Otenabant
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This drug entry is a stub and has not been fully annotated. It is scheduled to be annotated soon.
Explore a selection of our essential drug information below, or:
Identification
- Generic Name
- Otenabant
- DrugBank Accession Number
- DB11745
- Background
Otenabant has been investigated for the treatment of Obesity.
- Type
- Small Molecule
- Groups
- Investigational
- Structure
- Weight
- Average: 510.42
Monoisotopic: 509.1497639 - Chemical Formula
- C25H25Cl2N7O
- Synonyms
- Otenabant
- External IDs
- CP-945,598
- CP-945598
- CP-945598-01
Pharmacology
- Indication
Not Available
Reduce drug development failure ratesBuild, train, & validate machine-learning modelswith evidence-based and structured datasets.Build, train, & validate predictive machine-learning models with structured datasets.- Contraindications & Blackbox Warnings
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- Pharmacodynamics
Not Available
- Mechanism of action
Pre-clinical and clinical trial data suggest that CB-1 antagonists may have favorable effects on glucose metabolism in patients with type 2 diabetes and may also be an effective therapy for the treatment of obesity.
Target Actions Organism ACannabinoid receptor 1 antagonistHumans - Absorption
Not Available
- Volume of distribution
Not Available
- Protein binding
Not Available
- Metabolism
- Not Available
- Route of elimination
Not Available
- Half-life
Not Available
- Clearance
Not Available
- Adverse Effects
- Improve decision support & research outcomesWith structured adverse effects data, including: blackbox warnings, adverse reactions, warning & precautions, & incidence rates. View sample adverse effects data in our new Data Library!Improve decision support & research outcomes with our structured adverse effects data.
- Toxicity
Not Available
- Pathways
- Not Available
- Pharmacogenomic Effects/ADRs
- Not Available
Interactions
- Drug Interactions
- This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.Not Available
- Food Interactions
- Not Available
Products
- Drug product information from 10+ global regionsOur datasets provide approved product information including:dosage, form, labeller, route of administration, and marketing period.Access drug product information from over 10 global regions.
- Product Ingredients
Ingredient UNII CAS InChI Key Otenabant hydrochloride X2166Z319O 686347-12-6 KPYUQCJBZGQHPL-UHFFFAOYSA-N
Categories
- Drug Categories
- Chemical TaxonomyProvided by Classyfire
- Description
- This compound belongs to the class of organic compounds known as alpha amino acid amides. These are amide derivatives of alpha amino acids.
- Kingdom
- Organic compounds
- Super Class
- Organic acids and derivatives
- Class
- Carboxylic acids and derivatives
- Sub Class
- Amino acids, peptides, and analogues
- Direct Parent
- Alpha amino acid amides
- Alternative Parents
- Phenylimidazoles / 6-alkylaminopurines / Piperidinecarboxamides / Dialkylarylamines / Aminopiperidines / Aminopyrimidines and derivatives / Chlorobenzenes / N-substituted imidazoles / Imidolactams / Aryl chlorides show 8 more
- Substituents
- 1-phenylimidazole / 2-phenylimidazole / 4-aminopiperidine / 6-alkylaminopurine / 6-aminopurine / Alpha-amino acid amide / Amine / Aminopyrimidine / Aromatic heteropolycyclic compound / Aryl chloride show 31 more
- Molecular Framework
- Aromatic heteropolycyclic compounds
- External Descriptors
- Not Available
- Affected organisms
- Not Available
Chemical Identifiers
- UNII
- J8211Y53EF
- CAS number
- 686344-29-6
- InChI Key
- UNAZAADNBYXMIV-UHFFFAOYSA-N
- InChI
