PLX-4720

Name: PLX-4720
Brand: Selleck Chemicals
SKU: S1152
Rating: 5 (147 reviews)

For research use only.

Catalog No.S1152

147 publications

CAS No. 918505-84-7

PLX4720 is a potent and selective inhibitor of B-Raf^V600E 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.

Selleck's PLX-4720 has been cited by 147 publications

Cancer Cell, 2020, 37(1):85-103

PubMed: 31935375 ( click the link to review the publication )

Nature, 2019, 575(7781):203-209

PubMed: 31666698 ( click the link to review the publication )

Nat Med, 2018, 24(2):203-212

PubMed: 29334371 ( click the link to review the publication )

Nature, 2017, 548(7667):343-346

PubMed: 28792927 ( click the link to review the publication )

Cancer Cell, 2016, 12;30(3):485-498

PubMed: 27523909 ( click the link to review the publication )

Nature, 2015, 517(7536):583-8

PubMed: 25494202 ( click the link to review the publication )

Cell, 2015, 160(1-2):161-76

PubMed: 25594179 ( click the link to review the publication )

Cancer Discov, 2014, 4(1):94-109

PubMed: 24265153 ( click the link to review the publication )

Cancer Discov, 2014, 4(7):816-27

PubMed: 24771846 ( click the link to review the publication )

Nature, 2013, 6;498(7452):109-12.

PubMed: 23685455 ( click the link to review the publication )

Cell, 2013, 29;154(5):1036-1046.

PubMed: 23993095 ( click the link to review the publication )

Nat Biotechnol, 2013, 31(7):630-7

PubMed: 23811600 ( click the link to review the publication )

Cancer Discov, 2013, 3(3):350-62

PubMed: 23288408 ( click the link to review the publication )

Nature, 2012, 26;483(7387):100-3.

PubMed: 22281684 ( click the link to review the publication )

J Immunother Cancer, 2021, 9(1)e001179

PubMed: 33408093 ( click the link to review the publication )

Oncogene, 2021, 10.1038/s41388-020-01628-x

PubMed: 33500549 ( click the link to review the publication )

J Exp Clin Cancer Res, 2021, 40(1):34

PubMed: 33468157 ( click the link to review the publication )

Neoplasia, 2021, 23(3):304-325

PubMed: 33582407 ( click the link to review the publication )

J Cancer Res Clin Oncol, 2021, 10.1007/s00432-020-03484-4

PubMed: 33389075 ( click the link to review the publication )

Biomedicines, 2021, 9(2)E96

PubMed: 33498201 ( click the link to review the publication )

Nat Commun, 2021, 12(1):896

PubMed: 33563994 ( click the link to review the publication )

Cancer Biol Ther, 2021, 10.1080/15384047.2021.1883185

PubMed: 33602034 ( click the link to review the publication )

Sci Adv, 2020, 6(9):eaax3223

PubMed: 32133394 ( click the link to review the publication )

Genomics Proteomics Bioinformatics, 2020, 12 pii: S1672-0229(20)30052-8

PubMed: 32413516 ( click the link to review the publication )
Cancers (Basel), 2020, 27;12(5)pii: E1087

PubMed: 32349331 ( click the link to review the publication )

Pigment Cell Melanoma Res, 2020, 10.1111/pcmr.12932

PubMed: 33000894 ( click the link to review the publication )

Signal Transduct Target Ther, 2020, 5(1):191

PubMed: 32913191 ( click the link to review the publication )

Cancer Discov, 2020, 4;CD-20-0329

PubMed: 32499221 ( click the link to review the publication )

Biochim Biophys Acta Mol Basis Dis, 2020, S0925-4439(20)30409-9

PubMed: 33385518 ( click the link to review the publication )

J Transl Med, 2020, 11;18(1):192

PubMed: 32393282 ( click the link to review the publication )

J Biol Chem, 2020, 295(8):2407-2420

PubMed: 31929109 ( click the link to review the publication )

Transl Oncol, 2020, 13(2):355-364

PubMed: 31887630 ( click the link to review the publication )

Pharmaceuticals (Basel), 2020, 14(1)E23

PubMed: 33396632 ( click the link to review the publication )

Cell Rep, 2020, 30(2):510-524

PubMed: 31940493 ( click the link to review the publication )

Nat Cell Biol, 2019, 21(6):778-790

PubMed: 31160710 ( click the link to review the publication )

Mol Cell, 2019, S1097-2765(19)30838-X

PubMed: 31836388 ( click the link to review the publication )

Nat Commun, 2019, 10(1):5232

PubMed: 31745079 ( click the link to review the publication )

Nat Commun, 2019, 10(1):5167

PubMed: 31727888 ( click the link to review the publication )

Cell Syst, 2019, 9(4):366-374

PubMed: 31521607 ( click the link to review the publication )

Cell Syst, 2019, 8(2):97-108

PubMed: 30797775 ( click the link to review the publication )

Thyroid, 2019, 29(1):79-92

PubMed: 30398411 ( click the link to review the publication )

Oncogene, 2019, 38(22):4384-4396

PubMed: 30710146 ( click the link to review the publication )

J Invest Dermatol, 2019, 139(12):2506-2516

PubMed: 31229500 ( click the link to review the publication )

