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Medchemexpress LLC KB-R7943 mesylate | 182004-65-5 | C17H21N3O6S2 | 5 MG
SDP

Catalog No. 5000376841
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KB-R7943 mesylate is an inhibitor of the reverse Na+/Ca2+ exchanger (NCXrev) with an IC50 of 5.7±2.1 μM. It induces cancer cell death by activating the JNK pathway and blocking autophagic flux. It also blocks NMDAR-mediated ion currents, inhibits NMDA-induced increases in cytosolic Ca2+ (IC50 of 13.4±3.6 μM), and accelerates calcium deregulation in glutamate-treated neurons. Additionally, it depolarizes mitochondria in a Ca2+-independent manner and inhibits 2,4-dinitrophenol-stimulated respiration (IC50 of 11.4±2.4 μM) in cultured neurons.

  • Inhibits reverse Na+/Ca2+ exchanger (NCXrev)
  • Induces cancer cell death by activating JNK pathway
  • Blocks autophagic flux
  • Blocks NMDAR-mediated ion currents
  • Inhibits NMDA-induced increases in cytosolic Ca2+
  • Accelerates calcium deregulation and mitochondrial depolarization in glutamate-treated neurons
  • Depolarizes mitochondria in a Ca2+-independent manner

Catalog No. 50-003-76841 Supplier Medchemexpress LLC Supplier No. HY154155MG
May include imposed supplier surcharges.
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KB-R7943 mesylate is an inhibitor of the reverse Na+/Ca2+ exchanger (NCXrev) with an IC50 of 5.7±2.1 μM. It induces cancer cell death by activating the JNK pathway and blocking autophagic flux. It also blocks NMDAR-mediated ion currents, inhibits NMDA-induced increases in cytosolic Ca2+ (IC50 of 13.4±3.6 μM), and accelerates calcium deregulation in glutamate-treated neurons. Additionally, it depolarizes mitochondria in a Ca2+-independent manner and inhibits 2,4-dinitrophenol-stimulated respiration (IC50 of 11.4±2.4 μM) in cultured neurons.

  • Inhibits reverse Na+/Ca2+ exchanger (NCXrev)
  • Induces cancer cell death by activating JNK pathway
  • Blocks autophagic flux
  • Blocks NMDAR-mediated ion currents
  • Inhibits NMDA-induced increases in cytosolic Ca2+
  • Accelerates calcium deregulation and mitochondrial depolarization in glutamate-treated neurons
  • Depolarizes mitochondria in a Ca2+-independent manner

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