PD0325901

Licensed by Pfizer Catalog No.S1036

Molecular Weight(MW): 482.19

PD0325901 is a selective and non ATP-competitive MEK inhibitor with IC50 of 0.33 nM in cell-free assays, roughly 500-fold more potent than CI-1040 on phosphorylation of ERK1 and ERK2. Phase 2.

Cited by 81 Publications

Nature, 2018, 553(7686):96-100

PubMed: 29258294 ( click the link to review the publication )

Cell, 2018, 174(2):406-421

PubMed: 29887375 ( click the link to review the publication )

Nature, 2016, 539(7629):452-455

PubMed: 27783602 ( click the link to review the publication )

Nature, 2015, 10.1038/nature14413

PubMed: 25945737 ( click the link to review the publication )

Nature, 2015, 517(7534):391-5

PubMed: 25409143 ( click the link to review the publication )

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

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

Cell, 2012, 151(5):937-50

PubMed: 23178117 ( click the link to review the publication )

Nat Methods , 2011, 8(6):487-93

PubMed: 21516115 ( click the link to review the publication )

Cell Stem Cell, 2012, 10(2):210-7

PubMed: 22305570 ( click the link to review the publication )

Blood, 2017, 129(12):1691-1701

PubMed: 28159742 ( click the link to review the publication )

Blood, 2014, 123(18):2838-42

PubMed: 24553178 ( click the link to review the publication )

Blood, 2013, 122,215045

PubMed: ( click the link to review the publication )
Mol Cell, 2011, 43(5):723-37

PubMed: 21884975 ( click the link to review the publication )

Nat Protoc, 2017, 12(10):2097-2109

PubMed: 28880277 ( click the link to review the publication )

J Exp Med, 2014, 211(3):395-404

PubMed: 24516119 ( click the link to review the publication )

Clin Cancer Res, 2018, 24(10):2417-2429

PubMed: 29463558 ( click the link to review the publication )

Clin Cancer Res, 2018, 24(19):4771-4784

PubMed: 29563139 ( click the link to review the publication )

Clin Cancer Res, 2017, 23(21):6567-6579

PubMed: 28765329 ( click the link to review the publication )

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

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

Proc Natl Acad Sci USA, 2014, 111(29):10678-83

PubMed: 25002522 ( click the link to review the publication )

Proc Natl Acad Sci USA, 2014, 10.1073/pnas.1319738111

PubMed: 24623855 ( click the link to review the publication )

Proc Natl Acad Sci USA, 2013, 110(10):4015-20

PubMed: 23431193 ( click the link to review the publication )

Cancer Res, 2012, 72(13):3350-9

PubMed: 22573716 ( click the link to review the publication )

Cancer Res, 2009, 69(17):6839-47

PubMed: 19706763 ( click the link to review the publication )
EMBO Rep, 2015, 16(1):87-96

PubMed: ( click the link to review the publication )

Kidney Int, 2014, 10.1038/ki.2014.107

PubMed: 24786704 ( click the link to review the publication )

Oncogene, 2015, 10.1038/onc.2015.97

PubMed: 25867065 ( click the link to review the publication )

Oncogene, 2014, 33(14):1828-39

PubMed: 23624914 ( click the link to review the publication )

Oncogene, 2011, 30(11):1341-50

PubMed: 21057530 ( click the link to review the publication )

Stem Cell Rep, 2013, 1(4):360-9

PubMed: 24319670 ( click the link to review the publication )

Cancer Lett, 2014, 347(2):212-24

PubMed: 24576622 ( click the link to review the publication )

Cancer Lett, 2012, 324(1):98-108

PubMed: 22579651 ( click the link to review the publication )

Sci Signal, 2012, 5(224):rs4

PubMed: 22589389 ( click the link to review the publication )

Sci Signal, 2010, 3(149):ra84

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

J Bone Miner Res, 2011, 26(10):2486-97

PubMed: 21812026 ( click the link to review the publication )

Breast Cancer Res, 2011, 13(2):R36

PubMed: 21457548 ( click the link to review the publication )
J Neurosci, 2015, 35(9):3893-902

PubMed: 25740518 ( click the link to review the publication )

FASEB J, 2015, 10.1096/fj.14-267278

PubMed: 25857555 ( click the link to review the publication )

Stem Cells, 2015, 10.1002/stem.1990

PubMed: 25788415 ( click the link to review the publication )

Stem Cells, 2015, 33(3):686-98

PubMed: ( click the link to review the publication )

Development, 2013, 140(14):2961-71

PubMed: 23760955 ( click the link to review the publication )

Mol Cancer Ther, 2014, 13(8):2073-80

PubMed: 24899684 ( click the link to review the publication )

Mol Cancer Ther, 2014, 13(12):3098-106

PubMed: 25253779 ( click the link to review the publication )

Br J Haematol, 2012, 159(4):430-40

PubMed: 22985491 ( click the link to review the publication )

Radiother Oncol, 2012, 105(1):64-71

PubMed: 22682746 ( click the link to review the publication )

J Thromb Haemost, 2015, 10.1111/jth.12954

PubMed: 25858425 ( click the link to review the publication )

J Bone Joint Surg Am, 2014, 96(14):e117

PubMed: 25031379 ( click the link to review the publication )

J Immunol, 2014, 192(4):1351-5

PubMed: 24442443 ( click the link to review the publication )
Bone, 2013, 59:151-61

PubMed: 24269278 ( click the link to review the publication )

Antiviral Res, 2011, 92(2):195-203

PubMed: 21854809 ( click the link to review the publication )

J Genet Genomics, 2012, 39(12):643-51

PubMed: 23273768 ( click the link to review the publication )

Int J Biol Sci, 2015, 11(4):411-422

PubMed: ( click the link to review the publication )

J Biol Chem, 2014, 10.1074/jbc.M114.580076

PubMed: 25301940 ( click the link to review the publication )

J Biol Chem, 2011, 286(24):21062-72

PubMed: 21489997 ( click the link to review the publication )

J Biol Chem, 2010, 285(42):32370-7

PubMed: 20696763 ( click the link to review the publication )

Eur Cell Mater, 2013, 26:208-21

PubMed: 24146213 ( click the link to review the publication )

Cell Signal, 2014, 26(10):2276-2283

PubMed: 24905473 ( click the link to review the publication )

Cell Signal, 2012, 24(12):2360-8

PubMed: 22917534 ( click the link to review the publication )

Pharm Res, 2011, 28(12):3069-78

PubMed: 21879387 ( click the link to review the publication )

Stem Cells Dev, 2014, 23(17):2030-45

PubMed: 24742229 ( click the link to review the publication )
Stem Cells Dev, 2012, 21(14):2606-12

PubMed: 22455749 ( click the link to review the publication )

Exp Cell Res, 2013, 319(19):2928-37

PubMed: 24080014 ( click the link to review the publication )

Int J Biochem Cell Biol, 2015, 60C:34-42

PubMed: 25578563 ( click the link to review the publication )

Biol Reprod, 2015, 10.1095/biolreprod.114.127647

PubMed: 25947060 ( click the link to review the publication )

Biol Reprod, 2014, 91(4):88

PubMed: 25210127 ( click the link to review the publication )

Pancreas, 2014, 43(1):88-92

PubMed: 24263107 ( click the link to review the publication )

PLoS One, 2015, 10(3):e0119387

PubMed: 25803847 ( click the link to review the publication )