Cancers (Basel), 2019, 11(5)

PubMed: 31083627 ( click the link to review the publication )

Cell Death Dis, 2019, 10(4):281

PubMed: 30911007 ( click the link to review the publication )

Mol Oncol, 2019, 13(2):480-494

PubMed: 30582770 ( click the link to review the publication )

Mol Cell Proteomics, 2019, 18(6):1096-1109

PubMed: 30890564 ( click the link to review the publication )

Sci Rep, 2019, 9(1):7779

PubMed: 31123282 ( click the link to review the publication )
Transl Oncol, 2019, 12(7):932-950

PubMed: 31096110 ( click the link to review the publication )

Biomol Ther (Seoul), 2019, 27(3):302-310

PubMed: 30293252 ( click the link to review the publication )

Photodermatol Photoimmunol Photomed, 2019, 10.1111/phpp.12520

PubMed: 31618797 ( click the link to review the publication )

ACS Chem Biol, 2019, 14(7):1426-1435

PubMed: 31063355 ( click the link to review the publication )

Genes Genomics, 2019, 41(11):1273-1280

PubMed: 31388978 ( click the link to review the publication )

Exp Gerontol, 2019, 126:110691

PubMed: 31421186 ( click the link to review the publication )

Nat Commun, 2018, 9(1):1482

PubMed: 29662054 ( click the link to review the publication )

Genome Res, 2018, 28(9):1353-1363

PubMed: 30061114 ( click the link to review the publication )

J Control Release, 2018, 277:48-56

PubMed: 29550398 ( click the link to review the publication )

Cell Chem Biol, 2018, 25(2):175-184

PubMed: 29249695 ( click the link to review the publication )

Mol Cancer Ther, 2018, 17(10):2217-2225

PubMed: 30045926 ( click the link to review the publication )

Sci Rep, 2018, 8(1):10902

PubMed: 30026510 ( click the link to review the publication )

ACS Med Chem Lett, 2018, 9(12):1199-1204

PubMed: 30613326 ( click the link to review the publication )

Med Sci (Basel), 2018, 6(1)

PubMed: 29304009 ( click the link to review the publication )

J Exp Med, 2018, 215(1):319-336

PubMed: 29263218 ( click the link to review the publication )

Biophys J, 2018, 114(6):1499-1511

PubMed: 29590606 ( click the link to review the publication )

Nat Commun, 2017, 8(1):607

PubMed: 28928360 ( click the link to review the publication )

Nat Commun, 2017, 8;8:15617

PubMed: 28593995 ( click the link to review the publication )

Clin Cancer Res, 2017, 23(14):3953-3965

PubMed: 28096271 ( click the link to review the publication )

Cancer Res, 2017, 77(8):2161-2172

PubMed: 28242615 ( click the link to review the publication )

Oncogene, 2017, 36(32):4585-4596

PubMed: 28368422 ( click the link to review the publication )

Br J Cancer, 2017, 116(8):1065-1076

PubMed: 28301874 ( click the link to review the publication )

Mol Oncol, 2017,

PubMed: 28182330 ( click the link to review the publication )

Neoplasia, 2017, 19(11):932-940

PubMed: 28963969 ( click the link to review the publication )
Sci Rep, 2017, 7:44123

PubMed: 28276530 ( click the link to review the publication )

Colloids Surf B Biointerfaces, 2017, 154:350-356

PubMed: 28365424 ( click the link to review the publication )

Am J Physiol, Cell Physiol, 2017,

PubMed: 28100485 ( click the link to review the publication )

Cancer Res Treat, 2017, 49(4):947-959

PubMed: 28052651 ( click the link to review the publication )

EMBO Mol Med, 2017, 9(2):219-237

PubMed: 27974353 ( click the link to review the publication )

Oncotarget, 2017, 8(70):115140-115152

PubMed: 29383148 ( click the link to review the publication )

Proc Natl Acad Sci USA, 2016,

PubMed: 26787892 ( click the link to review the publication )

Cell Rep, 2016, 10.1016/j.celrep.2016.05.064

PubMed: 27320919 ( click the link to review the publication )

Elife, 2016, 10.7554/eLife.11414

PubMed: 26999821 ( click the link to review the publication )

Oncogene, 2016, 35(20):2675-80

PubMed: 26119932 ( click the link to review the publication )

Oncogene, 2016, 35(15):1909-18

PubMed: 26477313 ( click the link to review the publication )

Mol Cell Biol, 2016, 36(20):2612-25

PubMed: 27503857 ( click the link to review the publication )

Pharm Biol, 2016, 54(4):732-9

PubMed: 26931349 ( click the link to review the publication )

ACS Chem Biol, 2016, 11(10):2876-2888

PubMed: 27571413 ( click the link to review the publication )

Oncotarget, 2016, 7(50):81995-82012

PubMed: 27835901 ( click the link to review the publication )

Oncotarget, 2016, 7(31):49597-49610

PubMed: 27391062 ( click the link to review the publication )

Oncotarget, 2016, 7(8):9188-221

PubMed: 26802026 ( click the link to review the publication )

Nat Struct Mol Biol, 2015, 22(1):37-43

PubMed: 25437913 ( click the link to review the publication )

