Androgens
Genitalia, Male
Testosterone
Dihydrotestosterone
Androgen Receptor Antagonists
Receptors, Androgen
Metestrus
Anilides
Methyltestosterone
Antineoplastic Agents, Hormonal
Prostate
Hyaenidae
Tosyl Compounds
Hyperandrogenism
Cytochrome P-450 CYP1A2
Cryptorchidism
Pharmacokinetics of flutamide in patients with renal insufficiency. (1/384)
AIMS: The aim of this study was to determine the pharmacokinetic parameters of flutamide, a nonsteroidal antiandrogenic compound, and its pharmacologically active metabolite, hydroxyflutamide, in renal insufficiency. Haemodialysis (HD) clearance of flutamide and hydroxyflutamide was also determined. METHODS: Pharmacokinetic parameters were assessed for flutamide and hydroxyflutamide in 26 male subjects with normal renal function (creatinine clearance by 24 h urine collection, CLcr, greater than 80 ml min(-1) 1.73 m(-2); n=6) or reduced renal function; CLcr=50-80 (n=7), 30-49 (n=3), 5-29 (n=4), and <5 ml min(-1) 1.73 m(-2)-HD (n=6), following a single, oral 250 mg flutamide dose. Subjects undergoing HD received a second 250 mg dose of flutamide 4 h prior to HD; blood and dialysate were collected during HD to determine dialysability of flutamide and hydroxyflutamide. RESULTS: Cmax, tmax, AUC, t1/2, and renal clearance of flutamide and hydroxyflutamide did not differ between groups. Less than 1% of the dose appeared in dialysate as hydroxyflutamide. No serious adverse events were observed. CONCLUSIONS: Renal function did not affect flutamide nor hydroxyflutamide disposition. HD did not alter hydroxyflutamide pharmacokinetics. Dosing adjustments for renal impairment or HD are not indicated for flutamide. (+info)From HER2/Neu signal cascade to androgen receptor and its coactivators: a novel pathway by induction of androgen target genes through MAP kinase in prostate cancer cells. (2/384)
Overexpression of the HER2/Neu protooncogene has been linked to the progression of breast cancer. Here we demonstrate that the growth of prostate cancer LNCaP cells can also be increased by the stable transfection of HER2/Neu. Using AG879, a HER2/Neu inhibitor, and PD98059, a MAP kinase inhibitor, as well as MAP kinase phosphatase-1 (MPK-1), in the transfection assay, we found that HER2/Neu could induce prostate-specific antigen (PSA), a marker for the progression of prostate cancer, through the MAP kinase pathway at a low androgen level. Reporter assays and mammalian two-hybrid assays further suggest this HER2/Neu-induced androgen receptor (AR) transactivation may function through the promotion of interaction between AR and AR coactivators, such as ARA70. Furthermore, we found this HER2/Neu --> MAP kinase --> AR-ARAs --> PSA pathway could not be blocked completely by hydroxyflutamide, an antiandrogen used in the treatment of prostate cancer. Together, these data provide a novel pathway from HER2/Neu to AR transactivation, and they may represent one of the reasons for the PSA re-elevation and hormone resistance during androgen ablation therapy in prostate cancer patients. (+info)Selection for androgen receptor mutations in prostate cancers treated with androgen antagonist. (3/384)
The role of androgen receptor (AR) mutations in androgen-independent prostate cancer (PCa) was determined by examining AR transcripts and genes from a large series of bone marrow metastases. Mutations were found in 5 of 16 patients who received combined androgen blockade with the AR antagonist flutamide, and these mutant ARs were strongly stimulated by flutamide. In contrast, the single mutant AR found among 17 patients treated with androgen ablation monotherapy was not flutamide stimulated. Patients with flutamide-stimulated AR mutations responded to subsequent treatment with bicalutamide, an AR antagonist that blocks the mutant ARs. These findings demonstrate that AR mutations occur in response to strong selective pressure from flutamide treatment. (+info)Pharmacokinetics of flutamide and its metabolite 2-hydroxyflutamide in normal and hepatic injury rats. (4/384)
