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.

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In DMSO USD 156 In stock
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Cited by 46 Publications

9 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.

    (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.

  • 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.

    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 M2f1XGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVLCSm5iUUN3ME2wMlA4PDV5IN88US=> M13sNHNCVkeHUh?=
EoL-1-cell MoHHS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXHsXGFjUUN3ME2wMlE1OTZ4IN88US=> NFfXU5FUSU6JRWK=
C32 M3LkOWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXXJR|UxRTBwMUWxN|Eh|ryP MYTTRW5ITVJ?
M14 M1TwXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH;DZ3JKSzVyPUCuNlE4PTdizszN MmPWV2FPT0WU
CP50-MEL-B NX:0cY1WT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIXL[m1KSzVyPUCuNlk4QDRizszN MXLTRW5ITVJ?
A101D NV\jOpA2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkO0TWM2OD1yLkOyOVg6KM7:TR?= M1;lUHNCVkeHUh?=
G-361 NEmxcGlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUTYV3VWUUN3ME2wMlM1PjN5IN88US=> MkDIV2FPT0WU
HT-144 Mm\1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{XZWGlEPTB;MD6zOlMzQSEQvF2= NF7wNoNUSU6JRWK=
ACN NFjuVGRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYr6XZVTUUN3ME2wMlM5PDd5IN88US=> NXPkSoxWW0GQR1XS
COLO-829 MorxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFPzOnZKSzVyPUCuN|g6PjhizszN MnrsV2FPT0WU
MEL-HO MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWH1fW5jUUN3ME2wMlQyOTd7IN88US=> NFXDb|hUSU6JRWK=
SH-4 NWnMbFF1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NY\0NnNlUUN3ME2wMlQyPDJ{IN88US=> NInC[ZhUSU6JRWK=
SK-MEL-3 NYrtRXdvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHjMcYhKSzVyPUCuOVE2PjhizszN Mn7VV2FPT0WU
A375 NXrmUJpCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHHXd4pKSzVyPUCuOlc{PTlizszN MUDTRW5ITVJ?
MMAC-SF NYrIR453T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXT5Z2NGUUN3ME2wMlY5PjF2IN88US=> MW\TRW5ITVJ?
BHT-101 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX7JR|UxRTBwN{C3NFIh|ryP MnTUV2FPT0WU
K5 M3ntTWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkG5TWM2OD1yLke2NVQ5KM7:TR?= M3XXT3NCVkeHUh?=
BV-173 Ml;3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXrJR|UxRTBwN{m2OFQh|ryP MlXxV2FPT0WU
RVH-421 M3rRfGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGfMWIpKSzVyPUCuPFY4QTZizszN M{LQVnNCVkeHUh?=
HCC2218 M4rDNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYLabnNNUUN3ME2wMlg4QDR2IN88US=> NFTWdY1USU6JRWK=
WM-115 NGjqUppIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYHJR|UxRTBwOEi2PVIh|ryP M3[4VXNCVkeHUh?=
SK-MEL-28 NYTUS2RLT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYPDeotJUUN3ME2xMlA1PTZ7IN88US=> MYjTRW5ITVJ?
COLO-679 NYXN[mVwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVK1VXVPUUN3ME2xMlExPDZ2IN88US=> NFfSe2hUSU6JRWK=
MZ7-mel NEDhO49Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWTJR|UxRTFwMUS5OlMh|ryP NWTnTnhzW0GQR1XS
SK-MEL-30 NHPadodIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVnJR|UxRTFwM{OzPFYh|ryP NV:2enAxW0GQR1XS
NCI-H209 MVvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWe2UWZUUUN3ME2xMlYxQDZizszN NWjLSlM3W0GQR1XS
HTC-C3 NVvQWZN{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGj0R2NKSzVyPUGuOlYzQTRizszN NHW0W4FUSU6JRWK=
KARPAS-45 M4LTUmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGDLNJFKSzVyPUKuNFQ6PzhizszN NEXGZ2pUSU6JRWK=
NCI-SNU-5 M3zGVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkTnTWM2OD1{LkGxPVY6KM7:TR?= MX3TRW5ITVJ?
