Aromasin

Aromasin (exemestane)
Aromasin (exemestane) is an inhibitor of the steroidal aromatase suicide, which means that decreases the production of estrogen in the body by blocking the enzyme aromatase, an enzyme responsible for the synthesis of estrogen. (1) (2) (3) This document was prepared to fight against breast cancer in postmenopausal women who need special medical treatment and for which the first line of defense, such as SERM (tamoxifen), did not work. This must be our first key to the conclusion that this material is very strong, or at least stronger than other compounds, which are used to fight against breast cancer. Aromasin side effects Aromasin average 85% of the suppression of estrogen levels (4), which is clearly a very effective tool for bodybuilders and other athletes want to avoid estrogen related side effects such as gyno, acne or water retention caused by steroids aromatizing. In particular, the dose of exemestane that selectively prevents the activity of aromatase in the time-dependent and irreversible manner (hence the "suicide" of his name, I think). (7) As in most compounds of this class, but also led to a reasonable increase in testosterone (6), in May and as you guessed it, an increase of testosterone means that exemestane may also cause androgenic sides ( 8) (9) (10). As can be seen in the table below, exemestane is effective in reducing estrogen (estradiol) and the increase of testosterone: Fig. 1. Estrogen and androgen plasma D after 10 days by exemestane (25 or 50 mg) in young men (mean ± standard deviation, N = 9-11). To convert to Système International units: estradiol, picomole per liter (x3.671); estrone, picomole per liter (x3.699), androstenedione, nanomoles per liter (* 0.003492), and testosterone, nanomoles per liter (x0. 03467). (13) So we see that very 25mg of effective dose of this scheme, no? As an added benefit, exemestane, not only increases testosterone and estrogen decreases, but also increases the level of IGF (11). In addition, it should be noted that Aromasin May be less severe on blood lipids (14) than others (even) compounds we use in the world of bodybuilding and athletics (the other of Amnesty International). He also, at best, have no effect on the IGF, and in the worst case could be less than (13). Amnesty International is very difficult in terms of inconsistencies in the levels of IGF. Unfortunately, you need to exemestane for a week to ensure sustainable levels of blood plasma, and exemestane has a half life of 27 hours (12.). The ability of exemestane to lower estrogen levels in these 85% are a very good choice for use in the cycle where aromatizing used steroids. In addition, since it is not too hard for all blood lipid profiles, it is a very good choice for longer cycles. This is an opportunity to raise the level of testosterone is likely to indicate that it would be a very pleasant addition of a post-cycle therapy (PCT). References: A predictive model for exemestane pharmacokinetics / pharmacodynamics of the impact of food and formulation.Br J Clin Pharmacol. 2005 Mar; 59 (3) :355-64. Exemestane to prevent breast cancer: a feasible strategy? Clin Cancer Res. 2005 Jan 15; 11 (2 Pt 2): 24S-918s. Endocrinology and hormone therapy in breast cancer: aromatase inhibitors versus antioestrogen, Anthony Howell1 and Mitch Dowsett2. 1CRUK Department of Medical Oncology at the University of Manchester, Christie Hospital, Manchester, United Kingdom. 2Academic Department of Biochemistry, Royal Marsden Hospital, London, United Kingdom. Breast Cancer Res 2004, 6:269-274 DOI: 10.1186/bcr945. Published 6 October 2004 Eur. J. cancer. 2000 May 36 (8) :976-82 Breast Cancer Res Treatment. 1995, 36 (3) :287-97. J Clin Endocrinol Metab. December 2003, 88 (12) :5951-6. Nippon Yakurigaku Zasshi. October 2003, 122 (4) :345-54. Clin Cancer Res. January 2003, 9 (1 Pt 2): 468S-72S. J Clin Endocrinol Metab 2000 Jul; 85 (7) :2370-7 J Steroid Biochem Mol Biol 1997 Nov-Dec; 63 (4-6) :261-7 Anticancer Res. 2003 July-August, 23 (4) :3485-91 Clin Cancer Res. January 2003, 9 (1 Pt 2): 468S-72S Journal of Clinical Endocrinology and Metabolism Vol. 88, № 12 5951-5956 Copyright © 2003 Endocrine Society J Clin Endocrinol Metab. December 2003, 88 (12) :5951-6.