Clin Cancer Res, 2015, 21(7):1652-64

PubMed: 25617424 ( click the link to review the publication )

Proc Natl Acad Sci U S A, 2015, 112(6):E536-45

PubMed: 25624498 ( click the link to review the publication )

Cancer Res, 2015, 75(21):4573-81

PubMed: 26363009 ( click the link to review the publication )

Mol Ther, 2015, 23(5):931-942

PubMed: 25619724 ( click the link to review the publication )

J Med Chem, 2015, 58(4):1818-31

PubMed: 25611072 ( click the link to review the publication )

Pigment Cell Melanoma Res, 2015, 10.1111/pcmr.12364

PubMed: 25728708 ( click the link to review the publication )
Front Oncol, 2015, 10.3389/fonc.2015.00095

PubMed: ( click the link to review the publication )

Front Oncol, 2015, 5:95

PubMed: 26029660 ( click the link to review the publication )

J Cell Physiol, 2015, 10.1002/jcp.24888

PubMed: 25600161 ( click the link to review the publication )

J Dermatol Sci, 2015, 78(1):44-50

PubMed: 25726712 ( click the link to review the publication )

Exp Cell Res, 2015, 1;338(2):127-35

PubMed: 26384551 ( click the link to review the publication )

Biomol Ther (Seoul), 2015, 23(4):320-6

PubMed: 26157547 ( click the link to review the publication )

Oncotarget, 2015, 6(7):5118-33

PubMed: 25742786 ( click the link to review the publication )

J Invest Dermatol, 2015, 135(7):1863-1872

PubMed: 25789707 ( click the link to review the publication )

Mol Cancer Ther, 2015, 14(12):2700-11

PubMed: 26351322 ( click the link to review the publication )

Oncotarget, 2015,

PubMed: 26172302 ( click the link to review the publication )

Mol Cell, 2014, 55(6):904-15

PubMed: 25219500 ( click the link to review the publication )

Clin Cancer Res, 2014, 20(9):2410-23

PubMed: 24573550 ( click the link to review the publication )

Cancer Res, 2014, 74(23):7079-89

PubMed: 25320010 ( click the link to review the publication )

Cancer Res, 2014, 74(15):4122-32

PubMed: 25035390 ( click the link to review the publication )

Mol Syst Biol, 2014, 10:772

PubMed: 25538140 ( click the link to review the publication )

Cell Rep, 2014, 10.1016/j.celrep.2014.10.024

PubMed: ( click the link to review the publication )

Cell Rep, 2014, 9(4):1375-86

PubMed: 25456132 ( click the link to review the publication )

Cell Death Dis, 2014, 5:e1278

PubMed: 24901049 ( click the link to review the publication )

Mol Cancer Res, 2014, 12(9):1314-23

PubMed: 25061102 ( click the link to review the publication )

Antimicrob Agents Chemother, 2014, 58(5):2598-608

PubMed: 24550330 ( click the link to review the publication )

Biochem J, 2014, 459(3):513-24

PubMed: 24527759 ( click the link to review the publication )

Toxicol Lett, 2014, 10.1111/cmi.12305

PubMed: 24779413 ( click the link to review the publication )

J Pharm Pharm Sci, 2014, 17(1):154-68

PubMed: 24735766 ( click the link to review the publication )

Drug Des Devel Ther, 2014, 8:255-62

PubMed: 24600206 ( click the link to review the publication )
PLoS One, 2014, 9(1):e87457

PubMed: 24475291 ( click the link to review the publication )

PLoS One, 2014, 9(7):e101286

PubMed: 24983357 ( click the link to review the publication )

Oncotarget, 2014, 5(22):11237-51

PubMed: 25365078 ( click the link to review the publication )

Clin Cancer Res, 2013, 19(16):4383-91

PubMed: 23812671 ( click the link to review the publication )

Pigment Cell Melanoma Res, 2013, 27(1):124-33

PubMed: 24112705 ( click the link to review the publication )

Mol Cancer Ther, 2013, 12(7):1171-9

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Oncogenesis, 2013, 2:e44

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Clin Endocrinol, 2013, 81(1):109-16

PubMed: 24382015 ( click the link to review the publication )

Transl Oncol, 2013, 6(4):470-81

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Mol Cell Biochem, 2013, 372(1-2):65-74

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J Chromatogr B Analyt Technol Biomed Life Sci, 2013, 925:124-8

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J Biomol Screen, 2013, 19(4):526-37

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J Membr Biol, 2013, 247(2):137-45

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Sci Signal, 2013, 6(281):ra51

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Mol Cancer Res, 2013, 11(12):1530-41

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Clin Cancer Res, 2012, 18(12):3316-27

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Genes Dev, 2012, 26(10):1055-69

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Oncogene, 2012, 32(40):4836-44

PubMed: 23208503 ( click the link to review the publication )

J Invest Dermatol, 2012, 132(11):2652-60

PubMed: 22718120 ( click the link to review the publication )

Sci Signal, 2012, 5(224):rs4

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J Biol Chem, 2012, 287(1):91-104

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Biochem J, 2012, 450(2):285-94

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Oncotarget, 2012, 3(12):1688-99

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Mol Biol Cell, 2011, 22(23):4647-56

