167869-21-8 | PD98059

Chemical type

• Specific ERK inhibitor
• Small molecule MEK1/2 inhibitor

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• Mitogen-activated protein kinase (MAPK) inhibitor (specifically targets ERK1/2 pathway)

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Key properties

• Suppresses ERK activation and phosphorylation
• Reduces SU11274-induced autophagy, p53 activation, and Bcl-2 phosphorylation
• Decreases SU11274-mediated cell death and autophagic markers (Beclin-1, LC3-II)
• Used at micromolar concentrations (e.g., 5 µM)

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• Potent inhibitor of MAPK signaling
• Reduces NF-κB p65 activation and increases IκBα expression
• Suppresses production of inflammatory mediators (e.g., CCR6, CD14, GM-CSF, iNOS, IL-6, TNF-α) in B cells and brain tissue
• Administered at 5 mg/kg intraperitoneally in DMSO vehicle
• Ameliorates neuroimmune dysfunction in EAE model without reported toxicity in study

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• Inhibitor of MAPK/ERK pathway in cancer signaling studies
• Tool to dissect ERK's role in autophagy and apoptosis

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• Therapeutic agent for experimental autoimmune encephalomyelitis (EAE) in mice
• Potential treatment for multiple sclerosis (MS) by modulating neuroinflammation
• Suppresses inflammatory cytokine expression in spleen and brain
• Administered daily from day 14 to 28 post-EAE induction

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Classification by use

• Chemicals used as kinase inhibitors
• Chemicals used in signal transduction research

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• Chemicals used as kinase inhibitors
• Chemicals used in autoimmune disease treatment
• Chemicals used in neuroinflammation modulation

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A trustworthy factory and manufacturer

1. [Cite:1] Activation of ERK–p53 and ERK-Mediated Phosphorylation of Bcl-2 Are Involved in Autophagic Cell Death Induced by the c-Met Inhibitor SU11274 in Human Lung Cancer A549 Cells, Journal of Pharmacological Sciences, Volume 118, Issue 4, 2012, Pages 423-432
2. [Cite:2] Mitogen-activated protein kinase inhibitor PD98059 improves neuroimmune dysfunction in experimental autoimmune encephalomyelitis in SJL/J mice through the inhibition of nuclear factor-kappa B signaling in B cells, Brain Research Bulletin, Volume 194, March 2023, Pages 45-53