7-OH (7-Hydroxymitragynine)

Concentrated 7-hydroxymitragynine, how it differs from kratom leaf, why dependence builds fast, and what makes it taperable.

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

Regulatory news: on July 1, 2026, DEA filed 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. Dates, scope, and the public comment window: The Federal 7-OH Ban.

7-OH is the compound this site is named after, and the compound most people here are trying to get off of. It walks and talks like an opioid. Whatever the gas-station marketing says, whatever the “all-natural kratom alkaloid” framing implies, the practical reality is that 7-OH binds the mu-opioid receptor, produces opioid-class dependence, and goes through opioid-class withdrawal when you stop.

The good news, if there is good news: 7-OH’s pharmacology is favorable for coming off it. Short half-life, mu-dominant, fast clearance, the same things that make it easy to get hooked also make it tapereable in days rather than weeks once you commit to stopping.

Overview

7-hydroxymitragynine is one of the natural alkaloids of the kratom plant (Mitragyna speciosa), where it appears in trace amounts: typically well under 1% of total leaf alkaloid content. Mitragynine, the main alkaloid, dominates leaf at 40-66%. So 7-OH-as-it-exists-in-leaf is a minor character.

What’s sold as “7-OH” in tablet, shot, and liquid form is concentrated or semi-synthetic 7-hydroxymitragynine, extracted, isolated, or synthesized to deliver doses far above anything achievable from leaf. A single 5–15 mg 7-OH tablet contains more 7-OH than several grams of leaf would. The marketing language (“kratom enhanced”, “all-natural”) obscures this scale difference; the dependence reality doesn’t.

Pharmacology, briefly

Mu-opioid receptor: at the human µ-receptor, 7-OH binds with K_i around 78 nM and acts as a partial agonist (Hiranita et al. 2022, CHO-hMOR). Morphine binds tighter in the same assay (K_i ~4 nM), but it’s a full agonist with higher E_max. The “13× more potent than morphine” claim that circulates in secondary sources is from rodent antinociception assays (potency by weight in mouse tail-flick / hot-plate), not from human receptor binding. Mitragynine binds weakly at hMOR (K_i ~709 nM) with little to no agonism in the same assay.
Agonist character: partial agonist at the µ-receptor (E_max ~41% in [³⁵S]GTPγS at hMOR), with functional EC50 (~43 nM) about 3× lower than morphine’s (~125 nM). The lower E_max is part of why the recreational reputation focuses on the ceiling-vs-full-agonist distinction. Functionally, 7-OH produces opioid-class analgesia, sedation, euphoria, and (over time) dependence.
Receptor selectivity: mu-dominant. Little meaningful activity at κ or δ receptors at typical doses, and far less of the serotonergic and adrenergic activity that leaf carries via its other minor alkaloids (see Minor Alkaloids).

Plasma half-life

Short. No direct human PK study of standalone 7-OH has been published. The community-observed effect duration is roughly 90 minutes to a couple of hours, which fits the typical 3–6 hour redosing cadence. Published clinical PK reports the 7-OH metabolite (formed in the body after oral mitragynine) at a median ~4 hours single-dose and ~9 hours with repeated dosing (Tanna et al., 2024). Direct beagle-dog PK of 7-OH reports an elimination half-life of 3.6 ± 0.5 hours (Fan et al., 2020). The “~100 minutes” figure that circulates in community discussion describes effect duration, not a formally measured human plasma half-life.

7-OH is short by opioid standards, much shorter than MGM-15 or methadone’s 24+ hours.

The dosing pattern follows from the half-life: most habitual 7-OH users redose every 3–6 hours during waking hours, and many wake up at night needing a dose. That redosing cadence is the most visible behavioral signature of a 7-OH habit.

7-OH vs. kratom leaf

Calling 7-OH “kratom” is technically true and practically misleading. The differences that matter:

Property	Leaf kratom (mitragynine-dominant)	Concentrated 7-OH
Main active alkaloid	Mitragynine (~40-66% of leaf)	7-OH (isolated)
µ-receptor binding affinity	Weak (K_i ~709 nM at hMOR)	Moderate (K_i ~78 nM at hMOR)
µ-agonism efficacy	Minimal at hMOR	Partial agonist (E_max ~41%)
Serotonergic / adrenergic activity	Significant (via minor alkaloids)	Minimal
Typical use cadence	Every 4-6 h, often less	Every 3-6 h, often more
Dependence trajectory	Slow	Fast (weeks to months)
Withdrawal severity	Mild to moderate	Moderate to severe
Withdrawal duration (acute)	Several days	5-10 days
Bupe-induction profile	Straightforward	Straightforward (12-18 h)

The shorthand: kratom leaf is to 7-OH roughly what poppy tea is to heroin. Same plant family, vastly different concentration and delivery. The pharmacology that makes 7-OH attractive (faster onset, stronger effect, smaller dose to carry around) is the same pharmacology that makes dependence form quickly.

This is also why tapering off concentrated 7-OH using plain leaf is a planned protocol used by some people in this community. The leaf delivers vastly lower concentrations of the same family of alkaloids, so stepping down is a meaningful taper rather than a switch.

