Vemurafenib (PLX4032, RG7204)

Catalog No.S1267 Synonyms: RO5185426

Vemurafenib (PLX4032, RG7204) Chemical Structure

Molecular Weight(MW): 489.92

Vemurafenib (PLX4032, RG7204) is a novel and potent inhibitor of B-RafV600E with IC50 of 31 nM in cell-free assay.

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Cited by 69 Publications

16 Customer Reviews

  • The regressing tumour microenvironment stimulates the outgrowth, infiltration and metastasis of drug-resistant clones. b, Bioluminescent signal of drug-resistant A375RTGL cells in vemurafenib-sensitive, A375 tumours, treated with vehicle or vemurafenib for 5 days (vehicle, n = 36; vemurafenib, n = 15 tumours). D, day. c, EdU incorporation in A375R-TGL cells in A375/A375R-TGL tumours treated with vehicle or vemurafenib for 4 days, as determined by FACS (vehicle, n = 8; vemurafenib, n = 6 tumours). d, Bioluminescent signal of A375R-TGL tumours alone, treated with vehicle or vemurafenib for 5 days (vehicle, n 5 38; vemurafenib, n = 15 tumours). e, Bioluminescent signal of TGLexpressing drug-resistant cancer cells (A375R, M249R4, PC9 and H2030) in drug-sensitive tumours (Colo800, LOX, UACC62, M249, H3122 and HCC827) treated with vehicle or drugs (vemurafenib, crizotinib and erlotinib) for 5 days (n (from left to right on the graph) = 6, 7, 12, 12, 9, 9, 25, 26, 9, 12, 12, 12, 16 and 11 tumours). f, Spontaneous lung metastasis by A375R cells in mice bearing A375/A375R-TGL tumours treated with vehicle or vemurafenib (10 days), visualized by BLI (n = 4).

    Nature 2015 520(7547), 368-72. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

    FRA1 downregulation during RAFi treatment drives the reactive secretome. c, Relative mRNA levels of FRA1 during vemurafenib exposure [0.1-1 uM]. d, Representative immunofluorescence staining of A375/A375R tumours for GFP (A375R, green) and FRA1 (red) after vehicle or vemurafenib treatment (5 days). DAPI, 49,6-diamidino-2-phenylindole. Scale bars, 50 um.

    Nature 2015 520(7547), 368-72. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

  • Acquired EGFR expression in BRAF(V600E) mutant melanoma after vemurafenib resistance. Immunohistochemical (IHC) analysis (ultraView DAB stain, brown) showing increased EGFR expression in formalin-fixed paraffin embedded (FFPE) (Patient number 1-5) and frozen (Patient number 6) melanoma tissue sections from BRAF(V600E) mutant melanoma patients who developed resistance to vemurafenib, dabrafenib or trametinib as indicated. For each patient, the first biopsy is from the pre-treatment tumour; the second biopsy was performed after the tumour had progressed under treatment. For patient number 4, the first biopsy was performed when the patient was in partial response, but rapidly developed secondary resistance. Then 4.5 months later, the second biopsy was taken.

    Nature 2014 508(7494), 118-22. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

    Long-term colony formation assay of thyroid cancer (8505C), CRC (OXCO-1, COLO741 and WiDr) and melanoma (A375) cells. Cells were grown in the absence or presence of PLX4032 at the indicated concentrations for 10-14 days. For each cell line, all dishes were fixed at the same time, stained and photographed.

    Nature 2012 483(7387):100-3. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

  • Resistance to BRAF(V600E) inhibition in WiDr cells is mediated through feedback activation of EGFR. Biochemical responses of WiDr cells treated with PLX4032, cetuximab or gefitinib, or their combinations, were documented by western blot analysis. Cells were harvested at 6 h after drug treatment. BRAF(V600E) inhibition results in strong upregulation of Tyr1068 p-EGFR and Ser473 phosphorylated-AKT (p-AKT), which is abrogated by EGFR inhibitors. Furthermore, combination treatments result in complete inhibition of phosphorylated MEK (p-MEK) and phosphorylated ERK (p-ERK). Heat shock protein 90 (HSP90) served as a control.

    Nature 2012 483(7387):100-3. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

    Nature, 2016, 537(7620):422-426.. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

  • Science, 2014, 346(6205):1255784.. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

    Impact of BRAF and SYK/MEK inhibition on ERK activation in primary CLL cells. Representative Western blot analysis for pERK and tERK of the protein lysate at the indicated concentrations of vemurafenib and dabrafenib for patients 1 and 2. The experiment was performed 2 times with similar results.

