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Evista (Raloxifene)

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Generic Evista is the most effective preparation in struggle against female osteoporosis symptoms (bones weakness) after period of menopause. Generic Evista acts as up-to-date anti-osteoporosis remedy which provides bones strengths and health. Generic Evista acts improving bones states, their strength.

Other names for this medication:

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Also known as:  Raloxifene.


Generic Evista is created using perfect medical formula which is a magnificent weapon against women problem such as osteoporosis symptoms (bones weakness) after period of menopause. Target of Generic Evista is to make bones stronger.

Generic Evista acts as up-to-date anti-osteoporosis remedy which provides bones strengths and health. Generic Evista acts improving bones states, their strength.

Evista is also known as Raloxifene, Ralista.

Generic Evista is estrogen (woman hormone).

Generic Evista can't lead to vaginal bleeding, uterine or breast cancer, breast tenderness.

Generic name of Generic Evista is Estrogen.

Brand name of Generic Evista is Evista.


Generic Evista can be taken in form of tablets which should be taken by mouth with water.

Take Generic Evista every day at the same time and remember that its dosage depends on patient's health state.

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


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


Store at room temperature 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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The most common side effects associated with Evista 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 Generic Evista if you are allergic to Generic Evista components.

Do not take Generic Evista if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Generic Evista in case of using diazoxide such as Proglycem, diazepam such as Zetran,Valium, Valrelease, cholestyramine such as Questran, colestipol such as Colestid, estrogen or hormone replacement therapy such as ERT or HRT, warfarin such as Coumadin.

Be careful with Generic Evista in case of having of cancer, stroke, liver or heart disease, breast lumps, high blood cholesterol, blood clots, triglycerides, phlebitis in the leg.

Use Generic Evista with great care in case you want to undergo an operation (dental or any other).

Generic Evista can't lead to vaginal bleeding, uterine or breast cancer, breast tenderness.

If you take Generic Evista it is dangerous to smoke cigarettes.

Generic Evista can be dangerous for children.

Do not stop taking Generic Evista suddenly.

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The number of anterior cruciate ligament injuries in female athletes exceeds that in male athletes at similar competitive levels. This difference has been attributed by some authors to hormone-mediated alteration in knee laxity in women.

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The current study investigated the estrogen agonist-antagonist properties of the selective estrogen receptor modulator, raloxifene (Ral), on neuroprotection and neuronal markers of memory function. Low concentrations of raloxifene significantly reduced basal markers of membrane damage and had no deleterious effect on neuronal survival. However, high concentrations of raloxifene (1000-5000 ng/ml) induced a significant increase in markers of membrane damage and a significant decrease in neuronal survival. At subtoxic concentrations, raloxifene induced significant neuroprotection against beta amyloid(25-35)-, hydrogen peroxide- and glutamate-induced toxicity. Results of analyses to determine whether raloxifene acted competitively or synergistically with 17 beta-estradiol revealed that a postmenopausal level of 17 beta-estradiol exerted a significantly greater increase in neuronal survival against beta-amyloid- and glutamate-induced toxicity compared to 50 ng/ml raloxifene. The combined presence of raloxifene and 17 beta-estradiol was significantly neuroprotective against beta amyloid(25-35)- and glutamate-induced excitotoxicity but was significantly lower than 17 beta-estradiol alone while not significantly different than raloxifene alone. Morphologic analyses demonstrated that raloxifene significantly increased neuronal outgrowth of hippocampal neurons within a narrow dose range that was blocked by a glutamate NMDA receptor antagonist. Raloxifene did not promote the outgrowth of basal forebrain or cortical neurons. Results of this study indicate that raloxifene exerted partial estrogen agonist action in the absence of 17 beta-estradiol whereas in the presence of 17 beta-estradiol, raloxifene exerted a mixed estrogen agonist-antagonist effect.

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A 55-yr-old post-menopausal woman with osteopenia and no history of breast disease is presented. She was placed on raloxifene HCl 60 mg and soon after developed severe breast pain. The follow-up mammogram, performed prematurely at 6 months, showed a marked increase in breast density. Therapy was accordingly stopped and mastodynia subsided. The patient's mammogram regressed to pre-treatment status after 6 months off-therapy.

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The sodium iodide symporter (NIS) mediates active iodide uptake in lactating breast tissue, and when its levels are enhanced by all-trans retinoic acid (atRA), NIS has been proposed as a target for the imaging and radiotherapy of breast cancer. Importantly, the estrogen receptor α (ERα) is an important regulator of atRA induced NIS gene expression in breast cancer cells. In this study, we investigated the effect of an ER agonist (17β-estradiol, E(2)) or antagonist [trans-hydroxytamoxifen (TOT) or raloxifene (RAL)] treatment on the regulation of NIS gene expression and iodide uptake in an ERα-positive breast cancer (MCF-7) model.

