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The mean baseline levels of LH and FSH were 4.8 ± 2.2 and 1.3 ± 0.7 mIU/ml, respectively. The percent change from baseline up to 24 h is reported in Fig. 4. The LH levels initially decreased by 26% at 2 h; thereafter, there was a tendency for an increase to a maximum of 81% at 24 h. The levels of FSH were unchanged up to 12 h and increased by 49% at 24 h.

Complete article below


Suppression of estrogen, via estrogen receptor or aromatase blockade, is being investigated in the treatment of different conditions. Exemestane (Aromasin) is a potent and selective irreversible aromatase inhibitor. To characterize its suppression of estrogen and its pharmacokinetic (PK) properties in males, healthy eugonadal subjects (14–26 yr of age) were recruited. In a cross-over study, 12 were randomly assigned to 25 and 50 mg exemestane daily, orally, for 10 d with a 14-d washout period. Blood was withdrawn before and 24 h after the last dose of each treatment period. A PK study was performed (n = 10) using a 25-mg dose. Exemestane suppressed plasma estradiol comparably with either dose [25 mg, 38% (P 0.002); 50 mg, 32% (P 0.008)], with a reciprocal increase in testosterone concentrations (60% and 56%; P 0.003 for both). Plasma lipids and IGF-I concentrations were unaffected by treatment. The PK properties of the 25-mg dose showed the highest exemestane concentrations 1 h after administration, indicating rapid absorption. The terminal half-life was 8.9 h. Maximal estradiol suppression of 62 ± 14% was observed at 12 h. The drug was well tolerated. In conclusion, exemestane is a potent aromatase inhibitor in men and an alternative to the choice of available inhibitors. Long-term efficacy and safety will need further study.

THE BIOLOGICAL ACTIONS of estrogens in males have begun to be unraveled via prismatic cases of estrogen deficiency in adults (1, 2, 3), gene knockout experiments in mice (4, 5, 6), and metabolic studies in vivo (7). Experiments in both animals and humans, for example, have clearly shown that epiphyseal fusion and the completion of final adult height are processes regulated by estrogen, even in the male. Male patients with functional mutations in either the estrogen receptor gene (1) or the aromatase gene (2, 3) have demonstrated continued linear growth into adulthood, tall stature, and osteopenia. This information has lead to the investigation of pharmacologically induced estrogen deficiency as an adjunct in delaying epiphyseal fusion in males with short stature and potentially increasing final adult height (8, 9).

The biosynthesis of estrogens from C19 steroids is regulated by the aromatase cytochrome p450 (CYP19), a product of a single CYP19 gene. This enzyme, which catalyzes the conversion of androstenedione and testosterone to estrone and estradiol, is widely expressed in numerous tissues, including bone (10, 11). We have conducted detailed studies of the metabolic effects of selective estrogen suppression in young eugonadal males using anastrozole, a potent and selective nonsteroidal aromatase inhibitor, and have shown that specific blockade of the aromatase enzyme for 10 wk did not have catabolic effects on protein metabolism, body composition, measures of muscle strength, and bone calcium metabolism (7). The data suggest that estrogens do not contribute significantly to the changes in body composition and protein synthesis observed with changing androgen levels in males. It also suggested that this level of aromatase inhibition does not negatively impact markers of bone calcium metabolism, at least in the short term.

A new irreversible aromatase enzyme blocker, exemestane (Aromasin), offers an alternative to suppress estrogen concentrations. It is structurally related to the natural substrate androstenedione, and it is metabolized to an intermediate that binds to the active site of the enzyme and inactivates it. It is excreted in the urine and feces. It decreases estradiol concentrations in postmenopausal women, but has no effect on the synthesis of glucocorticosteroids or aldosterone (12, 13). All pharmacokinetic (PK) data available to date are from postmenopausal women, as it is presently used in this population for the treatment of metastatic breast cancer (12, 13, 14, 15). A daily dose of 25 mg has been shown to have no effect on circulating testosterone concentrations in females. This study was designed with two aims: first, to investigate the dose of exemestane that can be safely given in adolescent/young adult males with minimal or no side-effects, and second, to investigate the PK and pharmacodynamics of this aromatase inhibitor in males.

