KYL

• Supplier: Creative Peptides
• Product #: R0975
• CAS #: 676657-00-4
• LabelingTarget: EphA4 receptor tyrosine kinase
• MolecularFormula: C74H108N14O17
• MolecularWeight: 1465.75
• Sequence: KYLPYWPVLSSL
• Storage: -20°C
• Explanation: EphA4 receptor tyrosine kinase inhibitor (Kd = 0.8 μM), which 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. It shows neuroprotective effect.
• Activity: Inhibitor
• InChI: InChI=1S/C74H108N14O17/c1-40(2)31-52(64(94)84-59(39-90)68(98)85-58(38-89)67(97)83-57(74(104)105)33-42(5)6)80-71(101)62(43(7)8)86-70(100)61-19-14-30-88(61)73(103)56(36-46-37-77-51-17-10-9-15-49(46)51)82-66(96)54(35-45-22-26-48(92)27-23-45)79-69(99)60-18-13-29-87(60)72(102)55(32-41(3)4)81-65(95)53(34-44-20-24-47(91)25-21-44)78-63(93)50(76)16-11-12-28-75/h9-10,15,17,20-27,37,40-43,50,52-62,77,89-92H,11-14,16,18-19,28-36,38-39,75-76H2,1-8H3,(H,78,93)(H,79,99)(H,80,101)(H,81,95)(H,82,96)(H,83,97)(H,84,94)(H,85,98)(H,86,100)(H,104,105)/t50-,52-,53-,54-,55-,56-,57-,58-,59-,60-,61-,62-/m0/s1
• InChIKey: FZNPYIAZMDBRLC-RKNDTPCJSA-N
• IsomericSMILES: CC(C)C[C@@H](C(=O)N[C@@H](CO)C(=O)N[C@@H](CO)C(=O)N[C@@H](CC(C)C)C(=O)O)NC(=O)[C@H](C(C)C)NC(=O)[C@@H]1CCCN1C(=O)[C@H](CC2=CNC3=CC=CC=C32)NC(=O)[C@H](CC4=CC=C(C=C4)O)NC(=O)[C@@H]5CCCN5C(=O)[C@H](CC(C)C)NC(=O)[C@H](CC6=CC=C(C=C6)O)NC(=O)[C@H](CCCCN)N
• Reference:
  • KYL was also shown to prevent growth cone collapse in chicken retinal explants and dissociated cultures of rat cortical neurons, promote nerve regeneration and functional recovery in a rat model of spinal cord injury, and inhibit the adhesion of human T-cells to endothelial cells. Thus, KYL can target human, mouse, rat and chicken EphA4 and may be useful for promoting nerve regeneration after injury and modulating immune responses.
  • Distinctive Binding of Three Antagonistic Peptides to the Ephrin-Binding Pocket of the EphA4 Receptor
  • STI and KYL inhibitors prevented AβO-induced dendritic spine loss. Although the absence of EphA4 did not completely rescue the dendritic spine loss, EphA4-knockout neurons show a significant decrease in AβO-induced dendritic spine loss. Furthermore, protection was observed in mature neurons (with established synapses) transfected with either c-Abl shRNA or EphA4 shRNA.
  • EphA4 activation of c-Abl mediates synaptic loss and LTP blockade caused by amyloid-β oligomers