Nor binaltorphimine dihydrochloride

Manufactured by Merck Group

Sourced in United States

Nor-binaltorphimine dihydrochloride is a synthetic organic compound used as a laboratory research tool. It functions as a selective antagonist for the kappa opioid receptor.

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Lab products found in correlation

Naloxone, by Merck Group (4 mentions) β funaltrexamine hydrochloride, by Merck Group (2 mentions) Naloxone hydrochloride dihydrate, by Merck Group (2 mentions) Naltrindole hydrochloride, by Merck Group (2 mentions) Clocinnamox, by Merck Group (2 mentions) Naltrindole, by Bio-Techne (2 mentions) Naltrindole, by Merck Group (2 mentions) Apelin 13, by GL Biochem (1 mentions) Pyr apelin 13, by GL Biochem (1 mentions) Apelin 13 f13a, by GL Biochem (1 mentions) Scopolamine hydrochloride, by Merck Group (1 mentions) Prostaglandin e2, by Merck Group (1 mentions) Bestatin, by Bio-Techne (1 mentions) Planarians, by Carolina Biological Supply (1 mentions) Planarians dugesia dorotocephala, by Carolina Biological Supply (1 mentions) Naltrexone hydrochloride ntx, by Merck Group (1 mentions) U50488 hydrochloride, by Bio-Techne (1 mentions) Naloxone methiodide, by Merck Group (1 mentions) Carrageenan, by Merck Group (1 mentions) Am630, by Bio-Techne (1 mentions)

Spelling variants of this product

Nor-binaltorphimine (9 citations) Nor-Binaltorphimine dihydrochloride (norBNI), (2 citations)

8 protocols using nor binaltorphimine dihydrochloride

Peptide Apelin Receptor Antagonist Study

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The peptides, apelin-13, (pyr)apelin-13, and apelin-13(F13A) were obtained from GL Biochem (Shanghai) Ltd. (Shanghai, China). The amino acid sequence of (pyr)apelin-13 was “Pyr-Arg-Pro-Arg-Leu-Ser-His-Lys-Gly-Pro-Met-Pro-Phe,” and the amino acid sequence of apelin-13 was “Gln-Arg-Pro-Arg-Leu-Ser-His-Lys-Gly-Pro-Met-Pro-Phe.” apelin-13(F13A) was the APJ receptor antagonist. Morphine hydrochloride was supplied by The First Affiliated Hospital of Henan University (Kaifeng, China). Naloxone (opioid receptor antagonist) and nor-binaltorphimine dihydrochloride (nor-BNI, KOR antagonist) were purchased from Sigma-Aldrich (St. Louis, MO, United States). The chemicals were dissolved in sterile saline and stored at -20°C until the time of injection. The drugs were i.v. injected into mouse tail veins at a constant rate of 0.01 ml per second or were intramuscularly (i.m.) administered into buttock sites in a volume of 0.1 ml.

Lv S., Zhang X., Feng Y., Zhou Y., Cui B., Yang Y, & Wang X. (2020). Intravenous Administration of Pyroglutamyl Apelin-13 Alleviates Murine Inflammatory Pain via the Kappa Opioid Receptor. Frontiers in Neuroscience, 14, 929.

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Opioid Receptor Antagonists Evaluation

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Morphine hydrochloride was purchased from Takeda Chemical Industries (Osaka, Japan) and was dissolved in sterile saline (Otsuka Pharmaceutical Co. Ltd.). Naloxone hydrochloride dihydrate (a relatively non-selective opioid receptor antagonist), β-funaltrexamine hydrochloride ((E)-4-[[(5α,6β)-17-(cyclopropylmethyl)-4,5-epoxy-3,14-dihydroxy-morphinan-6-yl]amino]-4-oxo-2-butenoic acid methyl ester hydrochloride (a highly selective MOP antagonist), norbinaltorphimine dihydrochloride (a highly selective KOP antagonist), naltrindole hydrochloride (a highly selective DOP antagonist), and (−)-scopolamine hydrochloride (a muscarinic antagonist) were purchased from Sigma-Aldrich. Doses of all drugs refer to the weight of the salt. All reagents were dissolved in sterile saline. Drug solutions were prepared in such a way that the necessary dose could be injected in a volume of 0.1 mL/10 g of body weight by an intraperitoneal (i.p.) route. The doses of the drugs were chosen based on the literature.15 (link)–20 (link) In the present study, no reduced body weight in mice treated with naloxone, compared with mice treated with saline, was observed (data not shown).

