Aromasin, Armidex, Liquidex, Nolvadex, Gyno Issues

This shit seems to be great... check it out : http://www.pharmaciaoncology.com/products.asp?ptype=1
made by Upjohn pharmaceutical...3rd generation anti-estrogen. I've been taking it for TWO days and my lump has shrunk to almost NOTHING!! I'm very impressed! Nolva did NOTHING for me.. Don't know why, but i would think that Aromasin is actually better anyway because it gets rid of ALL estrogen whereas nolva just prevents attaching to receptors, but still leaves tons of estrogen floating around in your body which could cause other problems.

Anyone aware of anything that acts similar to nolva for DHT, in that it doesn't stop the CONVERSION to DHT or get rid of DHT, but ONLY blocks the attachment of DHT to hair follicles??? whenever i take things that prevent conversion to DHT it inhibits growth... what do you think of ALL of the above??

Tell me where I can get some of this. I have a little lump under the nip I would like to get rid of.

BUMP..................

that is good to hear about your gyno bro. check out nizoral or spironolactone for hairloss treatment. these are topical anti-androgens used to combat hairloss. these are the best choice when cycling since anti-dht only helps when using test. but there are some anti-dht topical solutions. but i'm not sure of the names of these products. do a search on a search engine for "topical anti-dht".

who knows anymore about this aromasin product?
like dose, half-life, benefits for bb's, etc............

keep this bumped, i will ask my pharmacist...

:rolleyes: yep :P

I want to know the benefits versus Arimadex.

Quote:

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I want to know the benefits versus Arimadex.

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its more effective as an anti-aromitic.... the drop in IGF-1 levels that is seen with aramidex is not with arom, in fact three studies show a rise in IGF-1 when arom or ferma are used...

bump
more info please
anyone know dose

bump for this shit, ... more info?..

"DESCRIPTION

Femara (letrozole tablets) for oral administration contain 2.5 mg of letrozole, a nonsteroidal aromatase inhibitor (inhibitor of estrogen synthesis). It is chemically described as 4,4'-(1H-1,2,4 -Triazol-1-ylmethylene) dibenzonitrile.

Letrozole is a white to yellowish crystalline powder, practically odorless, freely soluble in dichloromethane, slightly soluble in ethanol, and practically insoluble in water. It has a molecular weight of 285.31, empirical formula C17H11N5 and a melting range of 184o C-185o C.

Femara (letrozole tablets) is available as 2.5 mg tablets for oral administration.

Inactive Ingredients.

Colloidal silicon dioxide, ferric oxide, hydroxypropyl methylcellulose, lactose monohydrate, magnesium stearate, maize starch, microcrystalline cellulose, polyethylene glycol, sodium starch glycolate, talc, and titanium dioxide.


CLINICAL PHARMACOLOGY

Mechanism of Action

The growth of some cancers of the breast are stimulated or maintained by estrogens. Treatment of breast cancer thought to be hormonally responsive (i.e., estrogen and/or progesterone receptor positive or receptor unknown) has included a variety of efforts to decrease estrogen levels (ovariectomy, adrenalectomy, hypophysectomy) or inhibit estrogen effects (antiestrogens and progestational agents). These interventions lead to decreased tumor mass or delayed progression of tumor growth in some women.

In postmenopausal women, estrogens are mainly derived from the action of the aromatase enzyme, which converts adrenal androgens (primarily androstenedione and testosterone) to estrone and estradiol. The suppression of estrogen biosynthesis in peripheral tissues and in the cancer tissue itself can therefore be achieved by specifically inhibiting the aromatase enzyme.

Letrozole is a nonsteroidal competitive inhibitor of the aromatase enzyme system; it inhibits the conversion of androgens to estrogens. In adult nontumor- and tumorbearing female animals, letrozole is as effective as ovariectomy in reducing uterine weight, elevating serum LH, and causing the regression of estrogen-dependent tumors. In contrast to ovariectomy, treatment with letrozole does not lead to an increase in serum FSH. Letrozole selectively inhibits gonadal steroidogenesis but has no significant effect on adrenal mineralocorticoid or glucocorticoid synthesis.

Letrozole inhibits the aromatase enzyme by competitively binding to the heme of the cytochrome P450 subunit of the enzyme, resulting in a reduction of estrogen biosynthesis in all tissues. Treatment of women with letrozole significantly lowers serum estrone, estradiol and estrone sulfate and has not been shown to significantly affect adrenal corticosteroid synthesis, aldosterone synthesis, or synthesis of thyroid hormones.

