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Sufentanil is a fentanyl analog and one of the most potent opioids in clinical use, employed mainly in anesthesia and for severe pain. It is an extremely potent full mu-opioid agonist, producing profound analgesia, sedation and respiratory depression. Its sheer potency makes the margin for error tiny and overdose easy; naloxone reverses it, though repeat dosing is often needed.
- Profound pain relief
- Deep sedation
- Rapid, controllable onset in anesthesia
- Profound respiratory depression
- Chest-wall rigidity
- Extreme potency and easy overdose
- Dependence and withdrawal
Mechanism
Sufentanil is a fentanyl-class phenylpiperidine and a full at the mu-opioid receptor, the target underlying opioid analgesia, sedation and respiratory depression. It is far more potent than fentanyl itself and vastly more potent than morphine, so it is active at extraordinarily small amounts. As a mu-opioid drug it is reversible by the naloxone.
receptor fingerprint
Mu-opioid receptorFull agonist
Safetyrisks and cautions, not medical advice
Sufentanil's extreme potency is the core danger; the difference between an effective and a fatal amount is tiny, and outside controlled medical settings accurate dosing is essentially impossible. The main risk is profound respiratory depression, and it is deadly combined with other depressants such as benzodiazepines and alcohol. It can also cause chest-wall rigidity that impairs breathing. Naloxone can reverse an overdose but repeat doses are often required. Not medical advice.
Interactionsdocumented pairs only, not exhaustive
Sufentanil is cleared almost entirely by CYP3A4, which makes it unusually sensitive to inhibition of that enzyme. Modelling of ritonavir coadministration predicts more than a tenfold rise in sufentanil exposure, and ketoconazole, clarithromycin, itraconazole and cobicistat act the same way; the consequence is deeper and longer respiratory depression from a drug already given in micrograms. Strong inducers such as rifampin, carbamazepine and phenytoin run the other way and can leave analgesia inadequate.
The combination with benzodiazepines and other central nervous system depressants carries a boxed warning. Opioids and benzodiazepines suppress respiration through different receptors, and together they produce profound sedation, respiratory depression, coma and death far more readily than either alone; alcohol, gabapentinoids and sedating antihistamines add to the same picture.
Monoamine oxidase inhibitors are contraindicated within two weeks. Mixed agonist antagonists such as buprenorphine or nalbuphine displace sufentanil at the mu receptor and can precipitate withdrawal or reverse analgesia mid procedure.
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Subjective profileweighing the evidence above
A hospital drug and nothing else. Its extreme potency is a virtue under anesthesia and a lethal flaw anywhere else, because the gap between an effective and a fatal amount cannot be measured outside a clinic. Chest-wall rigidity and respiratory arrest are how that goes wrong.
Resources
No suppliers are provided for compounds like this. This entry is here for reference.
Research
- 1.Clinical pharmacokinetics of alfentanil, fentanyl and sufentanil. An update.
- 2.The risk of developing more potent fentanyl analogs: a mini review.
2 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
How potent is sufentanil?
It is one of the most potent opioids in clinical use, far stronger than fentanyl and vastly stronger than morphine, active at tiny amounts.
What is it used for?
Mainly in anesthesia and for severe pain in tightly controlled medical settings, given its extreme potency.
Does naloxone reverse it?
Yes, but because sufentanil is so potent, more than one dose of naloxone is often needed.
Adverse effects
- Profound respiratory depression
- Chest-wall rigidity
- Extreme potency and easy overdose
- Dependence and withdrawal