Kitanaka J., Kitanaka N., Hall F.S., Fujii M., Goto A., Kanda Y., Koizumi A., Kuroiwa H., Mibayashi S., Muranishi Y., Otaki S., Sumikawa M., Tanaka K.I., Nishiyama N., Uhl G.R, & Takemura M. (2015). Memory Impairment and Reduced Exploratory Behavior in Mice after Administration of Systemic Morphine. Journal of Experimental Neuroscience, 9, 27-35.

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Aripiprazole-Induced Plantar Hyperalgesia

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Aripiprazole was injected subcutaneously into the plantar surface of the right hind paw (25 and 100 μg). The substance was provided by Bristol-Myers Squibb (Syracuse, NY, USA) and Otsuka Pharmaceuticals (Naruto, Tokushima, Japan). It was dissolved in physiological saline containing 5% tween 80; prostaglandin E₂ (PGE₂; hyperalgesic agent; Sigma®) was diluted in ethanol [14 (link)]. All other drugs used were diluted in saline, naloxone (nonselective antagonist at opioid receptors, Sigma), bestatin (an aminopeptidase-N inhibitor, Tocris®), clocinnamox (selective μ-opioid receptor antagonist, Sigma), nor-Binaltorphimine dihydrochloride (nor-BNI, selective κ-opioid receptor antagonist, Sigma), and naltrindole (selective δ-opioid receptor antagonist, Tocris).

Ferreira R.C., Almeida-Santos A.F., Duarte I.D., Aguiar D.C., Moreira F.A, & Romero T.R. (2017). Peripheral Antinociception Induced by Aripiprazole Is Mediated by the Opioid System. BioMed Research International, 2017, 8109205.

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Planaria Opioid Receptor Pharmacology

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planarians (Dugesia dorotocephala) were purchased from Carolina Biological Supply (Burlington, NC, USA). Upon arrival in the laboratory, planarians were maintained in the aqueous solution provided by Carolina Biological Supply, acclimated to room temperature (21 °C), and tested within 3 days of receipt. DAMGO and the kappa agonist U50,488 hydrochloride was purchased from Tocris Biosciences (St. Louis, MO, USA). Naltrexone hydrochloride (NTX) and the kappa opioid receptor antagonist, nor-Binaltorphimine dihydrochloride (nBNI), were purchased from Sigma-Aldrich (St. Louis, MO, USA). Morphine sulfate was provided by NIDA Drug Supply (Bethesda, MD, USA). All drugs were dissolved in spring water, with stock and working solutions prepared daily, and concentrations were based on prior planarian work and Kd values of DAMGO (Tallarida et al., 2014 (link); Zhao et al., 2003 (link)). Behavioral experiments were conducted between 10 AM and 4 PM. Behavioral responses were quantified by a trained observer with a stopwatch who was blinded to drug treatment. planarians are large enough (average length about 3–15 mm) so that behavior can be observed and quantified with the naked eye, so behavioral responses were quantified without the aid of a microscope. Experiments and behavioral observations were conducted in ‘real time’, and no videotaping was used.

Dziedowiec E., Nayak S.U., Gruver K.S., Jennings T., Tallarida C.S, & Rawls S.M. (2018). Mu opioid receptor agonist DAMGO produces place conditioning, abstinence-induced withdrawal, and naltrexone-dependent locomotor activation in planarians. Neuroscience, 386, 214-222.

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Opioid Receptor Ligand Characterization

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Morphine sulfate pentahydrate, fentanyl hydrochloride, oxycodone hydrochloride, naltrexone hydrochloride, β-funaltrexamine hydrochloride, clocinnamox mesylate, SNC-80, naltrindole hydrochloride, U50,488H, and Salvinorin A were kindly provided by the National Institute on Drug Abuse Drug Supply Program. Naloxone hydrochloride dihydrate and nor-binaltorphimine dihydrochloride were purchased from Sigma-Aldrich Chemical Co. (St. Louis, MO, USA). All other chemicals used were purchased from commercial sources and are of analytical grade.

Hedrick S.L., Luo D., Kaska S., Niloy K.K., Jackson K., Sarma R., Horn J., Baynard C., Leggas M., Butelman E.R., Kreek M.J, & Prisinzano T.E. (2021). Design, synthesis, and preliminary evaluation of a potential synthetic opioid rescue agent. Journal of Biomedical Science, 28, 62.

