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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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.

    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 Mm\oS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NV:zVFJOUUN3ME2wMlA4PDV5IN88US=> Mmm0V2FPT0WU
EoL-1-cell NVXvcFhOT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mki5TWM2OD1yLkG0NVY3KM7:TR?= MnvhV2FPT0WU
C32 M{LCUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGHGU4JKSzVyPUCuNVUyOzFizszN NYHWT48zW0GQR1XS
M14 MkLhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIXiUnlKSzVyPUCuNlE4PTdizszN MnLWV2FPT0WU
CP50-MEL-B MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUjwXpl3UUN3ME2wMlI6Pzh2IN88US=> NXLFSpIyW0GQR1XS
A101D M3;le2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYnJR|UxRTBwM{K1PFkh|ryP MYLTRW5ITVJ?
G-361 NYjFdmJyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGOxe5pKSzVyPUCuN|Q3OzdizszN MWXTRW5ITVJ?
HT-144 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXfJR|UxRTBwM{[zNlkh|ryP MkHOV2FPT0WU
ACN NUj1O5I{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXHJR|UxRTBwM{i0O|ch|ryP MnHDV2FPT0WU
COLO-829 MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFPxWndKSzVyPUCuN|g6PjhizszN MlHqV2FPT0WU
MEL-HO M1LJb2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NV65bmdHUUN3ME2wMlQyOTd7IN88US=> MkPzV2FPT0WU
SH-4 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEO0[5hKSzVyPUCuOFE1OjJizszN NIfQNIxUSU6JRWK=
SK-MEL-3 MnfYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVPJR|UxRTBwNUG1Olgh|ryP MnzHV2FPT0WU
A375 MV;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGjoOWVKSzVyPUCuOlc{PTlizszN M4S5NXNCVkeHUh?=
MMAC-SF M3f4UGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHTDW2hKSzVyPUCuOlg3OTRizszN MXjTRW5ITVJ?
BHT-101 NUXybFBtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MX\JR|UxRTBwN{C3NFIh|ryP NY\TelFKW0GQR1XS
K5 NULhb2FjT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mm\4TWM2OD1yLke2NVQ5KM7:TR?= MWfTRW5ITVJ?
BV-173 NUHh[GUzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkS3TWM2OD1yLke5OlQ1KM7:TR?= M{W5bXNCVkeHUh?=
RVH-421 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYLuOGtYUUN3ME2wMlg3Pzl4IN88US=> M1e1RnNCVkeHUh?=
HCC2218 M370c2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXns[GkyUUN3ME2wMlg4QDR2IN88US=> NEjEbYxUSU6JRWK=
WM-115 M1;3[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4LQ[WlEPTB;MD64PFY6OiEQvF2= NWPIe3EzW0GQR1XS
SK-MEL-28 MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXjBNppWUUN3ME2xMlA1PTZ7IN88US=> MkLVV2FPT0WU
COLO-679 MnTnS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWnJR|UxRTFwMUC0OlQh|ryP MkTqV2FPT0WU
MZ7-mel MkjpS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIr0VWxKSzVyPUGuNVQ6PjNizszN MkXUV2FPT0WU
SK-MEL-30 M37ENWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MV3JR|UxRTFwM{OzPFYh|ryP NFzjPHNUSU6JRWK=
NCI-H209 NUP2UmxWT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVjLSoFbUUN3ME2xMlYxQDZizszN M2\pfHNCVkeHUh?=
HTC-C3 NXrNZZZLT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkHOTWM2OD1zLk[2Nlk1KM7:TR?= MoXiV2FPT0WU
KARPAS-45 M4r6T2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn3lTWM2OD1{LkC0PVc5KM7:TR?= M3HvcnNCVkeHUh?=
NCI-SNU-5 M{LLVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3[5e2lEPTB;Mj6xNVk3QSEQvF2= MXHTRW5ITVJ?
KP-4 MlzPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHe1R3pKSzVyPUKuN|A4QDdizszN Mne1V2FPT0WU
PA-1 MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NITEcZdKSzVyPUKuO|I3PzNizszN MVfTRW5ITVJ?
