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Record Information
Version2.0
Creation Date2009-07-21 20:27:27 UTC
Update Date2014-12-24 20:25:52 UTC
Accession NumberT3D2864
Identification
Common NameNaltrexone
ClassSmall Molecule
DescriptionDerivative of noroxymorphone that is the N-cyclopropylmethyl congener of naloxone. It is a narcotic antagonist that is effective orally, longer lasting and more potent than naloxone, and has been proposed for the treatment of heroin addiction. The FDA has approved naltrexone for the treatment of alcohol dependence. [PubChem]
Compound Type
  • Alcohol Antagonist
  • Amine
  • Anti-Craving Agent
  • Appetite Depressant
  • Central Nervous System Depressant
  • Depressant
  • Drug
  • Ether
  • Metabolite
  • Narcotic Antagonist
  • Opiate Antagonist
  • Organic Compound
  • Synthetic Compound
Chemical Structure
Thumb
Synonyms
Synonym
17-(Cyclopropylmethyl)-4,5-epoxy-3,14-dihydroxymorphinan-6-one
17-(Cyclopropylmethyl)-4,5alpha-epoxy-3,14-dihydroxymorphinan-6-one
Abernil
Adepend
Antaxon
Antaxone
Arrop
Celupan
Depade
Dependex
MorViva
N-Cyclopropylmethyl-14-hydroxydihydromorphinone
N-Cyclopropylmethylnoroxymorphone
Nalerona
Nalorex
Naltax
Naltrekson
Naltrexon
Naltrexona
Naltrexonum
Narcoral
Neksi
Nemexin
Opizone
PTI-555
Revez
Revia
Trexan
Vivitrex
Vivitrol
Chemical FormulaC20H23NO4
Average Molecular Mass341.401 g/mol
Monoisotopic Mass341.163 g/mol
CAS Registry Number16590-41-3
IUPAC Name(1S,5R,13R,17S)-4-(cyclopropylmethyl)-10,17-dihydroxy-12-oxa-4-azapentacyclo[9.6.1.0¹,¹³.0⁵,¹⁷.0⁷,¹⁸]octadeca-7(18),8,10-trien-14-one
Traditional Namenaltrexone
SMILES[H][C@@]12OC3=C(O)C=CC4=C3[C@@]11CCN(CC3CC3)[C@]([H])(C4)[C@]1(O)CCC2=O
InChI IdentifierInChI=1S/C20H23NO4/c22-13-4-3-12-9-15-20(24)6-5-14(23)18-19(20,16(12)17(13)25-18)7-8-21(15)10-11-1-2-11/h3-4,11,15,18,22,24H,1-2,5-10H2/t15-,18+,19+,20-/m1/s1
InChI KeyInChIKey=DQCKKXVULJGBQN-XFWGSAIBSA-N
Chemical Taxonomy
Description belongs to the class of organic compounds known as phenanthrenes and derivatives. These are polycyclic compounds containing a phenanthrene moiety, which is a tricyclic aromatic compound with three non-linearly fused benzene.
KingdomOrganic compounds
Super ClassBenzenoids
ClassPhenanthrenes and derivatives
Sub ClassNot Available
Direct ParentPhenanthrenes and derivatives
Alternative Parents
Substituents
  • Phenanthrene
  • Isoquinolone
  • Tetralin
  • Coumaran
  • 1-hydroxy-2-unsubstituted benzenoid
  • Alkyl aryl ether
  • Aralkylamine
  • Piperidine
  • Cyclic alcohol
  • Tertiary alcohol
  • 1,2-aminoalcohol
  • Ketone
  • Tertiary aliphatic amine
  • Tertiary amine
  • Ether
  • Oxacycle
  • Azacycle
  • Organoheterocyclic compound
  • Organonitrogen compound
  • Hydrocarbon derivative
  • Organic oxide
  • Organic nitrogen compound
  • Organopnictogen compound
  • Carbonyl group
  • Organooxygen compound
  • Alcohol
  • Organic oxygen compound
  • Amine
  • Aromatic heteropolycyclic compound
Molecular FrameworkAromatic heteropolycyclic compounds
External Descriptors
Biological Properties
StatusDetected and Not Quantified
OriginExogenous
Cellular Locations
  • Cytoplasm
  • Extracellular
  • Membrane
Biofluid LocationsNot Available
Tissue LocationsNot Available
PathwaysNot Available
Applications
Biological Roles
Chemical RolesNot Available
Physical Properties
StateSolid
AppearanceWhite powder.