AIM: To develop a new HPLC assay to study the pharmacokinetics of flutamide (Flu) and its active metabolite 2-hydroxyflutamide (HF) in rats. METHODS: Normal or hepatic injury rats were given i.g. Flu 50 mg.kg-1. Reverse phase HPLC was developed with a mu-Bondapak C 18 column. Internal standard was methyltestosterone. The mobile phase was a mixture of methanol:acetonitrile:water:diethyl ether = 40:20:35:1 (vol). Absorbance was measured at lambda 234 nm. RESULTS: The pharmacokinetic parameters of Flu were as follows: in normal rats, K = 0.62 +/- 0.16 h-1, Cl = 6.0 +/- 1.0 L.kg-1.h-1, AUC = 8.6 +/- 1.3 mg.L-1.h, Cmax = 2.4 +/- 0.7 mg.L-1; in hepatic injury rats, K = 0.16 +/- 0.03 h-1, Cl = 0.63 +/- 0.29 L.kg-1.h-1, AUC = 100 +/- 44 mg.L-1.h, Cmax = 6.7 +/- 2.8 mg.L-1. The pharmacokinetic parameters of HF were as follows: in normal rats, K(m) = 0.07 +/- 0.01 h-1, AUC = 219 +/- 22 mg.L-1.h, Cmax = 8.6 +/- 0.6 mg.L-1; in hepatic injury rats, K(m) = 0.05 +/- 0.01 h-1, AUC = 170 +/- 42 mg.L-1.h, Cmax = 3.8 +/- 0.8 mg.L-1. There were significant differences between the parameters of normal and hepatic injury rats (P < 0.01) except AUC of HF (P > 0.05). CONCLUSION: This HPLC assay was sensitive and precise, and the elimination of Flu and HF was inhibited significantly due to hepatic injury. (+info)Androgen and epidermal growth factor down-regulate cyclin-dependent kinase inhibitor p27Kip1 and costimulate proliferation of MDA PCa 2a and MDA PCa 2b prostate cancer cells. (5/384)
Low levels of p27Kip1 in primary prostate cancer specimens have been shown to be associated with higher rates of disease recurrence and poor rates of disease-free survival in patients with localized disease. In this study, we provide the first direct evidence showing that dihydrotestosterone (DHT), a major proliferation regulator of prostate cancer, can down-regulate p27Kip1 and stimulate cyclin-dependent kinase-2 (CDK2) activity in established prostate cancer cell lines. We investigated the cooperative effects of DHT and epidermal growth factor (EGF) on the proliferation of androgen-responsive MDA PCa 2a and MDA PCa 2b prostate cancer cells. DHT and EGF each stimulated proliferation of these cells, but exposure of the cells to DHT and EGF together stimulated greater proliferation. Stimulation of cell proliferation by DHT and/or EGF was associated with increased CDK2 activity and a decreased level of p27Kip1. There seems to be a positive feedback stimulation loop between androgen-induced gene transcription and EGF-stimulated signal transduction, as one could stimulate the synthesis of the receptors for the other. Dual blockade of androgen receptor function with the antiandrogen hydroxyflutamide and EGF receptor superfamily-mediated signal transduction with the anti-EGF receptor monoclonal antibody C225 and the anti-HER2 receptor monoclonal antibody Herceptin significantly enhanced growth inhibition of the MDA PCa 2a cells. Our results demonstrate the importance of counteracting both androgen receptors and EGF receptors in the development of novel therapies for prostate cancer. (+info)Detection of the environmental antiandrogen p,p-DDE in CD and long-evans rats using a tier I screening battery and a Hershberger assay. (6/384)
In this report, p,p'-DDE, a weak androgen receptor (AR) antagonist, has been examined in a Tier I screening battery designed to detect endocrine-active compounds (EACs). The screening battery that was used to examine p,p'-DDE was an abbreviated version of a proposed Tier I screening battery (Cook et al., 1997, Regul. ToxicoL Pharmacol. 26, 60-68) that consisted of a 15-day intact male in vivo battery and an in vitro yeast transactivation system (YTS). In addition, strain sensitivity differences were evaluated using male Crl:CDIGS BR (CD) and Long-Evans (LE) rats. Finally, p,p'-DDE was examined in a Hershberger assay designed to detect AR agonists. In the in vivo male battery using CD rats, responses to p,p'-DDE included organ weight changes (increased relative liver weight and decreased absolute epididymis weight) and hormonal alterations (increased serum estradiol [E2] levels and decreased serum FSH and T4 levels). Responses to p,p'-DDE in LE rats included organ weight changes (increased relative liver weight, absolute epididymis weight, relative accessory sex gland [ASG] unit weight, as