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 SERMs, which were developed as nuclear ER-alpha and ER-b

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

9 Perhaps a SERM used to prevent osteoporosis could simultaneously p

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

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

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

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

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

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

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

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

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

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

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

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

22 Although SERM-exposed DC exhibited increased ability to internali

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

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

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

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

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

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

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

30 nt target genes in response to estrogens and SERMs.

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

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

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

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

35 loped to generate a family of benzothiophene SERMs.

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

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

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

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

40 Estrogens and, consequently, SERMs regulate the synthesis of vasoactive nitric oxide

41 asing SERMs (NO-SERMs) and the corresponding SERMs (after NO release) derived from a triaryl olefin l

42 lpha, which is crucial for achieving desired SERM or SERD profiles.

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

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

45 the basis of the known response to different SERMs.

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

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

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

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

50 g PD-1 and CTLA-4 inhibition when evaluating SERMs as therapeutic agents.

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

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

53 activities in ESR1 mutant setting while few SERMs have been studied.

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

55 For SERMs, current evidence supports tamoxifen use for breas

56 valuable insights into the implications for SERMs in remyelination for MS and hormonal research at l

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

58 e show that nuclear ERs are not required for SERMs to mediate their potent effects on OPC differentia

59 y that could potentially act as a target for SERMs.

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

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

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

63 3 is a member of a series of next-generation SERMs with functional selectivity toward ER-alpha and a

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

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

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

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

68 tate to active (estrogen-bound) or inactive (SERM/SERD-bound) states remains unresolved.

69 itors of ERa signaling (aromatase inhibitors/SERMs/SERDs) used to treat ER+ breast cancer.

70 Ormeloxifene (ORM) is a well-known SERM of triphenylethylene family that has been approved

71 self-consistent expression recovery machine (SERM), to impute the missing expressions.

72 ing, and strain energy release maximization (SERM) theory.

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

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

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

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

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

78 selective estrogen receptor (ER) modulator (SERM) that could move quickly from bench to bedside.

79 selective estrogen receptor (ER) modulator (SERM), bazedoxifene (BZA), as a potent agent of oligoden

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

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

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

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

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

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

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

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

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

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

90 The selective estrogen receptor modulator (SERM) toremifene was previously identified from a screen

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

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

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

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

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

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

97 issue-selective estrogen receptor modulator (SERM).

98 enous selective estrogen receptor modulator (SERM).

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

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

101 the selective oestrogen-receptor modulators (SERM).

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

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

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

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

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

107 as selective oestrogen receptor modulators (SERMs) and downregulators (SERDs) also modulate oestroge

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

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

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

111 d 17 Selective Estrogen Receptor Modulators (SERMs) as inhibiting ligands for immune checkpoint prote

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

113 Selective estrogen receptor modulators (SERMs) extend estrogen receptor alpha (ERalpha) cellular

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

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

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

117 sing selective estrogen receptor modulators (SERMs) in cancer therapy, adverse effects such as endoth

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

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

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

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

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

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

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

125 that selective estrogen receptor modulators (SERMs) potently stabilize intracellular calcium and ther

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

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

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

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

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

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

132 nine selective estrogen receptor modulators (SERMs) via cellular and biochemical assays confirms taxa

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

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

135 The selective estrogen receptor modulators (SERMs), including 4-hydroxytamoxifen (4OHT), activate AF

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

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

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

139 the selective estrogen receptor modulators (SERMs), raloxifene and tamoxifen, and showed growth atte

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

141 lled selective estrogen receptor modulators (SERMs).

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

143 y of selective estrogen receptor modulators (SERMs).

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

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

146 Most SERMs are polyaromatic phenols susceptible to oxidative

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

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

149 nal release of (*)NO by the corresponding NO-SERM 4d.

150 nthesized a series of NO-releasing SERMs (NO-SERMs) and the corresponding SERMs (after NO release) de

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

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

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

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

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

156 l cancer prevention and individualization of SERM therapy.

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

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

159 pproach combining the antagonistic action of SERMs with a targeted (*)NO release could diminish vascu

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

161 alpha-dependent tissue-selective activity of SERMs.

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

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

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

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

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

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

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

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

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

171 ted to the tissue-selective functionality of SERMs.

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

173 We discuss the impact of SERMs on PD-1 and CTLA-4, suggesting that these SERMs co

174 Summarizing, the therapeutic index of SERMs might be improved by this bifunctional approach.

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

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

177 This study highlights the potential of SERMs as inhibitory ligands for immune checkpoint protei

178 ach to improve the therapeutic properties of SERMs.

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

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

181 263 represents a member of a novel series of SERMs that is structurally unrelated to SERMs currently

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

198 We synthesized a series of NO-releasing SERMs (NO-SERMs) and the corresponding SERMs (after NO r

199 ethylated Laso derivatives or representative SERMs and SERDs show that molecules that favor a highly

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

201 , raloxifene (a benzothiophene-type scaffold SERM) prevented the onset of photoreceptor apoptosis and

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

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

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

205 pharmacologic discovery of ovarian-targeted SERM.

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

207 We show that SERM improves the accuracy of gene imputation with order

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

209 Our study demonstrates that SERMs can modulate microtubule assembly and raises the p

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

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

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

213 in vivo biological assays reflective of the SERM profile.

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

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

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

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

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

219 differential impact in vivo In summary, the SERM raloxifene has structural and functional neuroprote

220 The SERMs investigated in this study include raloxifene, tam

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

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

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

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

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

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

227 Utilization of these SERMs in vivo closely resembled the sensitization predic

228 Ms on PD-1 and CTLA-4, suggesting that these SERMs could have therapeutic effects through immune chec

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

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

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

232 cruitment determine the cellular response to SERMs.

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

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

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

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

237 Unlike SERMs, the estrens induced reproductive organ hypertroph

238 by exploring the interaction between various SERMs and immune checkpoint pathways.

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

240 six possible candidate targets through which SERMs may mediate their effect on remyelination.

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

242 as significantly decreased by treatment with SERM 5d.