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Eulexin (Flutamide)

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Eulexin is a medication which belongs to a class of drugs known as antiandrogens. Eulexin is used along with drugs such as leuprolide. Eulexin blocks the effect of the male hormone testosterone. Taking Eulexin with leuprolide, which reduces the body's testosterone levels, you can treat prostate cancer.

Other names for this medication:
Andraxan, Asoflut, Curestat, Cytomid, Dedile, Drogenil, Elbat, Etaconil, Euflex, Eulexine, Farostat, Flimutal, Flucinom, Flulem, Flumid, Fluprosin, Fluprost, Fluta-cell, Fluta-gry, Flutabene, Flutahexal, Flutam, Flutamerck, Flutamid, Flutamida, Flutamidum, Flutamin, Flutan, Flutaplex, Flutasin, Flutastad, Flutepan, Flutrax, Fluxus, Ftda, Fugerel, Fuprostatel, Grisetin, Odyne, Oncosal, Palistop, Profamid, Prostacur, Prostadex, Prostadirex, Prostamid, Prostamide, Prostandril, Prostica, Tafenil, Tecnoflut, Tremexal

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Also known as:  Flutamide.


Eulexin is a medication belongs to a class of drugs known as antiandrogens.

Eulexin is used along with drugs such as leuprolide to treat prostate cancer.

Eulexin blocks the effect of the male hormone testosterone. Giving Eulexin with leuprolide, which reduces the body's testosterone levels, you can treat prostate cancer.

Generic name of Eulexin is Flutamid.

Brand name of Eulexin is Eulexin.


Take Eulexin orally.

Eulexin is best taken at evenly spaced intervals, and may be taken with or without food.

Eulexin daily dosage is 750 mg.

The recommended dosage of Eulexin: 2 capsules 3 times a day at 8-hour intervals.

This medicine is only for men.

If you want to achieve most effective results do not stop taking Eulexin suddenly.


If you overdose Eulexin and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of overdosage: loss of appetite, vomiting, slow breathing, decreased activity, trouble walking.


Store between 2 and 30 degrees C (36 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Eulexin are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Eulexin if you are allergic to Eulexin components.

Be careful with Eulexin if you have blood disorders, liver problems.

Be careful with Eulexin if you smoke.

Be careful with Eulexin if you take mibefradil, warfarin, sleep medicine, sedatives, tranquilizers, anti-anxiety drugs, narcotic pain relievers (e.g., codeine), psychiatric medicine, anti-seizure drugs, muscle relaxants, certain antihistamines (e.g., diphenhydramine).

Avoid alcohol.

Avoid driving machine.

Avoid exposuring to sunlight or artificial UV rays (sunlamps or tanning beds).

Avoid laboratory tests (e.g., liver function) are needed while taking Eulexin.

Do not stop taking Eulexin suddenly.

eulexin medication

Leflunomide, flutamide, nimodipine, mexiletine, sulindac, tranilast, 4-hydroxytamoxifen, and omeprazole are pharmaceuticals previously characterized as aryl hydrocarbon receptor (AHR) agonists in various cell lines and animal models. In this study, the eight AHR-active pharmaceuticals were investigated in highly aggressive aryl hydrocarbon (Ah)-responsive BT474 and MDA-MB-468 breast cancer cell lines, and their effects on AHR protein, CYP1A1 (protein and mRNA), CYP1B1 (mRNA), and cell migration were determined. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) was used as a positive control. The AHR agonist activities of the pharmaceuticals depended on structure, response, and cell context. Most compounds induced one or more AHR-mediated responses in BT474 cells, whereas in Ah-responsive MDA-MB-468 cells effects of the AHR-active pharmaceuticals were highly variable. 4-Hydroxytamoxifen, mexiletine, and tranilast did not induce CYP1A1 in MDA-MB-468 cells; moreover, in combination with TCDD, mexiletine was a potent AHR antagonist, tranilast was a partial antagonist, and 4-hydroxytamoxifen also exhibited some AHR antagonist activity. Omeprazole and, to a lesser extent, sulindac and leflunomide were full and partial AHR agonists, respectively, in both breast cancer cell lines. These data indicate that the AHR-active pharmaceuticals are selective AHR modulators, and applications of these drugs for targeting the AHR must be confirmed by studies using the most relevant cell context.

eulexin 125 mg

To evaluate the prognostic significance of pretreatment parameters and posttherapy declines in prostate-specific antigen (PSA) in relation to the survival of patients with hormone-refractory prostate cancer.

eulexin 500 mg

To investigate influence for the testicular development and to assess the usefulness as an animal model, cryptorchid rats were induced by exposure to flutamide during the fetal period and their testes examined histologically.

eulexin dosage

Effects of androgen and estrogen on proliferation of hypothalamic neurons were evaluated by a chicken hypothalamic neuron-glia coculture model. Hypothalamic cells were dispersed from 17-day-old embryos and challenged with testosterone (T) and 17beta-estradiol (E2) alone or combined with androgen receptor antagonist flutamide, estrogen receptor antagonist tamoxifen, or aromatase inhibitor letrozole for 48 h. The neuron number was counted and the proliferating cells were identified by immunocytochemistry of proliferating cell nuclear antigen (PCNA) and 5-bromo-2-deoxyuridine (BrdU) incorporation. Results showed that both E2 and T stimulated proliferation of hypothalamic neurons. E2 showed more intensive effect on females and this promoting effect was abrogated by tamoxifen. T played more intensive effect on males and the effect was inhibited by flutamide, tamoxifen, or letrozole. The above results indicated that E2 stimulated neuron proliferation through estrogenic actions with more sensitive effect on females and T promoted neuron proliferation through both androgenic and estrogenic actions with more intense effect on males. These observations suggested that steroid hormones influence the proliferation of hypothalamic neurons in a sexually dimorphic manner during the development of chicken embryos.

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• A biopsy Gleason score of 8-10 had an adjusted hazard ratio (AHR) of 1.56 (95% confidence interval [CI] 1.04, 2.34; P= 0.03) for a shorter time to testosterone normalization relative to Gleason 6. Specifically, the 51 men with biopsy Gleason score of 8-10 had a median time to testosterone normalization of 17.0 months compared with 22.1 months and 23.8 months for those with biopsy Gleason ≤ 6 and 7, respectively. • Increasing age was significantly associated with a longer duration of testosterone suppression (AHR of 0.95 [95% CI 0.92, 0.97; P < 0.001]) as was a higher baseline PSA (AHR 0.82 [95% CI 0.69, 0.97; P= 0.02]).

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It is well known that the sex difference in body growth at puberty is modulated by a complex interplay between sex steroids and somatotropic axis; however, the exact role played by sex steroids remains a matter of controversy. The aim of this study was to assess the mechanisms by which sex steroids regulate body growth during pubertal development. Flutamide, a non-steroid-blocking androgen receptor, was subcutaneously administered to 30-d-old male Wistar rats for 4 wk. The blockade of the androgen receptor led to a marked elevation in serum testosterone and an increment in serum estradiol. Flutamide administration decreased body weight gain, serum IGF-I levels, hepatic IGF-I mRNA, and GH receptor mRNA content. There were no significant changes in serum GH concentration, pituitary GH reserve, and pituitary GH mRNA content. Flutamide lowered hypothalamic somatostatin mRNA content and augmented hypothalamic immunoreactive somatostatin stores, but did not alter hypothalamic immunoreactive GH-releasing factor stores. Our findings indicate that during pubertal development of the male rat, the imbalance between androgen and estrogen actions determines an abnormal somatic growth, which is at least partly exerted through the peripheral or hepatic modification of the somatotropic axis that occurs under the high or exclusive action of estrogens. Potential implication of coincident sex-specific regulated mode of pulsatile GH secretion cannot be excluded from this random serum GH sample study.

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Endometrioid carcinoma of the prostate is an uncommon form of prostatic cancer. The authors present the case of a 77 year-old man and discuss the different particularities of this rare entity.

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This report describes the first observation of a direct mitogenic effect of androgens on isolated osteoblastic cells in serum-free culture. [3H]thymidine incorporation into DNA and cell counts were used as measures of cell proliferation. The percentage of cells that stained for alkaline phosphatase was used as a measure of differentiation. Dihydrotestosterone (DHT) enhanced mouse osteoblastic cell proliferation in a dose dependent manner over a wide range of doses (10(-8) to 10(-11) molar), and was maximally active at 10(-9) M. DHT also stimulated proliferation in human osteoblast cell cultures and in cultures of the human osteosarcoma cell line, TE89. Testosterone, fluoxymesterone (a synthetic androgenic steroid) and methenolone (an anabolic steroid) were also mitogenic in the mouse bone cell system. The mitogenic effect of DHT on bone cells was inhibited by antiandrogens (hydroxyflutamide and cyproterone acetate) which compete for binding to the androgen receptor. In addition to effects on cell proliferation, DHT increased the percentage of alkaline phosphatase (ALP) positive cells in all three bone cell systems tested, and this effect was inhibited by antiandrogens. We conclude that androgens can stimulate human and murine osteoblastic cell proliferation in vitro, and induce expression of the osteoblast-line differentiation marker ALP, presumably by an androgen receptor mediated mechanism.

eulexin 250 mg

Protein phosphorylation/dephosphorylation is an important posttranslational modification that plays a critical role in signal transduction. The androgen receptor (AR) is under such control. We demonstrate that androgen receptor phosphorylation determines whether or not AR ligands perform as agonists or antagonists in LNCaP cells. Androgen receptor ligands (such as dihydrotestosterone and beta-estradiol) stimulate receptor expression and phosphorylation and, as a result, they act as agonists or partial agonists. In contrast, agents such as bicalutamide and estramustine inhibit the receptor phosphorylation and act as antagonists. This model is supported by gene expression and transactivation assays. Significant increases in levels of both mRNA and protein of prostate-specific antigen (PSA), a natural AR target gene, occur following the treatment of LNCaP cells with DHT, beta-estradiol, or hydroxyflutamide. In contrast, exposure of LNCaP cells to bicalutamide or estramustine results in a sharp decrease of PSA expression. Agonistic or antagonistic effect of these compounds on PSA expression parallels the level of phosphorylated, but not dephosphorylated androgen receptors. These agonistic or antagonistic effects are also observed in HeLa cells transfected with wild-type AR expression plasmid (pAR0) and AR-driven luciferase expression plasmid GRE-tk-LUC in the presence of different groups of AR blockers. Our data indicate that the functional status of androgen receptors is strongly correlated with the phosphorylation status of the receptors, and that the phosphorylated androgen receptor is the form of the receptor transcriptionally active in regulation. Thus the androgen receptor phosphorylation/dephosphorylation may serve as a new molecular target for screening androgen antagonists for the treatment of prostate cancer.

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In 1941, Huggins and his colleagues discovered that testicular androgens exert a stimulatory effect on prostate cancer growth. Our group has made the key observations that the human adrenals, in addition to the tests, also secrete important amounts of androgens and cancer cells exhibit a marked heterogeneity of androgen sensitivity. In fact, human adrenals secrete large amounts of precursor steroids that are converted into active androgens in peripheral tissues (including the prostate), thus providing 40% to 50% of total androgens in adult men. The action of these androgens remaining after castration can be inhibited in prostatic cancer tissue by administering a pure antiandrogen that also decreases the local concentration of dihydrotestosterone (DHT). The castration levels of serum testosterone left in men after castration have an important stimulatory activity on the growth of androgen-sensitive normal as well as cancer tissues. Cancer cells have markedly different requirements for androgens. Some cell clones can grow in the presence of minimal amounts of androgens, requiring more complete androgen blockade and more potent antiandrogens for inhibiting growth. Among the compounds recommended as antiandrogens, the most unexpected finding is that many of them are devoid of any antiandrogenic activity. In fact, medroxyprogesterone acetate, chlormadinone acetate, and megestrol acetate have androgenic activity, but do not inhibit the peripheral action of DHT in prostatic tissue. These compounds should not be classified as antiandrogens. Cyproterone acetate, on the other hand, is a mixed agonist-antagonist. The only compounds showing pure antiandrogenic activity are Flutamide and its analogues. There is thus a need for a more complete blockade of androgens of both testicular and adrenal origins in order to exert a maximal inhibitory effect on cancer growth. We have therefore performed clinical studies in previously untreated stage D2 and C prostate cancer patients with the combination therapy using the LHRH agonist [D-Trp6, des Gly NH2(10)] LHRH ethylamide and the antiandrogen Flutamide. There was a significant increase in patients with a complete response, as compared with studies limited to the removal or blockade of testicular androgens. There was also a significant decrease in the number of non-responders, an increased duration of positive response, and a decrease in the death rate. This was achieved with minimal or no side effects, thus preserving a good quality of life.

