PLX4720 | Mutant B-Raf inhibitor
NMR (Conforms)
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 5 mg | $55.00 | ||
| 25 mg | $145.00 |
PLX4720 (918505-84-7) is a potent and selective inhibitor of B-Raf, V600E mutant, IC50=13 nM (Wild type IC50=160 nM).1 It induces cell cycle arrest and apoptosis in B-RafV600E-positive cells and suppresses growth of B-RafV600E-positive xenografts.1 It induces tumor regression and reverses cachexia in a mouse model of human thyroid cancer harboring the B-RafV600E mutation.2 Early stage autophagy inhibitors and ER stress inhibition with 4-phenylbutyric acid increases the sensitivity of resistant cells to PLX4720.3 PLX4720 induces cytoprotective autophagy in thyroid cancer cells via AMPK-ULK1 pathway.4
References/Citations:
- Tsai et al. (2008), Discovery of a selective inhibitor of oncogenic B-Raf kinase with potent antimelanoma activity; Proc. Natl. Acad. Sci. USA, 105 3041
- Nehs et al. (2012), Late intervention with anti-BRAF(V600E) therapy induces tumor regression in an orthotopic mouse model of human anaplastic thyroid cancer; Endocrinology, 153 985
- Yeom et al. (2021), Increase in the sensitivity to PLX4720 through inhibition of transcription factor EB-dependent autophagy in BRAF inhibitor-resistant cells; Toxicol. Res., 38 35
- Jimenez-Morah et al. (2021), V600EBRAF Inhibition Induces Cytoprotective Autophagy through AMPK in Thyroid Cancer Cells; Int. J. Mol. Sci. 22 6033
NMR (Conforms)
Safety Data Sheet:
Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
PLX4720 (918505-84-7) is a potent and selective inhibitor of B-Raf, V600E mutant, IC50=13 nM (Wild type IC50=160 nM).1 It induces cell cycle arrest and apoptosis in B-RafV600E-positive cells and suppresses growth of B-RafV600E-positive xenografts.1 It induces tumor regression and reverses cachexia in a mouse model of human thyroid cancer harboring the B-RafV600E mutation.2 Early stage autophagy inhibitors and ER stress inhibition with 4-phenylbutyric acid increases the sensitivity of resistant cells to PLX4720.3 PLX4720 induces cytoprotective autophagy in thyroid cancer cells via AMPK-ULK1 pathway.4
References/Citations:
- Tsai et al. (2008), Discovery of a selective inhibitor of oncogenic B-Raf kinase with potent antimelanoma activity; Proc. Natl. Acad. Sci. USA, 105 3041
- Nehs et al. (2012), Late intervention with anti-BRAF(V600E) therapy induces tumor regression in an orthotopic mouse model of human anaplastic thyroid cancer; Endocrinology, 153 985
- Yeom et al. (2021), Increase in the sensitivity to PLX4720 through inhibition of transcription factor EB-dependent autophagy in BRAF inhibitor-resistant cells; Toxicol. Res., 38 35
- Jimenez-Morah et al. (2021), V600EBRAF Inhibition Induces Cytoprotective Autophagy through AMPK in Thyroid Cancer Cells; Int. J. Mol. Sci. 22 6033
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