well as the individual component weights of the ASG [prostate and seminal vesicles]), and hormonal alterations (increased serum testosterone [T], E2, dihydrotestosterone [DHT], thyroid-stimulating hormone [TSH], and decreased T4 levels). These data demonstrate that there are considerable strain-sensitivity differences to p,p'-DDE exposure. The described in vivo male battery using CD rats did not identify p,p'-DDE as an EAC. In contrast, the in vivo male battery using LE rats identified p,p'-DDE as a EAC. Evaluation of the data for the LE rats demonstrate that p,p'-DDE appears to be acting as an AR antagonist whose primary effects are more potent centrally than peripherally. In the YTS for the AR, p,p'-DDE had an EC50 value of 3.5 x 10(-4) M; however, in the AR YTS competition assay, p,p'-DDE did not inhibit DHT binding to the AR. p,p'-DDE was inactive in the YTS containing the estrogen receptor or progesterone receptor at the concentrations evaluated. In the Hershberger assay, p,p'-DDE administration caused antiandrogen-like effects characterized by attenuation of the testosterone propionate-induced increases in reproductive-organ weights. In summary, these data suggest that strain selection will affect the ability to detect certain weak EACs. However, a Tier I screening battery consisting of both in vivo and in vitro endpoints would reduce the chance that weak-acting compounds such as p,p'-DDE would not be identified as potential EACs. (+info)Testosterone signaling through internalizable surface receptors in androgen receptor-free macrophages. (7/384)
Testosterone acts on cells through intracellular transcription-regulating androgen receptors (ARs). Here, we show that mouse IC-21 macrophages lack the classical AR yet exhibit specific nongenomic responses to testosterone. These manifest themselves as testosterone-induced rapid increase in intracellular free [Ca(2+)], which is due to release of Ca(2+) from intracellular Ca(2+) stores. This Ca(2+) mobilization is also inducible by plasma membrane-impermeable testosterone-BSA. It is not affected by the AR blockers cyproterone and flutamide, whereas it is completely inhibited by the phospholipase C inhibitor U-73122 and pertussis toxin. Binding sites for testosterone are detectable on the surface of intact IC-21 cells, which become selectively internalized independent on caveolae and clathrin-coated vesicles upon agonist stimulation. Internalization is dependent on temperature, ATP, cytoskeletal elements, phospholipase C, and G-proteins. Collectively, our data provide evidence for the existence of G-protein-coupled, agonist-sequestrable receptors for testosterone in plasma membranes, which initiate a transcription-independent signaling pathway of testosterone. (+info)Combined treatment with the 5 alpha-reductase inhibitor PNU 157706 and the antiandrogen flutamide on the Dunning R3327 prostatic carcinoma in rats. (8/384)
The steroid 5 alpha-reductase enzyme catalyzes the conversion of testosterone to the potent androgen 5 alpha-dihydrotestosterone (DHT). PNU 157706, a novel, potent and selective dual 5 alpha-reductase inhibitor, was reported to be effective in inhibiting the growth of established tumors in the Dunning R3327 rat prostatic carcinoma model. We have studied the efficacy of combined treatment with PNU 157706 and the antiandrogen flutamide in this prostatic tumor in rats. Rats with tumor diameters of about 1 cm were treated orally 6 days a week for 9 weeks with PNU 157706 (10 mg/kg per day) alone or in combination with flutamide (1 and 5 mg/kg per day). Animals were killed 24 h after the last treatment and ventral prostates were removed for testosterone and DHT determination. PNU 157706 reduced the growth of established tumors by 36%; flutamide showed a slight effect at 1 mg/kg per day (24% inhibition), while at the dose of 5 mg/kg per day it reduced tumor growth by 48%. The combination of PNU 157706 with the lower dose of flutamide caused an additive tumor growth inhibition (60%) and the combination with the higher dose of flutamide resulted in a better inhibition of tumor growth (68%) than did either treatment alone. Castration resulted in marked tumor