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 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 NYX3NYpIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHfB[YNKSzVyPUCuNFc1PTdizszN NGDHXY1USU6JRWK=
EoL-1-cell NI\Uc3dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVvJR|UxRTBwMUSxOlYh|ryP M2rUZnNCVkeHUh?=
C32 MUDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmXzTWM2OD1yLkG1NVMyKM7:TR?= NHHqR4JUSU6JRWK=
M14 NFXBfmRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXvJR|UxRTBwMkG3OVch|ryP NYjLSlBrW0GQR1XS
CP50-MEL-B MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn2xTWM2OD1yLkK5O|g1KM7:TR?= MXPTRW5ITVJ?
A101D NWi2WVhIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWnJR|UxRTBwM{K1PFkh|ryP NGW3ToFUSU6JRWK=
G-361 NH6yd5dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYHJR|UxRTBwM{S2N|ch|ryP M{LoU3NCVkeHUh?=
HT-144 NEizfmtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2i2eWlEPTB;MD6zOlMzQSEQvF2= NUnLTpBVW0GQR1XS
ACN MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mkn5TWM2OD1yLkO4OFc4KM7:TR?= NVHzZ403W0GQR1XS
COLO-829 NH3DfoJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MV;JR|UxRTBwM{i5Olgh|ryP MonxV2FPT0WU
MEL-HO NXXsTJBCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVXJR|UxRTBwNEGxO|kh|ryP NYi0XWQyW0GQR1XS
SH-4 M1\nNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUHWWVFJUUN3ME2wMlQyPDJ{IN88US=> NF;SXHhUSU6JRWK=
SK-MEL-3 M{jOeGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NV;5d5k{UUN3ME2wMlUyPTZ6IN88US=> MlrUV2FPT0WU
A375 MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3npXGlEPTB;MD62O|M2QSEQvF2= NHzBVnlUSU6JRWK=
MMAC-SF NWroblNMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3;FSGlEPTB;MD62PFYyPCEQvF2= NUHKdVM6W0GQR1XS
BHT-101 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWXsfHA3UUN3ME2wMlcxPzB{IN88US=> NXnzUphWW0GQR1XS
K5 NUDRO4ZnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVLz[oR5UUN3ME2wMlc3OTR6IN88US=> MWPTRW5ITVJ?
BV-173 MoXxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGLle4NKSzVyPUCuO|k3PDRizszN NXLRcFBtW0GQR1XS
RVH-421 M2jaUmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{T6SGlEPTB;MD64Olc6PiEQvF2= MnLjV2FPT0WU
HCC2218 MkewS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NULrfZh5UUN3ME2wMlg4QDR2IN88US=> NEjwVYVUSU6JRWK=
WM-115 MlLCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYrPUXlbUUN3ME2wMlg5Pjl{IN88US=> Ml\6V2FPT0WU
SK-MEL-28 Ml71S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXHJR|UxRTFwMES1Olkh|ryP MmDGV2FPT0WU
COLO-679 M3n1dmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVjJR|UxRTFwMUC0OlQh|ryP M3;xWHNCVkeHUh?=
MZ7-mel M4\KbGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MofmTWM2OD1zLkG0PVY{KM7:TR?= NGLLe4lUSU6JRWK=
SK-MEL-30 NYjDO25lT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mm\CTWM2OD1zLkOzN|g3KM7:TR?= MUjTRW5ITVJ?
