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Ravoxertinib

(別名: GDC-0994)
52 Cited Publications
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Based on 52 publication(s) in Google Scholar

Ravoxertinib (GDC-0994) is an orally active ERK1/2 inhibitor. Ravoxertinib inhibits the ERK1/2 MAPK signaling pathway and reduces the expression levels of c-Myc, HK2 and LDHA. Ravoxertinib decreases mammosphere formation, and exerts additive and/or superadditive cytotoxicity when combined with Ipatasertib (HY-15186) in 3D tumor sphere models. Ravoxertinib can be used in research related to various cancers including breast cancer, melanoma, head and neck cancer, non-small cell lung cancer, ovarian cancer and Merkel cell carcinoma.

商品は「研究用試薬」です。人や動物の医療用・臨床診断用・食品用の製品ではありません。
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  • 純度: 99.74%
  • CAS 番号: 1453848-26-4
  • 分子式: C21H18ClFN6O2
  • 分子量:440.86
  • 保管条件:
    Powder   -20°C, 3 years , 4°C, 2 years ; In solvent   -80°C, 2 years , -20°C, 1 year
  • Ravoxertinib Chemical Structure
    Ravoxertinib 構造式
  • Experimental Validation Results for Ravoxertinib
  • Experimental Validation Results for Ravoxertinib
  • Experimental Validation Results for Ravoxertinib
  • Experimental Validation Results for Ravoxertinib
  • Experimental Validation Results for Ravoxertinib
  • Experimental Validation Results for Ravoxertinib
CAS 番号: 1453848-26-4
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  • Ravoxertinib Chemical Structure
    Ravoxertinib Chemical Structure
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    Ravoxertinib purchased from MedChemExpress. Usage Cited in: Nat Commun. 2026 Jan 21;17(1):1902. [Abstract]

    Customer Validation
     U87, U251, and H1299 cells, with or without EGFR R252C mutation were treated with or without 5 μM Ravoxertinib. Cell proliferation was assessed at day 7. Relative proliferation was calculated using vehicle-treated EGFR WT cells as the control.

  • 1/16

    Ravoxertinib purchased from MedChemExpress. Usage Cited in: Nature. 2025 Jan;637(8046):726-735. [Abstract]

    Customer Validation
     Investigation of the signalling axis regulating LIF expression upon PDGF stimulation. Cells were treated with ERK inhibitor ravoxertinib (10 μM) for 24 h before cell lysis for total RNA extraction and measurement of LIF mRNA levels by real-time qPCR.

  • 1/16

    Ravoxertinib purchased from MedChemExpress. Usage Cited in: Cell Mol Immunol. 2023 Feb;20(2):175-188. [Abstract]

    Customer Validation
     Effects of kinase inhibitors on ISO-triggered inhibition of SeV-induced transcription of the IFNB1 gene. THP1 cells were treated with the ERK inhibitor GDC-0994 (1 μM) for 1 h and then were treated with ISO (10 μM) and infected with SeV (MOI = 1). Six hours later, a qPCR analysis to determine the mRNA levels of the IFNB1 gene was performed. The results are shown as the inhibition rate (%).

  • 1/16

    Ravoxertinib purchased from MedChemExpress. Usage Cited in: Nat Commun. 2023 Sep 30;14(1):6117. [Abstract]

    Customer Validation
     HCT116 cells were pretreated with PPP (1 μM), ARQ-092 (2 μM) and GDC-0994 (Ravoxertinib, 10 μM) for 1 h before being cultured under hypoxia for 12 h.

  • 1/16

    Ravoxertinib purchased from MedChemExpress. Usage Cited in: J Exp Clin Cancer Res. 2023 Jul 13;42(1):166. [Abstract]

    Customer Validation
     The effect of NF-κB, ERK, JNK and p38 inhibitors on IL-1β-induced Saa3 expression in vivo. One hour after intravenous administration of Ravoxertinib, IL-1β (20 ng in 100 ul saline) were i.v. administrated into the mice. Six hours later, lung Saa3 expression was detected by qPCR.

  • 1/16

    Ravoxertinib purchased from MedChemExpress. Usage Cited in: J Exp Clin Cancer Res. 2023 Jul 13;42(1):166. [Abstract]

    Customer Validation
     The effect of NF-κB, ERK, JNK and p38 inhibitors on IL-1β-induced Saa3 expression in MLE-12 cells. MLE-12 cells were pre-treated with Ravoxertinib for 1 h, then stimulated with IL-1β (10 ng/ml) for 6 h. Saa3 expression was detected by qPCR.

  • Ravoxertinib