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1 effect that was blocked by the MMP inhibitor marimastat.
2 e (AUC) tended to correlate with the dose of Marimastat.
3 -free form and in complex with the inhibitor marimastat.
4 ially inhibited by the hydroxamate inhibitor Marimastat.
5 ients were randomly assigned to receive oral marimastat (10 mg bid; n = 114) or a placebo (n = 65) wi
6  1-year survival rate for patients receiving marimastat 25 mg was similar to that of patients receivi
7 etween patients treated with gemcitabine and marimastat 5 and 10 mg (P <.003).
8 pancreatic cancer were randomized to receive marimastat 5, 10, or 25 mg bid or gemcitabine 1,000 mg/m
9 ignificantly less efficient (>100-fold) than marimastat, a broad-spectrum MMP inhibitor, in enhancing
10                     Plasma concentrations of Marimastat achieved at dose levels 2 and 3 (50 mg and 10
11                    Intracameral injection of Marimastat also suppressed basic fibroblast growth facto
12 e required for intravasation by showing that marimastat, an inhibitor of MMPs, reduced intravasation
13 rence in survival between 5, 10, or 25 mg of marimastat and gemcitabine (P =.19).
14    In view of the manageable tolerability of marimastat and its ease of administration, further studi
15 talytic domain in complex with the inhibitor marimastat and the inhibitor-free form.
16 ted dual inhibitor combination consisting of marimastat and varespladib prevents murine lethality cau
17 on of sVR-1 breakdown with the MMP inhibitor marimastat, and the provision of exogenous recombinant s
18 ,3-dimercapto-1-propanesulfonic acid (DMPS), marimastat, and varespladib, alone or in combination, in
19 he following synthetic MMPIs: batimastat and marimastat (BB-94 and BB-2516, respectively, British Bio
20  and pharmacokinetics of escalating doses of Marimastat (British Biotech, Inc, Oxford, United Kingdom
21                                              Marimastat does not prolong PFS when used after first-li
22 ific inhibitor), anakinra (IL-1R inhibitor), marimastat, exercise, supplements, and kidney transplant
23      Combining Wf-536 with the MMP inhibitor Marimastat greatly enhanced in vitro inhibition of endot
24 tudy provide evidence of a dose response for marimastat in patients with advanced pancreatic cancer.
25                         Patients with higher marimastat levels exhibited MST, and MST was associated
26 Z and the matrix metalloproteinase inhibitor marimastat (MRM) in patients with recurrent GBM was stud
27 10-30 mg of the broad-spectrum MMP inhibitor marimastat over a 2-week period via surgically implanted
28 loskeletal toxicity was severe in only 8% of marimastat patients).
29 ty of marimastat was musculoskeletal (44% of marimastat patients, compared with 12% of gemcitabine pa
30              In addition, patients who had a marimastat plasma concentration of at least 10 ng/mL at
31 I clinical trials initiated in 1997-98 using marimastat, prinomastat (AG3340), and BAY 12-9566 alone
32 ancreatic cancer performed to date, compares marimastat, the first of a new class of agents, with gem
33                  When comparing placebo with marimastat, there was no significant difference in PFS (
34 orted in 22% and 12% of the gemcitabine- and marimastat-treated patients, respectively.
35                              Histologically, marimastat-treated rat joints were characterized by soft
36                                              Marimastat-treated rats exhibited various clinical signs
37 he estimated plasma elimination half-life of Marimastat was 4 to 5 hours.
38                                              Marimastat was administered orally at 25, 50, or 100 mg
39                        The major toxicity of marimastat was musculoskeletal (44% of marimastat patien
40                                              Marimastat was well absorbed from the gastrointestinal t
41                        Patients treated with marimastat were more likely to develop grade 2 or 3 musc
42 the broad spectrum metalloprotease inhibitor marimastat, were independently bound to the catalytic do
43 -spectrum matrix metalloproteinase inhibitor Marimastat, which may result from decreased N-cadherin s
44  PC3 cells with a combination of Wf-536 plus Marimastat with or without Paclitaxel, significantly inh
45 the dual therapeutic combinations of DMPS or marimastat with varespladib significantly inhibit the de