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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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Estrogen 17beta-estradiol (E2) rapidly modulates several signaling pathways related to cell growth, preservation, and differentiation. The physiological role of these nongenomic effects with regard to downstream outcomes, and the relationship with transcriptional estrogen activity are unclear. Furthermore, the ability of selective estrogen receptor modulators (SERMs) to trigger nongenomic actions is largely unknown. To determine whether estrogen receptor (ER) ligands exert nongenomic activity in endometrial adenocarcinoma cells, and whether this activity affects transcription and DNA synthesis, we challenged human Ishikawa cells with E2 or partial ER agonists 4-hydroxytamoxifen (OHT) and raloxifene (ral). Serum-starved Ishikawa cells exposed for 5 min to 0.1 nM E2 showed induced phosphorylation of MAPK (ERK1/2). Ral and 4-OHT each at 1 nM also stimulated ERK in a rapid transient manner. E2 and 4-OHT induced proto-oncogene c-fos mRNA expression in Ishikawa cells within 30 min, but ral had no effect. In contrast to nongenomic action, only E2 stimulated expression of an estrogen response element (ERE)-driven luciferase (LUC) reporter gene. To examine DNA synthesis, [(3)H]-thymidine incorporation was measured in serum-starved cultures exposed to E2 or partial agonists for 2 d. E2 at 1 nM stimulated thymidine uptake in an ERK-dependent manner, but 1 nM 4-OHT, 1 nM ral, and 0.1-nM concentrations of E2 had no significant effects. Taken together, these data indicate that both nongenomic and direct transcriptional ER effects are likely required to promote DNA synthesis.

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GPR30 is required for the proliferation of hFOB cells induced by estradiol or raloxifene. This proliferative effect was at least partly mediated via MAP kinase activation. These findings revealed a novel function of GPR30 in osteoblasts and might lead to a better understanding of how estrogen and selective estrogen receptor modulators show their osteoprotective effects.

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175 bone biopsies of male and female osteoporotic patients (WHO criteria) were histologically classified in high- and low-turnover osteoporosis and associated with bone marker levels in serum and urine. Patients with any osteotropic therapy and with fractures were excluded.

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Recent genetic studies have identified common variation in susceptibility loci that stratify lifetime risks of breast cancer and may inform prevention and screening strategies. However, whether these loci have similar implications for women treated with tamoxifen or raloxifene (SERMs) is unknown. We conducted a matched case-control study of 592 cases who developed breast cancer and 1,171 unaffected women from 32,859 participants on SERM therapy enrolled on NSABP P-1 and P-2 breast cancer prevention trials. We formed a quantitative polygenic risk score (PRS) using genotypes of 75 breast cancer-associated single nucleotide polymorphisms and examined the PRS as a risk factor for breast cancer among women treated with SERMs. The PRS ranged from 3.98 to 7.74, with a one-unit change associated with a 42 % increase in breast cancer (OR = 1.42; P = 0.0002). The PRS had a stronger association with breast cancer among high-risk women with no first-degree family history (OR = 1.62) compared to those with a positive family history (OR = 1.32) (P intx = 0.04). There was also suggestion that PRS was a stronger risk factor for ER-positive (OR = 1.59, P = 0.0002) than ER-negative (OR = 1.05, P = 0.84) breast cancer (P intx = 0.10). Associations did not differ by tamoxifen or raloxifene treatment, age at trial entry, 5-year predicted Gail model risk or other clinical variables. The PRS is a strong risk factor for ER-positive breast cancer in moderate to high-risk individuals treated with either tamoxifen or raloxifene for cancer prevention. These data suggest that common genetic variation informs risk of breast cancer in women receiving SERMs.

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In summary, GH secretion was blunted by tamoxifen in women in the face of reduced IGF-I feedback inhibition but not in men in whom the gonadal axis was stimulated. We conclude that potential blunting of GH secretion in men by SERMs was counteracted by concomitant central stimulation of GH secretion by testosterone. In therapeutic doses, tamoxifen may induce detrimental metabolic effects in women, but not men.

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Recent studies documented that estrogen have antioxidant properties in-vitro, there are conflicting results on the effect of estrogen in vivo. We aimed to investigate the effects of estradiol and Raloxifene on the antioxidant enzyme [superoxide dismutase (SOD) and catalase (CAT)] activities and MDA levels in brain and liver homogenates of ovariectomized female rats. Twelve weeks after ovariectomy, female Sprague-Dawley rats (n = 26) were divided into three groups: (1) Ovariectomized placebo group (n = 6) was given physiologic saline. (2) Estrogen group (n = 10) was given Ethynyl estradiol, 0.1 mg/kg sc. (3) Raloxifene group (n = 10) was given raloxifene, 1 mg/kg sc during 8 weeks. Ten rats were used as naive controls without any treatment (Sham operated group, n = 10). Ovariectomy lead to an increase in the CAT activities in liver tissue samples compared to the sham group (p = 0.056, Mann-Whitney test). While estrogen treatment reversed to normal levels of CAT activities, raloxifene remained as ineffective. Superoxide dismutase activities and MDA levels in liver were remained unchanged in all groups. There was no significant change in the brain tissue SOD and CAT activities between the control ovariectomy, estrogen treated, and raloxifen treated groups. We determined an increase in MDA levels in brain of ovariectmised rat (p = 0.02). While raloxifene treatment reversed to normal levels of MDA (p = estrogen treatment failed. Our data showed that estrogen may play a role in regulation of CAT and SOD activities in liver due to its antioxidative effects. We can suggest estrogen and raloxifene exert their antioxidative effects in brain rather than liver. Since Raloxifene's effect is more clear than estradiol, raloxifene may be suggested primarily for treatment and/or prevention of diseases which can be resulted from oxidative stress in postmenopausal women.

