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 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 M1j0V2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmeyTWM2OD1yLkC3OFU4KM7:TR?= MUjTRW5ITVJ?
EoL-1-cell Ml\kS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFrxXlhKSzVyPUCuNVQyPjZizszN MXnTRW5ITVJ?
C32 M2P1ZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYfJR|UxRTBwMUWxN|Eh|ryP MnHnV2FPT0WU
M14 MmrmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYHNeoh3UUN3ME2wMlIyPzV5IN88US=> NVHQRlkzW0GQR1XS
CP50-MEL-B M2[4RWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGLUUYRKSzVyPUCuNlk4QDRizszN NXLiem1MW0GQR1XS
A101D MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmTJTWM2OD1yLkOyOVg6KM7:TR?= NF2zSGtUSU6JRWK=
G-361 MlHhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWDjNW1nUUN3ME2wMlM1PjN5IN88US=> NVHRbVBzW0GQR1XS
HT-144 M2jPR2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFvpbnNKSzVyPUCuN|Y{OjlizszN NWLPVpFVW0GQR1XS
ACN NEnaNGpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEDjUnBKSzVyPUCuN|g1PzdizszN MlnxV2FPT0WU
COLO-829 NXL2PZNxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYSx[ZlKUUN3ME2wMlM5QTZ6IN88US=> M2D3SXNCVkeHUh?=
MEL-HO NWewPGlYT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYrTclNTUUN3ME2wMlQyOTd7IN88US=> Mn:xV2FPT0WU
SH-4 NHXy[2JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NY\W[plRUUN3ME2wMlQyPDJ{IN88US=> MV;TRW5ITVJ?
SK-MEL-3 NYO0O2Z5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVvMOmp2UUN3ME2wMlUyPTZ6IN88US=> NYXhPGNGW0GQR1XS
A375 NV\Mflh4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHTCS3FKSzVyPUCuOlc{PTlizszN MVrTRW5ITVJ?
MMAC-SF MnPmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXrzOlRMUUN3ME2wMlY5PjF2IN88US=> MUjTRW5ITVJ?
BHT-101 NGXjfpBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVvJR|UxRTBwN{C3NFIh|ryP M1rHPHNCVkeHUh?=
K5 NXPMOFc6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEThSVRKSzVyPUCuO|YyPDhizszN MkSxV2FPT0WU
BV-173 MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWrJR|UxRTBwN{m2OFQh|ryP NH;hSIRUSU6JRWK=
RVH-421 MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFTWXY5KSzVyPUCuPFY4QTZizszN MV;TRW5ITVJ?
HCC2218 M4DXW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXHJR|UxRTBwOEe4OFQh|ryP NIjPbZZUSU6JRWK=
WM-115 MmTrS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHy0O5BKSzVyPUCuPFg3QTJizszN MoT3V2FPT0WU
SK-MEL-28 NW[zV49oT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1zwSGlEPTB;MT6wOFU3QSEQvF2= MXfTRW5ITVJ?
COLO-679 MmHHS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUfGSFhjUUN3ME2xMlExPDZ2IN88US=> M3nx[XNCVkeHUh?=
MZ7-mel M4\C[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NX7lZXlxUUN3ME2xMlE1QTZ|IN88US=> M1zlVnNCVkeHUh?=
SK-MEL-30 MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXGycXo3UUN3ME2xMlM{Ozh4IN88US=> MWDTRW5ITVJ?
NCI-H209 NH\X[mlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIjDPHFKSzVyPUGuOlA5PiEQvF2= MnzKV2FPT0WU
HTC-C3 MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXzjWZJYUUN3ME2xMlY3Ojl2IN88US=> MUfTRW5ITVJ?
