Sufentanil 30microgram sublingual tablets sugar free
Requires a prescription from a doctor or prescriber
Sufentanil is an opioid analgesic that is used as an adjunct in anesthesia, in balanced anesthesia, and as a primary anesthetic agent.
Strict controls: safe custody, register required
Legal requirements and restrictions
These are medicines with high potential for misuse but with accepted medical uses. Subject to the strictest controls.
Legal requirements
- Must be stored in a locked controlled drugs cabinet
- Pharmacy must keep a controlled drugs register
- Prescriptions valid for 28 days only
- Prescriptions must include specific details (dose, form, strength, total quantity)
- Cannot be emergency supplied by pharmacists
Other medicines in this category
Morphine, Oxycodone, Fentanyl, Methylphenidate (Ritalin), Amphetamines
Safety information for pregnancy and breastfeeding
Pregnancy
Sufentanil caused embryolethality in rats and rabbits treated for 10-30 days during pregnancy with 2.5 times the maximum human dose by intravenous administration.
May cause fetal harm [FDA label]
The Use in Lactation
Infants exposed to this drug through breast milk should be monitored for excess sedation and respiratory depression [FDA label].
Breastfeeding
May cause fetal harm [FDA label]
The Use in Lactation
Infants exposed to this drug through breast milk should be monitored for excess sedation and respiratory depression [FDA label].
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
Official documents, adverse reaction reporting, and safety monitoring
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Safety monitoring data
Yellow Card reports
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Suspected adverse reactions reported for Sufentanil
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
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Suspected adverse reactions reported for Sufentanil
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
1 branded products available
MHRA licensed products
View all licensed products for Sufentanil on the MHRA register
Dzuveo 30microgram sublingual tablets
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Supply & safety information
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 8 · Randomised trials: 42 · 2014–2026
Showing the 50 most relevant studies, sorted by most relevant.
C. Hutchings, K. Yadav, Warren J. Cheung, et al.
The American journal of emergency medicine, 2023
Manman Yao, Baoxia Fang, Jinguo Yang, et al.
Frontiers in Pharmacology, 2024
Objective: Patient-controlled intravenous analgesia (PCIA) can alleviate pain to some extent, and several randomized controlled trials (RCTs) have examined the efficacy of esketamine-assisted sufentanil in postoperative PCIA. In this research, we conducted a meta-analysis of relevant RCTs to compare the effect and safety of esketamine-sufentanil versus sufentanil alone for postoperative PCIA.Methods: We systematically searched the Cochrane Library, PubMed, Embase, Web of Science, CNKI, and other libraries up to December 2023 to screen out RCTs examining the use of esketamine combined with sufentanil for PCIA. We analysed analgesia scores, sedation scores, adverse drug reactions and postpartum depression scores as outcome indicators.Results: This meta-analysis included 32 RCTs. The results of the meta-analysis were as follows. 1) Visual Analog Scale: The VAS scores at 6, 12, 24, and 48 h were lower in the esketamine-sufentanil group than in the sufentanil alone group, and significant differences were found at all time points (p < 0.05). 2) Ramsay Sedation Scale: The sedation score of the esketamine-sufentanil group at 48 h after surgery was higher than that of the sufentanil group alone [mean difference (MD) = −0.09 points, confidence interval (CI): (−0.26, −0.07), p = 0.27], but this difference was not significant (p > 0.05). 3) Safety: Compared with sufentanil alone, the incidence rates of postoperative nausea-vomiting, dizziness-headache, skin pruritus and respiratory depression were significantly lower in the esketamine-sufentanil group. 4) Postartum depression: The reduction in postpartum depression scores were significantly greater in the esketamine-sufentanil group than in the sufentanil alone group at 3 days [MD = −1.35 points, CI: (−1.89, −0.81), p < 0.00001] and 7 days [MD = −1.29 points, CI: (−2.42, −0.16), p = 0.03].Conclusion: The meta-analysis showed that the use of esketamine combined with sufentanil for postoperative PCIA could improve postoperative analgesia, alleviate postpartum depression and reduce the rate of postoperative adverse reactions, but there was no significant difference in sedation.
Abstract licence: CC BY 4.0
Wan J, Li J, Liao L, et al.
