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1  a response with 4 mg and 54% with 5.5 mg of ixazomib.
2 alone, and half dose CsA (5 mg/kg per day) + ixazomib.
3  and 5%, respectively) received single-agent ixazomib 0.24 to 2.23 mg/m(2) (days 1, 4, 8, 11; 21-day
4 l dose cyclosporine (CsA, 10 mg/kg per day), ixazomib (0.25 mg/kg on days -5, -2 and +2) alone, and h
5 hase 1, we gave patients escalating doses of ixazomib (1.68-3.95 mg/m(2)) to establish the recommende
6 d toxicity of combining 2 different doses of ixazomib (4 mg and 5.5 mg given weekly for 3 of 4 weeks)
7               Compared to untreated animals, ixazomib alone or in combination with (1/2) dose CsA red
8 cycles, followed by maintenance therapy with ixazomib alone.
9  of an investigational proteasome inhibitor, ixazomib, alone and in a CNI minimization strategy in a
10 olid tumors led to the invention of MLN9708 (ixazomib), an orally bioavailable next-generation protea
11                                  Weekly oral ixazomib appears to be active in patients with relapsed/
12 t that CNI minimization strategies including ixazomib are effective to prevent AMR including in sensi
13 heral neuropathy, and treated them with oral ixazomib (days 1, 8, 15) plus lenalidomide 25 mg (days 1
14                            More importantly, ixazomib demonstrated potent anti-tumor efficacy in vivo
15 olled, 35 patients randomly assigned to each ixazomib dose.
16 m tolerated dose (MTD) of single-agent, oral ixazomib given weekly for 3 of 4 weeks.
17 e 4 severity occurred more frequently in the ixazomib group (12% and 7% of the patients, respectively
18 edian time to response was 1.1 months in the ixazomib group and 1.9 months in the placebo group, and
19 ence of peripheral neuropathy was 27% in the ixazomib group and 22% in the placebo group (grade 3 eve
20  similar in the two study groups (47% in the ixazomib group and 49% in the placebo group), as were th
21 he overall rates of response were 78% in the ixazomib group and 72% in the placebo group, and the cor
22         Rash occurred more frequently in the ixazomib group than in the placebo group (36% vs. 23% of
23 ree survival was significantly longer in the ixazomib group than in the placebo group at a median fol
24 ve ixazomib plus lenalidomide-dexamethasone (ixazomib group) or placebo plus lenalidomide-dexamethaso
25 atio for disease progression or death in the ixazomib group, 0.74; P=0.01); a benefit with respect to
26 ss the safety, tolerability, and activity of ixazomib in combination with lenalidomide and dexamethas
27 th creatinine clearance > 15 mL/min, whereas ixazomib in combination with lenalidomide and dexamethas
28 ormed the subsequent clinical development of ixazomib in multiple myeloma.
29 study illustrates the anti-tumor efficacy of ixazomib in NB both alone and in combination with dox, s
30 ficacy of the oral proteasome inhibitor (PI) ixazomib in patients with relapsed/refractory immunoglob
31 of a second-generation proteasome inhibitor, ixazomib, in T-cell lymphoma and Hodgkin lymphoma cells
32                         We demonstrated that ixazomib induced potent cell death in all cell lines at
33 dose CsA, the CNI minimization strategy with ixazomib inhibited AMR and allograft injury as evidenced
34                                              Ixazomib inhibits dox-induced NF-kappaB activity and sen
35                                              Ixazomib is an investigational, oral, proteasome inhibit
36                                              Ixazomib is an investigational, orally bioavailable 20S
37                                              Ixazomib is an oral proteasome inhibitor that is current
38                                              Ixazomib is the first investigational oral proteasome in
39                                              Ixazomib is the first oral proteasome inhibitor to enter
40 ment in progression-free survival (PFS) with ixazomib-lenalidomide-dexamethasone (IRd) compared with
41 t the second generation proteasome inhibitor ixazomib (MLN9708) not only inhibits NB cell proliferati
42 (Velcade(R)), carfilzomib (Kyprolis(R)), and ixazomib (Ninlaro(R)), confirms that proteasome inhibito
43 ents were noted in phase 1: one at a dose of ixazomib of 2.97 mg/m(2) and three at 3.95 mg/m(2).
44 possibilities (pomalidomide, carfilzomib and ixazomib, panobinostat, elotuzumab, and daratumumab).
45           The all-oral combination of weekly ixazomib plus lenalidomide and dexamethasone was general
46 d and refractory multiple myeloma to receive ixazomib plus lenalidomide-dexamethasone (ixazomib group
47 gression-free survival was observed with the ixazomib regimen, as compared with the placebo regimen,
48 in modification, and DNA repair processes in ixazomib-sensitive lymphoma cells.
49                                  Altogether, ixazomib significantly downregulates MYC and induces pot
50 genes from global transcriptome analysis for ixazomib strongly favored tumor inhibition via downregul
51 e, the second-generation PIs carfilzomib and ixazomib, the DACI panobinostat, and 2 mAbs, elotuzumab
52                              The addition of ixazomib to a regimen of lenalidomide and dexamethasone
53                              Furthermore, in ixazomib-treated lymphoma cells, we identified that CHK1
54                    The terminal half-life of ixazomib was 3.3 to 7.4 days; plasma exposure increased
55                                              Ixazomib was administered to adult patients with relapse
56                The maximum tolerated dose of ixazomib was established as 2.97 mg/m(2) and the recomme
57                                 Overall, the ixazomib with dexamethasone has good efficacy in relapse
58 uggesting that combination therapy including ixazomib with traditional therapeutic agents such as dox

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