ライフサイエンスコーパス: complement inhibitor

1 trophil elastase inhibitor), and eculizumab (complement inhibitor).

2 and the characterization of a novel targeted complement inhibitor.

3 n digestion with and without the addition of complement inhibitor.

4 ize of CR1, is a therapeutic candidate for a complement inhibitor.

5 arly suboptimal response/failure of previous complement inhibitor.

6 intracellular role relative to its role as a complement inhibitor.

7 evels and localization of intrinsic membrane complement inhibitors.

8 ications for the design of clinically useful complement inhibitors.

9 for the design of antiviral therapeutics and complement inhibitors.

10 phosphatidylinositol-anchored (GPI-anchored) complement inhibitors.

11 ntaneous activation of which is regulated by complement inhibitors.

12 y the lack of nontoxic and/or nonimmunogenic complement inhibitors.

13 pecies selectivity of endogenously expressed complement inhibitors.

14 ue to increased expression of membrane-bound complement inhibitors.

15 newed emphasis on development of therapeutic complement inhibitors.

16 erapy - and in patients who had not received complement inhibitors.

17 eceived anti-C5 therapy or have not received complement inhibitors.

18 ne thrombocytopenia, might also benefit from complement inhibitors.

19 rious disease-associated pathways, including complement inhibitors.

20 the complement system, including binding to complement inhibitors.

21 an additional 15% by blocking CD55 and CD59 complement inhibitors.

22 protein (C4BP) and factor H, which are both complement inhibitors.

23 rats and MCF7 cells expressing different rat complement inhibitors, a model of human breast cancer wa

24 Although the majority of staphylococcal complement inhibitors act on the alternative pathway to

25 e investigated a novel strategy to overwhelm complement inhibitor activity and amplify complement act

26 cipients were conditioned by combinations of complement inhibitors, adsorption of natural antibodies,

27 and those individuals who were treated with complement inhibitors all recovered with no adverse reac

28 Guianensin emerges as a novel complement inhibitor and a potential candidate for thera

29 ay revealed an increase in the expression of complement inhibitors and a decrease in the expression o

30 D19 chimeric antigen receptor T cells, novel complement inhibitors and agents that can target fibrosi

31 udies addressing therapeutic options such as complement inhibitors and anti-inflammatory agents.

32 hus, diabetes causes defective regulation of complement inhibitors and complement activation that pre

33 his model may be useful in the evaluation of complement inhibitors and other neuroprotectants intende

34 cooperation between membrane and fluid phase complement inhibitors and the body's ability to adaptive

35 e-group trial, patients who had not received complement inhibitors and who had lactate dehydrogenase

36 Treatment of xenograft recipients with complement inhibitors and xenoreactive natural antibody

37 sing new class of C3b-binding small-molecule complement inhibitors and, to our knowledge, provides th

38 h as statins, hydroxychloroquine, rituximab, complement inhibitors, and interventions aimed at disrup

39 ts, compares the results with those of other complement inhibitors, and summarizes potentially produc

40 receptors (TLR1-6-10 cluster), cytokine and complement inhibitors, and the kallikrein system.

41 Rate of TEs was halved in patients receiving complement inhibitors, and varied according to PNH granu

42 the clinician by providing several different complement inhibitors/antagonists for controlling comple

43 ctivation of complement (C4d and C5b-9), the complement inhibitor apolipoprotein J (apo J), and marke

44 Various novel complement inhibitors are being developed and several ar

45 While a few complement inhibitors are in clinical use, there is stil

46 er have been hampered by the fact that human complement inhibitors are not effective against rodent c

47 Complement inhibitors are now approved for use in atypic

48 cesses and in xenograft rejection, efficient complement inhibitors are of great interest.

49 ells from inadvertent complement attack, and complement inhibitors are often up-regulated on tumors,

50 ggest that soluble domains of membrane-bound complement inhibitors are potential candidates for preve

51 Because the membrane-associated complement inhibitors are very effective, recombinant so

52 t positions 4 and 7 of compstatin, a peptide complement inhibitor, are crucial for its interaction wi

53 found that IalphaI is not an essential human complement inhibitor as was reported for mice and that s

54 iscuss various injury site-specific targeted complement inhibitors as potential therapeutic agents fo

55 ational engineering approaches using natural complement inhibitors as potential therapeutics are high

56 om novel drug candidates, including SPMs and complement inhibitors as previously studied in animal mo

57 s for the development and therapeutic use of complement inhibitors as well as the interpretation of f

58 rcinomas of the lung, do express one or more complement inhibitors at a level likely to inhibit compl

59 ay suggest templates for the design of novel complement inhibitors based upon the SCIN structure.

