货号： T-6466-1 g 产品名称： Tivozanib, Free Base 品牌： LC 规格： 1 g
T-6466 Tivozanib, Free Base, 99% Synonyms: [AV-951] [KRN-951] M.W. 454.86 C22H19ClN4O5 [475108-18-0] Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO at 5 mg/mL with warming; very poorly soluble in ethanol; very poorly soluble in water; maximum solubility in plain water is estimated to be about 50-100 µM; buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •Tivozanib, also known as AV-951, is a VEGF receptor tyrosine kinase inhibitor. •Tivozanib strongly inhibited VEGFR-1, VEGFR-2, and VEGFR-3 tyrosine kinases with IC50 values of 30, 6.5, and 15 nM, respectively. It also inhibited EphB2, PDGFR-α, PDGFR-β, c-Kit, and Tie2 tyrosine kinases with IC50 values of 24, 40, 49, 78, and 78 nM, respectively. Furthermore, it inhibited several other tyrosine kinases with IC50 values greater than for VEGFR-2. Tivozanib markedly inhibited the ligand-induced phosphorylation of VEGFR-1, VEGFR-2, and VEGFR-3 in cellular assays, with IC50 values of 0.21, 0.16, and 0.24 nM, respectively. It strongly inhibited VEGF-dependent phosphorylation of MAPKs in HUVECs, with IC50 values of 0.13 and 0.18 nM for extracellular signal-regulated kinase 1 (ERK1) and ERK2, respectively. It also inhibited the VEGF-induced proliferation of HUVECs with an IC50 of 0.67 nM. Tivozanib inhibited tumor growth in vivo in athymic rat xenograft models of breast, colon, hepatic, lung, ovarian, pancreatic, and prostate tumors. Nakamura, K., et al. “KRN951, a highly potent inhibitor of vascular endothelial growth factor receptor tyrosine kinases, has antitumor activities and affects functional vascular properties.” Cancer Res. 66: 9134-9142 (2006). •A phase II clinical trial demonstrated an overall response rate of 25% and a median progression-free survival time of 11.8 months in patients with advanced renal cell carcinoma treated with tivozanib as a single agent. Hypertension and dysphonia were the most frequent side effects. De Luca, A. and Normanno, N. “Tivozanib, a pan-VEGFR tyrosine kinase inhibitor for the potential treatment of solid tumors.” IDrugs 13: 636-645 (2010). •Related CAS numbers: 682745-41-1 for the tivozanib monohydrochloride monohydrate. •Sold for laboratory or manufacturing purposes only; not for human, 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.
T-6466 Tivozanib, Free Base, 99% Synonyms: [AV-951] [KRN-951] M.W. 454.86 C22H19ClN4O5 [475108-18-0] Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO at 5 mg/mL with warming; very poorly soluble in ethanol; very poorly soluble in water; maximum solubility in plain water is estimated to be about 50-100 µM; buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •Tivozanib, also known as AV-951, is a VEGF receptor tyrosine kinase inhibitor. •Tivozanib strongly inhibited VEGFR-1, VEGFR-2, and VEGFR-3 tyrosine kinases with IC50 values of 30, 6.5, and 15 nM, respectively. It also inhibited EphB2, PDGFR-α, PDGFR-β, c-Kit, and Tie2 tyrosine kinases with IC50 values of 24, 40, 49, 78, and 78 nM, respectively. Furthermore, it inhibited several other tyrosine kinases with IC50 values greater than for VEGFR-2. Tivozanib markedly inhibited the ligand-induced phosphorylation of VEGFR-1, VEGFR-2, and VEGFR-3 in cellular assays, with IC50 values of 0.21, 0.16, and 0.24 nM, respectively. It strongly inhibited VEGF-dependent phosphorylation of MAPKs in HUVECs, with IC50 values of 0.13 and 0.18 nM for extracellular signal-regulated kinase 1 (ERK1) and ERK2, respectively. It also inhibited the VEGF-induced proliferation of HUVECs with an IC50 of 0.67 nM. Tivozanib inhibited tumor growth in vivo in athymic rat xenograft models of breast, colon, hepatic, lung, ovarian, pancreatic, and prostate tumors. Nakamura, K., et al. “KRN951, a highly potent inhibitor of vascular endothelial growth factor receptor tyrosine kinases, has antitumor activities and affects functional vascular properties.” Cancer Res. 66: 9134-9142 (2006). •A phase II clinical trial demonstrated an overall response rate of 25% and a median progression-free survival time of 11.8 months in patients with advanced renal cell carcinoma treated with tivozanib as a single agent. Hypertension and dysphonia were the most frequent side effects. De Luca, A. and Normanno, N. “Tivozanib, a pan-VEGFR tyrosine kinase inhibitor for the potential treatment of solid tumors.” IDrugs 13: 636-645 (2010). •Related CAS numbers: 682745-41-1 for the tivozanib monohydrochloride monohydrate. •Sold for laboratory or manufacturing purposes only; not for human, 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.
