PLX-4720

Catalog No.S1152

PLX-4720 Chemical Structure

Molecular Weight(MW): 413.83

PLX4720 is a potent and selective inhibitor of B-RafV600E with IC50 of 13 nM in a cell-free assay, equally potent to c-Raf-1(Y340D and Y341D mutations), 10-fold selectivity for B-RafV600E than wild-type B-Raf.

Size Price Stock Quantity  
In DMSO USD 156 In stock
USD 120 In stock
USD 270 In stock
USD 670 In stock
Bulk Discount

Free Overnight Delivery on orders over $ 500
Next day delivery by 10:00 a.m. Order now.

Cited by 49 Publications

10 Customer Reviews

  • Combinatorial knockdown of NF1 and C-RAF abrogates NF1-mediated resistance to B-RAF inhibition at the level of ERK phosphorylation. A375 cells were infected with NF1 shRNA and treated with either DMSO or PLX4720 for 16 h. Cell lysates were analyzed for the indicated proteins.

    Cancer Discov 2013 3, 350-62. PLX-4720 purchased from Selleck.

    Most of the resistant cells had higher levels of DCT compared with the parental cells. Cells were stained with a fluorescent-labeled DCT antibody (green) and counterstained with DAPI (blue).

    Genome Res, 2018, 28(9):1353-1363. PLX-4720 purchased from Selleck.

  • RAF inhibitors induce dimer formation between KSR and RAF, and activate KSR by CRAF. (A) GDC0879 but not PLX4720 induces BRAF/CRAF dimers. Cells overexpressing myc-CRAF and BRAF were treated with drug for 1 h and CRAF immunoprecipitates were immunoblotted for BRAF and CRAF (epitope tagged with myc). (B) GDC0879 but not PLX4720 enhances KSR/BRAF complexes. KSR immunoprecipitates were prepared from cells overexpressing FLAG-KSR and BRAF after treatment with the indicated drug for 1 h and immunoblotted using antibodies to BRAF. (C) Both GDC0879 and PLX4720 induce KSR/CRAF complexes.KSR immunoprecipitates were prepared from cells overexpressing FLAG-KSR and myc-CRAF after treatment with the indicated drug for 1 h and immunoblotted for CRAF using myc antibodies. (D and E) Requirement of KSR for drug-induced ERK activation. Lysates fromwild-type and KSR deficient fibroblasts, transfected with RASV12, were treated with the indicated doses of either GDC-0879 (D) or PLX4720 (E) for 1 h. Lysates were immunoblotted for phospho-ERK1 and 2, ERK2, and RASV12. (F) KSR and CRAF cooperate to activate MEK. Cells expressing the indicated constructs were treated with a 50 μM PLX4720 for 2 h before cell lysates were prepared and analyzed for pMEK by immunoblotting. CRAF(TM) refers to the T421M gatekeeper mutant that cannot bind to the drug(4). (G) KSR in vitro kinase reactions. Cells were cotransfected with WT or ATP binding deficient KSR and CRAF and immunoprecipitates prepared after cells were treated with an activating dose of PLX (10 μM) for 1 h. KSR immunoprecipitates were prepared, pretreated with 50 uM PLX4720 to inhibit coprecipitating RAF activity, and then tested for kinase activity using purified MEK. MEK phosphorylation was detected using a pMEK specific antibody.

    Proc Natl Acad Sci USA 2011 108, 6067-6072. PLX-4720 purchased from Selleck.

    (D)Melanoma cell lines were treated with 0.5 uM Pi-103 and/or 2 uM PLX4720 for 4 h. Samples were analyzed by Western blotting for the indicated proteins. β-Actin served as a loading control. (E) Melanoma cell lines were treated with a dilution series of Pi-103 either alone or in combination with the BRAFV600E inhibitor PLX4720 at a concentration of 3 uM (D10) or 1 uM (453A0) for 3 d. Total cell numbers were determined with a cell titer blue assay. The Y-axis represents the percentage of living cells.

    Genes Dev 2012 26, 1055-69. PLX-4720 purchased from Selleck.

  • PTEN predicts for PLX4720-induced apoptosis. A, basal PTEN and phospho-AKT(pAKT; S473, T308) expression in PTENt (WM164, 451Lu, SK-mel-28, WM983A, WM35, WM51) and PTEN (WM239A, WM266-4, WM793, M233, WM9, 1205Lu) melanoma cell lines. B, MTT assay of PTENt (gray)-expressing versus PTEN (black) cell lines. C, PTENt cells are more sensitive than PTEN cells to PLX4720-mediated apoptosis. Cells treated for 48 hours with 3 or 10 μmol/L PLX4720 before being stained for TMRM and Annexin-V. Apoptosis was measured by flow cytometry. Data shows mean SE mean of 3 independent experiments.*, PTENt cohort significantly different from PTEN cohort(P < 0.05).

    Cancer Res 2011 71, 2750-2760. PLX-4720 purchased from Selleck.

    Loss of PTEN is associated with PI3K/AKT signaling following BRAF inhibition. A, PTENt (WM35, WM164, WM983A) and PTEN (M233, WM9,WM793, 1205Lu) cells were treated with PLX4720 (24 hours: 0.03-3 μmol/L) and probed for phospho-PDK1 (pPDK1), total PDK1, phospho-AKT (pAKT), total AKT (tAKT), phospho-S6 (pS6), and total S6. Numbers indicate relative intensity of pPDK1 normalized to PDK1 and pAKT normalized to tAKT. B, PLX4720 increases pAKT following PTEN knockdown. WM35 cells were incubated with nontargeting siRNA (NT) or 2 different PTEN-specific siRNA's (PTEN) before treatment with either vehicle or PLX4720 (3 μmol/L). C, siRNA knockdown of BRAF increases pAKT in melanoma cell lines that are PTEN. WM164 (PTENt) and WM793 (PTEN) cells were incubated with lipofectamine alone (L), nontargeting siRNA (NT), or BRAF-specific siRNA (BRAF). Protein was extracted, resolved, and probed for BRAF, pAKT, total AKT, and GAPDH.

