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Medchemexpress LLC Licochalcone B | 58749-23-8 | 286.28 | 5 MG
SDP

Catalog No. 5000389121
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Licochalcone B is an extract from the root of Glycyrrhiza uralensis. It inhibits amyloid β (42) self-aggregation and disaggregates pre-formed Aβ42 fibrils. This compound can also reduce metal-induced Aβ42 aggregation through chelating metal ions, inhibit phosphorylation of NF-κB p65 in the LPS signaling pathway, and inhibit growth while inducing apoptosis of NSCLC cells. Additionally, it specifically inhibits the NLRP3 inflammasome by disrupting NEK7‐NLRP3 interaction.

  • Inhibits amyloid β (42) self-aggregation and disaggregates pre-formed Aβ42 fibrils.
  • Reduces metal-induced Aβ42 aggregation through chelating metal ions.
  • Inhibits phosphorylation of NF-κB p65 in the LPS signaling pathway.
  • Inhibits growth and induces apoptosis of NSCLC cells.
  • Specifically inhibits the NLRP3 inflammasome by disrupting NEK7‐NLRP3 interaction.
  • Alleviates oxidative stress of hepatotoxicity in mice induced by CCl4.

Catalog No. 50-003-89121 Supplier Medchemexpress LLC Supplier No. HYN03735MG
May include imposed supplier surcharges.
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Licochalcone B is an extract from the root of Glycyrrhiza uralensis. It inhibits amyloid β (42) self-aggregation and disaggregates pre-formed Aβ42 fibrils. This compound can also reduce metal-induced Aβ42 aggregation through chelating metal ions, inhibit phosphorylation of NF-κB p65 in the LPS signaling pathway, and inhibit growth while inducing apoptosis of NSCLC cells. Additionally, it specifically inhibits the NLRP3 inflammasome by disrupting NEK7‐NLRP3 interaction.

  • Inhibits amyloid β (42) self-aggregation and disaggregates pre-formed Aβ42 fibrils.
  • Reduces metal-induced Aβ42 aggregation through chelating metal ions.
  • Inhibits phosphorylation of NF-κB p65 in the LPS signaling pathway.
  • Inhibits growth and induces apoptosis of NSCLC cells.
  • Specifically inhibits the NLRP3 inflammasome by disrupting NEK7‐NLRP3 interaction.
  • Alleviates oxidative stress of hepatotoxicity in mice induced by CCl4.

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