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PD0325901MEK inhibitor


Catalog No. A3013
Size Price Stock Qty
10mM (in 1mL DMSO) $55.00 In stock
5mg $45.00 In stock
25mg $150.00 In stock
100mg $360.00 In stock
500mg $980.00 In stock

Tel: +1-832-696-8203


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Sample solution is provided at 25 µL, 10mM.

Quality Control

Quality Control & MSDS

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Chemical structure


Related Biological Data

Inhibition of the PI3K and MEK-ERK pathway enhances cell death in HCT116 cells. HCT116 cells stably transduced with control or PIK3CA inducible shRNA were treated with PD0325901 in the presence or absence of doxycycline. HCT116 cells grown in the presence or absence of doxycycline were treated with PD0325901 for 48 h. Cells were subsequently fixed with formaldehyde and stained with Hoechst 33342 to visualize fragmented nuclei. For each treatment condition, 1,500 cells were counted under a fluorescence microscope.

Biological Activity



Cell experiment: [1]

Cell lines

M14 (BRAFV600E) cells

Preparation method

The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months.

Reacting condition

1 μM, 48 hours for cell cycle accumulation ≥100 nM, 72 hours for DNA decrease


PD0325901 caused a dose- and time-dependent cell cycle accumulation at the G1/S boundary and depletion of cells in the S-phase. It also caused a dose- and time-dependent increase in the percentage of cellswith sub-G1 DNA content, thus indicating induction of apoptosis. Compared with the kinetics and dose-response curve of cell cycle inhibition, DNA decrease to sub-G1 levels required longer times of exposure (72 hours) and higher concentrations of the drug (≥100 nM).

Animal experiment: [1]

Animal models

Female CD-1 nude (nu/nu) mice injected with M14 (BRAFV600E) and ME8959 (wtBRAF) cells

Dosage form

Oral administration, 50 mg/kg per day for 21 days


Daily oral treatment of established tumors with 50 mg/kg per day of PD0325901 significantly impaired in vivo tumor growth (60%-65% inhibition compared with controls at the end of a 21-day treatment cycle) in both M14 and ME8959 xenografts. The effects of PD0325901 were reversible, and tumors grew back after treatment interruption.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.


[1] Ciuffreda L, Del Bufalo D, Desideri M, et al. Growth-inhibitory and antiangiogenic activity of the MEK inhibitor PD0325901 in malignant melanoma with or without BRAF mutations. Neoplasia, 2009, 11(8): 720-W6.

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Chemical Properties

Cas No. 391210-10-9 SDF Download SDF
Synonyms PD0325901,PD-0325901,PD 0325901,PD325901,PD 325901,PD-325901
Chemical Name N-[(2R)-2,3-dihydroxypropoxy]-3,4-difluoro-2-(2-fluoro-4-iodoanilino)benzamide
Canonical SMILES C1=CC(=C(C=C1I)F)NC2=C(C=CC(=C2F)F)C(=O)NOCC(CO)O
Formula C16H14F3IN2O4 M.Wt 482.19
Solubility Soluble in DMSO > 10 mM Storage Store at -20°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

Research Update

1. Modulation of endochondral ossification by MEK inhibitors PD 0325901 and AZD6244 (Selumetinib). Bone. 2014 Feb;59:151-61. doi: 10.1016/j.bone.2013.11.013. Epub 2013 Nov 20.
PD 0325901, a MEKi, affects chondrocyte hypertrophy, matrix resorption, fracture healing and bone architecture, where it expands the hypertrophic zone of th growth plate and reduces osteoclast surface systemically.
4. MEK inhibitor PD0325901 significantly reduces the growth of papillary thyroid carcinoma cells in vitro and in vivo. Mol Cancer Ther. 2010 Jul;9(7):1968-76. doi: 10.1158/1535-7163.MCT-10-0062. Epub 2010 Jun 29.
PD0325901, a MEK1/2 inhibitor, is an effective drug for the treatment of thyroid cancers with RET/PTC or BRAF mutation, where PTC cells with a BRAF mutation is more sensitive to PD0325901 than PTC cells with RET/PTC1 rearrangement.
5. Targeting mitogen-activated protein kinase kinase with the inhibitor PD0325901 decreases hepatocellular carcinoma growth in vitro and in mouse model systems. Hepatology. 2010 Apr;51(4):1218-25. doi: 10.1002/hep.23470.
PD0325901, a MEK inhibitor with possible inhibitory effects against HCC tumorigenesis, inhibited tumor growth and MEK activity in various HCC cells and HCC mouse models.


PD0325901 is a specific inhibitor of mitogen-activated protein kinase MEK. PD0325901 is a small molecular with the formula of C16H14F3IN2O4 and Molecular Weight of 482. MEK is a key component of the RAS/RAF/MEK/ERK signaling pathway that is frequently activated in human tumors, and MEK/ERK regulates cell proliferation, survival, and differentiation in response to extracellular signals. PD0325901 effectively reduces P-ERK levels and cell growth in vitro, and inhibits tumor growth in mouse model in vivo

1. Noninvasive imaging of cell proliferation following mitogenic extracellular kinase inhibition by PD0325901. J Leyton, G Smith, M Lees, M Peruma. Molecular cancer Therapeutics. 2008
2. Targeting mitogen‐activated protein kinase kinase with the inhibitor PD0325901 decreases hepatocellular carcinoma growth in vitro and in mouse model. M Hennig, MT Yip‐Schneider, S Wentz, H Wu. Hepatology. 2010