NCI-H209 NXmy[WloT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoruTWM2OD1zLk[wPFYh|ryP NI\nb4tUSU6JRWK=
HTC-C3 MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{X0NGlEPTB;MT62OlI6PCEQvF2= M2TsfXNCVkeHUh?=
KARPAS-45 M4PhbWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYjJR|UxRTJwMES5O|gh|ryP NGDPc4FUSU6JRWK=
NCI-SNU-5 NYe3SGZPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1nafWlEPTB;Mj6xNVk3QSEQvF2= NGjlSYdUSU6JRWK=
KP-4 NXLlWWZtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2HyfmlEPTB;Mj6zNFc5PyEQvF2= M3[5WnNCVkeHUh?=
PA-1 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGLOTXdKSzVyPUKuO|I3PzNizszN M3K4b3NCVkeHUh?=
HuO-3N1 NFT3d4RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYXJR|UxRTJwOEe5OFYh|ryP NYe3ZYQ5W0GQR1XS
NCI-H358 NVXMS2RlT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXTJR|UxRTJwOUKyN|Ih|ryP NHXDcFRUSU6JRWK=
CTB-1 NXHCWVdPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVzBZWxqUUN3ME2zMlQxOTd4IN88US=> NHru[ZpUSU6JRWK=
697 NYrEV2gxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGDZWphKSzVyPUOuOVUzPjZizszN Mn7jV2FPT0WU
CP66-MEL NF\kUmFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Ml;CTWM2OD12LkG1PVI4KM7:TR?= NXXpRpE4W0GQR1XS
NB13 NVSzeJpZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NInnUYpKSzVyPUSuOFkyPzlizszN M175UHNCVkeHUh?=
DBTRG-05MG NYXFZ5BFT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUjXN29jUUN3ME20MlU{OzJ3IN88US=> NVznSpNMW0GQR1XS
A2058 M2XqOWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXfJR|UxRTRwN{KxOlQh|ryP NIHKUWxUSU6JRWK=
KG-1 MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2HzXmlEPTB;ND63N|kxQCEQvF2= NWn6cHJZW0GQR1XS
8305C NGqxTXNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUnRc4ZkUUN3ME21MlE5PzNizszN NFHBfoZUSU6JRWK=
RPMI-7951 MmqyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWXhfYhXUUN3ME21MlgxOjh|IN88US=> M4PXcHNCVkeHUh?=
CHL-1 NGn1TYRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NInDbndKSzVyPUWuPVc3ODNizszN MVLTRW5ITVJ?
TI-73 M4DFd2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUDqTJp6UUN3ME22MlAxQTB{IN88US=> NEfvPW9USU6JRWK=
HT-1080 NEDBdIFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoLJTWM2OD14LkGwPVQ3KM7:TR?= MnPvV2FPT0WU
ES5 NHXyc|lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NH7ze|FKSzVyPU[uNVQ6OjRizszN MlexV2FPT0WU
8-MG-BA M2HoS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYHJR|UxRTZwMUixNlkh|ryP MojkV2FPT0WU
NB7 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFnHNlRKSzVyPU[uNlE{PzNizszN NVjCfYxQW0GQR1XS
H4 M{jSc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWWySJBMUUN3ME22MlIzPDl|IN88US=> NY[xNI4{W0GQR1XS
CAL-72 NWr1clBoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWnzNJVqUUN3ME22MlQ2PDJ|IN88US=> NIjETWxUSU6JRWK=
HCC1806 MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUfJR|UxRTZwOEG5N|Eh|ryP NV7IemR1W0GQR1XS
BCPAP MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlHnTWM2OD15LkKxO|Y1KM7:TR?= M3\OWnNCVkeHUh?=
LB2241-RCC M3XIdGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2HvPGlEPTB;Nz6zOlkxPyEQvF2= MXTTRW5ITVJ?
COLO-741 NY\3XVAyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlfhTWM2OD16LkCxOlc6KM7:TR?= MnL1V2FPT0WU
HSC-3 M2jKN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmrOTWM2OD16LkC3NFY5KM7:TR?= M3nW[3NCVkeHUh?=
SW982 M3PiOmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M13tNWlEPTB;OD60NVUyPiEQvF2= NYrxfZhCW0GQR1XS
GCT NHXjNJFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUXJR|UxRThwN{WzNVQh|ryP Mmr4V2FPT0WU
KY821 M13SbWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGrOe4pKSzVyPUmuNFUyPzhizszN MX3TRW5ITVJ?
JVM-3 M{PUeWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWLjflVNUUN3ME25MlU3QTl7IN88US=> M3GxW3NCVkeHUh?=
RS4-11 NVnRUYRyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1P3[2lEPTB;OT62NFQ5KM7:TR?= NGHKRmVUSU6JRWK=
VA-ES-BJ MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4XsWGlEPTB;MUCuNFE1QSEQvF2= MXnTRW5ITVJ?
