AZD4547

SKU: orb1307009

Description

AZD4547 is a potent and selective FGFR family inhibitor, suppressing cancer cell proliferation by blocking FGFR1-3 phosphorylation with low nanomolar IC50 values. It is widely used in preclinical research to study FGFR-driven tumor models both in vitro and in vivo, supporting investigations in oncology and targeted therapy development.

Research Area

Cardiovascular Research, Signal Transduction

Key Properties

• CAS Number: 1035270-39-3
• MW: 463.57
• Purity: 99.88% (May vary between batches)
• Formula: C₂₆H₃₃N₅O₃
• SMILES: COc1cc(CCc2cc(NC(=O)c3ccc(cc3)N3C[C@H](C)N[C@H](C)C3)n[nH]2)cc(OC)c1
• Target: VEGFR,FGFR
• Solubility: DMSO:252.5 mg/mL (544.69 mM);Ethanol:< 1 mg/mL (insoluble or slightly soluble);H2O:< 1 mg/mL (insoluble or slightly soluble);10% DMSO+40% PEG300+5% Tween-80+45% Saline:2.5 mg/mL (5.39 mM)

Bioactivity

• Target IC50:
  FGFR2:2.5 nM (cell free)|FGFR3:1.8 nM (cell free)|FGFR1:0.9 nM (cell free)|KDR:24 nM (cell free)
• In Vivo:
  METHODS: C57BL/6 mice were treated with LPS (15 mg/kg, intraperitoneal injection) and AZD4547 (40 mg/kg gavage 1 hour before LPS treatment) to investigate the renal protective effect of AZD4547 in LPS-induced acute kidney injury. Expression of the pro-apoptotic gene Bax and the anti-apoptotic gene Bcl-2 was measured to investigate whether the effect of AZD4547 on preserving renal function in AKI is mediated by regulating apoptosis. RESULTS AZD4547 prevented LPS-related renal dysfunction, apoptosis, and renal inflammation in mice.
• In Vitro:
  METHODS: NRK-52E cells were pretreated with 2.5, 5, 10, and 20 μM AZD4547 for 1 hour, and then exposed to 0.5 μg/mLLPS for the specified time, and the effect of AZD4547 on LPS-induced inflammation defects in NRK-52E cells was observed. RESULTS AZD4547 significantly inhibited cell proliferation in NRK-52E cells at a concentration of 20 μM. METHODS: NRK-52E cells were pretreated with 10 μM AZD4547 for 1 hour and then exposed to 0.5 μg/mL LPS for the indicated time. The levels of proinflammatory factors in NRK-52E cells were studied. RESULTS AZD4547 attenuated LPS-induced inflammatory factors by reducing the TAK1/NF-κB signaling pathway in NRK-52E cells.
• Cell Research:
  Cell lines were incubated with fixed concentrations of AZD4547 for 72 hours. For fluorescence-activated cell sorting (FACS), cells were fixed with 70% ethanol and then incubated with propidium iodide/RNase A labeling solution. Cell-cycle profiles were assessed with a FACSCalibur instrument and CellQuest analysis software. For apoptotic analysis, cells and media were gently harvested and centrifuged, followed by washing of cell pellets. Cells were then processed for Annexin V-fluorescein isothiocyanate (FITC) staining and propidium iodide uptake according to the manufacturer's instructions. The proportion of cells staining positive for Annexin V were then assessed with a FACSCalibur instrument and quadrant sorting was done by CellQuest analysis software .
• Animal Research:
  Tumor xenografts were established by s.c. injection into the left flank with 0.1 mL tumor cells (1 × 10^6 for LoVo, 1 × 10^7 for HCT-15, and 1 × 10^7 for Calu-6) or 0.2 mL (2 × 10^7 for KMS11 and KG1a) mixed 1:1 with Matrigel, with the exception of LoVo and HCT-15, which did not include Matrigel. Mice were randomized into control and treatment groups when tumors reached the determined size of more than 0.2 cm3. Tumor volume (measured by caliper), animal body weight, and tumor condition were recorded twice weekly for the duration of the study. Tumor volume was calculated as described previously .

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

inhibit, Inhibitor, KDR, Fibroblast growth factor receptor, FGFR4, FGFR, FGFR1, FGFR2, FGFR3, AZD4547, AZD-4547, AZD 4547

Compound Identifiers

PubChem CID

51039095