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PLoS One, 2011, 6(8):e23235

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PLoS One, 2011, 6(11):e26908

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Sci Signal, 2010, 3(149):ra84

PubMed: 21098728 ( click the link to review the publication )

Purity & Quality Control

Choose Selective Raf Inhibitors

Biological Activity

Description

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-Raf^V600E 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-Raf^V600E 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-Raf^V600E-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	Incubation Time	Activity Description	PMID
DU-4475	M3H5dWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7		M3\BeGlEPTB;MD6wO\|Q2PyEQvF2=	NEPqSnE9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;3e5cv\WKrLnHjMpVsN2OqZX3icE9kd22yb4Xu[H9z\XCxcoTfZ4Fz\C:FSFXNRmwyOjNyMEKwM{c,W0GQR1XSQE9iRg>?
EoL-1-cell	NFTzb5pIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=		NGO4SYJKSzVyPUCuNVQyPjZizszN	MWm8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQlyxNlMxODJyLze+V2FPT0WUPD;hQi=>
C32	M1:zVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7		MoLaTWM2OD1yLkG1NVMyKM7:TR?=	MWC8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQlyxNlMxODJyLze+V2FPT0WUPD;hQi=>
M14	M1[5SGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7		NED6do5KSzVyPUCuNlE4PTdizszN	M2LBUVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4f3e{5m[mlwYXOueYsw[2inbXLsM4NwdXCxdX7kY5JmeG:{dG;jZZJlN0OKRV3CUFEzOzByMkCvK\|5USU6JRWK8M4E,
CP50-MEL-B	M1jvfWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7		M3\tRmlEPTB;MD6yPVc5PCEQvF2=	MXS8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQlyxNlMxODJyLze+V2FPT0WUPD;hQi=>
A101D	MoDTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?		MnXzTWM2OD1yLkOyOVg6KM7:TR?=	NGfpb4I9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;3e5cv\WKrLnHjMpVsN2OqZX3icE9kd22yb4Xu[H9z\XCxcoTfZ4Fz\C:FSFXNRmwyOjNyMEKwM{c,W0GQR1XSQE9iRg>?
G-361	NF;nXoxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=		M1ToRmlEPTB;MD6zOFY{PyEQvF2=	NYrZcYJlRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:ve5d4NmWkaT7hZ{52cy:laHXtZoww[2:vcH;1coRgemWyb4L0Y4NiemRxQ1jFUWJNOTJ\|MECyNE8oRlODTlfFVlww[T5?
HT-144	NXriOXJMT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=		MX;JR\|UxRTBwM{[zNlkh\|ryP	Mn7QQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMNVI{ODB{MD:nQnNCVkeHUkyvZV4>
ACN	MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?		Ml3yTWM2OD1yLkO4OFc4KM7:TR?=	NV73UpRCRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:ve5d4NmWkaT7hZ{52cy:laHXtZoww[2:vcH;1coRgemWyb4L0Y4NiemRxQ1jFUWJNOTJ\|MECyNE8oRlODTlfFVlww[T5?
COLO-829	NGTPU25Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?=		M2\o[GlEPTB;MD6zPFk3QCEQvF2=	NIDL[mc9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;3e5cv\WKrLnHjMpVsN2OqZX3icE9kd22yb4Xu[H9z\XCxcoTfZ4Fz\C:FSFXNRmwyOjNyMEKwM{c,W0GQR1XSQE9iRg>?
MEL-HO	MnnLS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?		NYfDSHB{UUN3ME2wMlQyOTd7IN88US=>	MUi8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQlyxNlMxODJyLze+V2FPT0WUPD;hQi=>
SH-4	MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?		NX:0bo5wUUN3ME2wMlQyPDJ{IN88US=>	NIP4[WQ9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;3e5cv\WKrLnHjMpVsN2OqZX3icE9kd22yb4Xu[H9z\XCxcoTfZ4Fz\C:FSFXNRmwyOjNyMEKwM{c,W0GQR1XSQE9iRg>?
SK-MEL-3	NXvZeIFCT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=		NV;IfIxSUUN3ME2wMlUyPTZ6IN88US=>	MWK8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQlyxNlMxODJyLze+V2FPT0WUPD;hQi=>