HuO-3N1 MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2TqTmlEPTB;Mj64O|k1PiEQvF2= NXjzeoVmW0GQR1XS
NCI-H358 NXHmdJpGT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFS4bZBKSzVyPUKuPVIzOzJizszN NE\xdpZUSU6JRWK=
CTB-1 M{LPPGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUXlXYp7UUN3ME2zMlQxOTd4IN88US=> NEHxSIhUSU6JRWK=
697 MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWDJR|UxRTNwNUWyOlYh|ryP NVezUXNHW0GQR1XS
CP66-MEL NVjWdoNST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXzJR|UxRTRwMUW5Nlch|ryP MnLLV2FPT0WU
NB13 MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4Xzd2lEPTB;ND60PVE4QSEQvF2= MkHQV2FPT0WU
DBTRG-05MG MkLsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkXqTWM2OD12LkWzN|I2KM7:TR?= NXzEUGlrW0GQR1XS
A2058 NYHnSHp2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3jNUmlEPTB;ND63NlE3PCEQvF2= NFXwNXpUSU6JRWK=
KG-1 MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHzJTHhKSzVyPUSuO|M6ODhizszN MXjTRW5ITVJ?
8305C NVHa[286T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFzBUXZKSzVyPUWuNVg4OyEQvF2= MULTRW5ITVJ?
RPMI-7951 NGPvO3NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWm3Z2k4UUN3ME21MlgxOjh|IN88US=> MV;TRW5ITVJ?
CHL-1 NFzRdXpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYf6ZZdQUUN3ME21Mlk4PjB|IN88US=> NGrYeZVUSU6JRWK=
TI-73 M2jWbWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2DXVmlEPTB;Nj6wNFkxOiEQvF2= MX3TRW5ITVJ?
HT-1080 NUT1U|NHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1TWW2lEPTB;Nj6xNFk1PiEQvF2= MW\TRW5ITVJ?
ES5 MojjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXLJR|UxRTZwMUS5NlQh|ryP NYXsVY91W0GQR1XS
8-MG-BA NIPKelhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVnJR|UxRTZwMUixNlkh|ryP NWPqUIEyW0GQR1XS
NB7 M2HXZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MV3JR|UxRTZwMkGzO|Mh|ryP M{\RVHNCVkeHUh?=
H4 NV\BfVhPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHHQNFZKSzVyPU[uNlI1QTNizszN NUW3e|AyW0GQR1XS
CAL-72 M1nyNmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mnn2TWM2OD14LkS1OFI{KM7:TR?= NWrLNlZYW0GQR1XS
HCC1806 M4jobmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFzTdopKSzVyPU[uPFE6OzFizszN NFrLbndUSU6JRWK=
BCPAP NXGweHF4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2jRSWlEPTB;Nz6yNVc3PCEQvF2= M3;RWHNCVkeHUh?=
LB2241-RCC MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3;WSWlEPTB;Nz6zOlkxPyEQvF2= MVnTRW5ITVJ?
COLO-741 MoD0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnTiTWM2OD16LkCxOlc6KM7:TR?= NWf3cHM3W0GQR1XS
HSC-3 MlrsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFrFUW9KSzVyPUiuNFcxPjhizszN Mn3hV2FPT0WU
SW982 M1q1N2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFjSPZFKSzVyPUiuOFE2OTZizszN MXjTRW5ITVJ?
GCT M2K2c2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4TJRWlEPTB;OD63OVMyPCEQvF2= M2Hhe3NCVkeHUh?=
KY821 M3q4Smdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYPPV5IxUUN3ME25MlA2OTd6IN88US=> NIrlfIdUSU6JRWK=
JVM-3 M1;xWGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{\WZmlEPTB;OT61Olk6QSEQvF2= MXXTRW5ITVJ?
RS4-11 MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGPscI9KSzVyPUmuOlA1QCEQvF2= NUfEU2s{W0GQR1XS
VA-ES-BJ MkXDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NV\FS4s2UUN3ME2xNE4xOTR7IN88US=> NXzJXmlqW0GQR1XS
A431 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGOwV5RKSzVyPUGwMlQzOTJizszN NWTzWHd3W0GQR1XS
LXF-289 M3XaWWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1Pr[2lEPTB;MUCuOFU5KM7:TR?= NYHHeXV6W0GQR1XS
SK-MEL-24 NIPPeHVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVrJR|UxRTFyLkiyO|Qh|ryP MlrIV2FPT0WU
NOS-1 M4DUV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NITWWIlKSzVyPUGwMlg1PzJizszN NEjvUotUSU6JRWK=
KNS-62 NYHJ[nh1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkDTTWM2OD1zMT6yOFA1KM7:TR?= NX6xTmhVW0GQR1XS
SK-HEP-1 MnLOS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkHETWM2OD1zMT6zOVI4KM7:TR?= M4W2b3NCVkeHUh?=
A3-KAW NGH3fpdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVPJR|UxRTFzLkexO|gh|ryP M3vSZXNCVkeHUh?=
SK-LU-1 M3rKWmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlXkTWM2OD1zMj6yOlU2KM7:TR?= MW\TRW5ITVJ?
