Aromasin
 

(exemestane)

Aromasin (Exemestane) is a steroidal suicide aromatase inhibitor, which means that it lowers estrogen production in the body by blocking the aromatase enzyme, the enzyme responsible for estrogen synthesization. (1)(2)(3)
This stuff was developed to fight breast cancer in post-menopausal women, who need a particularly aggressive therapy, and for whom first line defenses such as SERMS (Tamoxifen) have not worked. This should be our first clue in inferring that this stuff is pretty strong, or at least stronger than some of the other compounds which are used to fight breast cancer.
Aromasin and Side Effects

Aromasin averages an 85% rate of estrogen suppression (4), so it´s clearly a very effective agent for bodybuilders and other athletes wanting to avoid estrogen related side effects such as gyno, acne, or water-retention brought on by aromatizing steroids. Specifically, Exemestane dose this by selectively inhibiting aromatase activity in a time-dependent and irreversible manner (hence the "suicidal" portion of it´s name, I guess).(7)
As with most of the compounds in this class, it also causes a reasonable rise in testosterone levels (6), and as you may have guessed, this rise in testosterone means that Exemestane can also cause androgenic sides(8)(9)(10). As you can see from the chart below, exemestane is very effective at both lowering estrogen (estradiol) and raising testosterone:
FIG. 1. Estrogen and androgen plasma levels after 10 d of daily exemestane (25 or 50 mg) in healthy young males (mean ± SD; n = 9-11). To convert to Systeme International units: estradiol, picomoles per liter (x3.671); estrone, picomoles per liter (x3.699); androstenedione, nanomoles per liter (*0.003492); and testosterone, nanomoles per liter (x0.03467). (13)
So we can see that 25mgs is a very effective dose from that chart, right? As an added benefit, exemestane not only increases testosterone and lowers estrogen, but it also increases IGF levels (11).Additionally Worth noting is that Aromasin may possibly be less harsh on blood lipids (14)than some of the other (similar) compounds we use in the world of bodybuilding or athletics (other AI´s). It also has, at best no effect on IGF, and at worst could lower (13) it. AI´s are very tricky with regards to inconsistencies in IGF levels.
Unfortunately, you need to take Exemestane for a week to reach steady blood plasma levels of it, and exemestane has a ½ life of 27 hours (12.).
The ability of exemestane to lower estrogen levels by the aforementioned 85% makes it a very nice choice for use in any cycle where aromatizing steroids are used. In addition, since it´s not too harsh at all on blood lipid profiles, it´s a very good choice for longer cycles. It´s ability to raise both testosterone levels also seem to suggest that it would be a very nice addition to a Post-Cycle-Therapy (PCT).
References:

1. A predictive model for exemestane pharmacokinetics/pharmacodynamics incorporating the effect of food and formulation.Br J Clin Pharmacol. 2005 Mar;59(3):355-64.
2. Exemestane for breast cancer prevention: a feasible strategy?Clin Cancer Res. 2005 Jan 15;11(2 Pt 2):918s-24s.
3. Endocrinology and hormone therapy in breast cancer: Aromatase inhibitors versus antioestrogens, Anthony Howell1 and Mitch Dowsett2. 1CRUK Department of Medical Oncology, University of Manchester, Christie Hospital, Manchester, UK. 2Academic Department of Biochemistry, Royal Marsden Hospital, London, UK. Breast Cancer Res 2004, 6:269-274 doi:10.1186/bcr945. Published 6 October 2004
4. Eur. J. Cancer. 2000, May;36(8):976-82
5. Breast Cancer Res Treat. 1995;36(3):287-97.
6. J Clin Endocrinol Metab. 2003 Dec;88(12):5951-6.
7. Nippon Yakurigaku Zasshi. 2003 Oct;122(4):345-54.
8. Clin Cancer Res. 2003 Jan;9(1 Pt 2):468S-72S.
9. J Clin Endocrinol Metab 2000 Jul;85(7):2370-7
10. J Steroid Biochem Mol Biol 1997 Nov-Dec;63(4-6):261-7
11. Anticancer Res. 2003 Jul-Aug;23(4):3485-91
12. Clin Cancer Res. 2003 Jan;9(1 Pt 2):468S-72S
13. The Journal of Clinical Endocrinology & Metabolism Vol. 88, No. 12 5951-5956Copyright © 2003 by The Endocrine Society
14. J Clin Endocrinol Metab. 2003 Dec;88(12):5951-6.