PLoS One, 2014, 9(4):e92304

PubMed: 24743237 ( click the link to review the publication )

PLoS One, 2014, 9(1):e85089

PubMed: 24465482 ( click the link to review the publication )

PLoS One, 2013, 8(12):e81156

PubMed: 24339907 ( click the link to review the publication )

PLoS One, 2013, 8(2):e56518

PubMed: 23437152 ( click the link to review the publication )

PLoS One, 2011, 6(10):e26755

PubMed: 22046344 ( click the link to review the publication )
Theriogenology, 2014, 82(2):283-93

PubMed: 24853281 ( click the link to review the publication )

J Surg Res, 2016, 206(2):371-379

PubMed: 27884331 ( click the link to review the publication )

Mol Med Rep, 2014, 10.3892/mmr.2014.2793

PubMed: 25352256 ( click the link to review the publication )

Tumour Biol, 2016, 37(4):4767-76

PubMed: 26518767 ( click the link to review the publication )

Methods Mol Biol, 2016, 1480:153-65

PubMed: 27659983 ( click the link to review the publication )

Cell Biology International Reports, 2015, 10.1002/cbi3.10019

PubMed: ( click the link to review the publication )

Oncotarget, 2014, 5(23):12189-202

PubMed: 25361008 ( click the link to review the publication )

Oncotarget, 2014, 5(2):351-62.

PubMed: 24504051 ( click the link to review the publication )

Genes Cancer, 2010, 1(10):994-1007

PubMed: 21442024 ( click the link to review the publication )

19 Customer Reviews

Phosphorylation of PPARg in epididymal white adipose tissue in ob/ob mice after treatment with MEK inhibitors. Gene expression in ob/ob epididymal white adipose tissue after treatment with vehicle or either of two MEK inhibitors, PD0325901 or GSK1120212 (n = 7, 7 and 8, respectively). Areas under the curve and gene expression were analysed by analysis of variance.

Nature 2015 517(7534), 391-5. PD0325901 purchased from Selleck.

c, Examples of CDK2 activity traces aligned to the end of mitosis. Each panel shows different time windows relative to mitosis when mitogens were withdrawn (marked in grey) in d. d, Probability of proliferation (defined as CDK2 activity > 1, 10 h after mitosis) represented as a function of time when inhibitors of MEK (MEKi; 100 nM PD0325901) or of CDK4 (CDK4i; 1 μ M palbociclib) were added or when mitogens were removed, relative to mitosis. Data are mean ± s.e.m. (n = 5 biological replicates).

Nature, 2017, 549(7672):404-408. PD0325901 purchased from Selleck.
Immunoblot analysis of Ser9-phosphorylated (that is, inactivated) or total GSK3β, active or total β-catenin Thr202- and Tyr204- phosphorylated or total Erk1/2, and Ser473-phosphorylated or total Akt in control; Bcl2 lymphoma cells treated with ADR for five days, together with pharmacological inhibitors targeting MAPK and PI3K kinase pathways.α -Tubulin was used as a loading control. MAPKi=PD325901.

Nature, 2018, 553(7686):96-100. PD0325901 purchased from Selleck.

Immunoblot analysis of Ser9-phosphorylated (that is, inactivated) or total GSK3β , active or total β -catenin (as in Extended Data Fig. 5c), Thr202- and Tyr204-phosphorylated or total Erk1/2, and Ser473-phosphorylated or total Akt in control;Bcl2 lymphoma cells treated with ADR for five days, together with pharmacological inhibitors targeting MAPK and PI3K kinase pathways. α -Tubulin was used as a loading control. One out of two independent experiments shown. MPAKi:PD325901

Nature, 2017, 553(7686):96-100. PD0325901 purchased from Selleck.
Rapamycin reduces VCAM expression in vivo. Expression of VCAM-1 mRNA (normalized to CD31) in aortas harvested from mice pretreated with vehicle, rapamycin, or rapamycin + MEK inhibitor (MEK-I; PD0325901) and then injected with TNF (n = 5 per group). Mice were treated as in D. Harvested aortas were analyzed for VCAM-1 expression via immunofluorescence.

J Exp Med 2014 211(3), 395-404. PD0325901 purchased from Selleck.

Plasma MEK inhibitor levels of PD325901 are plotted against % MEK inhibition in brain. One hundred percent pERK levels (0% MEK inhibition) were determined in vehicle-treated rats.Inhibition of pERK activity in brain, lung, and Colo205 tumor in nude xenograft mice treated with 10 mg/kg PD325901.

Cancer Res 2009 PD0325901 purchased from Selleck.
Pharmacological inhibition of MEK (PD0325901) suppresses DR5 expression in cancer cells; this effect is reversible upon stopping of the treatment. The indicated cancer cell lines were exposed to the given concentrations of the inhibitors as indicated for 16 h. TPC-1 cells were treated with 10 uM of the indicated inhibitors for different times as labeled.

Oncogene 2015 10.1038/onc.2015.97. PD0325901 purchased from Selleck.

(B)Effect of MAPK pathway inhibition on FGF9 mediated induction of Fgf23 expression. (D) Western blot analysis of FRS2 and ERK1/2 phosphorylation in UMR 106 cells. Cells were treated for 3h (Western blot) or 24h (qPCR analysis) with FGF9 (50ng/ml), EGF (50ng/ml), PD173074 (250nM), PD0325901 (100nM) and RAF265 (500nM) as indicated. Heparin (10g/ml) was added to all treatments with FGF9. Activation of Fgf23 is shown relative to transcript levels in vehicle treated cells (relative expression of 1). Expression values were normalized to Gapdh mRNA copies and are given as average with SEM (n3). Data were compared by 1 way ANOVA; asterisk indicates p<0.05 with respect to vehicle treated cells.

J Bone Miner Res 2011 26, 2486-2497. PD0325901 purchased from Selleck.
Assessment of in vivo toxicity to MEK inhibitor PD0325901. (A) Weight change in grams is shown for each PD0325901 (PD) treatment group in the MDA-MB-453 xenograft model. Weight change is the difference between pre- and post-treatment weight in each group. PD0325901 treatments were carried out at 5, 10, 15 and 20 mg/kg/day for 30 days, and daily gavage of carrier solution was used as control. *P < 0.01 for PD-5/PD-10 vs. control groups and PD-5/PD-10 vs. PD-15/PD-20 groups using Mann-Whitney U test. Error bars: ±2 SEM. (B) Number of days lost due to toxicity is shown for each PD0325901 treatment group in mouse xenograft model explained in Figure 5A. *P < 0.01 for PD-5/PD-10 vs. PD-15/PD-20 groups.

Breast Cancer Res 2011 13, R36. PD0325901 purchased from Selleck.

The therapeutic effect of AR and MEK inhibitors on in vivo angiogenesis. (A) Angiogenesis index for each in vivo treatment group. Angiogenesis was measured as the number of CD-31-positive blood vessels in a cross-section of each xenograft tumor. CTL: control group; FLU: flutamide; and PD: PD0325901. *P < 0.03 for PD0325901 monotherapy vs. control and **P < 0.03 for combination therapy vs. monotherapy groups using Mann-Whitney U test. Error bars: ±2 SEM. (B) Immunohistochemistry (IHC) was used to measure angiogenesis in a control xenograft tumor. Staining was performed using a CD31 rabbit polyclonal antibody. Original magnification, × 40. (C) IHC was used to measure angiogenesis in a PD0325901 monotherapy tumor. Original magnification, × 40. (D) IHC was used to measure angiogenesis in a xenograft tumor treated with combination therapy. Original magnification, × 40.