     

     

    Cancer Res 2011 71, 2750-2760. PLX-4720 purchased from Selleck.

  • Dual PI3K/BRAF inhibition upregulates BIM and enhances apoptosis in PTEN cells. A, left, Western blot of 1205Lu cells treated with PLX4720 (3 μmol/L, 48 hours), the PI3K inhibitor GDC-0941 (3 μmol/L, 48 hours), or both drugs in combination (PtG); right, immunofluorescence staining of BIM (green) and DAPI (blue) in PTEN cells following PLX4720 treatment (3 μmol/L, 48 hours), the PI3K inhibitor LY294002 (10 μmol/L, 48 hours), or both drugs in combination (PLXtLY). B, left, immunofluorescence staining of PTEN 1205Lu following combined inhibition (3 μmol/L PLX4720 t 10 μmol/L LY294002, 48hours) increases nuclear localization of FOXO3a (green). DAPI is shown in blue. Magnification 40. Right, combined inhibition (3 μmol/L PLX4720 t 10 μmol/L LY294002, 48 hours) increases PTEN WM793 BIM mRNA levels to those observed with single BRAF inhibition (3 μmol/L PLX4720, 48 hours) in the PTENt WM35. C, PTEN cells were treated with PLX4720 (3 μmol/L, 48 hours), GDC-0941 (3 μmol/L, 48hours), or a combination of the 2 drugs (3Pt3G) before Annexin-V staining was analyzed by flow cytometry (*, P < 0.05 between the drug combination and each inhibitor alone). D, combined BRAF/PI3K inhibitor treatment blocks the escape of 1205Lu cells (PTEN) from therapy. Spheroids of 1205Lu cells were treated with either PLX4720 alone (3 and 10 μmol/L: data shows 3 μmol/L), LY294002 (10 μmol/L) alone or a combination of the 2 drugs for 72 hours. In other studies, spheroids were treated with drugs for 72 hours and then allowed to recover for 120 hours. Micrograph shows viability staining (green ?live cells, red ?dead cells). Magnification 10.

    Cancer Res 2011 71, 2750-2760. PLX-4720 purchased from Selleck.

    LC-MRM identifies differential regulation of BIM in PTENt and PTEN cell lines following PLX4720 treatment. A, representative LC-MRM data showing the fold changes in the expression of Bak, Bax, Bcl-2, Bcl-w, Bcl-xL, BID, BIM, Bok, and Mcl-1 over internal standard in the WM164 (PTENt) and 1205Lu (PTEN) cell lines following treatment with PLX4720 (10 μmol/L, 0-48 hours). Statistical analysis of BIM fold change in PTEN versus PTENt. *, P < 0.05. B, Western blot showing BIM expression following PLX4720 treatment (10 μmol/L, 0-48 hours) in PTEN (WM793, 1205Lu) and WM164 cell lines (PTENt). C, immunofluorescence staining, showing expression of BIM and DAPI staining of PTEN (M233, WM9, WM793, 1205Lu) and PTENt (WM35, WM164, WM983A) cells following PLX4720 treatment (3 μmol/L, 48 hours).D, Western blot showing BAD phosphorylation following treatment with PLX4720 (0-48 hours) in PTEN (WM793,1205Lu) and PTENt WM164. Annexin V binding following treatment with 3 or 10 μmol/L PLX4720 (48 hours) showing increased apoptosis in WM793 stably overexpressing WT BAD. *, P < 0.05.

    Cancer Res 2011 71, 2750-2760. PLX-4720 purchased from Selleck.

  • B-RafV600E mutated melanoma line, SK-MEL-28, was treated with different doses of PLX-4720 for 4 h or 22 h.  Cell lysates were analyzed by Western blotting to determine the levels of phosphorylated MEK1/2 (pMEK1/2) and phosphorylated ERK1/2 (pERK1/2). MEK1/2 is the substrate of B-Raf while ERK1/2 is the substrate of MEK1/2.  Data show that phosphorylation of MEK1/2 and ERK1/2 was significantly inhibited by PLX-4720 treatment although total MEK1/2 or ERK1/2 protein levels were not affected. No pMEK1/2 or pERK1/2 signal was detected even after prolonged exposure, indicating that the inhibitor at 1 μM is very effective in blocking the constitutive kinase activity of B-RafV600E.  This data is consistent with the previous result demonstrating the effect of PLX-4720 in the B-RafV600E mutated melanoma line, A375 – Fig. 2A, Nature 464:431 (2010)

     

     

    Dr. Jong-In Park of Medical College of Wisconsin. PLX-4720 purchased from Selleck.

    A dose titration of PLX-4720 in A375 melanoma cells which possess a V600E B-Raf mutation.Effects of  increasing PLX-4720 dose on Erk phosphorylation and on tumor cell proliferation as determined by MTT  assay are shown.

     

     

    Dr. Daniel C.Cho of Harvard Medical School. PLX-4720 purchased from Selleck.