A431 NY\P[25pT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MortTWM2OD1zMD60NlEzKM7:TR?= NYf5R417W0GQR1XS
LXF-289 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWLJR|UxRTFyLkS1PEDPxE1? MYPTRW5ITVJ?
SK-MEL-24 MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWrJR|UxRTFyLkiyO|Qh|ryP NIfoXlZUSU6JRWK=
NOS-1 MorXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYPablFKUUN3ME2xNE45PDd{IN88US=> Mk\ZV2FPT0WU
KNS-62 MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlyyTWM2OD1zMT6yOFA1KM7:TR?= M2DueHNCVkeHUh?=
SK-HEP-1 NV3XS5Y4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXTXXHNmUUN3ME2xNU4{PTJ5IN88US=> M33VbHNCVkeHUh?=
A3-KAW MmfMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIfMd25KSzVyPUGxMlcyPzhizszN NWTPTZlDW0GQR1XS
SK-LU-1 NYPZfYpCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYfJR|UxRTF{LkK2OVUh|ryP MlnEV2FPT0WU
TYK-nu Mor2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NELKdoJKSzVyPUGyMlM6OzJizszN MUXTRW5ITVJ?
NMC-G1 MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXHGS3VpUUN3ME2xNk43ODZ{IN88US=> NIT6TWVUSU6JRWK=
BB65-RCC Mn\IS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4jmV2lEPTB;MUKuO|E3QSEQvF2= MVnTRW5ITVJ?
QIMR-WIL MkDmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXjJR|UxRTF{Lki4N|Mh|ryP MoDRV2FPT0WU
D-566MG NFLVOXlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVrJR|UxRTF|Lkm1O|Yh|ryP MXPTRW5ITVJ?
KYSE-140 M{KzVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnzvTWM2OD1zND6wO|U{KM7:TR?= MkewV2FPT0WU
SCC-4 NYrZdI5rT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NY\RVZlDUUN3ME2xOE4{OzV7IN88US=> M33tW3NCVkeHUh?=
U251 M3THeWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlrjTWM2OD1zND64OFkzKM7:TR?= NXiyTFFZW0GQR1XS
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LAMA-84 NES4blFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXrJR|UxRTF2Lkm5N|Ih|ryP MlTqV2FPT0WU
NCI-H720 NX3hcWtDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV3JR|UxRTF3LkK2PFQh|ryP MYnTRW5ITVJ?
DEL MoT0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWixd45oUUN3ME2xOU41Ojl|IN88US=> MnzTV2FPT0WU
SBC-1 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkjXTWM2OD1zNT60N|A2KM7:TR?= NH7m[2FUSU6JRWK=
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MZ2-MEL Ml;qS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHz3fndKSzVyPUG2MlA3PDZizszN MYfTRW5ITVJ?
CAL-12T MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXHTOHZwUUN3ME2xOk41QDZ{IN88US=> NGrTZ2hUSU6JRWK=
KE-37 M1;WcWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4T5T2lEPTB;MU[uPFExPyEQvF2= NEWwZVBUSU6JRWK=
LS-411N NHrOdlhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmjMTWM2OD1zNz6xNVgh|ryP M12yPHNCVkeHUh?=
NCI-H2228 NEXsZ2xIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUL4VGlqUUN3ME2xO{4{ODdzIN88US=> M4fpdHNCVkeHUh?=
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NCI-H1648 NEK4N2ZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MULJR|UxRTF5LkixPEDPxE1? MWTTRW5ITVJ?
IA-LM Mnn2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NV3QeIFJUUN3ME2xPE4{OTd{IN88US=> M3rWcnNCVkeHUh?=
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KNS-81-FD NVm2V|RTT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1;JNGlEPTB;MUmuOVg2QCEQvF2= NXjTc4ZIW0GQR1XS
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5637 MkXLS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1nqUmlEPTB;MkCuNFQ4QCEQvF2= NVjYSmExW0GQR1XS
NCI-H1755 NG[wWYNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYT2XoZ[UUN3ME2yNE41PzZ2IN88US=> MlHvV2FPT0WU
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TE-12 M33zO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlXYTWM2OD1{MD63NlAyKM7:TR?= NYrxbXAyW0GQR1XS
MOLT-4 NFWwbWtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{TFbGlEPTB;MkGuNVkyPSEQvF2= NXraUHFMW0GQR1XS
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LU-65 M2DUZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFnUbIhKSzVyPUKxMlg3OjRizszN MnTwV2FPT0WU
MS-1 M3\3emdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXTJR|UxRTJ{LkGyNFMh|ryP NYfEZoU2W0GQR1XS
LoVo M{\zOWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlO2TWM2OD1{Mj6yOFQh|ryP MWLTRW5ITVJ?
