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    Thread: Cabergoline (CABER)

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      Cabergoline (CABER)

      Cabergoline (aka Dostinex)
      (1-[(6-allelylergolin-8 beta-yl)carbonyl]-1-[3-(dimethylamino)propyl]-3-ethyl-urea)

      Cabergoline (pronounced ca-ber-goe-leen) is a long acting dopamine agonist which acts mainly on the D2 receptors. It is used to treat different types of medical problems that may occur when the body produces an excess of the hormone prolactin. It can also be used to treat menstrual problems in women, fertility problems in both men and women, and it also helps treat pituitary prolactinomas (pituitary gland tumors). Cabergoline is also reported to have some efficacy in patients with Nelson's syndrome and Cushing's disease, but data are available only for limited case reports.

      Cabergoline works by signaling the brain to stop the pituitary gland from producing and releasing the prolactin hormone. It is usually used for periods of up to six months after prolactin levels return to normal. You can of course start using it again if high prolactin symptoms reappear later. Prolactin is a single chain protein hormone, similar to growth hormone, that stimulates the secretion of milk by women. Prolactin also effects male libido by preventing erections.

      Below is a study done by the University of Naples in Italy, it compares treatment with cabergoline to bromocriptine.
      This study evaluated the effects of chronic treatment with cabergoline (CAB), a new, potent and long-lasting ergoline-derived dopamine agonist, on seminal fluid parameters and sexual and gonadal function in hyperprolactinemic males in comparison with the effect of bromocriptine (BRC) treatment. Seventeen males with macroprolactinoma were treated with CAB at a dose of 0.5-1.5 mg/week (n = 7), or BRC at a dose of 5-15 mg/day (n = 10) for 6 months. Baseline prolactin (PRL) was 925.7 +/- 522.6 microg/l in the CAB-treated group and 1059.4 +/- 297.6 microg/l in the BRC-treated group. All the patients suffered from libido impairment, ten from reduced sexual potency, and six had infertility. In five patients provocative bilateral galactorrhea was found. Seminal fluid analysis, functional seminal tests and penis rigidity and tumescence, measured by nocturnal penile tumescence (NPT) using Rigiscan equipment, were assessed before and after 1, 3 and 6 months of CAB or BRC treatment. Hormone profiles were assessed before and after 15, 30, 60, 90 and 180 days of both treatments. Before treatment, all patients had a low sperm count with oligoasthenospermia, reduced motility and rapid progression with an abnormal morphology and decreased viability, and a low number of erections. After 1 month, serum PRL levels were significantly reduced in both groups of patients (20.6 +/- 6.6 microg/l during CAB and 256.3 +/- 115.1 microg/l during BRC treatment) and were normalized after 6 months in all patients (CAB: 7.9 +/- 2.2 microg/l; BRC: 16.7 +/- 1.8 microg/l). After 6 months, a significant increase of number, total motility, rapid progression and normal morphology was recorded in patients treated with both CAB and BRC. An increase in the number of erections during the first 3 months of both treatments was noted by NPT. However, the improvements in seminal fluid parameters and sexual function were more evident and rapid in patients treated with CAB. The number of erections was normalized after 6 months of treatment in all patients submitted to CAB treatment, and in all patients but one treated by BRC. In addition, a significant increase of serum testosterone (from 3.7 +/- 0.3 to 5.3 +/- 0.2 microg/l) and dihydrotestosterone (from 0.4 +/- 0.1 to 1.1 +/- 0.1 nmol/l) was recorded. At the beginning of treatment, mild side-effects were recorded in two patients after CAB and mild-to-moderate side-effects in five patients after BRC administration. The treatment with CAB normalized PRL levels, improving gonadal and sexual function and fertility in males with prolactinoma, earlier than did BRC treatment, providing good tolerability and excellent patient compliance to medical treatment. Cabergoline is normally used were treatment with bromocriptine has failed.