KARPAS-45 MlqyS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWLOfXdrUUN3ME2yMlA1QTd6IN88US=> NVLoS3R2W0GQR1XS
NCI-SNU-5 Mmj2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVzWOpRCUUN3ME2yMlEyQTZ7IN88US=> Mn3zV2FPT0WU
KP-4 MmewS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXHJR|UxRTJwM{C3PFch|ryP NIrYdlFUSU6JRWK=
PA-1 NFLCb45Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3;PdWlEPTB;Mj63NlY4OyEQvF2= NVHUeldCW0GQR1XS
HuO-3N1 MlrLS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXPwe4VOUUN3ME2yMlg4QTR4IN88US=> MoTnV2FPT0WU
NCI-H358 NYqxNlFuT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{HaXmlEPTB;Mj65NlI{OiEQvF2= MmLaV2FPT0WU
CTB-1 M1vxeWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVnJR|UxRTNwNECxO|Yh|ryP MVXTRW5ITVJ?
697 NYnLPW41T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2nOUmlEPTB;Mz61OVI3PiEQvF2= M{Lt[3NCVkeHUh?=
CP66-MEL MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWPvSGF1UUN3ME20MlE2QTJ5IN88US=> M1[1TXNCVkeHUh?=
NB13 M1H1S2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYDJR|UxRTRwNEmxO|kh|ryP NEjWS5RUSU6JRWK=
DBTRG-05MG NXywTHNxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYf3SYNLUUN3ME20MlU{OzJ3IN88US=> MlX5V2FPT0WU
A2058 MlL0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnzHTWM2OD12LkeyNVY1KM7:TR?= NXrVN2xZW0GQR1XS
KG-1 MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3yzO2lEPTB;ND63N|kxQCEQvF2= MmTxV2FPT0WU
8305C M1\T[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NX7CXWVWUUN3ME21MlE5PzNizszN MmS3V2FPT0WU
RPMI-7951 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWi0So5jUUN3ME21MlgxOjh|IN88US=> M161SnNCVkeHUh?=
CHL-1 M2m1UGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGn0[ZpKSzVyPUWuPVc3ODNizszN NVXYS5J{W0GQR1XS
TI-73 NHzhcHZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVPJR|UxRTZwMEC5NFIh|ryP M3\senNCVkeHUh?=
HT-1080 NIHs[GFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWHJR|UxRTZwMUC5OFYh|ryP NUjTe3hCW0GQR1XS
ES5 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1zLTGlEPTB;Nj6xOFkzPCEQvF2= NH3xSotUSU6JRWK=
8-MG-BA NH\GWYZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYC1fmluUUN3ME22MlE5OTJ7IN88US=> NYLlVpVuW0GQR1XS
NB7 Mo\DS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXTJR|UxRTZwMkGzO|Mh|ryP M{fmSnNCVkeHUh?=
H4 NEnubm1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXvJR|UxRTZwMkK0PVMh|ryP NXTaTZkyW0GQR1XS
CAL-72 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4\GZWlEPTB;Nj60OVQzOyEQvF2= MXfTRW5ITVJ?
HCC1806 NIL5[5JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYHkfpRDUUN3ME22MlgyQTNzIN88US=> MUjTRW5ITVJ?
BCPAP NV3LV4dtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYPJR|UxRTdwMkG3OlQh|ryP NWX6XFZTW0GQR1XS
LB2241-RCC MoHxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUPPU252UUN3ME23MlM3QTB5IN88US=> MmLNV2FPT0WU
COLO-741 NVvjOGlET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3TTUWlEPTB;OD6wNVY4QSEQvF2= M1jLUXNCVkeHUh?=
HSC-3 NXXpcnNpT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlO4TWM2OD16LkC3NFY5KM7:TR?= MlzUV2FPT0WU
SW982 MmnZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX63XZQ{UUN3ME24MlQyPTF4IN88US=> MYnTRW5ITVJ?
GCT MnHTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mn76TWM2OD16Lke1N|E1KM7:TR?= M3q4O3NCVkeHUh?=
KY821 MmHqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MULJR|UxRTlwMEWxO|gh|ryP M1v3WXNCVkeHUh?=
JVM-3 M3PEWmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1v1PGlEPTB;OT61Olk6QSEQvF2= MXXTRW5ITVJ?
