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|Storage||Store at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 377.87. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||2.65 mL||13.23 mL||26.46 mL|
|5 mM||0.53 mL||2.65 mL||5.29 mL|
|10 mM||0.26 mL||1.32 mL||2.65 mL|
|50 mM||0.05 mL||0.26 mL||0.53 mL|
References are publications that support the biological activity of the product.
Gold et al (1982) Naltrexone, opiate addiction, and endorphins. Med.Res.Rev. 2 211 PMID: 6289026
Tempel et al (1982) Supersensitivity of brain opiate receptor subtypes after chronic naltr. treatment. Life Sci. 31 1401 PMID: 6292636
Zukin et al (1982) Naltrexone-induced opiate receptor supersensitivity. Brain Res. 245 285 PMID: 6289965
If you know of a relevant reference for Naltrexone hydrochloride, please let us know.
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Keywords: Naltrexone hydrochloride, Naltrexone hydrochloride supplier, Broad, spectrum, antagonists, Opioids, Receptors, Miscellaneous/Non-selective, 0677, Tocris Bioscience
9 Citations for Naltrexone hydrochloride
Citations are publications that use Tocris products. Selected citations for Naltrexone hydrochloride include:
Wang et al (2010) Coexpression of delta- and mu-opioid receptors in nociceptive sensory neurons. Proc Natl Acad Sci U S A 107 13117 PMID: 20615975
Cho et al (2019) Latent Sensitization in a Mouse Model of Ocular Neuropathic Pain. Transl Vis Sci Technol 8 6 PMID: 30937216
Tumati et al (2009) Sustained mor. treatment augments capsaicin-evoked calcitonin gene-related peptide release from primary sensory neurons in a protein kinase A- and Raf-1-dependent manner. J Pain 330 810 PMID: 19491327
Markkanen and Petäjä-Repo (2008) N-glycan-mediated quality control in the endoplasmic reticulum is required for the expression of correctly folded delta-opioid receptors at the cell surface. J Biol Chem 283 29086 PMID: 18703511
Yue et al (2008) Sustained mor. treatment augments basal CGRP release from cultured primary sensory neurons in a Raf-1 dependent manner. Eur J Pharmacol 584 272 PMID: 18328477
Smith et al (2016) Endogenous central amygdala mu-opioid receptor signaling promotes sodium appetite in mice. Proc Natl Acad Sci U S A 113 13893 PMID: 27849613
Leskelä et al (2012) Cys-27 variant of human δ-opioid receptor modulates maturation and cell surface delivery of Phe-27 variant via heteromerization. J Biol Chem 287 5008 PMID: 22184124
Chung et al (2010) Hyperbaric oxygen treatment induces a 2-phase antinociceptive response of unusually long duration in mice. Hum Mol Genet 11 847 PMID: 20418186
Jones et al (2010) Identification of a κ-opioid agonist as a potent and selective lead for drug development against human African trypanosomiasis. Biochem Pharmacol 80 1478 PMID: 20696141
Do you know of a great paper that uses Naltrexone hydrochloride from Tocris? Please let us know.
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Peptides Involved in Appetite Modulation Scientific Review
Written by Sonia Tucci, Lynsay Kobelis and Tim Kirkham, this review provides a synopsis of the increasing number of peptides that have been implicated in appetite regulation and energy homeostasis; putative roles of the major peptides are outlined and compounds available from Tocris are listed.
The key feature of drug addiction is the inability to stop using a drug despite clear evidence of harm. This poster describes the brain circuits associated with addiction, and provides an overview of the main classes of addictive drugs and the neurotransmitter systems that they target.
Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.