BEZ235 (NVP-BEZ235) Product Overview Product Name: BEZ235 (NVP-BEZ235) Alternate Name/Synonyms: NVP-BEZ235 Description: Orally active PI-3 kinase inhibitor; Dual PI3K/mTOR inhibition; BEZ235 showed high target specificity and demonstrated anti-proliferative activity against tumor cell lines in animal models of cancer. Peptide Sequence: N/A Appearance: Off-white to pale yellow solid Formulation: N/A CAS Number: 915019-65-7 Molecular Formula: C₃₀H₂₃N₅O Molecular Weight: 469.55 Purity: ≥99% by HPLC Solubility:DMSO (10 mM) Storage Temp.: -20°C Shipping Conditions: RT Handling: Protect from air and moisture SMILES: CC(C)(C#N)C1=CC=C(C=C1)N2C3=C4C=C(C=CC4=NC=C3N(C2=O)C)C5=CC6=CC=CC=C6N=C5 InChi: InChI=1S/C30H23N5O/c1-30(2,18-31)22-9-11-23(12-10-22)35-28-24-15-19(21-14-20-6-4-5-7-25(20)32-16-21)8-13-26(24)33-17-27(28)34(3)29(35)36/h4-17H,1-3H3 InChi Key: JOGKUKXHTYWRGZ-UHFFFAOYSA-N PubChem CID: 11977753 MDL Number: MFCD10565944 USAGE: For Research Use Only! Not For Use in Humans.
BEZ235 (NVP-BEZ235) Product Overview Product Name: BEZ235 (NVP-BEZ235) Alternate Name/Synonyms: NVP-BEZ235 Description: Orally active PI-3 kinase inhibitor; Dual PI3K/mTOR inhibition; BEZ235 showed high target specificity and demonstrated anti-proliferative activity against tumor cell lines in animal models of cancer. Peptide Sequence: N/A Appearance: Off-white to pale yellow solid Formulation: N/A CAS Number: 915019-65-7 Molecular Formula: C₃₀H₂₃N₅O Molecular Weight: 469.55 Purity: ≥99% by HPLC Solubility:DMSO (10 mM) Storage Temp.: -20°C Shipping Conditions: RT Handling: Protect from air and moisture SMILES: CC(C)(C#N)C1=CC=C(C=C1)N2C3=C4C=C(C=CC4=NC=C3N(C2=O)C)C5=CC6=CC=CC=C6N=C5 InChi: InChI=1S/C30H23N5O/c1-30(2,18-31)22-9-11-23(12-10-22)35-28-24-15-19(21-14-20-6-4-5-7-25(20)32-16-21)8-13-26(24)33-17-27(28)34(3)29(35)36/h4-17H,1-3H3 InChi Key: JOGKUKXHTYWRGZ-UHFFFAOYSA-N PubChem CID: 11977753 MDL Number: MFCD10565944 USAGE: For Research Use Only! Not For Use in Humans.
货号： N-4288-1 g 产品名称： NVP-BEZ235, Free Base 品牌： LC 规格： 1 g
N-4288 NVP-BEZ235, Free Base, >99%[New Generic Name: Dactolisib] [BEZ235 M.W. 469.54 C30H23N5O [915019-65-7] Storage: Store at or below -20 ºC. Solubility: Soluble in anhydrous dimethylformamide at 10 mg/mL after warming to 75 ºC and cooling; soluble in DMSO at 1.33 mg/mL with warming; soluble in 1-methyl-2-pyrrolidinone at about 2 mg/mL after warming to 75 ºC and cooling; very poorly soluble in ethanol; very poorly soluble in water; maximum solubility in plain water is estimated to be about 10-20 µM buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •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. NVP-BEZ235 is able to effectively and specifically block the dysfunctional activation of the PI3K pathway and induce G(1) arrest. It also inhibits the growth of human cancer in animal models. Maira, S.M., et al. “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.” Mol. Cancer Ther. 7: 1851-1863 (2008). •NVP-BEZ235 strongly inhibits VEGF-induced cell proliferation and survival in vitro and VEGF-induced angiogenesis in vivo. Schnell, C.R., et al. “Effects of the Dual Phosphatidylinositol 3-Kinase/Mammalian Target of Rapamycin Inhibitor NVP-BEZ235 on the Tumor Vasculature: Implications for Clinical Imaging.” Cancer Res. 68: 6598-6607 (2008). •NVP-BEZ235 abrogated phosphatidylinositol 3-kinase (PI3K)-induced lapatinib resistance. Eichhorn, P.J., et al. “Phosphatidylinositol 3-Kinase Hyperactivation Results in Lapatinib Resistance that Is Reversed by the mTOR/Phosphatidylinositol 3-Kinase Inhibitor NVP-BEZ235.” Cancer Res. 68: 9221-9230 (2008). •NVP-BEZ235 induced melanoma cells to arrest in the G1 phase of cell cycle, reduced cyclin D1 expression, and increased p27(KIP1), but had negligible apoptotic activity. In a syngeneic B16 mouse melanoma tumor model, NVP-BEZ235 significantly attenuated tumor growth at primary and lymph node metastatic sites without obvious toxicity. In addition, NVP-BEZ235 blocked neovascularization and increased tumoral necrosis. Marone, R., et al. “Targeting melanoma with dual phosphoinositide 3-kinase/mammalian target of rapamycin inhibitors.” Mol. Cancer Res. 7: 601-613 (2009). •NVP-BEZ235 inhibits the PI3K/mTOR pathway and results in inhibition of proliferation of cancer cells with both wild-type and mutated p110α. Serra, V., et al. “NVP-BEZ235, a dual PI3K/mTOR inhibitor, prevents PI3K signaling and