A375	M1XLNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7		MnjaTWM2OD1yLk[3N\|U6KM7:TR?=	NEDz[oc9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;3e5cv\WKrLnHjMpVsN2OqZX3icE9kd22yb4Xu[H9z\XCxcoTfZ4Fz\C:FSFXNRmwyOjNyMEKwM{c,W0GQR1XSQE9iRg>?
MMAC-SF	MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?		M{jxXWlEPTB;MD62PFYyPCEQvF2=	MnLzQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMNVI{ODB{MD:nQnNCVkeHUkyvZV4>
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UACC-257	MoDPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?		Mn;xTWM2OD1\|OD63PUDPxE1?	M4DMNVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4f3e{5m[mlwYXOueYsw[2inbXLsM4NwdXCxdX7kY5JmeG:{dG;jZZJlN0OKRV3CUFEzOzByMkCvK\|5USU6JRWK8M4E,
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T98G	MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?		NX32foJ[UUN3ME20NE41QTV5IN88US=>	Mo\nQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMNVI{ODB{MD:nQnNCVkeHUkyvZV4>
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LB1047-RCC	MmfUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?		NXjNbot3UUN3ME20OE46QTV7IN88US=>	NGHqSFA9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;3e5cv\WKrLnHjMpVsN2OqZX3icE9kd22yb4Xu[H9z\XCxcoTfZ4Fz\C:FSFXNRmwyOjNyMEKwM{c,W0GQR1XSQE9iRg>?
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EW-16	MnXkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?		NX7JU2tMUUN3ME20Ok44QDB4IN88US=>	MmPQQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMNVI{ODB{MD:nQnNCVkeHUkyvZV4>
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LN-405	M3SxNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7		MV3JR\|UxRTR6LkC4Nlch\|ryP	M1nnTlxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4f3e{5m[mlwYXOueYsw[2inbXLsM4NwdXCxdX7kY5JmeG:{dG;jZZJlN0OKRV3CUFEzOzByMkCvK\|5USU6JRWK8M4E,
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D-502MG	NXTZOYYyT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=		NUPON4syUUN3ME20PE46Pjd4IN88US=>	NYf4V2ZVRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:ve5d4NmWkaT7hZ{52cy:laHXtZoww[2:vcH;1coRgemWyb4L0Y4NiemRxQ1jFUWJNOTJ\|MECyNE8oRlODTlfFVlww[T5?
GMS-10	Mni2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?		NVvRWmNwUUN3ME20PU4zQTd2IN88US=>	NV\ucW94RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:ve5d4NmWkaT7hZ{52cy:laHXtZoww[2:vcH;1coRgemWyb4L0Y4NiemRxQ1jFUWJNOTJ\|MECyNE8oRlODTlfFVlww[T5?
MEL-JUSO	MlvWS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?		NXfqdZptUUN3ME20PU4{PDdizszN	NEfqSog9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;3e5cv\WKrLnHjMpVsN2OqZX3icE9kd22yb4Xu[H9z\XCxcoTfZ4Fz\C:FSFXNRmwyOjNyMEKwM{c,W0GQR1XSQE9iRg>?
insect cells	MVHGeY5kfGmxbjDhd5NigQ>?		NYTXUIVXUW6qaXLpeIlwdiCxZjDOMZRmem2rbnHsJGhqey22YXfn[YQhSlKDRjDWOlAxTSCvdYThcpQhMHWwa37ve44hd3KrZ3nuLUBmgHC{ZYPz[YQhcW5iYnHjeYxwfmm{dYOgbY5n\WO2ZXSgbY5{\WO2IHPlcIx{KGOxLXX4dJJme3OrbnegR2REOzdidYPpcoch[mmxdHnufYxifGWmLV3FT{BieyC\|dXLzeJJifGViYomgRYxxcGGVY4Ll[Y4h[XO\|YYmsJGlEPTBiPTCwMlAyOyEQvF2u	MlzjQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjl2NkG4NlcoRjJ7NE[xPFI4RC:jPh?=
A375	MnzJSpVv[3Srb36gZZN{[Xl?		NFvUZ5dKdmirYnn0bY9vKG:oIFLSRWYhXjZyMFWgcZV1[W62IHnuJIh2dWGwIFGzO\|Uh[2WubIOgZZN{\XO\|ZXSgZZMhemWmdXP0bY9vKGmwIFXST{BxcG:\|cHjvdplt[XSrb36gZpkhSWyyaHHTZ5Jm\W5iYYPzZZktKEmFNUCgQUAxNjB2NDFOwG0v	MnyxQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjl2NkG4NlcoRjJ7NE[xPFI4RC:jPh?=