Purity & Quality Control

Choose Selective Raf Inhibitors

Biological Activity

Description PLX4720 is a potent and selective inhibitor of B-RafV600E with IC50 of 13 nM in a cell-free assay, equally potent to c-Raf-1(Y340D and Y341D mutations), 10-fold selectivity for B-RafV600E than wild-type B-Raf.
Targets
C-Raf-1 (Y340D/Y341D) [1]
(Cell-free assay)
B-Raf (V600E) [1]
(Cell-free assay)
BRK [1]
(Cell-free assay)
B-Raf [1]
(Cell-free assay)
6.7 nM 13 nM 130 nM 160 nM
In vitro

PLX-4720 displays >10 times selectivity against wild type B-Raf, and >100 times selectivity over other kinases such as Frk, Src, Fak, FGFR, and Aurora A with IC50 of 1.3-3.4 μM. PLX-4720 significantly inhibits the ERK phosphorylation in cell lines bearing B-RafV600E with IC50 of 14-46 nM, but not the cells with wild-type B-Raf. PLX-4720 significantly inhibits the growth of tumor cell lines bearing the B-RafV600E oncogene, such as COLO205, A375, WM2664, and COLO829 with GI50 of 0.31 μM, 0.50 μM, 1.5 μM, and 1.7 μM, respectively. In addition, PLX-4720 treatment at 1 μM induces cell cycle arrest and apoptosis exclusively in the B-RafV600E-positive 1205Lu cells, but not in the B-Raf wild-type C8161 cells. [1] PLX-4720 treatment (10 μM) significantly induces >14-fold expression of BIM in the PTEN+ cells, compared with the PTEN- cell lines (4-fold), giving an explanation of the resistance of PTEN- cells to PLX-4720-induced apoptosis. [2]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
DU-4475 MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NX7zOIxKUUN3ME2wMlA4PDV5IN88US=> NFvo[IFUSU6JRWK=
EoL-1-cell NIj3bG5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmDkTWM2OD1yLkG0NVY3KM7:TR?= Mor1V2FPT0WU
C32 MnjwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Ml7YTWM2OD1yLkG1NVMyKM7:TR?= MXzTRW5ITVJ?
M14 NYH0cJRNT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MULJR|UxRTBwMkG3OVch|ryP Mo\rV2FPT0WU
CP50-MEL-B MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NU\2NXVoUUN3ME2wMlI6Pzh2IN88US=> MnTtV2FPT0WU
A101D M4jpRmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUDJR|UxRTBwM{K1PFkh|ryP NFTrPVdUSU6JRWK=
G-361 MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkSzTWM2OD1yLkO0OlM4KM7:TR?= NEjYZXhUSU6JRWK=
HT-144 M4Ppfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mlu2TWM2OD1yLkO2N|I6KM7:TR?= MnjFV2FPT0WU
ACN MknVS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX\JR|UxRTBwM{i0O|ch|ryP MXfTRW5ITVJ?
COLO-829 MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX\JR|UxRTBwM{i5Olgh|ryP M4rx[3NCVkeHUh?=
MEL-HO NVzyOng6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYDEOXU5UUN3ME2wMlQyOTd7IN88US=> MYfTRW5ITVJ?
SH-4 Ml6xS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3zzdGlEPTB;MD60NVQzOiEQvF2= M2POPHNCVkeHUh?=
SK-MEL-3 NWDU[lV[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnrKTWM2OD1yLkWxOVY5KM7:TR?= NUHZcItqW0GQR1XS
A375 M3;IeWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVrJR|UxRTBwNkezOVkh|ryP M1TZN3NCVkeHUh?=
MMAC-SF NUTaWm1FT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlX1TWM2OD1yLk[4OlE1KM7:TR?= MnnrV2FPT0WU
BHT-101 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGK0W3BKSzVyPUCuO|A4ODJizszN NWfZfZJjW0GQR1XS
K5 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWDme|VSUUN3ME2wMlc3OTR6IN88US=> NGLTR3RUSU6JRWK=
BV-173 NELENphIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHXkTmZKSzVyPUCuO|k3PDRizszN NGD0cm9USU6JRWK=
RVH-421 MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmC3TWM2OD1yLki2O|k3KM7:TR?= M2HiT3NCVkeHUh?=
HCC2218 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NITGXGZKSzVyPUCuPFc5PDRizszN MX3TRW5ITVJ?
WM-115 MojYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEHWSIZKSzVyPUCuPFg3QTJizszN MnPyV2FPT0WU
SK-MEL-28 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4\mcmlEPTB;MT6wOFU3QSEQvF2= NU\xVmdIW0GQR1XS
COLO-679 Mn;TS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGHqe2hKSzVyPUGuNVA1PjRizszN NXe4d2tkW0GQR1XS
MZ7-mel MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVLtUpZMUUN3ME2xMlE1QTZ|IN88US=> Mm\xV2FPT0WU
SK-MEL-30 M1q0TGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYnJR|UxRTFwM{OzPFYh|ryP MkjsV2FPT0WU
NCI-H209 MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2rVVGlEPTB;MT62NFg3KM7:TR?= M4fqZnNCVkeHUh?=
HTC-C3 M2W2[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1S2WmlEPTB;MT62OlI6PCEQvF2= MoLkV2FPT0WU
KARPAS-45 MlLBS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoPVTWM2OD1{LkC0PVc5KM7:TR?= MWrTRW5ITVJ?
NCI-SNU-5 MnLjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX\JR|UxRTJwMUG5Olkh|ryP M3LRcXNCVkeHUh?=
KP-4 NV;Xc5RoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmDtTWM2OD1{LkOwO|g4KM7:TR?= NY[5NVd{W0GQR1XS
PA-1 M{\EXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGe4RlhKSzVyPUKuO|I3PzNizszN NHXMXXpUSU6JRWK=
HuO-3N1 MoflS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlfnTWM2OD1{Lki3PVQ3KM7:TR?= MnrOV2FPT0WU
NCI-H358 NGfOUG9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWTJR|UxRTJwOUKyN|Ih|ryP M3TTe3NCVkeHUh?=