RS4-11 NXrre4N3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWfJR|UxRTlwNkC0PEDPxE1? MmHDV2FPT0WU
VA-ES-BJ NEnwdWdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NE\vUWhKSzVyPUGwMlAyPDlizszN NY\odGJpW0GQR1XS
A431 MkPtS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUXsVVVzUUN3ME2xNE41OjF{IN88US=> NEX6[2pUSU6JRWK=
LXF-289 MlfBS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlrJTWM2OD1zMD60OVgh|ryP MlzvV2FPT0WU
SK-MEL-24 M{fITmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3LrNmlEPTB;MUCuPFI4PCEQvF2= NHHTe21USU6JRWK=
NOS-1 NXfkXWtHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWnJR|UxRTFyLki0O|Ih|ryP M2H3cnNCVkeHUh?=
KNS-62 M1vRc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYT5XmJsUUN3ME2xNU4zPDB2IN88US=> NGjN[pBUSU6JRWK=
SK-HEP-1 Mk\BS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXO5[W5HUUN3ME2xNU4{PTJ5IN88US=> NUnlTYdoW0GQR1XS
A3-KAW MoLsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1PhPGlEPTB;MUGuO|E4QCEQvF2= NF;ZfldUSU6JRWK=
SK-LU-1 MoTGS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYLZe5prUUN3ME2xNk4zPjV3IN88US=> NWfXOXp7W0GQR1XS
TYK-nu M{[yemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHzzTWNKSzVyPUGyMlM6OzJizszN NHfOcVhUSU6JRWK=
NMC-G1 NX7LTVFVT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEXDSHZKSzVyPUGyMlYxPjJizszN MmrLV2FPT0WU
BB65-RCC M{LTSGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGq5cYxKSzVyPUGyMlcyPjlizszN NEL2b4FUSU6JRWK=
QIMR-WIL NV[1[JBTT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmPnTWM2OD1zMj64PFM{KM7:TR?= MnOyV2FPT0WU
D-566MG NYqzbWRbT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3\4e2lEPTB;MUOuPVU4PiEQvF2= NWC3WVd1W0GQR1XS
KYSE-140 NULJNWE4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEjlOGtKSzVyPUG0MlA4PTNizszN NV3wOHNbW0GQR1XS
SCC-4 MoPGS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NH7CRmtKSzVyPUG0MlM{PTlizszN MU\TRW5ITVJ?
U251 MlLtS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXnZOmV5UUN3ME2xOE45PDl{IN88US=> MnfSV2FPT0WU
D-542MG M{TZZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{\NZWlEPTB;MUSuPVIzOiEQvF2= NVjOdIF{W0GQR1XS
LAMA-84 M{TqSmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIe2c5FKSzVyPUG0Mlk6OzJizszN M3nyfnNCVkeHUh?=
NCI-H720 NVHtOo9{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmDNTWM2OD1zNT6yOlg1KM7:TR?= MULTRW5ITVJ?
DEL M3jr[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWDTRmhNUUN3ME2xOU41Ojl|IN88US=> M1u0PHNCVkeHUh?=
SBC-1 M{f6cWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGT6W4FKSzVyPUG1MlQ{ODVizszN M{TVTHNCVkeHUh?=
ECC10 MoHKS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYjJR|UxRTF3LkS0OVgh|ryP MXjTRW5ITVJ?
Daoy NG\IR4dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2Dib2lEPTB;MUWuO|YyPiEQvF2= Mmf1V2FPT0WU
SCH NHXTe3BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M17iSmlEPTB;MUWuO|g{PSEQvF2= MWnTRW5ITVJ?