A375	MkHKSpVv[3Srb36gZZN{[Xl?		NGHoZXRKdmirYnn0bY9vKG:oIHKtVoFnKGmwIHj1cYFvKEF\|N{WgZ4VtdHNiYYPz[ZN{\WRicHjvd5Bpd3K7bHH0bY9vKG:oIFXST{whUUN3MDC9JFAvODR4IN88UU4>	NGPy[lM9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{MkiwPFkyOSd-MkK4NFg6OTF:L3G+
A375	MXzBcpRqeHKxbHnm[ZJifGm4ZTDhd5NigQ>?		M2P4ZWFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iQUO3OUBk\WyuczDlfJBz\XO\|aX7nJGIuWmGoIG[2NFBGKG23dHHueEBidmRid3ns[EB1gXCnIGLhd{whUUN3MDC9JFAvPSEQvF2u	M{\ROFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ{OEC4PVEyLz5{MkiwPFkyOTxxYU6=
A375	M3X1bmN6fG:2b4jpZ4l1gSCjc4PhfS=>	NXXNR2NOPzJiaILz	MVjDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDBN\|c2KGOnbHzzJIhiemKxcnnu[{BDWkGIIG[2NFBGKG23dHHueEBi\nSncjC3NkBpenNiYomgR4VtdFSrdHXyMWdtdyCjc4PhfUwhUUN3MDC9JFAvPSEQvF2u	M{XYPVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ7NE[xPFI4Lz5{OUS2NVgzPzxxYU6=
HCT116	MVHBcpRqeHKxbHnm[ZJifGm4ZTDhd5NigQ>?		MVzBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKEiFVEGxOkBk\WyuczDlfJBz\XO\|aX7nJJdqdGRidInw[UBjNVKjZjDhcoQhU1KDUzDteZRidnRuIFnDOVAhRSB{NzFOwG0v	NHvuWI89[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{MkiwPFkyOSd-MkK4NFg6OTF:L3G+
A673	M3f2RpFJXFNiYYPzZZk>		M1TsOZFJXFNib3[gdIVlcWG2cnnjJINidmOncjDj[YxtKGyrbnXzJJRwKGmmZX70bYZ6KG23bITpdIxmKG:ycH;yeJVvcXSrZYOg[o9zKGS{dXegdoVxfXKyb4Ppcoc7KFC{aX3hdpkhe2O{ZXXuJIZweiCDNkezJINmdGy\|	MmLTQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjl2M{WxN\|koRjJ7NEO1NVM6RC:jPh?=
Saos-2	MlrmdWhVWyCjc4PhfS=>		NHXkcY5yUFSVIH;mJJBm\GmjdILpZ{Bk[W6lZYKgZ4VtdCCuaX7ld{B1dyCrZHXueIlngSCvdXz0bZBt\SCxcIDvdpR2dmm2aXXzJIZweiCmcoXnJJJmeHW{cH;zbY5oQiCScnntZZJ6KHOlcnXlckBnd3JiU3Hvd{0zKGOnbHzz	NEnnVm49[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{OUSzOVE{QSd-Mkm0N\|UyOzl:L3G+
RD	NFSzdI1yUFSVIHHzd4F6		MYDxTHRUKG:oIIDl[IlifHKrYzDjZY5k\XJiY3XscEBtcW6nczD0c{Bq\GWwdHnmfUBufWy2aYDs[UBweHCxcoT1col1cWW\|IH\vdkBlenWpIILldJVzeG:\|aX7nPkBRemmvYYL5JJNkemWnbjDmc5IhWkRiY3XscJM>	NGTNVnc9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{OUSzOVE{QSd-Mkm0N\|UyOzl:L3G+
SK-N-SH	M4PYZ5FJXFNiYYPzZZk>		NV3BZoJbeUiWUzDv[kBx\WSrYYTybYMh[2GwY3XyJINmdGxibHnu[ZMhfG9iaXTlcpRq\nlibYXseIlxdGVib4Dwc5J1fW6rdHnld{Bnd3JiZIL1[{Bz\XC3coDvd4lv\zpiUILpcYFzgSC\|Y4Ll[Y4h\m:{IGPLMW4uW0hiY3XscJM>	M3jFOVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ7NEO1NVM6Lz5{OUSzOVE{QTxxYU6=
NB1643	NWSwTmR4eUiWUzDhd5NigQ>?		MXfxTHRUKG:oIIDl[IlifHKrYzDjZY5k\XJiY3XscEBtcW6nczD0c{Bq\GWwdHnmfUBufWy2aYDs[UBweHCxcoT1col1cWW\|IH\vdkBlenWpIILldJVzeG:\|aX7nPkBRemmvYYL5JJNkemWnbjDmc5IhVkJzNkSzJINmdGy\|	NYTG[lZ[RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkm0N\|UyOzlpPkK5OFM2OTN7PD;hQi=>
OHS-50	M2PqcpFJXFNiYYPzZZk>		NWTTN4ZkeUiWUzDv[kBx\WSrYYTybYMh[2GwY3XyJINmdGxibHnu[ZMhfG9iaXTlcpRq\nlibYXseIlxdGVib4Dwc5J1fW6rdHnld{Bnd3JiZIL1[{Bz\XC3coDvd4lv\zpiUILpcYFzgSC\|Y4Ll[Y4h\m:{IF;IV{02OCClZXzsdy=>	NVjJSIJ{RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkm0N\|UyOzlpPkK5OFM2OTN7PD;hQi=>
SJ-GBM2	NGTNXnZyUFSVIHHzd4F6		MUXxTHRUKG:oIIDl[IlifHKrYzDjZY5k\XJiY3XscEBtcW6nczD0c{Bq\GWwdHnmfUBufWy2aYDs[UBweHCxcoT1col1cWW\|IH\vdkBlenWpIILldJVzeG:\|aX7nPkBRemmvYYL5JJNkemWnbjDmc5IhW0pvR1LNNkBk\Wyucx?=	MlfRQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjl2M{WxN\|koRjJ7NEO1NVM6RC:jPh?=
SK-N-MC	NVf5N3V7eUiWUzDhd5NigQ>?		MYnxTHRUKG:oIIDl[IlifHKrYzDjZY5k\XJiY3XscEBtcW6nczD0c{Bq\GWwdHnmfUBufWy2aYDs[UBweHCxcoT1col1cWW\|IH\vdkBlenWpIILldJVzeG:\|aX7nPkBRemmvYYL5JJNkemWnbjDmc5IhW0tvTj3NR{Bk\Wyucx?=	NVG3RmxqRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkm0N\|UyOzlpPkK5OFM2OTN7PD;hQi=>