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A total of 506 patients were included in the post hoc analysis. Both raloxifene monotherapy (RLX, n = 354) and active vitamin D3 cotreatment (COMBI, n = 152) significantly improved QOL and reduced pain from the baseline at Week 8 and Week 24. The COMBI group had significantly greater improvements in JOQOL total score and activity of daily living (total) domain at Week 24 and last observation carried forward (LOCF) than the RLX group. The COMBI group also had significantly greater improvements in SF-8 domains of general health (at Week 8, Week 24, and LOCF), role physical (at Week 24 and LOCF), and mental health (at LOCF) than the RLX group. The COMBI group also had significantly greater reduction in VAS pain at LOCF than the RLX group (mean [SD]: RLX = -0.99 [2.72], COMBI = -1.54 [2.21], P = 0.042).

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This study describes the inhibitory effect of 5 alpha-dihydrotestosterone (5 alpha-DHT) and its precursors testosterone (T) and androst-4-ene-3,17-dione (delta 4-DIONE) on the growth of the estrogen-sensitive human breast cancer cell line ZR-75-1. In the absence of estrogens, cell proliferation measured after a 12-day incubation period was 50-60% inhibited by maximal concentrations of 5 alpha-DHT, T, or delta 4-DIONE with half-maximal effects (IC50 values) observed at 0.10, 0.15 and 15 nM, respectively. This growth inhibition by androgens was due to an increase in generation time and a lowering of the saturation density of cell cultures. The antiestrogen LY156758 (300 nM) induced 25-30% inhibition of basal cell growth, its effect being additive to that of 5 alpha-DHT. The mitogenic effect of 1 nM estradiol (E2) was completely inhibited by increasing concentrations of 5 alpha-DHT with a potency (IC50 = 0.10 nM) similar to that measured when the androgen was used alone. E2 had a more rapid effect on cell proliferation than 5 alpha-DHT, the latter requiring at least 5 to 6 days to exert significant growth inhibition. As found in the absence of estrogens, maximal inhibition of cell proliferation in the presence of E2 was achieved by the combination of the antiestrogen and 5 alpha-DHT. Supraphysiological concentrations of E2 (up to 1 microM) were needed to completely reverse the growth inhibitory effect of a submaximal concentration of 5 alpha-DHT (1 nM). The antiproliferative effect of androgens was competitively reversed by the antiandrogen hydroxyflutamide, thus indicating an androgen receptor-mediated mechanism. The present data suggest the potential benefits of an androgen-antiestrogen combination therapy in the endocrine management of breast cancer.

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Inflammatory responses of mouse N9 microglial cells and rat primary hippocampal microglia to lipopolysaccharide (LPS) exposure were recorded by the secretion of nitric oxide (NO) and cytokine IL-6 in two models where SERM was added either 24 h before LPS addition or simultaneously or even after the LPS exposure. The responses of 17beta-estradiol, tamoxifen, raloxifene and ICI 182.780 were compared. Responses were recorded by ELISA, Northern and EMSA assays.

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Raloxifene is a selective oestrogen receptor modulator used clinically for the treatment and the prevention of osteoporosis in postmenopausal women. The drug has been evaluated in the Study of Tamoxifen and Raloxifene as an agent to reduce breast cancer incidence in postmenopausal women at high risk. However, about 30% of women who develop breast cancer do so in their premenopausal years. In this pilot study, salivary oestradiol and progesterone were determined throughout the menstrual cycle for a total of 22 subjects, 14 of whom completed pre- and postraloxifene (60 mg daily) salivary collections. The mean concentration of oestradiol during the menstrual cycle when subjects were taking raloxifene was significantly greater (P<0.001) than during baseline cycles. Neither salivary progesterone and cortisol nor menstrual cycle length were affected by raloxifene treatment. These data demonstrate that raloxifene administered to premenopausal women increases the concentration of oestradiol that diffuses into the salivary glands, and which presumably represents the concentration available to other organs as well. The results reflect increases in serum oestradiol reported earlier.

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Estrogens and selective estrogen receptor modulators (SERMs) interact with estrogen receptor (ER) alpha and beta to activate or repress gene transcription. To understand how estrogens and SERMs exert tissue-specific effects, we performed microarray analysis to determine whether ERalpha or ERbeta regulate different target genes in response to estrogens and SERMs. We prepared human U2OS osteosarcoma cells that are stably transfected with a tetracycline-inducible vector to express ERalpha or ERbeta. Western blotting, immunohistochemistry, and immunoprecipitation studies confirmed that U2OS-ERalpha cells synthesized only ERalpha and that U2OS-ERbeta cells expressed exclusively ERbeta. U2OS-ERalpha and U2OS-ERbeta cells were treated either with 17beta-estradiol (E2), raloxifene, and tamoxifen for 18 h. Labeled cRNAs were hybridized with U95Av2 GeneChips (Affymetrix). A total of 228, 190, and 236 genes were significantly activated or repressed at least 1.74-fold in U2OS-ERalpha and U2OS-ERbeta cells by E2, raloxifene, and tamoxifen, respectively. Most genes regulated in ERalpha cells in response to E2, raloxifene, and tamoxifen were distinct from those regulated in ERbeta cells. Only 38 of the 228 (17%) genes were regulated by E2 in both U2OS-ERalpha and U2OS-ERbeta cells. Raloxifene and tamoxifen regulated only 27% of the same genes in both the ERalpha and ERbeta cells. A subset of genes involved in bone-related activities regulated by E2, raloxifene, and tamoxifen were also distinct. Our results demonstrate that most genes regulated by ERalpha are distinct from those regulated by ERbeta in response to E2 and SERMs. These results indicate that estrogens and SERMs exert tissue-specific effects by regulating unique sets of targets genes through ERalpha and ERbeta

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PATIENTS were classified into the alendronate, calcitonin, or raloxifene group according to exposure after follow-up.