MZ2-MEL MWDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYHJR|UxRTF4LkC2OFYh|ryP M{Dib3NCVkeHUh?=
CAL-12T NIW2TFJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFrPNnBKSzVyPUG2MlQ5PjJizszN NH3pWXdUSU6JRWK=
KE-37 M1LUfGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2jvVGlEPTB;MU[uPFExPyEQvF2= NVS5bGJtW0GQR1XS
LS-411N M2rmT2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEHMTlZKSzVyPUG3MlEyQCEQvF2= Mn;RV2FPT0WU
NCI-H2228 MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MV;JR|UxRTF5LkOwO|Eh|ryP MXjTRW5ITVJ?
SK-MEL-2 M2jm[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlXWTWM2OD1zNz60PVY2KM7:TR?= NH2zPVVUSU6JRWK=
HN M{\DcWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkezTWM2OD1zNz63NlQ5KM7:TR?= MWrTRW5ITVJ?
NCI-H1648 MonwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Ml7sTWM2OD1zNz64NVgh|ryP NXrZe4tzW0GQR1XS
IA-LM MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXvLOlMyUUN3ME2xPE4{OTd{IN88US=> Mnr2V2FPT0WU
EW-13 MkLlS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYrJR|UxRTF6LkW3NFgh|ryP NYnifWQ1W0GQR1XS
YKG-1 MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3P0OmlEPTB;MUmuOVcyOSEQvF2= MoPhV2FPT0WU
KNS-81-FD M4nZdGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NILCcmxKSzVyPUG5MlU5PThizszN NGDoSJpUSU6JRWK=
23132-87 MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NF7KVphKSzVyPUG5Mlc3PDJizszN MlmxV2FPT0WU
NUGC-3 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGrvW5hKSzVyPUG5Mlk5QDdizszN MlTXV2FPT0WU
5637 NELkSGNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmS0TWM2OD1{MD6wOFc5KM7:TR?= M1zO[HNCVkeHUh?=
NCI-H1755 NXXofHliT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoXPTWM2OD1{MD60O|Y1KM7:TR?= NITP[2FUSU6JRWK=
RH-18 M2nteGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1nBbGlEPTB;MkCuOVc1QCEQvF2= MWDTRW5ITVJ?
RXF393 NETCcGdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYrJR|UxRTJyLk[3OVYh|ryP NUGxTW03W0GQR1XS
LU-134-A M2W3[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{OxWWlEPTB;MkCuO|A2PiEQvF2= M33jTXNCVkeHUh?=
TE-12 MlmzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF\CUYtKSzVyPUKwMlczODFizszN NInwfppUSU6JRWK=
MOLT-4 NFnLW2JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1ywNGlEPTB;MkGuNVkyPSEQvF2= NUXSUphGW0GQR1XS
IGR-1 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoPWTWM2OD1{MT6zO|k3KM7:TR?= M13lWXNCVkeHUh?=
HOP-92 Mn7JS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1LDWGlEPTB;MkGuOFk5PyEQvF2= M1rr[XNCVkeHUh?=
SK-MES-1 MoPhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmXGTWM2OD1{MT63N|gyKM7:TR?= M3vWUXNCVkeHUh?=
LU-65 NHPuU2dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmnpTWM2OD1{MT64OlI1KM7:TR?= NFvTWIVUSU6JRWK=
MS-1 MmD6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYH0R3pZUUN3ME2yNk4yOjB|IN88US=> NETiWYJUSU6JRWK=
LoVo NE[ydJhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYfOOHFQUUN3ME2yNk4zPDRizszN MonIV2FPT0WU
A704 NXjwOoZFT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnfuTWM2OD1{Mj61NVU2KM7:TR?= NV\TSmVoW0GQR1XS
HT-1376 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH\UN4xKSzVyPUKyMlYxPTlizszN MmTlV2FPT0WU
IST-MEL1 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEe3ZmhKSzVyPUKyMlY4PTFizszN NX71XplFW0GQR1XS
Ramos-2G6-4C10 NGrwXGxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVPZbGEzUUN3ME2yNk44OzZ4IN88US=> M{HKbHNCVkeHUh?=
T47D NITPUY5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEfTUXpKSzVyPUKyMlc6PzlizszN MX7TRW5ITVJ?