    J Clin Invest 2014 124(11), 5074-84. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

  • The B-Raf inhibitor PLX4032 decreases cell surface DR5 levels . BCPAP cells were treated with the indicated concentrations of PLX4032 for 12 h and then harvested for extraction of cellular total RNA and subsequent RT-PCR to detection of DR5.

    Oncogene 2015 10.1038/onc.2015.97. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

    Stat3 is activated in melanoma cells with acquired resistance to vemurafenib. Sensitive and resistant A375 melanoma cells were stimulated by different doses of vemurafenib as indicated. Total protein was collected 6 hours after stimulation. Protein expressions of phospho–ERK1/2, Stat3, phospho-Stat3, and paired box homeotic gene 3 (PAX3) were analyzed by western blot along with tubulin, which served as a loading control.

    J Invest Dermatol 2013 133, 2041. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

  • Clonogenic assays of VM21 (b) and VM1 (c) cells treated with 1 μM PD166866 (PD) and 0.1 μM RG7204 (RG) for 14 days. For VM21 cells, the combination index (CI) value indicating synergism is shown. For VM1 cells, inefficacy of 1 μM PD166866 alone precluded calculation of a CI value and P-values for reduction of clonal growth are shown instead. a, P<0.05 versus RG; b, P<0.01 versus PD.

    J Invest Dermatol 2011 131, 2087-95. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

    BRAF inhibition improves autologous tumor recognition by CD8+ tumor-infiltrating lymphocytes. (A and B) Tumor-infiltrating lymphocytes (TILs) were co-cultured with autologous BRAFV600E mutant melanoma target cell lines treated with vemurafenib (Vem) at low or high dose, or left untreated. (A) Frequency of tumor necrosis factor α (TNF α)-and interferon γ (IFN γ)-producing CD8+ TILs. (B) Frequency of CD8+ TILs producing TNF α and IFN γ and simultaneously mobilizing CD107a upon co-culture with autologous tumor cells. *p < 0.05; ** p < 0.01; ***p < 0.001.

    Oncoimmunology 2012 1, 1476-1483. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

  • Fig 1 represents the cell cytotoxicity assay to study the effect of Vemurafenib on ABCC10 (MRP7) overexpressing cells. Table 1 shows the data suggesting reversal of resistance ABCC10 overexpressing cells with Vemurafenib at 20 μM using Paclitaxel as a substrate. HEK293 is a human embryonic kidney cell line while HEK293/MRP7 is an MRP7 overexpressing cell line generated by MRP7 gene transfection. Cepharanthine is a positive control. Vemurafenib (20 μM) in combination with Paclitaxel can reverse MDR mediated by MRP7 over-expressing cells as it decreased the resistance fold from 24-fold to 1-fold.

    Dr. Zhe-Sheng Chen of St. John's University. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

    Fig 2 represents the cell cytotoxicity assay to study the effect of vemurafenib on ABCG2 (BCRP) overexpressing cells. Table 2 shows the data suggesting reversal of resistance ABCG2 overexpressing cells with vemurafenib at 20 μM using mitoxantrone as a substrate. H460 is a hepatic carcinoma cell line while H460/MX20 is an ABCG2 overexpressing cell line made resistant by drug selection with mitoxantrone. FTC (Fumitremorgin C) is a positive control. Vemurafenib (20 μM) in combination with Mitoxantrone can reverse MDR mediated by ABCG2 over-expressing cells as it decreased the resistance fold from 133-fold to 93-fold.

    Dr. Zhe-Sheng Chen of St. John's University. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

  • represents the effect of Vemurafenib on the accumulation of [3H]-Mitoxantrone. Vemurafenib increased the intra-cellular accumulation of Mitoxantrone in ABCG2 overexpressing H460/MX20 cells compared with parental H460 cells. From the figure, the accumulation in H460/MX20 control is decreased whereas in presence of Vemurafenib 20 μM, it is significantly increases the [3H]-Mitoxantrone accumulation.

    Dr. Zhe-Sheng Chen of St. John's University. Vemurafenib (PLX4032, RG7204) purchased from Selleck.