Breast Cancer Res 2011 13, R36. PD0325901 purchased from Selleck.
Effects of the MEK inhibitor (MEKi) PD0325901 (PD) and rhBMP-2 (BMP) treatment on histology in an NF1 open fracture model. Treatment with 10 mg/kg of PD0325901 on days 22 through 10 (PD alone) slightly improved bone volume and callus size. Delivery of 10 mg of rhBMP-2 in the collagen sponge (BMP alone) resulted in a large increase in bone volume and callus size. Combination treatment with local rhBMP-2 and systemic PD0325901 (PD 1 BMP) resulted in further increases in new bone volume and total callus volume.Picro Sirius Red and Alcian Blue staining to assess fibrous tissue.

J Bone Joint Surg Am 2015 96(14), e117. PD0325901 purchased from Selleck.

Bone 2014 59, 151-61. PD0325901 purchased from Selleck.
Characterization of rES cells. A: image of normal rES cell colonies on feeder layers. B: rES colonies were positive for AP staining. CeE: rES colonies readily expressed pluripotent markers, Sox2 (C), Oct4 (D), and SSEA-1 (E). Blue, DAPI. Scale bars: 100 um.

J Genet Genomics 2012 39, 643e651. PD0325901 purchased from Selleck.

Effect of small molecule inhibitors on reprogramming efficiency of myoblast cell derived from 5 different donors. (A) Reprogramming efficiency is shown as number of colonies from 10^5 starting cells on Y-axes. Ctrl, control condition and addition of small molecule inhibitors are marked. (B) AP staining of reprogrammed myoblast cell lines,from 5 different donors, in wells of 12-well plates at day 18. Ctrl, control condition and additions of small molecule inhibitors are marked.

Stem Cells Dev 2013 PD0325901 purchased from Selleck.
The effects of PD0325901 on the Akt/mTOR and MAPK pathways in the two DDLS cell lines as evaluated by western blotting

Tumour Biol, 2016, 37(4):4767-76.. PD0325901 purchased from Selleck.

PD0325901 inhibited the sorafenib-induced RAS/ERK pathway activation and enhanced the cytotoxic effects of sorafenib in resistant cell lines. (A) HUH-7 hepatoma cells treated with sorafenib (5 μM) for 24 h with or without pretreatment with specific kinase inhibitors (PD0325901, 10 μM). Expressions of p-AKT and cleaved PARP were revealed by Western blotting. (B) SK-HEP-1 hepatoma cells treated with sorafenib (5 μM) for 24 h with or without pretreatment with specific kinase inhibitors (PD0325901, 10 μM). Expressions of p-AKT and cleaved PARP were revealed by Western blotting. (C) HUH-7 hepatoma cells treated with sorafenib (5 μM) with or without the kinase inhibitors for 24 h. Proportions of apoptotic cells were evaluated by annexin V labeling. (D) SK-HEP-1 hepatoma cells treated with sorafenib (5 μM) with or without the kinase inhibitors for 24 h. Proportions of apoptotic cells were evaluated by annexin V labeling. (*P<0.05, HUH- 7, SK-HEP-1 are control groups, R-HUH-7, R-SK-HEP-1 are resistant groups).

J Surg Res, 2016, 206(2):371-379. PD0325901 purchased from Selleck.
Inhibition of anchorage-independent growth of lung tumor cell lines by selected inhibitors. Each selected cell line was treated with the indicated inhibitor at 0.1 μM and 1 μM concentrations for two weeks and cell colony size formation was scored under the Nikon inverted-phase microscope.

Int J Proteomics 2011 2011, Article ID 215496. PD0325901 purchased from Selleck.

Breast cancer cells were pretreated with 100ng/ml EGF for 15 min and then treated with the indicated concentrations of PD0325901 for 24 hours.

2010 Dr Zhang of Tianjin Medical University. PD0325901 purchased from Selleck.
Effects of PD0325901 on HT29 Xenograft tumors. PD0325901(1mg/kg carrier DMSO).Collection at 24h.

2010 Dr. Citrin, Deborah of NIH. PD0325901 purchased from Selleck.

Purity & Quality Control

Choose Selective MEK Inhibitors

Biological Activity

Description

Targets

MEK ^[1]
(Cell-free assay)

0.33 nM

In vitro

PD0325901 shows higher permeability than CI-1040, another MEK inhibitor. PD0325901 should be able to achieve higher systemic exposures than CI-1040. ^[1] PD0325901 is exquisitely specific and highly potent against purified MEK, revealing a K_i^app of 1 nM against activated MEK1 and MEK2. ^[2] PD0325901 is roughly 500-fold more potent than CI-1040 with respect to its cellular effects on phosphorylation of ERK1 and ERK2, displaying subnanomolar activity. ^[2] PD0325901 prevents the growth of melanoma cell lines. PD0325901 inhibits the growth of TPC-1 cells and K2 cells with GI50 of 11 nM and 6.3 nM, respectively. ^[3] PD0325901 significantly prevents the the growth of PTC cells harboring a BRAF mutation at very low concentration (10 nM) and only moderately increases the growth of the PTC cells carrying the RET/PTC1 rearrangement at the same concentration. PD0325901 effectively inhibits the phosphorylation of ERK1/2 in multiple PTC cell lines. ^[3]