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In the Multiple Outcomes of Raloxifene Evaluation (MORE) trial, 7705 postmenopausal women with osteoporosis, defined by low bone mineral density and/or prevalent vertebral fractures (VF), were randomized to placebo or raloxifene (60 or 120 mg/day). All women received daily calcium (500 mg) and vitamin D (400-600 IU) supplements. Our previous analyses found that changes in BMD and biochemical markers of bone turnover are poorly predictive of the reduction in VF risk observed with raloxifene. This present study evaluated the effects of raloxifene on type I procollagen N-terminal propeptide (PINP), a new marker of bone turnover. Logistic regression analysis models evaluated the relationships between the changes at 1 year in PINP, serum osteocalcin (OC), bone-specific alkaline phosphatase (BSAP), and urinary excretion of type I collagen C-telopeptide fragments normalized to creatinine (CTx/Cr), and the risk of new VF at 3 years for placebo and pooled raloxifene. A subset of 967 women (mean age = 68 years) from the MORE cohort had PINP, OC, BSAP, and CTx evaluated at baseline. Both doses of raloxifene significantly decreased (P < 0.001) all biochemical markers of bone turnover from baseline. Compared to baseline, PINP levels were decreased by medians of 11.0% and 40.8% in the placebo and pooled raloxifene groups, respectively. In addition, the placebo and pooled raloxifene groups decreased serum OC by 8.5% and 31.8%, BSAP by 15.8% and 34.6%, and urinary CTx/Cr excretion by 5.6% and 46.5%, respectively, from baseline. In the pooled raloxifene group, the logistic regression relationship between 3-year VF risk and 1-year percentage change for each biochemical marker was statistically significant with PINP (slope estimate = 0.0085, P = 0.009), OC (slope estimate = 0.0068, P = 0.035), and BSAP (slope estimate = 0.0056, P = 0.039), but not with CTx/Cr (slope estimate = 0.0027, P = 0.192). Furthermore, the percent decrease in PINP at 1 year could account for 28% of the total reduction in vertebral fracture risk. In conclusion, a 1-year decrease in PINP, BSAP, or OC, but not CTx/Cr, may be predictive of the 3-year VF risk reduction with raloxifene therapy in this subset of postmenopausal women with osteoporosis.

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At the beginning of the study, the chronological ages, menopausal ages, years of amenorrhea, weights, body mass indexes, and blood pressures were not significantly different between groups (P < 0.05). RAL treatment caused a significant decrease on serum IL-4 concentration (P < 0.001). Although HRT caused a 14% decrease in serum IL-4 concentration, this decrease was not statistically significant (P > 0.05). Serum TGF-beta1 concentrations were significantly decreased by HRT when compared to basal value (P < 0.001), and to control (P < 0.05). RAL treatment has no significant effect on serum TGF-beta1 concentration (P > 0.05).

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Tamoxifen had an oestrogen receptor dependent, direct, inhibitory effect on human osteoclast differentiation and bone resorption, whereas ospemifene and raloxifene required osteoblastic cells to achieve a similar inhibition. The effects of ospemifene and raloxifene were mediated by oestrogen receptors by a mechanism involving paracrine induction of osteoprotegerin in cultures with osteoblast derived osteosarcoma cells.

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Proteasome-mediated protein degradation has been implicated in playing a role in nuclear receptor-mediated gene expression; inhibition of the proteasome impairs the transcriptional activity of estrogen receptor alpha (ERalpha) and most other nuclear receptors. This coincides with blockage of agonist-dependent degradation of the receptor and elevation of the steady-state levels of SRC family coactivators and CBP. Here, we examined the effects that different ERalpha ligands have on coactivator protein steady-state levels and demonstrate that the selective ER modulators (SERMs) 4-hydroxytamoxifen (4HT) and raloxifene are able to elevate SRC-1 and SRC-3 protein levels. Using the HeLa cell line, we show that this effect is ERalpha dependent. Consistent with the observed increase in coactivator protein levels, we were also able to observe an increase in the transcriptional activity of other nuclear receptors in SERM-treated cells. Information presented here demonstrates an unexpected consequence of SERM treatment, which could help further define the complex tissue responses to 4HT and raloxifene, and suggests that these ligands can have a broad biological action, stimulating the transcriptional activity of other nuclear receptors.

evista usual dosage NCT00967824

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Female Wistar rats were OVX or subjected to sham surgery and received vehicle or RLX by gavage for 90 days. The treatment groups were as follows: sham surgery and treated with vehicle (SHAM-veh), OVX and treated with vehicle (OVX-veh), and OVX and treated with RLX (OVX-RLX). During treatment, the pulp of lower first molar was exposed to the oral environment for induction of periapical lesion that was analyzed 7 or 30 days after procedure. Blood samples were taken from jugular vein for measurement of estradiol, and the mandibles were removed and prepared for radiographic, histopathologic, histometric, and immunohistochemical analysis.

