For research use only. Not for therapeutic Use.
FM19G11 is a hypoxia-inducible factor-1-alpha (HIF-1α) inhibitor, and it inhibits hypoxia-induced luciferase activity with an IC50 of 80 nM in HeLa cells. FM19G11 modulates other signaling pathways, including mTOR and PI3K/Akt/eNOS, when the HIF-1α pathway is inactivated under normoxic conditions[1][2].
FM19G11 (30-300 nM) inhibits HIFα proteins in the HeLa cell lines[1].
FM19G11 (500 nM) promotes oligodendrocyte differentiation under hypoxia[1].
FM19G11 (300 nM; 3 days) suppresses the mRNA levels of O6-methylguanine DNA-methyltransferase (MGMT) significantly in hypoxic GBM‐XD, hypoxic T98G, and normoxic T98G cells[2].
M19G11 (300 nM; 3 days) significantly enhances the pro‐apoptotic effect of temozolomide (TMZ), although FM19G11 does not induce apoptosis by itself[2].
FM19G11 ( intramedullary injection; 1-8 weeks) improves locomotion in severe spinal cord injury (SCI)[3].
FM19G11 ( intramedullary injection; 8 weeks) induces the expression of GAP43, an axon growth marker, and RIP, a marker for myelinated oligodendrocytes at the injury[3].
| Catalog Number | I014828 |
| CAS Number | 329932-55-0 |
| Synonyms | [2-(4-methylphenyl)-2-oxoethyl] 3-[(2,4-dinitrobenzoyl)amino]benzoate |
| Molecular Formula | C23H17N3O8 |
| Purity | ≥95% |
| InChI | InChI=1S/C23H17N3O8/c1-14-5-7-15(8-6-14)21(27)13-34-23(29)16-3-2-4-17(11-16)24-22(28)19-10-9-18(25(30)31)12-20(19)26(32)33/h2-12H,13H2,1H3,(H,24,28) |
| InChIKey | XVUOIWIIQVGWAJ-UHFFFAOYSA-N |
| SMILES | CC1=CC=C(C=C1)C(=O)COC(=O)C2=CC(=CC=C2)NC(=O)C3=C(C=C(C=C3)[N+](=O)[O-])[N+](=O)[O-] |
| Reference | [1]. Victoria MM, et, al. FM19G11, a new hypoxia-inducible factor (HIF) modulator, affects stem cell differentiation status. J Biol Chem. 2010 Jan 8; 285(2): 1333-42. [2]. You CG, et, al. FM19G11 inhibits O 6 -methylguanine DNA-methyltransferase expression under both hypoxic and normoxic conditions. Cancer Med. 2018 May 15; 7(7): 3292-3300. [3]. Ana AA, et, al. FM19G11 and Ependymal Progenitor/Stem Cell Combinatory Treatment Enhances Neuronal Preservation and Oligodendrogenesis after Severe Spinal Cord Injury. Int J Mol Sci. 2018 Jan 9; 19(1): 200. |
