Sufentanil

Synonyms :
N-(4-(Methoxymethyl)-1-(2-(2-thienyl)ethyl)-4-piperidinyl)-N-phenylpropanamide, N-(4-(Methoxymethyl)-1-(2-(2-thienyl)ethyl)-4-piperidyl)propionanilide, Sufentanil, Sufentanilo, Sufentanilum, Sufentanyl

Status : approved

Category

Anesthetics, Intravenous

Therapeutic Classification

ANESTHETICS, GENERAL

NERVOUS SYSTEM
ANESTHETICS
ANESTHETICS, GENERAL
Analgesics, Opioid

Description

An opioid analgesic that is used as an adjunct in anesthesia, in balanced anesthesia, and as a primary anesthetic agent. [PubChem]

Used

Used as an analgesic adjunct in anesthesia and as a primary anesthetic drug in procedures requiring assisted ventilation and in the relief of pain.

Mechanism Of Action

Opiate receptors are coupled with G-protein receptors and function as both positive and negative regulators of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates 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. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine and noradrenaline is inhibited. Opioids also inhibit the release of vasopressin, somatostatin, insulin and glucagon. Sufentanil’s analgesic activity is, most likely, due to its conversion to morphine. Opioids open calcium-dependent inwardly rectifying potassium channels (OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability.

Dosage

Form Route Strength
Liquid intravenous 50 mcg
Liquid intravenous; epidural 50 mcg
Injection epidural; intravenous .05 mg/mL
Injection epidural; intravenous 50 ug/mL
Injection, solution epidural; intravenous 50 ug/mL
Solution intravenous; epidural 50 mcg

Pharmacodynamics

Sufentanil is a synthetic opioid analgesic. Sufentanil interacts predominately with the opioid mu-receptor. These mu-binding sites are discretely distributed in the human brain, spinal cord, and other tissues. In clinical settings, sufentanil exerts its principal pharmacologic effects on the central nervous system. Its primary actions of therapeutic value are analgesia and sedation. Sufentanil may increase the patient’s tolerance for pain and decrease the perception of suffering, although the presence of the pain itself may still be recognized. In addition to analgesia, alterations in mood, euphoria and dysphoria, and drowsiness commonly occur. Sufentanil depresses the respiratory centers, depresses the cough reflex, and constricts the pupils.

Toxic Effect

LD50: 18.7 mg/kg (IV in mice)

Half Life

265 minutes

Chemical Classification

This compound belongs to the class of organic compounds known as anilides. These are organic heterocyclic compounds derived from oxoacids RkE(=O)l(OH)m (l not 0) by replacing an OH group by the NHPh group or derivative formed by ring substitution.

Anilides

Organic compounds

Benzenoids

Benzene and substituted derivatives

Anilides

Salt : Sufentanil Citrate

Chemical Name

N-(4-(Methoxymethyl)-1-(2-(2-thienyl)ethyl)-4-piperidinyl)-N-phenylpropanamide

Brands

name Dosage form Country
Sufenta Inj 50mcg/ml liquid Canada
Sufenta Inj 50mcg/ml liquid Canada
Sufentanil Citrate injection, solution US
Sufentanil Citrate injection, solution US
Sufentanil Citrate injection US
Sufentanil Citrate injection US
Sufentanil Citrate injection US
Sufentanil Citrate injection US
Sufentanil Citrate Injection USP solution Canada

