NVP-AUY922 Product Overview Product Name: NVP-AUY922 Alternate Name/Synonyms: 5-(2,4-Dihydroxy-5-isopropylphenyl)-N-ethyl-4-(4-(morpholinomethyl)phenyl)isoxazole-3-carboxamide Description: A Hsp90 inhibitor. NVP-AUY922 has excellent potency against Hsp90 in a fluorescence polarization binding assay with an IC₅₀ of 21 nmol/L against the β-isoform and of 13 nmol/L for the α-isoform. Peptide Sequence: N/A Appearance: White to off-white solid Formulation: N/A CAS Number: 747412-49-3 Molecular Formula: C₂₆H₃₁N₃O₆ Molecular Weight: 465.54 Purity: ≥99% Solubility:DMSO (10 mM) Storage Temp.: -20°C Shipping Conditions: gel pack Handling: Protect from light and moisture SMILES: CCNC(=O)C1=C(C(=C2C=C(C(=CC2=O)O)C(C)C)ON1)C3=CC=C(C=C3)CN4CCOCC4 InChi: InChI=1S/C26H31N3O5/c1-4-27-26(32)24-23(18-7-5-17(6-8-18)15-29-9-11-33-12-10-29)25(34-28-24)20-13-19(16(2)3)21(30)14-22(20)31/h5-8,13-14,16,28,30H,4,9-12,15H2,1-3H3,(H,27,32)/b25-20- InChi Key: SWDZPNJZKUGIIH-QQTULTPQSA-N PubChem CID: 10096043 MDL Number: N/A 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.
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.
NVP-TAE684 Product Overview Product Name: NVP-TAE684 Alternate Name/Synonyms: 5-Chloro-N4-(2-(isopropylsulfonyl)phenyl-N2-(2-methoxy-4-(4-methylpiperazin-1-yl)-piperidin-1-yl)phenyl)pyrimidine-2,4-diamine Description: A potent and selective ALK (anaplastic lymphoma kinase) inhibitor that blocked the growth of ALCL (anaplastic large cell lymphoma)-derived and ALK-dependent cell lines with IC₅₀ = 2-10 nM. NVP-TAE684 treatment resulted in a rapid and sustained inhibition of phosphorylation of NPM-ALK (Nucleophosmin-anaplastic lymphoma kinase) and its downstream effectors and subsequent induction of apoptosis and cell cycle arrest. Peptide Sequence: N/A Appearance: Light yellow solid Formulation: N/A CAS Number: 761439-42-3 Molecular Formula: C₃₀H₄₀ClN₇O₃S Molecular Weight: 614.2 Purity: ≥98% by HPLC Solubility:DMSO Storage Temp.: -20°C Shipping Conditions: gel pack Handling: Protect from air and light SMILES: CC(C)S(=O)(=O)C1=CC=CC=C1NC2=NC(=NC=C2Cl)NC3=C(C=C(C=C3)N4CCC(CC4)N5CCN(CC5)C)OC InChi: InChI=1S/C30H40ClN7O3S/c1-21(2)42(39,40)28-8-6-5-7-26(28)33-29-24(31)20-32-30(35-29)34-25-10-9-23(19-27(25)41-4)37-13-11-22(12-14-37)38-17-15-36(3)16-18-38/h5-10,19-22H,11-18H2,1-4H3,(H2,32,33,34,35) InChi Key: QQWUGDVOUVUTOY-UHFFFAOYSA-N PubChem CID: 16038120 MDL Number: N/A USAGE: For Research Use Only! Not For Use in Humans.