T-6466 Tivozanib, Free Base, 99% Synonyms: [AV-951] [KRN-951] M.W. 454.86 C22H19ClN4O5 [475108-18-0] Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO at 5 mg/mL with warming; very poorly soluble in ethanol; very poorly soluble in water; maximum solubility in plain water is estimated to be about 50-100 µM; buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •Tivozanib, also known as AV-951, is a VEGF receptor tyrosine kinase inhibitor. •Tivozanib strongly inhibited VEGFR-1, VEGFR-2, and VEGFR-3 tyrosine kinases with IC50 values of 30, 6.5, and 15 nM, respectively. It also inhibited EphB2, PDGFR-α, PDGFR-β, c-Kit, and Tie2 tyrosine kinases with IC50 values of 24, 40, 49, 78, and 78 nM, respectively. Furthermore, it inhibited several other tyrosine kinases with IC50 values greater than for VEGFR-2. Tivozanib markedly inhibited the ligand-induced phosphorylation of VEGFR-1, VEGFR-2, and VEGFR-3 in cellular assays, with IC50 values of 0.21, 0.16, and 0.24 nM, respectively. It strongly inhibited VEGF-dependent phosphorylation of MAPKs in HUVECs, with IC50 values of 0.13 and 0.18 nM for extracellular signal-regulated kinase 1 (ERK1) and ERK2, respectively. It also inhibited the VEGF-induced proliferation of HUVECs with an IC50 of 0.67 nM. Tivozanib inhibited tumor growth in vivo in athymic rat xenograft models of breast, colon, hepatic, lung, ovarian, pancreatic, and prostate tumors. Nakamura, K., et al. “KRN951, a highly potent inhibitor of vascular endothelial growth factor receptor tyrosine kinases, has antitumor activities and affects functional vascular properties.” Cancer Res. 66: 9134-9142 (2006). •A phase II clinical trial demonstrated an overall response rate of 25% and a median progression-free survival time of 11.8 months in patients with advanced renal cell carcinoma treated with tivozanib as a single agent. Hypertension and dysphonia were the most frequent side effects. De Luca, A. and Normanno, N. “Tivozanib, a pan-VEGFR tyrosine kinase inhibitor for the potential treatment of solid tumors.” IDrugs 13: 636-645 (2010). •Related CAS numbers: 682745-41-1 for the tivozanib monohydrochloride monohydrate. •Sold for laboratory or manufacturing purposes only; not for human, 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.
T-6466 Tivozanib, Free Base, 99% Synonyms: [AV-951] [KRN-951] M.W. 454.86 C22H19ClN4O5 [475108-18-0] Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO at 5 mg/mL with warming; very poorly soluble in ethanol; very poorly soluble in water; maximum solubility in plain water is estimated to be about 50-100 µM; buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •Tivozanib, also known as AV-951, is a VEGF receptor tyrosine kinase inhibitor. •Tivozanib strongly inhibited VEGFR-1, VEGFR-2, and VEGFR-3 tyrosine kinases with IC50 values of 30, 6.5, and 15 nM, respectively. It also inhibited EphB2, PDGFR-α, PDGFR-β, c-Kit, and Tie2 tyrosine kinases with IC50 values of 24, 40, 49, 78, and 78 nM, respectively. Furthermore, it inhibited several other tyrosine kinases with IC50 values greater than for VEGFR-2. Tivozanib markedly inhibited the ligand-induced phosphorylation of VEGFR-1, VEGFR-2, and VEGFR-3 in cellular assays, with IC50 values of 0.21, 0.16, and 0.24 nM, respectively. It strongly inhibited VEGF-dependent phosphorylation of MAPKs in HUVECs, with IC50 values of 0.13 and 0.18 nM for extracellular signal-regulated kinase 1 (ERK1) and ERK2, respectively. It also inhibited the VEGF-induced proliferation of HUVECs with an IC50 of 0.67 nM. Tivozanib inhibited tumor growth in vivo in athymic rat xenograft models of breast, colon, hepatic, lung, ovarian, pancreatic, and prostate tumors. Nakamura, K., et al. “KRN951, a highly potent inhibitor of vascular endothelial growth factor receptor tyrosine kinases, has antitumor activities and affects functional vascular properties.” Cancer Res. 66: 9134-9142 (2006). •A phase II clinical trial demonstrated an overall response rate of 25% and a median progression-free survival time of 11.8 months in patients with advanced renal cell carcinoma treated with tivozanib as a single agent. Hypertension and dysphonia were the most frequent side effects. De Luca, A. and Normanno, N. “Tivozanib, a pan-VEGFR tyrosine kinase inhibitor for the potential treatment of solid tumors.” IDrugs 13: 636-645 (2010). •Related CAS numbers: 682745-41-1 for the tivozanib monohydrochloride monohydrate. •Sold for laboratory or manufacturing purposes only; not for human, 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.
T-6466 Tivozanib, Free Base, 99% Synonyms: [AV-951] [KRN-951] M.W. 454.86 C22H19ClN4O5 [475108-18-0] Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO at 5 mg/mL with warming; very poorly soluble in ethanol; very poorly soluble in water; maximum solubility in plain water is estimated to be about 50-100 µM; buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •Tivozanib, also known as AV-951, is a VEGF receptor tyrosine kinase inhibitor. •Tivozanib strongly inhibited VEGFR-1, VEGFR-2, and VEGFR-3 tyrosine kinases with IC50 values of 30, 6.5, and 15 nM, respectively. It also inhibited EphB2, PDGFR-α, PDGFR-β, c-Kit, and Tie2 tyrosine kinases with IC50 values of 24, 40, 49, 78, and 78 nM, respectively. Furthermore, it inhibited several other tyrosine kinases with IC50 values greater than for VEGFR-2. Tivozanib markedly inhibited the ligand-induced phosphorylation of VEGFR-1, VEGFR-2, and VEGFR-3 in cellular assays, with IC50 values of 0.21, 0.16, and 0.24 nM, respectively. It strongly inhibited VEGF-dependent phosphorylation of MAPKs in HUVECs, with IC50 values of 0.13 and 0.18 nM for extracellular signal-regulated kinase 1 (ERK1) and ERK2, respectively. It also inhibited the VEGF-induced proliferation of HUVECs with an IC50 of 0.67 nM. Tivozanib inhibited tumor growth in vivo in athymic rat xenograft models of breast, colon, hepatic, lung, ovarian, pancreatic, and prostate tumors. Nakamura, K., et al. “KRN951, a highly potent inhibitor of vascular endothelial growth factor receptor tyrosine kinases, has antitumor activities and affects functional vascular properties.” Cancer Res. 66: 9134-9142 (2006). •A phase II clinical trial demonstrated an overall response rate of 25% and a median progression-free survival time of 11.8 months in patients with advanced renal cell carcinoma treated with tivozanib as a single agent. Hypertension and dysphonia were the most frequent side effects. De Luca, A. and Normanno, N. “Tivozanib, a pan-VEGFR tyrosine kinase inhibitor for the potential treatment of solid tumors.” IDrugs 13: 636-645 (2010). •Related CAS numbers: 682745-41-1 for the tivozanib monohydrochloride monohydrate. •Sold for laboratory or manufacturing purposes only; not for human, 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.