TYK-nu NV3zV2MxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEXwXG1KSzVyPUGyMlM6OzJizszN MnLHV2FPT0WU
NMC-G1 Mki5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4PW[GlEPTB;MUKuOlA3OiEQvF2= MWLTRW5ITVJ?
BB65-RCC MlewS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVHJR|UxRTF{LkexOlkh|ryP MXTTRW5ITVJ?
QIMR-WIL NWPlN2dRT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVTJR|UxRTF{Lki4N|Mh|ryP MYHTRW5ITVJ?
D-566MG NGi2TnZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mn;QTWM2OD1zMz65OVc3KM7:TR?= MnvNV2FPT0WU
KYSE-140 M2\Mcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn;CTWM2OD1zND6wO|U{KM7:TR?= M2TVVHNCVkeHUh?=
SCC-4 NIDMUFVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{POVmlEPTB;MUSuN|M2QSEQvF2= MoDZV2FPT0WU
U251 M1[5fmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1\ydGlEPTB;MUSuPFQ6OiEQvF2= NVTCPWhiW0GQR1XS
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IA-LM NF6zWoNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1vjSWlEPTB;MUiuN|E4OiEQvF2= NIDYfZZUSU6JRWK=
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NCI-H526 M2DPbGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUXGOG1lUUN3ME2yOU4xODJ|IN88US=> NYS2VnBtW0GQR1XS
IST-SL1 M1jEWGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXzJR|UxRTJ3LkK3OVEh|ryP MkPvV2FPT0WU
HH M3TDcWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYfm[HJFUUN3ME2yOU4{OTl{IN88US=> MnrUV2FPT0WU
NCI-H82 NVLqeHN6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF\aclRKSzVyPUK1Mlk{QCEQvF2= NXG0S3hpW0GQR1XS
SNU-449 M1fjNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIj0boNKSzVyPUK3MlIxOThizszN NYnxNIpSW0GQR1XS
COR-L23 M17sUmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1HJT2lEPTB;MkeuNlgyOyEQvF2= MlnMV2FPT0WU
LOXIMVI Moq4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIWzcVZKSzVyPUK3MlM3QCEQvF2= NXfHZmNCW0GQR1XS
GR-ST NX;ZcXRUT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkPDTWM2OD1{Nz62O|A3KM7:TR?= NUH3R2FHW0GQR1XS
NCI-SNU-1 NWrMVJNIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXfJR|UxRTJ5Lkm0OEDPxE1? MX;TRW5ITVJ?
ALL-PO MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXq3UHpCUUN3ME2yPE4yPjB2IN88US=> MljXV2FPT0WU
ML-2 M3;BUmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2rvZ2lEPTB;MkiuNlgyPCEQvF2= MVfTRW5ITVJ?
HOP-62 NUHHd5JnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXXpUmFOUUN3ME2yPE44OTNizszN NV;SN5pPW0GQR1XS
EGI-1 NIr1dGNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnzrTWM2OD1{OD64PFQ2KM7:TR?= M{jqeHNCVkeHUh?=
TCCSUP NWTiVmNpT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXrNOpVnUUN3ME2yPE46Ojd{IN88US=> M3H1[XNCVkeHUh?=
LB996-RCC MWDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUm4TXhIUUN3ME2yPU42Pjh{IN88US=> MXzTRW5ITVJ?