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We divided New Zealand white rabbits into six groups (n = 6 per group): baseline control, sham operation, sham + 1% Met diet, ovariectomy (OVX), 1% Met diet + OVX, OVX + RLX (10 mg/kg/day), and 1% Met diet + OVX + RLX. RLX was administered for 16 weeks. We measured the amount of enzymatic immature and mature pyridinium cross-links and the nonenzymatic cross-link, Pen, and correlated the cross-link content to bone strength.

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IGF-I suppression in acromegaly obtained by tamoxifen, a selective estrogen receptor modulator (SERM), prompted us to evaluate the effects of the administration of a newer SERM, raloxifene (RAL), devoid of estrogenic activity at uterine level, on GH/IGF-I levels in patients with this disease.

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To analyze this phenomenon, female rats were injected daily with raloxifene (50, 100, 250 or 500 microg/rat per day) between days 1 and 5 of age. On day 23, hypothalamic gonadotropin-releasing hormone (LHRH) mRNA expression was assessed, and pituitary and plasma luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels were measured in basal and LHRH-stimulated conditions. In addition, LH and FSH responses to ovariectomy were evaluated in raloxifene-treated females. Finally, we monitored the ability of neonatal administration of a potent LHRH agonist ([d-Ala(6),d-Gly(10)]-LHRH ethylamide; 0.01 microg/kg per 12 h on days 1-5) to counteract the effects of raloxifene.

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This study included 20 postmenopausal women with invasive, stage II, estrogen receptor-positive ductal carcinoma diagnosed by incisional biopsy, who received 60 mg of raloxifene orally for 28 days prior to definitive surgery. On the 29th day of treatment, definitive surgery was performed and a second tumor sample was taken for analysis. The catalytic subunit of telomerase (hTERT) was evaluated semiquantitatively by immunohistochemistry in the tumor samples obtained prior to and following raloxifene use and the results were analyzed using the McNemar test (p<0.05).

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There is increasing evidence indicating that estrogen replacement therapy produces neuroprotective actions but has undesirable side effects on the reproductive system. Raloxifene is a selective estrogen receptor modulator that exerts estrogen agonist action in the brain while acting as an estrogen antagonist in the reproductive system. In the present study, we investigated whether raloxifene affected the glutamate-induced calcium (Ca2+) overload in rat cultured cortical neurons. The bulk cytosolic intracellular Ca2+ level was measured by using confocal microscopy with fluorescent Ca2+ probe fluo3. Whole-cell recording technique was used to observe the effects of raloxifene on N-methyl-D-aspartate (NMDA)-evoked and voltage-activated Ca2+ currents in cultured cortical neurons. Pre-exposure of cortical neurons to raloxifene (0.5 microM-10 microM) for 3 min attenuated intracellular Ca2+ increase induced by application of glutamate (300 microM) for 1 min. The action of raloxifene was reversible after washout. ICI 182,780 and thapsigargin did not block the action of raloxifene. In whole-cell recording experiments, raloxifene (10 microM) significantly reduced the amplitude of the high-voltage-activated Ca2+ current but had no effect on NMDA-evoked Ca2+ current. The present study demonstrates that raloxifene acutely reduces glutamate-induced intracellular Ca2+ increase probably via inhibition of high-voltage-activated calcium channels.

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This randomized, double-blind, placebo-controlled, multicenter, 8-week study evaluated short-term effects of raloxifene on bone turnover, serum lipids, and endometrium in healthy, postmenopausal women. A total of 251 women received either placebo, raloxifene HCl 200 or 600 mg/day, or conjugated estrogens (Premarin, 0.625 mg/day). Bone turnover (serum alkaline phosphatase, serum osteocalcin, urinary pyridinoline cross-links, urinary calcium excretion, urinary hydroxyproline) and serum lipids (total serum cholesterol, high- and low-density lipoprotein cholesterol [HDL-C and LDL-C]) were evaluated at weeks 0, 2, 4, and 8. Endometrial biopsies were performed at weeks 0 and 8. Treatment groups were compared for each parameter for baseline-to-endpoint changes. The estrogen and raloxifene groups experienced similar decreases in serum alkaline phosphatase (range 10-11%), serum osteocalcin (range 21-26%), urinary pyridinoline cross-links (range 20-26%), and urinary calcium excretion (range 45-72%). These decreases differed significantly compared with placebo-treated subjects for all markers except serum osteocalcin, the raloxifene HCl 200 mg group. LDL-C decreased significantly in the estrogen and both raloxifene groups (range 5-9%) compared with placebo-treated subjects. HDL-C increased significantly in the estrogen group (16%) but was unchanged in the raloxifene groups. HDL-C:LDL-C ratios increased significantly in the estrogen and raloxifene groups (range 9-29%). Serum cholesterol decreased significantly in both raloxifene groups (range 4-8%) but was unchanged in the estrogen group. Uterine biopsies of raloxifene-treated subjects showed no change in the endometrium during this short-term treatment. Biopsies of the estrogen group showed significant endometrial stimulation. The only adverse event possibly related to raloxifene was vasodilatation (hot flashes) which was most common in the raloxifene HCl 600 mg group. Study results indicate that raloxifene may provide beneficial effects to bone and serum lipids in humans without uterine stimulatory effects.

