REMIFENTANIL 1 mg ADCO
Remifentanil Hydrochloride equivalent to Remifentanil
What it does
Remifentanil is a powerful pain relief medicine used mainly during surgery.
Commonly used for: pain relief during surgery, anesthesia
Read more in plain English ↓Plain-language summary for general understanding - not medical advice. Always follow your pharmacist/doctor.
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Sourcing - Kenya onlyRegistration & product details
Source: South African Health Products Regulatory Authority · fetched 2026-04-15 21:13:02 · updated 2026-09-16 04:00:12
Drug Interactions
60Pharmacodynamic Warnings
Remifentanil appears in TABLE 6: Drugs that cause bradycardia
Remifentanil appears in TABLE 11: Drugs with CNS depressant effects
Severe (6)
Opioids - decreases concentration
Brigatinib potentially decreases the concentration of opioids (alfentanil, fentanyl). Avoid. Also see TABLE 6 p. 1518
Opioids - increases exposure
Ceritinib is predicted to increase the exposure to opioids (alfentanil, fentanyl). Avoid. Theoretical → Also see TABLE 6 p. 1518
Opioids - increases risk of cnstoxicity
Ritonavir increases the risk of CNS toxicity when given with opioids (pethidine). Avoid.
Opioids - decreases exposure
Lorlatinib is predicted to decrease the exposure to opioids (alfentanil, fentanyl). Avoid.
Opioids - increases risk of adverse effects
Selegiline increases the risk of adverse effects when given with opioids (pethidine). Avoid. Also see TABLE 13 p. 1520
Opioids - increases exposure
Selpercatinib is predicted to increase the exposure to opioids (alfentanil, buprenorphine). Avoid.
Moderate (31)
Opioids - increases exposure
Dronedaroneispredictedtoincreasetheexposuretoopioids (alfentanil,buprenorphine,fentanyl,oxycodone).Monitorand adjustdose.oStudy →AlsoseeTABLE6p.1518
Opioids - increases concentration
Amiodarone is predicted to increase the concentration of opioids (fentanyl). Monitor and adjust dose. Also see TABLE 6 p. 1518.
Opioids - decreases concentration
Carbamazepine decreases the concentration of opioids (tramadol). Adjust dose.
Opioids - increases exposure
Miconazole is predicted to increase the exposure to opioids (alfentanil). Use with caution and adjust dose.
Opioids - increases exposure
Antifungals, azoles (fluconazole, isavuconazole, posaconazole) are predicted to increase the exposure to opioids (alfentanil, buprenorphine, fentanyl, oxycodone). Monitor and adjust dose.
Unknown (23)
Drugs That Cause Serotonin Syndrome - increases risk of serotonin syndrome
Opioids (tapentadol) are predicted to increase the risk of serotonin syndrome when given with drugs that cause serotonin syndrome (see TABLE 13 p. 1520). Theoretical drugs that reduce serum potassium.
Opioids - additive effect
Clozapine can cause constipation, as can opioids; concurrent use might increase the risk of developing intestinal obstruction. Also see TABLE 11 p. 1519
Opioids - increases exposure
Asciminibispredictedtoincreasetheexposuretoopioids (alfentanil).rTheoretical
Opioids - increases exposure
Bictegravirispredictedtoincreasetheexposuretoopioids (methadone).oTheoretical
Opioids - increases exposure
Bulevirtideispredictedtoincreasetheexposuretoopioids (alfentanil).oTheoretical
Data from BNF 85 (British National Formulary). This is not a substitute for professional medical advice. Matched via: class
About this medicine
Remifentanil is a powerful pain relief medicine used mainly during surgery.
What it treats
- pain relief during surgery
- anesthesia
How it works
Remifentanil works by blocking pain signals in the brain, helping to reduce the sensation of pain.
Who it's for
This medicine is for patients undergoing surgery who need strong pain control.
Drug class
Opioids
Cautions
- • Be careful if you are taking medications that slow down your heart rate.
- • Avoid using with drugs that can cause drowsiness or sedation.
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
Clinical monograph: Remifentanil
BNF-referencedRemifentanil is an ultra-short-acting synthetic opioid analgesic, primarily used as an adjunct in anesthesia. It is a potent mu-opioid receptor agonist, providing rapid onset of analgesia and sedation. Due to its unique metabolism, it has a very short duration of action, making it suitable for procedures requiring quick recovery times and minimal post-operative pain management.
Indications
- Induction of anesthesia
- Maintenance of anesthesia
- Analgesia for surgical procedures
- Assisted ventilation in intensive care settings
Dosage
Children: Refer to the BNF for Children for specific paediatric dosing guidelines.
Adults: Initially 0.25–1 microgram/kg administered over at least 30 seconds for induction. For maintenance, an intravenous infusion starting at 2.4 micrograms/kg/hour, adjusted carefully according to response, with a usual range of 1.5–6 micrograms/kg/hour. Additional doses can be given every 2–5 minutes as needed.
Mechanism of action
Remifentanil acts as a selective mu-opioid receptor agonist, exhibiting greater affinity for the mu-receptors compared to delta- or kappa-receptors. Its action leads to analgesia and respiratory depression, with the latter potentially mediated by distinct mu2-receptors. The drug's rapid metabolism by plasma esterases results in a short duration of action that is independent of dose and infusion duration. Opioid activity can be reversed by antagonists such as naloxone.
Pharmacodynamics
Remifentanil demonstrates rapid onset and peak effects, with ultra-short duration of action. Its analgesic effects are dose-dependent, similar to other opioids, and its side effects include respiratory depression, which can occur even at therapeutic doses. The drug achieves quick blood-brain equilibration, contributing to its effectiveness in acute pain management during surgical procedures.