LCLC-97TM1 NVTIO4VkT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{\OfGlEPTB;M{KuNVk3PCEQvF2= NYrJbmo6W0GQR1XS
NCI-H1304 Mn\hS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYDJe5pyUUN3ME2zNk4{OzBzIN88US=> M4XUWXNCVkeHUh?=
KP-N-YS MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX7JR|UxRTN{LkW5O|Mh|ryP NY[1N4pLW0GQR1XS
NCI-H1770 NYD1NpI6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mkf4TWM2OD1|Mz6xOlQ5KM7:TR?= NVjqTVlbW0GQR1XS
EM-2 NYO2T5lET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYn1SW03UUN3ME2zN{43PTB2IN88US=> NXHQbY9FW0GQR1XS
ChaGo-K-1 NVHtNWxsT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3fCc2lEPTB;M{OuO|I{PiEQvF2= MlSzV2FPT0WU
ACHN NWfjNHh{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3rBfWlEPTB;M{OuPFM5PSEQvF2= MlHSV2FPT0WU
MN-60 NIjKcZZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXTJR|UxRTN|Lki1OFQh|ryP M3;1RXNCVkeHUh?=
EW-18 NVj5O25QT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4TScWlEPTB;M{OuPFk4OSEQvF2= NILIWIFUSU6JRWK=
KGN M4jlXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MX\JR|UxRTN3LkeyPVIh|ryP NFjMPIZUSU6JRWK=
U031 MmXVS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MW\JR|UxRTN3LkixN|Ih|ryP MVvTRW5ITVJ?
HMV-II NXfyTW5ST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYHJR|UxRTN4LkC3O|Qh|ryP MnvFV2FPT0WU
L-363 MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkLrTWM2OD1|Nz62OFU2KM7:TR?= NYjXfWdyW0GQR1XS
NCI-H1155 NVzWOnRHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVvJR|UxRTN6LkCwNVUh|ryP MWDTRW5ITVJ?
NCI-H1793 MnnWS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{TuRWlEPTB;M{iuNVAzPiEQvF2= NV7sWWxVW0GQR1XS
P30-OHK NYnyU4d[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3TCUmlEPTB;M{iuNVM{OiEQvF2= NV3BT|BpW0GQR1XS
AN3-CA MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{KwRmlEPTB;M{iuNVYyPSEQvF2= NEDKU2RUSU6JRWK=
UACC-257 M3vHNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{nibmlEPTB;M{iuO|kh|ryP MoTrV2FPT0WU
MCF7 MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4frSGlEPTB;M{muPFYzQSEQvF2= NEP6OnpUSU6JRWK=
KP-N-YN NFPPUFVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHHYWXVKSzVyPUSwMlQzQDVizszN NEPveopUSU6JRWK=
T98G M1jKS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkPkTWM2OD12MD60PVU4KM7:TR?= NYjvVVF7W0GQR1XS
HGC-27 MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVnJR|UxRTR|LkK3OEDPxE1? NV;0Z2NbW0GQR1XS
NCI-H1092 NV\TOXZ4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF\Z[YtKSzVyPUSzMlI5QTVizszN Mn[3V2FPT0WU
KARPAS-299 NGLwfVJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnXGTWM2OD12Mz6zNFcyKM7:TR?= MWjTRW5ITVJ?
LB1047-RCC NWDBVVE4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXXJR|UxRTR2Lkm5OVkh|ryP NUXubIlHW0GQR1XS
786-0 M{WxUmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWKySWlCUUN3ME20OU43PSEQvF2= Mn;1V2FPT0WU
HCC2157 Ml\DS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MV;JR|UxRTR4LkCzOVkh|ryP M4jNRnNCVkeHUh?=
NY NY\EVJJzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGnuS29KSzVyPUS2MlE4PzhizszN M4DobXNCVkeHUh?=
EFM-19 Mn61S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2r1fWlEPTB;NE[uO|U{OyEQvF2= NFXSZopUSU6JRWK=
EW-16 MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWTkSIFQUUN3ME20Ok44QDB4IN88US=> NFT2So1USU6JRWK=
UM-UC-3 NHPMbJFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHXrN41KSzVyPUS2MlgxPTlizszN NWXPU5ZwW0GQR1XS
HT-29 MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWTJR|UxRTR5Lki3PVIh|ryP NVH1PXprW0GQR1XS
LN-405 Moq2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M33oWWlEPTB;NEiuNFgzPyEQvF2= MnPSV2FPT0WU
NCI-H727 NX7P[YJ4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkLITWM2OD12OD63O|I3KM7:TR?= NEDvbIVUSU6JRWK=
D-502MG NX7Vb3pxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXvhc|RGUUN3ME20PE46Pjd4IN88US=> MnTMV2FPT0WU
GMS-10 NIrRbJFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWrKN|hVUUN3ME20PU4zQTd2IN88US=> NFWwcnFUSU6JRWK=
MEL-JUSO MV;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWfJR|UxRTR7LkO0O{DPxE1? NWL5VGhCW0GQR1XS

... 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(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

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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

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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