HT-1197 MnrjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIjoSZdKSzVyPUKzMlA5OTdizszN M2WzfnNCVkeHUh?=
LB2518-MEL NXj3UnhuT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUm0b2hWUUN3ME2yN{43PDF{IN88US=> NGPmUnVUSU6JRWK=
J-RT3-T3-5 MlLIS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Ml36TWM2OD1{ND63OVk2KM7:TR?= NFPKRWJUSU6JRWK=
SK-NEP-1 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NE\4XWdKSzVyPUK0Mlg4PDRizszN NVHtSXJSW0GQR1XS
NCI-H526 NG\sS3FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoDiTWM2OD1{NT6wNFI{KM7:TR?= M1\ufnNCVkeHUh?=
IST-SL1 NVnne2NIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVfJR|UxRTJ3LkK3OVEh|ryP MYLTRW5ITVJ?
HH NUnxcWZqT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NInvTWZKSzVyPUK1MlMyQTJizszN Mlj6V2FPT0WU
NCI-H82 MmLzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWrvZnZqUUN3ME2yOU46OzhizszN MmrGV2FPT0WU
SNU-449 NUXxc|VWT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mn3rTWM2OD1{Nz6yNFE5KM7:TR?= MmfTV2FPT0WU
COR-L23 NFn3doJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1TWS2lEPTB;MkeuNlgyOyEQvF2= M{jNV3NCVkeHUh?=
LOXIMVI NGTGcXBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEn1fIZKSzVyPUK3MlM3QCEQvF2= Ml3kV2FPT0WU
GR-ST M{i5cmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn3ITWM2OD1{Nz62O|A3KM7:TR?= MX3TRW5ITVJ?
NCI-SNU-1 MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4rNeGlEPTB;MkeuPVQ1KM7:TR?= MVTTRW5ITVJ?
ALL-PO MlnJS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmTBTWM2OD1{OD6xOlA1KM7:TR?= MkHWV2FPT0WU
ML-2 NIfVWmlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEG0NWZKSzVyPUK4MlI5OTRizszN MVnTRW5ITVJ?
HOP-62 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NILOS5VKSzVyPUK4MlcyOyEQvF2= NXv5VZNnW0GQR1XS
EGI-1 NV;PUmtET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2TzPGlEPTB;MkiuPFg1PSEQvF2= MknGV2FPT0WU
TCCSUP MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4XLe2lEPTB;MkiuPVI4OiEQvF2= NGXIfXVUSU6JRWK=
LB996-RCC NFLmU|JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MW\JR|UxRTJ7LkW2PFIh|ryP M4DJ[HNCVkeHUh?=
LCLC-97TM1 MkfGS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHq5W|dKSzVyPUOyMlE6PjRizszN M1v1cXNCVkeHUh?=
NCI-H1304 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkH5TWM2OD1|Mj6zN|AyKM7:TR?= NU\CXFhoW0GQR1XS
KP-N-YS NUDy[Yl3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmD2TWM2OD1|Mj61PVc{KM7:TR?= NF\4UmJUSU6JRWK=
NCI-H1770 MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlLCTWM2OD1|Mz6xOlQ5KM7:TR?= NHXoZmlUSU6JRWK=
EM-2 M3zZNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1S2ZmlEPTB;M{OuOlUxPCEQvF2= M3;CfnNCVkeHUh?=
ChaGo-K-1 NEPqWJlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkT4TWM2OD1|Mz63NlM3KM7:TR?= NYHQc4ZEW0GQR1XS
ACHN NUPLTlJjT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV\JR|UxRTN|LkizPFUh|ryP NImxNXNUSU6JRWK=
MN-60 NFWwOXFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NE\FcJNKSzVyPUOzMlg2PDRizszN MUPTRW5ITVJ?