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The primary endpoint in MORE was incidence of vertebral fracture, and the difference between the raloxifene and placebo groups for this endpoint widened during 4 years of therapy, with the relative risk reduction during the fourth year of the study being similar to the relative risk reduction during years 0 to 3 of the study. Continued raloxifene treatment is necessary to preserve bone mineral density (BMD). In MORE, raloxifene lowered markers of bone turnover to a premenopausal reference interval. Biopsies from three patients treated with raloxifene for 8 years showed normal bone and bone cells and double label in all specimens. Invasive breast cancer risk is a clinical consideration in postmenopausal women with osteoporosis, and invasive breast cancer risk reduction was the primary endpoint in CORE. In MORE and CORE, the benefit of raloxifene versus placebo in incidence of invasive breast cancer increased with greater duration of therapy up to 8 years.

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Effect of ormeloxifene, a multifunctional selective estrogen receptor modulator, on prevention of ovariectomy-induced bone resorption in retired breeder female rats, osteoclastogenesis using bone marrow cells from adult Balb/c mice cultured in presence of M-CSF and RANKL, osteoclast apoptosis using terminal deoxynucleotidyl transferase fragment end labeling and TGF beta-3 expression were investigated. Raloxifene, a benzothiophene reported to mimic effects of estrogen in bone, and estradiol were used for comparison. Ormeloxifene (10(-6) and 10(-8)M) significantly inhibited osteoclastogenesis (P<0.001 versus vehicle control) as evidenced by lower number of TRAP-positive osteoclasts in bone marrow cultures and caused apoptosis of osteoclasts. The effect was almost equivalent to that observed in presence of estradiol-17 beta, except that significant number of cells undergoing apoptosis was evident even at 10(-9)M concentration of estradiol-17 beta (P<0.001). Raloxifene, though inhibited osteoclastogenesis at much lower concentrations (10(-8) to 10(-12)M; P<0.001), failed to cause apoptosis of osteoclasts at any of the concentrations used. While ormeloxifene, raloxifene and ethynylestradiol significantly prevented ovariectomy-induced bone loss in vivo in retired breeder female rats, prevention of ovariectomy-induced decrease in BMD and trabecular network of proximal tibia, calcium and phosphorus levels in femur and tibia and prevention of ovariectomy-induced down-regulation of TGF beta-3 expression in lumbar vertebrae was of lower order in raloxifene- than ormeloxifene- or ethynylestradiol-supplemented females. Both the SERMs, however, produced considerable estrogenic effects at the uterine level as evidenced by increase in weight, total and endometrial area and luminal epithelial cell height; the effect being generally greater in raloxifene- than ormeloxifene-treated rats. Findings demonstrate that inhibition of estrogen-deficiency osteoporosis by ormeloxifene, as in case of estradiol, was mediated via inhibition of osteoclastogenesis, apoptosis of osteoclasts and up-regulation of TGF beta-3 expression. Raloxifene, though effective in inhibiting osteoclastogenesis in vitro at much lower concentrations, was not only less potent in preventing ovariectomy-induced bone loss in retired breeder female rats in vivo but also appeared to have a different mechanism of action than ormeloxifene and estradiol.

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Raloxifene reduces myocardial infarct size and the incidence of ventricular fibrillations by NO- and the opening of KCa channels-dependent mechanisms in canine hearts.

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Our results suggest that tamoxifen has more of an estrogenic effect on the gynecologic reproductive organs. These effects should be considered in counseling women on options for breast cancer prevention.

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Given raloxifene's mechanism of action and the preclinical evidence for its role in breast cancer prevention, a clinically favorable effect seems feasible. Results of ongoing clinical studies will provide evidence to support or refute the clinical findings of MORE and thus raloxifene's role in the breast cancer prevention.

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Large bladders with urinary retention developed in ERαWT and ERβWT litter mates treated with testosterone plus 17β-estradiol but such bladders did not develop in ERαKO mice treated with testosterone plus 17β-estradiol. ERβKO mice treated with testosterone plus 17β-estradiol had large bladders with urinary retention and increased bladder mass. Cotreatment with the estrogen receptor-α antagonist raloxifene resulted in decreased bladder mass compared to that in wild-type mice treated with testosterone plus 17β-estradiol. Bladders in mice treated with the estrogen receptor-β antagonist R,R-THC were similar to those in testosterone plus 17β-estradiol treated mice.