growth inhibition (76%). Ventral prostate weight was more markedly reduced by PNU 157706 treatment than by flutamide; combined treatment was as effective as castration. Prostatic DHT content was markedly reduced by PNU 157706 (93%), whereas prostatic testosterone increased (137%). Concomitant treatment with flutamide partially antagonized the testosterone increase induced by PNU 157706 and did not modify the already considerable suppression of DHT. These data show that the inhibitory effects of PNU 157706 and flutamide on Dunning prostatic tumor growth are additive, thus supporting the rationale of this combination therapy in advanced prostate cancer, in order to achieve adequate androgen blockade with minimal side-effects. (+info)Flutamide is a medication that is used to treat prostate cancer in men. It is a type of drug called an androgen receptor antagonist, which means that it blocks the effects of male hormones (androgens) on the prostate gland. Flutamide is usually used in combination with other medications or surgery to treat prostate cancer. It can help to slow the growth of cancer cells and reduce the risk of the cancer spreading to other parts of the body. Flutamide is usually taken by mouth as tablets, and the dosage and duration of treatment will depend on the individual patient's condition and response to the medication. It is important to follow the instructions of a healthcare professional when taking flutamide, as it can cause side effects such as breast tenderness, breast enlargement, and hot flashes.
Androgen antagonists are a class of drugs that block the effects of androgens, which are male sex hormones such as testosterone. These drugs are often used to treat conditions such as prostate cancer, acne, and hirsutism (excessive hair growth in women) by reducing the levels of androgens in the body. They work by binding to androgen receptors, preventing androgens from binding to these receptors and exerting their effects. Examples of androgen antagonists include flutamide, bicalutamide, and spironolactone.
Androgens are a group of hormones that are primarily responsible for the development and maintenance of male characteristics. They are produced by the testes in males and by the ovaries and adrenal glands in females. The most well-known androgen is testosterone, which is responsible for the development of male sexual characteristics such as facial hair, deep voice, and muscle mass. Other androgens include dihydrotestosterone (DHT), dehydroepiandrosterone (DHEA), and androstenedione. In addition to their role in sexual development, androgens also play a role in other bodily functions such as bone density, red blood cell production, and metabolism. They are also involved in the regulation of mood and behavior. Abnormal levels of androgens can lead to a variety of medical conditions, including androgen insensitivity syndrome, polycystic ovary syndrome (PCOS), and testicular feminization syndrome. Androgens are also used in medical treatment for conditions such as hypogonadism, breast cancer, and prostate cancer.
Testosterone is a hormone that is primarily produced in the testicles in males and in smaller amounts in the ovaries and adrenal glands in females. It is responsible for the development of male sexual characteristics, such as the growth of facial hair, deepening of the voice, and muscle mass. Testosterone also plays a role in bone density, red blood cell production, and the regulation of the body's metabolism. In the medical field, testosterone is often used to treat conditions related to low testosterone levels, such as hypogonadism (a condition in which the body does not produce enough testosterone), delayed puberty, and certain types of breast cancer in men. It can also be used to treat conditions related to low estrogen levels in women, such as osteoporosis and menopause symptoms. Testosterone therapy can be administered in various forms, including injections, gels, patches, and pellets. However, it is important to note that testosterone therapy can have side effects, such as acne, hair loss, and an increased risk of blood clots, and should only be prescribed by a healthcare professional.
