ライフサイエンスコーパス: factor Xa

1 ty related to an ability to bind and inhibit factor Xa.

2 on potency and selectivity over thrombin and factor Xa.

3 1)s(-1)) and selectively (> 20-fold) inhibit factor Xa.

4 t platelet subpopulations capable of binding factor Xa.

5 h inhibits both factor VIIa and its product, factor Xa.

6 e was changed to permit activation by bovine factor Xa.

7 atorial library based on its ability to bind factor Xa.

8 rotein, or protease activity of thrombin and Factor Xa.

9 inding site(s) on skeletal muscle myosin for factor Xa, 19 peptides (25-40 residues) representing the

10 , matrix metalloproteinase-9 (4.1-fold), and Factor Xa (3.8-fold)).

11 ies several features of the hydration of the factor Xa active site relevant to the structure-activity

12 single type of AT-binding site and high anti-factor Xa activity (137 +/- 36 units/mg).

13 ary outcomes were the percent change in anti-factor Xa activity after andexanet treatment and the per

14 from baseline of 39% in the measure of anti-factor Xa activity among patients receiving rivaroxaban

15 f edoxaban included endogenous and extrinsic factor Xa activity and edoxaban concentration.

16 re evaluated for changes in measures of anti-factor Xa activity and were assessed for clinical hemost

17 er the bolus administration, the median anti-factor Xa activity decreased by 89% (95% confidence inte

18 s who had received apixaban, the median anti-factor Xa activity decreased from 149.7 ng per millilite

19 sion of andexanet substantially reduced anti-factor Xa activity in patients with acute major bleeding

20 of 47 patients had a baseline value for anti-factor Xa activity of at least 75 ng per milliliter (or

21 h confirmed major bleeding and baseline anti-factor Xa activity of at least 75 ng per milliliter (or

22 Reduction in anti-factor Xa activity was not predictive of hemostatic effi

23 g the rivaroxaban-treated participants, anti-factor Xa activity was reduced by 92% among those who re

24 mong the apixaban-treated participants, anti-factor Xa activity was reduced by 94% among those who re

25 -terminal region of factor Va heavy chain to factor Xa activity within prothrombinase and demonstrate

26 eatment with andexanet markedly reduced anti-factor Xa activity, and 82% of patients had excellent or

27 outcome was the mean percent change in anti-factor Xa activity, which is a measure of factor Xa inhi

28 generated APC led to increased TF-dependent factor Xa activity.

29 Multiple direct anti-factor Xa agents are currently undergoing evaluation in

30 with anticoagulants that target thrombin or factor Xa alone.

31 With numerous novel factor Xa and direct thrombin inhibitor drugs completing

32 s from the ability of the aptamer to bind to factor Xa and exclude interactions between the proteinas

33 Factor Xa and factor IIa (thrombin) play roles in thromb

34 tially active prothrombinase complex between factor Xa and factor Va(2), compared with K(d)(app) for

35 100-fold accelerations of ZPI reactions with factor Xa and factor XIa to yield second order rate cons

36 ular-weight heparin: Potent activity against factor Xa and IIa, predictable pharmacokinetics after bo

37 Starting from compound 14, with low factor Xa and modest anti-thrombin inhibitory activities

38 red for the interaction of the cofactor with factor Xa and optimum rates of prothrombin cleavage.

39 methanol to multiple pockets on the proteins Factor Xa and p38 MAP kinase.

40 ral B domain which exposes binding sites for factor Xa and possibly prothrombin.

41 evealed that 16:0 acylcarnitine was bound to factor Xa and that binding did not require the gamma-car

42 ARC19499 blocks TFPI inhibition of both factor Xa and the TF/factor VIIa complex.

43 , which displays strong activity in vitro vs factor Xa and thrombin (with Ki's of 1 and 8 nM, respect

44 tralized the heparin-catalyzed inhibition of factor Xa and thrombin by AT in a Zn(2+)-dependent manne

45 ersibly inactivates the clotting proteinases factor Xa and thrombin by forming covalent complexes wit

46 ransgene-produced FVIII-SQ accelerated early factor Xa and thrombin formation, which may explain the

47 2: Direct-acting anticoagulants, such as the factor Xa and thrombin inhibitors, are relatively safe a

48 formation and markedly reduced generation of factor Xa and thrombin on platelets.

49 TF) and the downstream coagulation proteases factor Xa and thrombin significantly attenuates heme-ind

50 Antithrombin mainly inhibits factor Xa and thrombin.

51 specificity of FXIIa and its close homologue factor Xa and used these data, together with inhibitor-b

52 of the skeletal muscle myosin directly bind factor Xa and, with contributions from light chain resid

53 agulant drug that inhibits the activities of factors Xa and IIa (also known as thrombin) to prevent b

54 ly activates antithrombin as an inhibitor of factors Xa and IXa by enhancing the initial Michaelis co

55 assive 10-200-fold losses in reactivity with factors Xa and IXa in both unactivated and heparin-activ

56 determinant of antithrombin reactivity with factors Xa and IXa in the native as well as the heparin-

57 e variants exhibited basal reactivities with factors Xa and IXa, heparin affinities and thermal stabi

58 ed myosin-enhanced prothrombin activation by factors Xa and Va (50% inhibition at 1.2 mum), but it di

59 rombin generation due to binding coagulation factors Xa and Va and accelerating prothrombin activatio

60 was monitored using biolayer interferometry, factors Xa and Va each showed favorable binding interact

61 lants by providing membrane-like support for factors Xa and Va in the prothrombinase complex.

62 was bell-shaped for ZPI reactions with both factors Xa and XIa, consistent with a template-bridging

63 tor-dependent regulator of blood coagulation factors Xa and XIa.

64 Thrombin, Factor VIIa, Factor Xa, and activated protein C were not effective.

65 itor, enhances the inhibition of coagulation factor Xa, and protein Z-dependent protease inhibitor in

66 d not form stable complexes with thrombin or factor Xa, and the I207T/I207A variants inhibited both p

67 rate when enoxaparin sodium is dosed by anti-factor Xa (anti-Xa) trough level is not well described.

68 microscopy using a fluorophore-labeled anti-factor Xa antibody, which demonstrated the presence of d

69 coagulation enzymes thrombin (dabigatran) or factor Xa (apixaban, rivaroxaban, and edoxaban) and give

70 prolonged half-lives compared with wild-type factor Xa (approximately 60 minutes vs approximately 1 m

71 C6PE and C6PS binding sites of factor Xa are specific, distinct, and linked, because bi

72 Mutation of factor Xa Arg(143), Lys(148), and Arg(150) residues that

73 or Xa, heparin activates ZPI to inhibit free factor Xa as well as factor XIa and therefore may play a

74 cific fluorescence detection of thrombin and factor Xa at only 500 fM concentration.

75 t bind to the active site of factor VIIa and factor Xa based on its weak inhibition (IC50 >> 300 muM)

76 n factors, with those targeting thrombin and factor Xa being most advanced in development.

77 ed thrombin markedly increases Annexin V and factor Xa binding to platelets, consistent with the form

78 Inhibition of factor Xa by acylcarnitines was greater for longer acyl

79 consequence, heparin-catalyzed inhibition of factor Xa by antithrombin is compromised by fibrinogen t

80 ctivity of the exosite mutant inhibitor with factor Xa by approximately 2-fold but greatly increased

81 tor Va enhances activation of prothrombin by factor Xa by compressing Lnk2 and morphing prothrombin i

82 demonstrated through visualization of bound factor Xa by confocal microscopy using a fluorophore-lab

83 w that a specific and selective inhibitor of factor Xa can be engineered by incorporating factor Xa e

84 or, factor VIII, is activated by thrombin or factor Xa-catalyzed cleavage at three P1 residues: Arg-3

85 ngineered stalk with flexible linkers, and a Factor Xa cleavage site was inserted immediately in fron

86 e effects of dabigatran, the investigational factor Xa decoy andexanet alfa, and the synthetic small

87 (andexanet) is a recombinant modified human factor Xa decoy protein that has been shown to reverse t

88 Antithrombin III and anti-Factor Xa deficiencies and hypercoagulable TEG parameter

89 ally exacerbated by antithrombin III or anti-Factor Xa deficiencies and missed enoxaparin doses.

90 cidence of VTE, bleeding complications, anti-Factor Xa deficiency, and antithrombin III deficiency.

91 sue factor pathway inhibitor (TFPI) produces factor Xa-dependent feedback inhibition of factor VIIa/t

92 modified recombinant inactive form of human factor Xa developed for reversal of factor Xa inhibitors

93 to express PAI-1 in response to thrombin and factor Xa did not activate the PAR-1/PAR-2 complex.

94 congeneric ligand pairs for the test system factor Xa, elucidates physical properties of the active-

95 factor Xa can be engineered by incorporating factor Xa exosite and reactive site recognition determin

96 purified reaction mixtures composed only of factor Xa, factor Va, prothrombin, and calcium ions, myo

97 ell surface of monocytes, thereby liberating factor Xa for thrombin generation and protease activated

98 activation and forcing the release of bound factor Xa from the membrane at a venous shear rate (100

99 ibition of Factor VIIa (FVIIa)/tissue factor/Factor Xa (FVIIa/TF/FXa).

100 nformationally pliant variant of coagulation factor Xa (FXa(I16L)) rendered partially inactive by a d

101 Here we found that factor Xa (FXa) activated PAR1 at canonical Arg41 simila

102 doxaban dose, plasma concentration, and anti-Factor Xa (FXa) activity and compared efficacy and safet

103 so involved in the induction of TF-dependent factor Xa (FXa) activity by IgG-containing ICs by THP-1

104 A number of highly selective and potent factor Xa (FXa) and FIXa inhibitors were identified by s

105 nt (C3b, C5a, C5b-9) in baboons infused with factor Xa (FXa) and phospholipids (FXa/phosphatidylcholi

106 alivary anticoagulant that binds coagulation factor Xa (FXa) and zymogen FX, with formation of a quat

107 Current thought holds that factor Xa (FXa) bound in the prothrombinase complex is r

108 Protein S (PS) enhances the inhibition of factor Xa (FXa) by tissue factor pathway inhibitor-alpha

109 nt specific inhibitor of membrane-associated factor Xa (fXa) despite having an unfavorable P1 Tyr.

110 PIbeta inhibit both TF-factor VIIa-dependent factor Xa (FXa) generation and free FXa.

111 Factor Xa (FXa) has a prominent role in amplifying both

112 Inhibitors of coagulation factor Xa (fXa) have emerged as a new class of antithrom

113 of the tiger snake, Notechis scutatus, and a factor Xa (FXa) homolog.

114 ivative (6) showing poor thrombin (fIIa) and factor Xa (fXa) inhibition activities, anti-fIIa activit

115 The molecular mechanism of factor Xa (FXa) inhibition by Alboserpin, the major sali

116 approval of fondaparinux, a heparin-derived factor Xa (fXa) inhibitor, provided validation for the d

117 luding direct thrombin inhibitors (DTIs) and factor Xa (FXa) inhibitors, are emerging alternatives fo

118 -soluble phosphatidylserine (C6PS) to bovine factor Xa (FXa) leads to Ca2+-dependent dimerization in

119 Direct inhibitors of coagulation factor Xa (FXa) or thrombin are promising oral anticoagu

120 fied, and assessed for their ability to bind factor Xa (fXa) prior to and following incubation with t

121 The membrane-dependent interaction of factor Xa (FXa) with factor Va (FVa) forms prothrombinas

122 ombinase is composed of a catalytic subunit, factor Xa (fXa), and a regulatory subunit, factor Va (fV

123 ndicate that key clotting proteases, such as factor Xa (FXa), can promote atherosclerosis, presumably

124 an important anticoagulant role through the factor Xa (FXa)-dependent inhibition of tissue factor/fa

125 d physiological process culminating with the factor Xa (FXa)-mediated conversion of the prothrombin (

126 its tissue factor-factor VIIa (TF-fVIIa) and factor Xa (fXa).

127 converts it to an active cofactor (FVa) for factor Xa (FXa).

128 proved to be potent competitive inhibitor of factor Xa (fXa, Ki = 0.090 nM) and thrombin (fIIa, Ki =

129 ndent protease inhibitor (ZPI) inhibition of factors Xa (FXa) and XIa (FXIa) by a template mechanism.

130 rrower protease specificity, inhibiting only factors Xa (fXa) and XIa.

131 ctivity at 57 degrees C or in guanidinium by factor Xa generation assays.

132 Parameter values were determined by factor Xa generation assays.

133 reduced decay rates as part of the enzymatic factor Xa generation complex and retained their activiti

134 In addition, HPC TF initiated factor Xa generation without exogenous factor VIIa, and

135 nd D569A showed >80% reduction in k(cat) for factor Xa generation.

136 romote ZPI inhibition of membrane-associated factor Xa, heparin activates ZPI to inhibit free factor

137 chieved by tight binding ligands that target factor Xa in a discrete manner.

138 ites of cleavage at Arg(271) and Arg(320) to factor Xa in different orientations by pivoting the C-te

139 has been shown to reverse the inhibition of factor Xa in healthy volunteers.

140 rate constants of antithrombin inhibition of factor Xa in the presence and absence of the designed ac

141 lity to enhance ATIII-mediated inhibition of Factor Xa in vitro.

142 ors, and guanylate cyclase, respectively, in Factor Xa-inhibited (250 nM apixaban), diluted platelet

143 ion of AT activity is approximately 30nM for factor Xa inhibition and 90nM for thrombin inhibition.

144 scular bed and providing genetic support for Factor Xa inhibition as a therapeutic strategy for PAD.

145 ti-factor Xa activity, which is a measure of factor Xa inhibition by the anticoagulant.

146 OCKET AF (Rivaroxaban Once-daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism

147 ts in the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism

148 in the Rivaroxaban Once Daily, Oral, Direct Factor Xa Inhibition Compared With Vitamin K Antagonism

149 OCKET AF (Rivaroxaban Once-daily oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism

150 In the Rivaroxaban Once Daily, Oral, Direct Factor Xa Inhibition Compared With Vitamin K Antagonism

151 KET AF (Rivaroxaban Once-daily, oral, direct factor Xa inhibition Compared with vitamin K antagonism

152 KET AF (Rivaroxaban Once-Daily, Oral, Direct Factor Xa Inhibition Compared With Vitamin K Antagonism

153 In Rivaroxaban Once daily, oral, direct factor Xa inhibition Compared with vitamin K antagonism

154 KET AF (Rivaroxaban Once-Daily, Oral, Direct Factor Xa Inhibition Compared With Vitamin K Antagonism

155 aroxaban (Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared With Vitamin K Antagonism

156 rs in the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared With Vitamin K Antagonism

157 trial (Rivaroxaban Once-Daily, Oral, Direct Factor Xa Inhibition Compared With Vitamin K Antagonism

158 d that inhibition of thrombin generation via factor Xa inhibition may further reduce the risk of sten

159 ased binding to antithrombin, which enhanced Factor Xa inhibition, and binding of neuropilin-1.

160 eral anticoagulant that combines an indirect factor Xa inhibitor (fondaparinux analog) and a direct t

161 Apixaban, an oral factor Xa inhibitor administered in fixed doses, may sim

162 xtended-duration thromboprophylaxis with the factor Xa inhibitor betrixaban to reduce the risk of str

163 Whether the oral factor Xa inhibitor edoxaban can be an alternative to wa

164 The oral factor Xa inhibitor edoxaban has demonstrated safety and

165 a multinational randomized trial of the oral factor Xa inhibitor edoxaban in patients with atrial fib

166 rombolysis in Myocardial Infarction 48), the factor Xa inhibitor edoxaban was noninferior to warfarin

167 The use of an oral factor Xa inhibitor in patients stabilised after an acut

168 SAR107375), a novel potent dual thrombin and factor Xa inhibitor resulted from a rational optimizatio

169 Whether the direct factor Xa inhibitor rivaroxaban can prevent thromboembol

170 The factor Xa inhibitor rivaroxaban reduced mortality and is

171 (Alox12 or Alox15) or administration of the factor Xa inhibitor rivaroxaban significantly reduced AA

172 The oral factor Xa inhibitor rivaroxaban was noninferior to warfa

173 Apixaban, an oral factor Xa inhibitor that can be administered in a simple

174 Rivaroxaban is an oral direct factor Xa inhibitor that has been effective in preventio

175 Apixaban is a novel oral direct factor Xa inhibitor that has been shown to reduce the ri

176 Rivaroxaban is a factor Xa inhibitor that was recently reviewed by the Fo

177 of reproductive age who received direct oral factor Xa inhibitor therapy, of whom 57 had vaginal blee

178 in women of reproductive age on direct oral factor Xa inhibitor therapy.

179 luded because of the intake of a direct oral factor Xa inhibitor which has a strong impact on prothro

180 Edoxaban, an oral factor Xa inhibitor with 50% renal clearance, was noninf

181 erruption, or discontinuation of direct oral factor Xa inhibitor) and the remaining eight (14%) event

182 For each factor Xa inhibitor, a two-part randomized placebo-contr

183 A fixed-dose regimen of rivaroxaban, an oral factor Xa inhibitor, has been shown to be as effective a

184 Apixaban, an oral direct factor Xa inhibitor, is a novel anticoagulant that may r

185 Edoxaban, an oral factor Xa inhibitor, is non-inferior for prevention of s

186 Rivaroxaban, an oral factor Xa inhibitor, may provide more consistent and pre

187 Apixaban, an oral, direct factor Xa inhibitor, may reduce the risk of recurrent is

188 Rivaroxaban, an oral factor Xa inhibitor, might simplify treatment compared w

189 se rivaroxaban (2.5 mg twice-daily), an oral factor Xa inhibitor, plus acetylsalicylic acid reduced m

190 anticoagulation, the use of low doses of the factor Xa inhibitor, rivaroxaban, has shown benefit.

191 major bleeding associated with the use of a factor Xa inhibitor, treatment with andexanet markedly r

192 e clinical efficacy of PCCs in patients with factor Xa inhibitor-related ICH are needed.

193 evaluate the safety and efficacy of PCCs for factor Xa inhibitor-related ICH in a large, multicenter

194 Otamixaban is an intravenous direct factor Xa inhibitor.

195 ng within 18 hours after administration of a factor Xa inhibitor.

196 ithin 18 hours after the administration of a factor Xa inhibitor.

197 he effects of the DTI dabigatran, the direct factor Xa-inhibitor rivaroxaban, and of 2-O, 3-O desulfa

198 Factor Xa inhibitors and aspirin each reduce thrombotic

199 Compared with warfarin, factor Xa inhibitors are associated with a lower risk of

200 Two direct factor Xa inhibitors are emerging from phase II trials (

201 Oral direct factor Xa inhibitors are potentially well tolerated and

202 Is treatment with factor Xa inhibitors associated with better efficacy and

203 Compared with LMWH, lower doses of oral factor Xa inhibitors can achieve a small absolute risk r

204 Factor Xa inhibitors can prevent 4 instances of symptoma

205 onfatal pulmonary embolism, was reduced with factor Xa inhibitors compared with LMWH (4 fewer events

206 ived data from phase 3 trials of direct oral factor Xa inhibitors done at University Hospital Carl Gu

207 omplications during therapy with direct oral factor Xa inhibitors in a case series of women of reprod

208 ivaroxaban, apixaban, and edoxaban, the oral factor Xa inhibitors in the most advanced stages of deve

209 High, but not lower, doses of oral factor Xa inhibitors increased bleeding compared with LM

210 The direct factor Xa inhibitors may offer several promising alterna

211 in clinical trials suggest that direct oral factor Xa inhibitors might increase menstrual bleeding i

212 Therefore, development of the oral factor Xa inhibitors represents a translational science

213 thrombin inhibitor dabigatran etexilate and factor Xa inhibitors rivaroxaban and apixaban are new or

214 Recently, the oral factor Xa inhibitors rivaroxaban and apixaban have enter

215 In the secondary analysis, factor Xa inhibitors were associated with a reduced risk

216 Factor Xa inhibitors were associated with a reduction in

217 Factor Xa inhibitors were associated with lower rates of

218 se of anticoagulants (vitamin K antagonists, factor Xa inhibitors, and direct thrombin inhibitors) fo

219 s), including direct thrombin inhibitors and factor Xa inhibitors, are emerging options for thrombopr

220 Bleeding is a complication of treatment with factor Xa inhibitors, but there are no specific agents f

221 agulants (nOAC), which includes thrombin and factor Xa inhibitors, has been shown to be effective, bu

222 nhibitor, and rivaroxaban and apixaban, oral factor Xa inhibitors, have been found to be safe and eff

223 oral anticoagulants, such as factor IIa and factor Xa inhibitors, may provide a novel treatment appr

224 twice daily [BID], 110 mg BID), and the oral Factor Xa inhibitors, rivaroxaban and apixaban.

225 inhibitor, dabigatran etexilate, and the two factor Xa inhibitors, rivaroxaban and apixaban.

226 Since the approval of the oral factor Xa inhibitors, there have been concerns regarding

227 ts with acute major bleeding associated with factor Xa inhibitors, with effective hemostasis occurrin

228 gned to reverse the anticoagulant effects of factor Xa inhibitors.

229 atheter ablation in AF patients treated with factor Xa inhibitors.

230 arins, fondaparinux, thrombin inhibitors and factor Xa inhibitors.

231 of human factor Xa developed for reversal of factor Xa inhibitors.

232 available in the United States for the oral factor Xa inhibitors.

233 of reproductive age treated with direct oral factor Xa inhibitors: the non-interventional Dresden NOA

234 Various acylcarnitines inhibited factor Xa-initiated clotting.

235 of the protease domain of human coagulation factor Xa into a bacterial trypsin.

236 Va(2) (K(d) = approximately 6.5 mum) and to factor Xa (K(d) = approximately 91 mum).

237 ed by 100-fold the apparent Kd of myosin for factor Xa (Kd approximately 0.48 nM), primarily by reduc

238 trol group, respectively; p = 0.33) and anti-Factor Xa levels (0.4 international units/mL [0.3-0.5 in

239 Anti-Factor Xa levels in intervention patients were not highe

240 ay require laboratory confirmation with anti-factor Xa levels in patients treated with heparin, espec

241 ion suggest that novel zymogen-like forms of factor Xa might prove useful as new therapeutic procoagu

242 direct oral inhibitor of activated clotting factor Xa, might be more suitable than conventional anti

243 with a preferred IEG substrate sequence for factor Xa modestly enhanced the reactivity of the exosit

244 Here we show that factor Xa mutants with zymogen-like properties (FXa(I16L

245 (Effective aNticaoGulation with factor xA next Generation in Atrial Fibrillation [ENGAGE

246 E AF-TIMI 48 (Effective Anticoagulation with Factor Xa Next Generation in Atrial Fibrillation), SOLID

247 he ENGAGE AF (Effective Anticoagulation With Factor Xa Next Generation in Atrial Fibrillation)-TIMI 4

248 IMI 48 trial (Effective Anticoagulation With Factor Xa Next Generation in Atrial Fibrillation-Thrombo

249 E AF-TIMI 48 (Effective Anticoagulation with Factor Xa Next Generation in Atrial Fibrillation-Thrombo

250 E AF-TIMI 48 (Effective Anticoagulation With Factor Xa Next Generation in Atrial Fibrillation-Thrombo

251 E AF-TIMI 48 (Effective Anticoagulation With Factor Xa Next Generation in Atrial Fibrillation-Thrombo

252 IMI 48 trial (Effective Anticoagulation with Factor Xa Next Generation in Atrial Fibrillation-Thrombo

253 E AF-TIMI 48 (Effective Anticoagulation with factor Xa Next Generation in Atrial Fibrillation-Thrombo

254 IMI 48 trial (Effective Anticoagulation With Factor Xa Next Generation in Atrial Fibrillation-Thrombo

255 E AF-TIMI 48 (Effective Anticoagulation with Factor Xa Next Generation in Atrial Fibrillation-Thrombo

256 o regulate the function of blood coagulation factor Xa on membrane surfaces.

257 uding LMWH, vitamin K antagonists, or direct factor Xa or direct factor IIa inhibitors.

258 First, we found that factor Xa or thrombin activation of PAR-1 led to a rapid

259 n of exogenous recombinant TFshort inhibited factor Xa or thrombin generation, excluding a dominant-n

260 fibrin formation by selective inhibition of factor Xa or thrombin, has renewed the interest in dual-

261 vailable anticoagulants that directly target factor Xa or thrombin.

262 oagulants are a class of agents that inhibit factor Xa or thrombin.

263 f new oral anticoagulants that target either factor Xa or thrombin.

264 n, other coagulation proteases, such as fXa (factor Xa) or aPC (activated protein C), independently m

265 ated trypsin-like serine proteases thrombin, factor Xa, or activated protein C.

266 ed with low concentrations of tissue factor, factor Xa, or alpha-thrombin.

267 oteolytic activation of FVIII by thrombin or factor Xa, or with its binding to phospholipid surfaces,

268 d the selectivity of alpha1PI for inhibiting factor Xa over thrombin by approximately 1000-fold.

269 In response to thrombotic challenge with factor Xa/phospholipids, EPCR(R84A/R84A) mice generate m

270 Since factor Xa plays a central role in thrombosis, the inhibi

271 complex concentration and thereby attenuate factor Xa production.

272 I were strategically constructed with tandem factor Xa protease cleavage sites in the loop between th

273 rcome this difficulty via the insertion of a Factor Xa proteolytic cleavage site to acquire the optim

274 aelis complex through either ZPI-PZ-lipid or factor Xa-PZ-lipid intermediates was rate-limiting.

275 h independent kinetic analyses of ZPI-PZ and factor Xa-PZ-membrane complex formation suggested that a

276 own for heparin bridging of the antithrombin-factor Xa reaction.

277 lly to accelerate the membrane-dependent ZPI-factor Xa reaction.

278 Maximal accelerations of ZPI-factor Xa reactions required calcium, which augmented th

279 yptophan fluorescence changes and to enhance factor Xa reactivity in antithrombin, indicative of norm

280 ng proteolysis of the factor VIII mutants by factor Xa revealed modest rate reductions (<5-fold) in g

281 at directly inhibit thrombin (dabigatran) or factor Xa (rivaroxaban, apixaban) are effective and safe

282 Direct infusion of factor Xa should also restore hemostasis; however, it ha

283 tively cleaving the 3-4 loop (via introduced Factor Xa sites) we demonstrate that it plays a vital ro

284 The absence of the Arg173-like residue in factor Xa supported the observed selectivity of inhibiti

285 Secondary outcomes were anti-factor Xa, the incidence of hemorrhagic and thrombotic e

286 ing a protease recognition site specific for factor Xa, thrombin, or caspase 3.

287 deling in pulmonary fibrosis (PF); TGF-beta, Factor Xa, thrombin, plasmin and uPA all induced fibrobl

288 he MARCKS peptides antagonize the binding of factor Xa to phosphatidylserine and inhibit the enzymati

289 prothrombin is proteolytically converted by factor Xa to the active protease thrombin in a reaction

290 eviously, we found that a novel zymogen-like factor Xa variant (FXa-I16L) was effective in correcting

291 the K(m) for prothrombin conversion with the factor Xa variants assembled into prothrombinase was una

292 8]; warfarin vs dabigatran 0.88 [0.59-1.36]; factor Xa vs low-molecular-weight heparin 1.02 [0.42-2.7

293 th warfarin or low-molecular-weight heparin (factor Xa vs warfarin IRR 0.78 [95% CrI 0.47-1.08]; warf

294 Binding studies showed that purified factor Xa was bound to immobilized peptides HC796-835 an

295 The Gla domain of factor Xa was not required for myosin's prothrombinase e

296 ile the affinity of all mutant molecules for factor Xa was similar to that for factor Va(WT).

297 caspase 3, 1.0nM for thrombin, and 58nM for factor Xa were realized with a scanning fluorometer.

298 PARs) can activate HSCs through thrombin and factor Xa, which are known PAR agonists, and cause micro

299 The interaction of factor Xa with factor Va on membranes to form prothrombi

300 entral role in thrombosis, the inhibition of factor Xa with low-dose rivaroxaban might improve cardio

301 ly results from the binding of RNA(11F7t) to factor Xa with nanomolar affinity in a Ca(2+)-dependent