Aromazin (exemestane) tablets 25 mg. №30

active ingredient : exemestane;

1 tablet contains exemestane 25 mg

excipients: mannitol (E 421), hypromellose, polysorbate 80, crospovidone, aqueous silicon dioxide, microcrystalline cellulose, sodium starch (type A), magnesium stearate sugar shell (hypromellose, simethicone emulsion, macrogol 6000, sucrose, magnesium carbonate, titanium dioxide (E 171), methyl parahydroxybenzoate (E 218), polyvinyl alcohol, cetyl ether waxes, talc, carnauba wax) ink: shellac, iron oxide (E172), titanium oxide (E171), ethyl alcohol, isobutyl alcohol.

Sugar-coated tablets.

Basic physical and chemical properties : round, biconvex, sugar-coated tablets, from white to slightly grayish in color, about 6 mm in diameter, printed with numbers 7663 in black ink on one side.

Hormone antagonists and similar agents. aromatase inhibitors. ATX code L02B G06.

Mechanism of action

Exemestane is an irreversible steroidal aromatase inhibitor, similar in structure to the natural substance androstenedione. In postmenopausal women, estrogens are produced predominantly by converting androgens to estrogens by the action of the aromatase enzyme in peripheral tissues. Blocking estrogen production by inhibiting aromatase is an effective and selective treatment for hormone-dependent breast cancer in postmenopausal women. In postmenopausal women, exemestane significantly reduced the concentration of estrogen in the blood serum, starting with a dose of 5 mg, the maximum reduction (> 90%) is achieved with a dose of 10-25 mg. In postmenopausal patients diagnosed with breast cancer who received 25 mg daily, total aromatase levels were reduced by 98%.

Exemestane has no progestogenic and estrogenic activity. A small androgenic activity, probably related to the 17-hydroderivative, was observed mainly when the drug was used in high doses. In studies of long-term daily use, exemestane did not affect the biosynthesis of hormones such as cortisol or aldosterone in the adrenal glands, the level of which was measured before or after the ACTH test (ACTH), this demonstrated selectivity for other enzymes involved in steroid metabolism.

In this regard, there is no need for replacement therapy with glucocorticoids and mineralocorticoids. A slight, dose-independent increase in the level of LH and FSH in the blood serum is observed even at low doses; this effect, however, is expected for drugs of this pharmacological group; probably, it develops according to the feedback principle, at the level of the pituitary gland, as a result of a decrease in the concentration of estrogens, it stimulates the secretion of gonadotropins by the pituitary gland (also in postmenopausal women).