ライフサイエンスコーパス: batimastat

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1 ted by the metalloproteinase (MMP) inhibitor batimastat.

2 spase inhibitor and anti-alpha(2) but not by batimastat.

3 atment with the metalloproteinase inhibitor, batimastat.

4 inhibited by the metalloprotease inhibitor, batimastat.

5 is sensitive to a metalloprotease inhibitor, batimastat.

6 pounds such as the metalloprotease inhibitor batimastat ([4-(N-hydroxyamino)-2-(R)-isobutyl-3-(S)-(2-

7 e inhibited following incubation with BB-94 (batimastat), a specific inhibitor of matrix metalloprote

8 olytic activity was inhibited by EDTA and by batimastat, a selective MMP inhibitor.

9 Batimastat also reduced the expression of several inflam

10 ntibody to the alpha(2) integrin, but not by batimastat, an inhibitor of MMP-1 enzymatic activity.

11 ent manner by the following synthetic MMPIs: batimastat and marimastat (BB-94 and BB-2516, respective

12 ith two metalloproteinase inhibitors, BB-94 (Batimastat) and GM6001 (Ilomastat), suggesting that the

13 rosine kinase, the metalloprotease inhibitor batimastat, and methyl-beta-cyclodextrin and filipin, wh

14 rved with the PD98059 MEK1 inhibitor and the batimastat (BB-94) inhibitor of MMP activity, but not wi

15 targeted NPs could deliver the MMP inhibitor batimastat (BB-94) to the site of an aneurysm and preven

16 We have examined the interaction of batimastat (BB-94) with a metalloproteinase [atrolysin C

17 Chronic administration of batimastat (BB-94), a broad spectrum peptide inhibitor o

18 soenzymes or metalloproteinase inhibition by batimastat (BB94) showed that different regulatory signa

19 Other MMP inhibitors, such as Batimastat (British Bio-technology, Oxford, UK), are cur

20 as inhibited by the small molecule inhibitor batimastat but not by tissue inhibitor of metalloproteas

21 ic acid-type metalloprotease inhibitor BB94 (batimastat) but not to tissue inhibitors of metalloprote

22 nhibition ameliorates pathogenesis, and that batimastat could prove to be a significant candidate for

23 Batimastat dramatically inhibited the release of soluble

24 eatment with the metalloproteinase inhibitor Batimastat/GM6001, the EGFR phosphorylation inhibitor AG

25 ity, because the metalloproteinase inhibitor batimastat had no effect.

26 in a concentration-dependent fashion, while batimastat increased the surface expression of iCD23.

27 was blocked by the metalloprotease inhibitor batimastat, indicating that autocrine signaling through

28 The effect of batimastat on cell survival and colony formation was enh

29 y were inhibited by pretreatment with either batimastat or CRM197 or by pretreatment with rapamycin o

30 Treatment of cells with batimastat or GI254023X, inhibitors of the alpha-secreta

31 r CRM197 or the metalloproteinase inhibitors batimastat or phenanthroline, none of which had any effe

32 a broad spectrum metalloproteinase inhibitor batimastat reduced NT-induced MAP kinase activation.

33 Furthermore, inhibition of MMPs using batimastat reduced the activation of mitogen-activated p

34 The MMP inhibitor batimastat significantly reduced the GAG release and com

35 Moreover, treatment of batimastat-treated cells with recombinant sAPPalpha reve

36 on in isometric contraction was increased in batimastat-treated mdx mice compared with those treated

37 ADAM10 brought about similar results, as did batimastat treatment, thereby confirming that APP proces

38 ignaling induced by thrombin is inhibited by batimastat, which suggests a requirement for pro-HB-EGF

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