KP-4 MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUPJR|UxRTJwM{C3PFch|ryP MXHTRW5ITVJ?
PA-1 NVXKO|h5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NULjTVk2UUN3ME2yMlczPjd|IN88US=> MkTrV2FPT0WU
HuO-3N1 MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYKzfZhyUUN3ME2yMlg4QTR4IN88US=> MUnTRW5ITVJ?
NCI-H358 NHH6VopIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NY\tTJhSUUN3ME2yMlkzOjN{IN88US=> NGDaVnRUSU6JRWK=
CTB-1 MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVPJR|UxRTNwNECxO|Yh|ryP MXXTRW5ITVJ?
697 NFfSdYJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NU[4cXZmUUN3ME2zMlU2OjZ4IN88US=> MYfTRW5ITVJ?
CP66-MEL NIjYPFZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MULJR|UxRTRwMUW5Nlch|ryP MVLTRW5ITVJ?
NB13 MkT3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUnkNY1UUUN3ME20MlQ6OTd7IN88US=> MnTnV2FPT0WU
DBTRG-05MG NVfURWR[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHn6ZVdKSzVyPUSuOVM{OjVizszN M33leXNCVkeHUh?=
A2058 MkXQS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Moe2TWM2OD12LkeyNVY1KM7:TR?= NELaVoVUSU6JRWK=
KG-1 NWrud5ZyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWjJR|UxRTRwN{O5NFgh|ryP M13sPHNCVkeHUh?=
8305C MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIX1TFNKSzVyPUWuNVg4OyEQvF2= NGq0c|hUSU6JRWK=
RPMI-7951 MmnPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnW4TWM2OD13LkiwNlg{KM7:TR?= MojIV2FPT0WU
CHL-1 MmXPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHHVRolKSzVyPUWuPVc3ODNizszN NXTE[mdIW0GQR1XS
TI-73 NF[z[FhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmXKTWM2OD14LkCwPVAzKM7:TR?= MlzmV2FPT0WU
HT-1080 NYLrUYlIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3flNmlEPTB;Nj6xNFk1PiEQvF2= MnPCV2FPT0WU
ES5 NIjmTVdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGPFfHRKSzVyPU[uNVQ6OjRizszN M{fLZXNCVkeHUh?=
8-MG-BA MoOxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlS2TWM2OD14LkG4NVI6KM7:TR?= MVTTRW5ITVJ?
NB7 MkKzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2X6cGlEPTB;Nj6yNVM4OyEQvF2= MmXkV2FPT0WU
H4 NITwZotIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX3sZXFiUUN3ME22MlIzPDl|IN88US=> NIfERohUSU6JRWK=
CAL-72 MlewS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWXKV3RHUUN3ME22MlQ2PDJ|IN88US=> MlPqV2FPT0WU
HCC1806 MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYLiXFBRUUN3ME22MlgyQTNzIN88US=> MoewV2FPT0WU
BCPAP NIX1NGpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFviXoJKSzVyPUeuNlE4PjRizszN M{TKWnNCVkeHUh?=
LB2241-RCC MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVnJR|UxRTdwM{[5NFch|ryP M4jMdXNCVkeHUh?=
COLO-741 M1H1Wmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3HiSGlEPTB;OD6wNVY4QSEQvF2= NFLpdYNUSU6JRWK=
HSC-3 M2LrUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUHKN5hQUUN3ME24MlA4ODZ6IN88US=> MnvpV2FPT0WU
SW982 Ml\KS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWq5TGpsUUN3ME24MlQyPTF4IN88US=> NWDDNoQzW0GQR1XS
GCT MoDJS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4npZWlEPTB;OD63OVMyPCEQvF2= MXjTRW5ITVJ?
KY821 Mk\oS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MU\JR|UxRTlwMEWxO|gh|ryP MX\TRW5ITVJ?
JVM-3 NUPt[5Q1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYm5NpBbUUN3ME25MlU3QTl7IN88US=> NXzwbIRIW0GQR1XS
RS4-11 NWfUUWpbT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkTVTWM2OD17Lk[wOFgh|ryP MYfTRW5ITVJ?
VA-ES-BJ NH\SfINIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmH1TWM2OD1zMD6wNVQ6KM7:TR?= NYfWR3lFW0GQR1XS
A431 NGTI[HhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkfiTWM2OD1zMD60NlEzKM7:TR?= MYHTRW5ITVJ?
LXF-289 MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoqyTWM2OD1zMD60OVgh|ryP NIXiRnZUSU6JRWK=
SK-MEL-24 M2q2emdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkPtTWM2OD1zMD64Nlc1KM7:TR?= NIriOWZUSU6JRWK=