Cell Data

Cell Lines	Assay Type	Concentration	Incubation Time	Activity Description	PMID
human CHP-212 cell	NInJO29Iem:5dHigbY5pcWKrdHnvckBie3OjeR?=			NIm4SVFKdmirYnn0bY9vKG:oIHj1cYFvKEOKUD2yNVIh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0xNjV{NzDuUU4>	MUTTRW5ITVJ?
human M14 cell	NVnRRYtpT3Kxd4ToJIlvcGmkaYTpc44h[XO\|YYm=			NV;lSVhtUW6qaXLpeIlwdiCxZjDoeY1idiCPMUSgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xMlQ2KG6PLh?=	M3;4V3NCVkeHUh?=
human SK-MEL-28 cell	M13Wcmdzd3e2aDDpcohq[mm2aX;uJIF{e2G7			NHz1dpZKdmirYnn0bY9vKG:oIHj1cYFvKFONLV3FUE0zQCClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR\|UxRTFwNUKgcm0v	MYfTRW5ITVJ?
human NOMO-1 cell	MofXS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			NIPJd\|VKdmirYnn0bY9vKG:oIHj1cYFvKE6RTV:tNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVIvODdibl2u	NVzITY5ZW0GQR1XS
human A375 cell	MVfHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			NYT2[GU{UW6qaXLpeIlwdiCxZjDoeY1idiCDM{e1JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9Nk43QSCwTT6=	NGLVWXJUSU6JRWK=
human DU-4475 cell	NFXOVJJIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			Mnz2TY5pcWKrdHnvckBw\iCqdX3hckBFXS12NEe1JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9N{42PyCwTT6=	MmToV2FPT0WU
human C32 cell	MVrHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			MVfJcohq[mm2aX;uJI9nKGi3bXHuJGM{OiClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR\|UxRTNwNkegcm0v	MY\TRW5ITVJ?
human BPH-1 cell	MWLHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			MnXFTY5pcWKrdHnvckBw\iCqdX3hckBDWEhvMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG\|c3H5MEBKSzVyPUOuPVUhdk1w	M3vo[nNCVkeHUh?=
human CP50-MEL-B cell	MVzHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			M3TU[WlvcGmkaYTpc44hd2ZiaIXtZY4hS1B3MD3NSWwuSiClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR\|UxRTRwNUigcm0v	MmryV2FPT0WU
human H9 cell	MofDS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			MX3Jcohq[mm2aX;uJI9nKGi3bXHuJGg6KGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:PS55NzDuUU4>	NXfsb48xW0GQR1XS
human HTC-C3 cell	MVTHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			M37wUGlvcGmkaYTpc44hd2ZiaIXtZY4hUFSFLVOzJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9OU45QSCwTT6=	NV\LV5FjW0GQR1XS
human BHT-101 cell	MULHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			MWPJcohq[mm2aX;uJI9nKGi3bXHuJGJJXC1zMEGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME22Mlchdk1w	NYHVdHZrW0GQR1XS
human COLO-741 cell	NXL0b21nT3Kxd4ToJIlvcGmkaYTpc44h[XO\|YYm=			M{PLWmlvcGmkaYTpc44hd2ZiaIXtZY4hS0:OTz23OFEh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF04NjFibl2u	Mlv3V2FPT0WU
human OVCAR-5 cell	MnfES5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			NWrLN3lNUW6qaXLpeIlwdiCxZjDoeY1idiCRVlPBVk02KGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:Py56MjDuUU4>	NIXGcFZUSU6JRWK=
human A549 cell	NXLwb5ZsT3Kxd4ToJIlvcGmkaYTpc44h[XO\|YYm=			NVHGUpVNUW6qaXLpeIlwdiCxZjDoeY1idiCDNUS5JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9O{45QSCwTT6=	NV[4doZ[W0GQR1XS
human SH-4 cell growth	MlzpS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			MknlTY5pcWKrdHnvckBw\iCqdX3hckBUUC12IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO\|YYmsJGlEPTB;OD6yOkBvVS5?	NXq2bVZqW0GQR1XS
human SK-N-AS cell	NF\md2xIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			NFrxT\|hKdmirYnn0bY9vKG:oIHj1cYFvKFONLV6tRXMh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF05NjR2IH7NMi=>	MWHTRW5ITVJ?
human HT-144 cell	MmPFS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			M3;y[GlvcGmkaYTpc44hd2ZiaIXtZY4hUFRvMUS0JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9PE46PyCwTT6=	NX76NlhxW0GQR1XS
human MEL-HO cell	MlTXS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			NV7y[FNoUW6qaXLpeIlwdiCxZjDoeY1idiCPRVytTG8h[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF06NjR7IH7NMi=>	MU\TRW5ITVJ?
human COLO-679 cell	MVfHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			NV7oWHdbUW6qaXLpeIlwdiCxZjDoeY1idiCFT1zPMVY4QSClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR\|UxRTFyLkCxJI5O	MmHHV2FPT0WU
human HuP-T4 cell	MV7Hdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			NVywUWNUUW6qaXLpeIlwdiCxZjDoeY1idiCKdWCtWFQh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0yOC57ODDuUU4>	NUm2Vlh5W0GQR1XS
human H-EMC-SS cell	MmXTS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			MYLJcohq[mm2aX;uJI9nKGi3bXHuJGguTU2FLWPTJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NVEvODJibl2u	M{[3NXNCVkeHUh?=
human LB2518-MEL cell	NH\kUpZIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			NELmZYdKdmirYnn0bY9vKG:oIHj1cYFvKEyEMkWxPE1OTUxiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1zMT6xN{BvVS5?	MUfTRW5ITVJ?
human HL-60 cell	Mln6S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			NEnROXdKdmirYnn0bY9vKG:oIHj1cYFvKEiOLU[wJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NVEvOTVibl2u	M1r1bnNCVkeHUh?=
human NCI-H1666 cell	M1PCRmdzd3e2aDDpcohq[mm2aX;uJIF{e2G7			MV7Jcohq[mm2aX;uJI9nKGi3bXHuJG5EUS2KMU[2OkBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVEyNjF5IH7NMi=>	MkPoV2FPT0WU
human A101D cell	MVPHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			NWPYe3RMUW6qaXLpeIlwdiCxZjDoeY1idiCDMUCxSEBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVEyNjR3IH7NMi=>	NVPve\|ZzW0GQR1XS
human RVH-421 cell	Mlv6S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			M{XHO2lvcGmkaYTpc44hd2ZiaIXtZY4hWl[KLUSyNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVEzNjZ2IH7NMi=>	NFXPNIJUSU6JRWK=
human Hs-578-T cell	NWe5RopZT3Kxd4ToJIlvcGmkaYTpc44h[XO\|YYm=			MljnTY5pcWKrdHnvckBw\iCqdX3hckBJey13N{itWEBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVEzNjd7IH7NMi=>	M2Xl[3NCVkeHUh?=
human A375 cells	NGC5TJBRem:uaX\ldoF1cW:wIHHzd4F6		MYK3NkBp	MUDBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKEF\|N{WgZ4VtdHNiZYjwdoV{e2mwZzDCVmFHKFZ4MEDFJI12fGGwdDDh[pRmeiB5MjDodpMh[nliQ3XscEB1cXSncj3ncI8h[XO\|YYmsJGlEPTB;MUOgcm0v	M4O1RlI{PDd2M{i4
human DOK cell	M3zMNWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7			MU\Jcohq[mm2aX;uJI9nKGi3bXHuJGRQUyClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR\|UxRTF\|LkSgcm0v	NVXWN29[W0GQR1XS
human Mewo cell	MlLES5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			MVTJcohq[mm2aX;uJI9nKGi3bXHuJG1mf29iY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1zND60OUBvVS5?	M3u4Z3NCVkeHUh?=
human ONS-76 cell	NH7lUXNIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			M17ZZWlvcGmkaYTpc44hd2ZiaIXtZY4hV06VLUe2JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NVQvPTFibl2u	Ml;0V2FPT0WU
human UACC-257 cell	M124OWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7			NWfCS2JDUW6qaXLpeIlwdiCxZjDoeY1idiCXQVPDMVI2PyClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR\|UxRTF2Lk[yJI5ONg>?	NVj0SVJ2W0GQR1XS
human SW626 cell	MnSwS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			NX\PR41ZUW6qaXLpeIlwdiCxZjDoeY1idiCVV{[yOkBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVE1NjlzIH7NMi=>	MmjkV2FPT0WU