    Anti-ErbB3 mAbs differently counteract the increase of ErbB3-dependent AKT phosphorylation and potentiate growth inhibition induced by vemurafenib. LOX IMVI melanoma cells serum starved and treated with vemurafenib (0.3μ M) for 24 h were incubated or not with 20 μ g/ml of anti-ErbB3 mAbs A4 (a),A3orA2(d). Western blot analysis shows that A4 and A3, but not A2 mAbs abrogate receptor phosphorylation and ATK signaling. For densitometric analysis pErbB3/ErbB3, pERK/ERK and pAKT/ATK values are expressed as fold change with respect to the control unstimulated cells to which value = 1 was assigned. Results are expressed as mean values from three independent experiments. LOX IMVI cells were grown in the presence of different doses of vemurafenib alone or in combination with 20 μg/ml of A4 (b),A3 or A2(e) mAbs for 10 days. Cells were then fixed and stained with crystal violet(c). Cells were then dissolved in a Methanol/SDS solution and the adsorbance (595 nm) was read using a microplate ELISA reader (b, e). Quantitative analysis for curve fitting and for IC50 evaluation, performed by KaleidaGraph software, shows that the treatment with A4 and A3 but not with A2 enhances the inhibitory effect of vemurafenib on cell growth (IC50 vem = 155 nM; IC50 vem + A4 = 36 nM; IC50 vem + A3 = 62, IC50 vem + A2 = 146 nM). Results are reported as mean values±standard deviation (SD) from three independent experiments. p-values were calculated using Student ’s t test and significance level has been defined as p < 0,05. For IC50 vem + A4 and IC50 vem + A3 p < 0,001 vs IC50 vem; IC50 vem + A2 NS vs IC50 vem.

    Vemurafenib (PLX4032, RG7204) purchased from Selleck.

Purity & Quality Control

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2. For more details, such as half maximal inhibitory concentrations (IC50s) and working concentrations of each inhibitor, please click on the link of the inhibitor of interest.
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Biological Activity

Description Vemurafenib (PLX4032, RG7204) is a novel and potent inhibitor of B-RafV600E with IC50 of 31 nM in cell-free assay.
Features A novel and potent inhibitor of the B-RAFV600E oncoprotein.
SRMS [1]
(Cell-free assay)
ACK1 [1]
(Cell-free assay)
B-Raf (V600E) [1]
(Cell-free assay)
C-Raf [1]
(Cell-free assay)
MAP4K5 (KHS1) [1]
(Cell-free assay)
18 nM 19 nM 31 nM 48 nM 51 nM
In vitro

