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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)
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
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
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
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
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
33 dose CsA, the CNI minimization strategy with ixazomib inhibited AMR and allograft injury as evidenced
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
44 possibilities (pomalidomide, carfilzomib and ixazomib, panobinostat, elotuzumab, and daratumumab).
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,
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
58 uggesting that combination therapy including ixazomib with traditional therapeutic agents such as dox
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