The short version
Plant, body, lab — three places these compounds come from.
Kratom leaves contain naturally occurring alkaloids. Once kratom is ingested, the body can form additional active compounds from those alkaloids. Separately, researchers have synthesized stronger 7-OH analogs in the lab; those analogs are not known to occur naturally in kratom leaf.
What is naturally in the leaf
Kratom leaves contain many alkaloids. Two are most relevant here:
Mitragynine
The main kratom alkaloid. In some varieties, it may account for up to ~66% of the alkaloid fraction. It affects the brain in complex ways and is not the same as a classic opioid.
7-OH
7-hydroxymitragynine. Occurs naturally in kratom leaf in trace amounts. It has stronger opioid-receptor activity than mitragynine in lab and animal studies.
What your body can form
After kratom use, liver enzymes can convert some mitragynine into 7-OH:
More 7-OH
This can add to 7-OH exposure beyond the trace amount present in the leaf alone. The 7-OH formed in the body is the same chemical as the trace 7-OH found naturally in kratom leaf.
Mitragynine pseudoindoxyl
Another opioid-active metabolite formed through 7-OH pathways. It can have stronger opioid-receptor activity than mitragynine.
What can be synthesized
Researchers have synthesized 7-OH analogs with stronger opioid-receptor activity. These analogs are not known to occur naturally in kratom leaf.
MGM-15
Semi-synthetic analog of 7-OH. Also called dihydro-7-hydroxymitragynine, DH-7OH-MIT, or DHM. Early data suggest stronger opioid-receptor activity than 7-OH.
MGM-16
A 9-fluoro analog of MGM-15. In one mouse pain model, MGM-16 was reported to be ~240× as potent as morphine. This is not a human dose conversion.
What studies suggest about relative potency
Mitragynine
Reference point (1×)
7-OH
~5–9× mitragynine in selected assays
MGM-15
Early data: stronger opioid-receptor activity than 7-OH
MGM-16
~240× morphine in one mouse pain model
General pattern in cited studies — not to scale
Quick reference
Compound table.
| Compound | Where it comes from | What it is | Study-based potency signal |
|---|---|---|---|
| Mitragynine | Natural in kratom leaf (up to ~66% of leaf alkaloids) | Main kratom alkaloid; complex pharmacology | 1×reference point |
| 7-OH= 7-hydroxymitragynine | Trace amounts in leaf + body can form more from mitragynine | Natural minor alkaloid/metabolite with stronger opioid-receptor activity than mitragynine | ~5–9×mitragynine in selected assays |
| Dihydro-7-OH= MGM-15 = DH-7OH-MIT | Semi-synthetic analog of 7-OH | A semi-synthetic 7-OH analog; early data suggest higher opioid-receptor activity | Early data suggest> 7-OH; limited human data |
| MGM-16 | Synthetic 9-fluoro analog of MGM-15 | Experimental analog studied in animals | ~240×morphine in one mouse pain model |
Treatment context
Why buprenorphine/naloxone, often called Suboxone, can help with kratom and 7-OH dependence.
Buprenorphine is the part of buprenorphine/naloxone, often known by the brand name Suboxone, that acts at opioid receptors. It binds tightly to mu-opioid receptors. Opioid-active kratom compounds, including mitragynine and especially 7-hydroxymitragynine, also act on this receptor system.
When buprenorphine is started at the right time and dose, it can occupy those receptors in a steadier way and may help reduce opioid-like withdrawal symptoms and cravings in selected patients. Timing matters because buprenorphine binds tightly. If a larger dose is started too soon, before kratom or 7-OH effects have worn down enough, symptoms can suddenly worsen. This is called precipitated withdrawal.
Buprenorphine is a partial opioid agonist. In plain English, it turns the opioid receptor on only partway. That can be enough to help with withdrawal and cravings for some patients, but it does not activate the receptor in the same way as a full opioid agonist. Some effects level off at higher doses, which is often called the ceiling effect.
This partial-agonist effect is one reason many patients, once on a stable dose, feel steady rather than high or in withdrawal. Suboxone can still cause sleepiness, slowed breathing, or impairment, especially when starting treatment, after dose changes, or when combined with alcohol, benzodiazepines, gabapentin, pregabalin, or other sedating substances.
Using buprenorphine/naloxone for kratom or 7-OH dependence is off-label. The evidence is still limited, especially for concentrated 7-OH products, and comes mainly from case reports, case series, clinical experience, and opioid-receptor pharmacology. The decision should be individualized.