Dihydrotestosterone (DHT) is a hormone that is produced in the body from testosterone, a male sex hormone. DHT is a potent androgen, meaning that it has a strong effect on the development and maintenance of male characteristics. It is involved in the development of male reproductive organs, such as the prostate gland and testicles, and plays a role in the growth and maintenance of body hair, muscle mass, and bone density. In addition, DHT is thought to play a role in the development of prostate cancer. DHT is also found in women, but in lower levels than in men.
Androgen receptor antagonists are a class of drugs that block the action of androgens, which are male sex hormones such as testosterone. These drugs are used to treat a variety of conditions, including prostate cancer, acne, and hirsutism (excessive hair growth in women). They work by binding to the androgen receptor and preventing androgens from binding to it, which in turn prevents the androgens from exerting their effects on the body. Some examples of androgen receptor antagonists include flutamide, bicalutamide, and enzalutamide.
Receptors, Androgen are proteins found on the surface of cells that bind to and respond to androgens, a group of hormones that play a role in the development and maintenance of male characteristics. These receptors are primarily found in the prostate gland, testes, and reproductive organs, but they are also present in other parts of the body, such as the brain, bone, and muscle. Activation of androgen receptors by androgens can lead to a variety of effects, including the growth and development of male reproductive tissues, the maintenance of bone density, and the regulation of metabolism.
Anilides are a class of organic compounds that are derived from aniline, which is an aromatic amine. In the medical field, anilides are often used as intermediates in the synthesis of other drugs and pharmaceuticals. They can also be used as antiseptics, disinfectants, and as local anesthetics. Some specific examples of anilides that have medical applications include benzylamine, which is used as a local anesthetic, and chlorobenzylamine, which is used as a disinfectant.
Methyltestosterone is a synthetic androgenic anabolic steroid that is used in the medical field for the treatment of conditions such as delayed puberty, breast cancer in women, and muscle wasting diseases. It is also used to promote muscle growth and strength in athletes and bodybuilders. However, the use of methyltestosterone for these purposes is illegal without a prescription and can have serious side effects, including liver damage, high blood pressure, and infertility.
Antineoplastic agents, hormonal are a class of drugs that are used to treat cancer by targeting hormones that regulate cell growth and division. These drugs work by either blocking the production or action of hormones that promote cancer cell growth, or by stimulating the production of hormones that inhibit cancer cell growth. Examples of hormonal antineoplastic agents include tamoxifen, which is used to treat breast cancer, and leuprolide, which is used to treat prostate cancer. These drugs are often used in combination with other antineoplastic agents, such as chemotherapy or radiation therapy, to increase their effectiveness. It is important to note that hormonal antineoplastic agents are not effective for all types of cancer, and they may have side effects that can be serious or life-threatening. It is important for patients to discuss the potential risks and benefits of these drugs with their healthcare provider before starting treatment.
Tosyl compounds are a class of organic compounds that contain a tosyl group (-SO2CH3), which is derived from toluene. These compounds are commonly used in the medical field as intermediates in the synthesis of various drugs and pharmaceuticals. One example of a tosyl compound used in medicine is tosyl chloride, which is used as a reagent in the synthesis of a variety of drugs, including antibiotics, anti-inflammatory agents, and anticancer drugs. Another example is tosylate esters, which are used as intermediates in the synthesis of certain antibiotics and other drugs. Tosyl compounds can also be used as protecting groups in organic synthesis, where they are used to protect certain functional groups in a molecule during the synthesis process. This allows chemists to selectively modify other parts of the molecule without affecting the protected functional group. Once the desired modifications have been made, the protecting group can be removed to restore the original functional group.
