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1 biologic agents (infliximab, adalimumab, and natalizumab).
2 ts given fingolimod, and 1160 patients given natalizumab.
3 multiple sclerosis (MS) who are treated with natalizumab.
4 rials established the efficacy and safety of natalizumab.
5 onance imaging MS activity after 24 doses of natalizumab.
6 score remained stable for patients receiving natalizumab.
7 died of PML after receiving 45 infusions of natalizumab.
8 far unreported amongst patients treated with natalizumab.
9 atients treated with the monoclonal antibody natalizumab.
10 lateral blindness following his 44th dose of natalizumab.
11 cal leukoencephalopathy (PML) in patients on natalizumab.
12 or multiple sclerosis patients treated with natalizumab.
13 being treated or considering treatment with natalizumab.
14 atients with multiple sclerosis treated with natalizumab.
15 ultiple sclerosis (MS) patients treated with natalizumab.
16 ncreases with the duration of treatment with natalizumab.
17 ith multiple sclerosis who were treated with natalizumab.
18 lso showed significantly improved HRQoL with natalizumab.
19 nce imaging, and improved significantly with natalizumab.
20 (MS): glatiramer acetate, mitoxantrone, and natalizumab.
21 -339.3, p < 0.0001) in patients treated with natalizumab.
27 s received an initial i.v. bolus of placebo, natalizumab (30 mg/kg), or vedolizumab (30 mg/kg) before
28 ceived interferon beta-1a (IFN-beta-1a) plus natalizumab 300 mg (n = 589), or IFN-beta-1a plus placeb
29 Sclerosis (AFFIRM) study, patients received natalizumab 300 mg (n = 627) or placebo (n = 315); in th
30 centrations were randomized (1:1) to receive natalizumab 300 mg or placebo intravenously at Weeks 0,
37 alemtuzumab, interferon beta, fingolimod, or natalizumab), age 65 years or younger, Expanded Disabili
38 e, we review the bench-to-bedside journey of natalizumab, along with the lessons learned from postmar
43 risk of developing PML during treatment with natalizumab and detect early suspected PML using MRI inc
44 the disability-time curve) differed between natalizumab and fingolimod (-0.12 vs 0.04 per year, resp
45 d relapse rates decreased from 1.5 to 0.2 on natalizumab and from 1.3 to 0.4 on fingolimod, with 50%
47 ct the potential immunosuppressive effect of natalizumab and hence be associated with a reduced risk
52 ) or immunoabsorption to hasten clearance of natalizumab and shorten the period in which natalizumab
53 ed out, the shared reason for switching from natalizumab and the preferential use of either rituximab
54 modulatory monoclonal antibodies rituximab, natalizumab, and efalizumab have received regulatory app
56 e achieved within 1 day of the first dose of natalizumab, and similar levels were continuously mainta
58 responders among disabled MS subjects in the natalizumab arms than in the placebo or IM IFNbeta-1a ar
59 pse rates were observed in patients who used natalizumab as first MS therapy, in patients with lower
60 strating the early and sustained efficacy of natalizumab as induction therapy in patients with elevat
64 pattern facilitates an earlier diagnosis of natalizumab-associated PML in an asymptomatic stage asso
67 ients with multiple sclerosis, who developed natalizumab-associated PML or GCN with regard to JC vira
69 tudy assessing brain MRI of 26 patients with natalizumab-associated PML presenting with lesions sugge
72 more common and more severe in patients with natalizumab-associated PML than it is in patients with H
73 ancement is the most common earliest sign of natalizumab-associated PML-IRIS with a frequent imaging
79 constitution inflammatory syndrome (IRIS) in natalizumab-associated progressive multifocal leukoencep
80 lerosis who received 12 or more infusions of natalizumab at an academic multiple sclerosis center.
82 currently being treated with, or initiating, natalizumab, based on their anti-JCV antibody status.
85 nized anti-alpha4 integrin antibody known as Natalizumab, blocks homing of mononuclear cells to the C
87 We sought to determine whether exposure to natalizumab causes subclinical reactivation and neurotro
88 sitive multiple sclerosis (MS) patients from natalizumab clinical studies and postmarketing sources.