CTB-1 MofUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmO3TWM2OD1|LkSwNVc3KM7:TR?= M1G3SnNCVkeHUh?=
697 MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYXVWlE6UUN3ME2zMlU2OjZ4IN88US=> Mn\3V2FPT0WU
CP66-MEL MmiyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGXodohKSzVyPUSuNVU6OjdizszN Mmm0V2FPT0WU
NB13 MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYmwfIlwUUN3ME20MlQ6OTd7IN88US=> MYTTRW5ITVJ?
DBTRG-05MG NX76[YVET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEXFNnVKSzVyPUSuOVM{OjVizszN M{PYS3NCVkeHUh?=
A2058 NWXhcYtrT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFPZZWFKSzVyPUSuO|IyPjRizszN NX[xXoh4W0GQR1XS
KG-1 NEjlNnZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{DOZ2lEPTB;ND63N|kxQCEQvF2= MkLmV2FPT0WU
8305C MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{jPRWlEPTB;NT6xPFc{KM7:TR?= NGq4Z2hUSU6JRWK=
RPMI-7951 MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVrJR|UxRTVwOECyPFMh|ryP M4XYbnNCVkeHUh?=
CHL-1 M4HOdWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXzJR|UxRTVwOUe2NFMh|ryP MYnTRW5ITVJ?
TI-73 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoHDTWM2OD14LkCwPVAzKM7:TR?= MXPTRW5ITVJ?
HT-1080 M{exe2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVjJR|UxRTZwMUC5OFYh|ryP MnLuV2FPT0WU
ES5 M1PCOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MljzTWM2OD14LkG0PVI1KM7:TR?= MkCyV2FPT0WU
8-MG-BA NFu5NVNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4nrZmlEPTB;Nj6xPFEzQSEQvF2= MXLTRW5ITVJ?
NB7 MkO0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVrJR|UxRTZwMkGzO|Mh|ryP MonjV2FPT0WU
H4 NHmxN5lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnjCTWM2OD14LkKyOFk{KM7:TR?= M{KwW3NCVkeHUh?=
CAL-72 M{fxV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUXFU|ZVUUN3ME22MlQ2PDJ|IN88US=> Mnq3V2FPT0WU
HCC1806 MmnsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVz4VYptUUN3ME22MlgyQTNzIN88US=> NXzuOoNoW0GQR1XS
BCPAP MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mne1TWM2OD15LkKxO|Y1KM7:TR?= M3rzSXNCVkeHUh?=
LB2241-RCC NXfPflZjT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWXJR|UxRTdwM{[5NFch|ryP NUL1R4RkW0GQR1XS
COLO-741 MnXSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmD0TWM2OD16LkCxOlc6KM7:TR?= NYLpPXNEW0GQR1XS
HSC-3 MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWXJR|UxRThwMEewOlgh|ryP NH7lbHpUSU6JRWK=
SW982 MkDlS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mnv4TWM2OD16LkSxOVE3KM7:TR?= MX7TRW5ITVJ?
GCT NIjEcXBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVzJR|UxRThwN{WzNVQh|ryP NH3IT3JUSU6JRWK=
KY821 M2PxZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWXSO|JzUUN3ME25MlA2OTd6IN88US=> M2ryUXNCVkeHUh?=
JVM-3 NYH3OIV2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWT4b3A{UUN3ME25MlU3QTl7IN88US=> MXjTRW5ITVJ?
RS4-11 NIG4XmpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIX2UXdKSzVyPUmuOlA1QCEQvF2= M1fufHNCVkeHUh?=
VA-ES-BJ M1HCVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M37MSmlEPTB;MUCuNFE1QSEQvF2= NF;vVZlUSU6JRWK=
A431 M3\kN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1;5e2lEPTB;MUCuOFIyOiEQvF2= NYrBXmQ3W0GQR1XS
LXF-289 M4\ybmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHfkT4dKSzVyPUGwMlQ2QCEQvF2= MWfTRW5ITVJ?
SK-MEL-24 M4PZbGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MX3JR|UxRTFyLkiyO|Qh|ryP NH\ZSVdUSU6JRWK=
NOS-1 M3nzOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mo\yTWM2OD1zMD64OFczKM7:TR?= MXTTRW5ITVJ?
KNS-62 NWPGeIZlT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVTFSlVyUUN3ME2xNU4zPDB2IN88US=> NFjzOXBUSU6JRWK=
SK-HEP-1 NH7TZVVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUjJR|UxRTFzLkO1Nlch|ryP NGLIXnlUSU6JRWK=
A3-KAW M3PqVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn63TWM2OD1zMT63NVc5KM7:TR?= NVH4O4xHW0GQR1XS
SK-LU-1 MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NES0ZlhKSzVyPUGyMlI3PTVizszN NWLLbJc4W0GQR1XS
TYK-nu MkHBS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXq4SYRCUUN3ME2xNk4{QTN{IN88US=> NILxUo9USU6JRWK=
NMC-G1 NVWyUFhET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWTNVHlkUUN3ME2xNk43ODZ{IN88US=> MX3TRW5ITVJ?
BB65-RCC NFrGcmNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWLJR|UxRTF{LkexOlkh|ryP MY\TRW5ITVJ?
QIMR-WIL MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYDJR|UxRTF{Lki4N|Mh|ryP NV;Wd|FyW0GQR1XS
D-566MG MnPCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX;JR|UxRTF|Lkm1O|Yh|ryP NUXtOZR5W0GQR1XS
KYSE-140 MkP6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIX4dY1KSzVyPUG0MlA4PTNizszN NYrneJp7W0GQR1XS
SCC-4 MmTVS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX3JR|UxRTF2LkOzOVkh|ryP Mmr3V2FPT0WU
U251 NIPGV|ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{DlR2lEPTB;MUSuPFQ6OiEQvF2= NF\pcGRUSU6JRWK=
D-542MG NFPqfZBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3vVNmlEPTB;MUSuPVIzOiEQvF2= NGLV[|RUSU6JRWK=
LAMA-84 NESxe5ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWTJR|UxRTF2Lkm5N|Ih|ryP M3nwV3NCVkeHUh?=
NCI-H720 M{\JPWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXLFRpFrUUN3ME2xOU4zPjh2IN88US=> MXTTRW5ITVJ?