A704 MkC0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnfRTWM2OD1{Mj61NVU2KM7:TR?= M4GwNXNCVkeHUh?=
HT-1376 MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4LGeWlEPTB;MkKuOlA2QSEQvF2= NIfpcGlUSU6JRWK=
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T47D NV:2XGRST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVjhV2UyUUN3ME2yNk44QTd7IN88US=> NX;EbFZUW0GQR1XS
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LB2518-MEL NV2wVFI6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVHJR|UxRTJ|Lk[0NVIh|ryP M3L4OHNCVkeHUh?=
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SK-NEP-1 NY\PPZdkT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3fNd2lEPTB;MkSuPFc1PCEQvF2= NUnTNZpEW0GQR1XS
NCI-H526 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NX\RR|g1UUN3ME2yOU4xODJ|IN88US=> M3fwWnNCVkeHUh?=
IST-SL1 MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NX;PTVczUUN3ME2yOU4zPzVzIN88US=> NGHDcYFUSU6JRWK=
HH MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mlr5TWM2OD1{NT6zNVkzKM7:TR?= MVnTRW5ITVJ?
NCI-H82 MmfyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXvJR|UxRTJ3LkmzPEDPxE1? MmfhV2FPT0WU
SNU-449 M4Tlemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4C3NGlEPTB;MkeuNlAyQCEQvF2= NFv0N5NUSU6JRWK=
COR-L23 MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWLlSWF2UUN3ME2yO{4zQDF|IN88US=> MUHTRW5ITVJ?
LOXIMVI MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH\kSmJKSzVyPUK3MlM3QCEQvF2= MVrTRW5ITVJ?
GR-ST NI\xTndIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlTTTWM2OD1{Nz62O|A3KM7:TR?= NYHKeZlDW0GQR1XS
NCI-SNU-1 M2XLcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkTzTWM2OD1{Nz65OFQh|ryP NHLqVpVUSU6JRWK=
ALL-PO M1vkbWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MknRTWM2OD1{OD6xOlA1KM7:TR?= NHiyUI1USU6JRWK=
ML-2 MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVzJR|UxRTJ6LkK4NVQh|ryP NIq1PZBUSU6JRWK=
HOP-62 MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4nnfGlEPTB;MkiuO|E{KM7:TR?= MVnTRW5ITVJ?
EGI-1 MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NX35T5NvUUN3ME2yPE45QDR3IN88US=> MV\TRW5ITVJ?
TCCSUP NHfqZ2NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF;rRnZKSzVyPUK4MlkzPzJizszN MkD1V2FPT0WU
LB996-RCC M133R2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIjXRWpKSzVyPUK5MlU3QDJizszN MWnTRW5ITVJ?
LCLC-97TM1 NYrxWG4yT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M33KTmlEPTB;M{KuNVk3PCEQvF2= NEjwdItUSU6JRWK=
NCI-H1304 MV;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnPGTWM2OD1|Mj6zN|AyKM7:TR?= Mm\3V2FPT0WU
KP-N-YS M{\KNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlzCTWM2OD1|Mj61PVc{KM7:TR?= MYTTRW5ITVJ?
NCI-H1770 NU\o[FJjT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEi1dXBKSzVyPUOzMlE3PDhizszN MXrTRW5ITVJ?