- InChI=1S/C25H25Cl2N7O/c1-2-31-25(24(28)35)11-13-33(14-12-25)22-20-23(30-15-29-22)34(17-9-7-16(26)8-10-17)21(32-20)18-5-3-4-6-19(18)27/h3-10,15,31H,2,11-14H2,1H3,(H2,28,35)
- IUPAC Name
- 1-[8-(2-chlorophenyl)-9-(4-chlorophenyl)-9H-purin-6-yl]-4-(ethylamino)piperidine-4-carboxamide
- SMILES
- CCNC1(CCN(CC1)C1=C2N=C(N(C2=NC=N1)C1=CC=C(Cl)C=C1)C1=CC=CC=C1Cl)C(N)=O
References
- General References
- Heimann AS, Gomes I, Dale CS, Pagano RL, Gupta A, de Souza LL, Luchessi AD, Castro LM, Giorgi R, Rioli V, Ferro ES, Devi LA: Hemopressin is an inverse agonist of CB1 cannabinoid receptors. Proc Natl Acad Sci U S A. 2007 Dec 18;104(51):20588-93. Epub 2007 Dec 12. [Article]
- Buchweitz JP, Karmaus PW, Williams KJ, Harkema JR, Kaminski NE: Targeted deletion of cannabinoid receptors CB1 and CB2 produced enhanced inflammatory responses to influenza A/PR/8/34 in the absence and presence of Delta9-tetrahydrocannabinol. J Leukoc Biol. 2008 Mar;83(3):785-96. Epub 2007 Dec 11. [Article]
- Gerdeman GL, Schechter JB, French ED: Context-specific reversal of cocaine sensitization by the CB1 cannabinoid receptor antagonist rimonabant. Neuropsychopharmacology. 2008 Oct;33(11):2747-59. Epub 2007 Dec 5. [Article]
- External Links
- PubChem Compound
- 10052040
- PubChem Substance
- 347828103
- ChemSpider
- 8227602
- BindingDB
- 27337
- ChEMBL
- CHEMBL562668
- ZINC
- ZINC000003948997
- Wikipedia
- Otenabant
Clinical Trials
- Clinical Trials
Clinical Trial & Rare Diseases Add-on Data Package
Explore 4,000+ rare diseases, orphan drugs & condition pairs, clinical trial why stopped data, & more. Preview package Phase Status Purpose Conditions Count Start Date Why Stopped 100+ additional columns Unlock 175K+ rows when you subscribe.View sample data3 Terminated Treatment Obesity 4 somestatus stop reason just information to hide 2, 3 Completed Treatment Obesity 1 somestatus stop reason just information to hide 1 Completed Basic Science Non-Alcoholic Steatohepatitis (NASH) 1 somestatus stop reason just information to hide 1 Completed Diagnostic Healthy Volunteers (HV) 1 somestatus stop reason just information to hide 1 Completed Treatment Hepatic Insufficiency / Obesity 1 somestatus stop reason just information to hide
Pharmacoeconomics
- Manufacturers
- Not Available
- Packagers
- Not Available
- Dosage Forms
- Not Available
- Prices
- Not Available
- Patents
- Not Available
Properties
- State
- Not Available
- Experimental Properties
- Not Available
- Predicted Properties
Property Value Source Water Solubility 0.0107 mg/mL ALOGPS logP 3.66 ALOGPS logP 4.42 Chemaxon logS -4.7 ALOGPS pKa (Strongest Acidic) 15.89 Chemaxon pKa (Strongest Basic) 8.97 Chemaxon Physiological Charge 1 Chemaxon Hydrogen Acceptor Count 6 Chemaxon Hydrogen Donor Count 2 Chemaxon Polar Surface Area 101.96 Å2 Chemaxon Rotatable Bond Count 6 Chemaxon Refractivity 158.88 m3·mol-1 Chemaxon Polarizability 53.2 Å3 Chemaxon Number of Rings 5 Chemaxon Bioavailability 1 Chemaxon Rule of Five No Chemaxon Ghose Filter No Chemaxon Veber's Rule No Chemaxon MDDR-like Rule Yes Chemaxon - Predicted ADMET Features
- Not Available
Spectra
- Mass Spec (NIST)
- Not Available
- Spectra
- Chromatographic Properties
Collision Cross Sections (CCS)
Adduct CCS Value (Å2) Source type Source [M-H]- 205.45854 predictedDeepCCS 1.0 (2019) [M+H]+ 207.85411 predictedDeepCCS 1.0 (2019) [M+Na]+ 213.76662 predictedDeepCCS 1.0 (2019)
Targets
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Use our structured and evidence-based datasets to unlock newinsights and accelerate drug research.
Use our structured and evidence-based datasets to unlock new insights and accelerate drug research.