Experimental Properties
PropertyValue
Melting Point168-170°C
Boiling PointNot Available
Solubility100 mg/mL (as hydrochloride salt)
LogP1.92
Predicted Properties
PropertyValueSource
Water Solubility3.07 g/LALOGPS
logP2.07ALOGPS
logP1.36ChemAxon
logS-2ALOGPS
pKa (Strongest Acidic)7.39ChemAxon
pKa (Strongest Basic)11.54ChemAxon
Physiological Charge1ChemAxon
Hydrogen Acceptor Count5ChemAxon
Hydrogen Donor Count2ChemAxon
Polar Surface Area70 ŲChemAxon
Rotatable Bond Count2ChemAxon
Refractivity91.5 m³·mol⁻¹ChemAxon
Polarizability35.97 ųChemAxon
Number of Rings6ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
Spectra
Spectra
Spectrum TypeDescriptionSplash KeyDeposition DateView
Predicted GC-MSPredicted GC-MS Spectrum - GC-MS (Non-derivatized) - 70eV, Positivesplash10-0a4l-9032000000-f869731a6a6d2ba21fc92017-09-01View Spectrum
Predicted GC-MSPredicted GC-MS Spectrum - GC-MS (2 TMS) - 70eV, Positivesplash10-00bc-9601600000-928a74224d18c2ec3c942017-10-06View Spectrum
Predicted GC-MSPredicted GC-MS Spectrum - GC-MS (TBDMS_2_1) - 70eV, PositiveNot Available2021-10-12View Spectrum
Predicted GC-MSPredicted GC-MS Spectrum - GC-MS (Non-derivatized) - 70eV, PositiveNot Available2021-10-12View Spectrum
Predicted GC-MSPredicted GC-MS Spectrum - GC-MS ("Naltrexone,2TMS,#1" TMS) - 70eV, PositiveNot Available2021-10-14View Spectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-00di-0009000000-e30316dd5784a7100d382017-09-14View Spectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-0006-0009000000-2218214724e56047d52b2017-09-14View Spectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-0006-0009000000-bb047c719f3429eb44102017-09-14View Spectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-00di-0049000000-de9a717563978f22f02f2017-09-14View Spectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-00xr-0191000000-d2f2ff1e4eb93db46b5e2017-09-14View Spectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-03di-1390000000-091705f6f42bc0f1c2092017-09-14View Spectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-03di-1890000000-148c5608ef92c1dcaac42017-09-14View Spectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-0006-0009000000-6df03abdbdb7461f29452017-09-14View Spectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-0006-0009000000-059b1dffee7ef15b9e952017-09-14View Spectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-00di-0049000000-a20ede951b350fa97a312017-09-14View Spectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-00xr-0191000000-8a66ac92b4a1eadcc4052017-09-14View Spectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-03di-1490000000-0cfb621f77295ff438f22017-09-14View Spectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-03di-1980000000-63edda852273619df16c2017-09-14View Spectrum
LC-MS/MSLC-MS/MS Spectrum - LC-ESI-ITFT , positivesplash10-00di-0009000000-59ab0ef68d6e13a7d0852017-09-14View Spectrum
LC-MS/MSLC-MS/MS Spectrum - 60V, Positivesplash10-00xr-0191000000-8a66ac92b4a1eadcc4052021-09-20View Spectrum
LC-MS/MSLC-MS/MS Spectrum - 45V, Positivesplash10-00di-0049000000-02654ed4a592aa3f1d772021-09-20View Spectrum
LC-MS/MSLC-MS/MS Spectrum - 35V, Positivesplash10-00di-0009000000-5c4b68f88d13143d13c82021-09-20View Spectrum
LC-MS/MSLC-MS/MS Spectrum - 75V, Positivesplash10-03di-1490000000-0cfb621f77295ff438f22021-09-20View Spectrum
LC-MS/MSLC-MS/MS Spectrum - 75V, Positivesplash10-03di-1390000000-091705f6f42bc0f1c2092021-09-20View Spectrum