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Estrogen administration is associated with reduction in perimenopausal symptoms and the risk for several conditions affecting postmenopausal women. As estrogen administration also increases the risk for breast cancer, a common dilemma facing many women and their physicians is whether to use estrogen replacement therapy (ERT), a selective estrogen receptor modulator (SERM) that antagonises estrogenic effects in breast tissue but retains some estrogen agonist properties in other organs, or neither. For women with average to moderate risk of breast cancer and with perimenopausal symptoms, ERT may be the best short-term choice. For very high-risk women (>1% per year) with menopausal symptoms, alternatives to ERT might be offered and tried first. A diagnosis of ductal carcinoma in situ or invasive breast cancer within the last 2 to 5 years should be considered a relative contraindication for ERT unless the tumour was estrogen receptor negative. High-risk women without menopausal symptoms are the best candidates for the only currently approved drug for breast cancer risk reduction, tamoxifen. Although the drug is approved for women with a 5-year risk of breast cancer > or = 1.7% (0.34% per year), postmenopausal women most likely to experience a favourable benefit/risk ratio are those with a Gail estimated risk of >0.5% per year without a uterus or >1% per year if they retain their uterus. Tamoxifen should not be used in women with prior history of thromboembolic or precancerous uterine conditions. Tamoxifen is often used in Europe in conjunction with transdermal ERT in hysterectomised women without obvious loss of efficacy or increased risk of thromboembolism. Raloxifene is a second generation SERM with estrogen-like agonist effects on bone but with less uterine estrogen agonist activity than tamoxifen. Raloxifene may have less potent breast antiestrogenic effects than tamoxifen, particularly in a moderate- to high-estrogen environment. Raloxifene is approved for use in reducing risk of osteoporosis, but not breast cancer. Whether it is as effective as tamoxifen in reducing breast cancer risk in postmenopausal women is the subject of a current trial. All women regardless of breast cancer risk are advised to employ nonpharmacological risk reduction measures, including normalisation of bodyweight, exercise, adequate calcium and vitamin D intake, and avoidance of smoking and alcohol. The preventive options are best weighed during an individualised consultation where a woman's menopausal symptoms and risk for breast cancer and other diseases can be examined, and the options for improving postmenopausal health can be discussed.

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This study was undertaken to assess persistence with bisphosphonates and raloxifene and to identify determinants of adherence (patient age, level of information, educational status, etc.) among women with osteoporosis in three different clinical settings in Denmark.

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Raloxifene, a selective estrogen receptor modulator used for the treatment of osteoporosis, undergoes extensive conjugation to the 6-beta- and 4'-beta-glucuronides in vivo. This paper investigated raloxifene glucuronidation by human liver and intestinal microsomes and identified the responsible UDP-glucuronosyltransferases (UGTs). UGT1A1 and 1A8 were found to catalyze the formation of both the 6-beta- and 4'-beta-glucuronides, whereas UGT1A10 formed only the 4'-beta-glucuronide. Expressed UGT1A8 catalyzed 6-beta-glucuronidation with an apparent K(m) of 7.9 microM and a V(max) of 0.61 nmol/min/mg of protein and 4'-beta-glucuronidation with an apparent K(m) of 59 microM and a V(max) of 2.0 nmol/min/mg. Kinetic parameters for raloxifene glucuronidation by expressed UGT1A1 could not be determined due to limited substrate solubility. Based on rates of raloxifene glucuronidation and known extrahepatic expression, UGT1A8 and 1A10 appear to be primary contributors to raloxifene glucuronidation in human jejunum microsomes. For human liver microsomes, the variability of 6-beta- and 4'-beta-glucuronide formation was 3- and 4-fold, respectively. Correlation analyses revealed that UGT1A1 was responsible for 6-beta- but not 4'-beta-glucuronidation in liver. Treatment of expressed UGTs with alamethicin resulted in minor increases in enzyme activity, whereas in human intestinal microsomes, maximal increases of 8-fold for the 6-glucuronide and 9-fold for the 4'-glucuronide were observed. Intrinsic clearance values in intestinal microsomes were 17 microl/min/mg for the 6-glucuronide and 95 microl/min/mg for the 4'-isomer. The corresponding values for liver microsomes were significantly lower, indicating that intestinal glucuronidation may be a significant contributor to the presystemic clearance of raloxifene in vivo.

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Both preclinical and clinical data suggest a role for raloxifene in the prevention of breast cancer. Like tamoxifen, raloxifene acts as an estrogen antagonist in breast tissue through competitive binding to the ER. Raloxifene may also inhibit breast tissue proliferation through mechanisms independent of the ER.

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Osteoporosis has been defined as "a progressive systemic disease characterized by low bone density and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture." Osteoporosis and the consequences of compromised bone strength--particularly vertebral and hip fractures--are a significant cause of frailty, and increased morbidity and even mortality and hence are a serious and costly public health problem in the elderly population. However, due to remarkable advances in basic and clinical research and in drug design, development, and testing, a number of efficacious, evidence-based options are available for the prevention and treatment of osteoporosis. These options extend far beyond estrogen/progestin therapy and include lifestyle and dietary changes such as increasing weight-bearing activity, enhancing calcium and vitamin D intake, as well as incorporating pharmacologic agents such as the bisphosphonates and selective estrogen receptor modulators (SERMs) such as raloxifene. In addition to its efficacy in increasing bone mineral density and reducing vertebral fractures by almost 40% in women with osteoporosis, the SERM raloxifene appears to promote a cardioprotective profile and to offer some protection against breast cancer. The potential of raloxifene to prevent or delay the development of a number of chronic diseases of aging such as osteoporosis, cardiovascular disease, and perhaps even Alzheimer's disease has stimulated the development and refinement of subsequent generations of SERMs aimed at maximizing beneficial effects in a wide variety of tissues while eliminating deleterious outcomes and side effects.