... Click to View More Cell Line Experimental Data

Assay

Methods	Test Index	PMID
Western blot	p-MEK / MEK / p-ERK / ERK / p-FAK(S910); PubMed: 23076151 J Biol Chem WM793 and WM793-Res NRAS cells were seeded overnight in the absence of PLX4720 and then treated with 1 μm PLX4720 for times ranging from 0 to 24 h. Samples were analyzed by Western blotting for phospho-MEK, total MEK, phospho-ERK1/2, total ERK1/2, phospho-S910 FAK, and total FAK. p-EGFR 1173 / EGFR / p-Akt / Akt; PubMed: 26023796 Oncotarget Three BRAF(V600E) glioma cell lines, NMC-G1, AM38 and DBTRG-05MG were subjected to a 24 hour time course treatment with 5 μM PLX4720 in the presence or absence of 1 μM HKI-272. These cells were serum starved for 16 hours before being stimulated with 10% FBS and harvested for immunoblotting analysis. Cells treated with PLX4720 alone showed an initial suppression of MEK and ERK phosphorylation followed by a profound rebound of MAPK pathway activation as early as one hour post-PLX4720 treatment. Elevated levels of EGFR phosphorylation were also observed in the PLX4720 treated cells. The extent of Akt phosphorylation increased upon PLX4720 treatment, although the extent varies between cell lines. In contrast, no reactivation of EGFR, MEK, ERK or Akt was observed in cells pre-treated with HKI-272. p27 / Cyclin D1 / pRb; PubMed: 21828154 Invest Ophthalmol Vis Sci Immunoblot analysis revealed that PLX4720 (3 μM) decreased levels of phosphorylated ERK, decreased levels of cyclin D1, increased levels of p27, and decreased levels of phosphorylated Rb in BRAF-mutant (OCM3) cells. On the contrary, in Gα-mutant (OMM1.3) UM cells, PLX4720 induced a paradoxical increase in phosphorylated ERK and Rb levels and an early increase in cyclin D1 levels but did not stimulate p27 levels. pAkt(Ser473) / pAkt(Thr308); PubMed: 21828154 Invest Ophthalmol Vis Sci Immunoblot analysis revealed that both AZD6244 and PLX4720 induced an early (within 2–6 hours of exposure) increase in the levels of phosphorylated Akt (at residues Ser473 and Thr308) in both BRAF-mutant OCM3 and Gα-mutant OMM1.3 cells. Eventually, and with prolonged drug exposure, the phosphorylation of Akt returned to baseline in Gα-mutant OMM1.3 cells and decreased even below baseline levels in BRAF-mutant OCM3 cells.	23076151 26023796 21828154
Immunofluorescence	LAMP1; PubMed: 30979895 Nat Commun Representative images of LysoTracker Red (red) and LAMP1 (green) immunostaining of PLX4720 (1 μM, 12 h-treated) A375 cells with depletion of the indicated genes. Note the reduced lysosome staining in PLX4720-treated cells upon TFEB depletion. ZKSCAN3 / TFEB ; PubMed: 30979895 Nat Commun Representative confocal images of subcellular translocation of endogenous TFEB (green) and ZKSCAN3 (red) in A375 cells treated with PLX4720 (1 μM, 12 h). n = 3 independent experiments.	30979895
Growth inhibition assay	Cell viability; PubMed: 27848137 J Neurooncol AM-38 and DBTRG-05MG cells were treated for 5 days. Media was changed once every 3 days. Cell viability was measured using WST-1 assay. Error bars indicate the variation between triplicate measurements. PLX4720 and PD0325901 alone or in combination reduced cell viability significantly. However, combined therapy led to the most significant cell viability reduction compared to either monotherapy in both AM-38 and DBTRG-05MG cell lines.	27848137
ELISA	mIFN-γ; PubMed: 23204132 Clin Cancer Res (C, D and E) IFN-γ secretion by pmel-1 T cells co-cultured with transduced melanoma cells (after cell sorting) that had been pre-treated with the indicated concentrations of PLX4720, as determined by ELISA. (P<0.05, * P<0.01) Data are representative of 3 independent experiments.	23204132

In vivo

Oral administration of PLX-4720 at 20 mg/kg/day induces significant tumor growth delays and regressions in B-Raf^V600E-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-Raf^V600E, 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]	- Collapse 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]	- Collapse 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]	- Collapse Animal Models: Female athymic mice (NCr nu/nu) implanted s.c. with COLO205 cells, and SCID mice with 1205Lu or C8161 cells Dosages: 5, 20, or 100 mg/kg Administration: Oral gavage once or twice daily (Only for Reference)

References

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 Download PLX-4720 SDF

Molecular Weight	413.83
Formula	C₁₇H₁₄ClF₂N₃O₃S
CAS No.	918505-84-7
Storage	3 years-20°C powder 2 years-80°C in solvent
Synonyms	N/A
Smiles	CCCS(=O)(=O)NC1=C(C(=C(C=C1)F)C(=O)C2=CNC3=C2C=C(C=N3)Cl)F

In vivo Formulation Calculator (Clear solution)

Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)

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Step 2: Enter the in vivo formulation (Different batches have different solubility ratios, please contact Selleck to provide you with the correct ratio)

% DMSO+ % + % Tween 80+ % ddH₂O

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Calculation results:

Working concentration： mg/ml；

Method for preparing DMSO master liquid: ： mg drug pre-dissolved in μL DMSO (Master liquid concentration mg/mL， Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation：Take μL DMSO master liquid, next addμL PEG300， mix and clarify, next addμL Tween 80，mix and clarify, next add μL ddH₂O，mix and clarify.