LC-MS/MSLC-MS/MS Spectrum - 60V, Positivesplash10-00xr-0191000000-d2f2ff1e4eb93db46b5e2021-09-20View Spectrum
LC-MS/MSLC-MS/MS Spectrum - 15V, Positivesplash10-0006-0009000000-f50bcaa6a045618a3c7d2021-09-20View Spectrum
LC-MS/MSLC-MS/MS Spectrum - 30V, Positivesplash10-0006-0009000000-acc2906c5a3c9b639ba82021-09-20View Spectrum
LC-MS/MSLC-MS/MS Spectrum - 45V, Positivesplash10-00di-0049000000-70f2ceb5abb36fef0fe62021-09-20View Spectrum
LC-MS/MSLC-MS/MS Spectrum - 30V, Positivesplash10-0006-0009000000-c9c1b724011247195d892021-09-20View Spectrum
LC-MS/MSLC-MS/MS Spectrum - 35V, Positivesplash10-00di-0009000000-cdd147bc699e82a0eabc2021-09-20View Spectrum
Toxicity Profile
Route of ExposureAlthough well absorbed orally, naltrexone is subject to significant first pass metabolism with oral bioavailability estimates ranging from 5 to 40%.
Mechanism of ToxicityNaltrexone is a pure opiate antagonist and has little or no agonist activity. The mechanism of action of naltrexone in alcoholism is not understood; however, involvement of the endogenous opioid system is suggested by preclinical data. Naltrexone is thought to act as a competitive antagonist at mc, kappa, and delta receptors in the CNS, with the highest affintiy for the mu receptor. Naltrexone competitively binds to such receptors and may block the effects of endogenous opioids. This leads to the antagonization of most of the subjective and objective effects of opiates, including respiratory depression, miosis, euphoria, and drug craving. The major metabolite of naltrexone, 6-beta-naltrexol, is also an opiate antagonist and may contribute to the antagonistic activity of the drug.
MetabolismHepatic. When administered orally, naltrexone undergoes extensive biotransformation and is metabolized to 6 beta-naltrexol (which may contribute to the therapeutic effect) and other minor metabolites. Route of Elimination: Both parent drug and metabolites are excreted primarily by the kidney (53% to 79% of the dose), however, urinary excretion of unchanged naltrexone accounts for less than 2% of an oral dose and fecal excretion is a minor elimination pathway. The renal clearance for naltrexone ranges from 30 to 127 mL/min and suggests that renal elimination is primarily by glomerular filtration. Half Life: 4 hours for naltrexone and 13 hours for the active metabolite 6 beta-naltrexol.
Toxicity ValuesLD50: 1,100-1,550 mg/kg (oral, mouse) LD50: 1,450 mg/kg (oral, rat) LD50: 1,490 mg/kg (oral, guinea pig)
Lethal DoseNot Available
Carcinogenicity (IARC Classification)No indication of carcinogenicity to humans (not listed by IARC).
Uses/SourcesUsed as an adjunct to a medically supervised behaviour modification program in the maintenance of opiate cessation in individuals who were formerly physically dependent on opiates and who have successfully undergone detoxification. Also used for the management of alcohol dependence in conjunction with a behavioural modification program.
Minimum Risk LevelNot Available
Health EffectsTolerance can develop, in which the person needs larger doses to achieve the desired effect; this can lead to overdose and death. Accidents or injury can also occur due to the side effects of loss of coordination, slowed reaction time, sleepiness and impaired judgment. Drugs in this category have a high potential for physical and psychological dependence.
SymptomsHigh doses of naltrexone (generally ≥1,000 mg/kg) produce salivation, depression/reduced activity, tremors, and convulsions.