NOS-1 MoXjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWTiSIFYUUN3ME2xNE45PDd{IN88US=> NFniW45USU6JRWK=
KNS-62 MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3WxNGlEPTB;MUGuNlQxPCEQvF2= MVjTRW5ITVJ?
SK-HEP-1 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGHuV29KSzVyPUGxMlM2OjdizszN NGPBeGZUSU6JRWK=
A3-KAW MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NV;pUZJ7UUN3ME2xNU44OTd6IN88US=> NGryTlJUSU6JRWK=
SK-LU-1 NYrCT5J3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NV\qO201UUN3ME2xNk4zPjV3IN88US=> M{f5WnNCVkeHUh?=
TYK-nu M1r2Omdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXn4cW96UUN3ME2xNk4{QTN{IN88US=> MlrJV2FPT0WU
NMC-G1 MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWDJR|UxRTF{Lk[wOlIh|ryP MUTTRW5ITVJ?
BB65-RCC NXTocJZ3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV3JR|UxRTF{LkexOlkh|ryP M1K2RXNCVkeHUh?=
QIMR-WIL MlzCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWnJR|UxRTF{Lki4N|Mh|ryP MUfTRW5ITVJ?
D-566MG M{TvNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmDtTWM2OD1zMz65OVc3KM7:TR?= M{DhN3NCVkeHUh?=
KYSE-140 NYjGdlhoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVfJR|UxRTF2LkC3OVMh|ryP NEjhZ|JUSU6JRWK=
SCC-4 NWHqXmJ2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlTaTWM2OD1zND6zN|U6KM7:TR?= NFHNXnJUSU6JRWK=
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NCI-H526 NHz3PWdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NI\qSYRKSzVyPUK1MlAxOjNizszN M3;TVXNCVkeHUh?=
IST-SL1 NEjlc3lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4fwTGlEPTB;MkWuNlc2OSEQvF2= MlXWV2FPT0WU
HH NX7BT|RkT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX;KNXFpUUN3ME2yOU4{OTl{IN88US=> NWLUNWpsW0GQR1XS
NCI-H82 NUH5UoxmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlTyTWM2OD1{NT65N|gh|ryP NUi0R3RuW0GQR1XS
SNU-449 MnK2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoG5TWM2OD1{Nz6yNFE5KM7:TR?= NUTP[ZRPW0GQR1XS
COR-L23 Mny5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1e0TmlEPTB;MkeuNlgyOyEQvF2= Mnr2V2FPT0WU
LOXIMVI M4jvdmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2LkfmlEPTB;MkeuN|Y5KM7:TR?= M1\CO3NCVkeHUh?=
GR-ST M{m0bWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVrJR|UxRTJ5Lk[3NFYh|ryP MlPNV2FPT0WU
NCI-SNU-1 NHnvVFhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXjJR|UxRTJ5Lkm0OEDPxE1? NF7jdplUSU6JRWK=
ALL-PO NFvQbnVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVf2bG9MUUN3ME2yPE4yPjB2IN88US=> NW\PfmNmW0GQR1XS
ML-2 NGLhW49Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mnn0TWM2OD1{OD6yPFE1KM7:TR?= NHnuXHlUSU6JRWK=
HOP-62 MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVPJR|UxRTJ6LkexN{DPxE1? MlrtV2FPT0WU
EGI-1 NWTxeVN3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmDkTWM2OD1{OD64PFQ2KM7:TR?= Mk\RV2FPT0WU
TCCSUP M2fXW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4rnb2lEPTB;MkiuPVI4OiEQvF2= M2S2WHNCVkeHUh?=
LB996-RCC MoPiS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2TK[GlEPTB;MkmuOVY5OiEQvF2= NULhbIhOW0GQR1XS
LCLC-97TM1 NH[1bolIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4[xWWlEPTB;M{KuNVk3PCEQvF2= MknpV2FPT0WU
NCI-H1304 MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUO1[5RjUUN3ME2zNk4{OzBzIN88US=> MWLTRW5ITVJ?
KP-N-YS Mo[3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYHWOllyUUN3ME2zNk42QTd|IN88US=> NYP2cIFvW0GQR1XS
NCI-H1770 M{LifWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnXrTWM2OD1|Mz6xOlQ5KM7:TR?= M1fJZXNCVkeHUh?=
EM-2 M3HrSWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYrVOlh3UUN3ME2zN{43PTB2IN88US=> NVr4UYNzW0GQR1XS
