CI-1040 (PD184352)

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Customer Reviews(12) in vivo invitation

Quality Control & MSDS

Related Compound Libraries

CI-1040 (PD184352) is available in the following compound libraries:

Chemical Library (96-well) Inhibitor Library (96-well) Kinase Inhibitor Library (96-well)

Product Information

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Research Area

Cat.No.	Product Name	Solubility (25°C)
S1008	AZD6244 (Selumetinib)	<1 mg/mL	92 mg/mL	<1 mg/mL
S1036	PD0325901	<1 mg/mL	96 mg/mL	40 mg/mL
S2673	GSK1120212 (JTP-74057)	<1 mg/mL	5 mg/mL	<1 mg/mL
S1102	U0126-EtOH	<1 mg/mL	85 mg/mL	<1 mg/mL
S1177	PD98059	<1 mg/mL	19 mg/mL	<1 mg/mL
S1020	CI-1040 (PD184352)	<1 mg/mL	96 mg/mL	14 mg/mL
S1531	BIX 02189	<1 mg/mL	88 mg/mL	88 mg/mL
S1475	AS703026 (pimasertib)	<1 mg/mL	86 mg/mL	<1 mg/mL
S2617	TAK-733	<1 mg/mL	101 mg/mL	<1 mg/mL
S1530	BIX 02188	<1 mg/mL	43 mg/mL	3 mg/mL
S2134	AZD8330	<1 mg/mL	92 mg/mL	92 mg/mL
S2310	Honokiol	53 mg/mL	53 mg/mL	<1 mg/mL
S1568	PD318088	<1 mg/mL	112 mg/mL	14 mg/mL
S1066	SL327	<1 mg/mL	4 mg/mL	7 mg/mL

Combination Therapy

Dr. Antonino Maria Sparta demonstrates a breakthrough in leukemia research by utilizing two inhibitors produced by Selleck Chemicals.

Product Description

Biological Activity Protocol Chemical Information Customer Reviews Product Citations Tech Support & FAQs

Biological Activity

Description	CI-1040 (PD 184352) is an ATP non-competitive MEK1/2 inhibitor with IC50 of 17 nM.
Targets	MEK1	MEK2
IC50	17 nM	17 nM ^[1]
In vitro	CI-1040 treatment produces a reduction of pMAPK levels in multiple tumor cells including Colon 26, BX-PC3 pancreatic, A431 cervical, HT-29 colon, ZR-25-1 breast and SKOV-3 ovarian carcinomas. CI-1040 treatment doesn't inhibit the phosphorylation of Jun kinase, p38 kinase or Akt, indicating CI-1040 specifically targets MEK. Inhibition of MAPK activation by CI-1040 prevents cell cycle progression and induces a G1 block. ^[1] The IC50 for inhibition of MEK1 by CI-1040 is 0.3 µM, 15-fold higher than the concentration required to inhibit the EGF-induced activation of ERK2 in Swiss 3T3 cells. These results indicate CI-1040 exerts its effects on cells by suppressing the activation of MKK1, and not by blocking its activity. 2 nM PD184352 inhibits the activation of MKK1 in Swiss 3T3 cells by 50%, while over 100-fold concentration of CI-1040 inhibits MEK1 in vitro. PD184352 also inhibits the Raf-catalysed phosphorylation of MEK1 without any effect on the Raf-catalysed phosphorylation of myelin basic protein. ^[2] CI-1040 inhibits 86% of papillary thyroid carcinoma (PTC) cell growth with the RET/PTC1 rearrangement at 10µM compared with cells treated with DMSO only. CI-1040 shows potent inhibition to PTC cells (BRAF mutation) with GI50 of 52 nM, but low activity to RET/PTC1 rearrangement type with GI50 of 1.1 µM. ^[3] A recent research indicates CI-1040 increases the apoptotic effect of BMS-214662 in a CML blast crisis cell line, K562, and in primary chronic phase CD34+ CML cells. ^[4]
In vivo	Oral dosing of CI-1040 impairs the growth of colon tumor xenografts of mouse and human with a wide dose range of 48-200 mg/kg per dose, but not of P388 leukemia. ^[1] CI-1040 inhibits the tumor xenografts from PTC cells carrying a BRAF mutation with 31.3% reduction, carrying the RET/PTC1 rearrangement with 47.5% reduction than in untreated (vehicle) mice after 3 weeks of oral administration (300 mg/kg/d). No toxic effects are observed in any mice when they are treated with CI-1040. ^[2] Transient exposure of mammary tumors to CI-1040 and UCN-01 causes tumor cell death in vivo and prolonged suppression of tumor regrowth. Combined treatment with CI-1040 (25 mg/kg) and UCN-01 (0.1-0.2 mg/kg) significantly reduces MDA-MB-231, and largely abolishs MCF7 tumor growth in implanted athymic mice, while either single treatment has no significant activity. The drug combination leads to profound tumor cell death which correlates with a reduction in the phosphorylation of ERK1/2 and the immuno-reactivity of Ki67 and of CD31. ^[5]
Clinical Trials	Currently under Phase II in breast cancer, colorectal cancer, lung cancer, and pancreatic cancer.
Features	First MEK inhibitor to begin clinical development.

