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Very potent antagonist at the glycine-NMDA site. Also available as part of the NMDA Receptor - Glycine Site Tocriset™.
Sold with the permission of Merck Sharp and Dohme Ltd.
|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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 380.23. 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||2.63 mL||13.15 mL||26.3 mL|
|5 mM||0.53 mL||2.63 mL||5.26 mL|
|10 mM||0.26 mL||1.31 mL||2.63 mL|
|50 mM||0.05 mL||0.26 mL||0.53 mL|
References are publications that support the biological activity of the product.
Leeson et al (1992) 4-Amido-2-carboxytetrahydroquinolines. Structure-activity relationship for antagonism at the glycine site of the NMDA receptor. J.Med.Chem. 35 1954 PMID: 1534584
Stone (2000) Development and therapeutic potential of kynurenic acid and kynurenine derivatives for neuroprotection. TiPS 21 149 PMID: 10740291
Leeson et al (1991) trans-2-Carboxy-4-substituted tetrahydroquinolines. Potent glycine-site NMDA receptor antagonists. Med.Chem.Res. 1 64
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Keywords: L-689,560, L-689,560 supplier, potent, NMDA, antagonists, glycine, site, Glutamate, Receptors, N-Methyl-D-Aspartate, iGluR, Ionotropic, L689560, merck, 0742, Tocris Bioscience
8 Citations for L-689,560
Citations are publications that use Tocris products. Selected citations for L-689,560 include:
Dargan et al (2009) ACET is a highly potent and specific kainate receptor antagonist: characterisation and effects on hippocampal mossy fibre function. Neuropharmacology 56 121 PMID: 18789344
Eales et al (2014) The MK2/3 cascade regulates AMPAR trafficking and cognitive flexibility. Nat Commun 5 4701 PMID: 25134715
Dennis et al (2016) Activation of Muscarinic M1 Acetylcholine Receptors Induces Long-Term Potentiation in the Hippocampus. Mol Brain 26 414 PMID: 26472558
Park et al (2016) Calcium-Permeable AMPA Receptors Mediate the Induction of the Protein Kinase A-Dependent Component of Long-Term Potentiation in the Hippocampus. J Neurosci 36 622 PMID: 26758849
Ng et al (2014) Rapid regulation of endoplasmic reticulum dynamics in dendritic spines by NMDA receptor activation. Mol Brain 7 60 PMID: 25242397
Potier et al (2010) Contribution of the d-Serine-Dependent Pathway to the Cellular Mechanisms Underlying Cognitive Aging. Front Aging Neurosci 2 1 PMID: 20552041
Fang et al (2015) Regulated internalization of NMDA receptors drives PKD1-mediated suppression of the activity of residual cell-surface NMDA receptors. Toxicol Lett 8 75 PMID: 26584860
Rouaud and Billard (2003) D-cycloserine facilitates synaptic plasticity but impairs glutamatergic neurotransmission in rat hippocampal slices. Br J Pharmacol 140 1051 PMID: 14530208
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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* or download your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
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.
Major depressive disorder is characterized by depressed mood and a loss of interest and/or pleasure. Updated in 2015 this poster highlights presynaptic and postsynaptic targets for the potential treatment of major depressive disorder, as well as outlining the pharmacology of currently approved antidepressant drugs.
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.
Huntington's Disease Poster
Huntington's disease (HD) is a monogenic neurodegenerative disorder, which is characterized by the prevalent loss of GABAergic medium spiny neurons (MSN) in the striatum. This poster summarizes the MSN intracellular signaling pathways implicated in the pathology of HD, as well as highlighting the use of iPSCs for HD modeling.
Learning & Memory Poster
Recognition memory enables us to make judgements about whether or not we have encountered a particular stimulus before. This poster outlines the cellular mechanisms underlying recognition memory and its links to long-term depression, as well as the use of pharmacological intervention to assess the role of neurotransmitters in recognition memory.
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.
Schizophrenia is a debilitating psychiatric disorder that affects 1% of the worldwide population. This poster describes the neurobiology of Schizophrenia, as well as highlighting the genetic and environmental factors that play a fundamental role in the etiology of the disease. The current and emerging drug targets are also discussed.