Withdrawal profile

Acute 7-OH withdrawal follows a recognizable opioid-withdrawal arc, compressed into days because of the short half-life:

Time since last dose	What’s happening
6-12 hours	First symptoms, anxiety, restlessness, sweating, runny nose, aches
12-24 hours	Symptoms climb, diarrhea, chills, goosebumps, insomnia, cravings
24-72 hours	Peak, body aches, restless legs, no sleep, profound discomfort
Days 3-5	Symptoms start lifting; sleep returns in fragments
Week 2 onward	Acute mostly done; welcome to PAWS

The peak is awful but time-limited. Most people are through the worst by day 5, into “functional but drained” by day 7, and out of acute by week 2. The post-acute tail (PAWS) is its own chapter and is usually much more manageable than peak acute.

The serotonergic and adrenergic overlay

7-OH itself isn’t particularly active at serotonergic or adrenergic receptors, but the concentrated kratom-derived products people use are rarely pure 7-OH. Many are stacked with mitragynine, other minor alkaloids, or undisclosed compounds. Two of those minor alkaloids, paynantheine and speciogynine, bind 5-HT_1A and 5-HT_2B receptors at low-nanomolar affinity (León et al., J Med Chem 2021), and corynantheidine binds α-1 and α-2 adrenergic receptors directly (corynantheidine α-1D Kᵢ 41.7 nM is selective and tight; mitragynine itself binds these receptors only weakly, at micromolar affinity; Obeng et al., J Med Chem 2020; Obeng et al., Eur J Pharmacol 2024). This is direct receptor activity, not SSRI/SNRI-style reuptake inhibition, but the resulting withdrawal symptom picture (brain zaps, wired-but-exhausted feeling, autonomic instability) looks a lot like SSRI/SNRI discontinuation because the same receptor families are involved. See Why Suboxone Might Not Be Working for why this overlay makes bupe alone feel insufficient for some people, and Helper Medications for what addresses the non-opioid side.

Tapereability, mechanistically

Counter-intuitively, the same pharmacology that makes 7-OH addictive is what makes coming off it relatively clean:

Short half-life means the drug leaves your system fast. Once you stop, plasma 7-OH is gone within ~10 hours. Receptor adaptation starts reversing immediately.
Mu-dominant binding means a mu-opioid medication like Suboxone (buprenorphine) substitutes cleanly. There’s no delta-receptor component left dangling (unlike MGM-15) and no unusually-tight binding that fights bupe induction (unlike pseudo).
Predictable bupe-induction window: COWS ≥ 12 usually arrives 12-18 hours after last dose, which fits well into a same-day telehealth Suboxone appointment.
Short receptor adaptation: because dependence on 7-OH typically develops over months (not years), the underlying receptor changes are less entrenched than they are with long-term full-agonist use.

This is why the rapid-taper protocol in Suboxone Rapid Taper works for so many people coming off 7-OH alone, and why this community leans toward short Suboxone tapers rather than indefinite maintenance for this population specifically. See Suboxone for the full overview, including the receptor-occupancy reason we start at low Suboxone doses rather than the clinical-default 16-24 mg.

Common forms

7-OH shows up in retail under a few names and formats:

Tablets / “7s”: typically 5-15 mg per tablet, often marketed as “tianeptine-free” or “kratom enhanced”. The dominant gas-station format.
Liquid shots: 1-2 oz bottles labeled by mg or by “potency”, often inconsistent between batches.
“Pseudo” tablets and shots: these are mitragynine pseudoindoxyl (MP), a different compound that binds even tighter than buprenorphine. Sometimes labeled or co-marketed with 7-OH; the pharmacology is different enough that you need to know which you’ve been on.
Stacked products: combinations of 7-OH, mitragynine, pseudoindoxyl, and sometimes MGM-15 or MIT-A/DHM. The label may say “kratom extract” and tell you nothing about what’s in it.
Raw 7-OH powder: less common in retail; more common in enthusiast communities. Tends to be the most concentrated form.

If you’re not sure what you’ve been on, that’s important to figure out before induction, the long-acting compounds (MGM-15, pseudo) have different timelines and different induction-window requirements. See the half-life table in COWS & SOWS Guide.

Marketing claims to be skeptical of

Retail 7-OH marketing tends toward a recurring set of claims, most of which don’t survive the pharmacology:

“Non-addictive”, false. The dependence profile is opioid-class. The withdrawal profile is opioid-class. The receptor mechanism is opioid-class.
“All-natural / just kratom”, technically the molecule exists in the plant, but the concentrations sold retail are orders of magnitude beyond what leaf delivers. Calling a 15 mg 7-OH tablet “natural” because the alkaloid is plant-derived is the same argument as calling pure morphine “natural” because poppies make it.
“Safer than opioids”, 7-OH binds the same mu-opioid receptors and produces the same dependence and withdrawal pattern as a classical opioid. The “safer” claim usually rests on the ceiling-effect-at-the- receptor argument, which has some truth at high doses but doesn’t change the dependence and withdrawal trajectory at typical use levels.
“Doesn’t cause respiratory depression”, disputed. Pure mitragynine in animal models has shown a respiratory ceiling effect, but real-world products are not pure mitragynine, are often stacked with other alkaloids, and are frequently combined by users with alcohol, benzos, or other depressants, any of which restores respiratory-depression risk. Get Narcan. See For Loved Ones for more.
“FDA approved” / “Doctor recommended”, almost always not true. Trace mitragynine appears in some research contexts, but no concentrated 7-OH product has FDA approval as of this writing.

If you’re trying to stop

See Paths Off 7-OH for the six ranked paths this community has used, in the order to try them. The Withdrawal Help page covers what to do hour-by-hour once you’ve picked one.

Whichever path you take, don’t try to navigate it without at least one other person knowing. The Discord and subreddit linked at Community are where most people in this position end up.