DEL NXvlTXVMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXztdokzUUN3ME2xOU41Ojl|IN88US=> MkfyV2FPT0WU
SBC-1 MoLKS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2O5dmlEPTB;MUWuOFMxPSEQvF2= NGPEXZVUSU6JRWK=
ECC10 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2LlemlEPTB;MUWuOFQ2QCEQvF2= NHzMUmlUSU6JRWK=
Daoy MkjvS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NE[ySFhKSzVyPUG1Mlc3OTZizszN M3rWbHNCVkeHUh?=
SCH NVT4TJhYT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NV\QZ5F7UUN3ME2xOU44QDN3IN88US=> MnLXV2FPT0WU
MZ2-MEL NEfl[4xIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NU\vZoZvUUN3ME2xOk4xPjR4IN88US=> NX3vdVRxW0GQR1XS
CAL-12T NEjzclNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF;zWYNKSzVyPUG2MlQ5PjJizszN NXjYZmtPW0GQR1XS
KE-37 M4\GZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M37XXGlEPTB;MU[uPFExPyEQvF2= MV3TRW5ITVJ?
LS-411N MkHPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NV31dYh5UUN3ME2xO{4yOThizszN NEDHVo1USU6JRWK=
NCI-H2228 M1;Lb2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVXHTHlLUUN3ME2xO{4{ODdzIN88US=> MWPTRW5ITVJ?
SK-MEL-2 MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXPiUId3UUN3ME2xO{41QTZ3IN88US=> NEH0W45USU6JRWK=
HN NYr2RmZCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWLPdoVWUUN3ME2xO{44OjR6IN88US=> NHXmVFVUSU6JRWK=
NCI-H1648 NHLMSGZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGjqeoZKSzVyPUG3MlgyQCEQvF2= NFvQelBUSU6JRWK=
IA-LM NY\UWWNTT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXPGeIQ2UUN3ME2xPE4{OTd{IN88US=> NXLzR5dNW0GQR1XS
EW-13 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWrJR|UxRTF6LkW3NFgh|ryP MoLFV2FPT0WU
YKG-1 M{jIVmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWfJR|UxRTF7LkW3NVEh|ryP NVfzeW9RW0GQR1XS
KNS-81-FD NELlUnBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1PEWWlEPTB;MUmuOVg2QCEQvF2= MVHTRW5ITVJ?
23132-87 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVzJR|UxRTF7Lke2OFIh|ryP MUfTRW5ITVJ?
NUGC-3 MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M13FNGlEPTB;MUmuPVg5PyEQvF2= NXO5XXBnW0GQR1XS
5637 M3nWcWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYrJR|UxRTJyLkC0O|gh|ryP MXLTRW5ITVJ?
NCI-H1755 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHvtVVNKSzVyPUKwMlQ4PjRizszN MnLSV2FPT0WU
RH-18 NI\LWpJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVPac3JzUUN3ME2yNE42PzR6IN88US=> NX7tdI8yW0GQR1XS
RXF393 M4LjcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWDSc4hsUUN3ME2yNE43PzV4IN88US=> MVfTRW5ITVJ?
LU-134-A NEm1TlFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmLnTWM2OD1{MD63NFU3KM7:TR?= NVzRbY82W0GQR1XS
TE-12 MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWTJR|UxRTJyLkeyNFEh|ryP MXrTRW5ITVJ?
MOLT-4 NUG3T5diT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkTmTWM2OD1{MT6xPVE2KM7:TR?= NF75NVJUSU6JRWK=
IGR-1 NELZc2lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHK3WYlKSzVyPUKxMlM4QTZizszN MmjRV2FPT0WU
HOP-92 NVTXSFR[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGrTZWFKSzVyPUKxMlQ6QDdizszN MYnTRW5ITVJ?
SK-MES-1 MkDVS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4i2TGlEPTB;MkGuO|M5OSEQvF2= NWn0WnEzW0GQR1XS
LU-65 M3HacWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWjJR|UxRTJzLki2NlQh|ryP NYDKZVlEW0GQR1XS
MS-1 NVj5VWVOT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MUXJR|UxRTJ{LkGyNFMh|ryP NH3pZ5lUSU6JRWK=
LoVo MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mkf3TWM2OD1{Mj6yOFQh|ryP Mn3yV2FPT0WU
A704 NWHrTnhNT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mny5TWM2OD1{Mj61NVU2KM7:TR?= M{\0dHNCVkeHUh?=
HT-1376 MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGX2O4FKSzVyPUKyMlYxPTlizszN MUXTRW5ITVJ?
IST-MEL1 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoDoTWM2OD1{Mj62O|UyKM7:TR?= NFH5fGFUSU6JRWK=
Ramos-2G6-4C10 NXPDdJJDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NE\WdYxKSzVyPUKyMlc{PjZizszN MVrTRW5ITVJ?
T47D M4jvXGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIG0OYNKSzVyPUKyMlc6PzlizszN M1rvR3NCVkeHUh?=
HT-1197 M1;0VGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHT1WnFKSzVyPUKzMlA5OTdizszN MX;TRW5ITVJ?
LB2518-MEL NETzc25Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3P6SGlEPTB;MkOuOlQyOiEQvF2= M4f6d3NCVkeHUh?=
J-RT3-T3-5 MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NV3VVY9QUUN3ME2yOE44PTl3IN88US=> MXXTRW5ITVJ?
SK-NEP-1 MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWS3NpBvUUN3ME2yOE45PzR2IN88US=> M{iwVnNCVkeHUh?=
NCI-H526 M{K2eWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHnUUpNKSzVyPUK1MlAxOjNizszN NGG2[m5USU6JRWK=
IST-SL1 MoPMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIXPfJpKSzVyPUK1MlI4PTFizszN MkTxV2FPT0WU
HH MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NILne45KSzVyPUK1MlMyQTJizszN Mki3V2FPT0WU
NCI-H82 MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3TOV2lEPTB;MkWuPVM5KM7:TR?= NU\3SY8xW0GQR1XS
SNU-449 NYLZdoVUT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX;6d5E3UUN3ME2yO{4zODF6IN88US=> M1XjSHNCVkeHUh?=
COR-L23 MmDsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVzWUldJUUN3ME2yO{4zQDF|IN88US=> NGjUXIhUSU6JRWK=
LOXIMVI MmTKS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnzoTWM2OD1{Nz6zOlgh|ryP M4O3ZnNCVkeHUh?=
GR-ST M3Tnd2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYPDV5ZqUUN3ME2yO{43PzB4IN88US=> M1LjTnNCVkeHUh?=
NCI-SNU-1 MmHUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUHDTIVbUUN3ME2yO{46PDRizszN MXvTRW5ITVJ?
ALL-PO MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUPPcXNHUUN3ME2yPE4yPjB2IN88US=> MYnTRW5ITVJ?
ML-2 NFTucmFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MofITWM2OD1{OD6yPFE1KM7:TR?= NV;xXW1[W0GQR1XS
HOP-62 MnuzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NImzRXpKSzVyPUK4MlcyOyEQvF2= NEm1eG9USU6JRWK=
EGI-1 NV7D[mhnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYLQTZN{UUN3ME2yPE45QDR3IN88US=> MnzDV2FPT0WU
TCCSUP NH7hbpJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlXLTWM2OD1{OD65NlczKM7:TR?= NHTUc5RUSU6JRWK=
LB996-RCC M2nQW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGLyZnhKSzVyPUK5MlU3QDJizszN NHzwS4hUSU6JRWK=
LCLC-97TM1 MnO0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXTJR|UxRTN{LkG5OlQh|ryP M4LTcnNCVkeHUh?=
NCI-H1304 M3f5WGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmjCTWM2OD1|Mj6zN|AyKM7:TR?= MWLTRW5ITVJ?
KP-N-YS NIroPYZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVLJR|UxRTN{LkW5O|Mh|ryP MXvTRW5ITVJ?
NCI-H1770 MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHXycWhKSzVyPUOzMlE3PDhizszN NV3nSIw4W0GQR1XS
EM-2 NYfrWHg1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGXsNpFKSzVyPUOzMlY2ODRizszN MX7TRW5ITVJ?
ChaGo-K-1 Mnu1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHP5eXhKSzVyPUOzMlczOzZizszN MlL0V2FPT0WU
ACHN MmTpS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NE[zcJlKSzVyPUOzMlg{QDVizszN NWHGdI51W0GQR1XS
MN-60 M{nzbWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUnreXpOUUN3ME2zN{45PTR2IN88US=> NEizVGJUSU6JRWK=
EW-18 Mo\3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXjJR|UxRTN|Lki5O|Eh|ryP NYrHdYltW0GQR1XS
KGN M4nYSmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NI\NPYZKSzVyPUO1MlczQTJizszN NHvOPGJUSU6JRWK=
U031 NFu0cYhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVTJR|UxRTN3LkixN|Ih|ryP Mlj5V2FPT0WU
HMV-II M{PhVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUXJR|UxRTN4LkC3O|Qh|ryP NHPJWoxUSU6JRWK=
L-363 M1mzfWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmS0TWM2OD1|Nz62OFU2KM7:TR?= NELOU2NUSU6JRWK=
NCI-H1155 M2\rc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXzrO2h3UUN3ME2zPE4xODF3IN88US=> NV;OPXRkW0GQR1XS
NCI-H1793 NWXqVGl6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWjZcW9vUUN3ME2zPE4yODJ4IN88US=> MUPTRW5ITVJ?
P30-OHK NVzQfVNoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUDEdmZ{UUN3ME2zPE4yOzN{IN88US=> NHfGTGlUSU6JRWK=
AN3-CA NGeyeYVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGP6N3dKSzVyPUO4MlE3OTVizszN M{TEbHNCVkeHUh?=
UACC-257 NYG5SFlXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEnSU|FKSzVyPUO4Mlc6KM7:TR?= MlnWV2FPT0WU
MCF7 MlrKS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mn;CTWM2OD1|OT64OlI6KM7:TR?= M3XoPHNCVkeHUh?=
KP-N-YN M{LkTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M12xUWlEPTB;NECuOFI5PSEQvF2= NYfkVZZWW0GQR1XS
T98G M2Xae2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEL1N2tKSzVyPUSwMlQ6PTdizszN MXjTRW5ITVJ?
HGC-27 NEXRbXZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NInQNWlKSzVyPUSzMlI4PCEQvF2= MVrTRW5ITVJ?
NCI-H1092 M17lbGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVfEUW9LUUN3ME20N{4zQDl3IN88US=> MkGwV2FPT0WU
KARPAS-299 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXvJR|UxRTR|LkOwO|Eh|ryP NHHtT4ZUSU6JRWK=
LB1047-RCC NVjs[JdkT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGHoV|NKSzVyPUS0Mlk6PTlizszN MWLTRW5ITVJ?
786-0 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NX3DeG41UUN3ME20OU43PSEQvF2= M1zORXNCVkeHUh?=
HCC2157 MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHfLRXVKSzVyPUS2MlA{PTlizszN MoO1V2FPT0WU
NY MmW2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVrHeWlFUUN3ME20Ok4yPzd6IN88US=> MV;TRW5ITVJ?
EFM-19 NHiwU|BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVvJR|UxRTR4Lke1N|Mh|ryP NYHORVVpW0GQR1XS
EW-16 NFXlSXJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmDmTWM2OD12Nj63PFA3KM7:TR?= NUK5ZlZPW0GQR1XS
UM-UC-3 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1;s[2lEPTB;NE[uPFA2QSEQvF2= NEPQSXhUSU6JRWK=
HT-29 NX\WVFJ2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVP3UGROUUN3ME20O{45Pzl{IN88US=> M1vLenNCVkeHUh?=
LN-405 MmTGS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHT6NYlKSzVyPUS4MlA5OjdizszN NHSwcIxUSU6JRWK=
NCI-H727 MlPZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M37iSmlEPTB;NEiuO|czPiEQvF2= Mnu5V2FPT0WU
D-502MG M3X5SWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHPLfoVKSzVyPUS4Mlk3PzZizszN M3\pOXNCVkeHUh?=
GMS-10 M2DRemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIXqdpVKSzVyPUS5MlI6PzRizszN MlHKV2FPT0WU
MEL-JUSO NIjUZW9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFOzb4VKSzVyPUS5MlM1PyEQvF2= MkW1V2FPT0WU