T-6466 Tivozanib, Free Base, 99% Synonyms: [AV-951] [KRN-951] M.W. 454.86 C22H19ClN4O5 [475108-18-0] Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO at 5 mg/mL with warming; very poorly soluble in ethanol; very poorly soluble in water; maximum solubility in plain water is estimated to be about 50-100 µM; buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •Tivozanib, also known as AV-951, is a VEGF receptor tyrosine kinase inhibitor. •Tivozanib strongly inhibited VEGFR-1, VEGFR-2, and VEGFR-3 tyrosine kinases with IC50 values of 30, 6.5, and 15 nM, respectively. It also inhibited EphB2, PDGFR-α, PDGFR-β, c-Kit, and Tie2 tyrosine kinases with IC50 values of 24, 40, 49, 78, and 78 nM, respectively. Furthermore, it inhibited several other tyrosine kinases with IC50 values greater than for VEGFR-2. Tivozanib markedly inhibited the ligand-induced phosphorylation of VEGFR-1, VEGFR-2, and VEGFR-3 in cellular assays, with IC50 values of 0.21, 0.16, and 0.24 nM, respectively. It strongly inhibited VEGF-dependent phosphorylation of MAPKs in HUVECs, with IC50 values of 0.13 and 0.18 nM for extracellular signal-regulated kinase 1 (ERK1) and ERK2, respectively. It also inhibited the VEGF-induced proliferation of HUVECs with an IC50 of 0.67 nM. Tivozanib inhibited tumor growth in vivo in athymic rat xenograft models of breast, colon, hepatic, lung, ovarian, pancreatic, and prostate tumors. Nakamura, K., et al. “KRN951, a highly potent inhibitor of vascular endothelial growth factor receptor tyrosine kinases, has antitumor activities and affects functional vascular properties.” Cancer Res. 66: 9134-9142 (2006). •A phase II clinical trial demonstrated an overall response rate of 25% and a median progression-free survival time of 11.8 months in patients with advanced renal cell carcinoma treated with tivozanib as a single agent. Hypertension and dysphonia were the most frequent side effects. De Luca, A. and Normanno, N. “Tivozanib, a pan-VEGFR tyrosine kinase inhibitor for the potential treatment of solid tumors.” IDrugs 13: 636-645 (2010). •Related CAS numbers: 682745-41-1 for the tivozanib monohydrochloride monohydrate. •Sold for laboratory or manufacturing purposes only; not for human, 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.