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Laparoscopic excision of lesions, including recording of lesion characteristics and surgical impression of the lesions.

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Raloxifene is approved for the treatment and prevention of postmenopausal osteoporosis. Previous studies have described a raloxifene-associated increase in hot flushes, reported as adverse events. This study was undertaken to provide a detailed evaluation of the potential of raloxifene to induce or exacerbate hot flushes in postmenopausal women.

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This article reviews lasofoxifene, a new-generation selective estrogen receptor modulator (SERM) that is currently in Phase III development for the prevention and treatment of osteoporosis in postmenopausal women. This compound selectively binds to both of the estrogen receptors with a high affinity and a median inhibitory concentration that is similar to that seen with estradiol and > or = 10-fold higher than those reported for other SERMs (raloxifene and tamoxifen). Lasofoxifene has a remarkably improved oral bioavailability with respect to other SERMs due to increased resistance to intestinal wall glucuronidation. In both preclinical and short-term studies, the compound showed a favourable safety profile and demonstrated a proven efficacy in preventing bone loss and lowering cholesterol levels. Dose modelling from Phase II studies allowed the selection of lasofoxifene 0.25 mg/day as the lowest fully effective dose.

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Experimental animal model.

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The risk of vertebral fractures was lower in women treated with raloxifene, regardless of prior HT use, but there was a suggestion that the effect was greater in women who had used HT. Women randomized to receive raloxifene exhibited a decreased incidence of invasive breast cancer, compared with women receiving placebo. No change occurred in the incidence of cardiovascular events, regardless of prior HT use.

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Overall, raloxifene use was associated with an increased VTE risk (HR 1.44, 95% CI 1.06-1.95) vs. placebo. Most women (72%) reported using aspirin, and 14.2% reported using nonaspirin antiplatelet agents during the study period. Users of antiplatelet agents were older, more likely to have CHD, and more likely to be hyperlipidemic. They had a higher VTE risk than nonusers. No difference in VTE risk was observed in women who used raloxifene alone vs. those who used raloxifene with antiplatelet agents during the study. The increase in VTE risk with raloxifene compared with placebo was not different between women who used antiplatelet agents at baseline (HR 1.44, 95% CI 0.98, 2.10) and those who did not use antiplatelet agents (HR 1.37, 95% CI 0.83, 2.27) (interaction p = 0.88). Similar conclusions were noted for aspirin and nonaspirin antiplatelet use.

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Cell culture for different incubation times.

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Ten healthy postmenopausal women and ten healthy men were randomized to 2-wk sequential treatment with tamoxifen (10 and 20 mg/d) and raloxifene (60 and 120 mg/d) with a washout of 2 wk between treatments.

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The UDP glucuronosyltransferase (UGT) 1A gene cluster encodes nine UGT1A family members via splicing of individual first exons to common exons 2 through 5. Each of these nine UGT1As can also undergo alternative splicing at their 3' ends by using an alternate exon 5, resulting in 27 different UGT1A mRNA species with each UGT1A gene encoding three different combinations of 5A and 5B UGT1A exons. To examine the importance of UGT1A exon 5 splice variants on overall UGT1A activity, a nested quantitative polymerase chain reaction assay was developed to accurately assess the combined expression of exon 5 splice variants (termed v2/v3) versus the expression of wild-type (termed v1) for each specific UGT1A. v1 expression was 16-, 17-, 57- and 29-fold higher than that observed for the levels of v2/v3 for UGTs 1A1, 1A4, 1A6, and 1A9, respectively, in normal human liver specimens. In a series of 58 normal human liver specimens, the expression of both UGT1A1 v1 and v2/v3 mRNAs was positively correlated with raloxifene glucuronidation activity in corresponding microsomes prepared from the same specimens (p < 0.0001, r² = 0.720; p = 0.0002, r² = 0.241, respectively), with expression of both variants lower in individuals homozygous for the UGT1A1*28 allele (42% for v1, p = 0.041; 53% for v2/v3, p = 0.0075). The expression of UGT1A1 v2/v3 was 1.6-fold higher than v1 (p = 0.03) in HepG2 cells, and short interfering RNA knockdown of HepG2 v2/v3 increased raloxifene glucuronidation activity by 83%. Together, these data suggest that hepatic UGT1A v2/v3 mRNA species are minor form variants in human livers from most individuals.

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Compared with continuous combined hormone replacement therapy, 6 and 12 months of raloxifene treatment do not lead to vaginal bleeding/spotting, are not associated with increased endometrial thickness or uterine volume and result in a significantly lower rate of early treatment discontinuations in asymptomatic women receiving treatment to prevent long term postmenopausal health risks.

