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Home > Products >  vx809, 99% in stock

vx809, 99% in stock CAS NO.936727-05-8

  • Min.Order: 1 Milligram
  • Payment Terms: T/T,Western Union,MoneyGram,Other
  • Product Details


  • vx809
  • Lumacaftor
  • vx-809 98%

Quick Details

  • ProName: vx809, 99% in stock
  • CasNo: 936727-05-8
  • Molecular Formula: C24H18F2N2O5
  • Appearance: -
  • Application: VX809;Lumacaftor;VX 809, For research ...
  • DeliveryTime: stock
  • Port: Shanghai; HK ; Shenzhen
  • ProductionCapacity: 100 Gram/Day
  • Purity: 99%
  • Storage: cool dry
  • Transportation: By air
  • LimitNum: 1 Milligram
  • Related Substances: -
  • Residue on Ignition: -
  • Heavy Metal: -


vx-809 is the second investigational oral candidate compound for the treatment of cystic fibrosis (cf).


vx-809 acts at the level of the er to allow a fraction of the f508del-cftr to adopt a properly folded form, to exit the er and mobilize to the cell surface for normal functioning. in fischer rat thyroid (frt) cells expressing f508del-cftr, vx-809 treatment significantly improves f508del-cftr maturation by 7.1 fold with an ec50 of 0.1 μm, and enhances f508del-cftr-mediated chloride transport by approximately 5 fold with ec50 of 0.5 μm, while vrt-768 has higher ec50 values of 7.9 μm and 16 μm, respectively. in hek-293 cells expressing f508del-cftr, vx-809 (3 μm) treatment increases f508del-cftr exit from the er by 6 fold, reaching levels comparable to 34% of cftr. in primary human bronchial epithelial (hbe) cells with f508del-cftr mutation, vx-809 increases cftr maturation and enhances chloride secretion with ec50 of 350 nm and 81 nm, respectively, more efficacious than corr-4a and vrt-325. f508del-cftr corrected by vx-809 exhibits single-channel open probability of 0.39 similar to normal cftr of 0.40. unlike vx-770, vx-809 is not a cftr potentiator, as acute addition of vx-809 has no effect on f508del-cftr function. in contrast to vrt-325 and corr-4a, vx-809 does not improve the processing of the normal or mutant forms of herg or p-gp, as well as other disease-causing mislocalized proteins, including α1-antitrypsin z mutant (e342k-α1-at) or n370s-β-glucosidase, suggesting that vx-809 is specific for cftr. vx-809 in combination with vrt-325 or corr-4a has additive effect on cftr-mediated chloride transport in cultured f508del-hbe.

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