TreatmentPatients should be treated symptomatically in a closely supervised environment. (5)
Normal Concentrations
Not Available
Abnormal Concentrations
Not Available
DrugBank IDDB00704
HMDB IDHMDB14842
PubChem Compound ID5360515
ChEMBL IDCHEMBL19019
ChemSpider ID4514524
KEGG IDC07253
UniProt IDNot Available
OMIM ID
ChEBI ID7465
BioCyc IDNot Available
CTD IDNot Available
Stitch IDNaltrexone
PDB IDNot Available
ACToR IDNot Available
Wikipedia LinkNaltrexone
References
Synthesis Reference

Bao-Shan Huang, Yansong Lu, Ben-Yi Ji, Aris P Christodoulou, “Preparation of naltrexone from codeine and 3-benzylmorphine.” U.S. Patent US6013796, issued March, 1990.

MSDSLink
General References
  1. Schmitz JM, Stotts AL, Rhoades HM, Grabowski J: Naltrexone and relapse prevention treatment for cocaine-dependent patients. Addict Behav. 2001 Mar-Apr;26(2):167-80. [11316375 ]
  2. Krystal JH, Gueorguieva R, Cramer J, Collins J, Rosenheck R: Naltrexone is associated with reduced drinking by alcohol dependent patients receiving antidepressants for mood and anxiety symptoms: results from VA Cooperative Study No. 425, "Naltrexone in the treatment of alcoholism". Alcohol Clin Exp Res. 2008 Jan;32(1):85-91. Epub 2007 Dec 7. [18070245 ]
  3. Ray LA, Chin PF, Miotto K: Naltrexone for the treatment of alcoholism: clinical findings, mechanisms of action, and pharmacogenetics. CNS Neurol Disord Drug Targets. 2010 Mar;9(1):13-22. [20201811 ]
  4. Drugs.com [Link]
  5. RxList: The Internet Drug Index (2009). [Link]
Gene Regulation
Up-Regulated GenesNot Available
Down-Regulated GenesNot Available

Targets

General Function:
Voltage-gated calcium channel activity
Specific Function:
Receptor for endogenous opioids such as beta-endorphin and endomorphin. Receptor for natural and synthetic opioids including morphine, heroin, DAMGO, fentanyl, etorphine, buprenorphin and methadone. 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. 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 extend to pertussis toxin-insensitive G alpha proteins GNAZ and GNA15. 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. Also couples to adenylate cyclase stimulatory G alpha proteins. The selective temporal coupling to G-proteins and subsequent signaling can be regulated by RGSZ proteins, such as RGS9, RGS17 and RGS4. Phosphorylation by members of the GPRK subfamily of Ser/Thr protein kinases and association with beta-arrestins is involved in short-term receptor desensitization. Beta-arrestins associate with the GPRK-phosphorylated receptor and uncouple it from the G-protein thus terminating signal transduction. The phosphorylated receptor is internalized through endocytosis via clathrin-coated pits which involves beta-arrestins. 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. 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. Receptor down-regulation pathways are varying with the agonist and occur dependent or independent of G-protein coupling. Endogenous ligands induce rapid desensitization, endocytosis and recycling whereas morphine induces only low desensitization and endocytosis. Heterooligomerization with other GPCRs can modulate agonist binding, signaling and trafficking properties. Involved in neurogenesis. Isoform 12 couples to GNAS and is proposed to be involved in excitatory effects. Isoform 16 and isoform 17 do not bind agonists but may act through oligomerization with binding-competent OPRM1 isoforms and reduce their ligand binding activity.