      The dose of cabergoline will vary do to the use it is needed for. The following information includes only the average doses of cabergoline in oral dose form. For high prolactin levels or pituitary tumors use 0.25mg/2xwk. This dose can be increased every four weeks if needed because of high sustaining prolactin levels. Usually no more than 1mg/2xwk is needed. The reason for the four week waiting period before adjusting the dose is due to the long half life of the drug. Unlike bromo which should be dosed twice a day, cabergoline is usually dosed once or twice a week.

      Men may get another added bonus when using cabergoline, as it has been found to substantially raise the chances of multiple orgasms in males during sex. Some men on the drug reported to have numerous multiple orgasms in rapid succession. In one study done by M. Schedlowski involved 60 male subjects between the ages of 20 to 30. It was found that they normally needed a break of approximately 20 minutes between sessions of sex. After receiving treatment with cabergoline they were able to have several orgasms within a span of a few minutes. Schedlowski said the drug raised the libido to enable the male to orgasm again more quickly. This is do to the fact that it reduces prolactin levels which is produced by men at the point of orgasm.

      Some of the most common side effects you may encounter when using this drug are abdominal pain, or vertigo (the feeling that you are weightless or objects are moving around you). Other side effects like constipation, headaches, nausea and weakness may occur, but will most likely stop after your body gets use to the drug. Some of the less common side effects are a change in vision, dizziness, feeling faint when standing up after sitting or lying down, loss of appetite, loss or gain in weight, your hands, feet, or legs may swell up, and rapid heartbeat. Other less common sides include burning, itching or a stinging feeling of the skin, diarrhea, cotton mouth, muscle and joint pain, sore throat, trouble sleeping and a runny nose. Most dopamine drugs are well tolerated by most so the above mentioned side effects are rare. To help prevent some sides, take your dose with food.

      Some symptoms of a possible overdose include fainting, hallucinations, lightheadedness, abnormally fast heart rate, and stuffy nose.

      An interaction may occur if you use cabergoline with any anti-psychotic medicine or metoclopramide (used to treat stomach problems). Cabergoline should not be used if you suffer from the ailments such as untreated high blood pressure, cabergoline usually decreases blood pressure but at times it may increase it maken your condidtion worse. Also if you suffer from mild to severe liver disease, cabergoline may make you condition worse. In this case a lower dose may be all that is required.

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      Dostinex
      DESCRIPTION

      DOSTINEX Tablets contain cabergoline, a dopamine receptor agonist. The chemical
      name for cabergoline is 1-[(6-allylergolin-8?-yl)-carbonyl]-1-[3-(dimethylamino)propyl]3-
      ethylurea. Its empirical formula is C26H37N5O2, and its molecular weight is 451.62. The
      structural formula is as follows:


      Cabergoline is a white powder soluble in ethyl alcohol, chloroform, and N, Ndimethylformamide
      (DMF); slightly soluble in 0.1N hydrochloric acid; very slightly
      soluble in n-hexane; and insoluble in water.

      DOSTINEX Tablets, for oral administration, contain 0.5 mg of cabergoline. Inactive
      ingredients consist of leucine, USP, and lactose, NF.

      CLINICAL PHARMACOLOGY
      Mechanism of Action: The secretion of prolactin by the anterior pituitary is mainly
      under hypothalamic inhibitory control, likely exerted through release of dopamine by
      tuberoinfundibular neurons. Cabergoline is a long-acting dopamine receptor agonist with
      a high affinity for D2 receptors. Results of in vitro studies demonstrate that cabergoline
      exerts a direct inhibitory effect on the secretion of prolactin by rat pituitary lactotrophs.
      Cabergoline decreased serum prolactin levels in reserpinized rats. Receptor-binding
      studies indicate that cabergoline has low affinity for dopamine D1, a1-and a2-adrenergic,
      and 5-HT1- and 5-HT2-serotonin receptors.

