you are correct. Adex has a longer life, in the blood stream however,
Aromasin (exemestane)

Exemestane is a steroidal suicide aromatase inhibitor. It isvery similar in structure and action to formestane, although it is significantly more potent in comparison. As a class of drugs, aromatase inhibitors offer an anti estrogenic effect by blocking the enzyme responsible for synthesizing estrogens. Exemestane is approved by the FDA for the treatment of breast cancer in women, specifically in post menopausal patients whose cancer has progressed following therapy with tamoxifen (nolvadex). Male bodybuilders and athletes often use the drug for non approved purposes, namely to counter the estrogenic side effects associated with the use of aromatizable anabolic/androgenic steroids. This may include gynecomastia, fat buildup, and water retention. Exemestane is one of the most potent aromatase inhibitors presently available. The most commonly cited date reports a lowering of estrogen around 85% on average in clinical studies with women. Exemestane was developed by Pharmacia & Upjohn, which gained FDA approval for sale of the drug in late 1999. They introduced it under the Aromasin brand name in early 2000. Although the drug proved to be effective in doses as low as 2.5mg per day in some patients, the company developed it in a standard and near universally effective dosage of 25mg per tablet. The company has since introduced the drug to many other nations under the same trade name of Aromasin.
It has been shown that 25 milligrams of exemestane is basically just as effective as 50 milligrams at suppressing estrogen, raising testosterone levels, and levels of IGF.

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. 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.

Products /aromatase inhibition/risudual aromatase%

formestance(4-androstenoldion) /91.6/8.1%

aromasin(exemestance)/97.9/2.1%

cytradren (aminoglutethimide)/90.6/9.4%

arimidex
(amastrozole)/96.7/3.1%

femera(letrozole)/98.7/1.3%

Produc/effect/percentage

formestance(4-androstenoldion) /increases IGF-1/26%

femera(letrozole)/increases IGF-1/24%

aromasin(exemestance)/increases IGF-1/28%

arimidex
(amastrozole)/decreases IGF-1/18%

nolvadex(tamoxifen citrate)/decreases IGF-1/23.5%

faslodex(fulvestrant)/decreases IGF-1/70%

cytradren (aminoglutethimide)/increases IGF-1/27%

Estrogen suppression in males: metabolic effects.
J Clin Endocrinol Metab 2000 Jul;85(7):2370-7 (ISSN: 0021-972X)
Mauras N; O'Brien KO; Klein KO; Hayes V [email protected].

We have shown that testosterone (T) deficiency per se is associated with marked catabolic effects on protein, calcium metabolism, and body composition in men independent of changes in GH or insulin-like growth factor I production. It is not clear,,however, whether estrogens have a major role in whole body anabolism in males. We investigated the metabolic effects of selective estrogen suppression in the male using a potent aromatase inhibitor, Arimidex (Anastrozole). First, a dose-response study of 12 males (mean age, 16.1 +/- 0.3 yr) was conducted, and blood withdrawn at baseline and after 10 days of oral Arimidex given as two different doses (either 0.5 or 1 mg) in random order with a 14-day washout in between. A sensitive estradiol (E2) assay showed an approximately 50% decrease in E2
concentrations with either of the two doses; hence, a 1-mg dose was selected for other studies. Subsequently, eight males (aged 15-22 yr; four adults and four late pubertal) had isotopic infusions of [(13)C]leucine and (42)Ca/(44)Ca, indirect calorimetry, dual energy x-ray absorptiometry, isokinetic dynamometry, and growth factors measurements performed before and after 10 weeks of daily doses of Arimidex. Contrary to the effects of T withdrawal, there were no significant changes in body composition (body mass index, fat mass, and fat-free mass) after estrogen suppression or in rates of protein synthesis or degradation; carbohydrate, lipid, or protein oxidation; muscle strength; calcium kinetics; or bone growth factors concentrations. However, E2 concentrations decreased 48% (P = 0.006), with
no significant change in mean and peak

GH concentrations, but with an 18% decrease in plasma insulin-like growth factor I concentrations.

There was a 58% increase in serum T (P = 0.0001), sex hormone-binding globulin did not change, whereas LH and FSH concentrations increased (P < 0.02, both). Serum bone markers, osteocalcin and bone alkaline phosphatase concentrations, and
rates of bone calcium deposition and resorption did not change. In conclusion, these data suggest that in the male 1) estrogens do not contribute significantly to the changes in body composition and protein
synthesis observed with changing androgen levels; 2) estrogen is a main regulator of the gonadal-pituitary feedback for the gonadotropin axis; and 3) this level of aromatase inhibition does not negatively impact either kinetically measured rates of bone calcium turnover or indirect markers of bone calcium turnover, at least in the short term. Further studies will provide valuable information on whether timed aromatase inhibition can be useful in increasing the height potential of pubertal boys with profound
growth retardation without the confounding negative effects of gonadal androgen suppression.