Gene Name:
OPRM1
Uniprot ID:
P35372
Molecular Weight:
44778.855 Da
Binding/Activity Constants
TypeValueAssay TypeAssay Source
Inhibitory0.002 uMNot AvailableBindingDB 50000787
References
  1. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [11752352 ]
  2. Oslin DW, Berrettini W, Kranzler HR, Pettinati H, Gelernter J, Volpicelli JR, O'Brien CP: A functional polymorphism of the mu-opioid receptor gene is associated with naltrexone response in alcohol-dependent patients. Neuropsychopharmacology. 2003 Aug;28(8):1546-52. Epub 2003 Jun 18. [12813472 ]
  3. Bartus RT, Emerich DF, Hotz J, Blaustein M, Dean RL, Perdomo B, Basile AS: Vivitrex, an injectable, extended-release formulation of naltrexone, provides pharmacokinetic and pharmacodynamic evidence of efficacy for 1 month in rats. Neuropsychopharmacology. 2003 Nov;28(11):1973-82. [12931140 ]
  4. Yoburn BC, Purohit V, Patel K, Zhang Q: Opioid agonist and antagonist treatment differentially regulates immunoreactive mu-opioid receptors and dynamin-2 in vivo. Eur J Pharmacol. 2004 Sep 13;498(1-3):87-96. [15363980 ]
  5. Roy S, Guo X, Kelschenbach J, Liu Y, Loh HH: In vivo activation of a mutant mu-opioid receptor by naltrexone produces a potent analgesic effect but no tolerance: role of mu-receptor activation and delta-receptor blockade in morphine tolerance. J Neurosci. 2005 Mar 23;25(12):3229-33. [15788780 ]
  6. Zhang C, Westaway SM, Speake JD, Bishop MJ, Goetz AS, Carballo LH, Hu M, Epperly AH: Tetrahydroquinoline derivatives as opioid receptor antagonists. Bioorg Med Chem Lett. 2011 Jan 15;21(2):670-6. doi: 10.1016/j.bmcl.2010.12.010. Epub 2010 Dec 8. [21193310 ]
  7. Wang D, Raehal KM, Bilsky EJ, Sadee W: Inverse agonists and neutral antagonists at mu opioid receptor (MOR): possible role of basal receptor signaling in narcotic dependence. J Neurochem. 2001 Jun;77(6):1590-600. [11413242 ]
General Function:
Not Available
Specific Function:
Not Available
Gene Name:
SIGMAR1
Uniprot ID:
Q5T1J1
Molecular Weight:
14852.655 Da
References
  1. Helm S, Trescot AM, Colson J, Sehgal N, Silverman S: Opioid antagonists, partial agonists, and agonists/antagonists: the role of office-based detoxification. Pain Physician. 2008 Mar-Apr;11(2):225-35. [18354714 ]
  2. Wee S, Orio L, Ghirmai S, Cashman JR, Koob GF: Inhibition of kappa opioid receptors attenuated increased cocaine intake in rats with extended access to cocaine. Psychopharmacology (Berl). 2009 Sep;205(4):565-75. doi: 10.1007/s00213-009-1563-y. Epub 2009 May 30. [19484223 ]
  3. Herz A: Endogenous opioid systems and alcohol addiction. Psychopharmacology (Berl). 1997 Jan;129(2):99-111. [9040115 ]
General Function:
Tumor necrosis factor receptor binding
Specific Function:
Cytokine that binds to TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR. It is mainly secreted by macrophages and can induce cell death of certain tumor cell lines. It is potent pyrogen causing fever by direct action or by stimulation of interleukin-1 secretion and is implicated in the induction of cachexia, Under certain conditions it can stimulate cell proliferation and induce cell differentiation. Impairs regulatory T-cells (Treg) function in individuals with rheumatoid arthritis via FOXP3 dephosphorylation. Upregulates the expression of protein phosphatase 1 (PP1), which dephosphorylates the key 'Ser-418' residue of FOXP3, thereby inactivating FOXP3 and rendering Treg cells functionally defective (PubMed:23396208). Key mediator of cell death in the anticancer action of BCG-stimulated neutrophils in combination with DIABLO/SMAC mimetic in the RT4v6 bladder cancer cell line (PubMed:22517918).The TNF intracellular domain (ICD) form induces IL12 production in dendritic cells.
