AEZS-112 - CAS 1214741-69-1
Catalog number: 1214741-69-1
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
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AEZS-112, also known as ZEN012, is an orally active small mol. anti-cancer drug which inhibits the polymn. of tubulin at low micromolar concns. AEZS 112 dose-dependently increased non-vital hypodiploid cells and the cytotoxic effect was least pronounced in G2 phase of the cell cycle. AEZS 112 showed anti-tumor activity in human ovarian and endometrial cancer cell lines at low micromolar concns., which could not be abrogated by caspase inhibition and is therefore a good candidate for in vivo studies in these tumors.
Solid powder
ZEN012; ZEN 012; ZEN-012; AEZS 112; AEZS112.
Current Developer:
AEterna Zentaris Inc.
1.Tubulin inhibitor AEZS 112 inhibits the growth of experimental human ovarian and endometrial cancers irrespective of caspase inhibition.
Engel JB1, Schönhals T, Weidler C, Häusler S, Krockenberger M, Rieger L, Dietl J, Wischhusen J, Honig A. Oncol Rep. 2009 Aug;22(2):361-7.
AEZS 112 is an orally active small molecule anticancer drug which inhibits the polymerization of tubulin at low micromolar concentrations. The current study investigates the anti-tumor effect and the mechanism of action of AEZS 112 in in vitro models of human ovarian and endometrial cancers. Four human ovarian and 2 endometrial cancer cell lines were incubated with increasing concentrations of AEZS 112 with and without multi-caspase inhibitor zVAD-FMK for 72 hours. Cytotoxic effects of AEZS 112 were analyzed using crystal violet staining, FACS analysis of DNA content as well as Annexin V/propidium iodide-double staining. AEZS 112 displayed anti-tumor activity in all six cell lines. The EC50 determined after 72-h incubation for Ishikawa and HEC 1A was 0.0312 and 0.125 microm, respectively. The EC50 was 5 microm for SKOV 3 cells, 1 microm for 0.5 microm for OAW 42 cells, 0.125 microm for OvW 1 cells and 0.0312 microm for PA 1 cells. Cytotoxic effects of AEZS 112 could not be abrogated by caspase inhibition with pan-caspase inhibitor zVAD-fmk.
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