DPP IV Inhibitor, NVP DPP 728 A potent DPP IV Inhibitor, Product Overview Product Name: DPP IV Inhibitor, NVP DPP 728 Alternate Name/Synonyms: 6-[[2-[[2-(2S)-2-Cyano-1-pyrrolidinyl]-2-oxoethyl]amino]ethyl]amino-3-pyridinecarbononitrile Dihydrochloride Description: A potent, selective, reversible, and slow binding dipeptidyl peptidase IV inhibitor (IC₅₀ = 14 nM). Displays >15,000 fold selectivity over DPP-II and a range of Proline-cleaving proteases. Displays anti-diabetic activity in vivo, improves glucose tolerance, increases glucagon-like peptide 1 (GLP-1) and insulin levels, and augments insulin secretion and GLUT-2 levels. Peptide Sequence: N/A Appearance: White solid Formulation: N/A CAS Number: 247016-69-9 Molecular Formula: C₁₅H₁₈N₆O.2HCl Molecular Weight: 371.27 Purity: ≥98% by HPLC Solubility:DMSO (~100 mM) or EtOH (~ 100 mM) Storage Temp.: -20°C Shipping Conditions: gel pack Handling: Protect from light and moisture SMILES: C1CC(N(C1)C(=O)CNCCNC2=NC=C(C=C2)C#N)C#N.Cl.Cl InChi: InChI=1S/C15H18N6O.2ClH/c16-8-12-3-4-14(20-10-12)19-6-5-18-11-15(22)21-7-1-2-13(21)9-17;;/h3-4,10,13,18H,1-2,5-7,11H2,(H,19,20);2*1H/t13-;;/m0../s1 InChi Key: VNACOBVZDCLAEV-GXKRWWSZSA-N PubChem CID: 9799555 MDL Number: N/A USAGE: For Research Use Only! Not For Use in Humans.
DPP IV Inhibitor, NVP DPP 728 A potent DPP IV Inhibitor, Product Overview Product Name: DPP IV Inhibitor, NVP DPP 728 Alternate Name/Synonyms: 6-[[2-[[2-(2S)-2-Cyano-1-pyrrolidinyl]-2-oxoethyl]amino]ethyl]amino-3-pyridinecarbononitrile Dihydrochloride Description: A potent, selective, reversible, and slow binding dipeptidyl peptidase IV inhibitor (IC₅₀ = 14 nM). Displays >15,000 fold selectivity over DPP-II and a range of Proline-cleaving proteases. Displays anti-diabetic activity in vivo, improves glucose tolerance, increases glucagon-like peptide 1 (GLP-1) and insulin levels, and augments insulin secretion and GLUT-2 levels. Peptide Sequence: N/A Appearance: White solid Formulation: N/A CAS Number: 247016-69-9 Molecular Formula: C₁₅H₁₈N₆O.2HCl Molecular Weight: 371.27 Purity: ≥98% by HPLC Solubility:DMSO (~100 mM) or EtOH (~ 100 mM) Storage Temp.: -20°C Shipping Conditions: gel pack Handling: Protect from light and moisture SMILES: C1CC(N(C1)C(=O)CNCCNC2=NC=C(C=C2)C#N)C#N.Cl.Cl InChi: InChI=1S/C15H18N6O.2ClH/c16-8-12-3-4-14(20-10-12)19-6-5-18-11-15(22)21-7-1-2-13(21)9-17;;/h3-4,10,13,18H,1-2,5-7,11H2,(H,19,20);2*1H/t13-;;/m0../s1 InChi Key: VNACOBVZDCLAEV-GXKRWWSZSA-N PubChem CID: 9799555 MDL Number: N/A 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.
货号： N-5300-1 g 产品名称： NVP-AUY922, Free Base 品牌： LC 规格： 1 g
N-5300 NVP-AUY922, Free Base, >99% Synonyms: [AUY922] [VER-52296] M.W. 465.54 C26H31N3O5 [747412-49-3] Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO at 100 mg/mL; soluble in ethanol at 100 mg/mL; very poorly soluble in water; maximum solubility in plain water is estimated to be about 25-50 µM; buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •NVP-AUY922 potently inhibited HSP90 with IC50 values of 7.8 nM and 21 nM, and Ki values of 9 nM and 8.2 nM for HSP90α and HSP90β, respectively. NVP-AUY922 showed a very high binding affinity to HSP90β with a Kd of 1.7 nM. NVP-AUY922 inhibited the proliferation of human tumor cells in vitro with GI50 values of approximately 2 to 40 nM, inducing G1-G2 arrest and apoptosis. Human endothelial cells were very sensitive to NVP-AUY922 with GI50s of 2.5-3.9 nM. NVP-AUY922 also exhibited potent antitumor efficacy in human tumor xenografts including BT474 breast, A2780 ovarian, U87MG glioblastoma, PC3 prostate, and WM266.4 melanoma. Eccles, S.A., et al. “NVP-AUY922: a novel heat shock protein 90 inhibitor active against xenograft tumor growth, angiogenesis, and metastasis.” Cancer Res. 68: 2850-2860 (2008). •NVP-AUY922 showed impressive synergistic inhibitory effect with histone deacetylase inhibitors, melphalan, doxorubicin, NVP-LBH589 (Panobinostat), and suberoylanilide hydroxamic acid (SAHA, Vorinostat) on the growth of multiple myeloma cell lines and primary myeloma cells. Kaiser, M., et al. “Synergistic action of the novel HSP90 inhibitor NVP-AUY922 with histone deacetylase inhibitors, melphalan, or doxorubicin in multiple myeloma.” Eur. J. Haematol. 84: 337-344 (2010). •NVP-AUY922 potently inhibited the proliferation of human breast cancer cell lines with GI50 values in the range of 3 to 126 nM. NVP-AUY922 induced proliferative inhibition concordant with HSP70 upregulation and client protein depletion. Significant growth inhibition of BT-474 tumor and good tolerability were observed in athymic mice when NVP-AUY922 was administered once per week. Therapeutic effects were also concurrent with changes in pharmacodynamic markers, including HSP90-p23 dissociation, decreases in ERBB2 and P-AKT, and increased HSP70 protein levels. Jensen, M.R., et al. “NVP-AUY922: a small molecule HSP90 inhibitor with potent antitumor activity in preclinical breast cancer models.” Breast Cancer Res. 10: R33 (2008). •Prostate-specific antigen (PSA) may serve as a sensitive biomarker of Hsp90 inhibition. Oikonomopoulou, K., et al. “Evaluation of prostate-specific antigen as a novel biomarker of Hsp90 inhibition.” Clin. Biochem. 42: 1705-1712 (2009). •89Zr-bevacizumab PET was concordant with the antiangiogenic response and direct antitumor effects after NVP-AUY922 treatment. It provided a noninvasive tool to monitor tumor VEGF levels. Nagengast, W.B., et al. “89Zr-bevacizumab PET of early antiangiogenic tumor response to treatment with HSP90 inhibitor NVP-AUY922.” J. Nucl. Med. 51: 761-767 (2010). •NVP-AUY922 effectively reduces human epidermal growth factor receptor-2 (HER2), which can be monitored with 89Zr-trastuzumab PET in vivo non-invasively. It might serve as an early biomarker for HSP90 inhibition in HER2 positive metastatic breast cancer patients. Oude Munnink, T.H., et al. “89Zr-trastuzumab PET visualises HER2 downregulation by the HSP90 inhibitor NVP-AUY922 in a human tumour xenograft.” Eur. J. Cancer 46: 678-684 (2010). •Hsp90 inhibitors NVP-AUY922 and NVP-BEP800 enhanced radiosensitivity in four tumor cell lines tested (A549, GaMG, HT 1080, and SNB19). Stingl, L., et al. “Novel HSP90 inhibitors, NVP-AUY922 and NVP-BEP800, radiosensitise tumour cells through cell-cycle impairment, increased DNA damage and repair protraction.” Br. J. Cancer 102: 1578-1591 (2010). •Sold for laboratory or manufacturing purposes only; not for huma
N-5300 NVP-AUY922, Free Base, >99% Synonyms: [AUY922] [VER-52296] M.W. 465.54 C26H31N3O5 [747412-49-3] Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO at 100 mg/mL; soluble in ethanol at 100 mg/mL; very poorly soluble in water; maximum solubility in plain water is estimated to be about 25-50 µM; buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •NVP-AUY922 potently inhibited HSP90 with IC50 values of 7.8 nM and 21 nM, and Ki values of 9 nM and 8.2 nM for HSP90α and HSP90β, respectively. NVP-AUY922 showed a very high binding affinity to HSP90β with a Kd of 1.7 nM. NVP-AUY922 inhibited the proliferation of human tumor cells in vitro with GI50 values of approximately 2 to 40 nM, inducing G1-G2 arrest and apoptosis. Human endothelial cells were very sensitive to NVP-AUY922 with GI50s of 2.5-3.9 nM. NVP-AUY922 also exhibited potent antitumor efficacy in human tumor xenografts including BT474 breast, A2780 ovarian, U87MG glioblastoma, PC3 prostate, and WM266.4 melanoma. Eccles, S.A., et al. “NVP-AUY922: a novel heat shock protein 90 inhibitor active against xenograft tumor growth, angiogenesis, and metastasis.” Cancer Res. 68: 2850-2860 (2008). •NVP-AUY922 showed impressive synergistic inhibitory effect with histone deacetylase inhibitors, melphalan, doxorubicin, NVP-LBH589 (Panobinostat), and suberoylanilide hydroxamic acid (SAHA, Vorinostat) on the growth of multiple myeloma cell lines and primary myeloma cells. Kaiser, M., et al. “Synergistic action of the novel HSP90 inhibitor NVP-AUY922 with histone deacetylase inhibitors, melphalan, or doxorubicin in multiple myeloma.” Eur. J. Haematol. 84: 337-344 (2010). •NVP-AUY922 potently inhibited the proliferation of human breast cancer cell lines with GI50 values in the range of 3 to 126 nM. NVP-AUY922 induced proliferative inhibition concordant with HSP70 upregulation and client protein depletion. Significant growth inhibition of BT-474 tumor and good tolerability were observed in athymic mice when NVP-AUY922 was administered once per week. Therapeutic effects were also concurrent with changes in pharmacodynamic markers, including HSP90-p23 dissociation, decreases in ERBB2 and P-AKT, and increased HSP70 protein levels. Jensen, M.R., et al. “NVP-AUY922: a small molecule HSP90 inhibitor with potent antitumor activity in preclinical breast cancer models.” Breast Cancer Res. 10: R33 (2008). •Prostate-specific antigen (PSA) may serve as a sensitive biomarker of Hsp90 inhibition. Oikonomopoulou, K., et al. “Evaluation of prostate-specific antigen as a novel biomarker of Hsp90 inhibition.” Clin. Biochem. 42: 1705-1712 (2009). •89Zr-bevacizumab PET was concordant with the antiangiogenic response and direct antitumor effects after NVP-AUY922 treatment. It provided a noninvasive tool to monitor tumor VEGF levels. Nagengast, W.B., et al. “89Zr-bevacizumab PET of early antiangiogenic tumor response to treatment with HSP90 inhibitor NVP-AUY922.” J. Nucl. Med. 51: 761-767 (2010). •NVP-AUY922 effectively reduces human epidermal growth factor receptor-2 (HER2), which can be monitored with 89Zr-trastuzumab PET in vivo non-invasively. It might serve as an early biomarker for HSP90 inhibition in HER2 positive metastatic breast cancer patients. Oude Munnink, T.H., et al. “89Zr-trastuzumab PET visualises HER2 downregulation by the HSP90 inhibitor NVP-AUY922 in a human tumour xenograft.” Eur. J. Cancer 46: 678-684 (2010). •Hsp90 inhibitors NVP-AUY922 and NVP-BEP800 enhanced radiosensitivity in four tumor cell lines tested (A549, GaMG, HT 1080, and SNB19). Stingl, L., et al. “Novel HSP90 inhibitors, NVP-AUY922 and NVP-BEP800, radiosensitise tumour cells through cell-cycle impairment, increased DNA damage and repair protraction.” Br. J. Cancer 102: 1578-1591 (2010). •Sold for laboratory or manufacturing purposes only; not for huma