Gene Name:
TNF
Uniprot ID:
P01375
Molecular Weight:
25644.15 Da
References
  1. Greeneltch KM, Haudenschild CC, Keegan AD, Shi Y: The opioid antagonist naltrexone blocks acute endotoxic shock by inhibiting tumor necrosis factor-alpha production. Brain Behav Immun. 2004 Sep;18(5):476-84. [15265541 ]
  2. Lin SL, Lee YM, Chang HY, Cheng YW, Yen MH: Effects of naltrexone on lipopolysaccharide-induced sepsis in rats. J Biomed Sci. 2005;12(2):431-40. [15917999 ]
  3. Davis RL, Buck DJ, Saffarian N, Stevens CW: The opioid antagonist, beta-funaltrexamine, inhibits chemokine expression in human astroglial cells. J Neuroimmunol. 2007 May;186(1-2):141-9. Epub 2007 May 1. [17475341 ]
General Function:
Opioid receptor activity
Specific Function:
G-protein coupled opioid receptor that functions as receptor for endogenous alpha-neoendorphins and dynorphins, but has low affinity for beta-endorphins. Also functions as receptor for various synthetic opioids and for the psychoactive diterpene salvinorin A. Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors, such as adenylate cyclase. 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.
Gene Name:
OPRK1
Uniprot ID:
P41145
Molecular Weight:
42644.665 Da
Binding/Activity Constants
TypeValueAssay TypeAssay Source
Inhibitory0.01 uMNot AvailableBindingDB 50000787
References
  1. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [11752352 ]
  2. Zhang C, Westaway SM, Speake JD, Bishop MJ, Goetz AS, Carballo LH, Hu M, Epperly AH: Tetrahydroquinoline derivatives as opioid receptor antagonists. Bioorg Med Chem Lett. 2011 Jan 15;21(2):670-6. doi: 10.1016/j.bmcl.2010.12.010. Epub 2010 Dec 8. [21193310 ]
General Function:
Opioid receptor activity
Specific Function:
G-protein coupled receptor that functions as receptor for endogenous enkephalins and for a subset of other opioids. Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors, such as adenylate cyclase. 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 and in opiate-mediated analgesia. Plays a role in developing analgesic tolerance to morphine.
Gene Name:
OPRD1
Uniprot ID:
P41143
Molecular Weight:
40368.235 Da
References
  1. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [11752352 ]
General Function:
Toxic substance binding
Specific Function:
After binding acetylcholine, the AChR responds by an extensive change in conformation that affects all subunits and leads to opening of an ion-conducting channel across the plasma membrane. The channel is blocked by alpha-bungarotoxin.
Gene Name:
CHRNA7
Uniprot ID:
P36544
Molecular Weight:
56448.925 Da
Binding/Activity Constants
TypeValueAssay TypeAssay Source
IC5025 uMNot AvailableBindingDB 50000787
IC5030 uMNot AvailableBindingDB 50000787
References
  1. Almeida LE, Pereira EF, Camara AL, Maelicke A, Albuquerque EX: Sensitivity of neuronal nicotinic acetylcholine receptors to the opiate antagonists naltrexone and naloxone: receptor blockade and up-regulation. Bioorg Med Chem Lett. 2004 Apr 19;14(8):1879-87. [15050620 ]
General Function:
Nociceptin receptor activity
Specific Function:
G-protein coupled opioid receptor that functions as receptor for the endogenous neuropeptide nociceptin. Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors. Signaling via G proteins mediates inhibition of adenylate cyclase activity and calcium channel activity. Arrestins modulate signaling via G proteins and mediate the activation of alternative signaling pathways that lead to the activation of MAP kinases. Plays a role in modulating nociception and the perception of pain. Plays a role in the regulation of locomotor activity by the neuropeptide nociceptin.
Gene Name:
OPRL1
Uniprot ID:
P41146
Molecular Weight:
40692.775 Da
Binding/Activity Constants
TypeValueAssay TypeAssay Source
Inhibitory>10 uMNot AvailableBindingDB 50000787
References
  1. Ghirmai S, Azar MR, Cashman JR: Synthesis and pharmacological evaluation of 6-naltrexamine analogs for alcohol cessation. Bioorg Med Chem. 2009 Sep 15;17(18):6671-81. doi: 10.1016/j.bmc.2009.07.069. Epub 2009 Aug 6. [19683449 ]