Metapristone - RU42633 | Desmethylmifepristone |
Catalog No.GB40275 |
Metapristone, the primary metabolite of RU486 , 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.
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Cas No.: 104004-96-8
Sample solution is provided at 25 µL, 10mM.
Metapristone, the primary metabolite of RU486 , 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.
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