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RX 821002 hydrochloride is a potent, selective α2-adrenoceptor antagonist with very low affinity for imidazoline sites. Displays selectivity for the α2D over the α2A subtypes (pKd values are 9.7 and 8.2 respectively).
RX 821002 hydrochloride is also offered as part of the Tocriscreen 2.0 Max. Find out more about compound libraries available from Tocris.
|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|
The following data is based on the product molecular weight 270.72. 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||3.69 mL||18.47 mL||36.94 mL|
|5 mM||0.74 mL||3.69 mL||7.39 mL|
|10 mM||0.37 mL||1.85 mL||3.69 mL|
|50 mM||0.07 mL||0.37 mL||0.74 mL|
References are publications that support the biological activity of the product.
Erdbrugger et al (1995) Does [3H]2-methoxy-idazoxan (RX 821002) detect more alpha-2-adrenoceptor agonist high-affinity sites than [3H]rauwolscine? A comparison of nine tissues and cell lines. J.Pharmacol.Exp.Ther. 273 1287 PMID: 7791100
O'Rourke et al (1994) Characterisation of [3H]RX 821002 binding to alpha-2 adrenergic receptor subtypes. J.Pharmacol.Exp.Ther. 268 1362 PMID: 7908054
Trendelenburg et al (1996) Antagonists that differentiate between α2A- and α2D-adrenoceptors. Naunyn Schmiedebergs Arch.Pharmacol. 353 245 PMID: 8692278
If you know of a relevant reference for RX 821002 hydrochloride, please let us know.
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Citations are publications that use Tocris products. Selected citations for RX 821002 hydrochloride include:
Staedtke et al (2018) Disruption of a self-amplifying catecholamine loop reduces cytokine release syndrome. Nature 564 273 PMID: 30542164
Hott et al (2012) Both α1- and β1-adrenoceptors in the bed nucleus of the stria terminalis are involved in the expression of conditioned contextual fear. Br J Pharmacol 167 207 PMID: 22506532
Li et al (2017) Pericytes impair capillary blood flow and motor function after chronic spinal cord injury. Nat Med 23 733 PMID: 28459438
Alves et al (2014) Both α1- and α2-adrenoceptors in the insular cortex are involved in the cardiovascular responses to acute restraint stress in rats. J Chem Biol 9 e83900 PMID: 24404141
Uchański et al (2019) An improved yeast surface display platform for the screening of nanobody immune libraries. Sci Rep 9 382 PMID: 30674983
Crestani et al (2008) Both alpha1 and alpha2-adrenoceptors mediate the cardiovascular responses to noradrenaline microinjected into the bed nucleus of the stria terminal of rats. Br J Pharmacol 153 583 PMID: 18037912
Deupree et al (2008) Alpha-2 adrenergic-induced changes in rectal temperature in adult and 13-day old rats following acute and repeated desipr. administration. BMC Pharmacol 8 17 PMID: 18831759
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Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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Major depressive disorder is characterized by depressed mood and a loss of interest and/or pleasure. Updated in 2015 this poster highlights presynaptic and postsynaptic targets for the potential treatment of major depressive disorder, as well as outlining the pharmacology of currently approved antidepressant drugs.
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.
Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.