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For the Continuing Outcomes Relevant to Evista (CORE) study population (n = 3,991; excluding women ≥86 y of age or with a history of ductal carcinoma in situ or lobular carcinoma in situ), the prevalence of risk factors to the overall IBC risk was calculated. To evaluate buy evista IBC incidence rates, the placebo arm of the CORE trial (n = 1,275) was pooled with the placebo arm of the Raloxifene Use for the Heart trial (n = 5,047; total of 6,322 women).

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Osteoporosis is a highly prevalent condition, characterized by compromised bone strength and fragility fractures and with an important associated socio-economic burden. Bisphosphonates are well established as the first line treatment for osteoporosis. However, while randomized control trials have in general demonstrated reasonable anti-fracture efficacy at the spine, they have shown moderate reduction in fracture incidence for non-vertebral sites. Furthermore, oral bisphosphonates are commonly associated with adverse gastrointestinal effects and both oral and parenteral bisphosphonates have been linked with osteonecrosis of the jaw and atypical femoral fracture, two rare but debilitating side effects. In addition, bisphosphonates are not recommended in patients with GFR <35 ml/min/1.73 m(2). Hence, there is a clear requirement for newer agents, which are able to reduce fracture risk further, whilst overcoming the limitations of bisphosphonates. Over the past 20 years, knowledge and a deeper understanding of the various signalling pathways involved in bone remodelling has increased, enabling identification of additional targets for therapy. This review focuses on these newer therapies and includes anti-resorptive agents such as raloxifene and other selective oestrogen receptor modulators, the monoclonal antibody denosumab (which inhibits the RANKL pathway), odanacatib, a cathepsin K inhibitor and the anabolic agents, PTH analogue; PTH (1-34) and anti-sclerostin antibodies (activator of the Wnt pathway). Strontium ranelate will not be reviewed as recent reports highlight concerns surrounding its cardiovascular safety and together with an apparent increased risk of thrombosis, its future use remains uncertain. Some of these agents such as raloxifene, denosumab and teriparatide are already in clinical use whilst others are at varying stages of development. This review will provide an overview of the mechanisms of action of these therapeutic agents on the skeleton and assess their efficacy in osteoporosis buy evista and fracture prevention.

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The Study of Tamoxifen and Raloxifene (STAR) demonstrated that raloxifene was as effective as tamoxifen in reducing the risk of invasive breast cancer (IBC) in postmenopausal women and had lower risks of thromboembolic events, endometrial cancer, and cataracts but had a nonstatistically significant higher risk of noninvasive breast cancer. There is a need Trileptal Drug Rash to summarize the risks and benefits of these agents.

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Several meta-analyses confirm that physical exercise can slow down postmenopausal bone loss, but it is not clear whether physical exercise alone can increase bone mass Cleocin Pill . Our intent was to evaluate high-impact exercises (including jumping) and combined balance and leg-strength training, with and without raloxifene treatment, in three healthy elderly women, age 68-71 years. The 40-week study period consisted of two 17-week exercise periods with a 6-week rest period in between. The jumping exercises were performed both vertically and in different directions. Effects were measured in bone mineral density (BMD), balance, maximal gait speed, and leg extensor strength. BMD (g/cm(2)) was measured with dual-energy X-ray photon absorptiometry (DXA) at the proximal femur, lumbar spine, and total body. After the first exercise period, large losses of trochanteric BMD (8.1%-10.8%) were seen in all subjects. After both 6 weeks of rest and the second exercise period, which included both exercise and raloxifene, BMD increased in all subjects. During both exercise periods, the balance, gait speed, and leg extensor strength increased in all subjects. The results show that this kind of high-impact exercise had limited effects on BMD, but had large positive effects on balance, gait speed, and leg extensor strength. In conclusion, high-impact exercise in elderly women improves their fall risk factors, but, at least without raloxifene treatment, the trochanteric fracture risk might even increase because of reduction in the regional bone mass.

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A rapid, sensitive and selective method for the determination of raloxifene hydrochloride (RLX) in pure drug and in tablets was developed using gradient high performance liquid chromatography (HPLC). The devised method involved separation of RLX on a reversed phase Hypersil ODS column and determination with UV detection at 284 nm. The standard curve was linear (R = 0.999) over the concentration range of 50-600 microg mL-1 with a detection limit of 0.04 microg mL-1 and a quantification limit of 0.16 microg mL-1. Intra-day and inter-day precision and accuracy of the method were established according to the current ICH guidelines. Intra-day RSD values at three QC levels (250, 450 and 550 microg mL-1) were 0.2-0.5%, based on the peak area. The intra-day relative error (er) Singulair 10 Mg Cost was between 0.2 and 0.5%. The developed method was successfully applied to the determination of RLX in tablets and the results were statistically compared with those obtained by a literature method. Accuracy, evaluated by means of the spike recovery method, was the excellent with percent recovery in the range 97.7-103.2 with precision in the range 1.6-2.2%. No interference was observed from the co-formulated substances. The method was economical in terms of the time taken and the amount of solvent used.

