Ecsemarin (exemestane) coated tablets 25 mg. №30


Manufacturer: Spain

Adjuvant therapy in women with invasive early-stage breast cancer with a positive test for estrogen receptors in the postmenopausal period after 2-3 yEars and Nose of initial adjuvant therapy with tamoxifen. Treatment of advanced breast cancer in women with natural or induced postmenopausal status, in which the progression of the disease was detected after antiestrogen therapy. Ni has been shown to be effective in patients with a negative test for estrogen receptors.



Ecsemarin Storage:

active substance: exemestane;

1 tablet contains exemestane 25 mg;

Excipients: mannitol (E 421), copovidone (type A), crospovidone (type A), microcrystalline cellulose, colloidal anhydrous silica, sodium starch glycolate (type A), magnesium stearate (E 470);

shell Advantia Prime White 190100BA01: hypromellose (E 464), macrogol 400, titanium dioxide (E 171).

Ecsemarin Dosage form.

Film-coated tablets.

Main physical and chemical properties: white or almost white, round biconvex film-coated tablets marked “25” on one side and smooth on the other.

Pharmacotherapeutic group.

Hormone antagonists and similar drugs. Enzyme inhibitors. ATX code L02B G06.

Ecsemarin Pharmacological properties.


Exemestane is an irreversible steroid aromatase inhibitor, similar in structure to the natural substance androstenedione. In postmenopausal women, estrogens are produced primarily by the conversion of androgens to estrogens by the enzyme aromatase in peripheral tissues. Blocking estrogen production by aromatase inhibition is an effective and selective method of treating hormone-dependent breast cancer in postmenopausal women. In postmenopausal women, exemestane significantly reduces the concentration of estrogen in the serum, starting with a dose of 5 mg; the maximum reduction (> 90%) is reached at a dose of 10-25 mg. In postmenopausal patients diagnosed with breast cancer who received 25 mg daily, the overall level of aromatase was reduced by 98%.

Exemestane has no progestogenic or estrogenic activity. Low 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, the level of which changed before or after the ACTH test; this demonstrated selectivity for other enzymes involved in hormonal metabolism. Therefore, there is no need for glucocorticoid and mineralocorticoid replacement therapy.

A slight increase in serum levels of luteinizing and follicle-stimulating hormones is observed even at low doses; this effect, however, is expected for drugs of this pharmacological group; it probably develops on the principle of feedback at the level of the pituitary gland: a decrease in the concentration of estrogen stimulates the secretion of gonadotropins by the pituitary gland (also in postmenopausal women).


Absorption. After oral administration, exemestane is rapidly absorbed. The dose absorbed from the digestive tract is high. Absolute bioavailability has not been established, although distribution should be limited by the first-pass effect. At a single dose of 25 mg after a meal, the average level in blood plasma reaches a maximum after 2 hours and is equal to 17 ng / ml. The pharmacokinetics of exemestane are linear and independent of time, with long-term use no accumulation was observed. The terminal half-life of the drug is approximately 24 hours. It has been found that food improves absorption: the level in the blood plasma is 40% higher than in patients who took the drug on an empty stomach.

Distribution. The volume of distribution of exemestane is large. Plasma protein binding is approximately 90%; the degree of binding does not depend on the total concentration. Exemestane and its metabolites do not bind to erythrocytes.

Metabolism and excretion. Exemestane is metabolised by oxidation of the methylene group (6) to the isoenzyme CYP 3A4 and / or by reduction of the 17-keto group to aldoketoreductase and subsequent conjugation. The clearance of exemestane is 500 l / h. Regarding aromatase inhibition, these metabolites are either inactive or less active than the parent compound. After oral administration of a single dose of exemestane labeled with the radioactive isotope 14C, it was found that the elimination of the drug and its metabolites was mostly completed within a week, with equal portions of the dose excreted in urine and feces (40%). 0.1-1% of the radioactive dose was excreted in the urine as unchanged radiolabeled exemestane.

Special groups

Age. No significant correlation was observed between systemic excretion of exemestane and age.

Renal failure. In patients with impaired renal function (CLcr <30 ml / min), systemic excretion of exemestane was twice as high as in healthy volunteers.

Given the safety data of exemestane, no dose adjustment is required.

Liver dysfunction.

In patients with moderate or severe hepatic impairment, systemic excretion of exemestane is two to three times higher than in healthy volunteers. Given the safety data of exemestane, no dose adjustment is required.