Formestane은 2 세대의 돌이킬 수없는 스테로이드 성 아로마 타제입니다. 그것은 안드로겐을 에스트로겐으로 전환 시켜서 에스트로겐 생성을 예방하는 아로마 타제 효소를 억제합니다.
용도
Formestane oiwder 폐경 후 여성에서 에스트로겐 수용체 양성 유방암의 치료에 사용되는 제 1 형 선택적 I 형 스테로이드 아로마 타제 억제제였다. Formestane은 단백 동화 스테로이드 또는 프로 호르몬으로부터 에스트로겐 생성을 억제합니다.
개요
Formestane is a potent aromatase inhibitor launched in the UK as a second-line
endocrine treatment for breast cancer. As a synthetic derivative of androstanedione, the
natural substrate for the biosynthesis of estrogen by the enzyme aromatase, formastane
selectively inhibits aromatase and binds to its steroid receptor site to cause a rapid and
sustained fall in circulating estrogen level and, therefore, inhibits tumor growth. In patients
with existing bulky primary tumors, formestane effectively reduces the size of the tumors.
Formastane has apparent tolerability advantages and less side effects than other agents such
as aminoglutethimide.
화학적 성질
Needles
정의
ChEBI: A 17-oxo steroid that is androst-4-ene-3,17-dione in which the hydrogen at position 4 is replaced by a hydroxy group. Formestane was the first selective, type I steroidal aromatase inhibitor, suppressing oestrogen production from anabolic steroids or proho
mones. It was formerly used in the treatment of oestrogen-receptor positive breast cancer in post-meopausal women. As it has poor oral bioavailability, it had to be administered by (fortnightly) intramuscular injection. It fell out of use with the subseque
t development of cheaper, orally active aromatase inhibitors. Formestane is listed by the World Anti-Doping Agency as a substance prohibited from use by athletes.
Mechanism of action
Aromatase inhibitors such as formestane and letrozole reduce plasma estradiol levels by inhibiting the conversion of testosterone to estrogen. This compound was first described as a competitive inhibitor, but subsequent evidence proved that its binding to aromatase was irreversible. Hence, it is a suicide inhibitor. In the dog, but not rodents, this results in Leydig cell hypertrophy and hyperplasia. This is thought to be due to the differential sensitivity of the pituitary feedback mechanism to estrogens and androgens in the different species[1-2].