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eulexin 500 mg 2015-12-25

Overall, 25 studies considering disease flare were included: 9 randomized clinical trials with an LHRH agonist and an LHRH agonist/antiandrogen arm, 14 observational studies evaluating LHRH agonists only, and 2 case reports. The incidence of disease flare was reported between 0% and 83% owing to a wide set of clinical, biochemical, and radiological factors evaluated. In some of the randomized clinical trials, a statistically significant reduction of the incidence of disease flare by concomitant use of antiandrogens was reported. Most of these historical Zetia Drug Information studies report on subjective worsening of disease symptoms as outcome measure. More objective outcome measures such as the prostate-specific antigen level did not seem to increase to higher than the baseline values.

eulexin dose 2017-08-22

Men exhibit a higher incidence of cardiovascular diseases than do women. The cardiovascular actions of sex steroids have been suggested as primary factors in mediating this sex difference. The mechanisms by which sex steroids, androgens and estrogens, mediate cardiovascular actions remain unclear. Excess aldosterone secretion has been associated with cardiovascular diseases. The hypothesis tested in this study was that at physiological concentrations, androgens stimulate and estradiol inhibits aldosterone secretion by human adrenal cells. In contrast to our hypothesis, physiological concentrations of sex steroids did not modify aldosterone secretion by H295R human adrenocortical cells. However, supraphysiological concentrations (300-1000 nM) of dihydrotestosterone (DHT) significantly stimulated basal and Angiotensin II-mediated aldosterone secretion. The stimulatory effect of DHT on aldosterone secretion was not blocked by the classical androgen receptor blocker flutamide. The stimulatory effect of DHT on aldosterone secretion was also independent of the intra-adrenal renin-angiotensin system since it was neither modified by treatment with the Angiotensin II receptor type 1 blocker losartan or the angiotensin converting enzyme inhibitor captopril. Inhibitors of the calmodulin/calmodulin-dependent protein kinase (CaMK) and protein kinase C intracellular signaling pathways abolished the DHT stimulatory effect on aldosterone secretion by H295R cells. In conclusion, physiological concentrations of sex steroids did not Noroxin Tablet modify aldosterone secretion by human adrenal cells. However, supraphysiological concentrations of DHT-stimulated aldosterone secretion by human adrenal cells by the calmodulin/CaMK and protein kinase C intracellular signaling pathways but independently of the classical androgen receptor. Supraphysiological doses of androgen may promote cardiovascular diseases via stimulation of aldosterone secretion.

eulexin tablets 2017-03-01

Increasing evidence suggests that AR (androgen receptor) acetylation is critical for prostate cancer cell growth. In the present study, we identified Pro-B3 (procyanidin B3) as a specific HAT (histone acetyltransferase) inhibitor. Pro-B3 selectively inhibited the activity of HATs, but not other epigenetic enzymes. Pro-B3 substantially inhibited the p300-mediated AR acetylation, both in vitro and in vivo. Pro-B3 inhibited both p300-dependent and agonist-induced AR transcription. We demonstrate that the p300-mediated AR acetylation is critical for the hormone responsiveness of AR. Interestingly, B3 treatment efficiently enhanced the antagonist activity of flutamide through suppression of p300 HAT activity, demonstrating that relative p300 activity is critical for the antagonist action. Finally, Pro-B3 treatment inhibited acetylation-dependent prostate cell proliferation and expression of cell-cycle control genes, subsequently increasing cell death, indicating the functional importance of AR acetylation for Cytoxan 600 Mg prostate cancer cell growth.

eulexin capsules 2017-03-12

To determine the prognostic factors in patients with prostate cancer treated with hormone therapy and Singulair Generic radical prostatectomy.

eulexin 50 mg 2015-10-19

Expression profiling of microRNAs was performed by microarrays using RNA extracted from male fetal lungs isolated on gestational day (GD) 17.0 and GD 18.0 after daily injection of pregnant mice from GD 10.0 with the antiandrogen flutamide or vehicle only. To identify putative miRNA target genes, the data obtained Paxil Dosage Reduction here were combined with gene profiling data reported previously using the same RNA preparations. qPCR was used to confirm microarray data with fetal lungs from other litters than those used in microarrays.

eulexin 125 mg 2016-12-10

We report the use of laparoscopic bilateral adrenalectomy as a treatment for a 21 year old female with classic simple virilizing CAH and infertility. She presented as an adolescent with increasing weight gain, amenorrhea and elevated adrenal androgens despite the use of dexamethasone (250 mcg given twice daily), and fludrocortisone (150 mcg daily). An anti-androgen (flutamide 250 mg given twice daily) and a combined oral contraceptive pill were added to her regimen and Asacol Generic Availability prevented progressive virilization, but she eventually desired fertility. A bilateral laparoscopic adrenalectomy was performed at age 21. The right adrenal gland weighed 41.8 grams and the left gland 45.5 grams. There were no complications during the surgery. Since the surgery, she has had a total of three pregnancies, resulting in 3 healthy full-term infants. Follow-up 7 years later at age 27 revealed overall excellent health with a BMI of 25.1 kg/m(2), no evidence of adrenal rest tissue based on hormonal testing, above average quality-of-life based on 36-item short-form health survey and she has not experienced an adrenal crisis.

eulexin dosage 2017-12-22

The PSA Ziac Medication Bisoprolol normalized by week 12 in 71% of the patients receiving 500-mg dose and 75% of those receiving the standard dose. The percent change in PSA was 89% and 96%, respectively. The treatment groups were not significantly different with respect to the incidence of adverse events: 71% v 68% in the 500-mg and 250-mg arms, respectively (P = 0.337).

eulexin cost 2016-11-16

To investigate the effects of testosterone exposure on androgen receptor (AR) protein expression in vascular smooth muscle Geodon A Drug cells (VSMC) and the possible mechanisms mediating the effects.

eulexin drug 2015-10-03

This study is part of our first look at a novel class of nonsteroidal AR antagonists as positron emission tomography (PET) imaging agents, which are alternatives to steroidal Diovan Recommended Dosage AR agonist-based imaging agents. Although (76)Br- has a significant affinity for ARs, it showed limited promise as a PET imaging agent because of its poor target-tissue distribution properties.

eulexin medication 2017-03-29

A total of 72 Sprague-Dawley rats were divided into 9 different groups as follows: group 1: control (n = 10), group 2: metoprolol (Beloc) 100 mg/kg/d (n = 7), group 3: carvedilol (Dilatrend) 50 mg/kg/d (n = 7), group 4: nebivolol (Vasoxen) 10 mg/kg/d (n = 6), group 5: estrogen receptor (ER) antagonist ICI 182.780 (Fluvestrant) 50 microg/g (n = 10), group 6: nebivolol+ Flomax 400 Mg ER antagonist (n = 8), group 7: androgen receptor (AR) antagonist (flutamide) 20 mg/kg (n = 7), group 8: nebivolol+AR antagonist (n = 7), and group 9: DMSO (solvent for ER antagonist) (n = 10). All beta-blockers were applied with gastric gavage after dilution with 5 mL of serum physiological; ER and AR were both applied intraperitoneally (i.p.) for 14 days. In the isolated rat cavernous tissues, endothelial nitric oxide synthase (eNOS) and ER and AR immunoreactivity were analyzed quantitatively. One-way analysis of variance and Tukey test were used for statistical analysis.

eulexin 250 mg 2017-10-14

80 patients received hormone therapy with LH-RH agonists and flutamide before undergoing radical prostatectomy. The clinical stage and serum PSA were determined before and after hormone therapy. Prostate volume was determined by transrectal US.