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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:

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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 tablets

Hirsutism was assessed by measuring hair diameter. Follicle-stimulating hormone and LH responses to GnRH were evaluated. Basal plasma levels of T, androstenedione (A), 17-hydroxyprogesterone (17-OHP), DHEAS, cortisol (F), and sex hormone-binding globulin (SHBG) were evaluated. The same hormones were determined after a single dose of flutamide (250 or 500 mg) or placebo throughout a 12-hour period and in samples collected 60 and 120 minutes after ACTH intravenous injection.

eulexin dose

Recently we constructed yeast cells that either express the human estrogen receptor alpha or the human androgen receptor in combination with a consensus ERE or ARE repeat in the promoter region of a green fluorescent protein (yEGFP) read-out system. These bioassays were proven to be highly specific for their cognate agonistic compounds. In this study the value of these yeast bioassays was assessed for analysis of compounds with antagonistic properties. Several pure antagonists, selective estrogen receptor modulators (SERMs) and plant-derived compounds were tested. The pure antiestrogens ICI 182,780 and RU 58668 were also classified as pure ER antagonists in the yeast estrogen bioassay and the pure antiandrogen flutamide was also a pure AR antagonist in the yeast androgen bioassay. The plant-derived compounds flavone and guggulsterone displayed both antiestrogenic and antiandrogenic activities, while 3,3'-diindolylmethane (DIM) and equol combined an estrogenic mode of action with an antiandrogenic activity. Indol-3-carbinol (I3C) only showed an antiandrogenic activity. Coumestrol, genistein, naringenin and 8-prenylnaringenin were estrogenic and acted additively, while the plant sterols failed to show any effect. Although hormonally inactive, in vitro and in vivo metabolism of the aforementioned plant sterols may still lead to the formation of active metabolites in other test systems.

eulexin dosage

Two HPLC-DAD assays for the simultaneous quantitation of exemestane (EXE) and resveratrol (RES)-Mix 1-and EXE and luteolin (LUT)-Mix 2-in novel breast cancer therapy nanoformulations were developed. Calibration curves 15-30 µg/mL and samples were injected through an Inertsil ODS-3 (250 × 4.6 mm, 5 µm) column. The gradient elution for Mix 1 was methanol : 0.05% (v/v) acetic acid in water (60 : 40 to 80 : 20, linear over 2 min), and for Mix 2, it was methanol : water (60 : 40 for 4 min, then ramped linearly to 90 : 10, over 12 min) pumped at 1.5 mL/min for 4 min, then 1 mL/min till the end of run. EXE, RES, LUT and flutamide (internal standard (IS)) were measured at 246, 307, 350 and 300 nm, respectively. For Mix 1, RES, EXE and IS eluted at 3.5, 6.8 and 7.4 min, respectively, while for Mix 2, LUT, EXE and IS eluted at 7.5, 11.4 and 12.7 min, respectively. The mean r(2) for the standard curves was ≥0.99, and percentage coefficient of variation and % error of the mean were <2. Both assays successfully quantitated Mix 1 and Mix 2 in their nanoformulations. The two developed assays were sensitive and selective for the analysis of EXE-LUT and EXE-RES mixtures in nanoformulations according to International Conference on Harmonization guidelines.

eulexin capsules

This study included 35 Japanese men with advanced prostate cancer. Initial androgen ablation continued for 2 months after PSA levels decreased to <4.0 ng/ml, then was withdrawn. Androgen ablation was reinstituted 2 months after PSA reached levels >10 ng/ml, when indicated clinically or on patient request. Cycling continued until androgen independence was reached.

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Many patients with prostate cancer for whom hormonal therapy is indicated are still physically and sexually active; quality of life is therefore a vital issue when considering treatment options. Traditional castration-based therapies, although effective, have implications with respect to quality of life, causing loss of libido, impotence, fatigue, and reduced bone mineral density. Monotherapy with a nonsteroidal antiandrogen is an attractive therapeutic alternative to castration, offering effective therapy with potential quality-of-life benefits. Of the available nonsteroidal antiandrogens, bicalutamide has been most extensively evaluated in the monotherapy setting. Mature combined data (56% mortality) from 2 large randomized studies show no statistically significant difference in overall survival between bicalutamide 150-mg monotherapy and castration in patients with locally advanced, nonmetastatic (stage M0) disease. Survival outcome in patients with metastatic (stage M1) disease (43% mortality) favored castration, although the difference in median survival between the groups was only 6 weeks. Bicalutamide 150-mg monotherapy was associated with significant advantages compared with castration, in terms of sexual interest and physical capacity, in patients with either M0 and M1 stage disease. Data from a small subgroup of patients with stage M0 disease suggest that bicalutamide may also reduce the risk of osteoporosis compared with castration. Long-term therapy with bicalutamide 150-mg monotherapy is generally well tolerated, with a predictable side-effect profile. The most common side effects are male breast pain and gynecomastia. Emerging evidence also supports the use of bicalutamide 150 mg, both as immediate monotherapy and as adjuvant therapy in early stage (localized or locally advanced) prostate cancer.

eulexin drug

Sixty-two patients with clinical stage T3 and T4 N0,M0 prostate cancer were enrolled. Cases were classified by stage T3 vs T4 and by volume of disease (bulky >4 cm and nonbulky ≤ 4 cm).

eulexin 500 mg

It is known that expression of glial fibrillary acidic protein (GFAP) as an astrocyte-specific marker can be regulated by levels of circulating gonadal steroids during postnatal development. In addition, astrocytes play an important role in the physiology of the hippocampus, a brain region considered sexually dimorphic at the neuronal level in rodents. To evaluate the contribution of glial cells to gender-related differences in the hippocampus, we estimated the number of GFAP-immunoreactive (GFAP-IR) astrocytes in the hippocampus (CA1 and CA3 areas, dorsal and ventral regions) of male and female rats aged 30 days. Groups of 30-day-old masculinized females (TP-females; injected with testosterone propionate at birth) and feminized males (FLU-males, castrated and treated with flutamide, an androgen receptor antagonist) were included to assess the effects of gonadal hormones on these hippocampal astrocytes. Using the optical fractionator method, the total number of GFAP-IR cells found in CA1 and CA3 areas was significantly higher in males compared to that in age-matched females. This numerical pattern was reversed in TP-females and FLU-males in both hippocampal areas. In addition, more GFAP-IR cells were found in dorsal hippocampus than in the ventral region in the CA1 area from all experimental groups, whereas this result was found in the CA3 area from males and TP-females. Our results suggest an essential contribution of gonadal hormones to gender differences found in the astrocyte population of the rat hippocampus during development.

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Androgens are known to increase muscle mass, strength and muscle protein synthesis. However, the molecular mechanisms by which androgens regulate skeletal muscle development remain poorly understood. The ribosomal protein kinase p70(s6k) is a regulator of ribosome biogenesis and plays an important role in the regulation of growth-related protein synthesis. The phosphorylation of p70(s6k) has been implicated in load-induced skeletal muscle hypertrophy. In the current study, we determined the effect of DHT on the phosphorylation of p70(s6k) in the androgen-sensitive levator ani muscle of castrated rats. DHT induced a rapid increase in the phosphorylation of p70(s6k), which was detectable within 6 h after a single injection. Interestingly, DHT-induced phosphorylation of p70(s6k) occurred only in androgen-sensitive muscles, but not prostate and seminal vesicle. Co-administration of flutamide, an AR antagonist, inhibited DHT-induced p70(s6k) phosphorylation. While serum IGF-I levels were not changed by DHT treatment, IGF-I gene expression levels increased and the mRNA levels of IGFBP3 and IGFBP5 were suppressed in the LA muscle after DHT replacement in castrated rats. These results suggest that the phosphorylation of p70(s6k), likely via the IGF-I pathway, may play an important role in androgen-induced skeletal muscle hypertrophy.

eulexin 125 mg

From 10/88 to 12/93, 517 T1-T3 NXM0 patients with known pretreatment PSA level were treated at Fox Chase Cancer Center. Four hundred fifty-nine of those patients were treated with RT alone while 58 were treated with RT+H. The patients were categorized according to putative prognostic factors indicative of bNED control, which include the palpation stage, Gleason score, and pretreatment PSA. We compared actuarial bNED control rates according to treatment group within each of the prognostic groups. In addition, we devised a retrospective matched case/control selection of RT patients for comparison with the RT+H group. Five-year bNED control was compared for the two treatment groups, excluding the best prognosis group, using 56 RT+H patients and 56 matched (by stage, grade, and pretreatment PSA level) controls randomly selected from the RT alone group. bNED control for the entire group of 517 patients was then analyzed multivariately using step-wise Cox regression to determine independent predictors of outcome. Covariates considered for entry into the model included stage (T1/T2AB vs. T2C/T3), grade (2-6 vs. 7-10), pretreatment PSA (0-15 vs. > 15), treatment (RT vs. RT+H), and center of prostate dose. bNED failure is defined as PSA > or = 1.5 ngm/ml and rising on two consecutive determinations. The median follow-up for the 112 matched case/control patients was 41 months. The median follow-up was 46 months for the RT (range 11-102 months) and 37 months for the RT+H group (range 6-82 months).

eulexin medication

With a median follow-up of 37.9 and 46.0 months in the matched non-pT0 and pT0 cohort respectively, matched-pair analysis failed to demonstrate significant differences in crude PSA relapse-free survival between both groups (p=0.7758).

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eulexin 250 mg 2015-09-22

Flutamide (FLU) is an antiandrogen primarily used in the treatment of metastatic prostate cancer. It is an idiosyncratic hepatotoxicant that sometimes results in severe liver toxicity. FLU possesses a nitroaromatic group, which may be a contributor to its mechanism of toxicity. A nitro to cyano analogue buy eulexin of FLU (CYA) was synthesized and used to test this hypothesis in the TGFalpha-transfected mouse hepatocyte cell line (TAMH). MTT cell viability assays and confocal microscopy showed that hepatocytes are more sensitive to cytotoxicity caused by FLU than CYA (LD 50 75 vs 150 microM, respectively). Despite the structural modification, the antiandrogen activity of CYA is comparable to that of FLU. Comparisons of transcriptomic changes caused by FLU with those caused by a panel of known cytotoxicants [acetaminophen, tetrafluoroethylcysteine, diquat, and rotenone (ROT)] indicated that FLU results in a temporal gene expression pattern similar to ROT, a known inhibitor of complex I of the electron transport chain. A subsequent microarray analysis comparing FLU to CYA and ROT revealed many similarities among these three compounds; however, FLU and ROT result in more substantial changes than CYA in the expression of genes associated with oxidative phosphorylation, fatty acid beta-oxidation, antioxidant defense, and cell death pathways. Electron microscopy confirmed that FLU leads to mitochondrial toxicity that has some similarities to the mitochondrial effects of ROT, but the morphologic changes caused by FLU were greater in scope with both intra- and intercellular manifestations. Biochemical studies confirmed that both ROT and FLU deplete cellular ATP levels and inhibit complex I of the electron transport chain to a greater extent than CYA. Thus, as compared to CYA, the nitroaromatic group of FLU enhances cytotoxicity to hepatocytes, likely through mechanisms involving mitochondrial dysfunction and ATP depletion that include complex I inhibition.

eulexin 125 mg 2015-07-18

Status of androgen receptor (AR) in prostate carcinoma is biologically important. Therefore, more methods assessing AR abnormalities are warranted. Immunohistochemical (IHC) and ligand saturation buy eulexin (LSA) assays were not compared in details. AR in 53 cases were tested by monoclonal antibody (Ab) F39.4.1 (Biogenex), polyclonal Ab N-20 (Santa Cruz) and by ligand saturation analysis with (3)H-methyltrienolon. Statistical analyses were performed with Spearman's nonparametric rank test including neoadjuvant therapy subgroups treated by antiandrogens, combined androgen blockade (22 cases; flutamide with gosereline) or without therapy. By using monoclonal Ab we found AR positive tumor nuclei in 46 cases. Mean of positives was 64%, median 75%. The polyclonal Ab was not sufficiently specific. With LSA AR were found in 43 cases. Mean level was 6.6 fmol/mg, median 5.5 fmol/mg. Comparing IHC with LSA, we noted correlation trend only for the monoclonal Ab (r=0.35; p=0.02). With thresholds 70% positive nuclei for IHC and 6 fmol/mg for LSA, there were 66% and 43% cases positive with IHC and LSA, respectively. The LSA and IHC positives did not show significant agreement, concordance level being 58% only. We found significant IHC-LSA correlation (r=0.68; p=0.004) solely in combined androgen blockade subgroup with 82% level concordance. Our study has demonstrated that AR IHC and LSA are independent complementary methods. Significant correlation between LSA and IHC show only cases treated with combined androgen blockade. An explanation hypothesis is discussed concerning LH-RH influence on free AR capable of ligand binding. IHC as well as LSA have specific biologic significance and may be useful for prostate cancer diagnostic and therapy.

eulexin medication 2015-08-21

Gender-specific disparities have been observed in myocardium Aggrenox Medication exposed to tumor necrosis factor-α (TNF). Male myocardium demonstrates greater loss in cardiac function in the presence of a given TNF level compared to female. In addition, we have previously demonstrated that estrogen has little influence on reducing TNF-caused myocardial dysfunction in female hearts, suggesting that male hormone - testosterone may be responsible for gender differences in TNF-mediated myocardial damage. Therefore, in this study, we hypothesize that endogenous testosterone plays a detrimental role in TNF-induced myocardial injury in male hearts.

eulexin dosage 2017-01-17

Since that time, a large body of information has been published regarding the mechanism of androgen-mediated action. With the understanding of androgen-mediated action has come the opportunity to develop drugs targeted to block specific steps in the sequence of androgen action, beginning in the hypothalamus-pituitary area and extending down to the Suprax Generic intracellular processes of enzymatic reduction, receptor binding, and nuclear translocation of the hormone receptor complexes. The major focus in prostate cancer therapy currently is the role of the adrenal androgens.

