Ravoxertinib  (Synonyms: GDC-0994)

Ravoxertinib GMP is Ravoxertinib (HY-15947) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. 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^[1][2][3][4].

In relevant in vitro experiments on stem cell-like human glioma stem cells, Ravoxertinib GMP completely abrogates Humanin (HY-P1928)-induced Temozolomide (HY-17364) resistance, restores the growth inhibitory effect of Temozolomide on tumor cells, and inhibits the Humanin-induced upregulation of Hus1 protein expression^[1].
Combination of Ravoxertinib GMP (0.1-10 μM; 7 d) and ipatasertib induces additive to superadditive cytotoxicity in multiple human tumor organoid spheres, with over 2-log cell killing achieved in the 417821-307-R-J1 lung squamous cell carcinoma organoid spheres^[2].
Ravoxertinib GMP (1 μM; 72 h) does not significantly inhibit the LMCD1-mediated enhancement of cell proliferation in human dermal fibroblasts^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Ravoxertinib GMP (20-30 mg/kg; p.o.) is well tolerated at 20 mg/kg and 30 mg/kg in NSG mice bearing 171881-019-R-J1 breast carcinoma PDX, but its combination with ipatasertib does not control tumor growth, leading to progressive disease^[2].
Ravoxertinib GMP (20-30 mg/kg; p.o.) is well tolerated at 20 mg/kg and 30 mg/kg in NSG mice bearing 845751-090-R-J2 head and neck squamous cell carcinoma PDX, but its combination with ipatasertib does not control tumor growth, leading to progressive disease^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

440.86

C₂₁H₁₈ClFN₆O₂

1453848-26-4

O=C1C=C(C2=NC(NC3=CC=NN3C)=NC=C2)C=CN1[C@@H](C4=CC=C(Cl)C(F)=C4)CO

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Cheng J, et al. Myeloid cells coordinately induce glioma cell-intrinsic and cell-extrinsic pathways for chemoresistance via GP130 signaling[J]. Cell Reports Medicine, 2024, 5(8).

  [2]. Teicher BA, et al. Targeted therapy combinations with ipatasertib in multi-cell type 3D tumor spheroid models. Acad Oncol. 2025;2(2):10.20935/acadonco7726.

  [3]. Ye Z, et al. LMCD1 facilitates the induction of pluripotency via cell proliferation, metabolism, and epithelial-mesenchymal transition. Cell Biol Int. 2022;46(9):1409-1422.

  [4]. Hunt BG, et al. RON-augmented cholesterol biosynthesis in breast cancer metastatic progression and recurrence. Oncogene. 2023;42(21):1716-1727.