Lenvatinib

SKU: orb1310532

Description

Lenvatinib

Research Area

Cardiovascular Research, Cell Biology, Signal Transduction

Key Properties

• CAS Number: 417716-92-8
• MW: 426.85
• Purity: 99.96%
• Formula: C₂₁H₁₉ClN₄O₄
• SMILES: O(C=1C2=C(C=C(OC)C(C(N)=O)=C2)N=CC1)C3=CC(Cl)=C(NC(NC4CC4)=O)C=C3
• Target: PDGFR,c-Kit,VEGFR,FGFR,c-RET
• Solubility: DMSO:42 mg/mL (98.4 mM);Ethanol:< 1 mg/mL (insoluble or slightly soluble);10% DMSO+40% PEG300+5% Tween 80+45% Saline:1.9 mg/mL (4.45 mM)

Bioactivity

• Target IC50:
  VEGFR3/FLT4:5.2 nM|c-Kit:100 nM|VEGFR2/KDR:4.0 nM|FGFR1:46 nM|VEGFR1/FLT1:22 nM|PDGFRβ:39 nM|PDGFRα:51 nM
• In Vivo:
  METHODS: To assay antitumor activity in vivo Lenvatinib (30-100 mg/kg in 0.5% methylcellulose) was orally administered twice daily for twenty-one days to BALB/c nude mice harboring human s All cell lung cancer tumor H146. Results: Oral administration of Lenvatinib inhibite the growth of H146 tumors in a dose-dependent manner and caused tumor regression at 100 mg/kg. METHODS: To tes the antitumor activity in vivo Lenvatinib (100 mg/kg) was orally administered once daily for eight weeks to nude mice harboring human mammary carcinoma tumor MDA-MB-231. Results: Lenvatinib inhibited metastasis to regional lymph nodes and distant lungs in the MDA-MB-231 xenograft model.Lenvatinib decreased angiogenesis and lymphangiogenesis in established metastatic nodes of MDA-MB-231 tumors in lymph nodes.
• In Vitro:
  METHODS: Six human tumor cells, A375, DU145, DX3, KM12C, SK23, and U2OS, were treated with Lenvatinib (1-100 μM) for 72 h. Cell viability was measured by MTT. Results: In most cell lines, Lenvatinib inhibited proliferation only at high concentration IC50 23.6-44.17 μM), whil the IC50 in the KM12C cell line was 9.54 μM. METHODS: Human umbilical vein endothelial cells HUVECs were treated with Lenvatinib (0.16-20 nM) for 1 h, followed by stimulation with SCF or VEGF (20 ng/mL) for 5 min, an the expression levels of target proteins were detected by Western Blot. Results: Li and-induced phosphorylation of both KIT and KDR was inhibited by Lenvatinib.
• Cell Research:
  HUVECs (1,000 cells in Each well in serum-free medium containing 2% fetal bovine serum) and L6 rat skeletal musclee myoblasts (5,000 cells in Each well in serum-free DMEM) are dispensed in a 96-well plate and incubated overnight. E7080 and either VEGF (20 ng/mL) or FGF-2 (20 ng/mL) containing 2% fetal bovine serum and PDGFβ (40 ng/mL) are added to Each well. Cells are incubated for 3 days and the The ratios of surviving cells are measured by WST-1 reagent. For proliferation assay, Samples are duplicated and three separate experiments are done. (Only for Reference)

Storage & Handling

• Storage: store at low temperature,The compound is unstable in solution. Please use soon | Powder: -20°C for 3 years | Shipping with blue ice/Shipping at ambient temperature.
• Disclaimer: For research use only

Alternative Names

CD117, c-Kit, cKit, cRET, E 7080, E-7080, E7080, inhibit, Platelet-derived growth factor receptor, PDGFR, Inhibitor, Lenvatinib, FGFR1, FGFR, Fibroblast growth factor receptor, RET, SCFR, PDGFRβ, VEGFR2/KDR, VEGFR3/FLT4, Vascular endothelial growth factor receptor, VEGFR1/FLT1, VEGFR

Compound Identifiers

PubChem CID

9823820