Pharmacognosy · April 2026
Kratom alkaloids — the whole picture.
Direct answer
Kratom contains 40+ alkaloids; two dominate pharmacologically: mitragynine (~66% of alkaloid content, primary driver of effects) and 7-hydroxymitragynine (trace amount native, ~13× more potent, formed in higher quantities as mitragynine is metabolized in your liver). Both bind the mu-opioid receptor but with biased signaling that differs from classical opioids.
The major alkaloids
Mitragynine
~66% of total alkaloidsPrimary kratom alkaloid. Partial mu-opioid agonist with selective downstream signaling (biased agonism). Responsible for the bulk of kratom's analgesic and stimulant properties.
7-Hydroxymitragynine
< 0.02% in fresh leafMetabolite of mitragynine formed by cytochrome P450 in the body, and a trace native compound. ~13× more potent than mitragynine at the mu-opioid receptor. Isolated products are pharmacologically different from leaf kratom.
Speciogynine
~7%Smooth muscle relaxant properties. Minor contribution to overall profile.
Paynantheine
~9%Spasmolytic; theorized contribution to muscle relaxation and anti-nausea effects.
Mitraphylline
traceImmunomodulatory effects observed in vitro; unknown clinical relevance.
Speciociliatine
~1–5%Minor alkaloid with unknown pharmacological significance.
Biased agonism — why kratom isn't morphine
Mu-opioid receptors can signal through two downstream pathways: G-protein coupling (produces analgesia and mild euphoria) and β-arrestin recruitment (drives respiratory depression, constipation, tolerance, and dependence). Traditional opioids like morphine activate both pathways strongly.
Mitragynine demonstrates functional selectivity — it activates G-protein signaling disproportionately more than β-arrestin. This biased agonism is hypothesized to underlie kratom's reduced respiratory depression risk relative to morphine at equivalent analgesic doses. However, at extreme doses — or when co-administered with other CNS depressants — respiratory depression does occur.
Why vein color matters (and doesn't)
The red/white/green vein distinction is a post-harvest drying phenomenon. Extended outdoor drying oxidizes mitragynine to 7-OH in greater quantities, producing a more sedating profile characteristic of "red" kratom. Indoor, quick drying preserves higher mitragynine (more stimulating, "white"). It is NOT a genetic difference — leaves from the same branch can be processed into any vein color.
Yellow vein is a fermentation or blending artifact; not a true leaf color.
The 7-OH problem
Isolated 7-hydroxymitragynine products (sold as shots, tablets, tinctures) contain concentrations thousands of times higher than what you would extract from leaf kratom. These are pharmacologically closer to concentrated opioids than to kratom. The FDA has signaled intent to schedule isolated 7-OH. See our 7-OH watchlist.
FAQ
What makes kratom work?
Primarily mitragynine — a partial agonist at mu-opioid receptors with biased signaling toward G-protein pathways rather than beta-arrestin. This biased agonism is hypothesized to underlie kratom's lower respiratory depression risk compared to classical opioids.
Is 7-OH the "active ingredient"?
Partially. 7-OH is ~13× more potent at the mu-opioid receptor than mitragynine, but it is present at < 0.02% in fresh leaf. In your body, mitragynine is metabolized to 7-OH, so some of the effect comes from endogenous conversion. Isolated 7-OH products skip the leaf and are pharmacologically closer to concentrated opioids.
What is biased agonism?
Mu-opioid receptors activate two downstream pathways: G-protein (analgesia + euphoria) and beta-arrestin (respiratory depression + constipation). Mitragynine selectively activates G-protein signaling much more than beta-arrestin, which theoretically produces analgesia with less respiratory depression than morphine. Research is ongoing.
Does kratom contain psychoactive tryptamines?
No. Kratom alkaloids are indole-based but they are NOT tryptamines like psilocin or LSD. There is no hallucinogenic or serotonergic 5-HT2A activity. Kratom is not a psychedelic.
Why do red, white, and green veins feel different?
Drying conditions alter the mitragynine-to-7-OH ratio. Red veins are dried longer, converting more mitragynine to 7-OH (more sedating). White veins are dried faster and indoors (higher mitragynine, more stimulating). Green veins are middle-ground.