PLX4032 inhibits B-RAFV600E, C-RAF, as well as wildtype B-RAF, with IC50 of 31 nM, 48 nM and 100 nM, respectively. PLX4032 also inhibits several non-RAF kinases, including ACK1, KHS1, and SRMS, with IC50 of 18 nM to 51 nM. [1] In melanoma cell lines, the inhibitory effect by PLX4032 depends on B-RAF mutational status, because PLX4032 potently inhibits those harboring B-RAF V600 mutants, including V600E, V600D, V600K, and V600R, but not wildtype or other mutants. The IC50 values of PLX4032 on these cells, including MALME-3M, Colo829, Colo38, A375, SK-MEL28, and A2058, ranges from 20 nM to 1 μM. In these cells, PLX4032 (0.1 μM to 30 μM) also inhibits the phosphorylation of both MEK1/2 and ERK1/2. [2] PLX4032 is highly effective in the treatment of melanoma, for its ability of inhibiting B-RAFV600E. However, PLX4032 displays limited effect in colon cancer patients that also carrying B-RAFV600E oncoprotein. The reason for this is that, in colon cancer cells, B-RAFV600E inhibition by PLX4032 results in a rapid feedback EGFR activation, which compensates for the PLX4032-inhibited cell proliferation. [3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
A375 NIq1[JZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIr4TY4yODBizszN M4PHSlk3KGh? MYLEUXNQ NXvhWo5QUUN3ME20O{BvVQ>? NGrZcIYyQDR3OEC1Ny=>
ARO M{fPXGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NV:wVW4xOTByIN88US=> MknMPVYhcA>? MWXEUXNQ Mn3RTWM2OD1{MEWgcm0> M17o[|E5PDV6MEWz
NPA MlnIS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmfiNVAxKM7:TR?= MWS5OkBp NG\nd|lFVVOR M{L1SmlEPTB;Mk[gcm0> Mlm4NVg1PThyNUO=
TPCI MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{Psb|ExOCEQvF2= NV7pVW1YQTZiaB?= MojHSG1UVw>? MWnJR|UxRTFyLke3JO69VQ>? MYixPFQ2QDB3Mx?=
A375 MlPGRZBweHSxc3nzJGF{e2G7 NYSzPXFVOTBizszN MlvySG1UVw>? NIfINodRem:vb4Tld{BieG:ydH;0bYMh\GWjdHi= M3fyRlE5PDV6MEWz
ARO M2\YOGZ2dmO2aX;uJGF{e2G7 NVjBNYJtOTBizszN M2rIPVczKGh? MYHEUXNQ MU\JcoR2[2W|IITo[UBz\WW6cILld5Nqd25ib3[geIhmKE6LUzDweY1x MnK3NVg1PThyNUO=
8505C (BRAF V600E/V600E) MnHtS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIXudWE6PiCq MWjJR|UxRTV5IH7NJC=> NF;ER2MzODF2OUGzOi=>
SW1736 (BRAF WT/V600E) MmDYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXPX[ndqQTZiaB?= MnnlTWM2OD1{OTDuUS=> NU\aTnJ3OjBzNEmxN|Y>
BHT101 (BRAF WT/V600E) MnrMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX\tcZNSQTZiaB?= M3vKdmlEPTB;OUegcm0> MWWyNFE1QTF|Nh?=
BCPAP (BRAF WT/V600E) MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVToS5ViQTZiaB?= M3X2[mlEPTB;N{igcm0> M174W|IxOTR7MUO2
C643 (HRAS G13R)≥ 500 NG[xT21Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVryV2xiQTZiaB?= MnnJTWM2OCEkibWgOVAxKG6P MWmyNFE1QTF|Nh?=
HTH7 (NRAS Q61R) NF[5[IxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1vkOVk3KGh? MVjJR|Ux6onnIEGwNFAhdk1? MVOyNFE1QTF|Nh?=
CAL62 (KRAS G12R) > 1000 > 1000 NH3SXlhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoLzPVYhcA>? NXfMSI8xUUN3ME6gNVAxOCCwTR?= MoO4NlAyPDlzM{[=
TPC-1 (RET/PTC1) MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NELQUG86PiCq MVjJR|Ux6onnMUCwNEBvVQ>? NEnROm4zODF2OUGzOi=>
PC MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1\LXVk3KGh? MmPqTWM2OD5iMUCwNEBvVQ>? MWKyNFE1QTF|Nh?=
Calu-6 M4jZXmZ2dmO2aX;uJGF{e2G7 NH;1OJgy6oDLzszN MXGxJIg> M3njVGROW09? MXHBZ5RqfmG2ZYOgUWVMN0WUSzDpckBk\WyuczD3bZRpKHerbHSteJlx\SCEUlHG NIPHb3EzODF5OUewOS=>
C4 NYTufGlKTnWwY4Tpc44hSXO|YYm= M2HmU|Mh|ryP NX[1SllMPDhiaB?= Ml71SG1UVw>? NHHRPZBKdmO{ZXHz[ZMh[2:ubHHn[Y4he3mwdHjld4l{KGGwZDDk[YNz\WG|ZYOgTWwuQCCneIDy[ZN{cW:w MnzvNlU6QDl3ME[=
VMM12 MnPHSpVv[3Srb36gRZN{[Xl? MnvkN{DPxE1? M4P6Z|Q5KGh? M3XFcWROW09? MYjJcoNz\WG|ZYOgZ49tdGGpZX6gd5lvfGinc3nzJIFv\CCmZXPy[YF{\XNiSVytPUBmgHC{ZYPzbY9v Mny1NlU6QDl3ME[=
SKMEL19 M4e1eWZ2dmO2aX;uJGF{e2G7 MUS2JO69VQ>? MWG0PEBp M1;Ye2ROW09? NFX4SG9VemmpZ3Xyd{BGWiC|dILld5M> MWCyN|M3OjJ2MB?=
UKF-NB-3 (ABCB1) M2G1dGZ2dmO2aX;uJGF{e2G7 M2T4T|EvOjViwsXN M1HZdlIhcA>? NW\xNJFETE2VTx?= NF3l[|FGdmijbnPld{Bi[2O3bYXsZZRqd25ib3[geIhmKG[udX;y[ZNk\W62IFHCR2IyKHO3YoP0doF1\SC{aH;kZY1qdmViMUKz MlnhNlQ4OzV5Nk[=
UKF-NB-3 NV3GWHpMTnWwY4Tpc44hSXO|YYm= NITOOJQyNjJ3INM1US=> MUOyJIg> MXzEUXNQ NUjzV4lsW2mpbnnmbYNidnSueTDh[oZm[3S|IH;uJIFk[3WvdXzheIlwdiCxZjD0bIUh\my3b4Lld4NmdnRiQVLDRlEhe3Wkc4TyZZRmKHKqb3ThcYlv\SBzMkO= MX[yOFc{PTd4Nh?=
A375 (BRAFV600E) MVjGeY5kfGmxbjDBd5NigQ>? NYfyXXVHQCCq NVn0VHlJTE2VTx?= M4DTUmlv[3KnYYPld{BqdnS{YXPlcIx2dGG{IGLPV{BidmRiTl:gcIV3\Wy|IB?= MlfvNlU{PjN4NES=