human SW620 cell	NHvWVVdIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			MV\Jcohq[mm2aX;uJI9nKGi3bXHuJHNYPjJyIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO\|YYmsJGlEPTB;MUSuPVUhdk1w	M1e1fXNCVkeHUh?=
human TYK-nu cell	MmOxS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			M1ixZmlvcGmkaYTpc44hd2ZiaIXtZY4hXFmNLX71JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NVUvOTNibl2u	MVTTRW5ITVJ?
human ACN cell	M2\UcGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7			MXrJcohq[mm2aX;uJI9nKGi3bXHuJGFEViClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR\|UxRTF3Lke2JI5ONg>?	NEHIW\|ZUSU6JRWK=
human MIAPaCa2 cells	M1zGfHBzd2yrZnXyZZRqd25iYYPzZZk>			MkjvRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6\|dDDoeY1idiCPSVHQZWNiOiClZXzsd{whUUN3ME2xO{BvVS5?	Mn7aNlM1PzR\|OEi=
human T-24 cell	MnLTS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			MoPQTY5pcWKrdHnvckBw\iCqdX3hckBVNTJ2IHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO\|YYmsJGlEPTB;MUmuO\|Ehdk1w	MkfyV2FPT0WU
human AGS cell	NHfJWmVIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			MkfpTY5pcWKrdHnvckBw\iCqdX3hckBCT1NiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1{MD60NUBvVS5?	M4njUnNCVkeHUh?=
human SW872 cell	NE[1NoFIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			NHu5O5NKdmirYnn0bY9vKG:oIHj1cYFvKFOZOEeyJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NlcvQTlibl2u	Mlz4V2FPT0WU
human C2BBe1 cell	NUfjdoRVT3Kxd4ToJIlvcGmkaYTpc44h[XO\|YYm=			MYHJcohq[mm2aX;uJI9nKGi3bXHuJGMzSkKnMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG\|c3H5MEBKSzVyPUK4MlU1KG6PLh?=	M37E[nNCVkeHUh?=
human MZ7-mel cell	NIHtW\|BIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			NYHEOnZJUW6qaXLpeIlwdiCxZjDoeY1idiCPWketcYVtKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OjlwNEOgcm0v	M1z1NnNCVkeHUh?=
human HCC2998 cell	MV7Hdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			NGS5ZZhKdmirYnn0bY9vKG:oIHj1cYFvKEiFQ{K5PVgh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0{Oy54NjDuUU4>	M1fI[3NCVkeHUh?=
human HO-1-N-1 cell	MorSS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			NEfsOZdKdmirYnn0bY9vKG:oIHj1cYFvKEiRLUGtUk0yKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OzRwNEOgcm0v	MXLTRW5ITVJ?
human SW756 cell	NHGxR5pIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			NHPtWXRKdmirYnn0bY9vKG:oIHj1cYFvKFOZN{W2JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9N\|QvPDVibl2u	MmXrV2FPT0WU
human NCI-H1437 cell	NVLVcWVDT3Kxd4ToJIlvcGmkaYTpc44h[XO\|YYm=			M3\QW2lvcGmkaYTpc44hd2ZiaIXtZY4hVkOLLVixOFM4KGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:OzRwNEmgcm0v	MYHTRW5ITVJ?
human NCI-H747 cell	M17UT2dzd3e2aDDpcohq[mm2aX;uJIF{e2G7			MYjJcohq[mm2aX;uJI9nKGi3bXHuJG5EUS2KN{S3JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9N\|QvQThibl2u	MXPTRW5ITVJ?
human SK-MEL-2 cell	NV3BPWFtT3Kxd4ToJIlvcGmkaYTpc44h[XO\|YYm=			MVTJcohq[mm2aX;uJI9nKGi3bXHuJHNMNU2HTD2yJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9N\|UvOiCwTT6=	M1jsbXNCVkeHUh?=
human MZ2-MEL cell	MVzHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			MnPsTY5pcWKrdHnvckBw\iCqdX3hckBOYjJvTVXMJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9N\|UvPjVibl2u	NVfnR5c6W0GQR1XS
human PSN1 cell	NIrxfYxIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			NWLyfllyUW6qaXLpeIlwdiCxZjDoeY1idiCSU16xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9N\|gvPDVibl2=	NETDblNUSU6JRWK=
human CAL-39 cell	MmHoS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			NVTJWGNWUW6qaXLpeIlwdiCxZjDoeY1idiCFQVytN\|kh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF0{QS5yNDDuUU4>	M4jXfXNCVkeHUh?=
human LOXIMVI cell	Mn62S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			MX7Jcohq[mm2aX;uJI9nKGi3bXHuJGxQYEmPVlmgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2zPU4{QSCwTT6=	MXPTRW5ITVJ?
human COLO-792 cell	NFfneXRIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			MoPKTY5pcWKrdHnvckBw\iCqdX3hckBEV0yRLUe5NkBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVQ{NjF3IH7NMi=>	MWTTRW5ITVJ?
human CAL-27 cell	MX3Hdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			NEHrXZlKdmirYnn0bY9vKG:oIHj1cYFvKEODTD2yO{Bk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVQ1NjlzIH7N	M1;sVXNCVkeHUh?=
human AsPC-1 cell	MmHJS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			Mn72TY5pcWKrdHnvckBw\iCqdX3hckBCe1CFLUGgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME20OU4zQCCwTT6=	MoXDV2FPT0WU
human NCI-H2291 cell	NWrWZmhUT3Kxd4ToJIlvcGmkaYTpc44h[XO\|YYm=			MknCTY5pcWKrdHnvckBw\iCqdX3hckBPS0lvSEKyPVEh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF01Pi52NjDuUU4>	MknRV2FPT0WU
human RCM-1 cell	MXPHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			MXHJcohq[mm2aX;uJI9nKGi3bXHuJHJEVS1zIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO\|YYmsJGlEPTB;NE[uPFUhdk1w	NGTCS3lUSU6JRWK=
human NCI-H292 cell	NGjFXHlIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			NYW0PFg2UW6qaXLpeIlwdiCxZjDoeY1idiCQQ1mtTFI6OiClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR\|UxRTR5LkO5JI5ONg>?	NF\EeJZUSU6JRWK=
human WM-115 cell	MVPHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			M4j2[mlvcGmkaYTpc44hd2ZiaIXtZY4hX01vMUG1JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9OFgvPSCwTT6=	MkftV2FPT0WU
human RT-112 cell	MnP0S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			MULJcohq[mm2aX;uJI9nKGi3bXHuJHJVNTFzMjDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG\|c3H5MEBKSzVyPUS4Mlg1KG6PLh?=	NYe1eXk{W0GQR1XS
human HT-29 cell	M1zt[Wdzd3e2aDDpcohq[mm2aX;uJIF{e2G7			NWTOfZFqUW6qaXLpeIlwdiCxZjDoeY1idiCKVD2yPUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVUxNjR7IH7NMi=>	NET2b5ZUSU6JRWK=
human RKO cell growth	NHvQNZBIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			NFexZY5KdmirYnn0bY9vKG:oIHj1cYFvKFKNTzDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG\|c3H5MEBKSzVyPUWyMlAzKG6PLh?=	NF\xOZhUSU6JRWK=
human KY821 cell	MmqwS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			MUTJcohq[mm2aX;uJI9nKGi3bXHuJGt[QDJzIHPlcIwh\3Kxd4ToJIlvKGFiY3XscEB3cWGkaXzpeJkh[XO\|YYmsJGlEPTB;NUOuN{BvVS5?	M{\r[3NCVkeHUh?=
human LB1047-RCC cell	NEi3dVZIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			M{P3S2lvcGmkaYTpc44hd2ZiaIXtZY4hVEJzMES3MXJESyClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR\|UxRTV7Lk[1JI5ONg>?	NX7scVFlW0GQR1XS
human SW1116 cell	MnfRS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			MXXJcohq[mm2aX;uJI9nKGi3bXHuJHNYOTFzNjDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG\|c3H5MEBKSzVyPU[wMlQ6KG6PLh?=	M1LheXNCVkeHUh?=
human P12-ICHIKAWA cell	NGHmWXVIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			MVjJcohq[mm2aX;uJI9nKGi3bXHuJHAyOi2LQ1jJT2FYSSClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR\|UxRTZ{LkK3JI5ONg>?	MlHHV2FPT0WU
human HCC70 cell	NGj4TFNIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			MkXxTY5pcWKrdHnvckBw\iCqdX3hckBJS0N5MDDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG\|c3H5MEBKSzVyPU[zMlAyKG6PLh?=	MYPTRW5ITVJ?
