Plain language summary

Buprenorphine/naloxone (Suboxone) is a medication used to treat opioid dependence — it reduces withdrawal and cravings. This card is a prescribing reference for doctors. If you are a patient, your doctor will guide you through starting and continuing this treatment.

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Medication Reference Card — Opioid Use Disorder

Buprenorphine/Naloxone Sublingual

Suboxone® & generic · S100 (MATOD) · Induction: COWS ≥8–12 · Maintenance: 8–24 mg/day

Dr Basanth Kenchaiah
FRANZCP · MBBS · DPM · DNB (Psychiatry) · Cert. Addiction Psych. Addiction Psychiatrist v1.0 · May 2026
Audience Clinicians
Purpose Prescribing quick-reference for sublingual buprenorphine/naloxone (Suboxone®) in opioid use disorder (OUD).
Key messages
  • Partial mu-agonist with naloxone deterrent — reduces withdrawal, craving and illicit opioid use
  • Induction when COWS ≥8–12; start 2–4 mg sublingual; titrate to 8–24 mg/day maintenance
  • S100 (MATOD) in Victoria — confirm enrolment and dispensing pharmacy before initiation

For Patients

Buprenorphine is a medication that partially activates opioid receptors, reducing cravings and withdrawal symptoms without producing the high of stronger opioids. The naloxone component discourages misuse by injection. It is taken as a film or tablet under the tongue and can be prescribed by authorised GPs and specialists.

Particularly useful when comorbid with:
Prescription opioid analgesic dependence (analgesic activity — dual benefit) Chronic pain with opioid use disorder Depression / anxiety (kappa antagonism — antidepressant properties) Pregnancy (mono buprenorphine preferred — consult specialist) Previous overdose / high relapse risk Unable to attend daily methadone dosing

For Clinicians

Mechanism

Buprenorphine: Partial mu-opioid agonist with very high receptor affinity, slow dissociation (long half-life 24–60 hrs), and ceiling effect for respiratory depression. Displaces full agonists — precipitates withdrawal if initiated before patient is in moderate withdrawal (COWS ≥8–12). Naloxone: short-acting antagonist; minimally absorbed sublingually but active if injected (abuse deterrent). Combination produces stable opioid receptor occupancy, eliminates cravings, and blocks the reinforcing effects of additional opioids.

Dosing & Induction

Standard induction: 2–4 mg SL when COWS ≥8–12 (moderate withdrawal) — observe 1 hour, re-dose if tolerated. Titrate to 8–16 mg on day 1. Maintenance: 8–24 mg/day (most patients 12–16 mg/day). Low-dose induction (Bernese method): begin 0.5–1 mg while patient still on full agonist, increase gradually over days — avoids precipitated withdrawal entirely. S100 in Australia — requires MATOD enrolment and prescriber authority.

Evidence

Strong evidence. Fudala et al. NEJM 2003: buprenorphine/naloxone significantly superior to placebo for opioid use disorder. NIDA CTN 0003: comparable to methadone for prescription opioid dependence. Lee et al. Lancet 2018 (X:BOT trial): extended-release naltrexone vs buprenorphine — both effective; buprenorphine easier to initiate (lower induction failure rate).

Cautions
  • Precipitated withdrawal risk — use COWS scale; wait for score ≥8–12 before first dose (or use Bernese method)
  • QTc prolongation: less concern than methadone, but baseline ECG reasonable in high-risk patients
  • Concurrent benzodiazepines: significant respiratory depression risk — risk vs benefit discussion, consider supervised dispensing
  • S100 in Australia — requires MATOD enrolment (authorised prescriber or addiction specialist)
  • Hepatotoxicity rare but documented — monitor LFTs at baseline and periodically
  • In pregnancy: mono buprenorphine (without naloxone) preferred — consult addiction medicine/obstetrics specialist