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1 ctivation was inhibited by the MMP inhibitor ilomastat.
2 y, minimal scar tissue was seen with MMC and ilomastat.
3 the matrix metalloproteinase (MMP) inhibitor ilomastat.
4 t proliferation was found in the presence of ilomastat.
5 talloproteinases, as they were reproduced by ilomastat.
7 day of failure was 46.2 (range, 42-60) with ilomastat, 51.3 (range, 49-60) with MMC, and 16 (range,
8 movement was inhibited by local delivery of Ilomastat, a general matrix metalloproteinase inhibitor,
9 ibition of matrix metalloproteinases because ilomastat, a synthetic inhibitor of these enzymes, had n
10 spectrum metalloproteinase inhibitor, GM6001/Ilomastat, acted synergistically with Abeta to enhance n
11 his study we show that CMT-300, CMT-308, and Ilomastat, agents initially characterized as matrix meta
15 o exposure to cells, while the CMTs, but not Ilomastat, are also effective when added after LF has al
16 A hydroxamate class inhibitor (GM6001, or Ilomastat) blocked activation of MT1-MMP in MCF7 cells b
17 rations of the broad-spectrum MMP inhibitors ilomastat, CellTech (Slough, UK), and BB-94 were added t
19 roughout the course of the experiment in the ilomastat group compared with the vehicle group (P < 0.0
20 All three inhibitors, CMT-300, CMT-308, and Ilomastat, inhibit LF-mediated cleavage of a synthetic p
25 e inhibitors, BB-94 (Batimastat) and GM6001 (Ilomastat), suggesting that the cleavage is mediated by
26 l outcome was significantly prolonged in the ilomastat-treated group compared with the vehicle-treate
27 all the blebs had survived except two in the ilomastat-treated group, whereas no blebs survived to da
28 eration in the presence of concentrations of ilomastat was measured by using the reagent water-solubl
30 e matrix metalloproteinase inhibitor GM6001 (ilomastat), which is currently in clinical development,
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