60 Microbial complement inhibitor-binding molecules can be promising

61 The targeted complement inhibitors bound to C3-opsonized cells, and a

62 pplement the activity of membrane-associated complement inhibitors by release of soluble forms of DAF

63 eterozygous deficiency of first component of complement-inhibitor (C1INH).

64 el, hitherto unknown interaction between the complement inhibitor C4b-binding protein (C4BP) and plas

65 type, uses exclusively protein H to bind the complement inhibitor C4b-binding protein (C4BP).

66 serum killing by recruiting to its surface a complement inhibitor C4b-binding protein, which is also

67 study, PRELP was found to interact with the complement inhibitor C4b-binding protein, which was sugg

68 The structurally related soluble complement inhibitors C4b-binding protein (C4BP) and fac

69 The complement inhibitors C4b-binding protein and factor H a

70 As a complement inhibitor, C4BP also promotes apoptotic cell

71 These data suggest that complement inhibitors can enhance the immunocompatibilit

72 tion and suggests that GPI-anchored membrane complement inhibitors can regulate T cell immunity to vi

73 t difference in the expression of individual complement inhibitor CD46 (mean channel fluorescence [MC

74 tumor effect of rituximab, the expression of complement inhibitors CD46, CD55, and CD59 was analyzed

75 g neovessel clearance by down-regulating the complement inhibitor Cd55 specifically on neovessels, al

76 neovessels, decreased the expression of the complement inhibitor Cd55.

77 ion-selective channel protein 3 (VDAC3), and complement inhibitor CD55.

78 y in follicular lymphoma cells in vitro, and complement inhibitors CD55 and CD59 may regulate this pr

79 Expression of the complement inhibitors Cd55 and Cd59 was significantly de

80 These proteins include the complement inhibitors CD55 and CD59, and this explains t

81 By contrast, mRNAs for the complement inhibitor CD59 and the cytokine IL-1beta were

82 internalization and rapid degradation of the complement inhibitor CD59, and highlights the potential

83 wn that for effective functioning of soluble complement inhibitor CD59, binding of CD59 to the cell s

84 ked surface proteins, including the terminal complement inhibitor CD59, on hematopoietic stem cells.

85 ions of the heterodimeric apolipoprotein and complement inhibitor, clusterin (CL, 80 kDa), with activ

86 combinant soluble form of the mouse membrane complement inhibitor complement receptor-related gene y

87 o efficiently compete with the physiological complement inhibitor, complement factor H (CFH), for lig

88 ormation, we developed/characterized a novel complement inhibitor composed of single-chain antibody (

89 We describe a targeted complement inhibitor, comprising complement receptor of

90 14 inhibition alone and combined with the C3 complement inhibitor compstatin (Cp40), on the bacteria-

91 of C3, which contains a binding site for the complement inhibitor compstatin and is considered critic

92 cal evidence showing that treatment with the complement inhibitor compstatin Cp40 inhibited the expre

93 Pretreatment of plasma with the complement inhibitor compstatin reduced opsonization >2-

94 le cystathionine (thioether) analogue of the complement inhibitor compstatin.

95 y-Ig), whether exogenous administration of a complement inhibitor could lessen renal injury.

96 Disruption of the ability of NiV to recruit complement inhibitors could form the basis for the devel

97 Recipient mice were treated with the complement inhibitor CR2-Crry or vehicle control (n=6).

98 ermore, treatment of wild-type mice with the complement inhibitor CR2-Crry provided protection equiva

99 ice were treated with the targeted murine C3 complement inhibitor, CR2-Crry, from 16 to 24 wk of age

100 combinant soluble form of the mouse membrane complement inhibitor Crry (complement receptor-related g

101 Viral overexpression of the complement inhibitor Crry at C3-bound synapses decreased

102 erfering RNA-mediated down-regulation of the complement inhibitor Crry on MB49 murine bladder cancer

103 h H(2)O(2) reduced surface expression of the complement inhibitors DAF, CD55, and CD59, and impaired

104 ive and retro-oriented versions of the human complement inhibitor decay-accelerating factor (DAF), as

105 -12 levels in mice deficient in the membrane complement inhibitor decay-accelerating factor (DAF).

106 C terminus of soluble forms of the membrane complement inhibitors decay accelerating factor (DAF) or

107 roteins, we examined the distribution of the complement inhibitors decay-accelerating factor (DAF), C

108 tructural and functional analog of the human complement inhibitors decay-accelerating factor and memb

109 t study, we investigated the consequences of complement inhibitor down-regulation on the effector and

110 components (e.g., Factor B) and infusion of complement inhibitors (e.g., Crry, anti-C5 Ab) protect a

111 lthough early reports of the efficacy of the complement inhibitor eculizumab are promising, the outco

112 In the last year the complement inhibitor eculizumab has been used successful

113 he regulatory approval of the first-in-class complement inhibitor eculizumab revolutionized the clini

114 The terminal complement inhibitor eculizumab was recently shown to be

115 es of UNbC5-1 and UNbC5-2 overlap with known complement inhibitors eculizumab and RaCI3, respectively

116 These data indicate that complement inhibitors expressed on a tumor cell can supp

117 It has been hypothesized that complement inhibitors expressed on the surface of tumor

118 Complement inhibitors expressed on tumor cells provide a

119 Complement inhibitors expressed on tumor cells provide a

120 pendent of a requirement to target and block complement inhibitor expression or function, which is di

121 of carcinomas and showed no correlation with complement inhibitor expression.

122 n proteins combining the alternative-pathway complement inhibitor factor H (fH(1-5)) with an anti-C3d

123 he outer surface protein CspZ that binds the complement inhibitor factor H (FH) to facilitate bacteri

124 Binding of the complement inhibitor factor H (fH) to the surface of Nei

125 e evolutionarily and structurally related to complement inhibitor factor H (FH), the initial assumpti

126 subvert complement, including binding of the complement inhibitor factor H (FH).

127 that NspA is a human-specific ligand of the complement inhibitor factor H (FH).

128 enhances binding of the alternative pathway complement inhibitor factor H and renders otherwise seru

129 paper we report that the ability to bind the complement inhibitor factor H is a general characteristi

130 our results suggest that, in contrast to the complement inhibitor factor H, CFHR4 acts as an enhancer

131 activates complement, but it also binds the complement inhibitor factor H.

132 g a mutation abrogating binding to the human complement inhibitor factor H. The resulting vaccine can

133 Gonococci bind the complement inhibitors factor H (FH) and C4b-binding prot

134 the Lyme disease spirochete, binds the host complement inhibitors factor H (FH) and FH-like protein

135 Furthermore, IAPP also bound complement inhibitors factor H and C4b-binding protein (

136 lter C1q interaction but affected binding of complement inhibitors factor H and C4b-binding protein.

137 oproteins on its surface that bind the human complement inhibitors factor H and factor H-like protein

138 gonorrhoeae to bind the alternative pathway complement inhibitor, factor H (fH), and evade killing b

139 g outer surface proteins that bind to a host complement inhibitor, factor H (FH).

140 specifically interacts with the soluble host complement inhibitor, factor H.

141 idal activity (SBA) and block binding of the complement inhibitor fH.

142 ctural homology with the alternative pathway complement inhibitor FH.

143 t approval of eculizumab as a first-in-class complement inhibitor for the treatment of PNH validates

144 this review, possible applications of these complement inhibitors for treatment of complement-mediat

145 substitutions that occur in the more potent complement inhibitor from Variola (small pox) virus.

146 hese data support a hypothesis that blocking complement inhibitor function on tumor cells will not on

147 ypothesis, the species-selective activity of complement inhibitors has been a hindrance to investigat

148 A key hurdle in the development of complement inhibitors has been the determination of thei

149 These data suggest that sLex-decorated complement inhibitors have enhanced antiinflammatory eff

150 As such, complement inhibitors have enormous potential to allevia

151 Complement inhibitors have entered clinical use and have

152 pite promising preclinical results, systemic complement inhibitors have not significantly improved DG

153 was engineered to express the human terminal complement inhibitor hCD59.

154 a family of tick-derived alternative pathway complement inhibitors, hereafter termed CirpA.

155 Recombinant soluble complement inhibitors hold promise for the treatment of

156 s This protein is composed of two domains of complement inhibitor human FH (FH complement control pro

157 The effects of a complement inhibitor, IgG-FH(1-5) (factor H-immunoglobul

158 tigated the therapeutic effect of a targeted complement inhibitor in recipients of BD donor hearts an

159 dardized monitoring of patients treated with complement inhibitors in clinical practice is needed.

160 ess to treatment, and the next generation of complement inhibitors in complement-mediated HUS.

161 retinal vessels and the decreased levels of complement inhibitors in diabetic rats, as well as the l

162 Transgenic expression of human complement inhibitors in donor cells and organs has sign

163 s and provides a rationale for investigating complement inhibitors in future clinical trials.

164 We propose an approach for sequencing complement inhibitors in PNH.

165 d against C1s and a full pipeline of several complement inhibitors in preclinical and clinical develo

166 to investigate the role of these endogenous complement inhibitors in renal IRI.

167 to investigating the role of membrane-bound complement inhibitors in rodent models of human cancer.

168 utic implications for use of MCP isoforms as complement inhibitors in such areas as xenotransplantati

169 ed to investigate the role of complement and complement inhibitors in tumor progression.

170 lement receptor-related protein y (sCrry), a complement inhibitor, in the brains of hAPP mice.

171 with ongoing or published clinical trials of complement inhibitors include paroxysmal nocturnal hemog

172 To date several complement inhibitors, including recombinant forms of co

173 Intravitreal complement inhibitors injections (IVCIs) slowed progress

174 l needs that have thrust a new generation of complement inhibitors into clinical development for a va

175 viruses SV5 and MuV incorporate cell surface complement inhibitors into progeny virions as a mechanis

176 role and suggest that targeted therapy using complement inhibitors is a potential therapeutic option

177 088, BIVV020), a second-generation classical complement inhibitor, is a humanized monoclonal antibody

178 recombinant fusion proteins consisting of a complement inhibitor linked to a C3 binding region of co

179 the retinal levels of CD55 and CD59, the two complement inhibitors linked to the plasma membrane by g

180 e, we describe the function of an endogenous complement inhibitor, mannan-binding lectin (MBL)-associ

181 The targeting of systemically administered complement inhibitors markedly enhanced their efficacy a

182 Complement inhibitors may be useful therapeutically in a

183 of the TMA samples, suggesting that terminal complement inhibitors may have a beneficial effect in th

184 and strongly suggest that in disease flares complement inhibitors might have therapeutic value.

185 ed the efficacy and safety of ravulizumab in complement inhibitor-naive children (under 18 years) wit

186 meters with no unexpected safety concerns in complement inhibitor-naive children with atypical hemoly

187 ucted in 12 hospitals from eight countries), complement inhibitor-naive patients with paroxysmal noct

188 Endogenous membrane-associated complement inhibitors normally protect endothelial cells

189 emic inhibition, CR2-mediated targeting of a complement inhibitor of activation improved bioavailabil

190 )S(-) cells displayed potent binding of host complement inhibitors of C3 convertase, viz.

191 compared functional profiles of the poxviral complement inhibitors of smallpox, vaccinia, and monkeyp

192 hibits different relative affinities for the complement inhibitors of various potential animal hosts.

193 eutic effect to that of Ornithodoros moubata complement inhibitor (OmCI), a known inhibitor of C5 act

194 eukotriene B4 inhibitor Ornithodoros moubata complement inhibitor (OmCI; also known as coversin) alon

195 data show directly that the expression of a complement inhibitor on a tumor cell promotes tumor grow

196 These results show that expression of complement inhibitors on a tumor cell has functional con

197 to determine the effect of pexelizumab, a C5 complement inhibitor, on infarct size in patients with S

198 plicating IalphaI as a potentially important complement inhibitor once enriched onto hyaluronan moiet

199 ch a chimaera has therapeutic potential as a complement inhibitor or immune modulator.

200 Supplementing an exogenous complement inhibitor, or up-regulating MSC expression le

201 cophore models have been constructed for the complement inhibitor peptide compstatin, using first pri

202 To determine whether complement inhibitors play a role in regulating the anti

203 t model, neither of two potent soluble-phase complement inhibitors prevented complement activation or

204 study suggested that eculizumab, a terminal complement inhibitor, produced clinically meaningful imp

205 Membrane-bound complement inhibitors protect host cells from inadverten

206 ting the efficacy and safety of the terminal complement inhibitor ravulizumab in adult patients with

207 MG to investigate the efficacy of a novel C5 complement inhibitor rEV576, recombinantly produced prot

208 The staphylococcal complement inhibitor (SCIN) protein exhibits a particula

209 One of these, the staphylococcal complement inhibitor (SCIN), acts at the level of the C3

210 Among these are the staphylococcal complement inhibitors (SCIN), which are composed of thre

211 Staphylococcal complement inhibitors (SCINs) are one important class of

212 Thus, rMil2, particularly combined with complement inhibitors, should be well suited for in vivo

213 The complement inhibitor soluble complement receptor type 1

214 Thus, pneumococci bind complement inhibitors such as C4b-binding protein (C4BP)

215 Certain pathogens recruit host complement inhibitors such as factor H (fH) to evade the

216 f inadequate reticulocyte counts, use of the complement inhibitor sutimlimab for relapsed cold AIHA,

217 ing a single chain Ab fragment and show that complement inhibitors targeted to the tubular epithelium

218 fore, mini-FH could potentially be used as a complement inhibitor targeting host surfaces, as well as

219 es in an enzyme-like fashion, stoichiometric complement inhibitors targeting C3, C5, factor B, and fa

220 d both C3b and C4b but is also a more potent complement inhibitor than other recombinant CR1-based th

221 Mirococept is a potent membrane-localizing complement inhibitor that can be administered ex vivo to

222 The triple fusion approach yielded a potent complement inhibitor that efficiently inhibits all three

223 ARGX-117 is a promising new complement inhibitor that is uniquely positioned to targ

224 C4b-binding protein (C4BP) is a fluid-phase complement inhibitor that prevents uncontrolled activati

225 main protein SRPX2 is a neuronally expressed complement inhibitor that regulates complement-dependent

226 sotype and, when fused to Crry, results in a complement inhibitor that should not be recognized as fo

227 an (LNP023) is an oral, proximal alternative complement inhibitor that specifically binds to Factor B

228 ety of iptacopan (LNP023), an oral, proximal complement inhibitor that targets factor B to selectivel

229 Compstatin peptides are complement inhibitors that bind and inhibit cleavage of

230 ne system, and the rational design of potent complement inhibitors that might be used as therapeutic

231 ogical diseases, but whether neurons express complement inhibitors that protect synapses against comp

232 The number of available complement inhibitor therapies has also increased during

233 t treatment is plasma infusion/exchange, but complement inhibitor therapy provides hope for the futur

234 st successful phase 3 clinical trial data of complement inhibitor therapy to date.

235 amined the capability of a novel therapeutic complement inhibitor to prevent pathological complement

236 nd that it fulfills this role by acting as a complement inhibitor to prevent virus-triggered compleme

237 gous for hemoglobin S (HbSS) mouse model and complement inhibitors to determine whether anaphylatoxin

238 In a strategy to specifically target complement inhibitors to sites of complement activation

239 come these limitations, approaches to target complement inhibitors to specific sites have been invest

240 ent years have not only introduced the first complement inhibitors to the clinic but also filled the

241 Targeting complement inhibitors to the site of complement activati

242 onectin, the human adhesive glycoprotein and complement inhibitor, to facilitate attachment to epithe

243 Such a triple fusion complement inhibitor (TriFu) was recombinantly expressed

244 nal (anti-C5 ravulizumab and crovalimab) and complement inhibitors upstream C5 (anti-C3 pegcetacoplan

245 eakthrough hemolysis and briefly discuss new complement inhibitors upstream of C5 that are in clinica

246 ribe a strategy for Ag-specific targeting of complement inhibitors using a single chain Ab fragment a

247 Eculizumab, the first-in-class complement inhibitor, was approved for PNH in 2007.

248 In a therapeutic paradigm using targeted complement inhibitors, we investigated the role of compl

249 Subsequently, complement inhibitors were tested on serum from the pati

250 stance is a unique protein, FACIN (F. alocis complement inhibitor), which binds to C3, resulting in s

251 enotypes via CD55, an intrinsic cell surface complement inhibitor, which was identified in a comparat

252 CD46 is a cell surface complement inhibitor widely expressed in human tissues,

253 Whether complement inhibitors will be useful to treat TSEs remai

254 ction and the use of new therapies including complement inhibitors will contribute to increasing succ

255 e use of complement receptor 2 (CR2)-Crry, a complement inhibitor with the ability to target C3 break

256 nearly natural sequences that act as potent complement inhibitors with greatly improved therapeutic

257 reclinical model will allow testing of novel complement inhibitors with the aim of developing precise

258 In particular, BTH may occur with all complement inhibitors, with a frequency of 10% to 15% ov

259 Thus, altered expression of a complement inhibitor within the tubular epithelium appea

260 However, expression of complement inhibitors without eliminating xenogeneic nat