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Most patients who initiate a medication for osteoporosis do not continue to take it as prescribed. Although several patient characteristics significantly correlated with compliance, adjusted models explained little of the variation.

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The groundwork for making the concept of breast cancer chemoprevention a clinical reality began over a century ago. Although tamoxifen's first clinical use was for the treatment of breast cancer, the earliest animal studies with the drug provided the scientific basis for chemoprevention. The extensive clinical experience, safety and laboratory data have made tamoxifen the current standard-of-care for the prevention of breast cancer in women at elevated risk. The STAR trial will address the value of raloxifene as a chemopreventative in postmenopausal women. Results will be available by 2005. Newer compounds are under development which hold the promise of expanded efficacy and narrower side-effect profile. These compounds will function as multifunctional medicines and will hold the promise of preventing breast and endometrial cancer, while providing the beneficial effects of preventing osteoporosis and coronary heart disease.

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The selective estrogen receptor modulator raloxifene (RAL), used to treat and prevent osteoporosis, is under investigation for its use in the treatment and prevention of breast cancer. RAL in combination with the antimetabolites methotrexate (MTX) and 5-fluorouracil (5-FU) has not been extensively studied. Because RAL and the antimetabolites target different phases of the cell cycle and exhibit different mechanisms of action and clinical toxicity, the effects of sequence of administration on the growth inhibition of MCF-7 human breast cancer cells were investigated.

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Bone mineral density (BMD) of the spine and hip was measured semiannually. Serum lipids and biochemical bone markers were determined at each visit. To eliminate interindividual differences, all values were calculated as individual percentage change from baseline.

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evista cost comparison 2016-07-12

Overall, the incidence of AEs, serious AEs, and discontinuations due to AEs in the bazedoxifene groups was not different from that seen in the placebo group. The incidence of hot flushes and leg cramps was higher with bazedoxifene or raloxifene compared with placebo. The rates of cardiac disorders buy evista and cerebrovascular events were low and evenly distributed among groups. Venous thromboembolic events, primarily deep vein thromboses, were more frequently reported in the active treatment groups compared with the placebo group; rates were similar with bazedoxifene and raloxifene. Bazedoxifene showed a neutral effect on the breast and an excellent endometrial safety profile. The incidence of fibrocystic breast disease was lower with bazedoxifene 20 and 40 mg versus raloxifene or placebo. Reductions in total and low-density lipoprotein levels and increases in high-density lipoprotein levels were seen with bazedoxifene versus placebo; similar results were seen with raloxifene. Triglyceride levels were similar among groups.

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Healthy postmenopausal women with a BMD T-score at the lumbar spine or femoral neck between -1.0 buy evista and -2.5 or clinical risk factors for osteoporosis were randomly assigned to one of five groups: bazedoxifene 10, 20, or 40 mg/d, placebo, or raloxifene 60 mg/d. All women received elemental calcium. Efficacy outcomes included changes from baseline through 24 mo in BMD of the lumbar spine, hip, femoral neck, and femoral trochanter and biomarkers of bone metabolism.

evista drug class 2017-11-26

About 40% of women who reach the age of 50 are expected to suffer from osteoporosis during their remaining life. The morbidity associated with hip, spinal and wrist fractures, resulting from osteoporosis, and the mortality resulting from hip fractures justify the development of prevention strategies. Optimal management of osteoporosis consists of maximizing peak bone mass in early adulthood and preventing the rapid bone loss that occurs soon after the menopause. Peak bone mass will be reached in most women if adequate nutrition is taken and exercise is encouraged, while major risk factors are avoided. At the menopause, prescription of hormone replacement therapy (HRT) constitutes the primary prevention strategy. There are, however, questions that remain unanswered or debated. What is the optimal dose of HRT, when should it be started, and for how long should it be maintained? In women who do not, or may not, take HRT, and who have osteoporosis, alternative therapeutic options include diphosphonates (e.g., alendronate) and Selective buy evista Estrogen Receptor Modulators (such as raloxifene). Other treatments to restore bone strength in women with established disease may also reduce the risk of fractures. Some of them, such as calcitonin, may not be cost effective. Others have produced conflicting data (fluoride) and others are still under evaluation (PTH or strontium). In sunlight-deprived, vitamin D-deficient elderly nursing home residents, dietary supplementation of calcium and vitamin D has been shown to prevent bone loss and fractures. Strategies to avoid falls should also be encouraged for these patients.

evista generic pricing 2015-02-07

Among the 615 women with data, the mean (SD) age was 61.5 (8.3) years. Using the 2006 guidelines of The North American Menopause Society, 41.3% (253 of 612) of the women who had DXA testing did not meet the criteria for such screening. Of these women, 25.5% (157 of 615) were not taking calcium, 31.1% (191 of 614) were not taking vitamin D, and 59.8% (343 of 574) were not exercising at least half an hour per week. Of the women with any of the approved indications for treatment, 15.7% (16 of 102) were not taking calcium, 18.6% (19 of 102) were not taking vitamin D, 52.7% (49 buy evista of 93) were not exercising at least 2 hours per week, and 35.3% (36 of 102) were not receiving therapy. In contrast, of those women without an indication for treatment, 17.8% (83 of 467) were receiving bisphosphonate, raloxifene, or calcitonin therapy.

