Letromara coated tablets 2.5 mg. №30


Manufacturer: Ukraine

Adjuvant therapy for hormone-positive invasive breast cancer in early stages in postmenopausal women. Extended adjuvant therapy for invasive breast cancer in the early stages in postmenopausal women who received standard adjuvant therapy with tamoxifen for 5 years. First-line therapy for hormone-dependent advanced breast cancer in postmenopausal women.



Letromara Storage
active substance: letrozole;

1 tablet contains letrozole 2.5 mg in terms of 100% of the substance;

Excipients: lactose monohydrate, corn starch, microcrystalline cellulose 101, hydroxypropylmethylcellulose (15), sodium starch glycolate (type A), magnesium stearate; film coating composition: SepifilmTM 050 (methylhydroxypropylcellulose, microcrystalline cellulose, acetylated (or acetate esters) mono- and diglycerides), SepisperseTM Dry 3214 Jaune (hydroxypropylmethylcellulose), microcrystalline cellulose

Letromara Dosage form
Film-coated tablets.

Main physical and chemical properties: round tablets with a biconvex surface, film-coated brownish-yellow or orange-yellow.

Letromara Pharmacotherapeutic group
Means used for hormone therapy. Hormone antagonists and similar drugs. Aromatase inhibitors. Letrozole.

ATX code L02B G04.

Letromara Pharmacological properties

Letrozole – a non-steroidal aromatase inhibitor (inhibitor of estrogen biosynthesis); antitumor drug.

In cases where the growth of tumor tissue depends on the presence of estrogen, the elimination of the stimulant effect mediated by them is a prerequisite for inhibition of tumor growth.
In postmenopausal women, estrogens are produced primarily by the enzyme aromatase, which converts androgens synthesized in the adrenal glands (primarily androstenedione and testosterone) to estrone (E1) and estradiol (E2). Therefore, with the help of specific inhibition of the enzyme aromatase, it is possible to achieve inhibition of estrogen biosynthesis in peripheral tissues and in tumor tissue.

Letrozole inhibits aromatase by competitively binding to a subunit of this enzyme, cytochrome P 450 heme, which reduces estrogen biosynthesis in all tissues.

In healthy postmenopausal women, a single dose of letrozole, which is 0.1 mg or 0.5 mg or 2.5 mg, reduces the level of estrone and estradiol in the serum (compared to baseline) by 75-78% and 78% in accordance. The maximum reduction is achieved in 48-78 hours.

In women with advanced postmenopausal breast cancer, daily administration of letrozole 0.1 mg to 5 mg reduces plasma estradiol, estrone and estrone sulphate levels by 75-95% from baseline. When using the drug at a dose of 0.5 mg or more in many cases, the concentrations of estrone and estrone sulfate are below the sensitivity limit of the method used to determine hormones. This indicates that with these doses of the drug is a more pronounced inhibition of estrogen synthesis. Estrogen suppression was maintained during treatment in all patients.

Letrozole is a highly specific inhibitor of aromatase activity. Disorders of steroid hormone synthesis in the adrenal glands were not detected. No clinically significant changes in plasma concentrations of cortisol, aldosterone, 11-deoxycortisol, 17-hydroxyprogesterone, ACTH, and renin activity were observed in postmenopausal patients treated with letrozole at a daily dose of 0.1-5 mg. Conducting an ACTH stimulation test after 6 and 12 weeks of letrozole therapy at a daily dose of 0.1 mg; 0.25 mg; 0.5 mg; 1 mg; 2.5 mg and 5 mg did not show any significant decrease in aldosterone or cortisol synthesis. Thus, there is no need to prescribe glucocorticoids and mineralocorticoids.