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Western blot
p-MEK / MEK / p-ERK / ERK / p-FAK(S910); 

PubMed: 23076151     


WM793 and WM793-Res NRAS cells were seeded overnight in the absence of PLX4720 and then treated with 1 μm PLX4720 for times ranging from 0 to 24 h. Samples were analyzed by Western blotting for phospho-MEK, total MEK, phospho-ERK1/2, total ERK1/2, phospho-S910 FAK, and total FAK.

p-EGFR 1173 / EGFR / p-Akt / Akt; 

PubMed: 26023796     


Three BRAF(V600E) glioma cell lines, NMC-G1, AM38 and DBTRG-05MG were subjected to a 24 hour time course treatment with 5 μM PLX4720 in the presence or absence of 1 μM HKI-272. These cells were serum starved for 16 hours before being stimulated with 10% FBS and harvested for immunoblotting analysis. Cells treated with PLX4720 alone showed an initial suppression of MEK and ERK phosphorylation followed by a profound rebound of MAPK pathway activation as early as one hour post-PLX4720 treatment. Elevated levels of EGFR phosphorylation were also observed in the PLX4720 treated cells. The extent of Akt phosphorylation increased upon PLX4720 treatment, although the extent varies between cell lines. In contrast, no reactivation of EGFR, MEK, ERK or Akt was observed in cells pre-treated with HKI-272.

p27 / Cyclin D1 / pRb; 

PubMed: 21828154     


Immunoblot analysis revealed that PLX4720 (3 μM) decreased levels of phosphorylated ERK, decreased levels of cyclin D1, increased levels of p27, and decreased levels of phosphorylated Rb in BRAF-mutant (OCM3) cells. On the contrary, in Gα-mutant (OMM1.3) UM cells, PLX4720 induced a paradoxical increase in phosphorylated ERK and Rb levels and an early increase in cyclin D1 levels but did not stimulate p27 levels.

pAkt(Ser473) / pAkt(Thr308); 

PubMed: 21828154     


Immunoblot analysis revealed that both AZD6244 and PLX4720 induced an early (within 2–6 hours of exposure) increase in the levels of phosphorylated Akt (at residues Ser473 and Thr308) in both BRAF-mutant OCM3 and Gα-mutant OMM1.3 cells. Eventually, and with prolonged drug exposure, the phosphorylation of Akt returned to baseline in Gα-mutant OMM1.3 cells and decreased even below baseline levels in BRAF-mutant OCM3 cells.

23076151 26023796 21828154
Immunofluorescence
LAMP1; 

PubMed: 30979895     


Representative images of LysoTracker Red (red) and LAMP1 (green) immunostaining of PLX4720 (1 μM, 12 h-treated) A375 cells with depletion of the indicated genes. Note the reduced lysosome staining in PLX4720-treated cells upon TFEB depletion. 

ZKSCAN3 / TFEB ; 

PubMed: 30979895     


Representative confocal images of subcellular translocation of endogenous TFEB (green) and ZKSCAN3 (red) in A375 cells treated with PLX4720 (1 μM, 12 h). n = 3 independent experiments. 

30979895
Growth inhibition assay
Cell viability; 

PubMed: 27848137     


AM-38 and DBTRG-05MG cells were treated for 5 days. Media was changed once every 3 days. Cell viability was measured using WST-1 assay. Error bars indicate the variation between triplicate measurements. PLX4720 and PD0325901 alone or in combination reduced cell viability significantly. However, combined therapy led to the most significant cell viability reduction compared to either monotherapy in both AM-38 and DBTRG-05MG cell lines.

