PD0325901 MEK inhibitor |
Sample solution is provided at 25 µL, 10mM.
Quality Control & MSDS
- View current batch:
Chemical structure

Related Biological Data

Targets | ||||||
IC50 |
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. |
Reaction Conditions |
1 μM, 48 hours for cell cycle accumulation ≥100 nM, 72 hours for DNA decrease |
Applications |
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 |
Applications |
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. |
References: [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. |

PD0325901 Dilution Calculator

PD0325901 Molarity Calculator
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 | >24.1mg/mL in DMSO | 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 |
Abstract
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.
Abstract
The MEK inhibitor PD-0325901 prevented PF-04880594-induced hyperplasia and ERK hyperphosphorylation at clinically well-tolerated doses.
Abstract
The tolerability and antitumor activity of PD-0325901 have been assessed in cancer patients.
Abstract
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.
Abstract
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
References:
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