These studies were approved by the Nemours Children’s Clinic clinical research review committee and Baptist Medical Center/Wolfson Children’s Hospital institutional review board. Healthy lean male volunteers between 14–26 yr of age were recruited after giving informed written consent to participate in study I or II (see below). Their clinical characteristics are summarized in Table 1.

Study I: dose finding
Two different doses of exemestane (Aromasin, 25-mg tablets) were administered orally in random order for 10 d with a 14-d washout in between. Twelve subjects were divided into 2 groups (treatment sequences): group I received 25 mg in period 1 and 50 mg in period 2, and group II received 50 mg in period 1 and 25 mg in period 2. Blood was withdrawn in the morning, between 0800–0900 h at the beginning of each treatment cycle and 24 h after the last dose of each treatment cycle (4 blood draws) for various pharmacodynamic assays. These included estradiol, estrone, estrone sulfate, androstenedione, testosterone, free testosterone, dehydroepiandrosterone sulfate, cortisol, SHBG, IGF-I, IGF-binding protein-3, and plasma lipid profiles [triglycerides, total cholesterol, high density lipoprotein (HDL) cholesterol, and low density lipoprotein (LDL) cholesterol]. Safety data, including general chemistries, cell blood count (CBC), urinalysis, and liver profiles, were measured as well. All adverse events were recorded.

Study II: PK study

Ten male volunteers participated in this study arm. They came to the Clinical Research Center at 0700 h after an overnight fast. An iv heparin lock was placed in a forearm vein for the blood drawing after numbing the skin with a topical anesthetic (EMLA, AstraZeneca, Wilmington, DE). In addition to safety laboratories (CBC, chemistry profile, and urinalysis), blood was withdrawn for determining exemestane, its metabolite 17-hydroexemestane, estradiol, testosterone, LH, and FSH concentrations. A regular breakfast was served that contained 30% of the total calories as fat, and a single dose of 25 mg exemestane was given with the meal. Blood was withdrawn at 0, 1, 2, 3, 4, 8, 12, 24, 48, 72, 144, and 240 h after the administration of exemestane for the same assays as at baseline. The subjects were fed a regular diet and were free to move around. After the 24 h sample was withdrawn, subjects were discharged home, and the 48, 72, 144, and 240 h samples were obtained as out-patients. LH and FSH were only measured up to 24 h.


As exemestane is a steroid, to eliminate any confounding interference of this compound and its metabolites on the assays of related endogenous steroidal hormones (androgens and estrogens), careful separation of the given compounds in the plasma samples was performed using HPLC, followed by RIA, as described by Johannessen et al. (16). Plasma estradiol, estrone, estrone sulfate, testosterone, and androstenedione concentrations were measured by a validated HPLC-RIA method at Aster-Cephac Laboratories (Saint-Benoit, Cedex, France). Briefly, a 2-ml plasma sample was loaded onto Amprep C18 cartridge and the fraction containing estrone sulfate or free steroids (estradiol, estrone, androstenedione, and testosterone) were eluted with 4 ml 24% acetonitrile in water or 100% acetonitrile, respectively. Estrone sulfate was hydrolyzed with arylsulfatase, and the deconjugated estrone was further extracted with a C18 cartridge. The extracted fractions were injected into a reverse phase HPLC system. The eluates corresponding to estradiol, estrone, androstenedione, and testosterone or to deconjugated estrone (to measure estrone sulfate) were collected and subjected to specific RIAs using commercial kits. The collected fractions were evaporated and reconstituted using an assay buffer before RIA. Appropriate plasma samples, spiked with each of the tritiated hormones, were included in each analytical run to calculate overall recoveries to correct results measured by RIA. All extractions were performed singly, and all RIA analysis were performed in duplicate. The lower limit of sensitivity was 0.7 pg/ml for estradiol, 1.8 pg/ml for estrone, 6 pg/ml for estrone sulfate, 40 pg/ml for androstenedione, and 30 pg/ml for testosterone. The overall interassay coefficients of variation were: estradiol, 6.2%; estrone, 12.9%; estrone sulfate, 8.2%; androstenedione, 12.6%; and testosterone, 8.6%. Free testosterone was measured by a validated gas chromatography/mass spectrometry bioanalytical method at Taylor Technology, Inc. (Princeton, NJ). LH and FSH were measured by RIA at the Nemours Biomedical Research Laboratory using commercial kits from Diagnostic Systems Laboratories, Inc. (Webster, TX). All other hormones were measured at a contract laboratory by RIAs using commercial kits. All samples were run in the same assay run. Concentrations of plasma lipids, chemistry profile, and CBC were measured using automated analyzers at Baptist Medical Center (Jacksonville, FL). Exemestane and 17-hydroexemestane plasma levels were measured at Pharma Bio Research (Assen, The Netherlands) using a validated liquid chromatography method with tandem mass spectrometry detection (17). The lower limit of sensitivity was 0.1 ng/ml for both assays.