Pharmacokinetics

Letrozole is rapidly and completely absorbed from the gastrointestinal tract and absorption is not affected by food. It is metabolized slowly to an inactive metabolite whose glucuronide conjugate is excreted renally, representing the major clearance pathway. About 90% of radiolabeled letrozole is recovered in urine. Letrozole’s terminal elimination half-life is about 2 days and steady-state plasma concentration after daily 2.5mg dosing is reached in 2-6 weeks. Plasma concentrations at steady-state are 1.5 to 2 times higher than predicted from the concentrations measured after a single dose, indicating a slight nonlinearity in the pharmacokinetics of letrozole upon daily administration of 2.5mg. These steady-state levels are maintained over extended periods, however, and continuous accumulation of letrozole does not occur. Letrozole is weakly protein bound and has a large volume of distribution (approximately 1.9 L/kg).

Metabolism and Excretion

Metabolism to a pharmacologically-inactive carbinol metabolite (4, 4'-methanol-bisbenzonitrile) and renal excretion of the glucuronide conjugate of this metabolite is the major pathway of letrozole clearance. Of the radiolabel recovered in urine, at least 75% was the glucuronide of the carbinol metabolite, about 9% was two unidentified metabolites, and 6% was unchanged letrozole.

In human microsomes with specific CYP isozyme activity, CYP 3A4 metabolized letrozole to the carbinol metabolite while CYP 2A6 formed both this metabolite and its ketone analog. In human liver microsomes, letrozole strongly inhibited CYP 2A6 and moderately inhibited CYP 2C19.

Special Populations

Pediatric, Geriatric and Race: In the study populations (adults ranging in age from 35 to >80 years), no change in pharmacokinetic parameters was observed with increasing age. Differences in letrozole pharmacokinetics between adult and pediatric populations have not been studied. Differences in letrozole pharmacokinetics due to race have not been studied.

Renal Insufficiency: In a study of volunteers with varying renal function (24-hour creatinine clearance: 9-116 mL/min), no effect of renal function on the pharmacokinetics of single doses of 2.5mg of Femara (letrozole tablets) was found. In addition, in a study of 347 patients with advanced breast cancer, about half of whom received 2.5mg Femara and half 0.5mg Femara, renal impairment (calculated creatinine clearance: 20-50 mL/min) did not affect steady-state plasma letrozole concentration.

Hepatic Insufficiency: In a study of subjects with varying degrees of non-metastatic hepatic dysfunction (e.g., cirrhosis, Child-Pugh classification A and B), the mean AUC values of the volunteers with moderate hepatic impairment were 37% higher than in normal subjects, but still within the range seen in subjects without impaired function. Patients with severe hepatic impairment (Child-Pugh classification C) have not been studied (see DOSAGE AND ADMINISTRATION, Hepatic Impairment).

Drug/Drug Interactions

A pharmacokinetic interaction study with cimetidine showed no clinically significant effect on letrozole pharmacokinetics. An interaction study with warfarin showed no clinically significant effect of letrozole on warfarin pharmacokinetics.

There is no clinical experience to date on the use of Femara in combination with other anti-cancer agents.

Pharmacodynamics

In postmenopausal patients with advanced breast cancer, daily doses of 0.1 mg to 5 mg Femara suppress plasma concentrations of estradiol, estrone, and estrone sulfate by 75%-95% from baseline with maximal suppression achieved within two-three days. Suppression is dose-related, with doses of 0.5 mg and higher giving many values of estrone and estrone sulfate that were below the limit of detection in the assays. Estrogen suppression was maintained throughout treatment in all patients treated at 0.5 mg or higher.

Letrozole is highly specific in inhibiting aromatase activity. There is no impairment of adrenal steroidogenesis. No clinically-relevant changes were found in the plasma concentrations of cortisol, aldosterone, 11-deoxycortisol, 17-hydroxy-progesterone, ACTH or in plasma renin activity among post-menopausal patients treated with a daily dose of Femara 0.1 mg to 5 mg. The ACTH stimulation test performed after 6 and 12 weeks of treatment with daily doses of 0.1, 0.25, 0.5, 1, 2.5, and 5 mg did not indicate any attenuation of aldosterone or cortisol production. Glucocorticoid or mineralocorticoid supplementation is, therefore, not necessary.