Hyperandrogenism is a medical condition characterized by an excess of androgens, which are male sex hormones such as testosterone. This excess can lead to a variety of symptoms and health problems, particularly in women and girls. In women, hyperandrogenism can cause symptoms such as acne, excess hair growth (hirsutism), irregular menstrual periods, and infertility. It can also lead to conditions such as polycystic ovary syndrome (PCOS), which is a hormonal disorder that affects women of reproductive age. In boys, hyperandrogenism can cause symptoms such as early puberty, excessive growth, and acne. It can also lead to conditions such as precocious puberty, which is the early onset of puberty. Hyperandrogenism can be caused by a variety of factors, including genetic disorders, certain medications, and certain medical conditions such as Cushing's syndrome or adrenal gland tumors. Treatment for hyperandrogenism depends on the underlying cause and may include medications to lower androgen levels, lifestyle changes, or surgery.
Linuron is a herbicide that is used to control broadleaf weeds in various crops, including cereals, vegetables, and fruits. It is a systemic herbicide, which means that it is absorbed by the plant and transported throughout its tissues, ultimately killing the plant. In the medical field, Linuron is not used as a treatment for any medical condition. However, it is important to note that exposure to Linuron or other herbicides can have potential health effects on humans, including skin irritation, respiratory problems, and damage to the liver and kidneys. Therefore, it is important to follow proper safety precautions when handling and using herbicides, including wearing protective clothing and gloves, and avoiding contact with the skin or eyes.
Prostatic neoplasms refer to tumors that develop in the prostate gland, which is a small gland located in the male reproductive system. These tumors can be either benign (non-cancerous) or malignant (cancerous). Benign prostatic neoplasms, also known as benign prostatic hyperplasia (BPH), are the most common type of prostatic neoplasm and are typically associated with an increase in the size of the prostate gland. Malignant prostatic neoplasms, on the other hand, are more serious and can spread to other parts of the body if left untreated. The most common type of prostate cancer is adenocarcinoma, which starts in the glandular cells of the prostate. Other types of prostatic neoplasms include sarcomas, which are rare and start in the connective tissue of the prostate, and carcinoid tumors, which are rare and start in the neuroendocrine cells of the prostate.
Cytochrome P-450 CYP1A2 is an enzyme that plays a crucial role in the metabolism of various drugs and toxins in the human body. It is a member of the cytochrome P450 family of enzymes, which are responsible for the oxidation of a wide range of substrates, including drugs, hormones, and environmental pollutants. CYP1A2 is primarily expressed in the liver, but it is also found in other tissues such as the lungs, kidneys, and gastrointestinal tract. It is involved in the metabolism of many commonly used drugs, including caffeine, theophylline, and certain antidepressants, as well as some environmental pollutants, such as polycyclic aromatic hydrocarbons (PAHs) and dioxins. The activity of CYP1A2 can be influenced by a variety of factors, including genetic polymorphisms, age, sex, and exposure to certain chemicals. Variations in CYP1A2 activity can affect the metabolism and clearance of drugs, leading to differences in drug response and toxicity among individuals. Therefore, understanding the role of CYP1A2 in drug metabolism is important for optimizing drug therapy and minimizing adverse effects.
Cryptorchidism is a medical condition in which one or both testicles fail to descend from the abdomen into the scrotum, the pouch of skin that hangs behind the penis. This can occur in newborns, infants, and children, and is more common in males than females. In some cases, the testicles may descend into the scrotum within the first few months of life, but in others, the testicles may remain in the abdomen or inguinal canal (the canal that connects the abdomen to the scrotum) throughout life. Cryptorchidism can have a number of potential health consequences, including an increased risk of testicular cancer, infertility, and problems with sexual development. Treatment typically involves surgical intervention to move the testicles into the scrotum.
