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Selective κ-opioid agonist. At higher concentrations blocks Na+ channels.
|Storage||Desiccate 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 405.79. 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|
|0.25 mM||9.86 mL||49.29 mL||98.57 mL|
|1.25 mM||1.97 mL||9.86 mL||19.71 mL|
|2.5 mM||0.99 mL||4.93 mL||9.86 mL|
|12.5 mM||0.2 mL||0.99 mL||1.97 mL|
References are publications that support the biological activity of the product.
Pao-Luh Tao et al (1994) U-50,488 blocks the development of mor. tolerance and dependence at a very low dose in guinea pigs. Eur.J.Pharmacol. 256 281 PMID: 8045272
Suarez-Roca and Maixner (1993) Activation of kappa opioid receptors by U-50488H and mor. enhances the release of substance P from rat trigeminal nucleus slices. J.Pharmacol.Exp.Ther. 264 648 PMID: 7679733
Pugsley et al (1992) Cardiovascular actions of the κ-agonist, U-50-488H, in the absence and presence of opioid receptor blockade. Br.J.Pharmacol. 105 521 PMID: 1320979
Su et al (1998) Blockade of the development of mor. tolerance by U-50,488, an AVP antagonist or MK 801 in the rat hippocampal slice. Br.J.Pharmacol. 123 625 PMID: 9517380
If you know of a relevant reference for (±)-U-50488 hydrochloride, please let us know.
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Keywords: (±)-U-50488 hydrochloride, (±)-U-50488 hydrochloride supplier, selective, agonists, κ-opioid, kappa-opioid, KOP, Receptors, OP2, Kappa, Opioid, 0495, Tocris Bioscience
7 Citations for (±)-U-50488 hydrochloride
Citations are publications that use Tocris products. Selected citations for (±)-U-50488 hydrochloride include:
Grachev et al (2012) GPR54-dependent stimulation of luteinizing hormone secretion by neurokinin B in prepubertal rats. Pain 7 e44344 PMID: 23028524
Dziedowiec et al (2018) sMu opioid receptor agonist DAMGO produces place conditioning, abstinence-induced withdrawal, and naltrexone-dependent locomotor activation in planarians. Neuroscience 386 214 PMID: 29958944
Liu (2018) In vivo brain GPCR signaling elucidated by phosphoproteomics. Science 360 eaao4927 PMID: 29930108
Marchant et al (2010) Medial dorsal hypothalamus mediates the inhibition of reward seeking after extinction. J Neurosci 30 14102 PMID: 20962231
Polter (2017) Constitutive activation of kappa opioid receptors at ventral tegmental area inhibitory synapsesfollowing acute stress Elife 6 e23785 PMID: 28402252
Zhou et al (2013) Development of functionally selective, small molecule agonists at kappa opioid receptors. J Biol Chem 288 36703 PMID: 24187130
Kharmate et al (2013) Inhibition of tumor promoting signals by activation of SSTR2 and opioid receptors in human breast cancer cells. Cancer Cell Int 13 93 PMID: 24059654
Do you know of a great paper that uses (±)-U-50488 hydrochloride from Tocris? Please let us know.
Reviews for (±)-U-50488 hydrochloride
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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* or download your copy today!
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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.