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1 improved over that of the parental compound TNP-470.
2 (HPMA) copolymer, Gly-Phe-Leu-Gly linker and TNP-470.
3 nically without the toxicities observed with TNP-470.
4 s data were based on the chemically reactive TNP-470.
5 xed paclitaxel dose with escalating doses of TNP-470.
6 also were reduced by 50% in the presence of TNP-470.
7 t in p53 and p21(WAF1/CIP1) are resistant to TNP-470.
8 are resistant to the cytostatic activity of TNP-470.
9 ncephalitozoonidae and treated at day 3 with TNP-470.
10 is known of the molecular mode of action of TNP-470.
13 20 mg.kg-1.d-1; group 2, fumagillin analogue TNP-470, 30 mg/kg every other day; and group 3, control
17 One day after the last dose of vehicle or TNP-470, a steady-state dosing regimen of TMZ was admini
18 pients of Lewis allografts were treated with TNP-470, a synthetic fumagillin derivative and a well-es
19 y administration of an antiangiogenic agent, TNP-470, abolished this increase and reduced local tumor
22 GM-1470,O-chloroacetyl-carbamoyl-fumagillol (TNP-470), after two-thirds hepatectomy to prevent hepati
25 ined this possibility for the combination of TNP-470, an angiogenesis inhibitor, and temozolomide (TM
26 C tumor concentrations were not different in TNP-470 and control treatment groups in s.c. tumors.
27 f human methionine aminopeptidase-2 bound to TNP-470 and its analogs fumagillin and ovalicin revealed
29 okinetics (PK) of the angiogenesis inhibitor TNP-470 and secondarily to evaluate tumor response in pa
30 on the mechanism of cell cycle inhibition by TNP-470 and suggest an alternative method of activating
32 tor O-(N-chloroacetyl-carbamoyl)-fumagillol (TNP-470) and the alkylating agent temozolomide (TMZ), in
33 ay following tumor implantation, control (no TNP-470) and treated rats received 40 mg/kg of TMZ intra
34 2 (0.503 to 0.838; n=12) for the endostatin, TNP-470, and control groups, respectively (P</=0.0001).
35 e relative to the earlier clinical candidate TNP-470, and has advanced into phase I clinical studies
36 evious reports that sunitinib, sorafenib and TNP-470 are teratogenic and demonstrate that axitinib, p
37 uch as O-(chloracetyl-carbamoyl) fumagillol (TNP-470), are thus emerging as a new class of anticancer
38 1, fumagillin, and its synthetic derivative, TNP-470, are potent inhibitors of endothelial cell proli
40 bination of endostatin and either DI-TSPa or TNP-470, at doses that were ineffective when used alone,
42 iogenic agent fumagillin (Fg) and its analog TNP-470 bind to intracellular metalloprotease methionine
44 urine tumors with the angiogenesis inhibitor TNP-470 caused near-complete ablation, with reduced prol
47 f angiogenesis such as the dipeptide IM 862, TNP-470, Col-3, and thalidomide; 2) topical and systemic
49 ently described water-soluble HPMA copolymer-TNP-470 conjugate (caplostatin), which showed comparable
50 rsely, animals treated with both DI-TSPa and TNP-470 demonstrated a modest effect on both tumor growt
51 Here, we show that the antiangiogenic drug TNP-470 displays striking cell-type specificity insofar
55 weight and volume observed between the PDT + TNP-470 group and the control group suggests that the co
57 , animals in all groups, except in the PDT + TNP-470 group, had a weight loss of >3 g at the time of
59 Although the direct molecular target for TNP-470 has been identified as the type 2 methionine ami
63 ed a phase II study of the fumigillin analog TNP-470 in previously treated patients with metastatic r
64 ore, these data are suggestive of a role for TNP-470 in selection for less leaky vascular segments wi
65 resistant to the antiangiogenic activity of TNP-470 in the basic fibroblast growth factor corneal mi
73 cancer therapy because the anticancer agent TNP-470 irreversibly inactivates the catalytic activity
74 data suggest that the fumagillin derivative TNP-470 is a promising agent for the treatment of micros
75 (WAF1/CIP1) for the cell cycle inhibition by TNP-470 is underscored by the observation that cells def
77 several antiangiogenic compounds, including TNP-470, matrix metalloproteinase inhibitors, carboxyami
79 mation in vitro, and the antiangiogenic drug TNP-470 (NSC 642492) inhibits endothelial but not tumor
81 enic inhibitors endostatin, angiostatin, and TNP-470 on tumor growth dynamics are experimentally and
85 om pre-existing vessels after treatment with TNP-470 (P < 0.05), consistent with induction of transie
89 Immunohistochemistry revealed that bFGF and TNP-470 primarily affected the endothelial compartment.
91 Further studies in this population using TNP-470 schedules that produce more prolonged drug level
93 tor Lodamin, an oral nontoxic formulation of TNP-470, significantly decreased EPC levels while suppre
96 tion of the angiogenesis inhibitor AGM-1470 (TNP-470), the antibiotic minocycline, and interferon alp
98 thrombospondin-mimetic peptide (DI-TSPa) and TNP-470 (TNP) were very similar, whereas endostatin had
100 tration-time curve was reduced by 25% in the TNP-470-treated group compared to the control (5450 +/-
101 harmacodynamic end points in the control and TNP-470 treatment groups were completed by nonparametric
102 n both the s.c. and intracerebral V+ models, TNP-470 treatment produced significant reductions in TMZ
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