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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.
11                                              TNP-470 (30 mg/kg) was given s.c. on days 6, 8, 10, 12,
12 traperitoneal) or the angiogenesis inhibitor TNP-470 (30 mg/kg/qod subcutaneous).
13 20 mg.kg-1.d-1; group 2, fumagillin analogue TNP-470, 30 mg/kg every other day; and group 3, control
14 combined with the systemic administration of TNP-470, a conventional angiogenesis inhibitor.
15                                              TNP-470, a fumagillin analog, is among the most potent a
16                                              TNP-470, a semisynthetic analogue of fumagillin, was stu
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
20                           The combination of TNP-470 administered at 60 mg/m(2) three times per week
21                                              TNP-470, administered as a weekly, 1-hour infusion to pa
22 GM-1470,O-chloroacetyl-carbamoyl-fumagillol (TNP-470), after two-thirds hepatectomy to prevent hepati
23                                              TNP-470 alone resulted in some prolongation of graft sur
24                                              TNP-470 also demonstrated in vivo activity against Encep
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
28                           The combination of TNP-470 and paclitaxel, each at full single-agent dose,
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
31  one strain demonstrating resistance to both TNP-470 and thalidomide.
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
39 codynamic end point and the effectiveness of TNP-470 as an angiogenesis inhibitor.
40 bination of endostatin and either DI-TSPa or TNP-470, at doses that were ineffective when used alone,
41         On the other hand, administration of TNP-470 before PDT was less effective at local tumor con
42 iogenic agent fumagillin (Fg) and its analog TNP-470 bind to intracellular metalloprotease methionine
43               Thirty-eight patients received TNP-470 by weekly intravenous infusion over 1 hour at on
44 urine tumors with the angiogenesis inhibitor TNP-470 caused near-complete ablation, with reduced prol
45                              It appears that TNP-470 caused this reduction in the tumor uptake of TMZ
46                               Treatment with TNP-470 caused weight loss and neurotoxic effects in mic
47 f angiogenesis such as the dipeptide IM 862, TNP-470, Col-3, and thalidomide; 2) topical and systemic
48                           MVD was reduced by TNP-470 compared with vehicle control in the V+ tumors,
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
52                       Arm A involved a fixed TNP-470 dose with escalating doses of paclitaxel, and Ar
53                Polymer conjugation prevented TNP-470 from crossing the blood-brain barrier (BBB) and
54                                       Unlike TNP-470, fumarranol does not covalently bind to MetAP2.
55 weight and volume observed between the PDT + TNP-470 group and the control group suggests that the co
56 fice; the weight of the animals in the PDT + TNP-470 group did not change.
57 , animals in all groups, except in the PDT + TNP-470 group, had a weight loss of >3 g at the time of
58                                      Because TNP-470 has been associated with neurotoxicity, we teste
59     Although the direct molecular target for TNP-470 has been identified as the type 2 methionine ami
60                                              TNP-470 has been shown to block endothelial cell cycle p
61                       Long-term therapy with TNP-470 has manageable toxicities and is feasible in pat
62        The leading anti-angiogenic compound, TNP-470, has proven to be effective in in vitro and in a
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
66 ially enhanced and prolonged the activity of TNP-470 in vivo in tumor and hepatectomy models.
67                                              TNP-470, in contrast, inhibited endothelial cell prolife
68                             We conclude that TNP-470 induces p53 activation through a unique mechanis
69 ents were treated at a dose of 60 mg/m(2) of TNP-470 infused over 1 hour three times per week.
70                                              TNP-470 inhibited hepatic regeneration by 46%, 74%, 67%,
71                    Therefore, endostatin and TNP-470 inhibited plaque growth during the treatment per
72                                   Therefore, TNP-470 interrupts the progression of CAV when given lat
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
76            A synthetic analog of fumagillin, TNP-470, is currently undergoing clinical trials for tre
77  several antiangiogenic compounds, including TNP-470, matrix metalloproteinase inhibitors, carboxyami
78 ese issues and report an oral formulation of TNP-470, named Lodamin.
79 mation in vitro, and the antiangiogenic drug TNP-470 (NSC 642492) inhibits endothelial but not tumor
80  increased in the urine of mice treated with TNP-470 on day 8.
81 enic inhibitors endostatin, angiostatin, and TNP-470 on tumor growth dynamics are experimentally and
82            An analog of fumagillin, known as TNP-470 or AGM-1470, has been undergoing clinical trials
83 s synergistically antiangiogenic with either TNP-470 or DI-TSPa.
84 ministered either a multiple-dose regimen of TNP-470 or vehicle control.
85 om pre-existing vessels after treatment with TNP-470 (P < 0.05), consistent with induction of transie
86                    Using a derivative of the TNP-470 parent compound, the fungal metabolite, fumagill
87                               Paclitaxel and TNP-470 pharmacokinetics were evaluated along with toxic
88                                              TNP-470 potently inhibits angiogenesis (EC(50) = 88 pmol
89  Immunohistochemistry revealed that bFGF and TNP-470 primarily affected the endothelial compartment.
90                                              TNP-470 reduced the permeability of BEVs at the leading
91     Further studies in this population using TNP-470 schedules that produce more prolonged drug level
92                                              TNP-470 should be evaluated further in patients with AID
93 tor Lodamin, an oral nontoxic formulation of TNP-470, significantly decreased EPC levels while suppre
94                          In clinical trials, TNP-470 slowed tumor growth in patients with metastatic
95                               HPMA copolymer-TNP-470 substantially enhanced and prolonged the activit
96 tion of the angiogenesis inhibitor AGM-1470 (TNP-470), the antibiotic minocycline, and interferon alp
97                                              TNP-470, the first anti-angiogenic small molecule to ent
98 thrombospondin-mimetic peptide (DI-TSPa) and TNP-470 (TNP) were very similar, whereas endostatin had
99 e not significantly different in control and TNP-470-treated animals.
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
103                                However, when TNP-470 was administered from day 30 to 120 after discon
104                                         When TNP-470 was administered in combination with CsA from da
105                                              TNP-470 was administered with paclitaxel to adults with
106                                              TNP-470 was conjugated to monomethoxy-polyethylene glyco
107 dies suggested that the antiangiogenic agent TNP-470 was synergistic with cytotoxic therapy.
108         When another angiogenesis inhibitor, TNP-470, was added to the antiangiogenic schedule of cyc
109                           Further studies of TNP-470 with chemotherapy regimens are warranted in NSCL

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