EW-18 MoTwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NULnVWh6UUN3ME2zN{45QTdzIN88US=> NWfYe|hlW0GQR1XS
KGN M4W0bmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUjJR|UxRTN3LkeyPVIh|ryP NELOcnBUSU6JRWK=
U031 NFrybIZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFT0UJhKSzVyPUO1MlgyOzJizszN NYfKbYhXW0GQR1XS
HMV-II MkftS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWTJR|UxRTN4LkC3O|Qh|ryP Ml\VV2FPT0WU
L-363 M{jHfGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MV\JR|UxRTN5Lk[0OVUh|ryP NVLk[5Z1W0GQR1XS
NCI-H1155 NX[5UFNFT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlrVTWM2OD1|OD6wNFE2KM7:TR?= MVnTRW5ITVJ?
NCI-H1793 MmPtS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NH;0VGNKSzVyPUO4MlExOjZizszN NHfGeGtUSU6JRWK=
P30-OHK M{T5dGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFH1VmlKSzVyPUO4MlE{OzJizszN MonmV2FPT0WU
AN3-CA NUPB[ohsT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NU\lOHB1UUN3ME2zPE4yPjF3IN88US=> MlK0V2FPT0WU
UACC-257 NWjPNlI5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1jHfWlEPTB;M{iuO|kh|ryP NUnvVZRjW0GQR1XS
MCF7 NFPiPJhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFnIOmFKSzVyPUO5Mlg3OjlizszN MYPTRW5ITVJ?
KP-N-YN NX3kOHR2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWjJR|UxRTRyLkSyPFUh|ryP NHPhdpFUSU6JRWK=
T98G MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1HtOGlEPTB;NECuOFk2PyEQvF2= M3fkR3NCVkeHUh?=
HGC-27 NFK4RlhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1[yTWlEPTB;NEOuNlc1KM7:TR?= MmfXV2FPT0WU
NCI-H1092 NXWxRm9oT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGnwcphKSzVyPUSzMlI5QTVizszN MlvnV2FPT0WU
KARPAS-299 Moj0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWPPe4dUUUN3ME20N{4{ODdzIN88US=> NWLTVppnW0GQR1XS
LB1047-RCC NET4TG9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGTLNIJKSzVyPUS0Mlk6PTlizszN NHzSdppUSU6JRWK=
786-0 NW\hPVVkT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVv0T3FRUUN3ME20OU43PSEQvF2= NGrn[IpUSU6JRWK=
HCC2157 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3XhV2lEPTB;NE[uNFM2QSEQvF2= NImzU5BUSU6JRWK=
NY NHfveFdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWTJR|UxRTR4LkG3O|gh|ryP NVnReldjW0GQR1XS
EFM-19 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGfyOIVKSzVyPUS2Mlc2OzNizszN NX71UJdJW0GQR1XS
EW-16 NXXw[49pT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXXJR|UxRTR4Lke4NFYh|ryP NH\nO4dUSU6JRWK=
UM-UC-3 M2S2U2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYDJR|UxRTR4LkiwOVkh|ryP M4fRdHNCVkeHUh?=
HT-29 NVixVmw5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1S4XmlEPTB;NEeuPFc6OiEQvF2= MmPBV2FPT0WU
LN-405 NUnyRXZ6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnHWTWM2OD12OD6wPFI4KM7:TR?= MUXTRW5ITVJ?
NCI-H727 NFfP[nZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX3uUGh[UUN3ME20PE44PzJ4IN88US=> NHryUHdUSU6JRWK=
D-502MG NFixfGdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1X0fGlEPTB;NEiuPVY4PiEQvF2= NFewU5BUSU6JRWK=
GMS-10 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYe2ZpZqUUN3ME20PU4zQTd2IN88US=> NWq2T4w3W0GQR1XS
MEL-JUSO Mny3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUTJR|UxRTR7LkO0O{DPxE1? NWHiS3RQW0GQR1XS

... 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 individually and in order:
2% DMSO+50% PEG 300+5% Tween 80+ddH2O
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

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.

Related Antibodies

Raf Signaling Pathway Map

Raf Inhibitors with Unique Features

Related Raf Products

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