EM-2 MofaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVK3S4NPUUN3ME2zN{43PTB2IN88US=> MoLyV2FPT0WU
ChaGo-K-1 NWXzSXNVT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoPGTWM2OD1|Mz63NlM3KM7:TR?= M2X6dHNCVkeHUh?=
ACHN NWLpO5JIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1zGWGlEPTB;M{OuPFM5PSEQvF2= MoG5V2FPT0WU
MN-60 Ml25S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYPJR|UxRTN|Lki1OFQh|ryP MoDDV2FPT0WU
EW-18 NXvOOHRbT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkPqTWM2OD1|Mz64PVcyKM7:TR?= NVTFcWxtW0GQR1XS
KGN M{HQTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Ml;HTWM2OD1|NT63NlkzKM7:TR?= NVzndnJTW0GQR1XS
U031 MorRS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWLVemxOUUN3ME2zOU45OTN{IN88US=> MXLTRW5ITVJ?
HMV-II MmHhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NV7pVY06UUN3ME2zOk4xPzd2IN88US=> NGr1blRUSU6JRWK=
L-363 MnLlS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NITXdo9KSzVyPUO3MlY1PTVizszN M1vDdHNCVkeHUh?=
NCI-H1155 MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYnLUVI2UUN3ME2zPE4xODF3IN88US=> NFOxe2ZUSU6JRWK=
NCI-H1793 NH6zeotIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmfPTWM2OD1|OD6xNFI3KM7:TR?= MWrTRW5ITVJ?
P30-OHK M4PV[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlHzTWM2OD1|OD6xN|MzKM7:TR?= M3zxW3NCVkeHUh?=
AN3-CA MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1:2NGlEPTB;M{iuNVYyPSEQvF2= M1fubHNCVkeHUh?=
UACC-257 NEPiepZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoKyTWM2OD1|OD63PUDPxE1? M3G4XXNCVkeHUh?=
MCF7 NELQ[IxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGXKdYNKSzVyPUO5Mlg3OjlizszN NVnkcFF4W0GQR1XS
KP-N-YN MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmnqTWM2OD12MD60Nlg2KM7:TR?= M3jhfXNCVkeHUh?=
T98G NXXxUpk1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoflTWM2OD12MD60PVU4KM7:TR?= MXzTRW5ITVJ?
HGC-27 MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mmf3TWM2OD12Mz6yO|Qh|ryP MWrTRW5ITVJ?
NCI-H1092 NIPx[IhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF;sVIlKSzVyPUSzMlI5QTVizszN NFXtNpNUSU6JRWK=
KARPAS-299 NUnNb5NIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MUTJR|UxRTR|LkOwO|Eh|ryP NVzsbJl{W0GQR1XS
LB1047-RCC Mn7mS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXHJR|UxRTR2Lkm5OVkh|ryP M{HkNHNCVkeHUh?=
786-0 M17KR2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXvJR|UxRTR3Lk[1JO69VQ>? M3XmU3NCVkeHUh?=
HCC2157 NF6yTHVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHnO[VlKSzVyPUS2MlA{PTlizszN NV\GTG5tW0GQR1XS
NY NWn4bpVpT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGnqdFBKSzVyPUS2MlE4PzhizszN MmXhV2FPT0WU
EFM-19 NGLVTmtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnTuTWM2OD12Nj63OVM{KM7:TR?= M2jzTXNCVkeHUh?=
EW-16 NIe4dG1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2fYOWlEPTB;NE[uO|gxPiEQvF2= MWnTRW5ITVJ?
UM-UC-3 MoW0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1nTVGlEPTB;NE[uPFA2QSEQvF2= MkXLV2FPT0WU
HT-29 MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mny3TWM2OD12Nz64O|kzKM7:TR?= NYnPcppNW0GQR1XS
LN-405 MoTJS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIq3WppKSzVyPUS4MlA5OjdizszN MWDTRW5ITVJ?
NCI-H727 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXTJR|UxRTR6Lke3NlYh|ryP MYPTRW5ITVJ?
D-502MG Mmi5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmfETWM2OD12OD65Olc3KM7:TR?= Mkm2V2FPT0WU
GMS-10 Ml3nS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHPnUlhKSzVyPUS5MlI6PzRizszN MknWV2FPT0WU
MEL-JUSO NEC0TGNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWjPeYRSUUN3ME20PU4{PDdizszN MWfTRW5ITVJ?

... 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

Bio Calculators

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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

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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.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID