ライフサイエンスコーパス: SERM

1 SERM, used in treatment of breast cancer and osteoporosi

2 SERM-membrane interactions were probed under multiple pH

3 SERMs bind ER, alter receptor conformation, and facilita

4 SERMs may be preferable to estrogens given their efficac

5 SERMs reduced the cellular sphingosine and subsequently

6 SERMs, which interact with estrogen receptor-alpha and e

7 In this study, we compared the effects of a SERM (PSK3471) and 2 estrens (estren-alpha and estren-be

8 Perhaps a SERM used to prevent osteoporosis could simultaneously p

9 the contention that trioxifene represents a SERM with potential antimetastatic efficacy for the trea

10 ndings demonstrate for the first time that a SERM other than tamoxifen can induce glioma cell apoptos

11 eoadjuvant trials of hormonal therapy with a SERM (tamoxifen or idoxifene) or an aromatase inhibitor

12 Depending on their functional activities, SERMs could then be developed for a variety of clinical

13 To identify additional SERMs, a method to classify compounds based on different

14 rther development in order to obtain dual AI/SERM agents for breast cancer treatment.

15 he antiestrogenic SERM activity of a dual AI/SERM could act synergistically with AI activity to enhan

16 ue the estrogenic SERM activity of a dual AI/SERM could attenuate the undesired effects stemming from

17 etion caused by the AI activity of a dual AI/SERM, while in breast cancer tissue the antiestrogenic S

18 For all SERMs, incidence of invasive oestrogen (ER)-positive bre

19 creases N-CoR binding in the presence of all SERMs blocks AF-1 activity.

20 events were significantly increased with all SERMs (odds ratio 1.73, 95% CI 1.47-2.05; p<0.0001).

21 Although SERM-exposed DC exhibited increased ability to internali

22 Although SERMs have been available for clinical use for 50 years,

23 ng can discern fundamental differences among SERMs and provides insight into the distinct biologies o

24 is benzothiophene derivative demonstrated an SERM profile in preclinical studies.

25 ancer compared with both tamoxifen users and SERM nonusers, suggesting a role for raloxifene in endom

26 se regulated by ERbeta in response to E2 and SERMs.

27 These results indicate that estrogens and SERMs exert tissue-specific effects by regulating unique

28 To understand how estrogens and SERMs exert tissue-specific effects, we performed microa

29 nt target genes in response to estrogens and SERMs.

30 ed increase in uterine weight, while another SERM, tamoxifen, increased uterine weight.

31 e in breast cancer tissue the antiestrogenic SERM activity of a dual AI/SERM could act synergisticall

32 zothiophene SERM, raloxifene, the benzopyran SERM, (S)-3-(4-hydroxyphenyl)-4-methyl-2-[4-[2-(1-piperi

33 -alpha ethinyl estradiol, the benzothiophene SERM, raloxifene, the benzopyran SERM, (S)-3-(4-hydroxyp

34 loped to generate a family of benzothiophene SERMs.

35 ity in vivo, and suggest that benzothiophene SERMs may exert estrogen-like beneficial effects on chol

36 rocedure is reported yielding benzothiophene SERMs wherein redox activity and ER affinity are modulat

37 SHG measurements of the interactions between SERMs and artificial cell membranes and independent obse

38 is incidental biological activity induced by SERMs could be a plausible mechanism as to their inhibit

39 on profiles after ER activation by different SERMs in MDA-MB-231 human breast cancer cells stably tra

40 were treated with estradiol, four different SERMs, and the pure antiestrogen ICI 182,780.

41 the basis of the known response to different SERMs.

42 ether, our results suggest that differential SERM effects on corepressor binding can explain differen

43 This suggests that differential SERM repression of AF-1 involves HDAC-dependent corepres

44 on of NF-kappaB activation markedly enhances SERM-induced apoptosis, suggesting a role for NF-kappaB

45 esis is that in normal tissue the estrogenic SERM activity of a dual AI/SERM could attenuate the unde

46 ogen action can no longer be used to explain SERM action at different sites around the body.

47 molecular mechanisms potentially explaining SERM resistance in ER-positive/PR-negative tumors have b

48 was renamed raloxifene and became the first SERM for the treatment and prevention of osteoporosis as

49 For SERMs, current evidence supports tamoxifen use for breas

50 association constants (Ka) were measured for SERMs using varying lipid compositions to examine how li

51 or NF-kappaB in protecting glioma cells from SERM-induced cytotoxicity.

52 Furthermore, SERMs did not induce the AF-1-mediated activity from the

53 Whereas the first generation SERMs/SERDs were discovered in a serendipitous manner, t

54 3 is a member of a series of next-generation SERMs with functional selectivity toward ER-alpha and a

55 impact on the discovery of second generation SERMs, some of which are in late stage clinical developm

56 king density, and cholesterol content impact SERM-membrane interactions.

57 repressor binding can explain differences in SERM effects on ERalpha activity.

58 ional activity of other nuclear receptors in SERM-treated cells.

59 ifen, selective estrogen receptor modifiers [SERMs], diet, and exercise) likely to favorably influenc

60 the recognition of selective ER modulation (SERM) that created a new dimension in therapeutics.

61 EDC is a non-nuclear selective ER modulator (SERM) in vivo, and in mice, non-nuclear ER signaling pro

62 as estradiol and the selective ER modulator (SERM) tamoxifen promote p53 antagonism.

63 respond less well to selective ER modulator (SERM) therapy than ER-positive/PR-positive tumors.

64 f the selective estrogen receptor modulator (SERM) family, is widely used in the treatment of estroge

65 A selective estrogen receptor modulator (SERM) for the potential treatment of hot flushes is desc

66 novel selective estrogen receptor modulator (SERM) for the potential treatment of uterine leiomyoma i

67 is a Selective Estradiol Receptor Modulator (SERM) from soy.

68 of a selective estrogen receptor modulator (SERM) in the general population and characterize the end

69 f the selective estrogen receptor modulator (SERM) tamoxifen were synthesized and evaluated for their

70 of a selective estrogen receptor modulator (SERM) that has a dihydrobenzoxathiin core structure bear

71 ation selective estrogen receptor modulator (SERM) that has been approved for the prevention and trea

72 is a selective estrogen receptor modulator (SERM) that is a potent estrogen antagonist in mammary an

73 16), selective estrogen receptor modulator (SERM) therapy (n = 8), and no (hormone replacement) ther

74 is a selective estrogen receptor modulator (SERM) which is currently under clinical evaluation for t

75 is a selective estrogen receptor modulator (SERM) with competitive binding activity against estradio

76 en, a selective estrogen receptor modulator (SERM), represents the standard of care for many patients

77 ation selective estrogen receptor modulator (SERM), tamoxifen, and raloxifene side-by-side in in vitr

78 issue-selective estrogen receptor modulator (SERM), which acts as an antiestrogen in the mammary tiss

79 ation selective estrogen receptor modulator (SERM)-because this benzothiophene derivative demonstrate

80 issue-selective estrogen receptor modulator (SERM).

81 enous selective estrogen receptor modulator (SERM).

82 cause breast cancer selective ER modulators (SERM) are therapeutically ineffective in EOC, we suggest

83 utic selective estrogen receptor modulators (SERM), raloxifene and tamoxifen, can perturb DC developm

84 the selective oestrogen-receptor modulators (SERM).

85 emonstrate that the selective ER modulators (SERMs) 4-hydroxytamoxifen (4HT) and raloxifene are able

86 ring treatment with selective ER modulators (SERMs) such as tamoxifen.

87 Selective estrogen-receptor (ER) modulators (SERMs) are synthetic nonsteroidal compounds that switch

88 selective estrogen receptor (ER) modulators (SERMs) tamoxifen and raloxifene, cause antagonistic and

89 and selective estrogen receptor modulators (SERMs) activated the AF-2 mutants.

90 ding selective estrogen receptor modulators (SERMs) and selective androgen receptor modulators (SARMs

91 ding selective estrogen receptor modulators (SERMs) and/or aromatase inhibitors (AIs).

92 Selective Estrogen Receptor Modulators (SERMs) are a new class of drugsthat bind to estrogen rec

93 Selective estrogen receptor modulators (SERMs) demonstrate tissue-specific estrogen receptor (ER

94 s or selective estrogen receptor modulators (SERMs) has not been determined.

95 Selective estrogen receptor modulators (SERMs) have been defined as compounds that display tissu

96 y of selective estrogen receptor modulators (SERMs) have relied on ER binding and cell-based estrogen

97 t as selective estrogen receptor modulators (SERMs) in women, with estrogen-like activities on some p

98 and selective estrogen receptor modulators (SERMs) interact with estrogen receptor (ER) alpha and be

99 s of selective estrogen receptor modulators (SERMs) is thought to underlie their clinical use.

100 Selective estrogen receptor modulators (SERMs) mimic estrogen action in certain tissues while op

101 of selective oestrogen receptor modulators (SERMs) on breast cancer incidence.

102 t of selective estrogen receptor modulators (SERMs) on the brain.

103 Selective estrogen receptor modulators (SERMs) partially avoid such unwanted effects, but their

104 Selective estrogen receptor modulators (SERMs) show differential effects upon ERalpha activation

105 Selective estrogen receptor modulators (SERMs) such as tamoxifen are effective in the treatment

106 ther selective estrogen receptor modulators (SERMs) such as tamoxifen have estrogen-like effects in t

107 the Selective Estrogen Receptor Modulators (SERMs) tamoxifen and raloxifene, so called for their abi

108 n as selective estrogen receptor modulators (SERMs) that possess estrogen agonist-like actions on bon

109 Selective estrogen receptor modulators (SERMs) that suppress bone remodeling will change trabecu

110 n of selective estrogen receptor modulators (SERMs) with lipid membranes has been measured at clinica

111 gen, selective estrogen receptor modulators (SERMs), and bisphosphonates has been well described.

112 t of selective estrogen receptor modulators (SERMs), novel chromene scaffolds, benzopyranobenzoxapane

113 ding selective estrogen receptor modulators (SERMs), possess selective anti-Ebola activities.

114 lude selective estrogen receptor modulators (SERMs), prophylactic surgery, and lifestyle change.

115 Selective estrogen receptor modulators (SERMs), such as tamoxifen (4-OHT), bind to the ER and af

116 (AI)/selective estrogen receptor modulators (SERMs).

117 lled selective estrogen receptor modulators (SERMs).

118 y of selective estrogen receptor modulators (SERMs).

119 our selective oestrogen receptor modulators (SERMs; tamoxifen, raloxifene, arzoxifene, and lasofoxife

120 tor (selective estrogen receptor modulators (SERMs]); or (2) inhibit estrogen-synthesizing enzymes, t

121 Most SERMs are polyaromatic phenols susceptible to oxidative

122 Several new SERM agents are in clinical development in an attempt to

123 Lasofoxifene and arzoxifene are two newer SERMs that have recently been demonstrated to improve bo

124 A novel SERM (selective estrogen receptor modulators), 1-(R), a

125 These data identify 4c as a novel SERM with greater potency to antagonize estrogen in uter

126 ermined the differential response of a novel SERM, SP500263, on estrogen receptor (ER) alpha and the

127 Under active evaluation are novel SERMs, aromatase inhibitors/inactivators, gonadotrophin-

128 re demonstrates an unexpected consequence of SERM treatment, which could help further define the comp

129 l cancer prevention and individualization of SERM therapy.

130 LBD structure reveals an unexpected mode of SERM-mediated ER antagonism, in which the stability of E

131 DC differentiated in the presence of SERM were assessed for their capacity to internalize flu

132 antiestrogen-like (apoptosis) activities of SERMs on the basis of their gene expression profiles is

133 in, we demonstrated that the same dosages of SERMs which induced cholesterol accumulation also inhibi

134 The effect of SERMs on the coronary vasculature is unknown.

135 verses the differential inhibitory effect of SERMs upon AF-1 activity in MCF-7 cells.

136 tored the growth-inhibitory effectiveness of SERMs in endocrine-resistant cells.

137 The therapeutic effectiveness of SERMs such as tamoxifen and raloxifene in breast cancer

138 Effects of SERMs on men with coronary artery disease (CAD) have not

139 propose a model for differential effects of SERMs on N-CoR binding.

140 nd in vivo and that the clinical efficacy of SERMs for the treatment of malignant gliomas could poten

141 data strongly support clinical evaluation of SERMs for the treatment of men with CAD.

142 in the development of the next generation of SERMs/SERDs, some of which are likely to have a major im

143 arified the specific anti-Ebola mechanism of SERMs, even the cationic amphiphilic drugs (CADs), this

144 The sometimes surprising pharmacology of SERMs has resulted in a growing interest in the developm

145 ach to improve the therapeutic properties of SERMs.

146 specific or represents a general property of SERMs is unknown.

147 Conversely, the redox reactivity of SERMs may contribute to antioxidant and chemopreventive

148 263 represents a member of a novel series of SERMs that is structurally unrelated to SERMs currently

149 By analyzing the structures of SERMs and their incidental biological activity (choleste

150 serum cholesterol values compared with older SERMs in smaller clinical trials.

151 er EFP values than did women receiving NT or SERM therapy (6.2 mL . 100 g(-1) . min(-1)+/- 2.4 and 5.

152 .1) (P = .012 and P = .008, respectively) or SERM therapy (3.9 mL . 100 g(-1) . min(-1)+/- 1.1) (P =

153 ticle by Spurgeon et al which evaluates oral SERM raloxifene as a potential therapeutic agent for HPV

154 Other SERMs are in development, with the goal of reducing toxi

155 ively elicited by tamoxifen but not by other SERMs, such as raloxifene or ICI182,780 (Fulvestrant).

156 ngs indicate that BZA is distinct from other SERMs in its ability to inhibit hormone-independent brea

157 terized the effects of BZA and several other SERMs on the proliferation of hormone-dependent MCF-7 an

158 Tamoxifen, the pioneering SERM, blocks estrogen action by binding to the ER in bre

159 M raloxifene, 7-(R) was found to be a potent SERM that behaved as antagonist in the uterus and exhibi

160 pounds, LY357489,4, is among the most potent SERMs described to date with in vivo efficacy on bone an

161 To discover new classes of potential SERMs, we have employed a cell-free microsphere-based bi

162 A promiscuous SERM ER complex creates a stimulatory signal in growth f

163 the antiestrogenic effect of this prototype SERM, we performed an analysis of the cofactors that int

164 Raloxifene, a prototypical SERM, has ER agonist properties in bone and on cholester

165 These events cause drug-resistant, SERM-stimulated growth.

166 centers in the monkey, suggesting that some SERMs may share estrogen's neuroprotective potential for

167 e developed an in vitro system in which some SERMs (4-hydroxytamoxifen and resveratrol) demonstrate e

168 able, with some (bisphosphonates, tamoxifen, SERMs, and exercise) likely to favorably influence breas

169 pharmacologic discovery of ovarian-targeted SERM.

170 These results imply that SERM activity is dependent on a conformational change of

171 These observations suggest that SERM may depress immunity when given to healthy individu

172 n addition to statins, our screen found that SERMs, antifungals, and several antipsychotic medication

173 Recent clinical trials indicate that SERMs are useful in treatment of disorders of bone and m

174 estrogen agonist (ethynyl estradiol) and the SERM raloxifene, 7-(R) was found to be a potent SERM tha

175 in vivo biological assays reflective of the SERM profile.

176 We therefore investigated the effects of the SERM raloxifene on isolated rabbit coronary arteries.

177 no effect on the potency or efficacy of the SERM raloxifene.

178 Furthermore, the selective ability of the SERM tamoxifen but not raloxifene to regulate miR-451 an

179 l (BCPT) demonstrated the superiority of the SERM tamoxifen to placebo in reducing breast cancer risk

180 higher concentrations than estradiol or the SERM, and acted for the most part through the AR.

181 The SERMs investigated in this study include raloxifene, tam

182 is of gene stimulation and inhibition by the SERMs trans-hydroxytamoxifen (TOT) and raloxifene (Ral)

183 embranes and independent observations of the SERMs efficacy from clinical studies suggests that quant

184 We found that all of the SERMs inhibited the growth of MCF-7, T47D, and MCF-7:2A

185 In addition to the SERMs, however, have emerged the Selective Estrogen Degr

186 Theoretically, SERMs could be synthesized that would exhibit nearly com

187 This phenotype indicates that these SERM act to maintain DC in an immature state by inhibiti

188 estrogen receptor (ER) ligand binding, this SERM family was shown to provide both a range of ERalpha

189 ic capsules concurrently with the last three SERM injections (immediate, group 1).

190 ast cancers may be specifically resistant to SERMs, whereas they may be less resistant to estrogen wi

191 cruitment determine the cellular response to SERMs.

192 s of SERMs that is structurally unrelated to SERMs currently on the market or in clinical development

193 ng efficacy as well as toxicity of these two SERMs in a similar high-risk population, will be availab

194 Of these two SERMs, raloxifene is preferred because it has markedly l

195 roperties may be important for understanding SERM action in vivo.

196 Unlike SERMs, the estrens induced reproductive organ hypertroph

197 ng the average length of the cracks, whereas SERM treatments lead to a more ductile fracture and main

198 ifen and CC-8490, a novel benzopyranone with SERM activity, induce glioma cell apoptosis in a dose- a