime Southeast Asia: southern Thailand, peninsular Malaysia, Indonesia (particularly Kalimantan/Borneo), the Philippines and New Guinea. It is also reported from Myanmarâs Tanintharyi Region. In Thailand it is a plant of the deep South, part of local farming and social life long before anyone wrote a law about it.
Leaves are the part used. They are harvested from mature trees, dried, and then used whole, milled to powder, or processed further into extracts.
The alkaloids
Kratom leaf contains dozens of alkaloids. Only a handful matter for the plantâs effects:
- Mitragynine: the main alkaloid in the leaf by mass, and the one the pharmacology is built around
- Speciociliatine, speciogynine, paynantheine: structurally related, present in meaningful amounts
- Corynoxine, corynantheidine, isocorynantheidine, mitraphylline: minor constituents
- 7-hydroxymitragynine (7-OH): the compound everyone talks about, and the one almost everyone misunderstands
The single most important thing to understand about 7-OH
A controlled cultivation study in PLOS One grew kratom under three light regimes and measured the alkaloid profile of the leaves. Mitragynine, paynantheine, corynoxine and the rest were all measurable, and all varied with treatment.
7-hydroxymitragynine was below the limit of quantification in every sample.
The authors took this as support for the view that 7-OH is not mainly made by the living plant. On that view, it forms after harvest, as an oxidation product of mitragynine, during drying, storage and processing. Keep the limits of this evidence in mind. It is one study of a single clonal genotype grown for about three and a half months, and the post-harvest explanation comes from earlier literature rather than from anything this study tested. The finding is important, but it does not settle the question on its own.
The body makes 7-OH too. In laboratory studies, mouse and human liver preparations converted mitragynine into 7-OH, and the conversion was carried out by CYP3A enzymes. In mice, the 7-OH formed this way reached brain levels that the researchers judged sufficient to explain most of mitragynineâs opioid-receptor-mediated pain relief. So when someone swallows leaf that contains almost no 7-OH, their liver will still produce some. âThe leaf is mitragynine, not 7-OHâ is therefore an oversimplification.
This is why so much public discussion of kratom is confused. A claim that âkratom is many times more potent than morphineâ is really about 7-OH measured in isolation. Dried leaf delivers mostly mitragynine plus a little 7-OH from the drying process. More 7-OH then forms gradually in the liver, at a rate that depends on each personâs metabolism. A tablet sold as âkratomâ but enriched with isolated 7-OH delivers a large amount of that compound directly. That is a very different exposure from leaf.
Fresh leaf, dried leaf, standardised extract and 7-OH-enriched products are best treated as different products with different 7-OH exposure. Any statement about âkratomâ that does not say which one it means is not a useful statement.
Mechanism
Mitragynine acts as a partial agonist at the mu-opioid receptor. It has comparatively low efficacy, which is the pharmacological basis for the observation that leaf preparations produce something quite different from a conventional opioid at ordinary intakes.
7-OH is a mu-opioid partial agonist that is considerably more potent than mitragynine. The numbers you see repeated online come from different kinds of measurement, so read them carefully:
- Potency in animal tissue. In isolated guinea-pig ileum (gut tissue), Horie et al. (Planta Medica, 2005) found 7-OH about 30 times more potent than mitragynine and about 17 times more potent than morphine. The widely repeated â13 times morphine, 46 times mitragynineâ figures also come from guinea-pig ileum potency assays. They are not receptor-affinity measurements, and none of these figures were measured in humans.
- Receptor affinity. In binding studies on a cloned mu-opioid receptor, VĂĄradi et al. (Journal of Medicinal Chemistry, 2016) found that 7-OH had only moderate affinity, about 5 times higher than mitragynine.
Potency and affinity are different properties. Quoting one as if it were the other is a common error in kratom writing.
A 2026 review in Current Addiction Reports also describes interactive effects at alpha-2 adrenergic receptors alongside the mu-opioid activity. Kratom shares this mechanism with clonidine-class drugs, and simplified accounts often leave it out.
Biased signalling. Cell-based studies (Kruegel et al., Journal of the American Chemical Society, 2016) reported that both alkaloids activate G-protein signalling while recruiting little or no beta-arrestin. In opioid pharmacology, beta-arrestin recruitment has been linked to respiratory depression and severe constipation. That âbiasedâ profile is the mechanistic reason some people argue kratom is less dangerous than a classical opioid.
That interpretation is disputed. Later work on other âbiasedâ opioid agonists (Gillis et al., Science Signaling, 2020) argued that their apparent bias and milder side effects can be explained by low intrinsic efficacy: they activate the receptor only weakly, rather than steering it towards one signalling pathway. Whether beta-arrestin drives opioid side effects at all is itself still debated.