Flutamide
Effects of hormones on sexual motivation
Estrogen (medication)
Comparison of bicalutamide with other antiandrogens
Hirsutism
Pharmacology of bicalutamide
List of EORTC trials
Bicalutamide
ZM-182345
Gynecomastia
Medical uses of bicalutamide
Management of hair loss
Acne
Side effects of cyproterone acetate
Feminizing hormone therapy
Discovery and development of antiandrogens
Pharmacology of cyproterone acetate
Nilutamide
Hydroxyflutamide
Antiandrogen
Gonadotropin-releasing hormone agonist
Spironolactone
Side effects of bicalutamide
Androgen
Supernumerary nipples-uropathies-Becker's nevus syndrome
Megestrol acetate
Ramesh C. Deka
Pharmacodynamics of spironolactone
Cyproterone acetate
Allylestrenol
Flutamide: MedlinePlus Drug Information
Eulexin (Flutamide): Uses, Dosage, Side Effects, Interactions, Warning
Flutamide - Health Information Library | PeaceHealth
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EULEXIN9
- Eulexin (flutamide) Capsules is an antiandrogen used to treat prostate cancer . (rxlist.com)
- Our Eulexin (flutamide) Capsules Side Effects Drug Center provides a comprehensive view of available drug information on the potential side effects when taking this medication. (rxlist.com)
- EULEXIN Capsules contain flutamide, an acetanilid, nonsteroidal, orally active anti- androgen having the chemical name, 2-methyl-N-[4-nitro-3 (trifluoromethyl) phenyl] propanamide. (rxlist.com)
- The inactive ingredients for EULEXIN (flutamide) Capsules include: corn starch, lactose, magnesium stearate, povidone, and sodium lauryl sulfate. (rxlist.com)
- EULEXIN (flutamide) Capsules are indicated for use in combination with LHRH agonists for the management of locally confined Stage B 2 -C and Stage D 2 metastatic carcinoma of the prostate . (rxlist.com)
- Treatment with EULEXIN (flutamide) Capsules and the LHRH agonist should start 8 weeks prior to initiating radiation therapy and continue during radiation therapy. (rxlist.com)
- To achieve benefit from treatment, EULEXIN (flutamide) Capsules should be initiated with the LHRH agonist and continued until progression. (rxlist.com)
- Treatment with EULEXIN (flutamide) Capsules and the LHRH agonist did not add substantially to the toxicity of radiation treatment alone. (rxlist.com)
- The following adverse experiences were reported during a multicenter clinical trial comparing EULEXIN (flutamide) Capsules + LHRH-A +radiation versus radiation alone. (rxlist.com)
Nilutamide1
- Prior treatment with first-generation AR antagonists (i.e., bicalutamide, nilutamide, flutamide) before abiraterone or enzalutamide is allowed. (mayo.edu)
Antiandrogen2
- Flutamide, a nonsteroidal antiandrogen drug widely used in the treatment of prostate cancer, has been associated with rare incidences of hepatotoxicity in patients. (unboundmedicine.com)
- The first and only case report of AKI associated with ADT (the oral antiandrogen flutamide) was published in 2002 by Turkish clinicians ( Med Oncol . (medscape.com)
Nonsteroidal1
- Flutamide is in a class of medications called nonsteroidal antiandrogens. (medlineplus.gov)
Combination with LHRH agonists1
- Flutamide tablets may be given in combination with LHRH agonists. (mrmed.in)
LHRH1
- Continue to take flutamide along with the LHRH agonist treatment even if you feel well. (medlineplus.gov)
Dosage1
- You may not be able to take flutamide, or you may require a dosage adjustment or special monitoring during treatment if you have any of the conditions listed above. (us.org)
Human liver2
- NADPH- and GSH-supplemented human liver microsomal incubations of flutamide gave rise to a novel GSH conjugate where GSH moiety was conjugated to the flutamide molecule via the amide nitrogen, resulting in a sulfenamide. (unboundmedicine.com)
- Interestingly, the same adduct was formed when flutamide was incubated with human liver microsomes in the presence of GSSG and NADPH. (unboundmedicine.com)
