The Experts below are selected from a list of 1980 Experts worldwide ranked by ideXlab platform
Kevin Schoemaker - One of the best experts on this subject based on the ideXlab platform.
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identification and characterization of nvp bez235 a new orally available dual phosphatidylinositol 3 kinase mammalian target of rapamycin inhibitor with potent in vivo antitumor activity
Molecular Cancer Therapeutics, 2008Co-Authors: Sauveur Michel Maira, Christian Schnell, Saskia Brachmann, Christine Fritsch, Frederic Stauffer, Josef Brueggen, Pascal Furet, Patrick Chene, Alain De Pover, Kevin SchoemakerAbstract:The phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin inhibitor (mTOR) pathway is often constitutively activated in human tumor cells, providing unique opportunities for anticancer therapeutic intervention. NVP-BEZ235 is an imidazo[4,5-c]Quinoline Derivative that inhibits PI3K and mTOR kinase activity by binding to the ATP-binding cleft of these enzymes. In cellular settings using human tumor cell lines, this molecule is able to effectively and specifically block the dysfunctional activation of the PI3K pathway, inducing G(1) arrest. The cellular activity of NVP-BEZ235 translates well in in vivo models of human cancer. Thus, the compound was well tolerated, displayed disease stasis when administered orally, and enhanced the efficacy of other anticancer agents when used in in vivo combination studies. Ex vivo pharmacokinetic/pharmacodynamic analyses of tumor tissues showed a time-dependent correlation between compound concentration and PI3K/Akt pathway inhibition. Collectively, the preclinical data show that NVP-BEZ235 is a potent dual PI3K/mTOR modulator with favorable pharmaceutical properties. NVP-BEZ235 is currently in phase I clinical trials.
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identification and characterization of nvp bez235 a new orally available dual phosphatidylinositol 3 kinase mammalian target of rapamycin inhibitor with potent in vivo antitumor activity
Molecular Cancer Therapeutics, 2008Co-Authors: Sauveur Michel Maira, Christian Schnell, Saskia Brachmann, Christine Fritsch, Frederic Stauffer, Josef Brueggen, Pascal Furet, Patrick Chene, Alain De Pover, Kevin SchoemakerAbstract:The phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin inhibitor (mTOR) pathway is often constitutively activated in human tumor cells, providing unique opportunities for anticancer therapeutic intervention. NVP-BEZ235 is an imidazo[4,5- c ]Quinoline Derivative that inhibits PI3K and mTOR kinase activity by binding to the ATP-binding cleft of these enzymes. In cellular settings using human tumor cell lines, this molecule is able to effectively and specifically block the dysfunctional activation of the PI3K pathway, inducing G1 arrest. The cellular activity of NVP-BEZ235 translates well in in vivo models of human cancer. Thus, the compound was well tolerated, displayed disease stasis when administered orally, and enhanced the efficacy of other anticancer agents when used in in vivo combination studies. Ex vivo pharmacokinetic/pharmacodynamic analyses of tumor tissues showed a time-dependent correlation between compound concentration and PI3K/Akt pathway inhibition. Collectively, the preclinical data show that NVP-BEZ235 is a potent dual PI3K/mTOR modulator with favorable pharmaceutical properties. NVP-BEZ235 is currently in phase I clinical trials. [Mol Cancer Ther 2008;7(7):1–13 [Mol Cancer Ther 2008;7(7):1851–13]
Sauveur Michel Maira - One of the best experts on this subject based on the ideXlab platform.