evista medication guide 2015-11-19

Raloxifene decreased the incidence of vertebral fracture and invasive breast cancer while increasing the incidence of venous thromboembolism. All treatment by vertebral fracture status interaction p-values were greater than 0.13, indicating that the effect of raloxifene on these outcomes was not significantly different between patients without versus those with vertebral fractures. In women without baseline vertebral fracture, absolute risk differences between the raloxifene and placebo group buy evista included vertebral fracture -2.83%, invasive breast cancer -1.21%, and venous thromboembolism +0.28%. In women with baseline vertebral fracture, absolute risk differences between raloxifene and placebo group included vertebral fracture -8.21%, invasive breast cancer -0.75% and venous thromboembolism +0.91%. The analysis had limited power to test whether raloxifene had a significantly different effect on venous thromboembolism in women without versus those with a vertebral fracture.

evista reviews 2017-04-09

In postmenopausal women, estrogen may have a beneficial effect on cognition or reduce the risk of decline in cognitive function. Whether raloxifene, a selective estrogen-receptor modulator buy evista , might have similar actions is not known.

evista alternative medicine 2017-04-03

Menopause is characterized by amenorrhea for 1 year due to the cessation of ovarian function. The hormonal treatment of menopause has significantly altered since the publication of initial results from the Women's Health Initiative continuous, combined, conjugated equine estrogen with medroxyprogesterone acetate study arm in 2002. Current studies suggest that treatment should be individualized and that the lowest dose of estrogen providing relief should be used for the shortest period of time in buy evista menopausal women who experience vasomotor symptoms or urogenital atrophy. Future studies into different delivery mechanisms such as transdermal applications and different agents, such as tibolone and raloxifene, will help refine the treatment of menopause.

generic evista osteoporosis 2016-12-09

Estrogen exerts biphasic effects on progesterone biosynthesis by swine granulosa cells, such that initial transient inhibition is followed by delayed but sustained stimulation. We have tested the functional role of the estradiol receptor in these biphasic responses by utilizing the highly selective estrogen-receptor antagonist, LY156758, and the synthetic estrogen agonist, moxestrol. The acute inhibitory action of estradiol was mimicked in a dose-dependent action by moxestrol (half-maximally inhibitory dose: 54.3 +/- 25 ng/ml), but was not antagonized by LY156758. Rather, the antiestrogen alone significantly suppressed basal progesterone synthesis, and accentuated the suppressive effect of submaximally inhibitory doses of estradiol. Inhibition was accompanied by increased pregnenolone accumulation, with a consequently augmented ratio of pregnenolone to progesterone. Moreover, in cell-free sonicates of granulosa cells, LY156758 directly inhibited 3 beta-hydroxysteroid dehydrogenase activity in a dose-dependent fashion, with half-maximal inhibition expressed at a drug concentration of 2.44 +/- 0.31 micrograms/ml compared with 85 +/- 19 ng/ml for estradiol. In addition, the combination of LY156758 and submaximally inhibitory doses of estradiol resulted in further suppression of 3 beta-hydroxysteroid dehydrogenase activity. The sustained stimulatory phase of estrogen action was also mimicked by moxestrol in a dose-dependent fashion. However, in contrast to its acute inhibitory effects, longer-term treatment with LY156758 slightly enhanced basal progesterone accumulation, and effectively antagonized estradiol's stimulatory actions. In summary, our results with moxestrol demonstrate that both the inhibitory and the stimulatory actions of estradiol are effectively mimicked by this synthetic estrogen agonist. Results with the selective anti-estrogen LY156758 indicate a small degree of intrinsic estrogen agonist activity (approx 4% that of estradiol), which is reflected by its acute and direct inhibition of 3 beta-hydroxysteroid dehydrogenase activity. However, under longer-term conditions in which estradiol's stimulation of progesterone production is buy evista expressed, LY156758 significantly antagonizes estradiol's trophic actions. Accordingly, we suggest that the acute suppressive effects of estradiol on progesterone production are mediated predominantly by direct inhibition of 3 beta-hydroxysteroid dehydrogenase activity, while delayed stimulatory effects are transduced via estrogen-receptor mechanisms.(ABSTRACT TRUNCATED AT 400 WORDS)

evista 60mg tablets 2017-03-05

The results of this prospective study show for the first time that raloxifene use is associated with a significant reduction in plasma antithrombin activity. This effect buy evista may contribute to a procoagulant state and partly explain the increased risk of venous thromboembolism in raloxifene users.

evista user reviews 2017-11-29

Forty-nine patients with cirrhotic ESLD (26 men, 23 women; median age 54 years) had dual energy x-ray absorptiometry preformed at baseline and 4 and 12 months after OLT. Immunosuppression therapy after OLT included a standard transplant protocol of daily tacrolimus to maintain plasma levels between 0.2 to 0.5 ng/mL and daily oral prednisone tapered over 4 months. BMD was measured at the lumbar spine (L-BMD) and left hip (hip BMD) and buy evista reported as raw density (g/cm2) and T score (standard deviations from gender-matched young healthy subjects). Results represent total hip measurements. Two-sided paired t test and analysis of variance methods were used for statistical comparisons.

evista usual dose 2017-08-19

The aim was to investigate patient compliance with different osteoporosis medications commonly prescribed in clinical practice, to determine risk factors associated with discontinuation and to evaluate quality buy evista of life changes.

evista dosage 2017-11-07

Not much is known about cross-geographic region differences in quality of life (QoL) in women with and without prevalent vertebral fractures (VFX). QoL differed between continents, countries, and ethnicities. The buy evista observed differences in QoL mostly appeared larger than the difference in QoL between women with or without mild to moderate VFX.

evista prices canada 2017-12-18

RLX treatment reduced CAVI value at 6 months which was superior in buy evista relatively younger group.