No changes were noted in plasma concentrations of androgens (androstenedione and testosterone) among healthy postmenopausal women after 0.1, 0.5, and 2.5 mg single doses of Femara or in plasma concentrations of androstenedione among postmenopausal patients treated with daily doses of 0. 1 mg to 5 mg. This indicates that the blockade of estrogen biosynthesis does not lead to accumulation of androgenic precursors. Plasma levels of LH and FSH were not affected by letrozole in patients, nor was thyroid function as evaluated by TSH levels, T3 uptake, and T4 levels.


__________________
Zyg the Zealot
[email protected]
[email protected]
----------------
http://anamarketing.net for anastrozole/letrozole


"

"DESCRIPTION

AROMASIN Tablets for oral administration contain 25 mg of exemestane, an irreversible, steroidal aromatase inactivator. Exemestane is chemically described as 6-methylenandrosta-1,4-diene-3, 17-dione. Its molecular formula is C20H24O2.

The active ingredient is a white to slightly yellow crystalline powder with a molecular weight of 296.41. Exemestane is freely soluble in N, N-dimethylformamide, soluble in methanol, and practically insoluble in water.

Each AROMASIN Tablet contains the following inactive ingredients: mannitol, crospovidone, polysorbate 80, hydroxypropyl methylcellulose, colloidal silicon dioxide, microcrystalline cellulose, sodium starch glycolate, magnesium stearate, simethicone, polyethylene glycol 6000, sucrose, magnesium carbonate, titanium dioxide, methylparaben, and polyvinyl alcohol.


CLINICAL PHARMACOLOGY

Mechanism of Action

Breast cancer cell growth may be estrogen-dependent. Aromatase (exemestane) is the principal enzyme that converts androgens to estrogens both in pre- and postmenopausal women. While the main source of estrogen (primarily estradiol) is the ovary in premenopausal women, the principal source of circulating estrogens in postmenopausal women is from conversion of adrenal and ovarian androgens (androstenedione and testosterone) to estrogens (estrone and estradiol) by the aromatase enzyme in peripheral tissues. Estrogen deprivation through aromatase inhibition is an effective and selective treatment for some postmenopausal patients with hormone-dependent breast cancer.

Exemestane is an irreversible, steroidal aromatase inactivator, structurally related to the natural substrate androstenedione. It 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.” Exemestane significantly lowers circulating estrogen concentrations in postmenopausal women, but has no detectable effect on adrenal biosynthesis of corticosteroids or aldosterone. Exemestane has no effect on other enzymes involved in the steroidogenic pathway up to a concentration at least 600 times higher than that inhibiting the aromatase enzyme.

Pharmacokinetics

Following oral administration to healthy postmenopausal women, exemestane is rapidly absorbed. After maximum plasma concentration is reached, levels decline polyexponentially with a mean terminal half-life of about 24 hours. Exemestane is extensively distributed and is cleared from the systemic circulation primarily by metabolism. The pharmacokinetics of exemestane are dose proportional after single (10 to 200 mg) or repeated oral doses (0.5 to 50 mg). Following repeated daily doses of exemestane 25 mg, plasma concentrations of unchanged drug are similar to levels measured after a single dose.

Pharmacokinetic parameters in postmenopausal women with advanced breast cancer following single or repeated doses have been compared with those in healthy, postmenopausal women. Exemestane appeared to be more rapidly absorbed in the women with breast cancer than in the healthy women, with a mean tmax of 1.2 hours in the women with breast cancer and 2.9 hours in the healthy women. After repeated dosing, the average oral clearance in women with advanced breast cancer was 45% lower than the oral clearance in healthy postmenopausal women, with corresponding higher systemic exposure. Mean AUC values following repeated doses in women with breast cancer (75.4 ng•h/mL) were about twice those in healthy women (41.4 ng•h/mL).

Absorption: Following oral administration of radiolabeled exemestane, at least 42% of radioactivity was absorbed from the gastrointestinal tract. Exemestane plasma levels increased by approximately 40% after a high-fat breakfast.

Distribution: Exemestane is distributed extensively into tissues. Exemestane is 90% bound to plasma proteins and the fraction bound is independent of the total concentration. Albumin and a1-acid glycoprotein both contribute to the binding. The distribution of exemestane and its metabolites into blood cells is negligible.