91 from nearly 1,400 patients participating in natalizumab clinical trials were tested for JCV DNA usin
93 izumab (n = 81), with a protective effect of natalizumab continuation on both outcomes (odds ratio [O
94 ect of natalizumab on the risk of relapse in natalizumab continuers compared with natalizumab quitter
96 .03) MS activity was significantly lower in natalizumab continuers than in natalizumab switchers or
97 ncephalopathy (PML) following treatment with natalizumab develop IRIS which carries a high morbidity
98 unotherapies, including cyclophosphamide and natalizumab, did not improve her cognitive deficits, nec
104 alemtuzumab, and dimethyl fumarate, whereas natalizumab disproportionally increases them in the bloo
107 utcomes for all RRMS patients switching from natalizumab due to JC virus antibody positivity at 3 Swe
111 ive multiple sclerosis who were treated with natalizumab during their third trimester of pregnancy, w
113 -infected CD8-depleted macaques treated with natalizumab either early (the day of infection) or late
114 ur l'Introduction du Fingolimod en Relais au Natalizumab (ENIGM) study, a survey-based, observational
117 alence was similar in patients regardless of natalizumab exposure or prior immunosuppressant use, p =
118 mpared the effectiveness of alemtuzumab with natalizumab, fingolimod, and interferon beta in patients
119 We review each of the newly approved agents-natalizumab, fingolimod, teriflunomide, dimethyl fumarat
122 mple was drawn from 23 MS patients receiving natalizumab for more than 24 months and from 18 healthy
124 diction of risk of PML in patients receiving natalizumab for multiple sclerosis, supporting yearly be
125 s review article summarizes the evolution of natalizumab from target molecule discovery through regul
130 e Sclerosis [AFFIRM], Safety and Efficacy of Natalizumab in Combination With Interferon Beta-1a in Pa
131 ebo (n = 315); in the Safety and Efficacy of Natalizumab in Combination with Interferon Beta-1a in Pa
132 regression was observed after the switch to natalizumab in comparison to fingolimod (p < 0.001).
133 anisms that may contribute to the benefit of natalizumab in MS, as well as candidate therapeutics tha
134 rapeutic choices is needed after 24 doses of natalizumab in patients with multiple sclerosis (MS).
135 e use of intense immunosuppressant drugs and natalizumab in patients with rapidly worsening MS and pr
137 o-controlled trial evaluated the efficacy of natalizumab induction therapy in patients with Crohn's d
138 e modifying therapy (DMT) following the last natalizumab infusion, while the TG received two more nat
140 natalizumab to fingolimod after a mean of 31 natalizumab infusions (female to male ratio, 2.36; mean
142 mab infusion, while the TG received two more natalizumab infusions, at 6 and 8 weeks (14 weeks from s
148 r median Expanded Disability Status Scale at natalizumab interruption was 3.0 and increased to 6.0 du
153 le disease-modifying therapies, switching to natalizumab is more effective than switching to fingolim
155 cases occurred during the first two years of natalizumab marketing but, by the end of November, 2009,
157 CV-seropositive MS patients, including 32 on natalizumab monotherapy >18 months, 6 on interferon beta
159 s significantly lower in patients continuing natalizumab (n = 43) than in patients interrupting natal
160 zumab (n = 43) than in patients interrupting natalizumab (n = 81), with a protective effect of natali
163 eated group, natalizumab continuers received natalizumab, natalizumab switchers changed to different
165 modifying treatments for multiple sclerosis, natalizumab (NTZ) is highly effective, well tolerated an
170 quitters, confirming a protective effect of natalizumab on the risk of relapse in natalizumab contin
171 ing infusions of the CD49d-blocking antibody natalizumab) on levels of circulating HSPCs after a sing
174 andomly assigned (1:1) to 300 mg intravenous natalizumab or placebo with stratification by treatment
175 ith multiple sclerosis who were treated with natalizumab over an 18-month period, performing quantita
180 apse in natalizumab continuers compared with natalizumab quitters (OR, 4.40; 95% CI, 1.72-11.23) and
181 witchers changed to different therapies, and natalizumab quitters discontinued natalizumab during the
183 spended pending a safety review when several natalizumab recipients were diagnosed as having progress
184 opeller and thigh domain fragment shows that natalizumab recognizes human-mouse differences on the ci
185 In a 48-week study testing the safety of natalizumab redosing, JCV DNA was detected in plasma of
187 ongitudinal clinical course of patients with natalizumab-related progressive multifocal leukoencephal
188 natalizumab and shorten the period in which natalizumab remains active (usually several months).
189 Therapy discontinuation after 24 doses in natalizumab-responding patients should be considered onl
190 d treatment with the CD49d-blocking antibody natalizumab resulted in significantly decreased migratio
191 ebrospinal fluid of MS patients treated with natalizumab revealed that transmigration of this subset
194 tively analyzed data from 3 clinical trials (Natalizumab Safety and Efficacy in Relapsing-Remitting M
197 Treatment decisions between alemtuzumab and natalizumab should be primarily governed by their safety
201 sclerosis (RRMS) patients who are stable on natalizumab switch to other therapies to avoid progressi
202 quitters (OR, 4.40; 95% CI, 1.72-11.23) and natalizumab switchers (OR, 3.28; 95% CI, 0.99-10.79).
203 natalizumab continuers received natalizumab, natalizumab switchers changed to different therapies, an
204 ntly lower in natalizumab continuers than in natalizumab switchers or quitters, confirming a protecti
207 with multiple sclerosis (MS) who had been on natalizumab therapy >/=24 months and were contemplating
209 n the 12 months prior to baseline to 0.31 on natalizumab therapy (p<0.0001), remaining low at 5 years
210 lopathy risk associated with >/=24 months of natalizumab therapy against the benefits of disease cont
213 immunosuppressants before the initiation of natalizumab therapy, and had received 25 to 48 months of
217 In total, 333 patients with MS switched from natalizumab to fingolimod after a mean of 31 natalizumab
218 The safety and efficacy of switching from natalizumab to fingolimod have not yet been evaluated in
222 A was detectable within cell compartments of natalizumab-treated MS patients after treatment inceptio
223 In this retrospective review, the first 40 natalizumab-treated MS patients diagnosed with PML in th
224 sive multifocal leukoencephalopathy (PML) in natalizumab-treated MS patients is linked to JC virus (J
225 NA was detected in the CSF of 2 of 27 (7.4%) natalizumab-treated MS patients who had no symptoms or m
230 ring JC virus (JCV) DNA in blood or urine of natalizumab-treated multiple sclerosis (MS) patients to
233 sustained through Week 12 occurred in 48% of natalizumab-treated patients and 32% of patients receivi
238 characteristics of PML-IRIS manifestation in natalizumab-treated patients with multiple sclerosis and
240 istry to estimate the incidence of PML among natalizumab-treated patients with multiple sclerosis, ac
241 sociated with distinct levels of PML risk in natalizumab-treated patients with multiple sclerosis.
242 eactivation of JC virus occurs frequently in natalizumab-treated patients with multiple sclerosis.
243 pse rate and stabilised disability levels in natalizumab-treated patients with RRMS in clinical pract
246 ted >6 months prior to PML diagnosis from 71 natalizumab-treated PML patients and 2,522 non-PML anti-
247 rmine the presence of anti-JCV antibodies in natalizumab-treated PML patients where serum samples wer
251 le sclerosis patient who developed PML under natalizumab treatment and a vigorous immune response aga
252 therapy, and had received 25 to 48 months of natalizumab treatment had the highest estimated risk (in
254 ve multifocal leukoencephalopathy (PML) with natalizumab treatment is associated with the presence of
255 ver, severe disease activity may return once natalizumab treatment is withdrawn, as recommended durin
257 orted here sought to determine the effect of natalizumab treatment on relapse activity in the minorit
259 ults, close clinical vigilance is indicated, natalizumab treatment should be suspended, and JCV polym
261 itive patients who wish to begin or continue natalizumab treatment to be managed with a more individu
263 mmunosuppressants, and increased duration of natalizumab treatment, alone or in combination, were ass
264 (JC) antibodies, with prolonged duration of natalizumab treatment, and with prior exposure to immuno
267 eveloped, progressive cerebellar signs under natalizumab treatment, especially in cases where cerebel
268 thology showed diminished DRG pathology with natalizumab treatment, including decreased inflammation,
279 f FAE and bsAb formation using Hz6F4-2v3 and natalizumab, two humanized IgG4s which bind to human Jun
280 at target the cell adhesion molecules VLA-4 (natalizumab; Tysabri for multiple sclerosis and Crohn's
283 in patients being treated with rituximab or natalizumab warrants early assessment for JCV infection.
289 us success of a molecular targeted approach, natalizumab was the first mAb approved for the treatment
291 wever, only a few months after its approval, natalizumab was withdrawn from the market because of an
292 ML probability over 6 years (72 infusions of natalizumab) was 2.7% (95% CI 1.8-4.0) in patients with
293 unders (age, sex, disability status, time on natalizumab, washout time, follow-up time, and study cen
294 pha(4)beta(1) and alpha(4)beta(7) antagonist natalizumab were compared with those of the alpha(4)beta
295 n patients with multiple sclerosis receiving natalizumab were stratified by three risk factors: anti-
299 sis patients treated with the anti-VLA-4 mAb natalizumab, which selectively inhibits cell migration a
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