Fig. 1 · Structure

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PD318088

Cat. No. A10704 CAS 391210-00-7

MEK Inhibitor

PD318088 is an inhibitor of MEK1 AND MEK2.

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Biological Activity

Target & Activity

Target Activity Value
MEK1/2

In Vitro Studies

In PC12 cells incubated with PD318088 in a design including glucose/glucose oxidase, MEK inhibitors demonstrated similarly high cell death rates to the DMSO control. In SW480–7TFP, PD318088 produced a dose-dependent increase in TCF-Wnt reporter levels. In ACHN, PD318088 showed limited single-agent activity as assessed by cell viability. [1,2,3]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Cell death in PC12 cells

Cell-based study · PC12 cells (Neuroscreen-1 sub cell line) [1]

PC-12 cells were separately incubated with PD318088 (200 nM) for 1 h. Against oxidative stress induced by 0.01 units of glucose oxidase in glucose-supplemented medium for 12 h, MEK inhibitors demonstrate similar high cell death rates as to the DMSO control.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
percentage of dead cellsReported result PD318088 (200 nM); 12 h for glucose/glucose oxidase (0.01 units of glucose oxidase with one-fifth of the medium exchanged to high glucose DMEM): MEK inhibitors demonstrate similar high cell death rates as to the DMSO control.[1]

Literature-Reported Treatment Conditions

Treatment concentration
200 nM
Exposure duration
for 1 h
Method
incubated
Vehicle
DMSO
Co-treatment
Other interventions in this design: glucose/glucose oxidase 0.01 units of glucose oxidase with one-fifth of the medium exchanged to high glucose DMEM. Compound effect isolated by the comparison: MEK inhibitors demonstrate similar high cell death rates as to the DMSO control.
Methods and source locations

Compound reported in the paper: PD318088

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Methods > Materials (S4); Methods > Cell Culture (S5); Methods > Cell Death Assay (S10, S12, S13, S18); Figure 1 legend (S44, S53)

percentage of dead cells: percentage of dead cells; comparator: DMSO control — Methods > Cell Death Assay (S10, S12, S18); Figure 1 legend (S53)

Dose-dependent increase in TCF-Wnt reporter levels

Cell-based study · SW480–7TFP [2]

In the SW480–7TFP model, treatment at different concentrations was evaluated against DMSO controls using TCF/Wnt-luciferase and CellTiterGlo signals. TCF-Wnt reporter levels increased in a dose-dependent manner.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
TCF/Wnt-luciferase and CellTiterGlo signalsReported result dose-dependent increase of TCF-Wnt reporter levels[2]

Literature-Reported Treatment Conditions

Treatment concentration
different concentrations
Reported limits
Not stated in the sentences used: route, schedule, vehicle.
Methods and source locations

Compound reported in the paper: PD318088

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results > Trametinib is a potent activator of canonical Wnt signalling (S20, S21); Fig. 2 legend (S338, S339)

TCF/Wnt-luciferase and CellTiterGlo signals: TCF/Wnt-luciferase and CellTiterGlo signals; comparator: DMSO controls — Results > Trametinib is a potent activator of canonical Wnt signalling (S20, S21); Fig. 2 legend (S339)

Limited Single-Agent Activity in the ACHN Model

Cell-based study · ACHN [3]

Single-agent treatment in the ACHN model showed limited activity in the cell viability readout.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
cell viabilityReported result limited single-agent activity[3]

Literature-Reported Treatment Conditions

Reported limits
Not stated in the sentences used: dose, route, schedule, vehicle, control.
Methods and source locations

Compound reported in the paper: PD318088

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results > Integration of transcriptomic and phosphoproteomic datasets reveals coordinated inhibition of the MAPK-ERK pathway (S63, S65)

cell viability: cell viability — Results > Integration of transcriptomic and phosphoproteomic datasets reveals coordinated inhibition of the MAPK-ERK pathway (S65)

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 391210-00-7
Applications MEK Inhibitor
Formula C16H13BrF3IN2O4
Molecular Weight 561.1
SMILES
C1=CC(=C(C=C1I)F)NC2=C(C(=C(C=C2C(=O)NOCC(CO)O)Br)F)F

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 105 mg/mL (187.13 mM)
Water Insoluble
Ethanol 13 mg/mL (23.17 mM)

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Ong Q, Guo S, Zhang K, et al. U0126 protects cells against oxidative stress independent of its function as a MEK inhibitor. ACS Chem Neurosci (2015). PMID: 25544156 DOI: 10.1021/cn500288n Source material
  2. [2] Zhan T, Ambrosi G, Wandmacher AM, et al. MEK inhibitors activate Wnt signalling and induce stem cell plasticity in colorectal cancer. Nat Commun (2019). PMID: 31097693 DOI: 10.1038/s41467-019-09898-0 Source material
  3. [3] Lue HW, Derrick DS, Rao S, et al. Cabozantinib and dasatinib synergize to induce tumor regression in non-clear cell renal cell carcinoma. Cell Rep Med (2021). PMID: 34095877 DOI: 10.1016/j.xcrm.2021.100267 Source material

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