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To evaluate the relationship between bone mass and risk of breast cancer and to determine the effect Cleocin 300 Mg Dose of raloxifene therapy on breast cancer incidence in women categorized by bone mass into low bone mass and osteoporosis subgroups.

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The aim of this study was to investigate the effects of 17β-estradiol (E2), the selective ERα agonist 16α-LE2, and the selective estrogen receptor modulator (SERM) raloxifene on remodeling processes during the development of myocardial hypertrophy (MH) in a mouse model of pressure overload. Myocardial hypertrophy in ovariectomized female C57Bl/6J mice was induced by transverse aortic constriction (TAC). Two weeks after TAC, placebo treated mice developed left ventricular hypertrophy and mild systolic dysfunction. Estrogen treatment, but not 16α-LE2 or raloxifene reduced TAC induced MH compared to placebo. E2, 16α-LE2 and raloxifene supported maintenance of cardiac function in comparison with placebo. Nine weeks after induction of pressure overload, Norvasc Drug Classification MH was present in all TAC groups, most pronounced in the raloxifene treated group. Ejection fraction (EF) was decreased in all animals. However, 16α-LE2 treated animals showed a smaller reduction of EF than animals treated with placebo. E2 and 16α-LE2, but not raloxifene diminished the development of fibrosis and reduced the TGFβ and CTGF gene expression. Treatment with E2 or 16α-LE2 but not with raloxifene reduced survival rate after TAC significantly in comparison with placebo treatment. In conclusion, E2 and 16α-LE2 slowed down the progression of MH and reduced systolic dysfunction after nine weeks of pressure overload. Raloxifene did not reduce MH but improved cardiac function two weeks after TAC. However, raloxifene was not able to maintain EF in the long term period.

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In RUTH, postmenopausal women treated with raloxifene had an increased risk of VTE Flagyl Pediatric Dose compared with placebo. Concomitant use of aspirin or nonaspirin antiplatelet agents along with raloxifene did not change VTE risk.

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Between January and August 2000, 75 Italian osteoporotic women were enrolled and treated with raloxifene at a dose of 60 mg/day. At entry and after 1 year of treatment, lumbar bone mineral density (BMD), serum osteocalcin (OC) and urinary creatinine-corrected free deoxypyridinoline (DPD) levels were evaluated. DNA was extracted from Duphaston Tab Indication blood and analysed with restriction endonuclease BsmI for VDR gene.

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Raloxifene hydrochloride therapy reduces the risk Valtrex Generic Cost With Insurance for vertebral fractures at 3 years, but the effects on clinical vertebral fractures in the first year are not known.

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Human ER-negative MDA-MB231 breast cancer cells were treated with different doses of Levitra Online Canada Tam and Ral. Gln uptake was monitored by using [(3)H]Gln assay. The effect of Tam and Ral on Gln transporter ASCT2 expression, glutathione (GSH) levels and cellular proliferation was determined.

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Single doses of warfarin (20 mg) were administered prior to and during 2 weeks of dosing with raloxifene 120 mg/day. Each Propecia Generic Online warfarin dose was followed by pharmacokinetic sampling and prothrombin time measurements.

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Before treatment, endometrial thickness was 3.38 +/- 0.73 mm, and similar values were observed after 1, 3 and 6 months of treatment (3. Asacol Foam Enema Dose 04 +/- 0.82; 3.3 +/- 0.83; and 3.37 +/- 0.79, respectively) (P > 0.05). No significant differences in uterine volume were observed between the pre- and post-treatment periods. Uterine artery perfusion as indicated by RI and PI measured by Doppler also showed no significant variation, with a high impedance flow being maintained throughout treatment.

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Oestrogens are involved in the growth, development and homeostasis of a number of tissues. The physiological effects of these steroids are mediated by a ligand-inducible nuclear transcription factor, the oestrogen receptor (ER). Hormone binding to the ligand-binding domain (LBD) of the ER initiates a series of molecular events culminating in the activation or repression of target genes. Transcriptional regulation arises from the direct interaction of the ER with components of the cellular transcription machinery. Here we report the crystal structures of the LBD of ER in complex with the endogenous oestrogen, 17beta-oestradiol, and the selective antagonist raloxifene, at resolutions of 3.1 and 2.6 A, respectively. The structures provide a molecular basis for the distinctive pharmacophore of the ER and its catholic binding properties. Agonist and antagonist bind at the same site within the core of the LBD but demonstrate different binding modes. In addition, each class of ligand induces a distinct conformation in the transactivation domain of the LBD, providing Levaquin 250 Mg Iv structural evidence of the mechanism of antagonism.

