Discontinued Product

cis-ACBD (Cat. No. 0271) has been withdrawn from sale for commercial reasons.
Description: Potent, selective L-glutamate uptake inhibitor
Chemical Name: cis-1-Aminocyclobutane-1,3-dicarboxylic acid
Citations (1)
Literature (1)

Biological Activity for cis-ACBD

cis-ACBD is a potent, competitive and selective inhibitor of glutamate uptake. Certain confusion exists over the naming of this compound because of apparent contradictions in the literature. This is the isomer which has the carboxylic acid and the amino groups on the same side of the cyclobutyl ring.

Technical Data for cis-ACBD

M. Wt 159.14
Formula C6H9NO4
Storage Store at RT
CAS Number 73550-55-7
PubChem ID 1214
Smiles [H][C@@]1([C@@](O)=O)C[C@@](N)([C@](O)=O)C1

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 cis-ACBD

Certificate of Analysis / Product Datasheet
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Keywords: cis-ACBD, cis-ACBD supplier, Potent, selective, competitive, L-glutamate, uptake, inhibitors, inhibits, EAAT, Excitatory, Amino, Acid, Transporters, GLAST, GLT-1, Glutamate, Monoamine, Neurotransmitter, 0271, Tocris Bioscience

1 Citation for cis-ACBD

Citations are publications that use Tocris products. Selected citations for cis-ACBD include:

Lee et al (2010) Characterisation of the expression of NMDA receptors in human astrocytes. PLoS One 5 e14123 PMID: 21152063

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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 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.