inhibits the growth of cancer cells with activating PI3K mutations.” Cancer Res. 68: 8022-8030 (2008). •Sold for laboratory or manufacturing purposes only; not for human, medical, veterinary, food, or household use. •This product is offered for R&D use in accordance with (i) 35 USC 271(e)+A13(1) in the U.S.; (ii) Section 69.1 of Japanese Patent Law in Japan; (iii) Section 11, No. 2 of the German Patent Act of 1981 in Germany; (iv) Section 60, Paragraph 5b of the U.K. Patents Act of 1977 in the U.K.; (v) Sections 55.2(1) and 55.2(6) and other common law exemptions of Canadian patent law; (vi) Section 68B of the Patents Act of 1953 in New Zealand together with the amendment of same by the Statutes Amendment Bill of 2002; (vii) such related legislation and/or case law as may be or become applicable in the aforementioned countries; and (viii) such similar laws and rules as may apply in various other countries. •Not available in some countries; not available to some institutions; not available for some uses.
N-4288 NVP-BEZ235, Free Base, >99%[New Generic Name: Dactolisib] [BEZ235 M.W. 469.54 C30H23N5O [915019-65-7] Storage: Store at or below -20 ºC. Solubility: Soluble in anhydrous dimethylformamide at 10 mg/mL after warming to 75 ºC and cooling; soluble in DMSO at 1.33 mg/mL with warming; soluble in 1-methyl-2-pyrrolidinone at about 2 mg/mL after warming to 75 ºC and cooling; very poorly soluble in ethanol; very poorly soluble in water; maximum solubility in plain water is estimated to be about 10-20 µM buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •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. NVP-BEZ235 is able to effectively and specifically block the dysfunctional activation of the PI3K pathway and induce G(1) arrest. It also inhibits the growth of human cancer in animal models. Maira, S.M., et al. “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.” Mol. Cancer Ther. 7: 1851-1863 (2008). •NVP-BEZ235 strongly inhibits VEGF-induced cell proliferation and survival in vitro and VEGF-induced angiogenesis in vivo. Schnell, C.R., et al. “Effects of the Dual Phosphatidylinositol 3-Kinase/Mammalian Target of Rapamycin Inhibitor NVP-BEZ235 on the Tumor Vasculature: Implications for Clinical Imaging.” Cancer Res. 68: 6598-6607 (2008). •NVP-BEZ235 abrogated phosphatidylinositol 3-kinase (PI3K)-induced lapatinib resistance. Eichhorn, P.J., et al. “Phosphatidylinositol 3-Kinase Hyperactivation Results in Lapatinib Resistance that Is Reversed by the mTOR/Phosphatidylinositol 3-Kinase Inhibitor NVP-BEZ235.” Cancer Res. 68: 9221-9230 (2008). •NVP-BEZ235 induced melanoma cells to arrest in the G1 phase of cell cycle, reduced cyclin D1 expression, and increased p27(KIP1), but had negligible apoptotic activity. In a syngeneic B16 mouse melanoma tumor model, NVP-BEZ235 significantly attenuated tumor growth at primary and lymph node metastatic sites without obvious toxicity. In addition, NVP-BEZ235 blocked neovascularization and increased tumoral necrosis. Marone, R., et al. “Targeting melanoma with dual phosphoinositide 3-kinase/mammalian target of rapamycin inhibitors.” Mol. Cancer Res. 7: 601-613 (2009). •NVP-BEZ235 inhibits the PI3K/mTOR pathway and results in inhibition of proliferation of cancer cells with both wild-type and mutated p110α. Serra, V., et al. “NVP-BEZ235, a dual PI3K/mTOR inhibitor, prevents PI3K signaling and inhibits the growth of cancer cells with activating PI3K mutations.” Cancer Res. 68: 8022-8030 (2008). •Sold for laboratory or manufacturing purposes only; not for human, medical, veterinary, food, or household use. •This product is offered for R&D use in accordance with (i) 35 USC 271(e)+A13(1) in the U.S.; (ii) Section 69.1 of Japanese Patent Law in Japan; (iii) Section 11, No. 2 of the German Patent Act of 1981 in Germany; (iv) Section 60, Paragraph 5b of the U.K. Patents Act of 1977 in the U.K.; (v) Sections 55.2(1) and 55.2(6) and other common law exemptions of Canadian patent law; (vi) Section 68B of the Patents Act of 1953 in New Zealand together with the amendment of same by the Statutes Amendment Bill of 2002; (vii) such related legislation and/or case law as may be or become applicable in the aforementioned countries; and (viii) such similar laws and rules as may apply in various other countries. •Not available in some countries; not available to some institutions; not available for some uses.
