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EphA4 receptor tyrosine kinase inhibitor (Kd = 0.8 μM); inhibits EphA4-EphrinA5 interactions (IC50 = 6.34 μM). Prevents AβO induced synaptic damage, dendritic spine loss and prevents the blocking of LTP in hippocampal CA3-CA1 transmissions. Exhibits a long half life in cell culture media (8 and 12 hours in PC3 and C2C12 media respectively). Neuroprotective.
|Storage||Store at -20°C|
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.
|Solubility||Soluble to 2 mg/ml in water|
References are publications that support the biological activity of the product.
Lamberto et al (2012) Distinctive binding of three antagonistic peptides to the ephrin-binding pocket of the EphA4 receptor. Biochem. J. 445 47 PMID: 22489865
Vargas et al (2014) EphA4 activation of c-Abl mediates synaptic loss and LTP blockade caused by amyloid-β oligomers. PLoS One. 9 e92309 PMID: 24658113
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Keywords: KYL, KYL supplier, Ephrins, EphA4, receptor, tyrosine, kinase, antagonists, promotes, axon, regeneration, long, term, potentiation, Eph, Receptors, 5290, Tocris Bioscience
1 Citation for KYL
Citations are publications that use Tocris products. Selected citations for KYL include:
Defourny et al (2019) EphA4-ADAM10 Interplay Patterns the Cochlear Sensory Epithelium through Local Disruption of Adherens Junctions. iScience 11 246 PMID: 30639848
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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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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.