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Aromasin - Exemestane

Chemical Name: Exemestane
Drug Class: Type-I Aromatase Inhibitor


Aromasin Profile

exemestane aromasin chemical structureAromasin (Exemestane) is a Type-I aromatase inhibitor, or suicidal aromatase inhibitor. It’s called this because it lowers estrogen production in the body by attaching to the aromatase enzyme, and permanently deactivating it. [1]

Personally, I find this to be a very interesting mechanism of action when compared to type-II aromatase inhibitors, which bind competitively to the aromatase enzyme, and eventually unbind, rendering it active again. In the case of Aromasin, this doesn’t happen, and once it does its job on the enzyme, those particular enzymes will no longer function. Your body will eventually create more of the aromatase enzyme, so this isn’t dangerous, despite the really odd “suicide” thing in the first paragraph. As with all aromatase inhibitors, Aromasin was developed to fight breast cancer primarily in post-menopausal women, but we in the athletic community use it to combat estrogenic side effects from aromatizable steroids, or for post cycle therapy.

Estrogen is responsible for many of the effects we’re trying to avoid when we’re on a cycle, including excess water retention and development of gynocomastia (breast tissue development in males. Thus, limiting the conversion of testosterone into estrogen is of use for steroid using athletes, when they’re trying to avoid side effects. In this case, the advantage of using a suicidal aromatase inhibitor is that it really won’t cause much, if any, noticeable “rebound” in estrogen when you cease using it.

The hard numbers on Aromasin are reasonably impressive, as it averages an 85% rate of estrogen suppression [2], and this translates to an overall reduction in estradiol levels of about 50%, as well as raising testosterone to a significant degree.[3].

It is also known as a “steroidal” aromatase inhibitor. This is really interesting, because it has been known to actually cause side effects (androgenic sides) that include increased aggressiveness and a pretty decent hardening effect. [3] I wouldn’t usually suggest that women should use Aromasin in large doses for any extended period of time, for this reason (possible virilization, or development of male sexual characteristics could occur with its use). It should, therefore, be reserved for use by women to brief periods of time in a possible pre-contest phase or for a form of post cycle therapy after a cycle.

aromasin vs nolvade chart
Fig 1. Aromasin vs. Nolvadex Comparison

Interestingly (and almost paradoxically) exemestane not only increases testosterone and lowers estrogen, but it also increases levels of insulin-like growth Factor (IGF). [5] I find this to be interesting, because although the rise in testosterone is most likely responsible for the increase in IGF levels, IGF is known to be an aggravating factor in the growth of breast tumors, like the kind found in breast cancer. However, since estrogen is the primary culprit in breast cancer, the large reduction in estrogen levels, even when combined with a rise in IGF, is enough to make Aromasin a very effective breast cancer medication. Aromasin isn’t too harsh on blood lipids [6] (cholesterol), unlike some of the other AIs’ like Letrozole.

Exemestane reaches steady blood plasma levels of after a week of administration and this is also when we see it begin its maximal effect on reducing circulating estrogen levels. It’s also has a ½ life of 27 hours [4], so taking it once per day is going to build up blood plasma levels to a very effective level.


aromasin tablets
aromasin pfizer


Climacteric. 2012 Oct;15(5):460-6. Epub 2012 Feb 9.
Effects of exemestane and tamoxifen on hormone levels within the Tamoxifen Exemestane Adjuvant Multicentre (TEAM) Trial: results of a German substudy.
Hadji P, Kauka A, Bauer T, Tams J, Hasenburg A, Kieback DG.

University Hospital of Giessen and Marburg , Marburg.

Drug Insert


  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. ^ Eur. J. Cancer. 2000, May;36(8):976-82
  3. ^ The Journal of Clinical Endocrinology & Metabolism Vol. 88, No. 12 5951-5956Copyright © 2003 by The Endocrine Society
  4. ^ Clin Cancer Res. 2003 Jan;9(1 Pt 2):468S-72S
  5. ^ Anticancer Res. 2003 Jul-Aug;23(4):3485
  6. ^ J Clin Endocrinol Metab. 2003 Dec;88(12):5951-6.

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