货号： N-4288-2 g 产品名称： NVP-BEZ235, Free Base 品牌： LC 规格： 2 g
N-4288 NVP-BEZ235, Free Base, >99%[New Generic Name: Dactolisib] [BEZ235 M.W. 469.54 C30H23N5O [915019-65-7] Storage: Store at or below -20 ºC. Solubility: Soluble in anhydrous dimethylformamide at 10 mg/mL after warming to 75 ºC and cooling; soluble in DMSO at 1.33 mg/mL with warming; soluble in 1-methyl-2-pyrrolidinone at about 2 mg/mL after warming to 75 ºC and cooling; very poorly soluble in ethanol; very poorly soluble in water; maximum solubility in plain water is estimated to be about 10-20 µM buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •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. NVP-BEZ235 is able to effectively and specifically block the dysfunctional activation of the PI3K pathway and induce G(1) arrest. It also inhibits the growth of human cancer in animal models. Maira, S.M., et al. “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.” Mol. Cancer Ther. 7: 1851-1863 (2008). •NVP-BEZ235 strongly inhibits VEGF-induced cell proliferation and survival in vitro and VEGF-induced angiogenesis in vivo. Schnell, C.R., et al. “Effects of the Dual Phosphatidylinositol 3-Kinase/Mammalian Target of Rapamycin Inhibitor NVP-BEZ235 on the Tumor Vasculature: Implications for Clinical Imaging.” Cancer Res. 68: 6598-6607 (2008). •NVP-BEZ235 abrogated phosphatidylinositol 3-kinase (PI3K)-induced lapatinib resistance. Eichhorn, P.J., et al. “Phosphatidylinositol 3-Kinase Hyperactivation Results in Lapatinib Resistance that Is Reversed by the mTOR/Phosphatidylinositol 3-Kinase Inhibitor NVP-BEZ235.” Cancer Res. 68: 9221-9230 (2008). •NVP-BEZ235 induced melanoma cells to arrest in the G1 phase of cell cycle, reduced cyclin D1 expression, and increased p27(KIP1), but had negligible apoptotic activity. In a syngeneic B16 mouse melanoma tumor model, NVP-BEZ235 significantly attenuated tumor growth at primary and lymph node metastatic sites without obvious toxicity. In addition, NVP-BEZ235 blocked neovascularization and increased tumoral necrosis. Marone, R., et al. “Targeting melanoma with dual phosphoinositide 3-kinase/mammalian target of rapamycin inhibitors.” Mol. Cancer Res. 7: 601-613 (2009). •NVP-BEZ235 inhibits the PI3K/mTOR pathway and results in inhibition of proliferation of cancer cells with both wild-type and mutated p110α. Serra, V., et al. “NVP-BEZ235, a dual PI3K/mTOR inhibitor, prevents PI3K signaling and inhibits the growth of cancer cells with activating PI3K mutations.” Cancer Res. 68: 8022-8030 (2008). •Sold for laboratory or manufacturing purposes only; not for human, medical, veterinary, food, or household use. •This product is offered for R&D use in accordance with (i) 35 USC 271(e)+A13(1) in the U.S.; (ii) Section 69.1 of Japanese Patent Law in Japan; (iii) Section 11, No. 2 of the German Patent Act of 1981 in Germany; (iv) Section 60, Paragraph 5b of the U.K. Patents Act of 1977 in the U.K.; (v) Sections 55.2(1) and 55.2(6) and other common law exemptions of Canadian patent law; (vi) Section 68B of the Patents Act of 1953 in New Zealand together with the amendment of same by the Statutes Amendment Bill of 2002; (vii) such related legislation and/or case law as may be or become applicable in the aforementioned countries; and (viii) such similar laws and rules as may apply in various other countries. •Not available in some countries; not available to some institutions; not available for some uses.
N-4288 NVP-BEZ235, Free Base, >99%[New Generic Name: Dactolisib] [BEZ235 M.W. 469.54 C30H23N5O [915019-65-7] Storage: Store at or below -20 ºC. Solubility: Soluble in anhydrous dimethylformamide at 10 mg/mL after warming to 75 ºC and cooling; soluble in DMSO at 1.33 mg/mL with warming; soluble in 1-methyl-2-pyrrolidinone at about 2 mg/mL after warming to 75 ºC and cooling; very poorly soluble in ethanol; very poorly soluble in water; maximum solubility in plain water is estimated to be about 10-20 µM buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •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. NVP-BEZ235 is able to effectively and specifically block the dysfunctional activation of the PI3K pathway and induce G(1) arrest. It also inhibits the growth of human cancer in animal models. Maira, S.M., et al. “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.” Mol. Cancer Ther. 7: 1851-1863 (2008). •NVP-BEZ235 strongly inhibits VEGF-induced cell proliferation and survival in vitro and VEGF-induced angiogenesis in vivo. Schnell, C.R., et al. “Effects of the Dual Phosphatidylinositol 3-Kinase/Mammalian Target of Rapamycin Inhibitor NVP-BEZ235 on the Tumor Vasculature: Implications for Clinical Imaging.” Cancer Res. 68: 6598-6607 (2008). •NVP-BEZ235 abrogated phosphatidylinositol 3-kinase (PI3K)-induced lapatinib resistance. Eichhorn, P.J., et al. “Phosphatidylinositol 3-Kinase Hyperactivation Results in Lapatinib Resistance that Is Reversed by the mTOR/Phosphatidylinositol 3-Kinase Inhibitor NVP-BEZ235.” Cancer Res. 68: 9221-9230 (2008). •NVP-BEZ235 induced melanoma cells to arrest in the G1 phase of cell cycle, reduced cyclin D1 expression, and increased p27(KIP1), but had negligible apoptotic activity. In a syngeneic B16 mouse melanoma tumor model, NVP-BEZ235 significantly attenuated tumor growth at primary and lymph node metastatic sites without obvious toxicity. In addition, NVP-BEZ235 blocked neovascularization and increased tumoral necrosis. Marone, R., et al. “Targeting melanoma with dual phosphoinositide 3-kinase/mammalian target of rapamycin inhibitors.” Mol. Cancer Res. 7: 601-613 (2009). •NVP-BEZ235 inhibits the PI3K/mTOR pathway and results in inhibition of proliferation of cancer cells with both wild-type and mutated p110α. Serra, V., et al. “NVP-BEZ235, a dual PI3K/mTOR inhibitor, prevents PI3K signaling and inhibits the growth of cancer cells with activating PI3K mutations.” Cancer Res. 68: 8022-8030 (2008). •Sold for laboratory or manufacturing purposes only; not for human, medical, veterinary, food, or household use. •This product is offered for R&D use in accordance with (i) 35 USC 271(e)+A13(1) in the U.S.; (ii) Section 69.1 of Japanese Patent Law in Japan; (iii) Section 11, No. 2 of the German Patent Act of 1981 in Germany; (iv) Section 60, Paragraph 5b of the U.K. Patents Act of 1977 in the U.K.; (v) Sections 55.2(1) and 55.2(6) and other common law exemptions of Canadian patent law; (vi) Section 68B of the Patents Act of 1953 in New Zealand together with the amendment of same by the Statutes Amendment Bill of 2002; (vii) such related legislation and/or case law as may be or become applicable in the aforementioned countries; and (viii) such similar laws and rules as may apply in various other countries. •Not available in some countries; not available to some institutions; not available for some uses.
N-4288 NVP-BEZ235, Free Base, >99%[New Generic Name: Dactolisib] [BEZ235 M.W. 469.54 C30H23N5O [915019-65-7] Storage: Store at or below -20 ºC. Solubility: Soluble in anhydrous dimethylformamide at 10 mg/mL after warming to 75 ºC and cooling; soluble in DMSO at 1.33 mg/mL with warming; soluble in 1-methyl-2-pyrrolidinone at about 2 mg/mL after warming to 75 ºC and cooling; very poorly soluble in ethanol; very poorly soluble in water; maximum solubility in plain water is estimated to be about 10-20 µM buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •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. NVP-BEZ235 is able to effectively and specifically block the dysfunctional activation of the PI3K pathway and induce G(1) arrest. It also inhibits the growth of human cancer in animal models. Maira, S.M., et al. “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.” Mol. Cancer Ther. 7: 1851-1863 (2008). •NVP-BEZ235 strongly inhibits VEGF-induced cell proliferation and survival in vitro and VEGF-induced angiogenesis in vivo. Schnell, C.R., et al. “Effects of the Dual Phosphatidylinositol 3-Kinase/Mammalian Target of Rapamycin Inhibitor NVP-BEZ235 on the Tumor Vasculature: Implications for Clinical Imaging.” Cancer Res. 68: 6598-6607 (2008). •NVP-BEZ235 abrogated phosphatidylinositol 3-kinase (PI3K)-induced lapatinib resistance. Eichhorn, P.J., et al. “Phosphatidylinositol 3-Kinase Hyperactivation Results in Lapatinib Resistance that Is Reversed by the mTOR/Phosphatidylinositol 3-Kinase Inhibitor NVP-BEZ235.” Cancer Res. 68: 9221-9230 (2008). •NVP-BEZ235 induced melanoma cells to arrest in the G1 phase of cell cycle, reduced cyclin D1 expression, and increased p27(KIP1), but had negligible apoptotic activity. In a syngeneic B16 mouse melanoma tumor model, NVP-BEZ235 significantly attenuated tumor growth at primary and lymph node metastatic sites without obvious toxicity. In addition, NVP-BEZ235 blocked neovascularization and increased tumoral necrosis. Marone, R., et al. “Targeting melanoma with dual phosphoinositide 3-kinase/mammalian target of rapamycin inhibitors.” Mol. Cancer Res. 7: 601-613 (2009). •NVP-BEZ235 inhibits the PI3K/mTOR pathway and results in inhibition of proliferation of cancer cells with both wild-type and mutated p110α. Serra, V., et al. “NVP-BEZ235, a dual PI3K/mTOR inhibitor, prevents PI3K signaling and inhibits the growth of cancer cells with activating PI3K mutations.” Cancer Res. 68: 8022-8030 (2008). •Sold for laboratory or manufacturing purposes only; not for human, medical, veterinary, food, or household use. •This product is offered for R&D use in accordance with (i) 35 USC 271(e)+A13(1) in the U.S.; (ii) Section 69.1 of Japanese Patent Law in Japan; (iii) Section 11, No. 2 of the German Patent Act of 1981 in Germany; (iv) Section 60, Paragraph 5b of the U.K. Patents Act of 1977 in the U.K.; (v) Sections 55.2(1) and 55.2(6) and other common law exemptions of Canadian patent law; (vi) Section 68B of the Patents Act of 1953 in New Zealand together with the amendment of same by the Statutes Amendment Bill of 2002; (vii) such related legislation and/or case law as may be or become applicable in the aforementioned countries; and (viii) such similar laws and rules as may apply in various other countries. •Not available in some countries; not available to some institutions; not available for some uses.
N-4288 NVP-BEZ235, Free Base, >99%[New Generic Name: Dactolisib] [BEZ235 M.W. 469.54 C30H23N5O [915019-65-7] Storage: Store at or below -20 ºC. Solubility: Soluble in anhydrous dimethylformamide at 10 mg/mL after warming to 75 ºC and cooling; soluble in DMSO at 1.33 mg/mL with warming; soluble in 1-methyl-2-pyrrolidinone at about 2 mg/mL after warming to 75 ºC and cooling; very poorly soluble in ethanol; very poorly soluble in water; maximum solubility in plain water is estimated to be about 10-20 µM buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •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. NVP-BEZ235 is able to effectively and specifically block the dysfunctional activation of the PI3K pathway and induce G(1) arrest. It also inhibits the growth of human cancer in animal models. Maira, S.M., et al. “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.” Mol. Cancer Ther. 7: 1851-1863 (2008). •NVP-BEZ235 strongly inhibits VEGF-induced cell proliferation and survival in vitro and VEGF-induced angiogenesis in vivo. Schnell, C.R., et al. “Effects of the Dual Phosphatidylinositol 3-Kinase/Mammalian Target of Rapamycin Inhibitor NVP-BEZ235 on the Tumor Vasculature: Implications for Clinical Imaging.” Cancer Res. 68: 6598-6607 (2008). •NVP-BEZ235 abrogated phosphatidylinositol 3-kinase (PI3K)-induced lapatinib resistance. Eichhorn, P.J., et al. “Phosphatidylinositol 3-Kinase Hyperactivation Results in Lapatinib Resistance that Is Reversed by the mTOR/Phosphatidylinositol 3-Kinase Inhibitor NVP-BEZ235.” Cancer Res. 68: 9221-9230 (2008). •NVP-BEZ235 induced melanoma cells to arrest in the G1 phase of cell cycle, reduced cyclin D1 expression, and increased p27(KIP1), but had negligible apoptotic activity. In a syngeneic B16 mouse melanoma tumor model, NVP-BEZ235 significantly attenuated tumor growth at primary and lymph node metastatic sites without obvious toxicity. In addition, NVP-BEZ235 blocked neovascularization and increased tumoral necrosis. Marone, R., et al. “Targeting melanoma with dual phosphoinositide 3-kinase/mammalian target of rapamycin inhibitors.” Mol. Cancer Res. 7: 601-613 (2009). •NVP-BEZ235 inhibits the PI3K/mTOR pathway and results in inhibition of proliferation of cancer cells with both wild-type and mutated p110α. Serra, V., et al. “NVP-BEZ235, a dual PI3K/mTOR inhibitor, prevents PI3K signaling and inhibits the growth of cancer cells with activating PI3K mutations.” Cancer Res. 68: 8022-8030 (2008). •Sold for laboratory or manufacturing purposes only; not for human, medical, veterinary, food, or household use. •This product is offered for R&D use in accordance with (i) 35 USC 271(e)+A13(1) in the U.S.; (ii) Section 69.1 of Japanese Patent Law in Japan; (iii) Section 11, No. 2 of the German Patent Act of 1981 in Germany; (iv) Section 60, Paragraph 5b of the U.K. Patents Act of 1977 in the U.K.; (v) Sections 55.2(1) and 55.2(6) and other common law exemptions of Canadian patent law; (vi) Section 68B of the Patents Act of 1953 in New Zealand together with the amendment of same by the Statutes Amendment Bill of 2002; (vii) such related legislation and/or case law as may be or become applicable in the aforementioned countries; and (viii) such similar laws and rules as may apply in various other countries. •Not available in some countries; not available to some institutions; not available for some uses.