T-6466 Tivozanib, Free Base, 99% Synonyms: [AV-951] [KRN-951] M.W. 454.86 C22H19ClN4O5 [475108-18-0] Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO at 5 mg/mL with warming; very poorly soluble in ethanol; very poorly soluble in water; maximum solubility in plain water is estimated to be about 50-100 µM; buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •Tivozanib, also known as AV-951, is a VEGF receptor tyrosine kinase inhibitor. •Tivozanib strongly inhibited VEGFR-1, VEGFR-2, and VEGFR-3 tyrosine kinases with IC50 values of 30, 6.5, and 15 nM, respectively. It also inhibited EphB2, PDGFR-α, PDGFR-β, c-Kit, and Tie2 tyrosine kinases with IC50 values of 24, 40, 49, 78, and 78 nM, respectively. Furthermore, it inhibited several other tyrosine kinases with IC50 values greater than for VEGFR-2. Tivozanib markedly inhibited the ligand-induced phosphorylation of VEGFR-1, VEGFR-2, and VEGFR-3 in cellular assays, with IC50 values of 0.21, 0.16, and 0.24 nM, respectively. It strongly inhibited VEGF-dependent phosphorylation of MAPKs in HUVECs, with IC50 values of 0.13 and 0.18 nM for extracellular signal-regulated kinase 1 (ERK1) and ERK2, respectively. It also inhibited the VEGF-induced proliferation of HUVECs with an IC50 of 0.67 nM. Tivozanib inhibited tumor growth in vivo in athymic rat xenograft models of breast, colon, hepatic, lung, ovarian, pancreatic, and prostate tumors. Nakamura, K., et al. “KRN951, a highly potent inhibitor of vascular endothelial growth factor receptor tyrosine kinases, has antitumor activities and affects functional vascular properties.” Cancer Res. 66: 9134-9142 (2006). •A phase II clinical trial demonstrated an overall response rate of 25% and a median progression-free survival time of 11.8 months in patients with advanced renal cell carcinoma treated with tivozanib as a single agent. Hypertension and dysphonia were the most frequent side effects. De Luca, A. and Normanno, N. “Tivozanib, a pan-VEGFR tyrosine kinase inhibitor for the potential treatment of solid tumors.” IDrugs 13: 636-645 (2010). •Related CAS numbers: 682745-41-1 for the tivozanib monohydrochloride monohydrate. •Sold for laboratory or manufacturing purposes only; not for human, 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.
T-6466 Tivozanib, Free Base, 99% Synonyms: [AV-951] [KRN-951] M.W. 454.86 C22H19ClN4O5 [475108-18-0] Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO at 5 mg/mL with warming; very poorly soluble in ethanol; very poorly soluble in water; maximum solubility in plain water is estimated to be about 50-100 µM; buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •Tivozanib, also known as AV-951, is a VEGF receptor tyrosine kinase inhibitor. •Tivozanib strongly inhibited VEGFR-1, VEGFR-2, and VEGFR-3 tyrosine kinases with IC50 values of 30, 6.5, and 15 nM, respectively. It also inhibited EphB2, PDGFR-α, PDGFR-β, c-Kit, and Tie2 tyrosine kinases with IC50 values of 24, 40, 49, 78, and 78 nM, respectively. Furthermore, it inhibited several other tyrosine kinases with IC50 values greater than for VEGFR-2. Tivozanib markedly inhibited the ligand-induced phosphorylation of VEGFR-1, VEGFR-2, and VEGFR-3 in cellular assays, with IC50 values of 0.21, 0.16, and 0.24 nM, respectively. It strongly inhibited VEGF-dependent phosphorylation of MAPKs in HUVECs, with IC50 values of 0.13 and 0.18 nM for extracellular signal-regulated kinase 1 (ERK1) and ERK2, respectively. It also inhibited the VEGF-induced proliferation of HUVECs with an IC50 of 0.67 nM. Tivozanib inhibited tumor growth in vivo in athymic rat xenograft models of breast, colon, hepatic, lung, ovarian, pancreatic, and prostate tumors. Nakamura, K., et al. “KRN951, a highly potent inhibitor of vascular endothelial growth factor receptor tyrosine kinases, has antitumor activities and affects functional vascular properties.” Cancer Res. 66: 9134-9142 (2006). •A phase II clinical trial demonstrated an overall response rate of 25% and a median progression-free survival time of 11.8 months in patients with advanced renal cell carcinoma treated with tivozanib as a single agent. Hypertension and dysphonia were the most frequent side effects. De Luca, A. and Normanno, N. “Tivozanib, a pan-VEGFR tyrosine kinase inhibitor for the potential treatment of solid tumors.” IDrugs 13: 636-645 (2010). •Related CAS numbers: 682745-41-1 for the tivozanib monohydrochloride monohydrate. •Sold for laboratory or manufacturing purposes only; not for human, 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.