Protocol(Only for Reference)

Kinase Assay:
^[2]

MEK1 Assay	MAP kinase is activated after phosphorylation by MEK; the activated MAP kinase subsequently phosphorylates myelin basic protein (MBP).Incorporation of ³²P into myelin basic protein (MBP) is assayed in the presence of glutathione S-transferase (GST) fusion proteins containing the 44-kDa MAPK (GST-MAPK) or the 45-kDa MEK (GST-MEK1). Assays are conducted in 50μL of 50 mM Tris, pH 7.4/10 mM MgCl₂ /2 mM EGTA/10 μM [γ-³²P]ATP containing 10 μg of GST-MEK1, 0.5 μg of GST-MAPK, and 40 μg of MBP. After incubation at 30°C for 15 minutes, reactions are stopped by addition of Laemmli SDS sample buffer. Phosphorylated MBP is resolved by SDS/10% PAGE. This screening effort leads to the discovery of several small-molecule inhibitors of MEK, i.e. CI-1040. Experiments assessing the order of addition shows that CI-1040 directly inhibits MEK1 with a 50% inhibitory concentration (IC50) of 17 nM, without affecting the activity of MAPK.

MEK1 Assay

MAP kinase is activated after phosphorylation by MEK; the activated MAP kinase subsequently phosphorylates myelin basic protein (MBP).Incorporation of ³²P into myelin basic protein (MBP) is assayed in the presence of glutathione S-transferase (GST) fusion proteins containing the 44-kDa MAPK (GST-MAPK) or the 45-kDa MEK (GST-MEK1). Assays are conducted in 50μL of 50 mM Tris, pH 7.4/10 mM MgCl₂ /2 mM EGTA/10 μM [γ-³²P]ATP containing 10 μg of GST-MEK1, 0.5 μg of GST-MAPK, and 40 μg of MBP. After incubation at 30°C for 15 minutes, reactions are stopped by addition of Laemmli SDS sample buffer. Phosphorylated MBP is resolved by SDS/10% PAGE. This screening effort leads to the discovery of several small-molecule inhibitors of MEK, i.e. CI-1040. Experiments assessing the order of addition shows that CI-1040 directly inhibits MEK1 with a 50% inhibitory concentration (IC50) of 17 nM, without affecting the activity of MAPK.

Cell Assay:
^[1]

Cell lines	Colon 26 carcinoma cells
Concentrations	0.1-10 μM
Incubation Time	24 hours
Method	Cells are planted seeded in T-75 cm ² flasks and treated the next day for 24 hous with either DMSO or CI-1040. Single-cell suspensions are collected, and pellets are fixed in ice-cold ethanol (70%) for 30 minutes. After centrifugation of the samples, propidium iodide (50 μg/mL) and RNase (30 units/mL) are added to the pellets for 20 minutes at 37 °C. After filtration, samples are analyzed by flow cytometry.

Animal Study:
^[3]

Animal Models	PTC cells in athymic mice
Formulation	Cremophor EL–95% ethanol (50:50) and dilutes with water
Dosages	150 mg/kg
Administration	Orally twice daily via p.o.

