Amlexanox

SKU: orb1307931

Description

Amlexanox is a small molecule therapeutic agent that accelerates the healing of aphthous ulcers and alleviates associated pain. It functions by suppressing inflammatory mediator release from mast cells and neutrophils while acting as a phosphodiesterase inhibitor and leukotriene antagonist, making it relevant for immunology and inflammation research in both cellular and animal models.

Research Area

Cardiovascular Research, Immunology & Inflammation, Signal Transduction

Key Properties

• CAS Number: 68302-57-8
• MW: 298.29
• Purity: >99.99% (May vary between batches)
• Formula: C₁₆H₁₄N₂O₄
• SMILES: CC(C)C1=CC=C2OC3=NC(N)=C(C=C3C(=O)C2=C1)C(O)=O
• Target: IκB/IKK,IL Receptor,FGFR
• Solubility: 10% DMSO+40% PEG300+5% Tween 80+45% Saline:4 mg/mL (13.41 mM);DMSO:127 mg/mL (425.76 mM)

Bioactivity

• Target IC50:
  IKKε:1-2 μM|TBK1:1-2 μM
• In Vivo:
  AmLexanox (100 mg/kg, p.o.) prevents and reverses diet-induced or genetic obesity, and produces reversible weight loss in obese mice. AmLexanox also causes a significant decrease in adipose tissue mass in these mice, and an increase in circulating adiponectin. AmLexanox (25 mg/kg) significantly improves insulin sensitivity in mice with established DIO,and after four weeks of treatment, amLexanox produces marked improvements in glucose. AmLexanox before the first application of the paste and at each has been shown to suppress both immediate and evaluation thereafter. A categorical scale is also delayed-type hypersensitivity reactions. AmLexanox (20 mg/kg) enhances osteoblast differentiation of BMSCs. In ovariectomized (OVX) mouse model, amLexanox prevents OVX-induced bone loss by suppressing osteoclast activity.
• In Vitro:
  AmLexanox increases phosphorylation of TBK1 on Ser172 in 3T3-L1 adipocytes, and blocks polyinosinic:polycytidylic acid (poly I:C)-stimulated phosphorylation of interferon responsive factor-3 (IRF3), a presumed substrate of IKKε and TBK1. AmLexanox potently inhibits the release of histamine and leukotrienes from mast cells, basophils and neutrophils in in vitro settings, possibly through increasing intracellular cyclic AMP content in inflammatory cells, a mem-brane-stabilising effect or inhibition of calcium influx. In primary bone marrow derived macrophages (BMMs), amLexanox inhibits osteoclast formation and bone resorption. At the molecular level, amLexanox suppresses RANKL-induced activation of nuclear factor-κB (NF-κB), mitogen-activated protein kinase (MAPKs), c-Fos and NFATc1. AmLexanox decreases the expression of osteoclast-specific genes, including TRAP, MMP9, Cathepsin K and NFATc1.
• Cell Research:
  To examine cell proliferation, a Cell Counting Kit-8 is used according to the manufacturer's instructions. BMMs are seeded at a density of 5×103 cells/well in 96-well plates. After 24 hours, cells are treated with different concentrations of AmLexanox (0, 1.5, 3, 6, 12, 25 μM) every 2 days in the presence of M-CSF (30 ng/mL) for 7 days. After 1, 3, 5 and 7 days, the culture medium is replaced by the medium containing 10% CCK-8 and cells are incubated at 37°C for an additional 2 h. The absorbance is then measured at a wavelength of 450 nm on an ELX800 absorbance microplate reader.

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

FGFR1, IL Receptor, IKKε, IkB/IKK, IkB, IKK, Inhibitor, I kappa B kinase, inhibit, IκB, IκB kinase, IL-3, ILReceptor, Amlexanox, Amoxanox, AA 673, AA673, AA-673, CHX 3673, CHX3673, CHX-3673, Protein S100-P, TBK1

Compound Identifiers

PubChem CID

2161