27848137
ELISA
mIFN-γ; 

PubMed: 23204132     


(C, D and E) IFN-γ secretion by pmel-1 T cells co-cultured with transduced melanoma cells (after cell sorting) that had been pre-treated with the indicated concentrations of PLX4720, as determined by ELISA. (*P<0.05, ** P<0.01) Data are representative of 3 independent experiments.

23204132
In vivo Oral administration of PLX-4720 at 20 mg/kg/day induces significant tumor growth delays and regressions in B-RafV600E-dependent COLO205 tumor xenografts, without obvious adverse effects in mice even at dose of 1 g/kg. PLX-4720 at 100 mg/kg twice daily almost completely eliminates the 1205Lu xenografts bearing B-RafV600E, while has no activity against C8161 xenografts bearing wild-type B-Raf. The anti-tumor effects of PLX-4720 correlate with the blockade of MAPK pathway in those cells harboring the V600E mutation. [1] PLX-4720 treatment at 30 mg/kg/day significant inhibits the tumor growth of 8505c xenografts by >90%, and dramatically decreases distant lung metastases. [3]

Protocol

Kinase Assay:[1]
+ Expand

In vitro Raf kinase activities:

The in vitro kinase activities of wild type Raf and mutants are determined by measuring phosphorylation of biotinylated-MEK protein using Perkin-Elmer's AlphaScreen Technology. For each enzyme (0.1 ng), 20-μL reactions are carried out in 20 mM Hepes (pH 7.0), 10 mM MgCl2, 1 mM DTT, 0.01% Tween-20, 100 nM biotin-MEK protein, various ATP concentrations, and increasing concentrations of PLX-4720 at room temperature. Reactions are stopped at 2, 5, 8, 10, 20, and 30 minutes with 5 μL of a solution containing 20 mM Hepes (pH 7.0), 200 mM NaCl, 80 mM EDTA, and 0.3% BSA. The stop solution also includes phospho-MEK Antibody, Streptavidin-coated Donor beads and Protein A Acceptor beads from the AlphaScreen Protein A Detection Kit. The antibody and beads are preincubated in stop solution in the dark at room temperature for 30 minutes. The final dilution of antibody is 1/2,000, and the final concentration of each bead is 10 μg/mL. The assay plates are incubated at room temperature for one hour then are read on a PerkinElmer AlphaQuest reader.
Cell Research:[1]
+ Expand
  • Cell lines: COLO205, A375, WM2664, COLO829, HT716, SW620, H460, Calu-6, HCT116, SK-MEL2, SK-MEL3, Lovo, H1299, 1205Lu, and C8161 cells
  • Concentrations: Dissolved in DMSO, final concentrations ~1 mM
  • Incubation Time: 24, 48, and 72 hours
  • Method: Cells are treated with various concentrations PLX-4720 for 24, 48, and 72 hours. Cell proliferation is measured by using the CellTiter-Glo Luminescent Cell Viability Assay or MTT assay. For cell cycle analysis, supernatant and cells are collected, pelleted, and fixed with 70% ethanol. Before staining with propidium iodide (10 μg/mL), cells are incubated for 1 hour at 37 °C in 0.5 mg/mL RNase I to rid samples of residual RNA contamination. Samples are then analyzed by using the EPICS XL apparatus. For the assessment of apoptosis, media and cells are harvested and pelleted before staining with annexin-FITC and propidium iodide. Samples are subsequently analyzed by using the EPICS XL apparatus.
    (Only for Reference)
Animal Research:[1]
+ Expand
  • Animal Models: Female athymic mice (NCr nu/nu) implanted s.c. with COLO205 cells, and SCID mice with 1205Lu or C8161 cells
  • Formulation: Suspended in vehicle (5% DMSO, 1% methylcellulose)
  • Dosages: 5, 20, or 100 mg/kg
  • Administration: Oral gavage once or twice daily
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 83 mg/mL (200.56 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+50% PEG 300+5% Tween 80+ddH2O
For best results, use promptly after mixing.
5mg/mL

* 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 413.83
Formula

C17H14ClF2N3O3S

CAS No. 918505-84-7
Storage powder
in solvent
Synonyms N/A

Bio Calculators

Molarity Calculator

Molarity Calculator

Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

  • Mass
    Concentration
    Volume
    Molecular Weight

*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).

Dilution Calculator

Dilution Calculator

Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

Concentration (start) x Volume (start) = Concentration (final) x Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

  • C1
    V1
    C2
    V2

* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).

The Serial Dilution Calculator Equation

  • Serial Dilutions

  • Computed Result

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):
Molecular Weight Calculator

Molecular Weight Calculator

Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

Total Molecular Weight: g/mol

Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2

Instructions to calculate molar mass (molecular weight) of a chemical compound:

To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Mass Concentration Volume Molecular Weight

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

  • * Indicates a Required Field

Frequently Asked Questions

  • Question 1:

    What would you recommend to make working solution for intraperitoneal injection into mice?

  • Answer:

    PLX4720 has very limited solubility in aqueous solution and for this reason, we recommend oral gavage to administer this compound as not fully dissolved suspension can be used in oral gavage feeding.

Raf Signaling Pathway Map

Raf Inhibitors with Unique Features

Related Raf Products3

Tags: buy PLX-4720 | PLX-4720 supplier | purchase PLX-4720 | PLX-4720 cost | PLX-4720 manufacturer | order PLX-4720 | PLX-4720 distributor
×
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID