ライフサイエンスコーパス: MTX

1 MTX (0.75 mg/kg per day) was administered for 5 days, an

2 MTX AUC0-48h was a significant predictor of overall toxi

3 MTX concentrations in a patient's serum undergoing chemo

4 MTX induces death in rapidly replicating cells and is us

5 MTX inhibits 5-aminoimidazole-4-carboxamide ribonucleoti

6 MTX inhibits thymidine synthesis by targeting dihydrofol

7 MTX is the 'anchor drug' in all rheumatoid arthritis tre

8 MTX use was associated with a 70% reduction in mortality

9 MTX use was associated with reduced risk of death (adjus

10 MTX-ARG rats demonstrated greater jejunal and ileal bowe

11 MTX-inducible changes in DHFR(FS) and TYMS(SS) expressio

12 MTX-related clinical neurotoxicity is transient, and mos

13 co-2 vs. co-culture cell model: Caco-2:HT-29-MTX (90:10%) and colonic fermentation were determined fo

14 etter to mucus-producing cells such as HT-29-MTX than to the parental HT-29 cells.

15 olon cancer cell line and was effective in a MTX-transport resistant leukemic cell line.

16 single-agent methotrexate and folinic acid (MTX-FA; SIR, 0.7; 95% CI, 0.5 to 1.1) and also for patie

17 replications via interaction with Cdt1 after MTX treatment, and DHFR amplification proceeded in v-K-r

18 nths with folinic acid rescue 24 hours after MTX administration.

19 lative risk of early menopause was low after MTX-FA but was substantial after EMA-CO, reaching 13% by

20 o overall increased risk of malignancy after MTX-FA or EMA-CO.

21 NR could deliver the chemotherapeutic agent, MTX to tumor cells and induce effective cell killing.

22 Inclusion of low-dose prednisone in an MTX-based treatment strategy for tight control in early

23 ssed transgenes is similarly decreased in an MTX-inducible manner.

24 rthermore, enforced expression of Cks1 in an MTX-resistant breast cancer cell line was found to resto

25 This has led to the development of an MTX-resistant DHFR, DHFR L22F, F31S (DHFR(FS)), to rescu

26 Patients were randomly assigned to an MTX-based, tight control strategy starting with either M

27 Cotherapy with AICAR and MTX could represent a novel strategy to treat metabolic

28 ith the adenosine binding domain of DHFR and MTX interacting with the loop domain.

29 imab in combination with a TNF inhibitor and MTX was consistent with the safety profile of rituximab

30 ated with a single dose of methotrexate, and MTX-ARG rats were treated with oral ARG following inject

31 onditions, a decrease in the IC50 of MTX and MTX-loaded MSNR was observed when compared to normoxic c

32 ions allowed the locations of the NADPH and MTX ligands to be mapped, with NADPH associated with the

33 ibitor methotrexate (MTX), or both NADPH and MTX were characterized by 193 nm ultraviolet photodissoc

34 of MTX plus etanercept, triple therapy, and MTX monotherapy among patients with early RA with active

35 the MTX plus etanercept, triple therapy, and MTX monotherapy arms.

36 vity significantly decreased during UDCA and MTX-treatment and also after OLT.

37 (parSlo) is inherently insensitive to MTX as MTX shifted the activation of heterologously expressed p

38 ab or placebo in combination with background MTX and a TNF inhibitor.

39 for AMPK as a direct molecular link between MTX and energy metabolism in skeletal muscle.

40 ion levels of CHEK2 and RANGAP1 mRNA between MTX-treated and non-MTX-treated patients.

41 the notion that this pathway is activated by MTX in vivo and may contribute to the efficacy of MTX in

42 was to explore the induction of apoptosis by MTX.

43 while CHEK2 and RANGAP1 were not induced by MTX.

44 otrexate (HD-MTX) or Capizzi methotrexate (C-MTX) during interim maintenance (IM) or prednisone or de

45 vs 58% +/- 4% for MRD-negative vs positive C-MTX subjects; 88% +/- 2% vs 68% +/- 4% for HD-MTX subjec

46 Although HD-MTX was superior to C-MTX, MRD retained prognostic significance in both groups

47 loading, in vitro MTX release, and cellular MTX delivery under hypoxic conditions.

48 PB compared with BM: 34% versus 38% with CNI-MTX and 27% versus 20% with CNI-MMF GVHD prophylaxis.

49 lacebo in patients with active RA continuing MTX treatment.

50 Compared with a normal control, MTX increased the density of osteoclasts within the meta

51 In tissue culture, MTX induced expression of both p53 and p21 by JNK-2- and

52 e testing during MTX therapy, the cumulative MTX dose corresponded to a statistically significant ass

53 Fourteen patients (3.8%) developed MTX-related clinical neurotoxicity.

54 UVPD of the binary DHFR.NADPH and DHFR.MTX complexes led to an unprecedented number of fragment

55 ic progression significantly better than did MTX alone in the GO-BEFORE study.

56 d improvement in physical function than does MTX alone.

57 TX with leucovorin rescue or escalating dose MTX with PEG asparaginase without leucovorin rescue.

58 tudy that included five courses of high-dose MTX and 13 to 25 doses of triple intrathecal therapy.

59 data on safety of intrathecal and high-dose MTX rechallenge in patients with neurotoxicity.

60 uence the kinetics and response to high-dose MTX therapy in childhood ALL.

61 were randomly assigned to receive high-dose MTX with leucovorin rescue or escalating dose MTX with P

62 challenged with intrathecal and/or high-dose MTX, 12 did not experience recurrence of neurotoxicity.

63 = .009), a frequent side effect of high-dose MTX.

64 evels in patients with RA receiving low-dose MTX supports the notion that this pathway is activated b

65 ceiving MTX than in those receiving low-dose MTX, with no difference in expression levels of CHEK2 an

66 ictor of overall toxic adverse events during MTX courses (R(2) = 0.043; P < .001), whereas the thymid

67 onitor for risk of worsening fibrosis during MTX therapy.

68 worsening of hepatic fibrosis scores during MTX therapy.

69 ars) underwent NASH FibroSure testing during MTX therapy and were eligible for correlation analysis.

70 who underwent NASH FibroSure testing during MTX therapy, the cumulative MTX dose corresponded to a s

71 tight control strategy starting with either MTX and prednisone or MTX and placebo.

72 All major treatments except MTX-FA increased the risk of early menopause.

73 The conjugate G5-FA-MTX acted as a potent antiinflammatory agent and reduced

74 evaluate the therapeutic potential of G5-FA-MTX.

75 apoptosis were determined 72 hours following MTX injection.

76 y and improves intestinal recovery following MTX- injury in the rat.

77 ompared with no GC use, after adjustment for MTX and TNF inhibitor use (HR(adj) 3.1 [95% CI 2.0, 4.7]

78 he binding constant (K) value calculated for MTX was 3.821x10(5)M(-1).

79 The sensor was calibrated for MTX in phosphate buffer at different dynamic range by va

80 Our results demonstrate mechanisms for MTX-induced osteoclastogenesis and show that MTX induces

81 to generate individual propensity scores for MTX use at study entry and during followup in a time-var

82 rolling for individual propensity scores for MTX use.

83 We found MTX markedly reduced the threshold for AICAR-induced AMP

84 ne plus hydroxychloroquine), or step-up from MTX monotherapy to one of the combination therapies (MTX

85 ediate combination treatment or step-up from MTX monotherapy.

86 Furthermore, MTX activated AMPK in wild-type HEK-293 cells.

87 ative affinities: raltitrexed > pemetrexed > MTX) at low pH.

88 Although HD-MTX was superior to C-MTX, MRD retained prognostic signi

89 TX subjects; 88% +/- 2% vs 68% +/- 4% for HD-MTX subjects).

90 to receive either high-dose methotrexate (HD-MTX) or Capizzi methotrexate (C-MTX) during interim main

91 HT29-MTX cells contained >1000-fold higher levels of UGT1A8 m

92 In the intestinal Caco-2/HT29-MTX co-culture model, overall relative glucuronidation r

93 es, Caco-2 (colorectal adenocarcinoma), HT29-MTX-E12 (colorectal adenocarcinoma) and HepG2 (hepatocel

94 of living cultured human colonic cells (HT29-MTX) and human colonic tissue explants.

95 lateral parts of the plasma membrane of HT29-MTX cells.

96 l geometries of the MTX(Glu)5 and hydrolyzed MTX(Glu)1 in the mutant complexes differ significantly f

97 tant complexes with MTX(Glu)5 and hydrolyzed MTX(Glu)1, revealing the complete set of key residues in

98 (TYMS(SS)) is resistant to MTX and improves MTX resistance of DHFR(FS) in primary T cells.

99 The interindividual variability in MTX kinetics had a substantial genetic component between

100 EGylated MSNR (PMSNR) demonstrated increased MTX release compared to non-PEGylated particles.

101 amine outcomes of a blinded trial of initial MTX monotherapy with the option to step-up to combinatio

102 demonstrate in a blinded trial that initial MTX monotherapy with the option to step-up to combinatio

103 he 370 evaluable participants in the initial MTX group, 28% achieved low levels of disease activity a

104 Participants assigned to initial MTX who required step-up to combination therapy at 24 we

105 re and 72 hours following vehicle injection, MTX rats were treated with a single dose of methotrexate

106 actory to high-dose systemic and intrathecal MTX plus IV rituximab.

107 Interventions: Intravenous MTX (4 mg/kg) monthly for 5 months with folinic acid res

108 during IM with vincristine and escalating IV MTX improved EFS.

109 1.2% and 96.5% +/- 0.8% for those on the IV MTX arms (P = .009, P = .66).

110 ificantly from those of the previously known MTX(Glu)1, providing polymorphic information.

111 LEF, and particularly those on combined LEF+MTX, should be monitored closely for hepatotoxicity.

112 tent activator of BK channels is mallotoxin (MTX), which produces a very large hyperpolarizing shift

113 Methotrexate (MTX) can cause significant clinical neurotoxicity and as

114 Methotrexate (MTX) is a widely used anticancer and antirheumatic drug

115 Methotrexate (MTX) is an anti-folate that inhibits de novo purine and

116 Methotrexate (MTX) taken as monotherapy is recommended as the initial

117 Methotrexate (MTX), a tight binding inhibitor of DHFR, is one of the m

118 mutually exclusive cohorts: 1) methotrexate (MTX) monotherapy users, and 2) multiple nonbiologic DMAR

119 ecially hydroxychloroquine and methotrexate (MTX) have positive effects on cardiovascular risk factor

120 h as 5-Fluorouracil (5-FU) and methotrexate (MTX) leading to enhanced sensitivity in vitro and in viv

121 lates and antifolates, such as methotrexate (MTX), a widely used anticancer drug.

122 nistered along with background methotrexate (MTX), for the treatment of RA.

123 amine the relationship between methotrexate (MTX) use and mortality in RA, after controlling for indi

124 ological inhibition of DHFR by methotrexate (MTX) causes severe defects in oligodendrocyte survival a

125 cacy and safety data comparing methotrexate (MTX) and leflunomide (LEF) monotherapy, in combination w

126 amined the impact of different methotrexate (MTX) and corticosteroid treatment strategies on neurocog

127 Low-dose methotrexate (MTX) is an effective therapy for rheumatoid arthritis (R

128 alysis of an anti-cancer drug, methotrexate (MTX) as a potential analytical tool used in clinical che

129 in inhibitor (CNI) with either methotrexate (MTX) or mycophenolate mofetil (MMF).

130 ration and apoptosis following methotrexate (MTX)-induced intestinal damage in a rat.

131 therapy regimens that included methotrexate (MTX), cisplatin (CDP), and doxorubicin (ADM) with or wit

132 ning cofactor NADPH, inhibitor methotrexate (MTX), or both NADPH and MTX were characterized by 193 nm

133 tically relevant drug molecule methotrexate (MTX) and its metabolites 7-hydroxy methotrexate (7-OH MT

134 The pharmacogenetics of methotrexate (MTX) was investigated in a large cohort of pediatric pat

135 ed to study the interaction of methotrexate (MTX) with DNA immobilized on the bare surface of glassy

136 effects of v-K-ras and p53 on Methotrexate (MTX)-mediated DHFR amplification.

137 gh-dose intravenous (IV) pulse methotrexate (MTX) as a treatment for EF.

138 etrexed influx [in contrast to methotrexate (MTX), folic acid, and reduced folates] could be detected

139 Exposures to methotrexate (MTX), TNF inhibitors, and oral glucocorticoids (GCs) wer

140 eight received during a trial methotrexate (MTX).

141 -NPY conjugates containing two methotrexate (MTX) molecules are presented.

142 Treatment with methotrexate (MTX) and tumor necrosis factor (TNF) inhibitors was cate

143 ministered in combination with methotrexate (MTX) during the second treatment each week.

144 Cancer chemotherapy with methotrexate (MTX) is known to cause bone loss.

145 , 36 of whom were treated with methotrexate (MTX).

146 other week in combination with methotrexate (MTX).

147 otherapy (rituximab, high-dose methotrexate [MTX], vincristine, procarbazine) followed by a novel con

148 4 mug subcutaneously 3 times weekly or 20 mg MTX subcutaneously once weekly.

149 ian (range) monthly dose of 288 (230-336) mg MTX.

150 emolysis, colloidal stability, mitoxantrone (MTX) loading, in vitro MTX release, and cellular MTX del

151 In a multiple regression model, MTX area under the concentration time curve (AUC)0-48h i

152 At 300 muM MTX, influx was one-third that of pemetrexed; influx of

153 e conformational changes upon binding NADPH, MTX, or both ligands.

154 observed upon UVPD of the ternary DHFR.NADPH.MTX complex.

155 and RANGAP1 mRNA between MTX-treated and non-MTX-treated patients.

156 ry protein strongly inhibited the ability of MTX to activate BK channels, we found that it had only a

157 act with immobilized hDHFR in the absence of MTX and this interaction was inhibited in the presence o

158 26 channels were resistant to the actions of MTX.

159 ot account for the protective association of MTX use with mortality.

160 ic shifts in the maximum absorption bands of MTX after interaction with DNA.

161 TNF-alpha antagonists can be used in case of MTX failure.

162 Treatment with the combination of MTX plus etanercept resulted in a statistically signific

163 ter) 2000 trial who received 1996 courses of MTX at 5 g/m(2) were genotyped for 8 single nucleotide p

164 MTX) therapy, monitor for the development of MTX-induced hepatotoxic effects, and monitor for worseni

165 tigated whether selective discontinuation of MTX immediately prior to death altered the risk of morta

166 ents continued to receive a stable dosage of MTX.

167 nts with active RA receiving stable doses of MTX (10-25 mg weekly) were randomized to receive intrave

168 Patients receiving stable doses of MTX were randomized to receive 2 infusions of placebo (n

169 d we examined the association of duration of MTX use with survival.

170 n vivo and may contribute to the efficacy of MTX in inflammatory disease.

171 p53, amplification of DHFR and formation of MTX-resistant colonies occurred.

172 ics bands of C=O, N-H, C-H and O-H groups of MTX endow evidence for the interaction of MTX with DNA s

173 ypoxic conditions, a decrease in the IC50 of MTX and MTX-loaded MSNR was observed when compared to no

174 Here, the identification of MTX, 7-OH MTX and DAMPA are based on their unique SERS s

175 ease in enterocyte apoptosis in the ileum of MTX-ARG rats (vs MTX) was accompanied by decreased bax m

176 eased comparably shortly after initiation of MTX plus etanercept, triple therapy, and MTX monotherapy

177 treated with oral ARG following injection of MTX.

178 of MTX endow evidence for the interaction of MTX with DNA supporting the intercalative binding betwee

179 FT-IR investigations of MTX-DNA interaction revealed significant changes in the

180 TNF inhibitor use (irrespective of MTX) resulted in a similar rate of infection as use of M

181 r plasma MTX to leucovorin ratio (measure of MTX exposure) was associated with increased risk of leuk

182 The binding mechanism of MTX with DNA was elucidated by using constant current po

183 Here we find that a known mechanism of MTX-induced increase in DHFR expression persists with DH

184 Results The method of MTX delivery and corticosteroid assignment were unrelate

185 interaction was inhibited in the presence of MTX.

186 absence of cranial radiation, regardless of MTX delivery or corticosteroid type.

187 hain of Phe20 and the 6-methylpterin ring of MTX(Glu)5 invoke pi-pi interactions to promote distinct

188 his study investigated the potential role of MTX-induced pro-inflammatory cytokines and activation of

189 nstrated a safety profile similar to that of MTX monotherapy, data from a large population study sugg

190 Initial use of MTX monotherapy with the addition of sulfasalazine plus

191 The use of MTX to treat cancer also causes bone marrow suppression

192 ted in a similar rate of infection as use of MTX without a TNF inhibitor (HR(adj) 1.2 [95% CI 0.8, 1.

193 Here, the identification of MTX, 7-OH MTX and DAMPA are based on their unique SERS spectra, pr

194 its metabolites 7-hydroxy methotrexate (7-OH MTX) and 2,4-diamino-N(10)-methylpteroic acid (DAMPA) in

195 njugates revealed higher potency than MTX on MTX-resistant cells.

196 A negative effect of PEGylation on MTX loading was observed but PEGylated MSNR (PMSNR) demo

197 Only MTX use for >1 year was associated with lower risks of m

198 y to determine the effects of vitamin B12 or MTX on fitness and the epigenome.

199 ombination therapies (MTX plus etanercept or MTX plus sulfasalazine plus hydroxychloroquine) at week

200 combination therapy (MTX plus etanercept or MTX plus sulfasalazine plus hydroxychloroquine).

201 y starting with either MTX and prednisone or MTX and placebo.

202 nation approaches, whether triple therapy or MTX plus etanercept, were similar.

203 e trial support superiority of IFN beta over MTX in the treatment of macular edema in the setting of

204 Patients' MTX pharmacokinetics, MTX toxicities, and outcomes were

205 Patients' MTX pharmacokinetics, MTX toxicities, and outcomes were correlated with the ge

206 A high 42-hour plasma MTX to leucovorin ratio (measure of MTX exposure) was as

207 0.29 and 0.34 with tocilizumab 8 mg/kg plus MTX and 4 mg/kg plus MTX, respectively, versus 1.13 with

208 ocilizumab 8 mg/kg plus MTX and 4 mg/kg plus MTX, respectively, versus 1.13 with placebo plus MTX (P

209 respectively, versus 1.13 with placebo plus MTX (P < 0.0001 for both comparisons).

210 ngs of this study show that tocilizumab plus MTX results in greater inhibition of joint damage and im

211 kg or 4 mg/kg) or placebo every 4 weeks plus MTX.

212 for a second DI; however, replacement of PO MTX, PO mercaptopurine, vincristine, and dexamethasone d

213 and overall survival for patients on the PO MTX arms were 88.7% +/- 1.4% and 96% +/- 0.9% versus 92.

214 ty and effects of monthly high-dose IV pulse MTX in EF.

215 onclusions and Relevance: High-dose IV pulse MTX is a safe and effective treatment option in EF.

216 poor-prognosis RA were randomized to receive MTX monotherapy or combination therapy (MTX plus etanerc

217 Participants randomized to receive MTX monotherapy stepped-up to combination therapy at 24

218 8-102 between subjects randomized to receive MTX plus etanercept and those randomized to triple thera

219 iple therapy and those randomized to receive MTX plus etanercept.

220 Participants who received MTX monotherapy had less radiographic progression at wee

221 nisone (n = 117) than in the group receiving MTX and placebo (n = 119).

222 was limited and less in the group receiving MTX and prednisone (n = 117) than in the group receiving

223 ts from baseline between the group receiving MTX plus etanercept and the group receiving oral triple

224 CDKN1B was greater in patients not receiving MTX than in those receiving low-dose MTX, with no differ

225 After 1 visit, 24-37% of patients receiving MTX monotherapy who had moderate disease activity and a

226 s score in patients with psoriasis receiving MTX.

227 e of CNS NHL with intraventricular rituximab/MTX, including 1 with CNS lymphoma refractory to high-do

228 Selective MTX cessation immediately before death did not account f

229 rmining eligibility for methotrexate sodium (MTX) therapy, monitor for the development of MTX-induced

230 ent NASH FibroSure testing prior to starting MTX; 19 of those patients (27.5%) had elevated fibrosis

231 nt, and most patients can receive subsequent MTX without recurrence of acute or subacute symptoms.

232 DAS28-ESR in participants continuing to take MTX monotherapy at week 102 was 2.7 +/- 1.2, which is si

233 e of infection as those not currently taking MTX (HR(adj) 1.2 [95% CI 0.9, 1.7]).

234 , JIA patients who were not currently taking MTX or TNF inhibitors had an increased rate of infection

235 For those taking MTX without TNF inhibitor use, the SIR was 3.9 (95% CI 0

236 patients with psoriasis receiving long-term MTX therapy.

237 with either strategy was more effective than MTX monotherapy prior to the initiation of step-up thera

238 antagonists seemed to be more effective than MTX.

239 ore, conjugates revealed higher potency than MTX on MTX-resistant cells.

240 However, we found that MTX shifted the steady-state activation of BK channels i

241 Our findings support the notion that MTX restores some, but not all, of the proteins contribu

242 MTX-induced osteoclastogenesis and show that MTX induces osteoclast differentiation by generating a p

243 The MTX and prednisone strategy was also more effective in r

244 n both groups, but some occurred less in the MTX and prednisone group.

245 n (range, 0.12 to -0.38, 4.7 letters) in the MTX arm (P = .0435, Mann-Whitney U test).

246 sed by 47 mum (range, 108 to -28 mum) in the MTX group (P < .0001).

247 Attrition at 24 weeks was similar in the MTX monotherapy and combination groups.

248 increases in mean cholesterol levels in the MTX plus etanercept, triple therapy, and MTX monotherapy

249 commendations; after 2 visits, 34-56% of the MTX monotherapy group received care consistent with the

250 Gene silencing of the MTX target ATIC activated AMPK and stimulated lipid oxid

251 The structural geometries of the MTX(Glu)5 and hydrolyzed MTX(Glu)1 in the mutant complex

252 de polymorphisms in 5 candidate genes of the MTX/folate pathway.

253 Then, MTX was introduced at positions four and 22 of [F(7),P(3

254 therapy to one of the combination therapies (MTX plus etanercept or MTX plus sulfasalazine plus hydro

255 and did not step-up to combination therapy (MTX monotherapy group).

256 eive MTX monotherapy or combination therapy (MTX plus etanercept or MTX plus sulfasalazine plus hydro

257 s etanercept, immediate oral triple therapy (MTX plus sulfasalazine plus hydroxychloroquine), or step

258 atients not receiving TNF inhibitor therapy, MTX users had a similar rate of infection as those not c

259 ation with tetrahydrobiopterin blocked these MTX-induced effects.

260 okinetic, and genetic risk factors for these MTX-related toxicities during childhood acute lymphoblas

261 This MTX assay was subsequently adapted to a fully integrated

262 Even though MTX had a minimal effect on steady-state activation of p

263 IFO added to MTX, CDP, and ADM from the preoperative phase does not i

264 es have re-examined LEF as an alternative to MTX and demonstrated comparable clinical and radiographi

265 ileum and crypt depth in ileum, compared to MTX animals.

266 Safety data on LEF compared to MTX are less conclusive.

267 s an alternative with comparable efficacy to MTX as both monotherapy and, as preliminary data suggest

268 ents whose disease responded inadequately to MTX.

269 soform (parSlo) is inherently insensitive to MTX as MTX shifted the activation of heterologously expr

270 Conversely, exposing D. magna to MTX negatively influenced the fitness of the animals and

271 Ten were randomized to MTX, and 9 were randomized to IFN beta.

272 t TYMS T51S, G52S (TYMS(SS)) is resistant to MTX and improves MTX resistance of DHFR(FS) in primary T

273 gic agents and had an inadequate response to MTX were randomly assigned to receive 125 mg SC abatacep

274 ients who have a poor histologic response to MTX, CDP, and ADM.

275 postoperatively when pathologic response to MTX-CDP-ADM was poor (arm A) or given in the primary pha

276 levels of select target genes in response to MTX.

277 ogenesis may contribute to susceptibility to MTX-related neurotoxicity.

278 acebo every other week, as add-on therapy to MTX.

279 th 13,003 person-years of followup; 36% took MTX and 16% took TNF inhibitors.

280 bility, mitoxantrone (MTX) loading, in vitro MTX release, and cellular MTX delivery under hypoxic con

281 e apoptosis in the ileum of MTX-ARG rats (vs MTX) was accompanied by decreased bax mRNA and protein e

282 Our results support a model whereby MTX inhibits reduction of dihydrobiopterin to tetrahydro

283 We explored whether MTX promotes AMPK activation in cultured myotubes and is

284 56 variant was significantly associated with MTX kinetics.

285 determine the risk of death associated with MTX use, modeled in time-varying Cox regression models.

286 en in the primary phase of chemotherapy with MTX-CDP-ADM (arm B).

287 ety profile of rituximab in combination with MTX in other RA trials without a TNF inhibitor, with no

288 Golimumab in combination with MTX inhibited radiographic progression significantly bet

289 traventricular rituximab in combination with MTX is feasible and highly active in the treatment of dr

290 mab biweekly, both given in combination with MTX, in a 2-year study.

291 nanoparticles (FA-AuNP) in competition with MTX for the bioreceptor, human dihydrofolate reductase (

292 from zebrafish and the mutant complexes with MTX(Glu)5 and hydrolyzed MTX(Glu)1, revealing the comple

293 the rate of infection was not increased with MTX or TNF inhibitor use, but was significantly increase

294 ortance, combination treatment of NADPS with MTX displayed significant synergy in a metastatic colon

295 is RA validate the strategy of starting with MTX monotherapy.

296 hort of patients with psoriasis treated with MTX who underwent NASH FibroSure testing between January

297 ued cell-cycle progression when treated with MTX.

298 f 4 treatment arms: immediate treatment with MTX plus etanercept, immediate oral triple therapy (MTX

299 nts with psoriasis undergoing treatment with MTX, 69 (53.5%) underwent NASH FibroSure testing prior t

300 nts with psoriasis undergoing treatment with MTX, while 107 patients (57 women and 50 men; mean [SD]