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Cat. No. M2102

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VX-809 Structure


Size Price Availability Quantity
Free Sample (0.5-1 mg)  USD 0 In stock
10mM*1mL in DMSO USD 53  USD53 In stock
5mg USD 50  USD50 In stock
10mg USD 70  USD70 In stock
25mg USD 104  USD104 In stock
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Quality Control & Documentation
Biological Activity

VX-809 is a CFTR modulator with EC50 of 0.1 μM. VX-809 increases chloride secretions by 14% in human bronchial epithelial cells. Unlike VX-770, VX-809 is not a CFTR potentiator, as acute addition of VX-809 has no effect on F508del-CFTR function. VX-809 has been shown to correct the folding and processing of CFTR in F508del mutation cells in vitro. Pharmacodynamic data showed that VX-809 improved CFTR function in at least one organ (sweat gland). VX-809 reduced elevated sweat chloride values in a dose-dependent manner (p=0.0013) that was statistically significant in the 100 and 200 mg dose groups. VX-809 was more efficacious and selective for CFTR than previously reported CFTR correctors. VX-809 is currently in a phase II study alone and in combination with VX-770 in cystic fibrosis (CF) patients with the F508del-CFTR mutation.

Product Citations
Customer Product Validations & Biological Datas
Source Br J Pharmacol (2016). Figure 4. VX-809 (lumacaftor) was purchased from AbMole BioScience (Houston, USA)
Method Immunoblot
Cell Lines HeLa-F508del cells
Concentrations 10 µM
Incubation Time 24 h
Results VX-809 treatment induced maturation of CFTR F508del (Figure 4A) and inhibited NF-κB activity and IL-8 promoter activity (Figure 4C and 4D). HeLa-F508del cells transiently transfected with reporter system were corrected with VX-809, treated with vehicle or sulindac and inflammation was induced by TNF-α as shown figure 4B.
Protocol (for reference only)
Cell Experiment
Cell lines FRT, HEK-293 and HBE cells
Preparation method CFTR Immunoblot Analysis.
FRT, HEK-293, or HBE cells expressing CFTR or F508del-CFTR were incubated for 24 h at 37 °C with or without VX-809 in the assay media. After incubation, cells were harvested in ice-cold D-PBS solution (without calcium and magnesium) and pelleted at 1,000 × g at 4 °C. Cell pellets were lysed in 1% Nonidet P-40, 0.5% sodium deoxycholate, 200 mM NaCl, 10 mM Tris, pH 7.8, and 1 mM EDTA plus protease inhibitor mixture (1:250; Roche) for 30 min on ice. Lysates were spun for 10 min at 10,000 × g at 4 °C to pellet nuclei and insoluble material. Approximately 12 μg total protein was heated in Laemmli buffer with 5% β mercaptoethanol at 37 °C for 5 min and loaded onto a 3% to 8% Tris-acetate gel (Invitrogen). The gel was transferred to nitrocellulose and processed for Western blotting by using monoclonal CFTR antibody 769 (gift from John R. Riordan, University of North Carolina, Chapel Hill, NC) or polyclonal to GAPDH (Santa Cruz Biotechnology). Blots were developed by enhanced chemiluminescence. Quantification of the relative amounts of bands C and GAPDH was performed by using NIH ImageJ analysis of scanned films.
Concentrations 0~100μM
Incubation time 48 h
Animal Experiment
Animal models Male Sprague–Dawley rats model
Formulation 0.5% Tween80/0.5% methylcellulose/water
Dosages 1 mg/kg
Administration orally
Chemical Information
Molecular Weight 452.41
Formula C24H18F2N2O5
CAS Number 936727-05-8
Solubility (25°C) DMSO 60 mg/mL
Storage Powder          -20°C   3 years ;  4°C   2 years
In solvent       -80°C   6 months ;  -20°C   1 month

[1] Van Goor F, et al. Proc Natl Acad Sci U S A. Correction of the F508del-CFTR protein processing defect in vitro by the investigational drug VX-809.

[2] Clancy JP, et al. Thorax. Results of a phase IIa study of VX-809, an investigational CFTR corrector compound, in subjects with cystic fibrosis homozygous for the F508del-CFTR mutation.

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Keywords: VX-809, Lumacaftor supplier, CFTR, inhibitors, activators

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