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1 linically approved CFTR modulators ivacaftor/lumacaftor.
2 esponds to CFTR modulators like GLPG1837 and Lumacaftor.
3                            Children received lumacaftor 100 mg and ivacaftor 125 mg (bodyweight <14 k
4  and ivacaftor 125 mg (bodyweight <14 kg) or lumacaftor 150 mg and ivacaftor 188 mg (bodyweight >=14
5                               Treatment with lumacaftor 200 mg once daily and ivacaftor 250 mg every
6 ozygous patients randomly assigned to either lumacaftor 200 mg once per day for 14 days followed by a
7            Patients (N = 58) received 200 mg lumacaftor/250 mg ivacaftor orally every 12 hours for 24
8  mg once per day group -8.9 mmol/L, p<0.001; lumacaftor 400 mg every 12 h group -10.3 mmol/L, p=0.002
9  groups was generally similar to that of the lumacaftor 400 mg every 12 h/ivacaftor 250 mg every 12 h
10        340 patients continued treatment with lumacaftor 400 mg every 12 h/ivacaftor 250 mg every 12 h
11  or TRAFFIC studies initiated treatment with lumacaftor 400 mg every 12 h/ivacaftor 250 mg every 12 h
12 e treatment groups between day 1 and day 56 (lumacaftor 400 mg once per day group -9.1 mmol/L, p<0.00
13 aily) plus ivacaftor (250 mg every 12 h), or lumacaftor (400 mg every 12 h) plus ivacaftor (250 mg ev
14 FFIC were randomly assigned (1:1) to receive lumacaftor (400 mg every 12 h)/ivacaftor (250 mg every 1
15 percentage points [1.7-3.8; p<0.0001] in the lumacaftor [400 mg/12 h]-ivacaftor group).
16  percentage points [0.2-6.4; p=0.036] in the lumacaftor [400 mg/12 h]-ivacaftor group).
17       The efficacy and safety profile of the lumacaftor 600 mg once daily/ivacaftor 250 mg every 12 h
18  mg once per day group -9.1 mmol/L, p<0.001; lumacaftor 600 mg once per day group -8.9 mmol/L, p<0.00
19                             In cohort 2, the lumacaftor 600 mg once per day significantly improved FE
20 nts were randomly assigned to receive either lumacaftor (600 mg once daily or 400 mg every 12 hours)
21  response system (1:1:1) to receive placebo, lumacaftor (600 mg once daily) plus ivacaftor (250 mg ev
22 every 12 h)/ivacaftor (250 mg every 12 h) or lumacaftor (600 mg once daily)/ivacaftor (250 mg every 1
23 percentage points [2.3-4.4; p<0.0001] in the lumacaftor [600 mg per day]-ivacaftor group and 2.8 perc
24 tage points [95% CI 0.5-6.9; p=0.024] in the lumacaftor [600 mg/day]-ivacaftor group and 3.3 percenta
25 mbining ivacaftor (a gating potentiator) and lumacaftor (a folding corrector) have proven efficacious
26 sting of our EN523 OTUB1 recruiter linked to lumacaftor, a drug used to treat cystic fibrosis that bi
27          We also investigated the effects of lumacaftor, a drug used to treat cystic fibrosis, that p
28                                              Lumacaftor-a compound known to rescue HERG trafficking-s
29  tightness or dyspnoea during treatment with lumacaftor alone.
30 the combination of an anti-PD-1 antibody and Lumacaftor, an FDA-approved small molecule inhibitor of
31         We tested combination treatment with lumacaftor, an investigational CFTR corrector that incre
32 active web response system to receive 200 mg lumacaftor and 250 mg ivacaftor every 12 hours or placeb
33           Thirteen adults starting ivacaftor/lumacaftor and eight starting ivacaftor/tezacaftor were
34 re enrolled and randomly assigned to receive lumacaftor and ivacaftor (n=104) or placebo (n=102).
35   103 patients received at least one dose of lumacaftor and ivacaftor and 101 patients received at le
36 n children who received at least one dose of lumacaftor and ivacaftor and absolute changes from basel
37    The efficacy, safety, and tolerability of lumacaftor and ivacaftor are established in patients age
38 treptococcal throat infection and one in the lumacaftor and ivacaftor arm due to withdrawal based on
39 pport the further exploration of combination lumacaftor and ivacaftor as a treatment in this setting.
40                     We conclude that chronic lumacaftor and ivacaftor co-treatment restores stability
41                                              Lumacaftor and ivacaftor combination treatment showed ef
42 bation of F508del-CFTR-expressing cells with lumacaftor and ivacaftor deactivated macroscopic F508del
43              As a result, the combination of lumacaftor and ivacaftor delivered by lipid nanoparticle
44  reported in 13 (13%) of 103 patients in the lumacaftor and ivacaftor group and 11 (11%) of 101 patie
45  events in three (3%) of 103 patients in the lumacaftor and ivacaftor group and two (2%) of 101 patie
46 gs also suggest that early intervention with lumacaftor and ivacaftor has the potential to modify the
47         We provide evidence that combination lumacaftor and ivacaftor improves FEV1 for patients with
48 okinetics, pharmacodynamics, and efficacy of lumacaftor and ivacaftor in children aged 2-5 years.
