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Submit Review(2R,3R)-Chlorpheg
Discontinued Product
(2R,3R)-Chlorpheg (Cat. No. 0816) has been withdrawn from sale for commercial reasons.
Description: Inactive isomer of (0134)
Chemical Name: (2R,3R)-b-p-Chlorophenylglutamic acid
Biological Activity for (2R,3R)-Chlorpheg
Inactive stereoisomer.
Technical Data for (2R,3R)-Chlorpheg
| M. Wt | 257.67 |
| Storage | Store 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.
Product Datasheets for (2R,3R)-Chlorpheg
Certificate of Analysis is currently unavailable on-line.
Please contact Customer Service
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References for (2R,3R)-Chlorpheg
References are publications that support the biological activity of the product.
Chalmers et al (1995) Differential actions of 3-(4-chlorophenyl)glutamic acid stereoisomers and L-trans-pyrrolidine-2,4-dicarboxylic acid upon L-homocysteic acid and L-glutamic acid-induced responses from rat spinal motoneurones. Neuropharmacology 34 1589 PMID: 8788956
Jane et al (1996) Diastereoselective synthesis of all four isomers of 3-(4-chlorophenylglutamic acid: identification of the isomers responsible for the potentiation of L-homocysteic acid-evoked depolarizations in neonatal rat motoneurons. J.Med.Chem. 39 4738 PMID: 8941386
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Keywords: (2R,3R)-Chlorpheg, (2R,3R)-Chlorpheg supplier, Glutamate, Transporters, 0816, Tocris Bioscience
Citations for (2R,3R)-Chlorpheg
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Currently there are no citations for (2R,3R)-Chlorpheg.
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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!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Huntington's Disease Poster
Huntington's disease (HD) is a severe monogenic neurodegenerative disorder, which is characterized by the prevalent loss of GABAergic medium spiny neurons (MSN) in the striatum. This poster summarizes the effects of mutant huntingtin aggregation implicated in the pathology of HD, as well as highlighting the use of iPSCs for HD modeling.