Naltrexone HClopioid receptor antagonist CAS# 16676-29-2 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 16676-29-2 | SDF | Download SDF |
| PubChem ID | 5485201 | Appearance | Powder |
| Formula | C20H24ClNO4 | M.Wt | 377.86 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | Soluble to 100 mM in water | ||
| Chemical Name | (5α)-17-(Cyclopropylmethyl)-4,5-epox | ||
| SMILES | [Cl-].Oc1ccc2C[C@H]3N(CC[C@@]45[C@@H](Oc1c24)C(=O)CC[C@@]35O)CC6CC6.[H+] | ||
| Standard InChIKey | RHBRMCOKKKZVRY-ITLPAZOVSA-N | ||
| Standard InChI | InChI=1S/C20H23NO4.ClH/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;1H/t15-,18+,19+,20-;/m1./s1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Opioid antagonist. |
Naltrexone HCl Dilution Calculator
Naltrexone HCl Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.6465 mL | 13.2324 mL | 26.4648 mL | 52.9297 mL | 66.1621 mL |
| 5 mM | 0.5293 mL | 2.6465 mL | 5.293 mL | 10.5859 mL | 13.2324 mL |
| 10 mM | 0.2646 mL | 1.3232 mL | 2.6465 mL | 5.293 mL | 6.6162 mL |
| 50 mM | 0.0529 mL | 0.2646 mL | 0.5293 mL | 1.0586 mL | 1.3232 mL |
| 100 mM | 0.0265 mL | 0.1323 mL | 0.2646 mL | 0.5293 mL | 0.6616 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Naltrexone HCL is an opioid receptor antagonist and used in treatment of alcohol and opioid dependence.
Opioid receptor is a group of G protein-coupled receptors with opioids as ligands (e.g. proenkephalin, prodynorphin, pronociceptin etc, functioning in regulating pain perception, hormonal secretion and affecting temperature control etc.
In adult male Sprague-Dawley rats, ultra-low doses of naltrexone (16.7, 20.0, and 25.0 ng/kg) with morphine (1mg/kg) extended the duration of the morphine-induced conditioned place preference. [1] In male Wistar rats, naltrexone significantly inhibited ethanol self-adminnistration and prevented ethanol-activated increases in dialysate dopamine amount. [2] Subchronic treatment with naltrexone caused progressive decrease of ethanol self-administration. Single doses of naltrexone increased extinction and attenuated cue-induced reinstatement of ethanol-reinforced behavior. [3] In rhesus monkeys, naltrexone lowered behavior kept non-selectively by either ethanol or sucrose. [4]
References:
[1] Powell KJ, Abul-Husn NS, Jhamandas A, Olmstead MC, Beninger RJ, Jhamandas K. Paradoxical effects of the opioid antagonist naltrexone on morphine analgesia, tolerance, and reward in rats. J Pharmacol Exp Ther. 2002 Feb;300(2):588-96.
[2] Gonzales RA, Weiss F. Suppression of ethanol-reinforced behavior by naltrexone is associated with attenuation of the ethanol-induced increase in dialysate dopamine levels in the nucleus accumbens. J Neurosci. 1998 Dec 15;18(24):10663-71
[3] Bienkowski P, Kostowski W, Koros E. Ethanol-reinforced behaviour in the rat: effects of naltrexone. Eur J Pharmacol. 1999 Jun 25;374(3):321-7.
[4] Williams KL, Winger G, Pakarinen ED, Woods JH. Naltrexone reduces ethanol- and sucrose-reinforced responding in rhesus monkeys. Psychopharmacology (Berl). 1998 Sep;139(1-2):53-61.
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Physiologic and morphologic changes and incidence of neoplasms in mice and rats fed naltrexone HCl for 24 months.[Pubmed:6469931]
J Clin Psychiatry. 1984 Sep;45(9 Pt 2):11-4.
Short-term (acute oral LD50 and 90-day oral subchronic) studies in mice and long-term (24 months) carcinogenesis bioassays were performed in B6C3F1 mice and Fischer 344 rats given naltrexone. The oral LD50 was approximately 1500 mg/kg; convulsions, hypopnea, and cardiac failure were dose-related. Naltrexone mixed with feed over 90 days did not evoke definitive signs of gross toxicity, and histopathology was unrelated to drug treatment. Similar drug/feed admixtures given for 24 months to mice or rats did not disturb behavior. In mice, naltrexone reduced growth rates 5-10% and food intake 9-19%, but survival rates were 70-82% for treated mice and controls. The frequency and location of predominant tumors were similar in treated and untreated mice. In the rat, the same dosages had little effect on growth or food intake. The majority of all sacrificed rats had neoplasms. Neither neoplasms nor nonneoplastic lesions in mice or rats were associated with drug treatment. It is concluded that naltrexone is not a carcinogen.
Naltrexone-induced opiate receptor supersensitivity.[Pubmed:6289965]
Brain Res. 1982 Aug 12;245(2):285-92.
Chronic administration of the long-lived narcotic antagonist naltrexone resulted in a marked increase in brain opiate receptors. Similar changes in receptor density were observed for binding of the putative mu agonist [3H]dihydromorphine, the mu antagonist [3H]naloxone, the putative delta ligand [3H]D-Ala2,D-Leu5-enkephalin and [3H]etorphine. In addition, the sensitivity of agonist binding to guanyl nucleotide inhibition increased significantly. In contrast, no such changes in opiate binding were observed following acute administration of naltrexone. The increase in opiate receptor number following chronic naltrexone was highest in the mesolimbic and frontal cortex areas, and lowest in the dorsal hippocampus and periaqueductal gray. These results indicate a degree of plasticity in the opiate receptor system that may correlate with specific functional pathways.
