PD0325901

mRNA synthesis
In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail

Tyramide Signal Amplification (TSA)
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.

Phos Binding Reagent Acrylamide
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody

Cell Counting Kit-8 (CCK-8)
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay

SYBR Safe DNA Gel Stain
Safe and sensitive stain for visualization of DNA or RNA in agarose or acrylamide gels.

Inhibitor Cocktails
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
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
- 1. White SM, Avantaggiati ML, et al. "YAP/TAZ Inhibition Induces Metabolic and Signaling Rewiring Resulting in Targetable Vulnerabilities in NF2-Deficient Tumor Cells." Dev Cell. 2019 May 6;49(3):425-443.e9. PMID:31063758
- 2. Sima J, Chakraborty A, et al. "Identifying cis Elements for Spatiotemporal Control of Mammalian DNA Replication." Cell. 2019 Feb 7;176(4):816-830.e18. PMID:30595451
- 3. Wang Y, Li Y, et al. "The cerebral cavernous malformation disease causing gene KRIT1 participates in intestinal epithelial barrier maintenance and regulation." FASEB J. 2018 Sep 25:fj201800343R. PMID:30252535
- 4. Kopanitsa MV, Gou G, et al. "Chronic treatment with a MEK inhibitor reverses enhanced excitatory field potentials in Syngap1(+/-) mice." Pharmacol Rep. 2018 Jun 22;70(4):777-783. PMID:29940508
- 5. Potonjak I, Gobin I, et al. "Carvacrol induces cytotoxicity in human cervical cancer cells but causes cisplatin resistance: Involvement of MEK-ERK activation." Phytother Res. 2018 Feb 8. PMID:29417642
- 6. Sieber J, Wieder N, et al. "GDC-0879, a BRAF(V600E) Inhibitor, Protects Kidney Podocytes from Death." Cell Chem Biol. 2017 Dec 6. PMID:29249695
Physical Appearance | A solid |
Storage | Store at -20°C |
M.Wt | 482.19 |
Cas No. | 391210-10-9 |
Formula | C16H14F3IN2O4 |
Synonyms | PD0325901,PD-0325901,PD 0325901,PD325901,PD 325901,PD-325901 |
Solubility | ≥24.1 mg/mL in DMSO |
Chemical Name | N-[(2R)-2,3-dihydroxypropoxy]-3,4-difluoro-2-(2-fluoro-4-iodoanilino)benzamide |
SDF | Download SDF |
Canonical SMILES | C1=CC(=C(C=C1I)F)NC2=C(C=CC(=C2F)F)C(=O)NOCC(CO)O |
Shipping Condition | Evaluation sample solution: ship with blue ice. All other available sizes: ship with RT, or blue ice upon request. |
General tips | For obtaining a higher solubility, please warm the tube at 37°C and shake it in the ultrasonic bath for a while. Stock solution can be stored below -20°C for several months. |
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. |
Targets | ||||||
IC50 |
Quality Control & MSDS
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Chemical structure

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