2026
BackgroundOliceridine is a novel µ-opioid receptor agonist designed to reduce opioid-related adverse events while maintaining effective analgesia. However, randomized controlled trials comparing oliceridine with conventional opioids, such as sufentanil, have yielded inconsistent results. This systematic review and meta-analysis aims to compare the effects of oliceridine and sufentanil on postoperative nausea and vomiting.MethodsWe searched PubMed, Embase, and the Cochrane Library databases to identify all randomized controlled trials published from the inception through March 14, 2026, that examined the effects of oliceridine and sufentanil on postoperative nausea and vomiting. Data analysis was performed using RevMan 5.4 software. Binary outcomes were analyzed using risk ratios and 95% confidence intervals, while continuous variables were expressed as mean differences. The risk of bias in the included studies was assessed using the Cochrane Risk of Bias Tool.ResultsTen randomized controlled trials involving 1408 patients met the inclusion criteria. Compared with sufentanil, oliceridine was associated with a lower incidence of postoperative nausea and vomiting (RR = 0.46, 95% CI 0.36-0.58, P ConclusionsOliceridine may reduce the risk of postoperative nausea and vomiting and respiratory depression compared with sufentanil while maintaining comparable analgesic efficacy. These findings support the potential role of oliceridine as an alternative opioid for perioperative analgesia.
Abstract licence: CC BY-NC-ND
Miaomiao Feng, Xuhui Chen, Tongtong Liu, et al.
BMC Anesthesiology, 2019
BackgroundPrevious studies have demonstrated that dexmedetomidine improves the quality of postoperative analgesia. In the present study, we performed a meta-analysis of randomized controlled trials to quantify the effect of dexmedetomidine as an adjuvant to sufentanil for postoperative patient-controlled analgesia (PCA).MethodsPubMed, Embase, the Cochrane Library, and Web of Science were systematically searched for randomized controlled trials in which dexmedetomidine was used as an adjuvant for PCA with sufentanil. In the retrieved studies, we quantitatively analyzed pain intensity, sufentanil consumption, and drug-related side effects.ResultsNine studies with 907 patients were included in this meta-analysis. Compared with sufentanil alone, dexmedetomidine-sufentanil for postoperative intravenous PCA reduced pain intensity at 24 h (mean difference (MD) = − 0.70points; 95% confidence interval (CI): − 1.01, − 0.39; P < 0.00001) and 48 h postoperatively (MD = -0.61points; 95% CI: − 1.00, − 0.22; P = 0.002). Moreover, dexmedetomidine-sufentanil reduced sufentanil consumption during the first 24 h (MD = -13.77 μg; 95% CI: − 18.56, − 8.97; P < 0.00001) and 48 h postoperatively (MD = -20.81 μg; 95% CI: − 28.20, − 13.42; P < 0.00001). Finally, dexmedetomidine-sufentanil improved patient satisfaction without increasing the incidence of side effects.ConclusionsDexmedetomidine as an adjuvant to sufentanil for postoperative PCA can reduce postoperative pain score and sufentanil consumption.
Abstract licence: CC BY 4.0
Mengjia Zhi, Y. Diao, Shiyang Liu, et al.
European Journal of Clinical Pharmacology, 2020
Zhongbiao Nie, Zhi-Hong Li, Bing Lu, et al.
Medicine, 2022
Jiajia Hu, Chengliang Zhang, Jianqin Yan, et al.
PLoS ONE, 2016
Zhonglan Lin, Shuxin Li, Yun Zhou, et al.
BMC Anesthesiology, 2023
T. Melson, D. Boyer, H. Minkowitz, et al.
Pain Practice, 2014
Tao Zhang, Yulong Yu, Wang Zhang, et al.
Drug Design, Development and Therapy, 2019
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
64 found
Half-life
164 minutes
Mechanism
Sufentanil is a synthetic, potent opioid with highly selective binding to μ-opioid receptors [F2009].
Food interactions
2 warnings
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
52%
[A39629]
After…
Half-life
164 minutes
Protein binding
93%
Volume of distribution
1.4 minutes
Metabolism
Sufentanil…
Elimination
80%
Clearance
917 l
The…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Also known as Dsuvia, the sublingual form is used for the management of acute pain in adults that is severe to warrant the use of an opioid analgesic in certified medically supervised healthcare settings, including hospitals, surgical centers, and emergency departments [L4717]. Consideration may be made in the future for the use of the sublingual form in the US military in cases where analgesia is required immediately [L4718].
The sublingual form, manufactured by AcelRx Pharmaceuticals, Inc. (AcelRx), was approved on November 2, 2018 [L4717].
This route of administration is intended to be a simple, effective, non-invasive analgesic option to enable healthcare professionals to rapidly manage acute pain without difficult intravenous or epidural administration [L4717], [A39633].
1. As an analgesic adjunct in the maintenance of balanced general anesthesia in patients who are intubated and ventilated.
2. As a primary anesthetic agent for the induction and maintenance of anesthesia with 100% oxygen in patients undergoing major surgical procedures, in patients who are intubated and ventilated, such as cardiovascular surgery or neurosurgical procedures in the sitting position, to provide favorable myocardial and cerebral oxygen balance or when extended postoperative ventilation is anticipated.
3.
For epidural administration as an analgesic combined with low dose (usually 12.5 mg per administration) bupivacaine usually during labor and vaginal delivery
4. The sublingual form is indicated for the management of acute pain in adults that is severe to warrant the use of an opioid analgesic in certified medically supervised healthcare settings, including hospitals, surgical centers, and emergency departments.
