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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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