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Potent and highly selective histamine H3 receptor antagonist (pA2 = 8.4); displays > 30000-fold selectivity over H1 and H2 receptors. Can act as a partial agonist in SK-N-MC cells expressing human H3 receptors. Produces antinociception, possibly via a non-H1, -H2 or -H3 receptor-mediated mechanism, following central administration in vivo.
|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 315.05. 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||3.17 mL||15.87 mL||31.74 mL|
|5 mM||0.63 mL||3.17 mL||6.35 mL|
|10 mM||0.32 mL||1.59 mL||3.17 mL|
|50 mM||0.06 mL||0.32 mL||0.63 mL|
References are publications that support the biological activity of the product.
Hough et al (1999) Antinociceptive activity of impentamine, a histamine congener, after CNS administration. Life Sci. 64 PL79 PMID: 10072195
Vollinga et al (1995) Homologs of histamine as histamine H3 receptor antagonists: a new potent and selective H3 antagonist, 4(5)-(5-aminopentyl)-1H-imidazole. J.Med.Chem. 38 266 PMID: 7830269
Wieland et al (2001) Constitutive activity of histamine H3 receptors stably expressed in SK-N-MC cells: display of agonism and inverse agonism by H3 antagonists. J.Pharmacol.Exp.Ther. 299 908 PMID: 11714875
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Keywords: Impentamine dihydrobromide, Impentamine dihydrobromide supplier, Selective, H3, antagonists, Receptors, Histamine, histaminergic, VUF4702, VUF, 4702, 1858, Tocris Bioscience
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Alzheimer's disease (AD) is a degenerative brain disease and the most common cause of dementia, affecting approximately 47 million people worldwide. Updated in 2015, this poster summarizes the structural and functional changes observed in the progression of this neurodegenerative disease, as well as classic AD drug targets.