[FDA label]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1430 interactions
A Note on Respiratory Depression
Major, life-threatening, or fatal respiratory depression has been reported with the use of opioids, even in cases where it is used as recommended. Respiratory depression may lead to respiratory arrest and death if not diagnosed and treated appropriately. This drug should be administered only by persons specifically trained in the use of anesthetic drugs and the management of the respiratory effects of potent opioids, including respiration and cardiac resuscitation of patients in the age group being treated.
This training must include the establishment and maintenance of a patent airway and assisted ventilation [FDA label].
Carcinogenesis
Long-term studies in animals to evaluate the carcinogenic potential of sufentanil have not been conducted [FDA label].
Mutagenesis
Sufentanil was not found to be genotoxic in the in vitro bacterial reverse mutation assay (Ames assay) or in the in vivo rat bone marrow micronucleous assay [FDA label].
Reproductive Toxicity
Sufentanil caused embryolethality in rats and rabbits treated for 10-30 days during pregnancy with 2.5 times the maximum human dose by intravenous administration. The embryolethal effect was thought to be secondary to the toxicity for the mother animal model. No negative effects were noted in another study in rats that were treated with 20 times the maximum human dose in the period of organogenesis.
The preclinical effects were only seen following administrations of levels significantly above the maximum human dose, which is therefore of minimal relevance for clinical use [F2009].
Pregnancy
May cause fetal harm [FDA label]
The Use in Lactation
Infants exposed to this drug through breast milk should be monitored for excess sedation and respiratory depression [FDA label].
In general, opioids decrease cAMP (affecting neural signaling pathways), decrease neurotransmitter release, and cause membrane hyperpolarization, all of which contribute to the relief of painful symptoms [A39637].
Opiate receptors are coupled with G-protein receptors and function as both positive and negative regulators of synaptic neural transmission via G-proteins that activate effector proteins. Binding of the opiate receptor leads to the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP, located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. The release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine, and noradrenaline is then inhibited [A39637].
Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist), also preventing neurotransmitter release [A39637].
Sufentanil and other opioids open calcium-dependent inwardly rectifying potassium channels, resulting in hyperpolarization and reduced neuronal excitability [A39636], [A39637].
In clinical settings, sufentanil exerts its principal pharmacologic effects on the central nervous system. Its primary therapeutic actions are analgesia and sedation. Sufentanil may increase pain tolerance and decrease the perception of pain. This drug depresses the respiratory centers, depresses the cough reflex, and constricts the pupils [F2009], [A39637]. When used in balanced general anesthesia, sufentanil has been reported to be as much as 10 times as potent as fentanyl. When administered intravenously as a primary anesthetic agent with 100% oxygen, sufentanil is approximately 5 to 7 times as potent as fentanyl [FDA label]. High doses of intravenous sufentanil have been shown to cause muscle rigidity, likely as a result of an effect on the substantia nigra and the striate nucleus in the brain. Sleep-inducing (hypnotic) activity can be demonstrated by EEG alterations [FDA label].
Effects on the Respiratory System
Sufentanil may cause respiratory depression [FDA label].
Effects on the Cardiovascular System
Sufentanil causes peripheral vasodilation which may result in orthostatic hypotension or syncope. Bradycardia may also occur [F2009]. Clinical signs or symptoms of histamine release and/or peripheral vasodilation may include pruritus, flushing, red eyes and sweating and/or orthostatic hypotension [FDA label].
Effects on the Gastrointestinal Tract
Sufentanil causes a reduction in motility associated with an increase in smooth muscle tone in both the antrum of the stomach and duodenum. Digestion of food in the small intestine may be delayed and propulsive contractions are decreased. Propulsive peristaltic waves in the colon are decreased, while tone may be increased and lead to spasm, resulting in constipation. Other opioid-induced effects may include a reduction in biliary and pancreatic secretions, spasm of the sphincter of Oddi, as well as temporary elevations in serum amylase [FDA label].
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A39629]
After epidural administration of incremental doses totaling 5 to 40 mcg sufentanil during labor and delivery, maternal and neonatal sufentanil plasma concentrations were at or near the 0.05 to 0.1 ng/mL limit of detection, and were slightly higher in mothers than in their infants [FDA label].
After a single administration of a 15 microgram sufentanil sublingual tablet, mean terminal phase half-lives in the range of 6-10 hours have been observed. After multiple administrations, a longer average terminal half-life of up to 18 hours was measured, owing to the higher plasma concentrations of sufentanil achieved after repeated dosing and due to the possibility to quantify these concentrations over a longer time period [F2009].
The central volume of distribution after intravenous application of sufentanil is approximately 14 L and the volume of distribution at steady state is approximately 350 L [F2009].