Metabolism and Excretion: Following administration of radiolabeled exemestane to healthy postmenopausal women, the cumulative amounts of radioactivity excreted in urine and feces were similar (42 ± 3% in urine and 42 ± 6% in feces over a 1-week collection period). The amount of drug excreted unchanged in urine was less than 1% of the dose.

Exemestane is extensively metabolized, with levels of the unchanged drug in plasma accounting for less than 10% of the total radioactivity. The initial steps in the metabolism of exemestane are oxidation of the methylene group in position 6 and reduction of the 17-keto group with subsequent formation of many secondary metabolites. Each metabolite accounts only for a limited amount of drug-related material. The metabolites are inactive or inhibit aromatase with decreased potency compared with the parent drug. One metabolite may have androgenic activity (see Pharmacodynamics: Other Endocrine Effects, below). Studies using human liver preparations indicate that cytochrome P450 3A4 (CYP 3A4) is the principal isoenzyme involved in the oxidation of exemestane.

Special Populations

Geriatric: Healthy postmenopausal women aged 43 to 68 years were studied in the pharmacokinetic trials. Age-related alterations in exemestane pharmacokinetics were not seen over this age range.

Gender: The pharmacokinetics of exemestane following administration of a single, 25-mg tablet to fasted healthy males (mean age 32 years) were similar to the pharmacokinetics of exemestane in fasted healthy postmenopausal women (mean age 55 years).

Race: The influence of race on exemestane pharmacokinetics has not been evaluated.

Hepatic Insufficiency: The pharmacokinetics of exemestane have been investigated in subjects with moderate or severe hepatic insufficiency (Childs-Pugh B or C). Following a single 25-mg oral dose, the AUC of exemestane was approximately 3 times higher than that observed in healthy volunteers. (See PRECAUTIONS.)

Renal Insufficiency: The AUC of exemestane after a single 25-mg dose was approximately 3 times higher in subjects with moderate or severe renal insufficiency (creatinine clearance <35 mL/min/1.73 m2 ) compared with the AUC in healthy volunteers (see PRECAUTIONS).

Pediatric: The pharmacokinetics of exemestane have not been studied in pediatric patients.

Drug-Drug Interactions

Exemestane is metabolized by cytochrome P450 3A4 (CYP 3A4) and aldoketoreductases. It does not inhibit any of the major CYP isoenzymes, including CYP 1A2, 2C9, 2D6, 2E1, and 3A4. In a clinical pharmacokinetic study, ketoconazole showed no significant influence on the pharmacokinetics of exemestane. Although no other formal drug-drug interaction studies have been conducted, significant effects on exemestane clearance by CYP isoenzymes inhibitors appear unlikely. However, a possible decrease of exemestane plasma levels by known inducers of CYP 3A4 cannot be excluded.

Pharmacodynamics

Effect on Estrogens: Multiple doses of exemestane ranging from 0.5 to 600 mg/day were administered to postmenopausal women with advanced breast cancer. Plasma estrogen (estradiol, estrone, and estrone sulfate) suppression was seen starting at a 5-mg daily dose of exemestane, with a maximum suppression of at least 85% to 95% achieved at a 25-mg dose. Exemestane 25 mg daily reduced whole body aromatization (as measured by injecting radiolabeled androstenedione) by 98% in postmenopausal women with breast cancer. After a single dose of exemestane 25 mg, the maximal suppression of circulating estrogens occurred 2 to 3 days after dosing and persisted for 4 to 5 days.

Effect on Corticosteroids: In multiple-dose trials of doses up to 200 mg daily, exemestane selectivity was assessed by examining its effect on adrenal steroids. Exemestane did not affect cortisol or aldosterone secretion at baseline or in response to ACTH at any dose. Thus, no glucocorticoid or mineralocorticoid replacement therapy is necessary with exemestane treatment.

Other Endocrine Effects: Exemestane does not bind significantly to steroidal receptors, except for a slight affinity for the androgen receptor (0.28% relative to dihydrotestosterone). The binding affinity of its 17-dihydrometabolite for the androgen receptor, however, is 100-times that of the parent compound. Daily doses of exemestane up to 25 mg had no significant effect on circulating levels of testosterone, androstenedione, dehydroepiandrosterone sulfate, or 17-hydroxy-progesterone. Increases in testosterone and androstenedione levels have been observed at daily doses of 200 mg or more. A dose- dependent decrease in sex hormone binding globulin (SHBG) has been observed with daily exemestane doses of 2.5 mg or higher. Slight, nondose-dependent increases in serum lutenizing hormone (LH) and follicle-stimulating hormone (FSH) levels have been observed even at low doses as a consequence of feedback at the pituitary level.