Pharmacokinetics
Remifentanil is rapidly metabolized by plasma esterases, leading to a short half-life. Its effects are characterized by rapid onset and offset, with a mean blood-brain equilibration half-time of approximately 1 minute. It does not accumulate significantly with prolonged infusions, making it distinct from other opioids that have longer durations of action.
Contra-indications
- Hypersensitivity to remifentanil or any of its components
- Severe respiratory depression
- Acute or severe bronchial asthma
- Concurrent use with monoamine oxidase inhibitors (MAOIs)
Adverse effects
- Respiratory depression
- Hypotension
- Muscle rigidity
- Nausea
- Vomiting
- Bradycardia
- Cardiac arrest (rare)
- Agitation (uncommon)
- Atrioventricular block (rare)
- Hypertension (rare)
- Seizures (rare)
- Hypoxia (uncommon)
Interactions
- Caution with other central nervous system depressants (e.g., benzodiazepines, barbiturates)
- Increased effects with other opioids
- Potentially increased risk of respiratory depression with sedatives
- Opioid antagonists such as naloxone can reverse remifentanil's effects
Precautions
- Use with caution in patients with hepatic impairment
- Use with caution in patients with renal impairment
- Monitor for respiratory depression in opioid-naive patients
- Careful titration is advised, especially in elderly patients or those with significant comorbidities
Pregnancy
Remifentanil should only be used during pregnancy if the potential benefit justifies the potential risk to the fetus. Consult local guidelines.
Breast-feeding
Present in milk; withhold breastfeeding for 24 hours after administration.
Storage
Store at room temperature, protect from light. Discard any unused solution.
Formulations
- 5 mg/mL solution for injection
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Molecular reference: Remifentanil
PubChem CID 60815Molecular formula: C20H28N2O5
Mechanism of action
Remifentanil is a µ-opioid agonist with rapid onset and peak effect, and short duration of action. The µ-opioid activity of remifentanil is antagonized by opioid antagonists such as naloxone. Remifentanil is a selective mu-receptor agonist with similar potency to fentanyl; the drug shares the actions of the opiate agonists. The drug's precise mechanism of action has not been fully elucidated; opiate agonists act at several CNS sites, involving several neurotransmitter systems to produce analgesia. Remifentanil exhibits greater affinity for the mu-receptor than for the delta- or kappa-receptors; the drug does not substantially bind to other nonopiate receptors. Agonist activity at the opiate mu-receptor can result in analgesia and respiratory depression. Respiratory depression may be mediated by mu-receptors, possibly mu2-receptors (which may be distinct from mu1-receptors involved in analgesia); kappa- and delta-receptors may also be involved in respiratory depression. Remifentanil is a powerful mu-opioid (MOP) receptor agonist used in anesthesia with a very short half-life. However, per-operative perfusion of remifentanil was shown to increase morphine consumption during post-operative period to relieve pain. In the present study, we aimed to describe the cellular mechanisms responsible for this apparent reduction of morphine efficacy. For this purpose, we first examined the pharmacological properties of both remifentanil and morphine at the MOP receptor, endogenously expressed in the human neuroblastoma SH-SY5Y cell line, to regulate adenylyl cyclase and the MAP kinase ERK1/2 pathway, their potency to promote MOP receptor phosphorylation, arrestin 3-CFP (cyan fluorescent protein) recruitment and receptor trafficking during acute and sustained exposure. In the second part of this work, we studied the effects of a prior exposure of remifentanil on morphine-induced inhibition of cAMP accumulation, activation of ERK1/2 and analgesia. We showed that sustained exposure to remifentanil promoted a rapid desensitization of opioid receptors on both signalling pathways and a pretreatment with this agonist reduced signal transduction produced by a second challenge with morphine. While both opioid agonists promoted Ser(375) phosphorylation on MOP receptor, remifentanil induced a rapid internalization of opioid receptors compared to morphine but without detectable arrestin 3-CFP translocation to the plasma membrane in our experimental conditions. Lastly, a cross-tolerance between remifentanil and morphine was observed in mice using the hot plate test. Our in vitro and in vivo data thus demonstrated that remifentanil produced a rapid desensitization and internalization of the MOP receptor that would reduce the anti-nociceptive effects of morphine. Opioids are the most effective and widely used drugs in the treatment of severe acute and chronic pain. They act through opioid receptors that belong to the family of G protein-coupled receptors. Three classes of opioid receptors (mu, delta, kappa), expressed in the central and peripheral nervous system, have been identified. The analgesic effect of opioids is mediated through multiple pathways of opioid receptor signaling (e.g., G(i/o) coupling, cAMP inhibition, Ca(++) channel inhibition). The standard exogenous opioid analgesics used in the operating room are fentanyl, sufentanil, morphine, alfentanil, and remifentanil. The ultra-short-acting mu-opioid receptor (MOR) agonist remifentanil enhances postsurgical pain when used as main anesthetic in animal models and man. Although the mechanism/s involved are poorly characterized, changes in opioid receptor expression could be a relevant feature. Using a mouse model of postoperative pain, we assessed the expression of MOR and delta opioid receptors (DORs) and the efficacy of Herpes Simplex vector-mediated proenkephalin release (SHPE) preventing postoperative nociceptive sensitization induced by remifentanil or surgical incision. We dete
Pharmacodynamics
Remifentanil is an opioid agonist with rapid onset and peak effect and ultra-short duration of action. The opioid activity of remifentanil is antagonized by opioid antagonists such as naloxone. The analgesic effects of remifentanil are rapid in onset and offset. Its effects and side effects are dose dependent and similar to other opioids. Remifentanil in humans has a rapid blood-brain equilibration half-time of 1 ± 1 minutes (mean ± SD) and a rapid onset of action.
Biological pathways
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.
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The same active ingredient registered across other registries we cover - including different brands.