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identification and characterization of nvp bez235 a new orally available dual phosphatidylinositol 3 kinase mammalian target of rapamycin inhibitor with potent in vivo antitumor activity
Molecular Cancer Therapeutics, 2008Co-Authors: Sauveur Michel Maira, Christian Schnell, Saskia Brachmann, Christine Fritsch, Frederic Stauffer, Josef Brueggen, Pascal Furet, Patrick Chene, Alain De Pover, Kevin SchoemakerAbstract:The phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin inhibitor (mTOR) pathway is often constitutively activated in human tumor cells, providing unique opportunities for anticancer therapeutic intervention. NVP-BEZ235 is an imidazo[4,5-c]Quinoline Derivative that inhibits PI3K and mTOR kinase activity by binding to the ATP-binding cleft of these enzymes. In cellular settings using human tumor cell lines, this molecule is able to effectively and specifically block the dysfunctional activation of the PI3K pathway, inducing G(1) arrest. The cellular activity of NVP-BEZ235 translates well in in vivo models of human cancer. Thus, the compound was well tolerated, displayed disease stasis when administered orally, and enhanced the efficacy of other anticancer agents when used in in vivo combination studies. Ex vivo pharmacokinetic/pharmacodynamic analyses of tumor tissues showed a time-dependent correlation between compound concentration and PI3K/Akt pathway inhibition. Collectively, the preclinical data show that NVP-BEZ235 is a potent dual PI3K/mTOR modulator with favorable pharmaceutical properties. NVP-BEZ235 is currently in phase I clinical trials.
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identification and characterization of nvp bez235 a new orally available dual phosphatidylinositol 3 kinase mammalian target of rapamycin inhibitor with potent in vivo antitumor activity
Molecular Cancer Therapeutics, 2008Co-Authors: Sauveur Michel Maira, Christian Schnell, Saskia Brachmann, Christine Fritsch, Frederic Stauffer, Josef Brueggen, Pascal Furet, Patrick Chene, Alain De Pover, Kevin SchoemakerAbstract:The phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin inhibitor (mTOR) pathway is often constitutively activated in human tumor cells, providing unique opportunities for anticancer therapeutic intervention. NVP-BEZ235 is an imidazo[4,5- c ]Quinoline Derivative that inhibits PI3K and mTOR kinase activity by binding to the ATP-binding cleft of these enzymes. In cellular settings using human tumor cell lines, this molecule is able to effectively and specifically block the dysfunctional activation of the PI3K pathway, inducing G1 arrest. The cellular activity of NVP-BEZ235 translates well in in vivo models of human cancer. Thus, the compound was well tolerated, displayed disease stasis when administered orally, and enhanced the efficacy of other anticancer agents when used in in vivo combination studies. Ex vivo pharmacokinetic/pharmacodynamic analyses of tumor tissues showed a time-dependent correlation between compound concentration and PI3K/Akt pathway inhibition. Collectively, the preclinical data show that NVP-BEZ235 is a potent dual PI3K/mTOR modulator with favorable pharmaceutical properties. NVP-BEZ235 is currently in phase I clinical trials. [Mol Cancer Ther 2008;7(7):1–13 [Mol Cancer Ther 2008;7(7):1851–13]
Frederic Stauffer - One of the best experts on this subject based on the ideXlab platform.
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identification and characterization of nvp bez235 a new orally available dual phosphatidylinositol 3 kinase mammalian target of rapamycin inhibitor with potent in vivo antitumor activity
Molecular Cancer Therapeutics, 2008Co-Authors: Sauveur Michel Maira, Christian Schnell, Saskia Brachmann, Christine Fritsch, Frederic Stauffer, Josef Brueggen, Pascal Furet, Patrick Chene, Alain De Pover, Kevin SchoemakerAbstract:The phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin inhibitor (mTOR) pathway is often constitutively activated in human tumor cells, providing unique opportunities for anticancer therapeutic intervention. NVP-BEZ235 is an imidazo[4,5-c]Quinoline Derivative that inhibits PI3K and mTOR kinase activity by binding to the ATP-binding cleft of these enzymes. In cellular settings using human tumor cell lines, this molecule is able to effectively and specifically block the dysfunctional activation of the PI3K pathway, inducing G(1) arrest. The cellular activity of NVP-BEZ235 translates well in in vivo models of human cancer. Thus, the compound was well tolerated, displayed disease stasis when administered orally, and enhanced the efficacy of other anticancer agents when used in in vivo combination studies. Ex vivo pharmacokinetic/pharmacodynamic analyses of tumor tissues showed a time-dependent correlation between compound concentration and PI3K/Akt pathway inhibition. Collectively, the preclinical data show that NVP-BEZ235 is a potent dual PI3K/mTOR modulator with favorable pharmaceutical properties. NVP-BEZ235 is currently in phase I clinical trials.