Drug Drug Interactions

  •  Acetazolamide  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Alvimopan  : Analgesics (Opioid) may enhance the adverse/toxic effect of Alvimopan. This is most notable for patients receiving long-term (i.e., more than 7 days) opiates prior to alvimopan initiation.
  •  Amiloride  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Ammonium chloride  : May increase the excretion of Analgesics (Opioid).
  •  Amphetamine  : May enhance the analgesic effect of Analgesics (Opioid).
  •  Aprepitant  : May increase the serum concentration of CYP3A4 Substrates.
  •  Bendroflumethiazide  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Bretylium  : May enhance the bradycardic effect of Bradycardia-Causing Agents. Bretylium may also enhance atrioventricular (AV) blockade in patients receiving AV blocking agents.
  •  Bumetanide  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Cathinone  : May enhance the analgesic effect of Analgesics (Opioid).
  •  Ceritinib  : Bradycardia-Causing Agents may enhance the bradycardic effect of Ceritinib.
  •  Chlorothiazide  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Chlorthalidone  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Conivaptan  : May increase the serum concentration of CYP3A4 Substrates.
  •  Cyclothiazide  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Dasatinib  : May increase the serum concentration of CYP3A4 Substrates.
  •  Desmopressin  : Analgesics (Opioid) may enhance the adverse/toxic effect of Desmopressin.
  •  Doxylamine  : May enhance the CNS depressant effect of CNS Depressants.
  •  Dronabinol  : May enhance the CNS depressant effect of CNS Depressants.
  •  Dronabinol  : May enhance the CNS depressant effect of CNS Depressants.
  •  Droperidol  : May enhance the CNS depressant effect of CNS Depressants.
  •  Ethacrynic acid  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Ethoxzolamide  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Fosaprepitant  : May increase the serum concentration of CYP3A4 Substrates.
  •  Furosemide  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Hydrochlorothiazide  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Hydrocodone  : CNS Depressants may enhance the CNS depressant effect of Hydrocodone.
  •  Hydroflumethiazide  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Hydroxyzine  : May enhance the CNS depressant effect of CNS Depressants.
  •  Idelalisib  : May increase the serum concentration of CYP3A4 Substrates.
  •  Indapamide  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Ivabradine  : Bradycardia-Causing Agents may enhance the bradycardic effect of Ivabradine.
  •  Ivacaftor  : May increase the serum concentration of CYP3A4 Substrates.
  •  Lacosamide  : Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide.
  •  Luliconazole  : May increase the serum concentration of CYP3A4 Substrates.
  •  Magnesium Sulfate  : May enhance the CNS depressant effect of CNS Depressants.
  •  Methotrimeprazine  : CNS Depressants may enhance the CNS depressant effect of Methotrimeprazine. Methotrimeprazine may enhance the CNS depressant effect of CNS Depressants.
  •  Metolazone  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Metyrosine  : CNS Depressants may enhance the sedative effect of Metyrosine.
  •  Mifepristone  : May increase the serum concentration of CYP3A4 Substrates.
  •  Minocycline  : May enhance the CNS depressant effect of CNS Depressants.
  •  Mirtazapine  : CNS Depressants may enhance the CNS depressant effect of Mirtazapine.
  •  Nabilone  : May enhance the CNS depressant effect of CNS Depressants.
  •  Naltrexone  : May diminish the therapeutic effect of Analgesics (Opioid).
  •  Netupitant  : May increase the serum concentration of CYP3A4 Substrates.
  •  Orphenadrine  : CNS Depressants may enhance the CNS depressant effect of Orphenadrine.
  •  Palbociclib  : May increase the serum concentration of CYP3A4 Substrates.
  •  Paraldehyde  : CNS Depressants may enhance the CNS depressant effect of Paraldehyde.
  •  Pegvisomant  : Analgesics (Opioid) may diminish the therapeutic effect of Pegvisomant.
  •  Perampanel  : May enhance the CNS depressant effect of CNS Depressants.
  •  Pramipexole  : CNS Depressants may enhance the sedative effect of Pramipexole.
  •  Ropinirole  : CNS Depressants may enhance the sedative effect of Ropinirole.
  •  Rotigotine  : CNS Depressants may enhance the sedative effect of Rotigotine.
  •  Rufinamide  : May enhance the adverse/toxic effect of CNS Depressants. Specifically, sleepiness and dizziness may be enhanced.
  •  Ruxolitinib  : May enhance the bradycardic effect of Bradycardia-Causing Agents.
  •  Simeprevir  : May increase the serum concentration of CYP3A4 Substrates.
  •  Sodium oxybate  : May enhance the CNS depressant effect of CNS Depressants.
  •  Spironolactone  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Stiripentol  : May increase the serum concentration of CYP3A4 Substrates.
  •  Succinylcholine  : May enhance the bradycardic effect of Analgesics (Opioid).
  •  Suvorexant  : CNS Depressants may enhance the CNS depressant effect of Suvorexant.
  •  Tapentadol  : May enhance the CNS depressant effect of CNS Depressants.
  •  Thalidomide  : CNS Depressants may enhance the CNS depressant effect of Thalidomide.
  •  Ticrynafen  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Tofacitinib  : May enhance the bradycardic effect of Bradycardia-Causing Agents.
  •  Torasemide  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Triamterene  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Trichlormethiazide  : Analgesics (Opioid) may enhance the adverse/toxic effect of Diuretics.
  •  Zolpidem  : CNS Depressants may enhance the CNS depressant effect of Zolpidem.

Calculated Property

kind Value Source
logP 3.4 ALOGPS
logS -4.5 ALOGPS
Water Solubility 1.20e-02 g/l ALOGPS
logP 3.61 ChemAxon
IUPAC Name N-[4-(methoxymethyl)-1-[2-(thiophen-2-yl)ethyl]piperidin-4-yl]-N-phenylpropanamide ChemAxon
Traditional IUPAC Name sufentanil ChemAxon
Molecular Weight 386.551 ChemAxon
Monoisotopic Weight 386.202798904 ChemAxon
SMILES CCC(=O)N(C1=CC=CC=C1)C1(COC)CCN(CCC2=CC=CS2)CC1 ChemAxon
Molecular Formula C22H30N2O2S ChemAxon
InChI InChI=1S/C22H30N2O2S/c1-3-21(25)24(19-8-5-4-6-9-19)22(18-26-2)12-15-23(16-13-22)14-11-20-10-7-17-27-20/h4-10,17H,3,11-16,18H2,1-2H3 ChemAxon
InChIKey InChIKey=GGCSSNBKKAUURC-UHFFFAOYSA-N ChemAxon
Polar Surface Area (PSA) 32.78 ChemAxon
Refractivity 111.42 ChemAxon
Polarizability 43.85 ChemAxon
Rotatable Bond Count 8 ChemAxon
H Bond Acceptor Count 3 ChemAxon
H Bond Donor Count 0 ChemAxon
pKa (strongest basic) 8.86 ChemAxon
Physiological Charge 1 ChemAxon
Number of Rings 3 ChemAxon
Bioavailability 1 ChemAxon
Rule of Five 1 ChemAxon
Ghose Filter 1 ChemAxon
MDDR-Like Rule 1 ChemAxon

Affected organism

Humans and other mammals

Target within organism

  • Mu-type opioid receptor : in Human
  • Delta-type opioid receptor : in Human
  • Kappa-type opioid receptor : in Human