      Clinical Studies: The prolactin-lowering efficacy of DOSTINEX was demonstrated in
      hyperprolactinemic women in two randomized, double-blind, comparative studies, one
      with placebo and the other with bromocriptine. In the placebo-controlled study (placebo


      n=20; cabergoline n=168), DOSTINEX produced a dose-related decrease in serum
      prolactin levels with prolactin normalized after 4 weeks of treatment in 29%, 76%, 74%
      and 95% of the patients receiving 0.125, 0.5, 0.75, and 1.0 mg twice weekly respectively.

      In the 8-week, double-blind period of the comparative trial with bromocriptine
      (cabergoline n=223; bromocriptine n=236 in the intent-to-treat analysis), prolactin was
      normalized in 77% of the patients treated with DOSTINEX at 0.5 mg twice weekly
      compared with 59% of those treated with bromocriptine at 2.5 mg twice daily.
      Restoration of menses occurred in 77% of the women treated with DOSTINEX,
      compared with 70% of those treated with bromocriptine. Among patients with
      galactorrhea, this symptom disappeared in 73% of those treated with DOSTINEX
      compared with 56% of those treated with bromocriptine.

      Pharmacokinetics

      Absorption: Following single oral doses of 0.5 mg to 1.5 mg given to 12 healthy adult
      volunteers, mean peak plasma levels of 30 to 70 picograms (pg)/mL of cabergoline were
      observed within 2 to 3 hours. Over the 0.5-to-7 mg dose range, cabergoline plasma levels
      appeared to be dose-proportional in 12 healthy adult volunteers and nine adult
      parkinsonian patients. A repeat-dose study in 12 healthy volunteers suggests that steady-
      state levels following a once-weekly dosing schedule are expected to be twofold to
      threefold higher than after a single dose. The absolute bioavailability of cabergoline is
      unknown. A significant fraction of the administered dose undergoes a first-pass effect.
      The elimination half-life of cabergoline estimated from urinary data of 12 healthy
      subjects ranged between 63 to 69 hours. The prolonged prolactin-lowering effect of
      cabergoline may be related to its slow elimination and long half-life.

      Distribution: In animals, based on total radioactivity, cabergoline (and/or its metabolites)
      has shown extensive tissue distribution. Radioactivity in the pituitary exceeded that in
      plasma by >100-fold and was eliminated with a half-life of approximately 60 hours. This
      finding is consistent with the long-lasting prolactin-lowering effect of the drug. Whole
      body autoradiography studies in pregnant rats showed no fetal uptake but high levels in
      the uterine wall. Significant radioactivity (parent plus metabolites) detected in the milk of
      lactating rats suggests a potential for exposure to nursing infants. The drug is extensively
      distributed throughout the body. Cabergoline is moderately bound (40% to 42%) to
      human plasma proteins in a concentration-independent manner. Concomitant dosing of
      highly protein-bound drugs is unlikely to affect its disposition.

      Metabolism: In both animals and humans, cabergoline is extensively metabolized,
      predominately via hydrolysis of the acylurea bond or the urea moiety. Cytochrome P-450
      mediated metabolism appears to be minimal. Cabergoline does not cause enzyme
      induction and/or inhibition in the rat. Hydrolysis of the acylurea or urea moiety abolishes
      the prolactin-lowering effect of cabergoline, and major metabolites identified thus far do
      not contribute to the therapeutic effect.

      Excretion: After oral dosing of radioactive cabergoline to five healthy volunteers,
      approximately 22% and 60% of the dose was excreted within 20 days in the urine and


      f
      Food-Drug Interaction

      In 12 healthy adult volunteers, food did not alter cabergoline kinetics.

      Pharmacodynamics

      Dose response with inhibition of plasma prolactin, onset of maximal effect, and duration
      of effect has been documented following single cabergoline doses to healthy volunteers

      (0.05 to 1.5 mg) and hyperprolactinemic patients (0.3 to 1 mg). In volunteers, prolactin
      inhibition was evident at doses >0.2 mg, while doses =0.5 mg caused maximal
      suppression in most subjects. Higher doses produce prolactin suppression in a greater
      proportion of subjects and with an earlier onset and longer duration of action. In 12
      healthy volunteers, 0.5, 1, and 1.5 mg doses resulted in complete prolactin inhibition,
      with a maximum effect within 3 hours in 92% to 100% of subjects after the 1 and 1.5 mg
      doses compared with 50% of subjects after the 0.5 mg dose.
      In hyperprolactinemic patients (N=51), the maximal prolactin decrease after a 0.6 mg
      single dose of cabergoline was comparable to 2.5 mg bromocriptine; however, the
      duration of effect was markedly longer (14 days vs 24 hours). The time to maximal effect
      was shorter for bromocriptine than cabergoline (6 hours vs 48 hours).

      In 72 healthy volunteers, single or multiple doses (up to 2 mg) of cabergoline resulted in
      selective inhibition of prolactin with no apparent effect on other anterior pituitary
      hormones (GH, FSH, LH, ACTH, and TSH) or cortisol.

      INDICATIONS AND USAGE

      DOSTINEX Tablets are indicated for the treatment of hyperprolactinemic disorders,
      either idiopathic or due to pituitary adenomas.

      CONTRAINDICATIONS

      DOSTINEX Tablets are contraindicated in patients with uncontrolled hypertension or
      known hypersensitivity to ergot derivatives.


      WARNINGS

      Dopamine agonists in general should not be used in patients with pregnancy-induced
      hypertension, for example, preeclampsia and eclampsia, unless the potential benefit is
      judged to outweigh the possible risk.

      PRECAUTIONS
      General: Initial doses higher than 1.0 mg may produce orthostatic hypotension. Care
      should be exercised when administering DOSTINEX with other medications known to
      lower blood pressure.

      Postpartum Lactation Inhibition or Suppression: DOSTINEX is not indicated for the
      inhibition or suppression of physiologic lactation. Use of bromocriptine, another
      dopamine agonist for this purpose, has been associated with cases of hypertension,
      stroke, and seizures.

      Hepatic Impairment: Since cabergoline is extensively metabolized by the liver, caution
      should be used, and careful monitoring exercised, when administering DOSTINEX to
      patients with hepatic impairment.

      Information for Patients: A patient should be instructed to notify her physician if she
      suspects she is pregnant, becomes pregnant, or intends to become pregnant during
      therapy. A pregnancy test should be done if there is any suspicion of pregnancy and
      continuation of treatment should be discussed with her physician.

      Drug Interactions: DOSTINEX should not be administered concurrently with D2antagonists,
      such as phenothiazines, butyrophenones, thioxanthenes, or metoclopramide.

      Carcinogenesis, Mutagenesis, Impairment of Fertility: Carcinogenicity studies were
      conducted in mice and rats with cabergoline given by gavage at doses up to 0.98
      mg/kg/day and 0.32 mg/kg/day, respectively. These doses are 7 times and 4 times the
      maximum recommended human dose calculated on a body surface area basis using total
      mg/m2/week in rodents and mg/m2/week for a 50 kg human.

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      nice post pain.
      ALL THINGS SAID BY ME ARE FOR ENTERTAINMENT ONLY AND I DONT CONDONE STEROID USE. THAT-GOES FOR PM OR POSTS.


      BROTHERHOODOFPAIN.COM

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      You are a mind reader. I really am not well versed in this compound and I need to be. Big thanks, Great post.

      Peace and Love

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      One thing I've discovered is that dostinex doesn't inhibit progesterone conversion, so it is not really preventative. Arimidex seems to work much better in preventing the problems from arising to begin with.
      So I see ai use as much more important than the use of dost, caber, prami etc. Of course I would have it on hand when running tren, deca, NPP etc.
      Has that been anyone else's experience.

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      Quote Originally Posted by bufbiker View Post
      One thing I've discovered is that dostinex doesn't inhibit progesterone conversion, so it is not really preventative. Arimidex seems to work much better in preventing the problems from arising to begin with.
      So I see ai use as much more important than the use of dost, caber, prami etc. Of course I would have it on hand when running tren, deca, NPP etc.
      Has that been anyone else's experience.
      Not at all. AI are designed to inhibit estrogen not progesterone. That is exactly what dostinex, bromo, etc are designed for. You get gyno from Tren or Deca and an AI, like letro, a-sin, or a-dex will do nothing for you.
      It is good to have an end to journey toward; but it is the journey that matters, in the end.


      DISCLAIMER: "BrotherIron" is a fictitious character with the sole purpose to entertain. Any information/advice given out, stated, or implied by "BrotherIron" is for entertainment purposes only & should not be considered the advocation of any illegal activity.



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      Good read!!

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      Quote Originally Posted by BrotherIron View Post
      Not at all. AI are designed to inhibit estrogen not progesterone. That is exactly what dostinex, bromo, etc are designed for. You get gyno from Tren or Deca and an AI, like letro, a-sin, or a-dex will do nothing for you.

      If your estro is kept in check, proges is less likely to arise. Those drugs (caber, dost, prami) are more of anti depressants. I would have them on hand in case of someone being prone to it.

      Not mine, but a good read none the less.


      I would like to clear up a few misconceptions about progesterone and gynecomastia.

      Their is absolutely no steroid that aromatizes into progesterone. The reason for this is that progesteron does not have an aromatic A ring. So toss that myth out the window. Tren? Deca? Sorry but it just doesn't happen.

      Now Tren and Deca bind pretty well to the PR. They are progestins in their own right without undergoing any structural changes, but their affinity is MUCH weaker than progesterone itself. Even more so when nandrolone is reduced by 5-alpha reductase into DHN. Their is a small chance of progestogenic activity that could aid in manifesting a mass in the mammry IF estrogen is present in supraphysiological amounts, without proper ratio to testosterone but I have never see a documented case of progestogenic gynecomastia. The reason for this is that the PR has two isoforms. The PR-A and PR-B. PR-B mediates stimulatory effects of progestins; PR-A which is bound with progestins or anti-progestins inhibits PR-B, and PR-A is ***inant,. The response to progesterone is determined by the relative expression of the two isoforms.

      There is a direct relationship between the PR isoforms and steroid concentrations an this direct relationship suggests high progesterone concentrations, but this will induce the expression of PR-A, which represses transcription of PR-B, which in turn supresses PR function and progestin effect
      With initial administration of nandrolone or it's dirivitives, I could see an expression of PR-B but a rapid rise in PR-A will ultimately supress the function of the PR. IMO, you would need a high ratio of the two before concerns, and this is a bit more of a possiblity with the begining of administration. In this time of vulnerability, rest assured in aromatase inhibitors as progesterone is an E2 agonist so the utilization of an AI will help. I personally don't think the concern is warranted though

      Their are 4 combinations of hormones that cause gyno- Estrogen, Progesterone, Prolactin, and IGF. Nandrolone is a weak progestin, which agonizes the PRL, it also raises IGF. Progesterone induced gyno is not really of a concern given binding affinity to the PR and the mechanism of the two isoforms. The production of prolactin is a deffinate risk. Not only can it be an inductor for gyno along side estrogen, IGF, and pogesterone; this chance is increased as prolactn lowers testosterone. So you need to make sure to take proper precautions to not only keep estrogen in check, but prolactin as well.

      Also, basically from what I've read on the matter, prolactin or progesterone will not cause gyno unless there is excess estrogen that has been aromatized in the body and already beginning the stages of gyno. It just adds on to the problem and brings with it lactation. Having said that, if you are on nonaromatizing compounds along with tren, you should not get gyno. If you are on winny (and anti-progestagenic) you will not get gyno. If you are on aromatizing compounds and you supplement with anti-e's and AI, you should not get gyno because your estrogen level will be in check therefore not causing excess estrogen for the progesterone to team up with. Its all starting to make a little more sense to me now. If any of you have any conflicting or additional information to this topic, please post it. I am in the process of adding the Tren E back in my cycle as soon as I feel comfortable that I have my gyno in check.

