Lifirafenib (BGB-283)

For research use only.

Catalog No.S7926 Synonyms: Beigene-283

2 publications

Lifirafenib (BGB-283) Chemical Structure

Molecular Weight(MW): 478.42

Lifirafenib (BGB-283) potently inhibits RAF family kinases and EGFR activities in biochemical assays with IC50 values of 23, 29 and 495 nM for the recombinant BRAFV600E kinase domain, EGFR and EGFR T790M/L858R mutant.

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Selleck's Lifirafenib (BGB-283) has been cited by 2 publications

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Biological Activity

Description Lifirafenib (BGB-283) potently inhibits RAF family kinases and EGFR activities in biochemical assays with IC50 values of 23, 29 and 495 nM for the recombinant BRAFV600E kinase domain, EGFR and EGFR T790M/L858R mutant.
WT A-RAF [1]
(Cell-free assay)
C-RAF (Y340/341D) [1]
(Cell-free assay)
BRAF(V600E) [1]
(Cell-free assay)
EGFR [1]
(Cell-free assay)
(Cell-free assay)
1 nM 7 nM 23 nM 29 nM 32 nM
In vitro

In vitro, BGB-283 potently inhibits BRAFV600E-activated ERK phosphorylation and cell proliferation. It demonstrates selective cytotoxicity and preferentially inhibits proliferation of cancer cells harboring BRAFV600E and EGFR mutation/amplification. In BRAFV600E colorectal cancer cell lines, BGB-283 effectively inhibits the reactivation of EGFR and EGFR-mediated cell proliferation. It demonstrates selective cytotoxicity to cell lines harboring BRAFV600E or EGFR mutations. BGB-283 inhibits the EGF-induced EGFR autophosphorylation on Tyr1068 in A431 cells in a dose-dependent manner. In WiDr colorectal cancer cells, BGB-283 is shown to be able to inhibit the feedback activation of EGFR signaling and achieves sustained inhibition of pERK[1].

In vivo In vivo, BGB-283 treatment leads to dose-dependent tumor growth inhibition accompanied by partial and complete tumor regressions in both cell line-derived and primary human colorectal tumor xenografts bearing BRAFV600E mutation. BGB-283 is highly efficacious in BRAF(V600E) colorectal cancer xenograft models, including HT29, Colo205, and two primary tumor xenografts harboring BRAFV600E mutation. In addition, BGB-283 shows compelling efficacy in a WiDr xenograft model where EGFR reactivation is shown to be induced upon BRAF inhibition. BGB-283 induces tumor regression in HCC827 but not in A431 xenograft. BGB-283 inhibits phosphorylation of both ERK1/2 and EGFR and displays potent antitumor activity in WiDr tumor xenografts. BGB-283 does not induce EGFR feedback activation as reported for vemurafenib. BGB-283 potently inhibits MEK and ERK phosphorylation and DUSP6 expression in vivo when dosed repeatedly. There is no detectable difference on AKT phosphorylation[1].


Cell Research:


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  • Cell lines: A375 cells
  • Concentrations: 0.03, 1, 10 μM
  • Incubation Time: 3 days
  • Method:

    The number of cells seeded per well of a 96-well plate is optimized for each cell line to ensure logarithmic growth over the 3 days treatment period. Cells are left to attach for 16 hours and then treated with a 10-point dilution series in duplicate. Following a 3-day exposure to the compound, a volume of CellTiter-Glo reagent equal to the volume of cell culture medium present in each well is added. Mixture is mixed on an orbital shaker for 2 minutes to allow cell lysing, followed by 10 minutes incubation at room temperature to allow development and stabilization of luminescent signal. Luminescent signal is measured

    (Only for Reference)
Animal Research:


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  • Animal Models: NOD/SCID and BALB/c nude mice
  • Dosages: 2.5 to 30 mg/kg
  • Administration: p.o.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 95 mg/mL (198.57 mM)
Ethanol 95 mg/mL (198.57 mM)
Water Insoluble

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 478.42


CAS No. 1446090-79-4
Storage powder
in solvent
Synonyms Beigene-283

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Raf Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID