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Casodex (Bicalutamide)

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Generic Casodex is a high-quality medication which is taken in treatment of prostate cancer. Generic Casodex acts by killing the cancer cells growth.

Other names for this medication:

Similar Products:
Cenestin, Eligard, Enjuvia, Premarin, Lupron, Xeloda


Also known as:  Bicalutamide.


Generic Casodex is a perfect remedy in struggle against prostate cancer.

Generic Casodex acts by killing the cancer cells growth.

Casodex is also known as Bicalutamide, Cosudex, Calutide, Kalumid, Bicalox.

Generic name of Generic Casodex is Bicalutamide.

Brand name of Generic Casodex is Casodex.


Take Generic Casodex tablets orally with or without food.

Take Generic Casodex at the same time every day with water.

Do not crush or chew it.

This medicine is only for men.

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


If you overdose Generic Casodex and you don't feel good you should visit your doctor or health care provider immediately.


Store between 15 and 30 degrees C (59 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 in a container that small children cannot open.

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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 Generic Casodex if you are allergic to Generic Casodex components.

Use contraception and avoid vaccinations.

Try to be careful using Generic Casodex if you take warfarin (Coumadin), aspirin-substitute products, aspirin.

Be very careful with Generic Casodex if you suffer from or have a history of liver disease.

Do not stop taking Generic Casodex suddenly.

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We reported recently the induction of androgen-dependent iodide uptake activity in the human prostatic adenocarcinoma cell line LNCaP using a prostate-specific antigen (PSA) promoter-directed expression of the sodium iodide symporter (NIS) gene. This offers the potential to treat prostate cancer with radioiodine. In the current study, we examined the regulation of PSA promoter-directed NIS expression and therapeutic effectiveness of (131)I in LNCaP cells by all-trans-retinoic acid (atRA). For this purpose, NIS mRNA and protein expression levels in the NIS-transfected LNCaP cell line NP-1 were examined by Northern and Western blot analysis following incubation with atRA (10 (-9) to 10(-6) M) in the presence of 10(-9) M mibolerone (mib). In addition, NIS functional activity was measured by iodide uptake assay, and in vitro cytotoxicity of (131)I was examined by in vitro clonogenic assay. Following incubation with atRA, NIS mRNA levels in NP-1 cells were stimulated 3-fold in a concentration-dependent manner, whereas NIS protein levels increased 2.3-fold and iodide accumulation was stimulated 1.45-fold. This stimulatory effect of atRA, which has been shown to be retinoic acid receptor mediated, was completely blocked by the pure androgen receptor antagonist casodex (10(-6) M), indicating that it is androgen receptor dependent. The selective killing effect of (131)I in NP-1 cells was 50% in NP-1 cells incubated with 10(-9) M mib. This was increased to 90% in NP-1 cells treated with atRA (10(-7) M) plus 10(-9) M mib. In conclusion, treatment with atRA increases NIS expression levels and selective killing effect of (131)I in prostate cancer cells stably expressing NIS under the control of the PSA promoter. Therefore atRA may be used to enhance the therapeutic response to radioiodine in prostate cancer cells following PSA promoter-directed NIS gene delivery.

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The incremental cost per quality-adjusted life year gained for bicalutamide versus flutamide was 22,000 dollars and 16,000 dollars at 5 and 10 years, respectively. If a quality adjustment was not included, the incremental cost-effectiveness ratio for CAB with bicalutamide compared with CAB with flutamide was even more favorable (20,000 dollars/life year gained at 5 years). One-way sensitivity analysis demonstrated that the cost-effectiveness estimates were most sensitive to drug costs and survival (baseline survival was not significantly different between therapies). Multi-way uncertainty analysis revealed that the median value of the incremental cost-effectiveness ratio at 5 years was 13,637 dollars/quality-adjusted life year when all the parameters were varied over a clinically reasonable range.

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We discuss here the thyroid micropapillary carcinoma that was detected incidentally when investigating the primary focus of the left neck multiple lymph node metastases occurring 8 months later in a patient of ours, whose pathological examination of radical prostatectomy and bilateral inguinal lymph node dissection was reported to be pT3N0 and whole body scanning for metastases, was negative.

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Many patients with localised prostate cancer present with symptoms of benign prostatic hypertrophy (BPH) and require neoadjuvant hormone therapy to shrink the gland before brachytherapy. The impact of this hormone therapy has been evaluated in 667 patients treated with Iodine seed monotherapy.

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c-FLIP expression was increased in high-grade prostatic intraepithelial neoplasia and prostate cancer tissue relative to normal prostate epithelium (P < 0.001). Maximal c-FLIP expression was detected in castrate-resistant prostate cancer (CRPC; P < 0.001). In vitro, silencing of c-FLIP induced spontaneous apoptosis and increased 22Rv1 and LNCaP cell sensitivity to bicalutamide, determined by flow cytometry, PARP cleavage, and caspase activity assays. The histone deacetylase inhibitors (HDACi), droxinostat and SAHA, also downregulated c-FLIP expression, induced caspase-8- and caspase-3/7-mediated apoptosis, and increased apoptosis in bicalutamide-treated cells. Conversely, the elevated expression of c-FLIP detected in the CRPC cell line VCaP underpinned their insensitivity to bicalutamide and SAHA in vitro. However, knockdown of c-FLIP induced spontaneous apoptosis in VCaP cells, indicating its relevance to cell survival and therapeutic resistance.

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We collected diesel exhaust particles (DEPs) emitted from three diesel-engine vehicles--a car, a bus, and a truck--in daily use, and prepared DEP extracts (DEPEs), designated as EC, EB, or ET, respectively. The androgenic and antiandrogenic effects of the DEPE samples were examined by a luciferase reporter assay in human prostate carcinoma PC3/AR cells transiently transfected with a prostate specific antigen gene promoter-driven luciferase expression vector pGLPSA5.8. PC3/AR is a subline of human prostate carcinoma PC3 transformed to stably express wild-type human androgen receptor (AR). While DEPE samples did not exhibit any androgenic effect, they exerted antiandrogenic effect, inhibiting dihydrotestosterone (10 pM) -induced luciferase activity by 24 to 52% at an extract concentration of 10 microg/ml. The antiandrogenic effect was greater in the following order: ET > EB > EC. Co-treatment of PC3/AR cells with SKF-525A, a nonselective inhibitor of cytochrome P450 (CYP) enzymes, enhanced the antiandrogenic effect, indicating that the antiandrogenic effect is caused by intact species of DEPE constituents. The antiandrogenic effect of DEPE samples was reversed by alpha-naphthoflavone, an aryl hydrocarbon receptor (AhR) antagonist. The antiandrogenic activity of a DEPE sample correlated with its AhR agonist activity assayed in PC3/AR cells transiently transfected with CYP1A1 gene promoter-driven luciferase expression vector pLUC1A1. Equimolar mixtures of ten polycyclic aromatic hydrocarbons (PAHs) having four or more rings, structures found in the DEPEs, showed significant antiandrogenic effects and AhR agonist activity at concentrations equivalent to those found in DEPE samples. Further, DEPE samples elicited only antiandrogenic effects in recombinant yeast cells, which express beta-galactosidase in response to androgen. A competitive AR binding assay showed that AR-binding constituents exist in DEPE samples, indicating that greater part of AR-binding constituents in DEPEs are AR antagonists. All these findings show that DEPE samples exhibit significant antiandrogenic effect in cell-based transcription assay and that this effect is due in part to the constituents with AhR agonist activity including PAHs and to the constituents with AR antagonist activity.

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Prostate cancer patients at increased risk for relapse after prostatectomy were treated in a neoadjuvant study with androgen deprivation therapy (ADT) in combination with cixutumumab, an inhibitory fully human monoclonal antibody against IGF receptor 1 (IGF-IR).

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Leuprolide depot and bicalutamide were used in the study.

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A prospective phase II study enrolled men over 4 years with low-risk PCa and the following characteristics: PSA < 10 ng/mL, Gleason score of 6 (3 + 3) or less, three positive cores or less, and tumor stage T2a or less. Patients received a single sub-cutaneous injection of 22.5 mg of leuprolide acetate with Atrigel 3-month depot associated with a daily oral intake of bicalutamide 50 mg/day during 15 days around the injection. Follow-up included PSA and bioavailable testosterone blood tests every 3 months and yearly surveillance biopsies. Primary end point was the presence of PCa on biopsy at last follow-up. Secondary end points were detailed pathological features and adverse events.

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casodex pills 2015-08-06

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 buy casodex survival between both groups (p=0.7758).

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Different isomers of the β-amino-carbonyl compounds were obtained by chiral separation. The bioactivities of the isomers were evaluated by AR nuclear translocation, mammalian two-hybrid, competitive receptor binding and cell proliferation assays. The expression of genes downstream of AR was analyzed with real-time PCR. The therapeutic effects on tumor growth in vivo were observed in male SCID mice bearing LNCaP xenografts buy casodex .

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POSTN transfection stimulated LNCaP cell growth. While POSTN transfection did not interfere with the stimulatory effect Prilosec 80 Mg of DHT, BIC had an inhibitory effect on cell proliferation. However, exposure to either DHT and/or BIC was not able to interfere with POSTN expression per se.

casodex dosage form 2015-01-20

In the base-case analysis, the incremental cost-effectiveness ratio (ICER) for degarelix vs triptorelin plus antiandrogen was £59,000 per QALY gained Cymbalta Overdose Signs . The model was most sensitive to the rate of significant adverse events in the triptorelin plus antiandrogen group. The model was also sensitive to the assumed survival of patients with metastatic prostate cancer and the price of degarelix. The results of the probabilistic sensitivity analyses suggested that there was a low probability (9.6%) of degarelix being the most cost-effective treatment option when a willingness-to-pay threshold of £30,000 per QALY gained is assumed.

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The mean serum testosterone level was 29.1 ng/dl in patients undergoing MAB (group 2) and 29.5 ng/dl in patients treated with the LH-RH agonist (group 3; p > 0.05). In group 1, the mean serum testosterone was 445.2 ng/dl (p < 0.0001). The rate of patients with a serum testosterone level higher than 50 ng/dl was 10.9% in patients undergoing androgen suppression, 10% in patients with MAB treatment and 12.5% in those with LH-RH agonist therapy (p > 0.05). In group 1, 98. Suprax 600 Mg 9% of the patients had a serum testosterone level higher than 50 ng/dl.

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Evolution of the roles proposed for antiandrogenic agents in prostatic disease has been rapid. Since the early suggestions by Labrie and his colleagues that the nonsteroidal antiandrogen flutamide could be used in combination with medical or surgical castration to provide superior care for patients with metastatic prostate cancer, and subsequent substantiation of the theory in a number of clinical trials, we have observed an increasing tendency to test the Avapro 40 Mg use of antiandrogens (alone or in combination with other interventions) earlier in the disease process. At least in part, this tendency is a consequence of our increased ability to detect prostate cancer earlier in the disease process. At the present time, flutamide is the only nonsteroidal antiandrogen available for the treatment of prostate cancer in general clinical practice in the United States. However, two other nonsteroidal antiandrogens currently await decisions on their efficacy and safety by the Food and Drug Administration: nilutamide and bicalutamide. Will either of these agents offer clinical benefits beyond those offered by flutamide? Will the safety, activity, and dosing profiles of the nonsteroidal antiandrogens allow us to use them to treat even earlier stages of prostate cancer and perhaps even prostatic intraepithelial dysplasia in patients at high risk of prostate cancer? What are the potential future roles for bicalutamide and other nonsteroidal antiandrogens in the management of prostatic disorders? This article will attempt to lay out the key questions that await definitive answers as we expand our understanding of the possible future roles for antiandrogens in the management of prostate cancer and related conditions.