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      Quote Originally Posted by Shovel View Post
      If your estro is kept in check, proges is less likely to arise. Those drugs (caber, dost, prami) are more of anti depressants. I would have them on hand in case of someone being prone to it.

      Not mine, but a good read none the less.


      I would like to clear up a few misconceptions about progesterone and gynecomastia.

      Their is absolutely no steroid that aromatizes into progesterone. The reason for this is that progesteron does not have an aromatic A ring. So toss that myth out the window. Tren? Deca? Sorry but it just doesn't happen.

      Now Tren and Deca bind pretty well to the PR. They are progestins in their own right without undergoing any structural changes, but their affinity is MUCH weaker than progesterone itself. Even more so when nandrolone is reduced by 5-alpha reductase into DHN. Their is a small chance of progestogenic activity that could aid in manifesting a mass in the mammry IF estrogen is present in supraphysiological amounts, without proper ratio to testosterone but I have never see a documented case of progestogenic gynecomastia. The reason for this is that the PR has two isoforms. The PR-A and PR-B. PR-B mediates stimulatory effects of progestins; PR-A which is bound with progestins or anti-progestins inhibits PR-B, and PR-A is ***inant,. The response to progesterone is determined by the relative expression of the two isoforms.

      There is a direct relationship between the PR isoforms and steroid concentrations an this direct relationship suggests high progesterone concentrations, but this will induce the expression of PR-A, which represses transcription of PR-B, which in turn supresses PR function and progestin effect
      With initial administration of nandrolone or it's dirivitives, I could see an expression of PR-B but a rapid rise in PR-A will ultimately supress the function of the PR. IMO, you would need a high ratio of the two before concerns, and this is a bit more of a possiblity with the begining of administration. In this time of vulnerability, rest assured in aromatase inhibitors as progesterone is an E2 agonist so the utilization of an AI will help. I personally don't think the concern is warranted though

      Their are 4 combinations of hormones that cause gyno- Estrogen, Progesterone, Prolactin, and IGF. Nandrolone is a weak progestin, which agonizes the PRL, it also raises IGF. Progesterone induced gyno is not really of a concern given binding affinity to the PR and the mechanism of the two isoforms. The production of prolactin is a deffinate risk. Not only can it be an inductor for gyno along side estrogen, IGF, and pogesterone; this chance is increased as prolactn lowers testosterone. So you need to make sure to take proper precautions to not only keep estrogen in check, but prolactin as well.

      Also, basically from what I've read on the matter, prolactin or progesterone will not cause gyno unless there is excess estrogen that has been aromatized in the body and already beginning the stages of gyno. It just adds on to the problem and brings with it lactation. Having said that, if you are on nonaromatizing compounds along with tren, you should not get gyno. If you are on winny (and anti-progestagenic) you will not get gyno. If you are on aromatizing compounds and you supplement with anti-e's and AI, you should not get gyno because your estrogen level will be in check therefore not causing excess estrogen for the progesterone to team up with. Its all starting to make a little more sense to me now. If any of you have any conflicting or additional information to this topic, please post it. I am in the process of adding the Tren E back in my cycle as soon as I feel comfortable that I have my gyno in check.
      That's very interesting but my personal exp has me believing otherwise. I had issues even with a strong AI like letro from the pharm. The problem was resoved when I added caber into the mix @ .5mg Every 3rd. I would also say you should run T3 if you run Tren b/c Tren affects your thyroid (TSH) levels.
      It is good to have an end to journey toward; but it is the journey that matters, in the end.


      DISCLAIMER: "BrotherIron" is a fictitious character with the sole purpose to entertain. Any information/advice given out, stated, or implied by "BrotherIron" is for entertainment purposes only & should not be considered the advocation of any illegal activity.



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      Very interesting.

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