Statistical analysis

For the pharmacodynamic results of study I, descriptive statistics were generated for the assays measured by group (sequence) and by treatment. The mean concentrations at baseline and at the end of treatment were summarized by period and by treatment group for all assays. A paired t test was used to test the difference between baseline and day 10 concentrations for each assay. A cross-over ANOVA with factors for period, treatment, group (sequence), and subject within group was conducted (18). A baseline value was added to the model. A paired t test was used to test the difference in concentrations at baseline and on d 10 for all assays. Significance was established at P < 0.05.

PK analysis

The PK of exemestane were determined by noncompartmental analysis (19) using the computer program WinNonlin (Pharsight Corp., Mountain View, CA). The maximum plasma concentration was the highest concentration observed for each individual. The area under the curve (AUC) was calculated using the linear trapezoidal rule up to the last quantifiable concentration and extrapolated to infinite time (AUC0-inf). The half-life of the terminal decay phase, t1/2,z, was determined by linear regression analysis of the natural log concentration vs. time curve, where t1/2,z = ln2/Kel, where Kel is the slope of the regression line. Oral clearance was calculated as oral dose/AUC0-inf. Analogous calculations were performed on (c x t) vs. time plots to estimate the area under the first moment curve (AUMC0-inf). The mean residence time was calculated as AUMC/AUC PK parameters were summarized with descriptive statistics.

Study I: dose finding

Analysis of the data on hormone concentrations after the 25- and 50-mg doses showed no difference in any of the parameters measured due to an order effect; hence, the data were grouped for analysis by dose. The 25- and 50-mg doses of daily exemestane had comparable effects in suppressing circulating estrogen concentrations, with 38 ± 24% (mean ± SD; P = 0.002 vs. baseline) and 32 ± 29% (P = 0.008) decreases in estradiol concentrations, 71 ± 12% (P < 0.0001) and 74 ± 12% (P < 0.0001) decreases in estrone concentrations, and 45 ± 27% (P = 0.004) and 51 ± 20% (P = 0.02) decreases in estrone sulfate concentrations after doses of 25 and 50 mg, respectively. There was an increase in circulating testosterone concentrations after both 25 mg (60 ± 58%; P = 0.001) and 50 mg (56 ± 48%; P = 0.003) exemestane. Androstenedione concentrations were increased as well after 25 mg (32 ± 36%; P = 0.004) and 50 mg (47 ± 59%; P = 0.052) exemestane, respectively (Fig. 1 and Table 2). SHBG concentrations were decreased by 21 ± 7% (P = 0.0003) and 19 ± 39% (P = 0.18) at 25 and 50 mg exemestane, respectively. Free testosterone concentrations were increased by 117 ± 74% (P = 0.0001) and 154 ± 95% (P < 0.0001) at both doses, due to the decrease in SHBG and the increase in total testosterone. No effect on circulating dehydroepiandrosterone sulfate was observed at either dose. Serum cortisol concentrations increased significantly (38 ± 39%; P = 0.008) with the 25-mg dose, but not the 50-mg dose, yet the increase was well within the normal range of cortisol concentrations. Plasma IGF-I decreased significantly (-13 ± 11%; P = 0.008) after the 25-mg dose, but not the 50-mg dose. Similarly, IGF-binding protein-3 showed a trend toward lower concentrations after the 25-mg dose (-7 ± 13%; P = 0.09), but not the 50-mg dose. There were no changes in circulating serum triglycerides, cholesterol, or LDL or HDL cholesterol concentrations with either dose of exemestane. Table 2 summarizes the results of the hormonal and lipid data.

Study II: PK
As the level of suppression of circulating estrogens was comparable between doses, we elected to use 25 mg for the subsequent PK study. In all individuals, the highest concentrations of exemestane were observed in the first blood sample drawn 1 h after oral administration, indicating rapid absorption of the drug. Plasma concentration vs. time profiles in all subjects were characterized by a biexponential decline in exemestane (Fig. 2), with terminal half-life of 8.9 h. The other PK parameters are listed in Table 3. The mean maximal plasma concentration of the metabolite 17-hydroexemestane was 1.16 ± 0.36 ng/ml, a concentration achieved 1 h after the exemestane dose. These levels rapidly declined, and concentrations below the lower limit of sensitivity (0.1 ng/ml) were observed at a median time of 12 h (range, 4–24 h).

The mean baseline levels of estradiol and testosterone were 24.5 ± 8.8 pg/ml and 581 ± 165 ng/dl, respectively. Maximal suppression of estradiol (62 ± 14%) was observed 12 h after a single 25-mg dose of exemestane. Estradiol remained suppressed by 58 ± 21% at 24 h and returned to baseline 3–6 d after treatment (Fig. 3). At the time of maximal estradiol suppression, plasma testosterone levels were unchanged and thereafter tended to increase by 32% between 2–3 d; however, contrary to the significant increase in testosterone observed after 10-d daily dosing, this change did not achieve statistical significance after a single oral dose. Serum LH and FSH concentrations were measured up to 24 h at the same time intervals as the exemestane samples for the PK analysis. The mean baseline levels of LH and FSH were 4.8 ± 2.2 and 1.3 ± 0.7 mIU/ml, respectively. The percent change from baseline up to 24 h is reported in Fig. 4. The LH levels initially decreased by 26% at 2 h; thereafter, there was a tendency for an increase to a maximum of 81% at 24 h. The levels of FSH were unchanged up to 12 h and increased by 49% at 24 h.

Exemestane was well tolerated by the study subjects, with no serious adverse events reported. General chemistries, CBC, and differential urinalysis and liver profiles were measured and were unchanged during administration.

We report the first detailed study of the pharmacological effects of exemestane in male subjects. Doses of 25 and 50 mg were comparable in suppressing all circulating estrogens and had similar effects of increasing serum androstenedione and testosterone concentrations. There were 38%, 71%, and 45% decreases in estradiol, estrone, and estrone sulfate concentrations, respectively, after 10 d, approximately 24 h after administration of the last dose of 25 mg exemestane, coupled with 60% and 32% increases in testosterone and androstenedione concentrations. The rise in the aromatase substrates, testosterone and androstenedione, is probably secondary to substrate accumulation and/or to the feedback increase in gonadotropins caused by aromatase blockade. The 21% decrease in SHBG concentrations caused by 25 mg exemestane confirms the observation in postmenopausal women (20).

The maximum plasma concentration, time to achieve maximal concentrations and oral clearance for exemestane after oral administration of a single dose of 25 mg in the present study of males were similar to those reported for females (21, 22, 23). The terminal half-life in the present study (8.9 h) was considerably shorter than the published value of 27 h (23). The reason for this difference is not clear, but may be related to a true gender dependency possibly involving the volume of distribution (lower in males than females) and plasma or tissue protein binding (respectively, higher and lower in males). This finding may also be due to the lower sensitivity of the analytical methodology used in the previous studies (14 pg/ml by HPLC/RIA) (21).

The maximal suppression evoked by exemestane at the single dose of 25 mg in the present study was similar to published results in postmenopausal women, but the time course differed (24). Evans et al. (24) reported that a single 25-mg oral dose of exemestane maximally suppressed estradiol concentrations by 72% 3 d after administration, and estradiol levels returned to baseline only 8–11 d after drug administration. In the present study maximal suppression of estradiol of 62% was observed 12 h after exemestane administration and returned to baseline 3–6 d after administration. The reason for this difference is not clear, but may be related to the shorter half-life of exemestane in males, the lower exposure to exemestane, and the higher levels of the aromatase substrates androstenedione (1 ng/ml in young males vs. 0.5 ng/ml in postmenopausal women), particularly the much higher testosterone concentrations in young males than in postmenopausal women (700 ng/dl vs. 20 ng/dl, respectively) (25). This is supported by the observation that in the 10-d study in young males reported here, the suppression of estradiol is weaker (due to the very high levels of the precursor testosterone) than that of estrone (due to androstenedione levels not very different from those in postmenopausal women). A limited suppression of circulating estradiol (50%) has been reported in a similar study in young males treated with 1 mg daily anastrozole (7), a dose that reduces estradiol by 85% in postmenopausal women (23).

Aromatase inhibitors are being investigated in a variety of clinical situations besides breast cancer. As estrogen is the principal factor responsible for epiphyseal fusion, aromatase blockers are being studied in the treatment of severe short stature in boys (8, 9). This class of compounds has a theoretical advantage over using LHRH analogs to delay puberty, because they allow for progressive virilization while decreasing estrogens, potentially extending the time of epiphyseal fusion and thus the time for linear growth. Trials have not yet been performed in adolescent females due to the concerns that increased circulating gonadotropins, decreased estrogens, and increased testosterone could precipitate ovarian dysfunction and virilization, as is seen in the aromatase-deficient female (3, 26). Because of its properties of increasing circulating gonadotropins, it has been used as a treatment for oligospermic men with low testosterone/estradiol ratios with initial preliminary success (27). This class of compounds also has a theoretical application in the treatment of gynecomastia in those individuals with overexpressed aromatase activity as recently reported (28). In addition, studies conducted using estrogen receptor blockade in the treatment of gonadotropin-independent precocious puberty have shown encouraging results (29); hence, the use of aromatase blockers seems like a natural alternative worthy of clinical trials as well.

We conclude that exemestane is a potent aromatase inhibitor in men. Exemestane appears to be an alternative in the choice of inhibitors of the aromatase enzyme available for human studies. Further studies are underway to estimate dose and dosing intervals that will provide therapeutic suppression of estrogen concentrations in males. Long-term safety will also require further investigation.


We are grateful to Burnese Rutledge and the nursing staff of Wolfson Children’s Hospital Clinical Research Center, to Brenda Sager and the Biomedical Analysis Laboratory, and to Steve Fordham and Holly Murphy.


This work was supported by a grant from Amersham Pharmacia Biotech.

Abbreviations: AUC, Area under the curve; CBC, cell blood count; HDL, high density lipoprotein; LDL, low density lipoprotein; PK, pharmacokinetic.

Received July 23, 2003.

Accepted September 10, 2003.

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At doses of 25/50 it looks like Aromison raises LH and FSH by 81% and 49% after 24hrs, also does not affect circulating serum triglycerides, cholesterol, or LDL or HDL cholesterol concentrations.

There were 38%, 71%, and 45% decreases in estradiol, estrone, and estrone sulfate concentrations. A 60% and 32% increases in testosterone and androstenedione concentrations.

Also it looks like you could use aromison to delay growth plates being formed so you could grow as tall as you like!

Read the whole article it's pretty interesting.
yo that growing as tall as u like like shit is crazy. i wonder thou how it would fuk with your body composition, meaning i wonder if u would only have the genetic muscle potential for a smaller frame that u were suppost to have and now you would have trouble gaining size. Or i wonder how it would affect other body parts like your head size. what if u were mad tall and had a tiny ass head lol
just look at a few gigantism cases, normally everything grows but they do look a little odd...apparantly if your nads get chopped of before puberty you will grow forever as your growth plates never seal, infact vocal singers in the 1800's had there nads cut off to keep hitting the high notes and grew till they died....wish aromisan was around when I was 18 then I could have been 6ft3 :D