Cabozantinib S-malate

SKU: orb1307421

Description

Cabozantinib S-malate

Research Area

Cardiovascular Research, Cell Biology, Signal Transduction

Key Properties

• CAS Number: 1140909-48-3
• MW: 635.59
• Purity: 99.41%
• Formula: C₃₂H₃₀FN₃O₁₀
• SMILES: O[C@@H](CC(O)=O)C(O)=O.COc1cc2nccc(Oc3ccc(NC(=O)C4(CC4)C(=O)Nc4ccc(F)cc4)cc3)c2cc1OC
• Target: VEGFR,c-Met/HGFR,TAM Receptor,c-Kit,Apoptosis
• Solubility: Ethanol:< 1 mg/mL (insoluble or slightly soluble);DMSO:16.67 mg/mL (26.23 mM);H2O:< 1 mg/mL (insoluble or slightly soluble)

Bioactivity

• Target IC50:
  c-Met:1.3 nM|VEGFR2/KDR:0.035 nM
• In Vivo:
  Cabozantinib treatment at 30 mg/kg in RIP-Tag2 mice with spontaneous pancreatic islet tumors disrupts 83% o the tumor vasculature, reduces pericytes and empty basement membrane sleeves, causes widespread intratumoral hypoxia and extensive tumor cell apoptosis, and slows regrowth o the tumor vasculature after drug withdrawal, more significantly compared with XL999 that blocks VEGFR but not c-Met, leading to only 43% reduction in vascularity, suggesting that concurrent Inhibition of VEGFR and Other functionally relevant receptor tyrosine kinases (RTK) amplifies angiogenesis inhibition. Cabozantinib also decreases invasiveness of Primary tumors and reduces metastasis. Cabozantinib at 30 mg/kg/day significantly abrogates human MPNST xenografts growth and metastasis in SCID mice. Administration of Cabozantinib induces dose-dependent Inhibition of tumor growth in breast, lung, and glioma tumor models, in association with decreased tumor and endothelial cell proliferation as well as increased apoptosis. A Single oral dose of Cabozantinib is sufficient to induce sustained tumor growth Inhibition in MDA-MB-231 tumor-bearing mice and C6 tumor-bearing rats at 100 mg/kg and 10 mg/kg, respectively
• In Vitro:
  Cabozantinib has weak inhibitory activity against RON and PDGFRβ with IC50 of 124 nM and 234 nM, respectivey, and has low activity against FGFR1 with IC50 of 5.294 μM. Cabozantinib at low concentration (0.1-0.5 μM) is sufficient to induce marked Inhibition of constitutive and inducible Met phosphorylation and its resultant downstream signaling in MPNST cells, and inhibit HGF-induced MPNST cell migration and invasion. Cabozantinib also induces marked Inhibition of Met and VEGFR2 phosphorylation in cytokine-stimulated human umbilical vein endothelial cells (HUVECs). Although Cabozantinib has no significant effect on MPNST cell growth at 0.1 μM, Cabozantinib at 5-10 μM significantly inhibit the MPNST cell growth.
• Cell Research:
  Cells are exposed to various concentration of Cabozantinib for 48 hours. Cell growth is determined by MTS assays using CellTiter96 Aqueous Non-Radioactive Cell Proliferation Assay kit. Absorbance is measured at a wavelength of 490 nM, an the absorbance Values of treated cells are presented as a percentage o the absorbance of untreated cells. (Only for Reference)

Storage & Handling

• Storage: Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Disclaimer: For research use only

Alternative Names

XL-184, XL184, XL 184, TAMReceptor, TAM Receptor, VEGFR, VEGFR3/FLT4, VEGFR2/KDR, cMet, cMet/HGFR, c-Met, cKit, Apoptosis, AXL, Cabozantinib, Cabozantinib Malate, Cabozantinib S malate, Cabozantinib Smalate, Cabozantinib S-malate, BMS 907351, BMS907351, BMS-907351, Kit, HGFR

Compound Identifiers

PubChem CID

25102846