evista 70 mg 2015-06-26

The novel natural product DT56a (Tofupill/Femarelle), derived from soybean, has been shown to relieve menopausal vasomotor symptoms and to increase bone mineral density with no effect on sex steroid hormone levels or endometrial thickness. In the present study, we compared the effects of DT56a and estradiol-17beta (E2) on bone and cartilage (Ep) of immature or ovariectomized female rats, by measuring the changes in the specific activity of the BB isozyme of creatine kinase (CK). Single short-term buy evista injection of high doses of DT56a induced estrogenic activity in bones and uterus similar to that of E2. When administered in multiple oral doses, DT56a stimulated skeletal tissues similarly to E2, but whereas E2 increased CK specific activity in the uterus, DT56a did not. The selective estrogen receptor modulator (SERM) raloxifene (Ral) blocked the stimulation of CK by either DT56a or by E2 in all tissues tested. Our findings suggest that DT56a acts as a selective estrogen receptor modulator stimulating skeletal tissues without affecting the uterus. The effect of DT56a on other systems, such as the vascular and the central nervous system, are currently under investigation.

evista brand name 2015-05-04

Co-administration of apigenin with Tegretol And Alcohol raloxifene in a 1:2 ratio by weight resulted in a 55% and 37% increase in the C(max) and AUC of intact raloxifene, respectively. When equal proportions of raloxifene and apigenin (1:1) were administered, the C(max) and AUC of intact raloxifene were increased by 173% and 97% respectively. This increase in intact raloxifene was not associated with an increase in total raloxifene (intact plus conjugated raloxifene) because AUC and C(max) of total raloxifene when administered alone or in combination with apigenin were found to be similar. The results indicated that apigenin inhibited the glucuronidation and sulfation of raloxifene in the intestine bringing about an increased bioavailability of the drug.

evista medication 2015-12-06

Hypopituitarism is a well-known cause of secondary osteoporosis. However, patients receiving surgery for pituitary tumors or parasellar lesions have not been well studied for their bone sequel in Japan. We measured bone mineral density (BMD) and urinary type I collagen Elavil Lethal Dose N-telopeptide (uNTX) in 35 postoperative patients including 25 with pituitary tumor (PT), 6 with craniopharyngioma (CP), and 4 others who had not been on sex hormone replacement, raloxifene, or bisphosphonate therapy. Compared with patients with PT, patients with CP had lower BMD and higher uNTX. Five out of 6 patients with CP had BMD lower than 80% of young adult mean (YAM), whereas 11 out of 22 patients with PT had BMD less than 80% of YAM. Patients with CP had significantly lower serum levels of gonadotropins, and they also tended to have lower serum levels of sex steroids, although statistically not significantly. Two postoperative patients with CP on sex steroid replacement, who were not included in the current analysis, had normal BMD. Of all the subjects, the prominent difference between patients with normal BMD and normal value of uNTX and patients with low BMD and elevated uNTX value was that the latter received higher dose of hydrocortisone replacement. The present study confirms postsurgical patients with pituitary or parasellar lesions, especially those with CP, are at high risk for osteopenia. In designing replacement therapy for those patients, it is important to consider bone by minimizing the dose of glucocorticoid, including sex steroids, and using other drugs that protect bone.

evista cost 2017-12-28

The long-term use of raloxifene has Duricef Alcohol been evaluated through changes in fracture risk reduction, BMD, markers of bone turnover, iliac crest bone biopsies, and invasive breast cancer risk reduction.

evista drug dosage 2015-08-21

(1) Coagulation and anticoagulation indicators: it was observed (1.62 ± 0.22) g/L FIB at control group, (2.02 ± 0.54) g/L at RLX group, (1.97 ± 0.16) g/L at RLX and low CEE group, (2.00 ± 0.18) g/L at RLX and high CEE group. There was a statistically significant difference between control group and any one of treatment groups (P < 0.05) and no statistical significance among those three treatment groups (P > 0.05). No significant change was observed in plasma ATIII activity among groups (P > 0.05). (2) Fibrinolytic and anti-fibrinolytic indicators: it was observed (14.1 ± 2.8) µg/L PAI-1 at control Zoloft 6 Mg group, (20.0 ± 3.3) µg/L at RLX group, (41.5 ± 5.5) µg/L at RLX and low CEE group, (38.9 ± 6.0) µg/L at RLX and high CEE group. A remarkable increase was observed between control group and any one of treatment groups (P < 0.05) . But there was no significant difference of D-D among groups (P > 0.05) . (3) Endothelial function: it was (43 ± 7) % vWF at control group, (49 ± 5) % at RLX group, (46 ± 6) % at RLX and low CEE group, (36 ± 5) % at RLX and high CEE group. The vWF of RLX and high CEE group was the lowest among all groups (P < 0.05) . There was no difference of NO among groups (P > 0.05).

evista medication generic 2015-06-24

To investigate the association between diabetes and impaired fasting glucose (IFG) and cognition and risk of Amoxil Cost developing both dementia and mild cognitive impairment (MCI) in older women.

evista dosage instructions 2015-10-28

The oxidation of low-density lipoprotein (LDL) is an important factor in the Omnicef Dosing Pediatrics development of atherosclerosis. The antioxidant activity of some compounds buffers the free radicals generated either endogenously or exogenously, thus decreasing the potential damage mediated by oxidation. Estrogens are potent antioxidants of LDL, in vitro and in vivo, a mechanism that could probably influence the cardioprotection associated with hormone replacement therapy in postmenopause. We conducted an in vitro study of the antioxidant effect on LDL of two selective estrogen receptor modulators, raloxifene (RLX) and tamoxifen (TMX), comparing them with the known antioxidant effect of estradiol (E2 ).

