ROS 234 dioxalate

Discontinued Product

ROS 234 dioxalate (Cat. No. 2034) has been withdrawn from sale for commercial reasons.
Description: Potent H3 antagonist
Chemical Name: N-[3-(1H-Imidazol-4-yl)propyl]-1H-benzimidazol-2-amine dioxalate
Purity: ≥99% (HPLC)
Literature (2)

Biological Activity for ROS 234 dioxalate

ROS 234 dioxalate is a potent H3 antagonist (pKB at guinea-pig ileum H3-receptor = 9.46). Limited blood brain barrier permeability (ED50 = 19.12 mg/kg i.p.).

Technical Data for ROS 234 dioxalate

M. Wt 421.37
Formula C13H15N5.2C2H2O4
Storage Desiccate at RT
Purity ≥99% (HPLC)
CAS Number 1781941-93-2
PubChem ID 56972188
Smiles O=C(O)C(O)=O.O=C(O)C(O)=O.C1(CCCNC2=NC3=C(C=CC=C3)N2)=CNC=N1

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.

Product Datasheets for ROS 234 dioxalate

References for ROS 234 dioxalate

References are publications that support the biological activity of the product.

Ballabeni et al (2002) CNS access of selected H3-antagonists: ex vivo binding study in rats. Inflamm.Res. 51 S55 PMID: 12013409

Mor et al (2004) Synthesis, biological activity, QSAR and QSPR study of 2-aminobenzimidazole derivatives as potent H3-antagonists. Bioorg.Med.Chem.Lett. 12 663

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Citations for ROS 234 dioxalate

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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!

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Histamine Receptors Scientific Review

Histamine Receptors Scientific Review

Written by Iwan de Esch and Rob Leurs, this review provides a synopsis of the different histamine receptor subtypes and the ligands that act upon them; compounds available from Tocris are listed.

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Alzheimer's disease (AD) is a debilitating and progressive neurodegenerative disease and the most common cause of dementia, affecting approximately 30% of individuals aged over 85 years. This poster summarizes the cellular and molecular mechanisms of AD.