N-4288 NVP-BEZ235, Free Base, >99%[New Generic Name: Dactolisib] [BEZ235 M.W. 469.54 C30H23N5O [915019-65-7] Storage: Store at or below -20 ºC. Solubility: Soluble in anhydrous dimethylformamide at 10 mg/mL after warming to 75 ºC and cooling; soluble in DMSO at 1.33 mg/mL with warming; soluble in 1-methyl-2-pyrrolidinone at about 2 mg/mL after warming to 75 ºC and cooling; very poorly soluble in ethanol; very poorly soluble in water; maximum solubility in plain water is estimated to be about 10-20 µM buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •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. NVP-BEZ235 is able to effectively and specifically block the dysfunctional activation of the PI3K pathway and induce G(1) arrest. It also inhibits the growth of human cancer in animal models. Maira, S.M., et al. “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.” Mol. Cancer Ther. 7: 1851-1863 (2008). •NVP-BEZ235 strongly inhibits VEGF-induced cell proliferation and survival in vitro and VEGF-induced angiogenesis in vivo. Schnell, C.R., et al. “Effects of the Dual Phosphatidylinositol 3-Kinase/Mammalian Target of Rapamycin Inhibitor NVP-BEZ235 on the Tumor Vasculature: Implications for Clinical Imaging.” Cancer Res. 68: 6598-6607 (2008). •NVP-BEZ235 abrogated phosphatidylinositol 3-kinase (PI3K)-induced lapatinib resistance. Eichhorn, P.J., et al. “Phosphatidylinositol 3-Kinase Hyperactivation Results in Lapatinib Resistance that Is Reversed by the mTOR/Phosphatidylinositol 3-Kinase Inhibitor NVP-BEZ235.” Cancer Res. 68: 9221-9230 (2008). •NVP-BEZ235 induced melanoma cells to arrest in the G1 phase of cell cycle, reduced cyclin D1 expression, and increased p27(KIP1), but had negligible apoptotic activity. In a syngeneic B16 mouse melanoma tumor model, NVP-BEZ235 significantly attenuated tumor growth at primary and lymph node metastatic sites without obvious toxicity. In addition, NVP-BEZ235 blocked neovascularization and increased tumoral necrosis. Marone, R., et al. “Targeting melanoma with dual phosphoinositide 3-kinase/mammalian target of rapamycin inhibitors.” Mol. Cancer Res. 7: 601-613 (2009). •NVP-BEZ235 inhibits the PI3K/mTOR pathway and results in inhibition of proliferation of cancer cells with both wild-type and mutated p110α. Serra, V., et al. “NVP-BEZ235, a dual PI3K/mTOR inhibitor, prevents PI3K signaling and inhibits the growth of cancer cells with activating PI3K mutations.” Cancer Res. 68: 8022-8030 (2008). •Sold for laboratory or manufacturing purposes only; not for human, medical, veterinary, food, or household use. •This product is offered for R&D use in accordance with (i) 35 USC 271(e)+A13(1) in the U.S.; (ii) Section 69.1 of Japanese Patent Law in Japan; (iii) Section 11, No. 2 of the German Patent Act of 1981 in Germany; (iv) Section 60, Paragraph 5b of the U.K. Patents Act of 1977 in the U.K.; (v) Sections 55.2(1) and 55.2(6) and other common law exemptions of Canadian patent law; (vi) Section 68B of the Patents Act of 1953 in New Zealand together with the amendment of same by the Statutes Amendment Bill of 2002; (vii) such related legislation and/or case law as may be or become applicable in the aforementioned countries; and (viii) such similar laws and rules as may apply in various other countries. •Not available in some countries; not available to some institutions; not available for some uses.
N-4288 NVP-BEZ235, Free Base, >99%[New Generic Name: Dactolisib] [BEZ235 M.W. 469.54 C30H23N5O [915019-65-7] Storage: Store at or below -20 ºC. Solubility: Soluble in anhydrous dimethylformamide at 10 mg/mL after warming to 75 ºC and cooling; soluble in DMSO at 1.33 mg/mL with warming; soluble in 1-methyl-2-pyrrolidinone at about 2 mg/mL after warming to 75 ºC and cooling; very poorly soluble in ethanol; very poorly soluble in water; maximum solubility in plain water is estimated to be about 10-20 µM buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •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. NVP-BEZ235 is able to effectively and specifically block the dysfunctional activation of the PI3K pathway and induce G(1) arrest. It also inhibits the growth of human cancer in animal models. Maira, S.M., et al. “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.” Mol. Cancer Ther. 7: 1851-1863 (2008). •NVP-BEZ235 strongly inhibits VEGF-induced cell proliferation and survival in vitro and VEGF-induced angiogenesis in vivo. Schnell, C.R., et al. “Effects of the Dual Phosphatidylinositol 3-Kinase/Mammalian Target of Rapamycin Inhibitor NVP-BEZ235 on the Tumor Vasculature: Implications for Clinical Imaging.” Cancer Res. 68: 6598-6607 (2008). •NVP-BEZ235 abrogated phosphatidylinositol 3-kinase (PI3K)-induced lapatinib resistance. Eichhorn, P.J., et al. “Phosphatidylinositol 3-Kinase Hyperactivation Results in Lapatinib Resistance that Is Reversed by the mTOR/Phosphatidylinositol 3-Kinase Inhibitor NVP-BEZ235.” Cancer Res. 68: 9221-9230 (2008). •NVP-BEZ235 induced melanoma cells to arrest in the G1 phase of cell cycle, reduced cyclin D1 expression, and increased p27(KIP1), but had negligible apoptotic activity. In a syngeneic B16 mouse melanoma tumor model, NVP-BEZ235 significantly attenuated tumor growth at primary and lymph node metastatic sites without obvious toxicity. In addition, NVP-BEZ235 blocked neovascularization and increased tumoral necrosis. Marone, R., et al. “Targeting melanoma with dual phosphoinositide 3-kinase/mammalian target of rapamycin inhibitors.” Mol. Cancer Res. 7: 601-613 (2009). •NVP-BEZ235 inhibits the PI3K/mTOR pathway and results in inhibition of proliferation of cancer cells with both wild-type and mutated p110α. Serra, V., et al. “NVP-BEZ235, a dual PI3K/mTOR inhibitor, prevents PI3K signaling and inhibits the growth of cancer cells with activating PI3K mutations.” Cancer Res. 68: 8022-8030 (2008). •Sold for laboratory or manufacturing purposes only; not for human, medical, veterinary, food, or household use. •This product is offered for R&D use in accordance with (i) 35 USC 271(e)+A13(1) in the U.S.; (ii) Section 69.1 of Japanese Patent Law in Japan; (iii) Section 11, No. 2 of the German Patent Act of 1981 in Germany; (iv) Section 60, Paragraph 5b of the U.K. Patents Act of 1977 in the U.K.; (v) Sections 55.2(1) and 55.2(6) and other common law exemptions of Canadian patent law; (vi) Section 68B of the Patents Act of 1953 in New Zealand together with the amendment of same by the Statutes Amendment Bill of 2002; (vii) such related legislation and/or case law as may be or become applicable in the aforementioned countries; and (viii) such similar laws and rules as may apply in various other countries. •Not available in some countries; not available to some institutions; not available for some uses.
NVP-BEZ235 Cayman Chemical Item Number 10565 Description Phosphatidylinositol 3-kinase (PI3K) signaling through Akt/PKB and the mammalian target of rapamycin (mTOR) controls gene expression related to cell proliferation, differentiation, and apoptosis. Increased activity of this pathway is important in many types of cancer. NVP-BEZ235 is a potent dual inhibitor of PI3K and mTOR that is well tolerated, displays disease stasis when administered orally, and enhances the efficacy of other anticancer agents when used in in vivo combination studies.1↗,2↗ It inhibits PI3K isoforms and mutants with low nanomolar IC50 values, leading to growth arrest in the G1 phase.1↗,3↗ Through its effects on PI3K, NVP-BEZ235 inhibits VEGF-induced angiogenesis.4↗ By directly blocking cell growth and indirectly inhibiting angiogenesis, it has potential in both solid tumors and in metastatic melanoma therapy.5↗,6↗ Formal Name 4-[2,3-dihydro-3-methyl-2-oxo-8-(3-quinolinyl)-1H-imidazo[4,5-c]quinolin-1-yl]-α,α-dimethyl-benzeneacetonitrile CAS Number 915019-65-7 Molecular Formula C30H23N5O Formula Weight 469.5 Formulation A crystalline solid Purity ≥98% Stability 2 years Storage -20°C Shipping Room temperature in continental US; may vary elsewhere SMILES CC(C#N)(C)C(C=C1)=CC=C1N(C(N2C)=O)C3=C2C=NC4=CC=C(C5=CC(C=CC=C6)=C6N=C5)C=C43 InCHI Code 1S/C30H23N5O/c1-30(2,18-31)22-9-11-23(12-10-22)35-28-24-15-19(21-14-20-6-4-5-7-25(20)32-16-21)8-13-26(24)33-17-27(28)34(3)29(35)36/h4-17H,1-3H3 InCHI Key JOGKUKXHTYWRGZ-UHFFFAOYSA-N -20°C
NVP-BEZ235 Cayman Chemical Item Number 10565 Description Phosphatidylinositol 3-kinase (PI3K) signaling through Akt/PKB and the mammalian target of rapamycin (mTOR) controls gene expression related to cell proliferation, differentiation, and apoptosis. Increased activity of this pathway is important in many types of cancer. NVP-BEZ235 is a potent dual inhibitor of PI3K and mTOR that is well tolerated, displays disease stasis when administered orally, and enhances the efficacy of other anticancer agents when used in in vivo combination studies.1↗,2↗ It inhibits PI3K isoforms and mutants with low nanomolar IC50 values, leading to growth arrest in the G1 phase.1↗,3↗ Through its effects on PI3K, NVP-BEZ235 inhibits VEGF-induced angiogenesis.4↗ By directly blocking cell growth and indirectly inhibiting angiogenesis, it has potential in both solid tumors and in metastatic melanoma therapy.5↗,6↗ Formal Name 4-[2,3-dihydro-3-methyl-2-oxo-8-(3-quinolinyl)-1H-imidazo[4,5-c]quinolin-1-yl]-α,α-dimethyl-benzeneacetonitrile CAS Number 915019-65-7 Molecular Formula C30H23N5O Formula Weight 469.5 Formulation A crystalline solid Purity ≥98% Stability 2 years Storage -20°C Shipping Room temperature in continental US; may vary elsewhere SMILES CC(C#N)(C)C(C=C1)=CC=C1N(C(N2C)=O)C3=C2C=NC4=CC=C(C5=CC(C=CC=C6)=C6N=C5)C=C43 InCHI Code 1S/C30H23N5O/c1-30(2,18-31)22-9-11-23(12-10-22)35-28-24-15-19(21-14-20-6-4-5-7-25(20)32-16-21)8-13-26(24)33-17-27(28)34(3)29(35)36/h4-17H,1-3H3 InCHI Key JOGKUKXHTYWRGZ-UHFFFAOYSA-N -20°C
NVP-BEZ235 Cayman Chemical Item Number 10565 Description Phosphatidylinositol 3-kinase (PI3K) signaling through Akt/PKB and the mammalian target of rapamycin (mTOR) controls gene expression related to cell proliferation, differentiation, and apoptosis. Increased activity of this pathway is important in many types of cancer. NVP-BEZ235 is a potent dual inhibitor of PI3K and mTOR that is well tolerated, displays disease stasis when administered orally, and enhances the efficacy of other anticancer agents when used in in vivo combination studies.1↗,2↗ It inhibits PI3K isoforms and mutants with low nanomolar IC50 values, leading to growth arrest in the G1 phase.1↗,3↗ Through its effects on PI3K, NVP-BEZ235 inhibits VEGF-induced angiogenesis.4↗ By directly blocking cell growth and indirectly inhibiting angiogenesis, it has potential in both solid tumors and in metastatic melanoma therapy.5↗,6↗ Formal Name 4-[2,3-dihydro-3-methyl-2-oxo-8-(3-quinolinyl)-1H-imidazo[4,5-c]quinolin-1-yl]-α,α-dimethyl-benzeneacetonitrile CAS Number 915019-65-7 Molecular Formula C30H23N5O Formula Weight 469.5 Formulation A crystalline solid Purity ≥98% Stability 2 years Storage -20°C Shipping Room temperature in continental US; may vary elsewhere SMILES CC(C#N)(C)C(C=C1)=CC=C1N(C(N2C)=O)C3=C2C=NC4=CC=C(C5=CC(C=CC=C6)=C6N=C5)C=C43 InCHI Code 1S/C30H23N5O/c1-30(2,18-31)22-9-11-23(12-10-22)35-28-24-15-19(21-14-20-6-4-5-7-25(20)32-16-21)8-13-26(24)33-17-27(28)34(3)29(35)36/h4-17H,1-3H3 InCHI Key JOGKUKXHTYWRGZ-UHFFFAOYSA-N -20°C
NVP-BEZ235 Cayman Chemical Item Number 10565 Description Phosphatidylinositol 3-kinase (PI3K) signaling through Akt/PKB and the mammalian target of rapamycin (mTOR) controls gene expression related to cell proliferation, differentiation, and apoptosis. Increased activity of this pathway is important in many types of cancer. NVP-BEZ235 is a potent dual inhibitor of PI3K and mTOR that is well tolerated, displays disease stasis when administered orally, and enhances the efficacy of other anticancer agents when used in in vivo combination studies.1↗,2↗ It inhibits PI3K isoforms and mutants with low nanomolar IC50 values, leading to growth arrest in the G1 phase.1↗,3↗ Through its effects on PI3K, NVP-BEZ235 inhibits VEGF-induced angiogenesis.4↗ By directly blocking cell growth and indirectly inhibiting angiogenesis, it has potential in both solid tumors and in metastatic melanoma therapy.5↗,6↗ Formal Name 4-[2,3-dihydro-3-methyl-2-oxo-8-(3-quinolinyl)-1H-imidazo[4,5-c]quinolin-1-yl]-α,α-dimethyl-benzeneacetonitrile CAS Number 915019-65-7 Molecular Formula C30H23N5O Formula Weight 469.5 Formulation A crystalline solid Purity ≥98% Stability 2 years Storage -20°C Shipping Room temperature in continental US; may vary elsewhere SMILES CC(C#N)(C)C(C=C1)=CC=C1N(C(N2C)=O)C3=C2C=NC4=CC=C(C5=CC(C=CC=C6)=C6N=C5)C=C43 InCHI Code 1S/C30H23N5O/c1-30(2,18-31)22-9-11-23(12-10-22)35-28-24-15-19(21-14-20-6-4-5-7-25(20)32-16-21)8-13-26(24)33-17-27(28)34(3)29(35)36/h4-17H,1-3H3 InCHI Key JOGKUKXHTYWRGZ-UHFFFAOYSA-N -20°C