1. DetailsCannabinoid receptor 1
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Yes
- Actions
- Antagonist
- General Function
- G-protein coupled receptor for endogenous cannabinoids (eCBs), including N-arachidonoylethanolamide (also called anandamide or AEA) and 2-arachidonoylglycerol (2-AG), as well as phytocannabinoids, such as delta(9)-tetrahydrocannabinol (THC) (PubMed:15620723, PubMed:27768894, PubMed:27851727). Mediates many cannabinoid-induced effects, acting, among others, on food intake, memory loss, gastrointestinal motility, catalepsy, ambulatory activity, anxiety, chronic pain. Signaling typically involves reduction in cyclic AMP (PubMed:1718258, PubMed:21895628, PubMed:27768894). In the hypothalamus, may have a dual effect on mitochondrial respiration depending upon the agonist dose and possibly upon the cell type. Increases respiration at low doses, while decreases respiration at high doses. At high doses, CNR1 signal transduction involves G-protein alpha-i protein activation and subsequent inhibition of mitochondrial soluble adenylate cyclase, decrease in cyclic AMP concentration, inhibition of protein kinase A (PKA)-dependent phosphorylation of specific subunits of the mitochondrial electron transport system, including NDUFS2. In the hypothalamus, inhibits leptin-induced reactive oxygen species (ROS) formation and mediates cannabinoid-induced increase in SREBF1 and FASN gene expression. In response to cannabinoids, drives the release of orexigenic beta-endorphin, but not that of melanocyte-stimulating hormone alpha/alpha-MSH, from hypothalamic POMC neurons, hence promoting food intake. In the hippocampus, regulates cellular respiration and energy production in response to cannabinoids. Involved in cannabinoid-dependent depolarization-induced suppression of inhibition (DSI), a process in which depolarization of CA1 postsynaptic pyramidal neurons mobilizes eCBs, which retrogradely activate presynaptic CB1 receptors, transiently decreasing GABAergic inhibitory neurotransmission. Also reduces excitatory synaptic transmission (By similarity). In superior cervical ganglions and cerebral vascular smooth muscle cells, inhibits voltage-gated Ca(2+) channels in a constitutive, as well as agonist-dependent manner (PubMed:17895407). In cerebral vascular smooth muscle cells, cannabinoid-induced inhibition of voltage-gated Ca(2+) channels leads to vasodilation and decreased vascular tone (By similarity). Induces leptin production in adipocytes and reduces LRP2-mediated leptin clearance in the kidney, hence participating in hyperleptinemia. In adipose tissue, CNR1 signaling leads to increased expression of SREBF1, ACACA and FASN genes (By similarity). In the liver, activation by endocannabinoids leads to increased de novo lipogenesis and reduced fatty acid catabolism, associated with increased expression of SREBF1/SREBP-1, GCK, ACACA, ACACB and FASN genes. May also affect de novo cholesterol synthesis and HDL-cholesteryl ether uptake. Peripherally modulates energy metabolism (By similarity). In high carbohydrate diet-induced obesity, may decrease the expression of mitochondrial dihydrolipoyl dehydrogenase/DLD in striated muscles, as well as that of selected glucose/ pyruvate metabolic enzymes, hence affecting energy expenditure through mitochondrial metabolism (By similarity). In response to cannabinoid anandamide, elicits a pro-inflammatory response in macrophages, which involves NLRP3 inflammasome activation and IL1B and IL18 secretion (By similarity). In macrophages infiltrating pancreatic islets, this process may participate in the progression of type-2 diabetes and associated loss of pancreatic beta-cells (PubMed:23955712)
- Specific Function
- cannabinoid receptor activity
- Gene Name
- CNR1
- Uniprot ID
- P21554
- Uniprot Name
- Cannabinoid receptor 1
- Molecular Weight
- 52857.365 Da
References
- Zhou Y, Zhang Y, Zhao D, Yu X, Shen X, Zhou Y, Wang S, Qiu Y, Chen Y, Zhu F: TTD: Therapeutic Target Database describing target druggability information. Nucleic Acids Res. 2024 Jan 5;52(D1):D1465-D1477. doi: 10.1093/nar/gkad751. [Article]
Drug created at October 20, 2016 20:44 / Updated at August 26, 2024 19:22