1

References

Chemical Information

Download CI-1040 (PD184352) SDF

Molecular Weight (MW)	478.67
Formula	C₁₇H₁₄ClF₂IN₂O₂
CAS No.	212631-79-3
Synonyms	N/A

Solubility (25°C) DMSO 96 mg/mL Water <1 mg/mL Ethanol 14 mg/mL
Storage	2 years -20°CPowder
	2 weeks4°Cin DMSO
	6 months-80°Cin DMSO

Chemical Name	2-(2-chloro-4-iodophenylamino)-N-(cyclopropylmethoxy)-3,4-difluorobenzamide

Molarity Calculator Dilution Calculator Molecular Weight Calculator

Research Area

Customer Reviews (12)

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Rating

Source

SCIENCE, 2011, 331, 912-916. CI-1040 (PD184352) purchased from Selleck

Method

Immunohistochemistry

Cell Lines

Hand2d/d mice

Concentrations

Incubation Time

24h

Results

The epithelia of vehicle-treated horn showed prominent expression of p-FRS2 and p-ERK1/2(Fig.A,a and c). However, the levels of both p -FRS2 and p -ERK1/2 were reduced in the epithelia of PD173074-treated horn on day 4 of pregnancy (Fig. A, b and d). We also observed a marked decline in the proliferative activity of Hand2-null uterine epithelia, as indicated by decreased Ki-67 staining (Fig. A, e and f) . In parallel experiments, administration of PD184352, an inhibitor of the ERK1/2 pathway, to uterine horns of Hand2 d/d mice suppressed the level of pERK1/2 (Fig.B, a and b) , as well as luminal epithelial proliferation ( Fig. B, c and d).The ERK1/2-dependent phosphorylation of epithelial ERα at Ser118 is critical for the transcriptional activation of ERα. Administration of either PD173074 (Fig. C, a to d) or PD184352 (Fig. C, e to h) to Hand2-null uterine horns blocked the phosphorylation of epithelial ERα at Ser118 and the expression of Muc -1.

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Rating

Source

J Natl Cancer Inst, 2012, 104(21), 1673-9. CI-1040 (PD184352) purchased from Selleck

Method

Western Blot

Cell Lines

primary human melanocytes

Concentrations

1 uM

Incubation Time

18 h

Results

In BRAFV600E melanoma cells, the highly selective BRAFV600E inhibitor GDC-0879 and three selective MEK inhibitors [PD184352/CI-1040, U0126, PD98059] did not suppress c-Jun levels, although they effectively reduced phospho-ERK levels.

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Rating

Source

J Natl Cancer Inst, 2012, 104(21), 1673-9. CI-1040 (PD184352) purchased from Selleck

Method

Xenograft

Cell Lines

athymic nude Foxn1nu mice

Concentrations

3 mg/kg

Incubation Time

13 day

Results

CDK2/4 inhibition augmented statistically significant growth reduction of melanoma xenografts in vivo by the BRAF and MEK inhibitors (GDC-0879 and CI1040).

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Rating

Source

Proc Natl Acad Sci U S A, 2011, 108(39), 16392-7.. CI-1040 (PD184352) purchased from Selleck

Method

Western blot

Cell Lines

DU145/PC3 cells

Concentrations

10 μM

Incubation Time

12 h

Results

PI3K inhibition by LY294002 in-creased ERK activation in Her2-overexpressing DU145 cells, whereas treatment with the MEK inhibitor PD184352 in PC3 cells with Her2 overexpression resulted in increased AKT activation. This suggests a strong reciprocal feedback regulation of the PI3K/AKT and MEK/ERK signaling cascades (Fig. E)

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Rating

Source

Neoplasia, 2011, 13, 154–166. CI-1040 (PD184352) purchased from Selleck

Method

Western blot

Cell Lines

MDA-MB-453 cell lines, HCC-1954 cell lines

Concentrations

10 μM

Incubation Time

24 h

Results

We observed that CI-1040 at 10μM concentration almost completely inhibited ERK phosphorylation in both cell lines

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Rating

Source

Dr Zhang of Tianjin Medical University. CI-1040 (PD184352) purchased from Selleck

Method

Western blot

Cell Lines

Breast cancer cells

Concentrations

0-10 nM

Incubation Time

3 h

Results

Click to enlarge

Rating

Source

Breast Cancer Res, 2011, 13, R36. CI-1040 (PD184352) purchased from Selleck

Method

MTT assay

Cell Lines

MDA-MB-453 cell line, HCC-1954 cell line

Concentrations

2-25 μM

Incubation Time

48 h

Results

We observed that monotherapies with CI-1040 and other inhibitors reduced cell viability in a dose-dependent manner across these cell lines