human MIA-PaCa-2 cell	MXLHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			M{PzRWlvcGmkaYTpc44hd2ZiaIXtZY4hVUmDLWDhR4EuOiClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR\|UxRTZ\|LkWzJI5ONg>?	M1flfXNCVkeHUh?=
human LoVo cell	MYfHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			MWXJcohq[mm2aX;uJI9nKGi3bXHuJGxwXm9iY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD14NT6yPUBvVS5?	NEW3PJlUSU6JRWK=
human LB2241-RCC cell	MXTHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			MnfxTY5pcWKrdHnvckBw\iCqdX3hckBNSjJ{NEGtVmNEKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:PjVwNUKgcm0v	M2jLfnNCVkeHUh?=
human GAK cell	MXfHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			NXztWZdYUW6qaXLpeIlwdiCxZjDoeY1idiCJQVugZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME22Ok45PyCwTT6=	NGn0bWVUSU6JRWK=
human RD cell	NV7Nd\|A2T3Kxd4ToJIlvcGmkaYTpc44h[XO\|YYm=			MYXJcohq[mm2aX;uJI9nKGi3bXHuJHJFKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:PjdwMTDuUU4>	Mn3uV2FPT0WU
human KNS-62 cell	NHLhVnBIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			M2jaPGlvcGmkaYTpc44hd2ZiaIXtZY4hU06VLU[yJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9OlkvQTlibl2u	MoDOV2FPT0WU
human HD-MY-Z cell	NFfWXGxIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			M2DFSWlvcGmkaYTpc44hd2ZiaIXtZY4hUERvTWmtXkBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVcyNjF{IH7NMi=>	M1XFVnNCVkeHUh?=
human COR-L105 cell	MXTHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			NHjaXlVKdmirYnn0bY9vKG:oIHj1cYFvKEORUj3MNVA2KGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:PzFwN{Ggcm0v	Mlj3V2FPT0WU
human IA-LM cell	NWH0dFlqT3Kxd4ToJIlvcGmkaYTpc44h[XO\|YYm=			MkLDTY5pcWKrdHnvckBw\iCqdX3hckBKSS2OTTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG\|c3H5MEBKSzVyPUezMlI5KG6PLh?=	MV\TRW5ITVJ?
human EM-2 cell	NHL2fYRIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			NGXPPWxKdmirYnn0bY9vKG:oIHj1cYFvKEWPLUKgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME23OE44KG6PLh?=	MnnBV2FPT0WU
human NB69 cell	NF3zcZRIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			M{XFbmlvcGmkaYTpc44hd2ZiaIXtZY4hVkJ4OTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG\|c3H5	MUTTRW5ITVJ?
human HuP-T3 cell	M{DCTWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7			MlPyTY5pcWKrdHnvckBw\iCqdX3hckBJfVBvVEOgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME24N{46OyCwTT6=	NYXRVVFUW0GQR1XS
human BB30-HNC cell	M{HJSWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7			NVT4OHFDUW6qaXLpeIlwdiCxZjDoeY1idiCEQkOwMWhPSyClZXzsJIdzd3e2aDDpckBiKGOnbHygeoli[mmuaYT5JIF{e2G7LDDJR\|UxRTh3LkWxJI5ONg>?	NYjndYxHW0GQR1XS
human HT-1080 cell	MmjXS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			NIHQ[nVKdmirYnn0bY9vKG:oIHj1cYFvKEiWLUGwPFAh[2WubDDndo94fGhiaX6gZUBk\WyuII\pZYJqdGm2eTDhd5NigSxiSVO1NF05PS56ODDuUU4>	NUHybotFW0GQR1XS
human RMG-I cell	MXHHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			M3jxdGlvcGmkaYTpc44hd2ZiaIXtZY4hWk2JLVmgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME24O{4{PCCwTT6=	NELDe4lUSU6JRWK=
human HCC1419 cell	MkXjS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			MkDYTY5pcWKrdHnvckBw\iCqdX3hckBJS0NzNEG5JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9PVEvOzhibl2u	NUDLcotmW0GQR1XS
human SW780 cell	M2TWNGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7			NEXsN2RKdmirYnn0bY9vKG:oIHj1cYFvKFOZN{iwJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9PVIvOzJibl2u	NF7BRY9USU6JRWK=
human SNU-387 cell	MYPHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			MVTJcohq[mm2aX;uJI9nKGi3bXHuJHNPXS1\|OEegZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME25N{4{PiCwTR?=	NYjEVY1UW0GQR1XS
human LAMA-84 cell	MWjHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			MmjlTY5pcWKrdHnvckBw\iCqdX3hckBNSU2DLUi0JINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9PVQvPjhibl2u	MYDTRW5ITVJ?
human MV-4-11 cell	MUjHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			M4PremlvcGmkaYTpc44hd2ZiaIXtZY4hVVZvND2xNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVk1Njd\|IH7NMi=>	NInofmhUSU6JRWK=
human EGI-1 cell	NF22UZZIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			NVWw[FFvUW6qaXLpeIlwdiCxZjDoeY1idiCHR1mtNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVk2NjhzIH7NMi=>	MYrTRW5ITVJ?
human NCI-SNU-1 cell	M1fZVGdzd3e2aDDpcohq[mm2aX;uJIF{e2G7			M3Pt[mlvcGmkaYTpc44hd2ZiaIXtZY4hVkOLLWPOWU0yKGOnbHyg[5Jwf3SqIHnuJIEh[2WubDD2bYFjcWyrdImgZZN{[XluIFnDOVA:QTZwN{Ogcm0v	NGPqUXZUSU6JRWK=
human MEG-01 cell	MnrxS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			MU\Jcohq[mm2aX;uJI9nKGi3bXHuJG1GTy1yMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG\|c3H5MEBKSzVyPUm3Mlc4KG6PLh?=	MnTEV2FPT0WU
human OMC-1 cell	MVvHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			NWLydndNUW6qaXLpeIlwdiCxZjDoeY1idiCRTVOtNUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVExOC5{MzDuUU4>	MoDtV2FPT0WU
human NB10 cell	MYPHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			NGrHemFKdmirYnn0bY9vKG:oIHj1cYFvKE6EMUCgZ4VtdCCpcn;3eIghcW5iYTDj[YxtKH[rYXLpcIl1gSCjc4PhfUwhUUN3ME2xNFAvPDJibl2u	NIXoUIdUSU6JRWK=
human CAL-62 cell	NGH4NHRIem:5dHigbY5pcWKrdHnvckBie3OjeR?=			NHTuWXlKdmirYnn0bY9vKG:oIHj1cYFvKEODTD22NkBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVExOC55ODDuUU4>	M2q1U3NCVkeHUh?=
human NCI-H2087 cell	NYLDVJllT3Kxd4ToJIlvcGmkaYTpc44h[XO\|YYm=			NYnNd21QUW6qaXLpeIlwdiCxZjDoeY1idiCQQ1mtTFIxQDdiY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1zMEGuNVQhdk1w	MVPTRW5ITVJ?
human MDA-MB-175-VII cell	MV3Hdo94fGhiaX7obYJqfGmxbjDhd5NigQ>?			NWXOSFlOUW6qaXLpeIlwdiCxZjDoeY1idiCPRFGtUWIuOTd3LW\JTUBk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6	M2Tse3NCVkeHUh?=
human LS-513 cell	MmThS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			NGjSS3lKdmirYnn0bY9vKG:oIHj1cYFvKEyVLUWxN{Bk\WyuIHfyc5d1cCCrbjDhJINmdGxidnnhZoltcXS7IHHzd4F6NCCLQ{WwQVEyPC56MzDuUU4>	M1TWXHNCVkeHUh?=
human HN cell growth	MlewS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl?			M{fX[mlvcGmkaYTpc44hd2ZiaIXtZY4hUE5iY3XscEBoem:5dHigbY4h[SClZXzsJJZq[WKrbHn0fUBie3OjeTygTWM2OD1zMkKuOVkhdk1w	M1vBNHNCVkeHUh?=
human ABC-1 cell	M4HWXWdzd3e2aDDpcohq[mm2aX;uJIF{e2G7			Ml;6TY5pcWKrdHnvckBw\iCqdX3hckBCSkNvMTDj[YxtKGe{b4f0bEBqdiCjIHPlcIwhfmmjYnnsbZR6KGG\|c3H5MEBKSzVyPUGyN{4xOiCwTT6=	MWDTRW5ITVJ?
human SJSA-1 cell	NYLVXlVqT3Kxd4ToJIlvcGmkaYTpc44h[XO\|YYm=			M1izbmlvcGmkaYTpc44hd2ZiaIXtZY4hW0qVQT2xJINmdGxiZ4Lve5RpKGmwIHGgZ4VtdCC4aXHibYxqfHliYYPzZZktKEmFNUC9NVI{NjF7IH7NMi=>	MWXTRW5ITVJ?
human PANC1 cells	M13EPGZ2dmO2aX;uJIF{e2G7	NYeyUGJrOTBizszN	MWOxJIg>	M336eGlvcGmkaYTpc44hd2ZiTVXLNUBqdiCqdX3hckBRSU6FMTDj[YxteyCjc4Pld5Nm\CCjczDy[YR2[3Srb36gbY4heEW{a{GvNkBt\X[nbDDheEAyOCC3TTDh[pRmeiBzIHjyJIJ6KFenc4Tldo4h[myxdITpcoch[W6jbInzbZM>	NW\pcXJmOjV5Nk[2N\|M>
human MCF7 cells	NXTKb2RiTnWwY4Tpc44h[XO\|YYm=		M4DD[lc2KG2rboO=	Ml\mTY5pcWKrdHnvckBw\iCPRXuxM\|IhcW5iaIXtZY4hVUOINzDj[YxteyCjc4Pld5Nm\CCjczDk[YNz\WG\|ZTDpckBGWkticHjvd5Bpd3K7bHH0bY9vKGGodHXyJFc2KG2rboOgZpkhX2W\|dHXyckBjdG:2dHnu[{BidmGueYPpdy=>	M2rLelI{Ozl6NEWz

