Aminoglutethimide

2 years -20°C Powder, 2 weeks 4°C in DMSO, 2 months -80°C in DMSO

Injection

Adrenocortical tumor cell line NCI-h295

Dissolved in 65% ethanol as a stock solution, final concentrations 3, 30, 300 uM.

Dissolved in DMSO and diluted in saline.

Aminoglutethimide displays aromatase inhibition in vitro assay with human placental aromatase, which is an enzyme involved in the conversion of androgens into estrogens, and an important target for the endocrine treatment of breast cancer. [1] Aminoglutethimide inhibits ACTH receptor (ACTH-R) mRNA expression in ovine adrenocortical cells in a time-dependent fashion. Aminoglutethimide significantly suppresses steroid secretion and the baseline ACTH-R mRNA expression in a dose-dependent fashion (300 uM AG, 5+/-1%, 30 uM AG, 64+/-1%, 3 uM AG, 108+/-19% compared with control cells, 100+/-11%) by affecting the gene expression or by decreasing transcript accumulation via an effect on RNA stability, in the human NCI-h295 adrenocortical carcinoma cell line, which expresses functional ACTH receptors and produces steroids of the glucocorticoid, mineralocorticoid and androgen pathway. [2] Aminoglutethimide inhibits aromatase in a dose-dependent fashion with IC50 of 13 uM in 6 breast tumor homogenates, placental aromatase with IC50 of 6 uM and hypothalamic aromatase with IC50 of 8 uM. [3]

48 hours

The NCI-h295 tumor cell line is maintained in RPMI 1640 medium supplemented with transferrin (0.1 mg/mL), insulin (5 ug/mL), selenium (5.2 ug/mL) and 2% FCS. The cells are incubated for 48 hours with Aminoglutethimide (3, 30, 300 uM). Then cells are examined by trypan blue staining for cell viability, counted with a coulter counter. For the assessment of ACTH-R mRNA, cells are harvested, and total RNA is extracted, electrophoresed, blotted and hybridized with a human ACTH-R cDNA probe.

Aminoglutethimide (AMG, Cytadren) is an aromatase inhibitor with IC50 of 10 uM.