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Description:

ED50: 2.0 μM

Glandular kallikrein, a trypsin-like serine protease, has been identified as a major estrogen-induced protein in the rat anterior pituitary. This induction appears to be mediated by increased gene expression since glandular kallikrein mRNA is also estrogen-induced. Chlorotrianisene is classified as an estrogen agonist.

In vitro: The ED50 of chlorotrianisene were lowered by 3.9-fold. Chlorotrianisene inhibited the growth of both P388 and P388/ADR cells in a concentration-dependent manner [1].

In vivo: Chlorotrianisene markedly varied in its ability to elicit agonist responses on the three measures. On uterine weight and anterior pituitary prolactin, chlorotrianisene behaved as partial agonists. Chlorotrianisene also exhibited strikingly less agonist activity on glandular kallikrein than on PRL or the uterus. Further, the small agonist activity of chlorotrianisene on glandular kallikrein induction differed from that on the uterus or prolactin [2].

Clinical trial: Chlorotrianisene is a estrogen which is highly effective in the suppression of postpartum lactation when given orally in dosage of 48 mg/day for seven days. Recurrence of symptoms and appearance of withdrawal bleeding are virtually eliminated, probably because of the storage of chlorotrianisene in the body fat and its gradual release after cessation of therapy [3].

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