| Name | MX69 |
| Description | MX69 is the MDM2/XIAP inhibitor, blocking the MDM2 protein-XIAP RNA interaction, leading to MDM2 degradation. |
| Cell Research | The cytotoxic effect of leads is determined using the WST assay. Briefly, cells cultured in 96-well microtiter plates are treated with different concentrations of leads for a 20-hr period. WST (25 mg/well) is then added and incubation continued for an additional 4 hr, after which the optical density is read with a microplate reader.(Only for Reference) |
| In vitro | MX69 inhibits expression of both MDM2 and XIAP in a time- and dose-dependent manner. MX69 induces ubiquitination of endogenous MDM2 in cancer cells. Downregulation of MDM2 by MX69 is through induction of MDM2 self-ubiquitination and degradation. Half-life of MDM2 in control-treated EU-1 cells is greater than 90 min, whereas MX69 treatment decreases the MDM2 half-life to <30 min. In SK-N-SH cells with stably transfected either wild-type (WT)-MDM2 or mutant MDM2-C464A, Treatment with MX69 significantly inhibits expression and increased the turnover of WT-MDM2 but not MDM2-C464A. MX69 significantly enhances the p53 half-life in WT-MDM2 but not mutant MDM2-C464A-transfected SK-N-SH cells. p53 is stabilized and accumulates in MX69-treated cells. MX69-mediated inhibition of XIAP is MDM2 dependent. Treatment of MX69 activates caspases 3, 7, and 9 as well as the cleavage of the death substrate PARP. MX69 also exhibits a significant cytotoxic effect on both ALL and NB lines(cancer cell lines), particularly those lines with MDM2 overexpression and a WTp53 phenotype. MX69-induced cell death is indeed due to apoptosis. MX69-induced cell apoptosis and death are dependent on MDM2, p53, and XIAP expression. MX69 shows minimal inhibitory effect on normal human bone marrow in vitro[1]. |
| In vivo | MX69 has significant apoptotic and anti-proliferative effects on MDM2-expressing cancer cells in vivo. MX69 is well tolerated in animals due to the fact that normal cells/tissues express little or no MDM2. No evidence of toxicity after treatment with MX69 at the 100 mg/kg dose. MDM2-specific agent MX69 should not activate either on-target (e.g., p53 induction) or off-target signaling pathways in normal cells. Thus, specific MDM2 inhibitors such as MX69 may be excellent candidates for targeted therapy of refractory cancers expressing high levels of MDM2[1]. |
| Storage | Shipping with blue ice/Shipping at ambient temperature. |
| Solubility Information | DMSO : 88 mg/mL (185.43 mM), Sonication is recommended.
H2O : < 1 mg/mL (insoluble or slightly soluble)
Ethanol : 39 mg/mL (82.18 mM), Sonication is recommended.
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| Keywords | Ubiquitin ligase | Ubiquitin conjugating enzyme | Ubiquitin activating enzyme | MX-69 | MX69 | MX 69 | MDM-2/p53 | Mdm2 | Inhibitor | inhibit | IAP | E3Enzyme | E3 ligating enzyme | E3 Enzyme | E2Enzyme | E2 Enzyme | E2 conjugating enzyme | E1Enzyme | E1/E2/E3 Enzyme | E1 Enzyme | E1 activating enzyme |
| Inhibitors Related | 10-Hydroxydecanoic Acid | Flubendazole | Diuron | Gallium maltolate | D-(-)-3-Phosphoglyceric acid disodium | EN219 | Triglycidyl isocyanurate | Indole-3-carbinol | Methyl methanesulfonate | (E/Z)-10-Hydroxy-2-decenoic acid | Acacetin | 4-Methylsalicylic acid |
| Related Compound Libraries | Apoptosis Compound Library | Target-Focused Phenotypic Screening Library | Bioactive Compound Library | HIF-1 Signaling Pathway Compound Library | Pyroptosis Compound Library | Inhibitor Library | PPI Inhibitor Library | Anti-Aging Compound Library | Bioactive Compounds Library Max | Anti-COVID-19 Compound Library | Anti-Cancer Compound Library | Anti-Cancer Active Compound Library |
United States