eulexin capsules 2015-08-01

Mandibular growth was affected by ERβ antagonist injection in male mice at 4 and 8 weeks. In female mice, the growth was affected during all the experimental period, when ERβ was administered. Moreover, at 8 weeks, mandibular growth was also affected in male and female mice injected with ERα antagonist and in male mice injected with AR antagonist. Femoral growth was affected Famvir 500mg Medication during all the experimental period in male and female mice injected with ERβ antagonist. Moreover, at 8 weeks, the growth was affected in male and female mice injected with ERα antagonist and in male mice injected with AR antagonist.

eulexin 50 mg 2016-02-13

Antiandrogen flutamide, an antagonist of the wild-type androgen receptor (AR), is used in the clinics for treating metastatic prostate cancer. However, the T877A mutated AR is paradoxically activated by hydroxyflutamide, an active form of flutamide. Despite of crystallographic studies, how the T877A mutation results in antagonist-agonist conversion of hydroxyflutamide remains a puzzle. Here, started from a structural model of the apo form of AR ligand-binding domain (AR-LBD), we have investigated the impact of the T877A mutation on ligand-induced helix-12 positioning by replica-exchange molecular dynamics (REMD) simulations with an unique protocol, which is capable of simulating the H12 dynamics and keeping the main body of AR-LBD unchanged. Specifically, (i) we have computationally demonstrated that on the binding of hydroxyflutamide, the apo form of H12 rearranges into the agonistic form in the T877A mutant, but into the antagonistic forms in the wild-type receptor, shedding light on hydroxyflutamide agonism/antagonism; (ii) By REMD simulations, we have predicted antiandrogen SC184 is a non-agonist of the T877A mutant. This was confirmed by luciferase assays; and (iii) on the basis of the binding modes of hydroxyflutamide and SC184 from the simulations, we designed a novel flutamide derivative called SC333, which was subsequently predicted to be a pure antagonist of the T877A mutant. We then synthesized and experimentally confirmed SC333 is a pan-antiandrogen effective against the wild-type and the T877A and Cialis Medicine W741C mutated ARs, showing low micromolar cytotoxicity in LNCaP cells. Importantly, we demonstrated that distribution of the H12 conformations from REMD simulations is correlated with ligand agonist/antagonist activity.

eulexin 500 mg 2017-02-21

Esterases hydrolyze compounds containing ester, amide, and thioester bonds, causing prodrug activation or detoxification. Among esterases, carboxylesterases have been studied in depth due to their ability to hydrolyze a variety of drugs. However, there are several drugs for which the involved esterase(s) is unknown. We found that flutamide, phenacetin, rifamycins (rifampicin, rifabutin, and rifapentine), and indiplon are hydrolyzed by arylacetamide deacetylase (AADAC), which is highly expressed in human liver and gastrointestinal tissues. Flutamide hydrolysis is considered associated with hepatotoxicity. Phenacetin, a prodrug of acetaminophen, was withdrawn due to side effects such as methemoglobinemia and renal failure. It was demonstrated in vitro and in vivo using mice that AADAC is responsible for phenacetin hydrolysis, which leads to Paxil Starting Dose methemoglobinemia. In addition, it was shown that AADAC-mediated hydrolysis attenuates the cytotoxicity of rifamycins. Thus AADAC plays critical roles in drug-induced toxicity. Another orphan esterase, α/β hydrolase domain containing 10 (ABHD10), was found responsible for deglucuronidation of acyl-glucuronides including mycophenolic acid acyl-glucuronide and probenecid acyl-glucuronide. Because acyl-glucuronides appear associated with toxicity, ABHD10 would function as a detoxification enzyme. The roles of orphan esterases are becoming increasingly understood. Further studies will facilitate our knowledge of the pharmacologic and toxicological significance of orphan esterases in drug therapy.

eulexin cost 2015-10-29

Interleukin-1 beta was more potent than nifedipine in stimulating CTGF/CCN2 and procollagen alpha1(I) mRNA expression, and there was an additive effect of the two drugs. Healthy cells exhibited an equal or stronger response of procollagen alpha1(I) than Zofran Brand Name those with DIGO, but DIGO cells displayed a stronger response in the secretion of soluble collagen in the same conditions. Flutamide, an androgen receptor antagonist, inhibited stimulation by nifedipine or interleukin-1 beta. Additionally, the protein expressions of androgen receptor and type I collagen were higher in DIGO gingival tissue than those in healthy gingival tissue.