evista dosage forms 2017-10-10

Raloxifene is a selective estrogen receptor modulator approved for prevention of osteoporosis in postmenopausal women. It is selective by virtue of having estrogen agonistic effects in bone, vessels, and blood lipids, while it is antagonistic with mammary and uterine tissue. The aim of the study was to examine whether the raloxifene analogue LY117018 (LY) has estrogenic effects on the thymus, T cell responsiveness, and inflammation. Oophorectomized normal mice were treated with subcutaneous injections of equipotent antiosteoporotic doses of LY (3 mg/kg) and 17beta-estradiol (E2) (0.1 mg/kg) or vehicle as controls. Effects on thymus were studied by analyses of thymus weight, cellularity, and CD4 and CD8 phenotype expression and histology, while inflammation was determined as T-cell-mediated delayed-type hypersensitivity (DTH) and granulocyte-mediated footpad swelling. LY lacked the suppressive properties of E2 on DTH and granulocyte-mediated inflammation. Furthermore, LY induced only minor thymus atrophy compared with E2 and did not, in contrast to E2, alter the thymic CD4/CD8 phenotypes. These results clearly demonstrate that raloxifene principally lacks the modulatory effects of estrogen on T cell responsiveness and inflammation. Our data are discussed in the context of recent findings in estrogen receptor biology and also with respect to estrogen-mediated alteration of autoimmune rheumatic diseases.

evista medication uses 2015-07-26

To minimize potential controversies in determining the need for multiplicity adjustment for multiple hypotheses, we propose a decision rule based multiplicity adjustment strategy in this paper. Resorting to a predefined decision rule of a clinical trial, one may link the different hypotheses by their logical relationships and divide them into different families. A proper multiplicity adjustment procedure can then be developed by maintaining strong control of Type I error rate within each family. The paper applies the proposed multiplicity adjustment strategy to a published raloxifene clinical trial.

evista bone medicine 2017-10-20

Estrogens and selective estrogen receptor modulators (SERMs) interact with estrogen receptor (ER) alpha and beta to activate or repress gene transcription. To understand how estrogens and SERMs exert tissue-specific effects, we performed microarray analysis to determine whether ERalpha or ERbeta regulate different target genes in response to estrogens and SERMs. We prepared human U2OS osteosarcoma cells that are stably transfected with a tetracycline-inducible vector to express ERalpha or ERbeta. Western blotting, immunohistochemistry, and immunoprecipitation studies confirmed that U2OS-ERalpha cells synthesized only ERalpha and that U2OS-ERbeta cells expressed exclusively ERbeta. U2OS-ERalpha and U2OS-ERbeta cells were treated either with 17beta-estradiol (E2), raloxifene, and tamoxifen for 18 h. Labeled cRNAs were hybridized with U95Av2 GeneChips (Affymetrix). A total of 228, 190, and 236 genes were significantly activated or repressed at least 1.74-fold in U2OS-ERalpha and U2OS-ERbeta cells by E2, raloxifene, and tamoxifen, respectively. Most genes regulated in ERalpha cells in response to E2, raloxifene, and tamoxifen were distinct from those regulated in ERbeta cells. Only 38 of the 228 (17%) genes were regulated by E2 in both U2OS-ERalpha and U2OS-ERbeta cells. Raloxifene and tamoxifen regulated only 27% of the same genes in both the ERalpha and ERbeta cells. A subset of genes involved in bone-related activities regulated by E2, raloxifene, and tamoxifen were also distinct. Our results demonstrate that most genes regulated by ERalpha are distinct from those regulated by ERbeta in response to E2 and SERMs. These results indicate that estrogens and SERMs exert tissue-specific effects by regulating unique sets of targets genes through ERalpha and ERbeta

evista and alcohol 2015-05-10

To assess and compare the effect of conjugated estrogen and of the selective estrogen receptor modulator raloxifene on serum levels of insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding protein-3 (IGFBP-3) and on the IGF-I/IGFBP-3 ratio.

evista raloxifene tablets 2017-10-02

The goal of drug treatment of osteoporosis is to prevent fractures. Increase of bone density during therapy is not consistently associated with a clinical benefit. The purpose of this paper is to review the evidence of fracture prevention from published randomized controlled trials. Vitamin D, the bisphosphonate alendronate and the selective estrogen receptor modulator raloxifene have been evaluated in large randomized trials with clinical endpoints.

evista generic teva 2015-12-06

The clinical benefits of HRT are clearly established for the relief of menopausal symptoms, improving quality of life and the prevention of osteoporosis. Although research on the impact of HRT (oral, transdermal, tibolone, etc.) and on the effects of raloxifene on CVD is still ongoing, with certain unresolved controversies, studies using a variety of different HRT formulations have shown a clear benefit on surrogate markers of CHD and epidemiological and clinical, although not randomized, studies have demonstrated a CHD reduction in HRT-treated women. Today, HRT may be used for the primary prevention of CVD. Conversely, there is no clear reason to commence HRT solely or primarily to confer an immediate cardiovascular benefit in postmenopausal women with established CHD. Equally, there is no compelling evidence for discontinuing--or indeed not initiating--HRT in women without CVD because of concern about cardiovascular risk. In any case, all medical interventions should be individualized to the specific woman's age, characteristics and needs. The ultimate effects of different dosages, schedules and type of hormones used should be clarified, avoiding inferring the effects of one form of HRT to others. The importance of increased attention to life-style factors such as healthy diet, exercise and cessation of smoking should be underlined since these can confer specific benefits also to menopausal women. For women with known risks for CVD, HRT may contribute to the beneficial effects of life-style improvements and well-established therapies (including blood pressure control, cholesterol-lowering drugs, aspirin, etc.). New strategies, including lower dosages, new estrogens, progestins, and new estrogen-like substances may be designed to target specific needs.