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Rating

Source

Dr Zhang of Tianjin Medical University. CI-1040 (PD184352) purchased from Selleck

Method

Western blot

Cell Lines

Breast cancer cells

Concentrations

0-1 nM

Incubation Time

3 h

Results

Click to enlarge

Rating

Source

Dr Shuo Dong of Baylor College of Medicine. CI-1040 (PD184352) purchased from Selleck

Method

Cell colony formation assays

Cell Lines

primary hematopoietic cells

Concentrations

10 μM

Incubation Time

Results

Click to enlarge

Rating

Source

Neoplasia, 2011, 13, 154–166. CI-1040 (PD184352) purchased from Selleck

Method

RT-PCR

Cell Lines

MDA-MB-453 cell lines, HCC-1954 cell lines

Concentrations

10 μM

Incubation Time

24 h

Results

We assessed AR expression using RT-PCR and observed a significant reduction of AR transcript level after MEK inhibition by CI-1040 to 0.2- and 0.6-fold in MDA-MB- 453 and HCC-1954 cells, respectively, compared with the controls (P < .01; Figure A). This finding suggest that ERK signaling regulates AR expression in molecular apocrine cells.

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Rating

Source

Neoplasia, 2011, 13, 154–166. CI-1040 (PD184352) purchased from Selleck

Method

MTT assay

Cell Lines

MDA-MB-453 cell line, HCC-1954 cell line, HCC-202 cell line

Concentrations

5/10 μM

Incubation Time

48 h

Results

These data suggest that AR inhibitor flutamide and MEK inhibit or CI-1040 have synergy in reducing cell viability of molecular apocrine cell lines.

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Rating

Source

Breast Cancer Res, 2011, 13, R36. CI-1040 (PD184352) purchased from Selleck

Method

MTT assay/Western blot

Cell Lines

MDA-MB-453-R cell line

Concentrations

5/10 μM

Incubation Time

48 h

Results

"Flutamide and CI-1040 treatments were carried out at the same four dose combinations applied before in the nonresistant line (CI-1040(5μM)/flutamide(5μM), CI-1040 (10μM) /flutamide (5μM), CI-1040 (5μM)/flutamide (10μM), and CI-1040(10 μM)/f lutamide (10μM)). Importantly, we observed a synergy at all four dose combinations in MDA -MB-453-R line with CI values of 0.68 to 0.76 (Figure D). Combination therapies with CI-1040 (5μM)/f lutamide (5μM) and CI-1040 (5μM)/flutamide (10μM) completely abrogated ERK phosphorylationin MDA-MB-453-R line (Figure F).

Product Citations (22)

Exome sequencing identifies recurrent somatic MAP2K1 and MAP2K2 mutations in melanoma. [Nikolaev SI, et al. Nat Genet 2011;44(2):133-9]
PubMed: 22197931
The antiproliferative action of progesterone in uterine epithelium is mediated by Hand2. [Li Q, et al. Science 2011;331(6019), 912-916]
PubMed: 21330545
Constitutive intestinal NF-κB does not trigger destructive inflammation unless accompanied by MAPK activation. [Guma M, et al. J Exp Med 2011;208(9):1889-900]
PubMed: 21825016