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No significant differences existed between the tamoxifen and raloxifene groups in patient-reported outcomes for physical health, mental health, and depression, although the tamoxifen group reported better sexual function. Although mean symptom severity was low among these postmenopausal women, those in the tamoxifen group reported more gynecological problems, vasomotor symptoms, leg cramps, and bladder control problems, whereas women in the raloxifene group reported more musculoskeletal problems, dyspareunia, and weight gain Paracetamol Tablets Ip 500mg Uses .

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Participants were a subset of English-speaking women (n = 3798, mean age 66.7 yrs) from the Multiple Outcomes of Raloxifene Evaluation trial, who had low bone mineral density (BMD) and/or prevalent vertebral fractures. Vertebral fractures were measured at baseline by radiography using a semiquantitative technique. Depressive symptoms were assessed at baseline using the Geriatric Depression Scale (GDS), a valid and reliable Tegretol Reviews Bipolar Disorder scale for depression screening in elderly patients. Women were considered as probably depressed if > or = 6 symptoms of depression were reported.

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Prior studies have indicated an excess risk of gastroduodenal ulcers and esophagus perforations with the use of bisphosphonates. However, little is known about the contribution of comorbid conditions and concomitant drug use on this risk. We studied the risk of esophagus and gastric events in patients on a wide range of drugs against osteoporosis both before and after initiation of these drugs. We studied a nationwide register-based cohort from Denmark with all users of drugs against osteoporosis between 1996 and 2006 (n = 103,562) as cases and three age- and sex-matched controls from the general population (n = 310,683). In a crude analysis, most drugs were already associated with an increased risk of esophagitis, esophageal ulcerations, or esophageal perforations or gastroduodenal ulcers before initiation of the drugs. Upon adjustment, this excess risk disappeared for most drugs except parathyroid hormone and its analogues, etidronate and clodronate. Only for etidronate, alendronate, and raloxifene were sufficient data present for events after initiation of the drugs, and for these, an increased risk was present for all events except gastroduodenal ulcers with raloxifene. Several drugs against osteoporosis are associated with an increased risk of esophagitis, esophageal ulcers, esophageal perforation, and gastroduodenal ulcers. However, the increase was already present before initiation of the drug for several types of drugs against osteoporosis. This points at an effect of the underlying condition being treated or comorbid conditions and drugs being provided in patients with osteoporosis, such as nonsteroidal anti-inflammatory drugs and corticosteroids.

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The study was double-blinded, with a placebo run-in period of 28 to 50 days. Twenty-eight women received either 17beta-estradiol 2 mg + norethisterone acetate 1 mg (E2/NETA) or raloxifene HCL 60 mg for a period of 6 months. Total and active forms of MMP-2 and -9 were estimated at baseline and at month 6.

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The treatment of osteoporosis among postmenopausal women represents a major public health challenge since long-term therapy is needed to prevent fractures and chronic disability.

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The Multiple Outcomes of Raloxifene Evaluation trial included postmenopausal women with osteoporosis randomized to placebo, raloxifene 60 mg/day, or raloxifene 120 mg/day for 4 years. The protocol specified subgroups based on whether or not patients had a vertebral fracture at baseline. Absolute differences between placebo and raloxifene 60 mg/day (the approved dose) for endpoints in these groups were defined as the incidence in the raloxifene group minus the incidence in the placebo group.

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Twenty-four healthy postmenopausal women (six women in four groups) were randomly allocated to conventional-dose 17β-estradiol/norethisterone acetate (NETA), low-dose 17β-estradiol/NETA, tibolone, or raloxifene hydrochloride. RNA was isolated from whole blood before and after 6weeks of treatment. The changes in mRNA were assessed with a microarray chip.

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Participants were randomly assigned to receive 60 mg/d or 120 mg/d of raloxifene (n = 4843) or matching placebo (n = 2447) for 4 years.