... Click to View More Cell Line Experimental Data

In vivo

The improved potency of PD0325901 relative to CI-1040 is evident. A single oral dose of PD0325901 (25 mg/kg) inhibits phosphorylation of ERK by more than 50% at 24 hours post-dosing. In contrast, CI-1040 at a much higher dose (150 mg/kg) only inhibit pERK levels for roughly 8 hours, returning to control levels by 24 hours after treatment. ^[2] Therefore, the dose required to produce a 70% incidence of complete tumor responses (C26 model) is 25 mg/kg/day versus 900 mg/kg/day for PD0325901 and CI-1040, respectively. Anticancer activity of PD 0325901 has been demonstrated for a broad spectrum of human tumor xenografts. ^[2] After 1 week of oral administration of PD0325901 (20–25 mg/kg/day) in mice, no tumor growth is detected in mice inoculated with PTC cells bearing a BRAF mutation. ^[3] For PTC with the RET/PTC1 rearrangement, the average tumor volume of the orthotopic tumor is decreased by 58% as compared with controls. In conclusion, PTC cells carrying a BRAF mutation are more sensitive to PD0325901 than are PTC cells carrying the RET/PTC1 rearrangement. ^[3]

Protocol

Kinase Assay: ^[1]	+ Expand In vitro cascade assay: Incorporation of ³²P into myelin basic protein (MBP) is assayed in the presence of a glutathione S-transferase fusion protein containing p44MAP kinase (GST-MAPK) and a glutathione S-transferase protein containing p45MEK (GST-MEK). The assay solution contained 20 mM HEPES, pH 7.4, 10 mM MgCl₂, 1 mM MnCl₂, 1 mM EGTA, 50 mM [gamma-³²P]ATP, 10 mg GST-MEK, 0.5 mg GST-MAPK and 40 mg MBP in a final volume of 100 mL. Reactions are stopped after 20 minutes by addition of trichloroacetic acid and filtered through a GF/C filter mat. ³²P retained on the filter mat is determined using a 1205 Betaplate. PD0325901 is assessed at various dose ranges in order to determine dose response curves.
Cell Research: ^[3]	+ Expand Cell lines: PTC cells Concentrations: 0.1 nM- 1 μM Incubation Time: 48 hours Method: PTC cells (1 × 10⁴) are seeded in 24-well plates with 1 mL of medium for 4 days in a 37 °C incubator. MEK inhibitor PD0325901 at varying concentrations is added to the cells in triplicate on day 0. MTT dissolved in 0.8% NaCl solution at 5 mg/mL is added to each well (0.2 mL) on day 2 to test GI50 or every day for cell growth curves. The cells are incubated at 37 °C for 3 hours with MTT. The liquid is then aspirated from the wells and discarded. Stained cells are dissolved in 0.5 mL of DMSO and their absorption at 570 nm is measured using a Synergy HT multidetection microplate reader. For GI50, cell growth is calculated as 100 × (T − T₀)/(C − T₀), where T is the optical density of the wells treated with inhibitors after a 48-hour period, T₀ is the optical density at time zero, and C is the control optical density with DMSO only. (Only for Reference)
Animal Research: ^[3]	+ Expand Animal Models: Ncr-nu/nu mice bearing PTC cells Formulation: 80 mM citric buffer (pH 7) Dosages: 20-25 mg/kg Administration: Oral gavage (Only for Reference)

References

+ Expand

Solubility (25°C)

In vitro	DMSO	96 mg/mL (199.09 mM)
	Ethanol	40 mg/mL (82.95 mM)
	Water	Insoluble
In vivo	Add solvents to the product individually and in order(Data is from Selleck tests instead of citations): 30% PEG 400+5% Tween 80+ddH2O For best results, use promptly after mixing.	10mg/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 PD0325901 SDF

Molecular Weight	482.19
Formula	C₁₆H₁₄F₃IN₂O₄
CAS No.	391210-10-9
Storage	3 years -20°C powder
Storage	2 years -80°C in solvent
Synonyms	N/A

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 (g) = Concentration (mol/L) × Volume (L) × 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):
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

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

Clinical Trial Information (data from https://clinicaltrials.gov, updated on 2019-03-27)