HER2 overcomes PTEN (loss)-induced senescence to cause aggressive prostate cancer. [Ahmad I, et al. Proc Natl Acad Sci U S A 2011;108(39):16392-7]
PubMed: 21930937
RSK promotes G2 DNA damage checkpoint silencing and participates in melanoma chemoresistance. [Ray-David H, et al. Oncogene 2012;ahead of print]
PubMed: 23108403
BRAF gene amplification can promote acquired resistance to MEK inhibitors in cancer cells harboring the BRAF V600E mutation. [Corcoran RB, et al. Sci Signal 2010;3(149), ra84]
PubMed: 21098728
Cross-regulation between FOXA1 and ErbB2 signaling in estrogen receptor-negative breast cancer. [Naderi A, et al. Neoplasia 2012;14(4):283-96]
PubMed: 22577344
Synergy between inhibitors of androgen receptor and MEK has therapeutic implications in estrogen receptor-negative breast cancer. [Naderi A, et al. Breast Cancer Res 2011;13(2), R36]
PubMed: 21457548
A feedback loop between androgen receptor and ERK signaling in estrogen receptor-negative breast cancer. [Chia KM, et al. Neoplasia 2011;13(2), 154-166]
PubMed: 21403841
Ras mutation cooperates with β-catenin activation to drive bladder tumourigenesis. [Ahmad I, et al. Cell Death Dis 2011;2:e124]
PubMed: 21368895
Prolactin-induced protein mediates cell invasion and regulates integrin signaling in estrogen receptor-negative breast cancer. [Naderi A, et al. Breast Cancer Res 2012;14(4):R111]
PubMed: 22817771
Noonan syndrome gain-of-function mutations in NRAS cause zebrafish gastrulation defects. [Runtuwene V, et al. Dis Model Mech 2011;4(3):393-9]
PubMed: 21263000
Endothelial Nitric Oxide Synthase Activation Generates an Inducible Nitric Oxide Synthase-Like Output of Nitric Oxide in Inflamed Endothelium. [Lowry JL, et al. J Biol Chem 2012;ahead of print]
PubMed: 23255592
Acidosis promotes Bcl-2 family-mediated evasion of apoptosis: involvement of acid-sensing G protein-coupled receptor Gpr65 signaling to Mek/Erk. [Ryder C, et al. J Biol Chem 2012;287(33):27863-75]
PubMed: 22685289
Cigarette smoke components induce matrix metalloproteinase-1 in aortic endothelial cells through inhibition of mTOR signaling. [Lema顃re V, et al. Toxicol Sci 2011;123(2):542-9]
PubMed: 21742783
Research Resource: Identification of Novel Growth Hormone-Regulated Phosphorylation Sites by Quantitative Phosphoproteomics. [Ray BN, et al. Mol Endocrinol 2012;26(6):1056-73]
PubMed: 22570334
Antiviral activity of the MEK-inhibitor U0126 against pandemic H1N1v and highly pathogenic avian influenza virus in vitro and in vivo. [Droebner K, et al. Antiviral Res 2011;92(2), 195-203]
PubMed: 21854809
Molecular characterisation of MEK1/2- and MKK3/6-like mitogen-activated protein kinase kinases (MAPKK) from the fox tapeworm Echinococcus multilocularis. [Gelmedin V, et al. Int J Parasitol 2012;40(5), 555-567]
PubMed: 19887070
Arf6 promotes cell proliferation via the PLD-mTORC1 and p38MAPK pathways. [Knizhnik AV, et al. J Cell Biochem 2012;113(1):360-71]
PubMed: 21928324
Reactivation of ERK signaling causes resistance to EGFR kinase inhibitors. [Ercan D, et al. Cancer Discov 2012;2(10), 934-947]
PubMed: 22961667
Detection of Allosteric Kinase Inhibitors by Displacement of Active Site Probes. [Lebakken CS, et al. J Biomol Screen 2012;17(6):813-21]
PubMed: 22453235
Measurement of TLR-Induced Macrophage Spreading by Automated Image Analysis: Differential Role of Myd88 and MAPK in Early and Late Responses. [Wenzel J, et al. Front Physiol 2011;2, 71]
PubMed: 22028692

Tech Support & FAQs

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:3Monday–Friday 9:00 AM–5:00 PM (Central Time)

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Related MEK Inhibitors

AZD6244 (Selumetinib)

AZD6244 (Selumetinib, ARRY-142886) is highly potent to inhibit MEK1 with IC50 of 14 nM.
PD0325901

PD0325901 (PD325901) is selective and non ATP-competitive MEK inhibitor with IC50 of 0.33 nM.
SL327
SL327 is a selective inhibitor for MEK1 and MEK2 with IC50 of 0.18 μM and 0.22 μM, respectively.
U0126-EtOH

U0126-EtOH is a highly selective inhibitor of MEK1 and MEK2 with IC50 of 0.07 μM and 0.06 μM, respectively.
PD98059

PD98059 is a non-ATP competitive MEK inhibitor with IC50 of 2 μM.
AS703026 (pimasertib)

AS703026 is a highly selective and potent non-competitive inhibitor of MEK1/2 with IC50 of 5-11 nM.
BIX 02188
BIX02188 is a selective inhibitor of MEK5 with IC50 of 4.3 nM.
BIX 02189

BIX02189 is a selective inhibitor of MEK5 with IC50 of 1.5 nM.
PD318088

PD318088 is a non-ATP competitive allosteric MEK1/2 inhibitor.
AZD8330

AZD8330 (ARRY-424704) is a MEK 1/2 inhibitor with IC50 of 7 nM.