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identification and characterization of nvp bez235 a new orally available dual phosphatidylinositol 3 kinase mammalian target of rapamycin inhibitor with potent in vivo antitumor activity
Molecular Cancer Therapeutics, 2008Co-Authors: Sauveur Michel Maira, Christian Schnell, Saskia Brachmann, Christine Fritsch, Frederic Stauffer, Josef Brueggen, Pascal Furet, Patrick Chene, Alain De Pover, Kevin SchoemakerAbstract:The phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin inhibitor (mTOR) pathway is often constitutively activated in human tumor cells, providing unique opportunities for anticancer therapeutic intervention. NVP-BEZ235 is an imidazo[4,5- c ]Quinoline Derivative that inhibits PI3K and mTOR kinase activity by binding to the ATP-binding cleft of these enzymes. In cellular settings using human tumor cell lines, this molecule is able to effectively and specifically block the dysfunctional activation of the PI3K pathway, inducing G1 arrest. The cellular activity of NVP-BEZ235 translates well in in vivo models of human cancer. Thus, the compound was well tolerated, displayed disease stasis when administered orally, and enhanced the efficacy of other anticancer agents when used in in vivo combination studies. Ex vivo pharmacokinetic/pharmacodynamic analyses of tumor tissues showed a time-dependent correlation between compound concentration and PI3K/Akt pathway inhibition. Collectively, the preclinical data show that NVP-BEZ235 is a potent dual PI3K/mTOR modulator with favorable pharmaceutical properties. NVP-BEZ235 is currently in phase I clinical trials. [Mol Cancer Ther 2008;7(7):1–13 [Mol Cancer Ther 2008;7(7):1851–13]
Josef Brueggen - One of the best experts on this subject based on the ideXlab platform.
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identification and characterization of nvp bez235 a new orally available dual phosphatidylinositol 3 kinase mammalian target of rapamycin inhibitor with potent in vivo antitumor activity
Molecular Cancer Therapeutics, 2008Co-Authors: Sauveur Michel Maira, Christian Schnell, Saskia Brachmann, Christine Fritsch, Frederic Stauffer, Josef Brueggen, Pascal Furet, Patrick Chene, Alain De Pover, Kevin SchoemakerAbstract:The phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin inhibitor (mTOR) pathway is often constitutively activated in human tumor cells, providing unique opportunities for anticancer therapeutic intervention. NVP-BEZ235 is an imidazo[4,5-c]Quinoline Derivative that inhibits PI3K and mTOR kinase activity by binding to the ATP-binding cleft of these enzymes. In cellular settings using human tumor cell lines, this molecule is able to effectively and specifically block the dysfunctional activation of the PI3K pathway, inducing G(1) arrest. The cellular activity of NVP-BEZ235 translates well in in vivo models of human cancer. Thus, the compound was well tolerated, displayed disease stasis when administered orally, and enhanced the efficacy of other anticancer agents when used in in vivo combination studies. Ex vivo pharmacokinetic/pharmacodynamic analyses of tumor tissues showed a time-dependent correlation between compound concentration and PI3K/Akt pathway inhibition. Collectively, the preclinical data show that NVP-BEZ235 is a potent dual PI3K/mTOR modulator with favorable pharmaceutical properties. NVP-BEZ235 is currently in phase I clinical trials.
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identification and characterization of nvp bez235 a new orally available dual phosphatidylinositol 3 kinase mammalian target of rapamycin inhibitor with potent in vivo antitumor activity
Molecular Cancer Therapeutics, 2008Co-Authors: Sauveur Michel Maira, Christian Schnell, Saskia Brachmann, Christine Fritsch, Frederic Stauffer, Josef Brueggen, Pascal Furet, Patrick Chene, Alain De Pover, Kevin SchoemakerAbstract:The phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin inhibitor (mTOR) pathway is often constitutively activated in human tumor cells, providing unique opportunities for anticancer therapeutic intervention. NVP-BEZ235 is an imidazo[4,5- c ]Quinoline Derivative that inhibits PI3K and mTOR kinase activity by binding to the ATP-binding cleft of these enzymes. In cellular settings using human tumor cell lines, this molecule is able to effectively and specifically block the dysfunctional activation of the PI3K pathway, inducing G1 arrest. The cellular activity of NVP-BEZ235 translates well in in vivo models of human cancer. Thus, the compound was well tolerated, displayed disease stasis when administered orally, and enhanced the efficacy of other anticancer agents when used in in vivo combination studies. Ex vivo pharmacokinetic/pharmacodynamic analyses of tumor tissues showed a time-dependent correlation between compound concentration and PI3K/Akt pathway inhibition. Collectively, the preclinical data show that NVP-BEZ235 is a potent dual PI3K/mTOR modulator with favorable pharmaceutical properties. NVP-BEZ235 is currently in phase I clinical trials. [Mol Cancer Ther 2008;7(7):1–13 [Mol Cancer Ther 2008;7(7):1851–13]
Pascal Furet - One of the best experts on this subject based on the ideXlab platform.
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identification and characterization of nvp bez235 a new orally available dual phosphatidylinositol 3 kinase mammalian target of rapamycin inhibitor with potent in vivo antitumor activity
Molecular Cancer Therapeutics, 2008Co-Authors: Sauveur Michel Maira, Christian Schnell, Saskia Brachmann, Christine Fritsch, Frederic Stauffer, Josef Brueggen, Pascal Furet, Patrick Chene, Alain De Pover, Kevin SchoemakerAbstract:The phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin inhibitor (mTOR) pathway is often constitutively activated in human tumor cells, providing unique opportunities for anticancer therapeutic intervention. NVP-BEZ235 is an imidazo[4,5-c]Quinoline Derivative that inhibits PI3K and mTOR kinase activity by binding to the ATP-binding cleft of these enzymes. In cellular settings using human tumor cell lines, this molecule is able to effectively and specifically block the dysfunctional activation of the PI3K pathway, inducing G(1) arrest. The cellular activity of NVP-BEZ235 translates well in in vivo models of human cancer. Thus, the compound was well tolerated, displayed disease stasis when administered orally, and enhanced the efficacy of other anticancer agents when used in in vivo combination studies. Ex vivo pharmacokinetic/pharmacodynamic analyses of tumor tissues showed a time-dependent correlation between compound concentration and PI3K/Akt pathway inhibition. Collectively, the preclinical data show that NVP-BEZ235 is a potent dual PI3K/mTOR modulator with favorable pharmaceutical properties. NVP-BEZ235 is currently in phase I clinical trials.
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identification and characterization of nvp bez235 a new orally available dual phosphatidylinositol 3 kinase mammalian target of rapamycin inhibitor with potent in vivo antitumor activity
Molecular Cancer Therapeutics, 2008Co-Authors: Sauveur Michel Maira, Christian Schnell, Saskia Brachmann, Christine Fritsch, Frederic Stauffer, Josef Brueggen, Pascal Furet, Patrick Chene, Alain De Pover, Kevin SchoemakerAbstract:The phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin inhibitor (mTOR) pathway is often constitutively activated in human tumor cells, providing unique opportunities for anticancer therapeutic intervention. NVP-BEZ235 is an imidazo[4,5- c ]Quinoline Derivative that inhibits PI3K and mTOR kinase activity by binding to the ATP-binding cleft of these enzymes. In cellular settings using human tumor cell lines, this molecule is able to effectively and specifically block the dysfunctional activation of the PI3K pathway, inducing G1 arrest. The cellular activity of NVP-BEZ235 translates well in in vivo models of human cancer. Thus, the compound was well tolerated, displayed disease stasis when administered orally, and enhanced the efficacy of other anticancer agents when used in in vivo combination studies. Ex vivo pharmacokinetic/pharmacodynamic analyses of tumor tissues showed a time-dependent correlation between compound concentration and PI3K/Akt pathway inhibition. Collectively, the preclinical data show that NVP-BEZ235 is a potent dual PI3K/mTOR modulator with favorable pharmaceutical properties. NVP-BEZ235 is currently in phase I clinical trials. [Mol Cancer Ther 2008;7(7):1–13 [Mol Cancer Ther 2008;7(7):1851–13]