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Synthesis and Characterization of Opioid Compounds

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Morphine hydrochloride was produced by the Shenyang First Pharmaceutical Factory (Shenyang, China). Naloxone, Naloxone methiodide, β-funaltrexamine hydrochloride, nor-binaltorphimine dihydrochloride, and naltrindole were purchased from Sigma-Aldrich (St. Louis, MO, USA). All amino acids were purchased from GL Biochem Ltd. (Shanghai, China). All organic chemicals were purchased from J&K Scientific Ltd. (Beijing, China). Rink amide 4-methylbenzhydrylamine (MBHA) resin was purchased from Nankai Hecheng Science & Technology Co., Ltd. (Tianjin, China). The G-MOPS^TM PLUS was obtained from Vitrolife Sweden AB (Goteborg, Sweden). Drugs for mice were dissolved in physiological saline, and those for sperm were dissolved in G-MOPS^TM PLUS. All drugs were stored at −20 °C. G-MOPS ^TM PLUS was stored at 4 °C.

Li F., Yue F., Zhang W., Xu B., Wang Y, & Zhang X. (2023). A Novel Multi-Target Mu/Delta Opioid Receptor Agonist, HAGD, Produced Potent Peripheral Antinociception with Limited Side Effects in Mice and Minimal Impact on Human Sperm Motility In Vitro. Molecules, 28(1), 427.

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Analgesic Compounds: Purification and Preparation

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The following drugs and chemicals were used: δ-CNTX-Pn1a was purified by a combination of preparative reverse phase HPLC (RP-HPLC), ion exchange HPLC and analytical reverse phase HPLC as previously described [52 (link)]. µ-Conotoxin MVIIA was purchased from Latoxan (Valence, France). Carrageenan (Sigma, St Louis, MO, USA), Prostaglandin E₂ (Enzo Life Sciences, Farmingdale, NY, USA), AM251 (N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide; Tocris, Pittsburg, PA, USA), AM630 (6-iodo-2-methyl-1-[2-(4-morpholinyl)ethyl]-1H-indol-3-yl(4-ethoxyphenyl) methanone Tocris, Pittsburgh, PA, USA), Naloxone (Sigma, St. Louis, MO, USA), Clocinnamox (Tocris, Pittsburgh, PA, USA), Naltrindole (Tocris, Pittsburgh, PA, USA), Nor-BNI (Nor-Binaltorphimine dihydrochloride; Sigma, St. Louis, MO, USA) were dissolved as follows: PGE₂ (2% ethanol in saline); AM251 and AM630 (12% DMSO in saline); Carrageenan, δ-CNTX-Pn1a, µ-Conotoxin MVIIA (MVIIA), Naloxone, Clocinnamox, Naltrindole and Nor-BNI (saline).

Emerich B.L., Ferreira R.C., Cordeiro M.N., Borges M.H., Pimenta A.M., Figueiredo S.G., Duarte I.D, & de Lima M.E. (2016). δ-Ctenitoxin-Pn1a, a Peptide from Phoneutria nigriventer Spider Venom, Shows Antinociceptive Effect Involving Opioid and Cannabinoid Systems, in Rats. Toxins, 8(4), 106.

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Intrathecal Opioid Receptor Antagonist Pretreatment

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The following were obtained from the sources indicated: sialorphin (PH Japan, Hiroshima, Japan); and [Met 5 ]enkephalin (ME), amastatin, and phosphoramidon (The Peptide Institute, Inc., Minoh, Japan). The following were all purchased from SIGMA Japan (Tokyo, Japan): captopril, D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH 2 (CTOP, a mopioid receptor antagonist), nor-binaltorphimine dihydrochloride (nor-BNI, a k-opioid receptor antagonist), naltrindole hydrochloride (NTI, a d-opioid receptor antagonist), and BMS-986124 (a silent allosteric modulator of m-opioid receptor). The nonselective opioid receptor antagonist naloxone hydrochloride (NOX) was purchased from Daiichi-Sankyo Company, Limited (Tokyo, Japan). All of the above chemicals were dissolved in saline, except for nor-BNI and NTI, which were dissolved in water, and BMS-986124, which was dissolved in 50% DMSO and 50% saline. The desired concentration of each solution was prepared at the time it was to be used, and each was administered intrathecally at a volume of 10 ml. Administration of the PIs was performed at 10 minutes prior to that of the opioid receptor agonist or saline as a control.

Kan T., Yoshikawa M., Watanabe M., Miura M., Ito K., Matsuda M., Iwao K., Kobayashi H., Suzuki T, & Suzuki T. (2020). Sialorphin Potentiates Effects of [Met⁵]Enkephalin without Toxicity by Action other than Peptidase Inhibition. The Journal of pharmacology and experimental therapeutics, 375(1).

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