NCT Number	Recruitment	Conditions	Sponsor/Collaborators	Start Date	Phases
NCT02510001	Active not recruiting	Solid Tumor\|Colorectal Cancer	University of Oxford\|Queen''s University Belfast\|Oxford University Hospitals NHS Trust\|Velindre NHS Trust\|University Hospital Antwerp\|Hospital Vall d''Hebron\|Saint Antoine University Hospital\|European Georges Pompidou Hospital\|Pfizer\|University of Turin Italy\|Belfast Health and Social Care Trust\|Beaumont Hospital\|European Commission\|Array BioPharma\|University of Paris 5 - Rene Descartes	November 2014	Phase 1
NCT02510001	Active not recruiting	Solid Tumor\|Colorectal Cancer	University of Oxford\|Queen''s University Belfast\|Oxford University Hospitals NHS Trust\|Velindre NHS Trust\|University Hospital Antwerp\|Hospital Vall d''Hebron\|Saint Antoine University Hospital\|European Georges Pompidou Hospital\|Pfizer\|University of Turin Italy\|Belfast Health and Social Care Trust\|Beaumont Hospital\|European Commission\|Array BioPharma\|University of Paris 5 - Rene Descartes	November 2014	Phase 1
NCT02096471	Completed	Neurofibromatosis Type 1 and Growing or Symptomatic Inoperable PN	University of Alabama at Birmingham	June 2014	Phase 2
NCT02096471	Completed	Neurofibromatosis Type 1 and Growing or Symptomatic Inoperable PN	University of Alabama at Birmingham	June 2014	Phase 2
NCT02039336	Recruiting	Colorectal Cancer	The Netherlands Cancer Institute\|Pfizer	January 2014	Phase 1\|Phase 2
NCT02022982	Active not recruiting	KRAS Mutant Non-Small Cell Lung Cancer\|Solid Tumors	Dana-Farber Cancer Institute	January 2014	Phase 1\|Phase 2

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:
Whether the inhibitor PD0325901 interacts with other targets other than MEK?
Answer:
PD0325901 has very high selectivity to MEK. In addition, it can also inhibits VEGF activity according to the reference: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2713590/

MEK Signaling Pathway Map

MEK Inhibitors with Unique Features

Selective MEK Inhibitor

Selumetinib (AZD6244) : MEK1-selective, IC50=14 nM.
FDA-approved MEK Inhibitor

Trametinib (GSK1120212) : Approved by FDA against BRAF V600E mutated metastatic melanoma.
Newest MEK Inhibitor

Binimetinib (MEK162, ARRY-162, ARRY-438162) : Potent inhibitor of MEK1/2 with IC50 of 12 nM.
Classic MEK Inhibitor

SL-327 : Water soluble MEK1/2 inhibitor, which can cross the blood-brain barrier.

Related MEK Products4

Cobimetinib (GDC-0973, RG7420) ^New

Cobimetinib (GDC-0973, RG7420) is a potent and highly selective MEK1 inhibitor with IC50 of 4.2 nM, showing more than 100-fold selectively for MEK1 over MEK2 and showed no significant inhibition when tested against a panel of more than 100 of serine-threonine and tyrosine kinases. Phase 3.
BI-847325 ^New

BI-847325 is an orally bioavailable, and selective dual MEK/Aurora kinase inhibitor with IC50 of 3 nM, 25 nM, 15 nM, 25 nM, and 4 nM for Xenopus laevis Aurora B, human Aurora A and Aurora C, as well as human MEK1 and MEK2, respectively. Phase 1.
GDC-0623 ^New

GDC-0623 is a potent and ATP-uncompetitive MEK1 inhibitor with K_i of 0.13 nM. Phase 1.
Trametinib (GSK1120212)

Trametinib (GSK1120212) is a highly specific and potent MEK1/2 inhibitor with IC50 of 0.92 nM/1.8 nM in cell-free assays, no inhibition of the kinase activities of c-Raf, B-Raf, ERK1/2.

Features:More potent than PD0325901 or AZD6244.
Selumetinib (AZD6244)

Selumetinib (AZD6244) is a potent, highly selective MEK inhibitor with IC50 of 14 nM for MEK1 and Kd value of 530 nM for MEK2. It also inhibits ERK1/2 phosphorylation with IC50 of 10 nM, no inhibition to p38α, MKK6, EGFR, ErbB2, ERK2, B-Raf, etc. Phase 3.

Features:First MEK inhibitor being tested in Phase II clinical trials.
U0126-EtOH

U0126-EtOH is a highly selective inhibitor of MEK1/2 with IC50 of 0.07 μM/0.06 μM in cell-free assays, 100-fold higher affinity for ΔN3-S218E/S222D MEK than PD98059.

Features:A chemically synthesized and highly selective inhibitor of both MEK1 and MEK2.
PD98059

PD98059 is a non-ATP competitive MEK inhibitor with IC50 of 2 μM in a cell-free assay, specifically inhibits MEK-1-mediated activation of MAPK; does not directly inhibit ERK1 or ERK2.

Features:Does not inhibit c-Raf phosphorylated MEK1.
PD184352 (CI-1040)

PD184352 (CI-1040) is an ATP non-competitive MEK1/2 inhibitor with IC50 of 17 nM in cell-based assays, 100-fold more selective for MEK1/2 than MEK5. Phase 2.

Features:First MEK inhibitor to begin clinical development.
Binimetinib (MEK162, ARRY-162, ARRY-438162)

Binimetinib (MEK162, ARRY-162, ARRY-438162) is a potent inhibitor of MEK1/2 with IC50 of 12 nM in a cell-free assay. Phase 3.
Refametinib (RDEA119, Bay 86-9766)

Refametinib (RDEA119, Bay 86-9766) is a potent, ATP non-competitive and highly selective inhibitor of MEK1 and MEK2 with IC50 of 19 nM and 47 nM, respectively.

Choose Your Country or Region

By Signaling Pathways

By product type

PD0325901

Cited by 81 Publications

19 Customer Reviews

Purity & Quality Control

Choose Selective MEK Inhibitors

Biological Activity

Protocol

References

Solubility (25°C)

Chemical Information Download PD0325901 SDF

Bio Calculators

Molarity Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Dilution Calculator

Concentration _(start) x Volume _(start) = Concentration _(final) x Volume _(final)

The Serial Dilution Calculator Equation

Serial Dilutions

Computed Result

Molecular Weight Calculator

Total Molecular Weight: g/mol

Instructions to calculate molar mass (molecular weight) of a chemical compound:

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molarity Calculator

Clinical Trial Information (data from https://clinicaltrials.gov, updated on 2019-03-27)

Tech Support

Frequently Asked Questions

MEK Signaling Pathway Map

MEK Inhibitors with Unique Features

Related MEK Products4

Choose Your Country or Region

By Signaling Pathways

By product type

PD0325901

Cited by 81 Publications

19 Customer Reviews

Purity & Quality Control

Choose Selective MEK Inhibitors

Biological Activity

Protocol

References

Solubility (25°C)

Chemical Information Download PD0325901 SDF

Bio Calculators

Molarity Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Dilution Calculator

Concentration (start) x Volume (start) = Concentration (final) x Volume (final)

The Serial Dilution Calculator Equation

Serial Dilutions

Computed Result

Molecular Weight Calculator

Total Molecular Weight: g/mol

Instructions to calculate molar mass (molecular weight) of a chemical compound:

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molarity Calculator

Clinical Trial Information (data from https://clinicaltrials.gov, updated on 2019-03-27)

Tech Support

Frequently Asked Questions

MEK Signaling Pathway Map

MEK Inhibitors with Unique Features

Related MEK Products4

Concentration _(start) x Volume _(start) = Concentration _(final) x Volume _(final)