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.
All Tocris products are intended for laboratory research use only.
|Solubility||Soluble to 2 mg/ml in water|
Preparing Stock Solutions
The following data is based on the product molecular weight 1465.75. Batch specific molecular weights may vary from batch to batch due to solvent 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||0.68 mL||3.41 mL||6.82 mL|
|5 mM||0.14 mL||0.68 mL||1.36 mL|
|10 mM||0.07 mL||0.34 mL||0.68 mL|
|50 mM||0.01 mL||0.07 mL||0.14 mL|
References are publications that support the products' biological activity.
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
If you know of a relevant reference for KYL, please let us know.
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Keywords: KYL, supplier, Ephrins, EphA4, receptor, tyrosine, kinase, antagonists, promotes, axon, regeneration, long, term, potentiation, Eph, Receptors, Eph, Receptors, Tocris Bioscience
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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!
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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.