This argument is often overstated, so it is worth stating precisely. A signalling mechanism is a hypothesis about why harm might be lower. It does not show that harm is low. Treat it as an explanation to be tested, not as a safety guarantee.
Why the effects are dose-dependent â and why that is unusual
The most-repeated fact about kratom is that low intakes are stimulant-like and higher intakes are sedative and pain-relieving. That two-phase pattern is real and is documented in the clinical literature, including the StatPearls review.
The first human pharmacokinetic study (Trakulsrichai et al., Drug Design, Development and Therapy, 2015) studied nine regular users in Thailand. It found that mitragynineâs blood levels rose in proportion to dose, with a terminal half-life of about 23 hours (±16 hours). Blood was sampled for only 24 hours, though, so later authors regard that estimate as imprecise. Mitragynine is clearly not a short-acting compound, but its exact half-life in humans is not yet well established.
We are not going to reproduce a doseâeffect table. Tables of that kind circulate widely online, and they come from user self-reports rather than controlled studies. A table that looks precise and is not is worse than no table.
What changes the alkaloid content of a leaf
This is where the agronomy meets the chemistry, and where some of the marketing falls apart.
Growing conditions matter. In the PLOS One study, plants grown under different light conditions differed substantially in both mitragynine concentration and total leaf yield. Two leaves from the same genotype can differ chemically because of where and how the tree was grown.
âVein colourâ is the marketing claim with the weakest support. Red-vein, green-vein and white-vein kratom are sold as distinct products with distinct alkaloid profiles and distinct effects. We could not find controlled analytical work showing that vein colour predicts alkaloid composition once cultivar, leaf age, growing conditions and post-harvest handling are accounted for. Since growing conditions measurably shift alkaloid concentration, the simplest explanation has not been ruled out: vein colour may stand in for other factors, or mean nothing at all. If a vendor makes vein-colour claims, ask for the chromatogram, the lab test showing which alkaloids are present and in what amounts.
Post-harvest handling is not neutral. If most of the 7-OH in dried leaf forms after harvest, as current evidence suggests, then drying temperature, drying time, oxygen exposure and storage conditions are more than quality-control questions. They change how much 7-OH the product contains before the body adds its own. Two batches of the same leaf, dried differently, are not the same product.
What this means in Thailand specifically
Thailand regulates kratom through a dedicated law, the Kratom Plant Act B.E. 2565 (2022). Among other things, it prohibits selling kratom leaf, or food containing it, to people under 18 and to pregnant or breastfeeding women. Several neighbouring countries, including Malaysia and Indonesia, control or regulate kratom under other legislation, so Thailand is not unique in regulating the plant.
Where the science is genuinely unfinished
To be clear about the limits of the above:
- We could not find any published survey comparing the alkaloid content of Thai cultivars grown under standardised conditions
- The relationship between leaf age at harvest and alkaloid profile is not well characterised in the peer-reviewed literature
- Human pharmacokinetic data are thin, published half-life estimates are imprecise, and almost all of the data are for mitragynine rather than for whole-leaf preparations
- How much 7-OH the human liver produces from mitragynine, and how much that varies between people, is not well quantified
- The contribution of the minor alkaloids to overall effect is largely unknown
Anybody presenting kratom pharmacology as settled, in either direction, is going beyond the evidence.
Sources: Zhang et al., âPlant growth and phytoactive alkaloid synthesis in kratom [Mitragyna speciosa (Korth.)] in response to varying radianceâ, PLOS One 17(4): e0259326, 2022; Kruegel et al., â7-Hydroxymitragynine Is an Active Metabolite of Mitragynine and a Key Mediator of Its Analgesic Effectsâ, ACS Central Science, 2019; Kruegel et al., Journal of the American Chemical Society, 2016; Horie et al., Planta Medica 71(3): 231â236, 2005; VĂĄradi et al., Journal of Medicinal Chemistry, 2016; Gillis et al., âLow intrinsic efficacy for G protein activation can explain the improved side effect profiles of new opioid agonistsâ, Science Signaling, 2020; Trakulsrichai et al., âPharmacokinetics of mitragynine in manâ, Drug Design, Development and Therapy 9: 2421â2429, 2015; âKratomâ, StatPearls, NCBI Bookshelf; â7-Hydroxymitragynine (7-OH): Clinical Implications of a Potent, Unregulated Opioid Partial Agonist Derived from Kratomâ, Current Addiction Reports, 2026; Plants of the World Online (Royal Botanic Gardens, Kew), Mitragyna speciosa; Transnational Institute, âKratom in Myanmar and Southeast Asiaâ.