__________________
Zyg the Zealot
[email protected]
[email protected]
----------------
http://anamarketing.net for anastrozole/letrozole

"

thanks doofy..!

Damn... This shit looks good.

Definitely some good info. I would like to see some posts from people who have used femera and aromasin. It seems this might be a better choice instead of armidex; however I am yet to see too many people using it in their cycles so I am weary of trying it if there are not too many people who have done it before me.

No one has really used femara or aromasin? It seems to me like Aromasin might be a better choice but I am yet to see a single person who has used it. Any opinions? Experiences?

how does liquidex "stack" up?
Ripper

Don't forget guys, you body does need some estrogen, to help with joint lubrication and some AS will not work properly if some of them aren't converted to estrogen. So remember, that to much estrogen is the key here, not getting rid of it totally. Good read on this new drug however. I may have to start looking for it.

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Originally posted by Sicilian30
Don't forget guys, you body does need some estrogen, to help with joint lubrication and some AS will not work properly if some of them aren't converted to estrogen. So remember, that to much estrogen is the key here, not getting rid of it totally. Good read on this new drug however. I may have to start looking for it.

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I agree 100%. Too little estrogen will negatively impact your cholesterol ratios (HDL/LDL) as well as bone density.

This stuff is the rage in Pro BB ist was in the November MUSCLEMAG. In the uncensored colum.

I am prety sure that this stuff is to strong for what you want it for and just like arimidex is out of most poeple price range this and all newer drugs they are high dollar

though like stated above it you get gyno this will treat it very well.

It's not that expensive guys shop around! I'm seeing aromasin around for 3.50 per 25mg, which isn't that bad. Plus it's worth it imo if it will keep me healthy. Again would like to hear from those who have used aromasin or femara!!

I only had to use 15 tablets over a 45 day period and my gyno disappeard completely!!!! Nobules shrunk almost completely... Had used Nolvadex at high doses for two months before resorting to AROMASIN because the NOLVA did NOTHING FOR ME?????

I highly suggest grabbing some aromasin for those emergencies!!

Quote:

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Originally posted by Magnum357
I only had to use 15 tablets over a 45 day period and my gyno disappeard completely!!!! Nobules shrunk almost completely... Had used Nolvadex at high doses for two months before resorting to AROMASIN because the NOLVA did NOTHING FOR ME?????

I highly suggest grabbing some aromasin for those emergencies!!

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So Aromasin would take the place of using Nolvadex in case of emergency?? Is that right?????

-So you would still use Arimidex or Liquidex during the cycle, and just keep Aromasin on hand???

Even though aromasin SEEMS expensive, it is ACTUALLY INEXPENSIVE due to the long acting duration of the drug and it's effectiveness. Just ONE tab EOD works WONDERS like no other anti-E.

I believe the low estrogen levels also result in FAT LOSS. Even that hard to lose fat around your lower abdomen and love handles.

good luck bros. :lift:




ps...this is to ORIGINAL JASON... please PM me. I have read all your hairloss posts and i believe our experiences have been identical!!!

YOU GOT ME WANTING SOME NOW. I'M TALKING AMIDEX RIGHT NOW. DO US ALL A FAV AND POST WHERE WE CAN GET SOME.

Quote:

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Originally posted by Magnum357
I only had to use 15 tablets over a 45 day period and my gyno disappeard completely!!!! Nobules shrunk almost completely... Had used Nolvadex at high doses for two months before resorting to AROMASIN because the NOLVA did NOTHING FOR ME?????

I highly suggest grabbing some aromasin for those emergencies!!

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I am curious bro, how long did you have the gyno for? I've had a bit of gyno for about a year and a half due to a PH cycle (stupid stupid stupid :bw:) and I'm curious if this might help. How did you split up the dosages? It's really not even that expensive if you shop around. I've seen it fairly cheap. (Please no PM's or asking where).

Silly Question.... good way to get scammed.

Look around, think and do your research and you will find some.

could u get away with running a cycle with just femera and no nolva, just curious? suppose you had enough femera if symptoms occured, but u ran it from day 1 through to the end of post cycle therapy?

ive had alittle bit of gyno for a while now.....and if it works wonders like im reading about....feed me some :) ....id love to get rid of these lumps under my nips....good post!!....now i just need to find some