1.0 2009-07-21 20:27:40 UTC 2026-05-14 16:49:23 UTC T3D2894 Alfentanil SmallMolecule Alfentanil is an exogenous organic compound with the formula C21H32N6O3 and an average molecular weight of 416.52 g/mol. At room temperature, it exists as a solid. Alfentanil belongs to the anilides, a subclass of benzene and substituted derivatives within the organic compounds. This compound functions as an intravenous anaesthetic, a central nervous system depressant, a peripheral nervous system drug, and an opioid analgesic. Biologically, it acts as a mu-opioid receptor agonist. Its recorded protein targets include the mu-type opioid receptor (OPRM1), the kappa-type opioid receptor (OPRK1), alpha-1-acid glycoprotein 1 (ORM1), albumin (ALB), and ATP-dependent translocase ABCB1. 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 affecting the release of nociceptive neurotransmitter. Alfentanil is found in eight recorded sources, including anesthetics within healthcare, pharmaceuticals, and veterinary products. Other recorded sources include household cleaning and consumer products such as bleaching agents, cigar cigarettes, non-electric simulated smoking devices, and tobacco product cases, as well as electrical and electronic equipment such as antennas, electric switches, and electrically stimulated smoking devices. The recorded route of exposure for this compound is intravenous. Drug Synthetic Toxin Organic Compound Amine Ether Amide Drug Analgesic Analgesic, Opioid Narcotic Opiate Agonist Anesthetic Anesthetic, Intravenous Metabolite Synthetic Compound Alfenta Alfentanilum Alfentanyl N-(1-(2-(4-Ethyl-5-oxo-2-tetrazolin-1-yl)ethyl)-4-(methoxymethyl)-4-piperidyl)propionanilide Rapifen C21H32N6O3 416.5172 416.25358892 N-{1-[2-(4-ethyl-5-oxo-4,5-dihydro-1H-1,2,3,4-tetrazol-1-yl)ethyl]-4-(methoxymethyl)piperidin-4-yl}-N-phenylpropanamide alfentanil 71195-58-9 CCN1N=NN(CCN2CCC(COC)(CC2)N(C(=O)CC)C2=CC=CC=C2)C1=O InChI=1S/C21H32N6O3/c1-4-19(28)27(18-9-7-6-8-10-18)21(17-30-3)11-13-24(14-12-21)15-16-26-20(29)25(5-2)22-23-26/h6-10H,4-5,11-17H2,1-3H3 IDBPHNDTYPBSNI-UHFFFAOYSA-N Organic compounds Benzenoids Benzene and substituted derivatives Anilides Anilides Amino acids and derivatives Azacyclic compounds Carbonyl compounds Dialkyl ethers Heteroaromatic compounds Hydrocarbon derivatives Organic oxides Organopnictogen compounds Piperidines Tertiary carboxylic acid amides Tetrazoles Trialkylamines Amine Amino acid or derivatives Anilide Aromatic heteromonocyclic compound Azacycle Azole Carbonyl group Carboxamide group Carboxylic acid derivative Dialkyl ether Ether Heteroaromatic compound Hydrocarbon derivative Organic nitrogen compound Organic oxide Organic oxygen compound Organoheterocyclic compound Organonitrogen compound Organooxygen compound Organopnictogen compound Piperidine Tertiary aliphatic amine Tertiary amine Tertiary carboxylic acid amide Tetrazole Aromatic heteromonocyclic compounds monocarboxylic acid amide piperidines Detected and Not Quantified Exogenous Extracellular Membrane Alfentanil Action Pathway SMP0000413 Alfentanil Opioid Agonist Action Pathway SMP0124996 Alfentanil Metabolism Pathway SMP0125517 Alfentanil Drug Metabolism Action Pathway SMP0143241 Solid White powder. melting_point 140.8°C solubility 34.6 mg/L logp 2.16 logp 2.20 ALOGPS logs -3.22 ALOGPS solubility 2.52e-01 g/l ALOGPS logp 2.81 ChemAxon pka_strongest_basic 7.5 ChemAxon iupac N-{1-[2-(4-ethyl-5-oxo-4,5-dihydro-1H-1,2,3,4-tetrazol-1-yl)ethyl]-4-(methoxymethyl)piperidin-4-yl}-N-phenylpropanamide ChemAxon average_mass 416.5172 ChemAxon mono_mass 416.25358892 ChemAxon smiles CCN1N=NN(CCN2CCC(COC)(CC2)N(C(=O)CC)C2=CC=CC=C2)C1=O ChemAxon formula C21H32N6O3 ChemAxon inchi InChI=1S/C21H32N6O3/c1-4-19(28)27(18-9-7-6-8-10-18)21(17-30-3)11-13-24(14-12-21)15-16-26-20(29)25(5-2)22-23-26/h6-10H,4-5,11-17H2,1-3H3 ChemAxon inchikey IDBPHNDTYPBSNI-UHFFFAOYSA-N ChemAxon polar_surface_area 81.05 ChemAxon refractivity 118.59 ChemAxon polarizability 45.57 ChemAxon rotatable_bond_count 9 ChemAxon acceptor_count 6 ChemAxon donor_count 0 ChemAxon physiological_charge 1 ChemAxon formal_charge 0 ChemAxon For intravenous injection or infusion only. 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. Alfentanil's analgesic activity is, most likely, due to its conversion to morphine. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability. The liver is the major site of biotransformation. Route of Elimination: Only 1.0% of the dose is excreted as unchanged drug; urinary excretion is the major route of elimination of metabolites. Half Life: 90-111 minutes No indication of carcinogenicity to humans (not listed by IARC). For the management of postoperative pain and the maintenance of general anesthesia. #<HealthEffect::ActiveRecord_Associations_CollectionProxy:0x00007f72247a55b0> Symptoms of overexposure include characteristic rigidity of the skeletal muscles, cardiac and respiratory depression, and narrowing of the pupils. Intravenous administration of an opioid antagonist such as naloxone should be employed as a specific antidote to manage respiratory depression. The duration of respiratory depression following overdosage with ALFENTA may be longer than the duration of action of the opioid antagonist. Administration of an opioid antagonist should not preclude immediate establishment of a patent airway, administration of oxygen, and assisted or controlled ventilation as indicated for hypoventilation or apnea. If respiratory depression is associated with muscular rigidity, a neuromuscular blocking agent may be required to facilitate assisted or controlled ventilation. Intravenous fluids and vasoactive agents may be required to manage hemodynamic instability. (L1712) DB00802 HMDB14940 51263 CHEMBL634 46451 C08005 2569 Alfentanil Alfentanil Drugs.com: http://www.drugs.com/cons/Alfenta.html RxList: The Internet Drug Index (2009).: http://www.rxlist.com/ BE0000770 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. Alfentanil's analgesic activity is, most likely, due to its conversion to morphine. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability. IC50 0.015 uM BindingDB 50008979 BE0000925 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. Alfentanil's analgesic activity is, most likely, due to its conversion to morphine. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability. BE0002362 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. Alfentanil's analgesic activity is, most likely, due to its conversion to morphine. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability. BE0000530 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. Alfentanil's analgesic activity is, most likely, due to its conversion to morphine. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability. BE0001032 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. Alfentanil's analgesic activity is, most likely, due to its conversion to morphine. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability. IC50 112 uM BindingDB 50008979 BE0000632 IC50 >10 uM BindingDB 50008979