NVP-TAE 226

SKU: orb1307113

Description

NVP-TAE 226

Research Area

Cardiovascular Research, Cell Biology, Signal Transduction

Key Properties

• CAS Number: 761437-28-9
• MW: 468.94
• Purity: 98.07%
• Formula: C₂₃H₂₅ClN₆O₃
• SMILES: CNC(=O)c1ccccc1Nc1nc(Nc2ccc(cc2OC)N2CCOCC2)ncc1Cl
• Target: FAK,c-Met/HGFR,IGF-1R,PYK2,Apoptosis
• Solubility: DMSO:87 mg/mL (185.52 mM);10% DMSO+90% Corn Oil:1 mg/mL (2.13 mM);Ethanol:< 1 mg/mL (insoluble or slightly soluble);H2O:< 1 mg/mL (insoluble or slightly soluble)

Bioactivity

• Target IC50:
  PYK2:3.5 nM|FAK:5.5 nM
• In Vivo:
  NVP-TAE226 (0.1-10 μM) inhibits microtubule formation in HMEC1 cells and suppresses serum starvation-induced autophosphorylation of FAK(Tyr397) in U87 cells at concentrations below 1 μM. It also inhibits IGF-I-induced phosphorylation of IGF-1R and its downstream target gene activities, including MAPK and Akt in U87 and U251 cells at concentrations under 1 μM. Moreover, NVP-TAE226 at 1 μM inhibits tumor cell invasion by more than 50% in vitro assays on an artificial basement membrane for glioblastoma cell lines. It induces G(2)-M phase arrest in glioblastoma cell lines, including those with wild-type p53, while those bearing mutant p53 undertake apoptosis, evidenced by the activation of caspase-3/7, poly(ADP-ribose) polymerase cleavage, and annexin V apoptosis assays. In the neuroblastoma cell line SK-N-AS, NVP-TAE226 at 5 μM inhibits FAK phosphorylation and at concentrations below 10 μM decreases cell viability, induces cell cycle arrest, and increases apoptosis. In U87 and U251 cells, it impedes tumor cell growth and weakens the G(2)-M cell cycle process related to reduced expression of cyclin B1 and phosphorylated cdc2(Tyr15) proteins at concentrations below 10 μM.
• In Vitro:
  In in vivo models, NVP-TAE226 (100 mg/kg, p.o.) significantly hindered the growth of human pancreatic tumor MIA PaCa-2 without affecting body weight. Moreover, NVP-TAE226 demonstrated a dose-dependent inhibition of growth and lung metastasis in 4T1 murine mammary tumors, correlated with the suppression of FAK autophosphorylation on Y397 and Akt phosphorylation on serine 473. At a dosage of 75 mg/kg, NVP-TAE226 significantly increased the survival rate of mice bearing intracranial glioma xenografts. Additionally, in a human colorectal cancer SCID mouse model, NVP-TAE226 (100 mg/kg, p.o.) markedly reduced microvessel density.
• Cell Research:
  Cell cultures are harvested with 0.05% trypsin and seeded in triplicate at 2 × 104 in 24-well culture plates for 24 h before drug treatment. Culture medium is used for mock treatment. Cells are harvested at the indicated day after treatment, and viable cells are counted using the Vi-cell viability analyze(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.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

cMet, c-Met, cMet/HGFR, Apoptosis, inhibit, NVPTAE 226, NVP-TAE 226, NVP-TAE226, NVP-TAE-226, NVP TAE 226, HGFR, Insulin Receptor, Inhibitor, IGF-1R, IGF1R, Focal adhesion kinase, FAK, Pyk2, PYK2, PTK2 protein tyrosine kinase 2, PTK2, Proline-rich tyrosine kinase 2, TAE 226, TAE226, TAE-226

Compound Identifiers

PubChem CID

9934347