Discontinued Product6,7-Dichloro-3-hydroxy-2-quinoxalinecarboxylic acid (Cat. No. 0185) has been withdrawn from sale for commercial reasons.
Potent 'broad spectrum' excitatory amino acid receptor antagonist.
|Storage||Store at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
References are publications that support the biological activity of the product.
Frey et al (1988) 6,7-Dichloro-3-hydroxy-2-quinoxalinecarboxylic acid is a relatively potent antagonist at NMDA and kainate receptors. Neurosci.Lett. 91 194 PMID: 2847085
Watkins et al (1990) Experiments with kainate and quisqualate agonists and antagonists in relation to the sub-classification of 'non-NMDA' receptors. Excitatory Amino Acids and Synaptic Plasticity. E 49-55
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Keywords: 6,7-Dichloro-3-hydroxy-2-quinoxalinecarboxylic acid, 6,7-Dichloro-3-hydroxy-2-quinoxalinecarboxylic acid supplier, Non-selective, Ionotropic, Glutamate, 0185, Tocris Bioscience
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Literature in this Area
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Epilepsy is a brain disease that affects 60 million people globally. More than 20 anti-seizure drugs are currently available, but these do not address the underlying causes of the condition. This poster summarizes current knowledge about the development of the condition and highlights some approaches that have disease-modifying effects in proof-of-concept studies.
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.