49             We report efficacy and safety of lumacaftor and ivacaftor in patients with cystic fibrosi
50  units (95% CI -1.43 to -0.75, p<0.0001) for lumacaftor and ivacaftor versus placebo.
51               INTERPRETATION: Treatment with lumacaftor and ivacaftor was associated with statistical
52                                              Lumacaftor and ivacaftor were generally safe and well to
53 y and pharmacokinetics of the metabolites of lumacaftor and ivacaftor, and in part B included pharmac
54 o drugs with different mechanisms of action, lumacaftor and ivacaftor, has been recently proposed.
55 ane conductance regulator (CFTR) modulators, lumacaftor and ivacaftor, in patient-derived airway tiss
56 ith the well characterised safety profile of lumacaftor and ivacaftor.
57 n children who received at least one dose of lumacaftor and ivacaftor.
58  consistent with previous phase 3 studies of lumacaftor and ivacaftor.
59             Dual combinations like ivacaftor/lumacaftor and ivacaftor/tezacaftor brought together a p
60 macokinetics (part A) and safety (part B) of lumacaftor and ivacaftor; all analyses were done in chil
61  (e.g., using clinically approved modulators lumacaftor and tezacaftor) and demonstrated additivity o
62  site rendered DeltaF508-CFTR insensitive to lumacaftor and tezacaftor, underscoring the functional s
63 esponds robustly to CFTR correctors, such as lumacaftor and tezacaftor, with rescue in model systems
64      Two small molecules, the CFTR corrector lumacaftor and the potentiator ivacaftor, are now used c
65 1 was used in combination with the corrector lumacaftor and the potentiator ivacaftor, it showed an a
66  correction potency, additivity/synergy with lumacaftor, and a promising in vitro absorption, distrib
67 nt with CFTR modulators including ivacaftor, lumacaftor, and tezacaftor showed a high normalized peak
68     ORKAMBI, a combination of the corrector, lumacaftor, and the potentiator, ivacaftor, partially re
69          Our data showed that Simeprevir and Lumacaftor bind the receptor-binding domain of the Spike
70 monstrates that drugs such as remdesivir and lumacaftor can differently affect homomeric and heterome
71 ents, randomly assigned to either 56 days of lumacaftor (cohort 2: 200 mg, 400 mg, or 600 mg once per
72                                              Lumacaftor efficacy was also tested by ANEPPS, FluoVolt,
73 The addition of the small-molecule corrector Lumacaftor exerts a helix stabilization effect not only
74 stic fibrosis protein trafficking chaperone, lumacaftor, has been proposed as novel therapy for LQT2.
75                         These data show that lumacaftor in combination with ivacaftor provided a bene
76          However, remdesivir decreased while lumacaftor increased the current and cell-surface expres
77 18, an analog of the CFTR corrector compound Lumacaftor, induces almost no transcriptional perturbati
78                                        While lumacaftor is an effective hERG channel trafficking chap
79 y activating delayed rectifier K+ current by lumacaftor is the underlying mechanism of the LQT2 rescu
80                                        While lumacaftor is used to correct p.Phe508del mutation (the
81          With the discovery of Ivacaftor and Lumacaftor, it has been shown that administration of one
82  adverse events was generally similar in the lumacaftor-ivacaftor and placebo groups.
83 mprovements in the primary end point in both lumacaftor-ivacaftor dose groups; the difference between
84                   All patients who initiated lumacaftor-ivacaftor from January 1 to December 31, 2016
85  of intravenous antibiotics was lower in the lumacaftor-ivacaftor groups as well.
86 ary exacerbations was 30 to 39% lower in the lumacaftor-ivacaftor groups than in the placebo group; t
87  To evaluate the safety and effectiveness of lumacaftor-ivacaftor in adolescents (>=12 yr) and adults
88 ents, treatment with the CFTR modulator drug lumacaftor-ivacaftor increased the renal ability to excr
89 us antibiotic courses during the year before lumacaftor-ivacaftor initiation.
90                                   Rationale: Lumacaftor-ivacaftor is a CFTR (cystic fibrosis transmem
91                  Patients were evaluated for lumacaftor-ivacaftor safety and effectiveness over the f
92         Patients with continuous exposure to lumacaftor-ivacaftor showed an absolute increase in ppFE
93 e event was 4.2% among patients who received lumacaftor-ivacaftor versus 1.6% among those who receive
94  intravenous antibiotic courses.Conclusions: Lumacaftor-ivacaftor was associated with improvement in
95 92 adolescents and 553 adults) who initiated lumacaftor-ivacaftor, 18.2% (154 patients) discontinued
96                      Adults who discontinued lumacaftor-ivacaftor, often owing to adverse events, wer
97 reatment with the novel CFTR modulator drug, lumacaftor-ivacaftor.
98                  These analyses confirm that lumacaftor/ivacaftor combination therapy benefits patien
99                                              Lumacaftor/ivacaftor combination therapy has shown clini
100 erability, pharmacodynamics, and efficacy of lumacaftor/ivacaftor combination therapy in patients age
101              The long-term safety profile of lumacaftor/ivacaftor combination therapy was consistent
102 ERPRETATION: The long-term safety profile of lumacaftor/ivacaftor combination therapy was consistent
103           The 24-week safety and efficacy of lumacaftor/ivacaftor combination therapy was shown in tw
104 ry exacerbation events were observed in both lumacaftor/ivacaftor dose groups compared with placebo a
105 r the 15-day treatment period in part A, the lumacaftor/ivacaftor dose was based on weight at screeni
106 at week 24 in ppFEV1 were observed with both lumacaftor/ivacaftor doses in the subgroup with baseline
107                       RATIONALE: Combination lumacaftor/ivacaftor has been shown to improve lung func
108 y, pharmacokinetics, and pharmacodynamics of lumacaftor/ivacaftor in children aged 1 to <2 years with
109             These results support the use of lumacaftor/ivacaftor in this population.
110 e respiratory adverse events was higher with lumacaftor/ivacaftor than with placebo in all subgroups.
111 e aimed to assess the efficacy and safety of lumacaftor/ivacaftor therapy in these patients, defined
112 he long-term safety and efficacy of extended lumacaftor/ivacaftor therapy in this group of patients i
113 e potential for CF disease modification with lumacaftor/ivacaftor treatment.
114 generally similar to that observed in larger lumacaftor/ivacaftor trials with older patients.
115  be observed with longer-term treatment, and lumacaftor/ivacaftor was associated with a 42% slower ra
116                                 Conclusions: Lumacaftor/ivacaftor was generally safe and well tolerat
117 us phase 3 trials showed that treatment with lumacaftor/ivacaftor was safe and efficacious in people
118                                              Lumacaftor/ivacaftor was well tolerated in this young po
119                                              Lumacaftor/ivacaftor was well tolerated; the safety prof
120  Administation (FDA)-approved drugs Orkambi (lumacaftor/ivacaftor) and Trikafta (elexacaftor/tezacaft
121 ered the study using tezacaftor/ivacaftor or lumacaftor/ivacaftor, whereas 6.7% were using ivacaftor,
122 alised rate of ppFEV1 decline was reduced in lumacaftor/ivacaftor-treated patients compared with matc
123                                              Lumacaftor-mediated APD90 rescue was affected by rapidly
124  rescue effects of two drugs, remdesivir and lumacaftor, on trafficking-defective mutant hERG channel
125            In vitro application of ivacaftor/lumacaftor or ivacaftor/tezacaftor to CF monocytes showe
126  in complex with the FDA-approved correctors lumacaftor or tezacaftor.
127 he phenotype of KCNH2-N633S and KCNH2-R685P, lumacaftor paradoxically prolonged the APD90 in KCNH2-G6
128                                              Lumacaftor partially stabilized purified full-length F50
129 the hERG trafficking defect in TSA201 cells, lumacaftor rescued channel trafficking for all mutations
130 Our results show that neither remdesivir nor lumacaftor rescued the current or cell-surface expressio
131 2 knockdown with the corrector drug, VX-809 (lumacaftor) restored the mutant function to ~50% of the
132 onality of the mutant channel to be rescued, lumacaftor therapy could be harmful.
133 inding suggests a general mode of action for Lumacaftor through which this corrector efficiently impr
134  reduced in conditioned media from ivacaftor/lumacaftor treated CF MDMs.
135 presence of conditioned media from ivacaftor/lumacaftor treated CF MDMs.
136                                        While lumacaftor treatment failed to rescue the hERG trafficki
137                Here, we test the efficacy of lumacaftor treatment in patient-specific induced pluripo
138                                        While lumacaftor treatment rescued the phenotype of KCNH2-N633
139 receptor 1 (TfR1) was reduced with ivacaftor/lumacaftor treatment.
140 observation that clinically-approved VX-809 (Lumacaftor, Vertex Pharmaceuticals, Boston, MA, USA) and
141  that were designed to assess the effects of lumacaftor (VX-809), a CFTR corrector, in combination wi
142 y distinct correctors, corrector 4a (C4) and lumacaftor (VX-809), on I507-ATT and I507-ATC DeltaF508
143           Pharmacological chaperones such as lumacaftor (VX-809), tezacaftor (VX-661), and elexacafto
144 sion stabilized both wild-type (WT)-CFTR and Lumacaftor (VX-809)-rescued F508del-CFTR (where F508del

 
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