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Tissue-specific estrogen agonists may be useful in protecting against osteoporosis and the increased risk of coronary heart disease in postmenopausal women with minimal undesired effects on reproductive tissues. The actions of the mixed estrogen agonist/antagonist raloxifene on selected estrogen target tissues were determined in ovariectomized (OVX) rats immediately postovariectomy. Five groups of 75-day-old Sprague-Dawley rats were studied; baseline controls, sham-operated controls, OVX controls, OVX animals treated with estrogen (0.1 mg 17 alpha-ethynyl estradiol/, and OVX animals treated with raloxifene (3 mg/ Fluorochrome labels were given on days 1, 28, and 34. The baseline controls were killed on day 2, and the remaining groups on day 35. Ovariectomy increased tibial longitudinal growth rate as well as measurements related to radial growth and cancellous bone turnover. Ovariectomy decreased cancellous bone area and uterine weight, and increased serum cholesterol, bone elongation, and radial bone growth. Estrogen treatment prevented these changes in OVX rats. Raloxifene prevented cancellous osteopenia as well as the changes in radial bone growth, bone resorption, and blood cholesterol, but was less effective in reducing cancellous bone formation and did not prevent uterine atrophy. These findings suggest that raloxifene is a target-specific, mixed estrogen agonist/antagonist. At the concentration studied, raloxifene had potent estrogenic activity on bone resorption and serum cholesterol, a lesser effect on bone formation, and minimal activity on uterine wet weight.

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Among 956 women who were interviewed an average of 7 months after treatment initiation, 334 were taking hormone therapy, and 88 (26%) had discontinued; 256 were taking raloxifene, and 48 (19%) had discontinued (P = 0.03 vs. hormone therapy); and 366 were taking alendronate, and 70(19%) had discontinued (P = 0.02 vs. hormone therapy). Women with bothersome side effects (somewhat bothered: odds ratio [OR] = 4.0; 95% confidence interval [CI]: 2.5 to 6.5; very or extremely bothered: OR = 25; 95% CI: 16 to 39) or who thought that their bone density test results did not show osteoporosis (OR = 1.6; 95% CI: 1.0 to 2.5) were more likely to discontinue therapy, as compared with women reporting regular exercise (OR = 0.7; 95% CI: 0.4 to 1.0) or a willingness to take prescribed medications (OR = 0.6; 95% CI: 0.4 to 0.9). After adjustment for side effects and patient characteristics, the odds of early treatment discontinuation did not differ significantly among treatments.

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Two simple and sensitive spectrophotometric methods are described for the determination of raloxifene hydrochloride (RLX) in pure form and in tablets. The first method (method A) is based on the formation of a yellowish-brown chromogen peaking at 430 nm when RLX was reacted with permanganate in acetic acid medium. In the second method (method B), RLX was reacted with a measured excess of permanganate in H2SO4 medium followed by the spectrophotometric measurement of the unreacted KMnO4 at 550 nm. Under the optimized experimental conditions, Beer's law is obeyed in the concentration range 0.6-6.0 and 1.5-15.0 microg mL(-1) with molar absorptivity of 7.01 x 10(4) and 2.8 x 10(4) L mol(-1) cm(-1) for method A and method B, respectively. The limits of detection (LOD) and quantification (LOQ) have also been reported. The intra-day and inter-day RSD and RE values at three different concentrations were assessed. The proposed methods were applied to the commercially available tablets, and the results were statistically compared with those of the reference method. The accuracy and reliability of the methods were further ascertained by recovery studies.

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Selective estrogen receptor modulators (SERMs) inhibit constriction of mammalian conduit arteries. However, it is unknown whether SERMs at therapeutically achievable concentrations could reduce vascular tone in resistance arteries. The present study aimed to examine roles of Ca(2+) influx in endothelium and endothelial nitric oxide synthase (eNOS) activation in dilatations induced by raloxifene, a second-generation SERM in myogenically active arteries.

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The poor prognosis of patients with triple-negative breast cancer (TNBC) and the lack of targeted treatments have raised the need for alternative therapies. Previous studies have suggested an effect of raloxifene, a selective estrogen receptor modulator that is independent of the estrogen receptor (ER). Therefore, we assessed the therapeutic value of raloxifene in TNBC mouse models. Mice received a daily oral treatment with different doses of raloxifene. Tumor progression was monitored weekly; in addition microvessel density, proliferation, migration and invasion, apoptosis and tumorigenicity were analyzed. This study demonstrates that raloxifene (0.85 mg/kg) prevents TNBC tumor growth and induces tumor regression. The treated tumors showed a 54% decreased microvascular density and proliferation and a 7-fold increase in apoptosis. The underlying therapeutic mechanism of raloxifene was associated with a 27-fold decrease in the expression of the epidermal growth factor receptor (EGFR). Moreover, raloxifene promoted the translocation of EGFR into endosomes associated with decreased cell migration, cell invasion and tumorigenicity in vitro. Together, these data showed that raloxifene acts independently of the ER and may be relevant for the treatment as well as control the progression of TNBC.