Volume 5, Issue 3, Pages (March 2004)

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Volume 5, Issue 3, Pages 231-239 (March 2004) In vivo antitumor activity of NVP-AEW541—A novel, potent, and selective inhibitor of the IGF-IR kinase Carlos Garcı́a-Echeverrı́a, Mark A Pearson, Andreas Marti, Thomas Meyer, Juergen Mestan, Johann Zimmermann, Jiaping Gao, Josef Brueggen, Hans-Georg Capraro, Robert Cozens, Dean B Evans, Doriano Fabbro, Pascal Furet, Diana Graus Porta, Janis Liebetanz, Georg Martiny-Baron, Stephan Ruetz, Francesco Hofmann Cancer Cell Volume 5, Issue 3, Pages 231-239 (March 2004) DOI: 10.1016/S1535-6108(04)00051-0

Figure 1 Inhibition of IGF-IR signaling by NVP-AEW541 in NWT-21 cells Inhibition of IGF-IR-mediated signaling by NVP-AEW541 was determined in NWT-21 cells, a derivative of NIH3T3 mouse fibroblasts obtained upon overexpression of the human IGF-IR. Cells were grown as a monolayer, exposed to NVP-AEW541, and stimulated with IGF-I. IGF-IR and PKB phosphorylation, as well as their total protein levels, were determined by Western blot as described in the Experimental Procedures. Cancer Cell 2004 5, 231-239DOI: (10.1016/S1535-6108(04)00051-0)

Figure 2 Inhibition of IGF-IR signaling by NVP-AEW541 in a mouse pharmacodynamic model Inhibition of IGF-IR-mediated signaling by NVP-AEW541 in murine lung was determined ex vivo as described in the Experimental Procedures. NVP-AEW541 was administered p.o. at 50 mg/kg; one hour later, IGF-I at 0.1 mg/kg was injected i.v., and the tissue was collected 5 min thereafter. IGF-IR, PKB, and MAPK phosphorylation, as well as their total levels to ensure equal loading, were determined ex vivo by immunoprecipitation-Western blot (phospho-IGF-IR) or by Western blot. Cancer Cell 2004 5, 231-239DOI: (10.1016/S1535-6108(04)00051-0)

Figure 3 Inhibition of IGF-IR signaling by NVP-AEW541 in NWT-21 tumor xenografts Inhibition of IGF-IR-mediated signaling by NVP-AEW541 in subcutaneous NWT-21 tumors was determined ex vivo as described in the Experimental Procedures. NVP-AEW541 was administered p.o. at 50 mg/kg; one hour later, tumor tissue was collected with or without prior stimulation with IGF-I (0.1 mg/kg) by i.v. injection. IGF-IR, PKB, and MAPK phosphorylation, as well as their total levels to ensure equal loading, were determined ex vivo by Western blot. Cancer Cell 2004 5, 231-239DOI: (10.1016/S1535-6108(04)00051-0)

Figure 4 Inhibition of tumor growth by oral administration of NVP-AEW541 in a fibrosarcoma model Tumors were established in female nude mice (Hsd:Athymic Nude-nu) by subcutaneous implantation of NWT-21 tumor fragments (3 × 3 × 3 mm) obtained from donor mice. Seven days after implantation (day 0), treatment with NVP-AEW541 was started at doses of 20 mg/kg, 30 mg/kg, and 50 mg/kg p.o. bid, 7×/week. Vehicle controls received 25 mM L(+)-tartaric acid p.o. bid, 7×/week. Tumor volumes were determined according to the formula L × W × H × π / 6 and are shown in mm3 as mean ± SEM. Body weights are shown in g as mean ± SEM. The experiment was terminated 11 days after start of treatment. *p < 0.05 (Dunnett's) versus control vehicle. Cancer Cell 2004 5, 231-239DOI: (10.1016/S1535-6108(04)00051-0)