Note：1.Please make sure the liquid is clear before adding the next solvent.
2.Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.

Bio Calculators

Molarity Calculator

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

Mass (mg) = Concentration (mM) × Volume (mL) × Molecular Weight (g/mol)

*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

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 )

* 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
Concertration (start):
Dilution-folds:

Computed Result

C1=C0/X	C1:	LOG(C1):
C2=C1/X	C2:	LOG(C2):
C3=C2/X	C3:	LOG(C3):
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C6=C5/X	C6:	LOG(C6):
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C8=C7/X	C8:	LOG(C8):

Molecular Weight Calculator

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

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

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.

Frequently Asked Questions

Question 1:
What would you recommend to make working solution for intraperitoneal injection into mice?
Answer:
PLX4720 has very limited solubility in aqueous solution and for this reason, we recommend oral gavage to administer this compound as not fully dissolved suspension can be used in oral gavage feeding.

Raf Signaling Pathway Map

Raf Inhibitors with Unique Features

Pan Raf Inhibitor

AZ 628 : Pan-Raf inhibitor, BRAF, IC50=105 nM; BRAFV600E, IC50=34 nM; c-Raf-1, IC50=29 nM.
FDA-approved Raf Inhibitor

Sorafenib Tosylate : Approved by FDA for advanced renal cancer。
Newest Raf Inhibitor

TAK-632 ^New : Potent pan-Raf inhibitor with IC50 of 8.3 nM and 1.4 nM for B-Raf(wt) and C-Raf, respectively, showing less or no inhibition against other tested kinases.

Related Raf Products

LY3009120 ^New

LY03009120 (DP-4978) is a potent pan-Raf inhibitor with IC50 of 44 nM, 31-47 nM, and 42 nM for A-raf, B-Raf, and C-Raf in A375 cells, respectively. LY03009120 induces autophagy. Phase 1.
Ravoxertinib (GDC-0994) ^New

Ravoxertinib (GDC-0994) is a potent, orally available and highly selective ERK1/2 inhibitor with IC50 of 1.1 nM and 0.3 nM, respectively. Phase 1.
Ulixertinib (BVD-523) ^New

Ulixertinib (BVD-523, VRT752271) is a potent and reversible ERK1/ERK2 inhibitor with IC50 of <0.3 nM for ERK2. Phase 1.
Vemurafenib (PLX4032)

Vemurafenib (PLX4032, RG7204, RO5185426) is a novel and potent inhibitor of B-Raf^V600E with IC50 of 31 nM in cell-free assay. 10-fold selective for B-Raf^V600E over wild-type B-Raf in enzymatic assays and the cellular selectivity can exceed 100-fold. Vemurafenib (PLX4032, RG7204) induces autophagy.

Features:A novel and potent inhibitor of the B-RAF^V600E oncoprotein.
Dabrafenib (GSK2118436)

Dabrafenib (GSK2118436, GSK2118436A) is a mutant BRAFV600 specific inhibitor with IC50 of 0.7 nM in cell-free assays, with 7- and 9-fold less potency against B-Raf(wt) and c-Raf, respectively.
Sorafenib

Sorafenib (BAY 43-9006) is a multikinase inhibitor of Raf-1 and B-Raf with IC50 of 6 nM and 22 nM in cell-free assays, respectively. Sorafenib inhibits VEGFR-2, VEGFR-3, PDGFR-β, Flt-3 and c-KIT with IC50 of 90 nM, 20 nM, 57 nM, 59 nM and 68 nM, respectively. Sorafenib induces autophagy and apoptosis and activates ferroptosis with anti-tumor activity.
Sorafenib Tosylate

Sorafenib Tosylate (Bay 43-9006) is a multikinase inhibitor of Raf-1 and B-Raf with IC50 of 6 nM and 22 nM in cell-free assays, respectively. Sorafenib Tosylate inhibits VEGFR-2, VEGFR-3, PDGFR-β, Flt-3 and c-KIT with IC50 of 90 nM, 20 nM, 57 nM, 59 nM and 68 nM, respectively. Sorafenib Tosylate induces autophagy and apoptosis and activates ferroptosis with anti-tumor activity.
TAK-632

TAK-632 is a potent pan-Raf inhibitor with IC50 of 8.3 nM and 1.4 nM for B-Raf(wt) and C-Raf in cell-free assays, respectively, showing less or no inhibition against other tested kinases.
GDC-0879

GDC-0879 (AR-00341677) is a novel, potent, and selective B-Raf inhibitor with IC50 of 0.13 nM in A375 and Colo205 cells with activity against c-Raf as well; no inhibition known to other protein kinases.
GW5074

GW5074 is a potent and selective c-Raf inhibitor with IC50 of 9 nM, no effect on the activities of JNK1/2/3, MEK1, MKK6/7, CDK1/2, c-Src, p38 MAP, VEGFR2 or c-Fms is noted. GW5074 inhibits LK-induced apoptosis.

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PLX-4720