For research use only. Not for therapeutic Use.
Metapristone, the primary metabolite of RU486 (Axon 1502), suppressed NSCLC proliferation by promoting apoptosis via decrease the cellular EGFR-mediated PI3K/AKT pathways. In addition, metapristone inhibited anti-apoptotic marker Bcl-2, and activated pro-apoptotic key signaling proteins caspase-3, and poly (ADP-ribose) polymerase. Metapristone induced A549 and H1975 cell cycle via arrest at the G0-G1 stage. Moreover, metapristone inhibited endometrial cancer cell growth through suppressing cell proliferation and activating cell apoptosis-related signaling pathway. Mechanically, metapristone regulated miR-492 and its new target genes Klf5 and Nrf1 in vitro and in vivo to treat endometrial cancer.
KEYWORDS: Metapristone |Supplier | Metabolite Mifepristone | RU42633 | Desmethylmifepristone | RU 42633 | RU-42633 | CAS [104004-96-8] | Progesterone (PR) | Metabolite | Receptors
| Catalog Number | R009272 |
| CAS Number | 104004-96-8 |
| Molecular Formula | C28H33NO2 |
| Purity | ≥95% |
| IUPAC Name | (8S,11R,13S,14S,17S)-17-hydroxy-13-methyl-11-[4-(methylamino)phenyl]-17-prop-1-ynyl-1,2,6,7,8,11,12,14,15,16-decahydrocyclopenta[a]phenanthren-3-one |
| InChI | InChI=1S/C28H33NO2/c1-4-14-28(31)15-13-25-23-11-7-19-16-21(30)10-12-22(19)26(23)24(17-27(25,28)2)18-5-8-20(29-3)9-6-18/h5-6,8-9,16,23-25,29,31H,7,10-13,15,17H2,1-3H3/t23-,24+,25-,27-,28-/m0/s1 |
| SMILES | CC#C[C@@]1(CC[C@@H]2[C@@]1(C[C@@H](C3=C4CCC(=O)C=C4CC[C@@H]23)C5=CC=C(C=C5)NC)C)O |
| Reference | Y Chang et al. Metapristone (RU486-derivative) inhibits endometrial cancer cell progress through regulating miR-492/Klf5/Nrf1 axis. Cancer Cell Int. 2021 Jan 7;21(1):29. J Wang et al. Synthesis, spectral characterization, and in vitro cellular activities of metapristone, a potential cancer metastatic chemopreventive agent derived from mifepristone (RU486). AAPS J. 2014 Mar;16(2):289-98. |