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ACHN M4LZSGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIHqRZpKSzVyPUOzMlg{QDVizszN NHvzVWdUSU6JRWK=
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EW-18 MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Ml;yTWM2OD1|Mz64PVcyKM7:TR?= NXXHZnlqW0GQR1XS
KGN MkTDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4XTbGlEPTB;M{WuO|I6OiEQvF2= MUTTRW5ITVJ?
U031 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWnJR|UxRTN3LkixN|Ih|ryP MWXTRW5ITVJ?
HMV-II NIHjZ4NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MULJR|UxRTN4LkC3O|Qh|ryP MkPoV2FPT0WU
L-363 NUjadoh4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXe4bFI{UUN3ME2zO{43PDV3IN88US=> NWTQfWxNW0GQR1XS
NCI-H1155 M3fyNmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVGyUIhuUUN3ME2zPE4xODF3IN88US=> MnewV2FPT0WU
NCI-H1793 MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1vZemlEPTB;M{iuNVAzPiEQvF2= M3vjUHNCVkeHUh?=
P30-OHK M2\jb2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEnPZ2pKSzVyPUO4MlE{OzJizszN M{XITXNCVkeHUh?=
AN3-CA MkPjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NH:3XnlKSzVyPUO4MlE3OTVizszN MY\TRW5ITVJ?
UACC-257 NVe1XIFIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVPJR|UxRTN6Lke5JO69VQ>? M1PlbXNCVkeHUh?=
MCF7 NFjxT41Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4rRPGlEPTB;M{muPFYzQSEQvF2= MYnTRW5ITVJ?
KP-N-YN NEL2cnNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVrJR|UxRTRyLkSyPFUh|ryP MXzTRW5ITVJ?
T98G MkO1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{D4TmlEPTB;NECuOFk2PyEQvF2= NV6yZo5xW0GQR1XS
HGC-27 NITUOXJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NW\WT3lbUUN3ME20N{4zPzRizszN MV3TRW5ITVJ?
NCI-H1092 M{\pfGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3fnT2lEPTB;NEOuNlg6PSEQvF2= MYTTRW5ITVJ?
KARPAS-299 MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmXVTWM2OD12Mz6zNFcyKM7:TR?= NXTzRmg4W0GQR1XS
LB1047-RCC M2rRSGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmHpTWM2OD12ND65PVU6KM7:TR?= MV;TRW5ITVJ?
786-0 M2LO[Wdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYXJR|UxRTR3Lk[1JO69VQ>? M372N3NCVkeHUh?=
HCC2157 M3HhNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NX3ifFhiUUN3ME20Ok4xOzV7IN88US=> NGqyNFZUSU6JRWK=
NY MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUXJR|UxRTR4LkG3O|gh|ryP MlLZV2FPT0WU
EFM-19 NFq5S3BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIP0cXRKSzVyPUS2Mlc2OzNizszN MlKwV2FPT0WU
EW-16 MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnzVTWM2OD12Nj63PFA3KM7:TR?= NIjJVVBUSU6JRWK=
UM-UC-3 NIHGSWhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoDETWM2OD12Nj64NFU6KM7:TR?= MVzTRW5ITVJ?
HT-29 NUHubVluT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV;JR|UxRTR5Lki3PVIh|ryP Mmn5V2FPT0WU
LN-405 MlfPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Ml3zTWM2OD12OD6wPFI4KM7:TR?= M1y1fHNCVkeHUh?=
NCI-H727 Mn;2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYfJR|UxRTR6Lke3NlYh|ryP Mn7RV2FPT0WU
D-502MG M4HZNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHGzNYtKSzVyPUS4Mlk3PzZizszN MXzTRW5ITVJ?
GMS-10 MlmyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoewTWM2OD12OT6yPVc1KM7:TR?= Mm\uV2FPT0WU
MEL-JUSO M1OzO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUnMVoR7UUN3ME20PU4{PDdizszN MmTJV2FPT0WU

... Click to View More Cell Line Experimental Data

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:
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
Synonyms N/A

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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

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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

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID