| Name | Mitotane |
| Description | Mitotane (NCI-C04933) is a derivative of the insecticide DICHLORODIPHENYLDICHLOROETHANE that specifically inhibits cells of the adrenal cortex and their production of hormones. It is used to treat adrenocortical tumors and causes CNS damage, but no bone marrow depression. |
| In vitro | 10-40 μM Mitotane inhibited basal and cAMP-induced cortisol secretion but did not cause cell death.Mitotane inhibited basal expression of StAR and P450scc proteins.40 μM Mitotane significantly reduced mRNA expression of StAR, CYP11A1 and CYP21.In H295R cells, the mRNA expression of StAR, CYP11A1 and CYP21 was significantly reduced by Mitotane. In H295R cells, Mitotane in combination with gemcitabine showed antagonistic effects and interfered with gemcitabine-mediated S-phase inhibition of the cell cycle.Mitotane inhibited the expression and secretion of thyroid stimulating hormone (TSH), blocked TSH response to thyrotropin-releasing hormone (THRH), decreased cell viability, and induced apoptosis in the mouse TalphaT1 cell line.Mitotane inhibited the expression and secretion of pituitary thyrotropin secretory hormone (PTHS) and induced apoptosis in the pituitary thyrotropin secretory hormone (PSH) cells. Mitotane induced adrenocortical necrosis, mitochondrial membrane damage, and irreversible binding of the protein CYP in pituitary thyrotropin-secreting mouse cells, without interfering with thyroid hormones, and directly reduced secretory activity and cell viability. |
| In vivo | 10-40 μM Mitotane inhibited basal and cAMP-induced cortisol secretion but did not cause cell death.Mitotane inhibited basal expression of StAR and P450scc proteins.40 μM Mitotane significantly reduced mRNA expression of StAR, CYP11A1 and CYP21.In H295R cells, the mRNA expression of StAR, CYP11A1 and CYP21 was significantly reduced by Mitotane. In H295R cells, Mitotane in combination with gemcitabine showed antagonistic effects and interfered with gemcitabine-mediated S-phase inhibition of the cell cycle.Mitotane inhibited the expression and secretion of thyroid stimulating hormone (TSH), blocked TSH response to thyrotropin-releasing hormone (THRH), decreased cell viability, and induced apoptosis in the mouse TalphaT1 cell line.Mitotane inhibited the expression and secretion of pituitary thyrotropin secretory hormone (PTHS) and induced apoptosis in the pituitary thyrotropin secretory hormone (PSH) cells. Mitotane induced adrenocortical necrosis, mitochondrial membrane damage, and irreversible binding of the protein CYP in pituitary thyrotropin-secreting mouse cells, without interfering with thyroid hormones, and directly reduced secretory activity and cell viability. |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
| Solubility Information | H2O : < 1 mg/mL (insoluble or slightly soluble)
DMSO : 60 mg/mL (187.48 mM), Sonication is recommended.
Ethanol : 60 mg/mL (187.5 mM)
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| Keywords | drug-drug interactions | cholesterol | inhibit | Inhibitor | Apoptosis | antineoplastic | HepaRG | Mitotane | corticotroph cells | adrenocortical carcinoma | TαT1 | H295R | NCI-C 04933 | NCI-C-04933 |
| Inhibitors Related | Stavudine | Sodium 4-phenylbutyrate | Tributyrin |
| Related Compound Libraries | Bioactive Compound Library | EMA Approved Drug Library | Anti-Cancer Clinical Compound Library | Tobacco Monomer Library | Bioactive Compounds Library Max | Anti-Cancer Active Compound Library | Anti-Cancer Drug Library |
United States