... Click to View More Cell Line Experimental Data

In vivo In B-RAFV600E-mutant mice xenograft models, PLX4032 (6 mg/kg–20 mg/kg) inhibits tumor growth. [1] In mice xenograft models of LOX, Colo829, and A375 cells, PLX4032 (12.5 mg/kg–100 mg/kg) inhibits tumor growth and prolongs mice survival. [2]


Kinase Assay:[1]
+ Expand

RAF kinase activity measurements:

The kinase activities of wild-type RAF and mutants are determined by measuring phosphorylation of biotinylated-BAD protein. For each enzyme (0.01 ng), 20 μL reactions are carried out in 20 mM Hepes (pH 7.0), 10 mM MgCl2, 1 mM DTT, 0.01% (v/v) Tween-20, 50 nM biotin-BAD protein, and 1 mM ATP at room temperature. Reactions are stopped at 5 min with 5 μL of a solution containing 20 mM Hepes (pH 7.0), 200 mM NaCl, 80 mM EDTA, 0.3% (w/v) bovine serum albumin (BSA). The stop solution also includes phospho-BAD (Ser112) antibody, streptavidin-coated donor beads, and protein A acceptor beads. The antibody and beads are pre-incubated in stop solution in the dark at room temperature for 30 min. The final dilution of antibody is 1/2000 and the final concentration of each bead is 10 μg/mL. The assay plates are incubated at room temperature for one hour and then are read on a PerkinElmer AlphaQuest reader. Mutant activities are the average of two different batches of purified protein assayed in duplicate in three different experiments.
Cell Research:[2]
+ Expand
  • Cell lines: MALME-3M, Colo829, Colo38, A375, SK-MEL28, and A2058 cells
  • Concentrations: 0–10 μM , dissolved in DMSO
  • Incubation Time: 5 days
  • Method: Cellular proliferation is evaluated by MTT assay. Briefly, cells are plated in 96-well microtiter plates at a density of 1000 to 5000 cells per well in a volume of 180 μL. PLX4032 is prepared at 10 times the final assay concentration in media containing 1% DMSO. Twenty-four hours after cell plating, 20 μL of the appropriate dilution of PLX4032 are added to plates in duplicate. The plates are assayed for proliferation 6 days after the cells are plated. Percent inhibition is calculated and the IC50 is determined from the regression of a plot of the logarithm of the concentration versus percent inhibition.
    (Only for Reference)
Animal Research:[2]
+ Expand
  • Animal Models: Mice (athymic nude) xenograft models of LOX, Colo829, and A375 cells
  • Formulation: Formulated as microprecipitated bulk powder (MBP), suspended at the desired concentration in an aqueous vehicle containing 2% Klucel LF, and adjusted to pH 4 with dilute HCl
  • Dosages: 12.5 mg/kg–100 mg/kg
  • Administration: Oral gavage twice daily
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 97 mg/mL (197.99 mM)
Water <1 mg/mL
Ethanol <1 mg/mL
In vivo 4% DMSO+30% PEG 300+5% Tween 80+ddH2O 5mg/mL

* 1 mg/ml means slightly soluble or 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 489.92


CAS No. 918504-65-1
Storage powder
in solvent
Synonyms RO5185426

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01585415 Terminated Metastatic Cancer|Melanoma National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) April 9, 2012 Phase 1
NCT01843738 Not yet recruiting BRAFV600 Mutation|Stage IV Melanoma University of Utah January 2017 Phase 1
NCT02314481 Not yet recruiting Non-small Cell Lung Cancer University College, London|Hoffmann-La Roche January 2017 Phase 2
NCT03013491 Recruiting Solid Tumor|Lymphoma CytomX Therapeutics January 2017 Phase 1|Phase 2
NCT02908672 Recruiting Melanoma Hoffmann-La Roche January 2017 Phase 3
NCT03005639 Recruiting Stage IIIB-C Melanoma Inova Health Care Services|Genentech, Inc. December 2016 Phase 2

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID