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  1. #1
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    Default Aromasin~exemestane

    Aromasin

    (Exemestane)


    Aromasin is a steroidal aromatase inactivator used to lower circulating estrogen. It was developed to help fight breast cancer as estrogen plays a role in the growth of cancer cells. Aromasin binds irreversibly to the aromatase enzyme. This suppresses the conversion of androgens into estrogen. Circulating estrogen can be reduced by nearly 85% in women using Aromasin. A common misconception is that aromatase inhibition is similar in men than women. However in trials when males were administered 25mg of Aromasin daily maximal estradiol suppression of 62 ± 14% was observed at 12 hours. Aromasin acts as a false substrate for the aromatase enzyme, and is processed to an intermediate that binds irreversibly to the active site of the enzyme causing its inactivation, an effect also known as "suicide inhibition." In other words, Exemestane, by being structurally similar to the target of the enzymes, permanently binds to those enzymes, thereby preventing them from ever completing their task of converting androgens into estrogens. When we compare this mode of action against other AI’s the benefit becomes clear. Arimidex can unbind from the aromatase enzyme when you stop taking it but Aromasin will not therefore there is less chance of estrogen rebound with Aromasin.

    Aromasin can be employed during a steroid cycle when aromatizing compounds such as testosterone are administered in order to control estrogen from getting out of control. During the course of a typical steroid cycle estrogen can rise quite high. Estrogen has been measured as much as 7 times higher than normal in men on steroids. This is excessive and can potentially cause water retention, gynecomastia (the formation of female breast tissue) or benign prostatic hyperplasia. Therefore in order to avoid these side effects estrogen must be controlled.

    Aromasin not only lowers circulating estrogen and sex hormone binding globulin but it also increases free testosterone by a whopping 117%! Total testosterone increases about 60%. Check out the performance of Aromasin after just 10 days of treatment in males.


    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).

    Aromasin may be used during a steroid cycle with aromatizing compounds and during PCT to help keep the estrogen to testosterone balance in favor of testosterone. Out of all the medications to control estrogen, Aromasin seems to be the most well balanced. It raises testosterone slightly better than Arimidex and lowers estradiol about 12% better than arimidex in men and is likely to cause less estrogen rebound than Arimidex. Keep in mind that 50mg of Aromasin daily kept estradiol in the normal range for men so if you think using an aromatase inhibitor will crush estrogen too much this science supports the opposite. From the data I have read and my years of experience with this medication 25mg of Aromasin every other day is a good starting point on moderate doses of testosterone. If testosterone doses are raised then 25mg daily may be needed to control estrogen. Since either high and low estrogen can cause side effects such as low libido only labs can determine the appropriate dose of Aromasin.

    Written by heavyiron
    Last edited by heavyiron; 01-25-2010 at 08:36 PM.


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  2. #2
    Chemistry Experiment heavyiron's Avatar
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    Rationale for the Use of Aromasin with Tamoxifen During Post Cycle Therapy

    by Anthony Roberts

    Author of Anabolic Steroids: Ultimate Research Guide and Beyond Steroids; Co-Author with Christian Thibaudeau of Dr. Jekyll and Mr. Hyde - Body Transformation From Both Sides of the Force

    Publication Date: November 11, 2005
    Discussion of pharmaceutical agents below is presented for information only. Nothing here is meant to take the place of advice from a licensed health care practitioner. Consult a physician before taking any medication.

    Aromasin (Exemestane) is one of those weird compounds that nobody really knows what to do with. What we generally hear about it makes it very uninteresting…It’s a third generation Aromatase Inhibitor (AI) just like Arimidex (Anastrozole) and Femera (Letrozole). Both of those two drugs are very efficient at stopping the conversion of androgens into estrogen, and since we have them, why bother with Aromasin? It’s a little harder to get than the other two commonly used aromatase inhibitors, because it’s not in high demand, and there’s never been a readily apparent advantage to using it. And I mean…lets face it: It’s awkward-sounding. Aromasin doesn’t have much of a ring to it, and exemestane is even worse. Arimidex has a bunch of cool abbreviations ("A-dex" or just ‘dex) and even Letrozole is just "Letro" to most people. Where’s the cool nickname for

    Aromasin/exemestane? A-Sin? E-Stane? It just doesn’t work. It’s the black sheep of AIs. And why do we even need it when we have Letrozole, which is by far the most efficient AI for stopping aromatization (the process by which your body converts testosterone into estrogen)? Letro can reduce estrogen levels by 98% or greater; clinically a dose as low as 100mcgs has been shown to provide maximum aromatase inhibition (2)!

    So why would we need any other AIs? Well, first of all, estrogen is necessary for healthy joints (3) as well as a healthy immune system (4). So getting rid of 98% of the estrogen in your body for an extended period of time may not be the best of ideas. This may be useful on an extreme cutting cycle, leading up to a bodybuilding contest, or if you are particularly prone to gyno, but certainly can’t be used safely for extended periods of time without compromising your joints and immune system.

    That leaves us with Arimidex, which isn’t as potent as Letrozole, but at .5mgs/day will still get rid of around half (50%) of the estrogen in your body. Problem solved, right? Use Arimidex on your typical cycles, and if you are very prone to gyno or are getting ready for a contest, use Letro.

    But what about Post Cycle Therapy (PCT)?

    I think at this point most people are sold on the use of Nolvadex (Tamoxifen Citrate) instead of Clomid for post cycle therapy (PCT), since both compete estrogen at the receptor site, both increase serum test levels, and both drugs may also alter blood lipid profiles favorably (6). But since 20mgs of Tamoxifen is equal to 150mgs of clomid for purposes of testosterone elevation, FSH and LH, but Tamoxifen doesn’t decrease the LH response to LHRH (6) I think most people agree to Nolvadex’s superiority for PCT.

    Aromasin with Nolvadex

    I’ve always been in favor of using Nolvadex during PCT, along with an AI, because reducing estrogen levels has been positively correlated with an increase in testosterone (7) so in my mind, it’s be beneficial to increase testosterone by as many mechanisms as possible while trying to recover your endogenous testosterone levels after a cycle. SO which AI do we use? Letro or A-dex? Well, why don’t we just keep using whichever one we used during the cycle, and add in some Nolvadex? Unfortunately, Nolvadex will significantly reduce the blood plasma levels of both Letrozole as well as Arimidex (8). So if we choose to use one of them with our Nolvadex on PCT, we’re throwing away a bit of money as the Nolvadex will be reducing their effectiveness.

    This, of course, is where Aromasin comes in, at 20-25mgs/day.

    Aromasin, at that dose, will raise your testosterone levels by about 60%, and also help out your free to bound testosterone ratio by lowering levels of Sex Hormone Binding Globulin (SHBG), by about 20% (12)…SHBG is that nasty enzyme that binds to testosterone and renders it useless for building muscle. But what about using it along with Nolvadex for PCT?

    Difference Between Type-I and Type-II Aromatase Inhibitors

    To understand why Aromasin may be useful in conjunction with Nolvadex while both Letro and A-dex suffer reduced effectiveness, we’ll need to first understand the differences between a Type-I and Type-II Aromatase Inhibitor. Type I inhibitors (like Aromasin) are actually steroidal compounds, while type II inhibitors (like Letro and A-dex) are non-steroidal drugs. Hence, androgenic side effects are very possible with Type-I AIs, and they should probably be avoided by women. Of course, there are some similarities between the two types of AIs…both type I & type II AIs mimic normal substrates (essentially androgens), allowing them to compete with the substrate for access to the binding site on the aromatase enzyme. After this binding, the next step is where things differ greatly for the two different types of AI’s. In the case of a type-I AI, the noncompetitive inhibitor will bind, and the enzyme initiates a sequence of hydroxylation; this hydroxylation produces an unbreakable covalent bond between the inhibitor and the enzyme protein. Now, enzyme activity is permanently blocked; even if all unattached inhibitor is removed. Aromatase enzyme activity can only be restored by new enzyme synthesis. Now, on the other hand, competitive inhibitors, called type II AI’s, reversibly bind to the active enzyme site, and one of two things can happen: 1.) either no enzyme activity is triggered or 2.) the enzyme is somehow triggered without effect. The type II inhibitor can now actually disassociate from the binding site, eventually allowing renewed competition between the inhibitor and the substrate for binding to the site. This means that the effectiveness of competitive aromatase inhibitors depends on the relative concentrations and affinities of both the inhibitor and the substrate, while this is not so for noncompetitive inhibitors. Aromasin is a type-I inhibitor, meaning that once it has done its job, and deactivated the aromatase enzyme, we don’t need it anymore. Letrozole and Arimidex actually need to remain present to continue their effects. This is possibly why Nolvadex does not alter the pharmacokinetics of Aromasin (11).

    Conclusion

    Before we close the book on Aromasin, it’s worth noting that you can (and should) still use one of the non-steroidal AIs during your cycle to reduce estrogen, if necessary. When you are ready for PCT, you can then switch over to Aromasin and still experience the full effects of an AI, since there is no cross-over tolerance experienced between steroidal and non-steroidal AIs (9). Since Aromasin is about 65% efficient at suppressing estrogen (10), it’s certainly a very powerful agent, especially considering you won’t experience reduced effectiveness because of your concurrent use of Nolvadex or from any sort of tolerance developed by using other AIs on your cycle(9). There is also a decent amount of preclinical data suggesting that Aromasin has a beneficial effect on bone mineral metabolism that is not seen with non-steroidal agents, and it may also have beneficial effects on lipid metabolism that are not found in the non-steroidal Letro and A-dex (9).

    Finally, as we’re going to be using Nolvadex for PCT anyway, and we ought to be using an AI with it for maximum recovery…I think Aromasin- considering it’s compatibility with Nolvadex and beneficial effects on bone mineral content and lipid profile, has finally stopped being the black sheep of AIs and found a home in our cycles.

    References:

    1. Clin Cancer Res. 2005 Apr 15;11(8):2809-21.
    2. J Clin Endocrinol Metab. 1995 Sep;80(9):2658-60.
    3. [Clinical aspects of estrogen and bone metabolism] Clin Calcium. 2002 Sep;12(9):1246-51. Japanese.
    4. Science, Vol 283, Issue 5406, 1277-1278 , 26 February 1999
    5. J Clin Endocrinol Metab 2000 Jul;85(7):2370-7, "Estrogen Suppression in Males"
    6. Fertil Steril. 1978 Mar;29(3):320-7
    7. J Clin Endocrinol Metab. 2004 Mar;89(3):1174-80
    8. .J Steroid Biochem Mol Biol. 2001 Dec;79(1-5):85-91.
    9. The Oncologist, Vol. 9, No. 2, 126–136, April 2004
    10. Zilembo N., Noberasco C., Bajetta E., Martinetti A., Mariani L., Orefici S. Endocrinological and clinical evaluation of exemestane, a new steroidal aromatase inhibitor. Br. J. Cancer, 72: 1007-1012, 1995
    11. Clinical Cancer Research Vol. 10, 1943-1948, March 2004
    12. The Journal of Clinical Endocrinology & Metabolism Vol. 88, No. 12 5951-5956
    Copyright © 2003 by The Endocrine Society


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  3. #3
    Chemistry Experiment heavyiron's Avatar
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    Aromasin is an AI that has been studied in men. This is significant because circulating estradiol is reduced in differing percentages between genders.


    Pharmacokinetics and Dose Finding of a Potent Aromatase Inhibitor, Aromasin (Exemestane), in Young Males

    Nelly Mauras, John Lima, Deval Patel, Annie Rini, Enrico di Salle, Ambrose Kwok and Barbara Lippe
    Nemours Children’s Clinic and Research Programs (N.M., J.L., A.R.), Jacksonville, Florida 32207; and University of Florida Health Sciences Center (D.P.) and Amersham Pharmacia Biotech (E.d.S., A.K., B.L.), Peapack, New Jersey 07977

    Address all correspondence and requests for reprints to: Nelly Mauras, M.D., Nemours Children’s Clinic, 807 Children’s Way, Jacksonville, Florida 32207. E-mail: [email protected].

    Abstract

    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.

    full study;
    http://jcem.endojournals.org/cgi/con...ull/88/12/5951


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  4. #4
    Chemistry Experiment heavyiron's Avatar
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    In just 7 days steady-state plasma levels are reached with Aromasin. Because Aromasin raises testosterone so much it may exhibit androgenic side effects.


    Pharmacology and pharmacokinetics of the newer generation aromatase inhibitors.

    Buzdar AU.
    Department of Breast Medical Oncology, The University of Texas M D Anderson Cancer Center, Houston, Texas 77030, USA. [email protected]

    The newer generation aromatase inhibitors (AIs) as a class show efficacy and tolerability benefits over previously established treatments in postmenopausal women with advanced breast cancer. At clinically administered doses, the plasma half-lives of anastrozole (1 mg once daily), letrozole (2.5 mg once daily), and exemestane (25 mg once daily) are 41-48 h, 2-4 days, and 27 h, respectively. Time to steady-state plasma levels is 7 days for both anastrozole and exemestane and 60 days for letrozole. Androgenic side effects have only been reported with exemestane. Anastrozole treatment has no impact on plasma lipid levels, whereas both letrozole and exemestane have an unfavorable effect. From indirect comparisons, anastrozole shows the highest degree of selectivity compared with letrozole and exemestane, in terms of a lack of effect on adrenosteroidogenesis. To date, there are no data suggesting any major differences in clinical efficacy between the newer generation AIs anastrozole and letrozole. Based on the observed pharmacological profiles, however, it cannot be assumed that the AIs will display the same tolerability and safety profiles when given for extended periods of time in the adjuvant setting. The effects of anastrozole, letrozole, and exemestane are being investigated in the adjuvant setting, and these data will elucidate the possible long-term consequences of the pharmacological effects reported after short-term exposure.

    PMID: 12538502 [PubMed - indexed for MEDLINE]


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  5. #5
    GYM RAT rw0885's Avatar
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    i used this stuff for the first time as pct for the cycle i just got done with and had the best post cycle experience ever...no lathargy, no drop in strength (actually still getting stronger), no drop in sex drive and my last inj was over a month ago. the only thing i can notice from being off is that i actually get sore again. haha.

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    Quote Originally Posted by rw0885 View Post
    i used this stuff for the first time as pct for the cycle i just got done with and had the best post cycle experience ever...no lathargy, no drop in strength (actually still getting stronger), no drop in sex drive and my last inj was over a month ago. the only thing i can notice from being off is that i actually get sore again. haha.
    can you share what doses you were running? thanks

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    GYM RAT rw0885's Avatar
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    my cycle went like this
    week 1-2: 500 mgs sust
    week 2-3: 600 mgs test e
    week 4-10: 400 mgs test c / 300 mgs test p.

    i added in exemestane on week 3 and ran it till 3 weeks after my last injection at 12.5 mgs/day. i know everyone who sees this is gunna ask why i kept switching the compounds around like i did, i had about 5 ml's sust, about 5 ml's test e, and a few 10 ml bottles of test c and p and i was just trying to use it all up. so this is the cycle that i came up with.

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    Lol no worries on that do what you gotta do thanks for the dosing info im gonna get some asap for this cycle im on seems much better then Adex. thanks bro

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    NOVICE hooker's Avatar
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    It's always nice to see people reading my old articles.

  10. #10
    Chemistry Experiment heavyiron's Avatar
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    Quote Originally Posted by hooker View Post
    It's always nice to see people reading my old articles.
    Thank you for your willingness to allow me to post your thoughts on these meds. Your contributions to chemical enhancement over the years has been very much appreciated.


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  11. #11
    Chemistry Experiment heavyiron's Avatar
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    Effects of Tamoxifen and Exemestane on Cognitive Functioning of Postmenopausal Patients With Breast Cancer: Results From the Neuropsychological Side Study of the Tamoxifen and Exemestane Adjuvant Multinational Trial

    Christina M. Schilder, Caroline Seynaeve, Louk V. Beex, Willem Boogerd, Sabine C. Linn, Chad M. Gundy, Hilde M. Huizenga, Johan W. Nortier, Cornelis J. van de Velde, Frits S. van Dam, and Sanne B. Schagen*
    From the Departments of Psychosocial Research and Epidemiology, Neuro-oncology, and Medical Oncology, Netherlands Cancer Institute; Department of Neurology, Slotervaart Medical Center; Department of Psychology, University of Amsterdam, Amsterdam; Department of Medical Oncology, Erasmus Medical Center-Daniel den Hoed Cancer Center, Rotterdam; Department of Medical Oncology, Radboud University Medical Center, Nijmegen; and the Departments of Medical Oncology and Surgical Oncology, Leiden University Medical Center, the Netherlands.

    * To whom correspondence should be addressed. E-mail: [email protected]

    Purpose: To evaluate the influence of adjuvant tamoxifen and exemestane on cognitive functioning in postmenopausal patients with breast cancer (BC).
    Patients and Methods: Neuropsychological assessments were performed before the start (T1) and after 1 year of adjuvant endocrine treatment (T2) in Dutch postmenopausal patients with BC, who did not receive chemotherapy. Patients participated in the international Tamoxifen and Exemestane Adjuvant Multinational trial, a prospective randomized study investigating tamoxifen versus exemestane as adjuvant therapy for hormone-sensitive BC.
    Results: Participants included 80 tamoxifen users (mean age, 68.7 years; range 51 to 84), 99 exemestane users (mean age, 68.3 years; range, 50 to 82), and 120 healthy controls (mean age, 66.2 years; range, 49 to 86). At T2, after adjustment for T1 performance, exemestane users did not perform statistically significantly worse than healthy controls on any cognitive domain. In contrast, tamoxifen users performed statistically significantly worse than healthy controls on verbal memory (P < .01; Cohen's d = .43) and executive functioning (P = .01; Cohen's d = .40), and statistically significantly worse than exemestane users on information processing speed (P = .02; Cohen's d = .36). With respect to visual memory, working memory, verbal fluency, reaction speed, and motor speed, no significant differences between the three groups were found.
    Conclusion: After 1 year of adjuvant therapy, tamoxifen use is associated with statistically significant lower functioning in verbal memory and executive functioning, whereas exemestane use is not associated with statistically significant lower cognitive functioning in postmenopausal patients with BC. Our results accentuate the need to include assessments of cognitive effects of adjuvant endocrine treatment in long-term safety studies.


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  12. #12
    GYM RAT babybull's Avatar
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    Would you recommend a higher dose than 12.5mg ed for someone very gyno prone and on 600mg test a week?

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    Chemistry Experiment heavyiron's Avatar
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    Quote Originally Posted by babybull View Post
    Would you recommend a higher dose than 12.5mg ed for someone very gyno prone and on 600mg test a week?
    Yes, you could go 25mg daily but only labs can tell if your dose is dialed in. Estradiol is ideal at 10-25pg/ml.


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    GYM RAT babybull's Avatar
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    Quote Originally Posted by heavyiron View Post
    Yes, you could go 25mg daily but only labs can tell if your dose is dialed in. Estradiol is ideal at 10-25pg/ml.

    Ok bro!

    Ill keep it at 12.5, and if I need to bump it I can. Im good at a letro dose of 1.25 eod so I think Ill be ok.

    The letro works great but it kills my lipid panel along with the gyno.

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    Heavy, anythoughts on dosage if one was going to use this as a stand alone HCT type intervention. PA has an interesting article in MD last month suggesting good results just using this alone as a first phase intervention. Just wondering???

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  • bbcode_img_match
  • bbcode_parse_complete
  • postbit_display_complete
  • memberaction_dropdown
  • pagenav_page
  • pagenav_complete
  • tag_fetchbit_complete
  • forumrules
  • showthread_bookmarkbit
  • navbits
  • navbits_complete
  • build_navigation_data
  • build_navigation_array
  • check_navigation_permission
  • process_navigation_links_start
  • process_navigation_links_complete
  • set_navigation_menu_element
  • build_navigation_menudata
  • build_navigation_listdata
  • build_navigation_list
  • set_navigation_tab_main
  • set_navigation_tab_fallback
  • navigation_tab_complete
  • fb_publish_checkbox
  • fb_like_button
  • showthread_complete
  • page_templates