Sufentanil is rapidly metabolized to a number of inactive metabolites, with oxidative N- and O-dealkylation being the major routes of elimination [F2009].
The clearance of sufentanil in healthy neonates is approximately one-half that in adults and children. The clearance rate of sufentanil can be further reduced by up to a third in neonates with cardiovascular disease [FDA label].
Proteins and enzymes this drug interacts with in the body
PMID:10529478 PMID:12589820 PMID:7891175 PMID:7905839 PMID:7957926 PMID:9689128
Receptor for natural and synthetic opioids including morphine, heroin, DAMGO, fentanyl, etorphine, buprenorphin and methadone .
PMID:10529478 PMID:10836142 PMID:12589820 PMID:19300905 PMID:7891175 PMID:7905839 PMID:7957926 PMID:9689128
Also activated by enkephalin peptides, such as Met-enkephalin or Met-enkephalin-Arg-Phe, with higher affinity for Met-enkephalin-Arg-Phe (By similarity). Agonist binding to the receptor induces coupling to an inactive GDP-bound heterotrimeric G-protein complex and subsequent exchange of GDP for GTP in the G-protein alpha subunit leading to dissociation of the G-protein complex with the free GTP-bound G-protein alpha and the G-protein beta-gamma dimer activating downstream cellular effectors .
PMID:7905839
The agonist- and cell type-specific activity is predominantly coupled to pertussis toxin-sensitive G(i) and G(o) G alpha proteins, GNAI1, GNAI2, GNAI3 and GNAO1 isoforms Alpha-1 and Alpha-2, and to a lesser extent to pertussis toxin-insensitive G alpha proteins GNAZ and GNA15 .
PMID:12068084
They mediate an array of downstream cellular responses, including inhibition of adenylate cyclase activity and both N-type and L-type calcium channels, activation of inward rectifying potassium channels, mitogen-activated protein kinase (MAPK), phospholipase C (PLC), phosphoinositide/protein kinase (PKC), phosphoinositide 3-kinase (PI3K) and regulation of NF-kappa-B (By similarity). Also couples to adenylate cyclase stimulatory G alpha proteins (By similarity).
The selective temporal coupling to G-proteins and subsequent signaling can be regulated by RGSZ proteins, such as RGS9, RGS17 and RGS4 (By similarity). Phosphorylation by members of the GPRK subfamily of Ser/Thr protein kinases and association with beta-arrestins is involved in short-term receptor desensitization (By similarity). Beta-arrestins associate with the GPRK-phosphorylated receptor and uncouple it from the G-protein thus terminating signal transduction (By similarity).
The phosphorylated receptor is internalized through endocytosis via clathrin-coated pits which involves beta-arrestins (By similarity). The activation of the ERK pathway occurs either in a G-protein-dependent or a beta-arrestin-dependent manner and is regulated by agonist-specific receptor phosphorylation (By similarity). Acts as a class A G-protein coupled receptor (GPCR) which dissociates from beta-arrestin at or near the plasma membrane and undergoes rapid recycling (By similarity).
Receptor down-regulation pathways are varying with the agonist and occur dependent or independent of G-protein coupling (By similarity). Endogenous ligands induce rapid desensitization, endocytosis and recycling (By similarity). Heterooligomerization with other GPCRs can modulate agonist binding, signaling and trafficking properties (By similarity)
Inhibits neurotransmitter release by reducing calcium ion currents and increasing potassium ion conductance. Plays a role in the perception of pain and in opiate-mediated analgesia. Plays a role in developing analgesic tolerance to morphine
Signaling leads to the inhibition of adenylate cyclase activity. Inhibits neurotransmitter release by reducing calcium ion currents and increasing potassium ion conductance. Plays a role in the perception of pain.
Plays a role in mediating reduced physical activity upon treatment with synthetic opioids. Plays a role in the regulation of salivation in response to synthetic opioids. May play a role in arousal and regulation of autonomic and neuroendocrine functions
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC N01AH03
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Sufentanil
Additional database identifiers
Drugs Product Database (DPD)
12343
ChemSpider
38043
BindingDB
94503
Guide to Pharmacology
3534
ZINC
ZINC000000538386
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8156
GenAtlas
OPRM1
GeneCards
OPRM1
GenBank Gene Database
L25119
GenBank Protein Database
452073
Guide to Pharmacology
319
UniProt Accession
OPRM_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8153
GenAtlas
OPRD1
GeneCards
OPRD1
GenBank Gene Database
U07882
GenBank Protein Database
27545517
Guide to Pharmacology
317
UniProt Accession
OPRD_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8154
GenAtlas
OPRK1
GeneCards
OPRK1
GenBank Gene Database
U11053
GenBank Protein Database
532060
Guide to Pharmacology
318
UniProt Accession
OPRK_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72