MAPK Pathway Products

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CI-1040 (PD184352) + Rapamycin	CI-1040 in combination with mTOR inhibitor, Rapamycin, exhibits dose-dependent synergism in human lung cancer cell lines that is associated with suppression of proliferation rahter than enhancement of cell death. ^[6]
CI-1040 (PD184352) + Gefitinib	Combination of CI-1040 with Gefitinib effectively results in inhibition of the MAPK signaling pathway and exerts antitumor effects in vitro and in vivo in tumors resistant to each of the agents alone. Combined treatment in four tumor xenografts generated from patients with resected pancreatic cancer shows more effective than either single agent alone in this model. ^[8]
CI-1040 (PD184352) + Sorafenib-Tosylate	Combination of CI-1040 and Sorafenib synergistically inhibited ERK phosphorylation and cell growth and induced apoptosis in both HCC cells and HUVECs. Combination therapy inhibited tumor growth significantly better than either single agent in the xenograft models. ^[7]

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Product Categories

Validation & Quality Control

Product Citations(22)

Customer Reviews(12) in vivo invitation

Quality Control & MSDS

Related Compound Libraries

CI-1040 (PD184352) is available in the following compound libraries:

Product Information

Compare MEK Inhibitors

Research Area

Combination Therapy

Product Description

Biological Activity

Protocol(Only for Reference)

Kinase Assay:
^[2]

Cell Assay:
^[1]

Animal Study:
^[3]

References

Chemical Information

Research Area

Customer Reviews (12)

Product Citations (22)

Tech Support & FAQs

If you have any other enquiries, please leave a message.

Related MEK Inhibitors

MAPK Pathway Products

Recently Viewed Items

Cat.No.	Product Name	Solubility (25°C)
Cat.No.	Product Name	Water	DMSO	Ethanol
S1008	AZD6244 (Selumetinib)	<1 mg/mL	92 mg/mL	<1 mg/mL
S1036	PD0325901	<1 mg/mL	96 mg/mL	40 mg/mL
S2673	GSK1120212 (JTP-74057)	<1 mg/mL	5 mg/mL	<1 mg/mL
S1102	U0126-EtOH	<1 mg/mL	85 mg/mL	<1 mg/mL
S1177	PD98059	<1 mg/mL	19 mg/mL	<1 mg/mL
S1020	CI-1040 (PD184352)	<1 mg/mL	96 mg/mL	14 mg/mL
S1531	BIX 02189	<1 mg/mL	88 mg/mL	88 mg/mL
S1475	AS703026 (pimasertib)	<1 mg/mL	86 mg/mL	<1 mg/mL
S2617	TAK-733	<1 mg/mL	101 mg/mL	<1 mg/mL
S1530	BIX 02188	<1 mg/mL	43 mg/mL	3 mg/mL
S2134	AZD8330	<1 mg/mL	92 mg/mL	92 mg/mL
S2310	Honokiol	53 mg/mL	53 mg/mL	<1 mg/mL
S1568	PD318088	<1 mg/mL	112 mg/mL	14 mg/mL
S1066	SL327	<1 mg/mL	4 mg/mL	7 mg/mL

Choose Your Country or Region

Product Categories

CI-1040 (PD184352)

Validation & Quality Control

Product Citations(22)

Customer Reviews(12) in vivo invitation

Quality Control & MSDS

Related Compound Libraries

CI-1040 (PD184352) is available in the following compound libraries:

Product Information

Compare MEK Inhibitors

Research Area

Combination Therapy

Product Description

Biological Activity

Protocol(Only for Reference)

Kinase Assay: [2]

Cell Assay: [1]

Animal Study: [3]

References

Chemical Information

Research Area

Customer Reviews (12)

Product Citations (22)

Tech Support & FAQs

If you have any other enquiries, please leave a message.

Related MEK Inhibitors

MAPK Pathway Products

Recently Viewed Items

E-newsletter

Kinase Assay:
^[2]

Cell Assay:
^[1]

Animal Study:
^[3]