Axitinib, Free Base

产品编号：	A-1107-1 g 查看说明书
产品名称：	Axitinib, Free Base .0 订购此产品
供应商：	LC
规格：	1 g
目录价：	16433
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CAS编号：	319460-85-0
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A-1107 Axitinib, Free Base, >99%M.W. 386.47 C22H18N4OS [319460-85-0] M.I. 14: 10304 Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO at 33 mg/mL; soluble in ethanol at 1.7 mg/mL with warming; very poorly soluble in water; maximum solubility in plain water is estimated to be about 10-50 µM; buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A •Axitinib (AG-013736) is an oral, potent, and selective inhibitor of vascular endothelial growth factor receptors 1 (VEGFR-1), 2 (VEGFR-2), and 3 (VEGFR-3), platelet derived growth factor receptor (PDGFR), and cKIT (CD117). •Axitinib inhibited growth of breast tumors in vivo at doses of 10-100 mg/kg and disrupted tumor microvasculature as measured by dynamic contrast-enhanced MRI. Wilmes, L.J., et al. "AG-013736, a novel inhibitor of VEGF receptor tyrosine kinases, inhibits breast cancer growth and decreases vascular permeability as detected by dynamic contrast-enhanced magnetic resonance imaging." Magn. Reson. Imaging. 25: 319-327 (2007). •Regrowth of blood vessels in spontaneous RIP-Tag2 tumors and implanted Lewis lung carcinomas in mice was studied after being treated with axitinib or AG-028262 for 7 days. Both agents inhibited 50%-60% of tumor neovasculature formation. Empty sleeves of basement membrane were left behind and surviving pericytes had less α-SMA immunoreactivity. Endothelial sprouts grew into empty sleeves of basement membrane one day after drug withdrawal, which was followed by vessel patency and connection to the bloodstream. Tumors were fully revascularized and the pericyte phenotype returned to baseline by 7 days. Mancuso, M.R., et al. "Rapid vascular regrowth in tumors after reversal of VEGF inhibition." J. Clin. Invest. 116: 2610-2621 (2006). •Axitinib inhibited angiogenesis significantly in rat 9L tumors grown s.c. in scid mice but only delayed tumor growth moderately. A combination of axitinib with metronomic cyclophosphamide completely blocked 9L tumor growth on initiation of drug treatment. However, metronomic cyclophosphamide alone required multiple treatment cycles to inhibit tumor growth. Ma, J. and Waxman, D.J. "Modulation of the antitumor activity of metronomic cyclophosphamide by the angiogenesis inhibitor axitinib." Mol. Cancer Ther. 7: 79-89 (2008). •Axitinib has clinical activity in patients with cytokine-refractory metastatic renal-cell cancer. Rixe, O., et al. "Axitinib treatment in patients with cytokine-refractory metastatic renal-cell cancer: a phase II study." Lancet Oncol. 8: 975-984 (2007). •Axitinib is the active ingredient in the drug sold under the trade name Inlyta®. This drug is currently approved in at least one country for the treatment of advanced renal cell carcinoma. NOTE: THE AXITINIB, FREE BASE RESEARCH COMPOUND SOLD BY LC LABORATORIES IS NOT INLYTA®, AND IS NOT FOR HUMAN USE. Inlyta® is a registered trademark of Pfizer Corporation. LC Laboratories is not affiliated with Pfizer Corporation, and the axitinib research compound sold by LC Laboratories is not manufactured by Pfizer Corporation. •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
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