Prostate2
Orally1
- Flutamide is an orally administered drug. (mrmed.in)
Capsule2
- Flutamide comes as a capsule to take by mouth. (medlineplus.gov)
- Each capsule contains 125 mg flutamide. (rxlist.com)
Allergic3
- tell your doctor and pharmacist if you are allergic to flutamide or any other medications. (medlineplus.gov)
- Do not take this medicine if you are allergic to Flutamide and its other ingredient. (mrmed.in)
- Serious side effects while taking Flutamide are liver problems (hepatitis), stomach pain, dark urine, allergic reaction swelling in the leg and other parts. (mrmed.in)
Room temperature2
Pregnant4
- If taken by pregnant women, flutamide can harm the fetus. (medlineplus.gov)
- Women who are or may become pregnant should not take flutamide. (medlineplus.gov)
- If you take flutamide while you are pregnant, call your doctor. (medlineplus.gov)
- Do not take flutamide if you are pregnant. (us.org)
Liver7
- Flutamide may cause liver damage that can be serious or life-threatening. (medlineplus.gov)
- Your doctor will order certain blood tests to check how well your liver is working before you begin taking flutamide, every month for the first 4 months of your treatment, and periodically for as long as your treatment continues. (medlineplus.gov)
- There have been postmarketing reports of hospitalization and rarely death due to liver failure in patients taking flutamide. (rxlist.com)
- If at any time a patient has jaundice, or their ALT rises above 2 times the upper limit of normal, flutamide should be immediately discontinued with close follow-up of liver function tests until resolution. (rxlist.com)
- Flutamide should be used cautiously in patients with liver problems. (mrmed.in)
- Your doctor will need to monitor your liver function with blood tests before starting treatment with flutamide, every month for the first 4 months of treatment, and periodically thereafter. (us.org)
- In rare cases, flutamide has caused severe liver damage resulting in death or hospitalization. (us.org)
Harm1
- Flutamide is in the FDA pregnancy category D. This means that it is known to harm an unborn baby. (us.org)
Treatment3
- Approximately half of the reported cases occurred within the initial 3 months of treatment with flutamide. (rxlist.com)
- Serum transaminase levels should be measured prior to starting treatment with flutamide. (rxlist.com)
- Short-term treatment with flutamide applied to adult rats exerts its primary effect on the basal ES, coexisting junctional complexes and their constituent proteins Cx43 and ZO-1, without any apparent morphological alterations in the seminiferous epithelium. (biomedcentral.com)
Women4
Talking to your doctor1
- Do not stop taking Flutamide without talking to your doctor. (mrmed.in)
Doctor3
- Talk to your doctor about the risks of taking flutamide. (medlineplus.gov)
- ask your doctor about the safe use of alcoholic beverages while you are taking flutamide. (medlineplus.gov)
- If you have overdosed on Flutamide tablets or someone accidentally takes your tablet, contact the hospital or a doctor immediately for medical advice. (mrmed.in)
Times1
- Flutamide is usually taken three times a day (every 8 hours). (us.org)
Effect2
- In contrast, estrogens (estradiol, bisphenol-A, and 4-tert-octylphenol), pure anti-estrogen ICI 182,780 (ICI), and anti-androgens (4-OH-flutamide or the vinclozolin metabolite M-2) had no effect on P production even at 1000 nM. (cdc.gov)
- flutamide reversed this effect. (bvsalud.org)
Breast2
- Although it is rare, some men taking flutamide have developed breast cancer. (medlineplus.gov)
- It is not known whether flutamide passes into breast milk. (us.org)
Patients1
- Flutamide is not recommended in patients whose ALT values exceed twice the upper limit of normal. (rxlist.com)
Male1
- Flutamide (50 mg/kg body weight) was administered to male rats daily from 82 to 88 postnatal day. (biomedcentral.com)