Clinical guide to 7-OH and kratom alkaloids
Five modules written for prescribers: what these compounds do at the receptor, what they turn into and how to detect them, the full compound-by-compound chemistry reference, what withdrawal looks like and how to treat it, and where the traps are. Read in order, or jump to what you need at the bedside.
Receptor pharmacology
The defensible activated-receptor map across μ, δ and κ. Why “7-OH is a partial μ-agonist” is the wrong sentence and what to say instead. Signalling efficacy, receptor reserve, and biased-agonism claims with their honest caveats. What should not go on the diagram. And the composite reason withdrawal from this class does not look like textbook opioid withdrawal.
Read module 01 → Module 02Kinetics, metabolism & testing
The metabolic map, core compounds and clinically important metabolites, elimination, and toxicology testing — what to order, why the routine opiate immunoassay will not find these compounds, and how to read the result you get back. Ends with an explicit inventory of what remains genuinely unknown.
Read module 02 → Module 03 · ReferenceChemistry & detection reference
The long-form working reference: every pharmacologically relevant alkaloid, active metabolite, and semisynthetic analogue, with category, why it matters clinically, and its human detection status. Built on an explicit evidence rule — a compound is called an active metabolite only when it is both a demonstrated metabolite and shown to be pharmacologically active.
Open the reference → Module 04Withdrawal course & treatment
Dependence phenomenology, the provisional timeline and why it is only provisional, the COWS problem, five-step intake and triage, standard versus low-dose buprenorphine initiation, alternatives, symptom-targeted adjuncts, what not to do, and the argument for using the least intensive setting that is safe.
Read module 04 → Module 05Toxicity, comorbidity & interactions
Evidence-ranked clinical manifestations of toxicity, emergency management including naloxone responsiveness and its limits, clinically significant drug interactions, and special populations — separated throughout into what is known, what is extrapolated, and where the data are insufficient.
Read module 05 → Bedside toolClinical assessment & disposition template
A printable worksheet covering exposure characterisation, dependence phenotype, current syndrome, coexposures and medication reconciliation, medical and social risk, a disposition screen, a treatment plan, and suggested note language. Adaptable, and explicitly not a validated instrument.
Open the worksheet → SourcesEvidence library
Every [E##] marker in these modules resolves to a record here: the citation, the evidence type, the key finding, and the limitations the source itself acknowledges. Graded A to D and filterable by domain.
Audit the sources →The evidence base is uneven: strong analytical chemistry and authoritative regulatory documents, useful but small human treatment data, and almost no controlled human work on the high-dose exposures that matter most clinically. Every claim therefore carries a certainty label — Established, Emerging, Mechanistically plausible, Practice-based synthesis, or Data insufficient.
This is a practice-based clinical framework, not a national guideline, and not a standard of care. It does not replace examination, local protocols, toxicology consultation, or individualised judgement. It is designed to be corrected as direct 7-OH evidence accumulates.
The five-minute version
If a patient is in front of you now and four modules is three too many, this is the compressed version. Everything in it is expanded and cited in the modules themselves.
| Question | Short answer | Detail |
|---|---|---|
| Is this real opioid withdrawal? | Yes. 7-OH is a high-potency μ-opioid receptor agonist. Treat it as opioid withdrawal, with modifications. | Module 01 |
| How do I ask about it? | By product, not by category. Ask about 7-OH, 7-hydroxy, kratom extract tablets, films, shots, gummies, and anything labelled MGM-15, MGM-16, or pseudoindoxyl. Ask the dosing interval, not just the daily total. | Module 04 |
| Will a urine opiate screen detect it? | No. Do not use a routine opiate immunoassay to exclude exposure. Targeted mass spectrometry is required. | Module 02 |
| Is buprenorphine appropriate? | It has the best direct published treatment signal so far, using either standard or clinician-directed low-dose initiation. | Module 04 |
| How many hours after the last dose? | There is no validated answer, and anyone giving you one is guessing. Use convincing clinical withdrawal and the whole exposure picture, not a stopwatch. | Module 04 |
| Does everyone need residential treatment? | No. Most patients can be managed as outpatients, and reserving beds for genuine indications is both a clinical and a public-health priority. | Module 04 |
| What makes this withdrawal atypical? | A composite syndrome with prominent autonomic, affective, and sleep features that COWS under-captures — a published high-dose patient remained substantially symptomatic at about 48 hours with a COWS of only 5. | Module 01 |
| What are the acute red flags? | Respiratory depression, altered mental status, seizure, cardiovascular instability, and sedative or alcohol co-ingestion. | Module 05 |
Clinician-to-clinician consultation is offered directly
Exposure history, withdrawal assessment, induction strategy, precipitated-withdrawal risk, differential diagnosis, level-of-care decisions. Collegial consultation, not a referral.
Educational content for licensed professionals. Not medical advice, not a standard of care, and no physician–patient relationship is created. Anyone experiencing withdrawal from or toxicity due to kratom or 7-OH products should be evaluated by an addiction medicine professional — start with the buprenorphine prescriber finder.