1                                     However, aminoglutethimide (50 mg/kg) produced an increase in max

2 ting result of this study was that 2 h after aminoglutethimide administration, when corticosterone le

3 ne whether combination hormonal therapy with aminoglutethimide (AG) and hydrocortisone (HC) plus mege

4  101003)], and four nonsteroidal inhibitors [aminoglutethimide (AG), CGS 20267, ICI D1033, and vorozo

5 101,003)], and four nonsteroidal inhibitors [aminoglutethimide (AG), CGS 20267, ICI D1033, and vorozo

6                         A Cyp11a1 inhibitor, aminoglutethimide (AMG), was administered to peanut-sens

7                      Even in the presence of aminoglutethimide, an inhibitor of P450scc, FeSO4 increa

8                                              Aminoglutethimide and ketoconazole were used to determin

9 s was not inhibited by CYP11A1 inhibitors DL-aminoglutethimide and ketoconazole.

10 1, two adrenocorticoid synthesis inhibitors, aminoglutethimide and metyrapone, were administered to f

11 ng megestrol, bicalutamide, glucocorticoids, aminoglutethimide, and ketoconazole, retain activity (14

12 nd 50 mg/kg for metyrapone, and 50 mg/kg for aminoglutethimide) being amnestic for the task.

13  101,003)] and four nonsteroidal inhibitors [aminoglutethimide, CGS 20267, ICI D1033, and vorozole (R

14 ds, and inhibitors of sex steroid synthesis (aminoglutethimide, ketoconazole, and fadrozole), or by a

15 esmolase activity that was not blocked by DL-aminoglutethimide or ketoconazole.

16 nhibition of Cyp11a1 enzymatic activity with aminoglutethimide or reduction in the expression of Cyp1

17 ibit either basal levels of corticosterone - aminoglutethimide - or treatment-induced stimulated cort

18                         Adoptive transfer of aminoglutethimide-treated CD8(+) T cells into sensitized