Amlexanox, also known as AA-673 and CHX 3673, is an anti-inflammatory antiallergic immunomodulator used to treat recurrent aphthous ulcers (canker sores), and (in Japan) several inflammatory conditions. Amlexanox inhibits the synthesis and release of inflammatory mediators, including leukotrienes and histamine, from mast cells, neutrophils, and mononuclear cells. Amlexanox also acts as a leukotriene D4 antagonist and a phosphodiesterase inhibitor. Amlexanox decreases the time ulcers take to heal as well as the pain associated with the ulcers.
CAS Number: 68302-57-8
Molecular Weight: 298.29
Chemical Name: 2-amino-5-oxo-7-(propan-2-yl)-5H-chromeno[2,3-b]pyridine-3-carboxylic acid
Appearance: Solid Power
Purity: ≥98% (or refer to the Certificate of Analysis)
Solubility: DMSO : 100 mg/mL (335.24 mM; Need ultrasonic)
Shipping Condition: Shipped under ambient temperature as non-hazardous chemical or refer to Certificate of Analysis
Storage Condition: Dry, dark and -20 oC for 1 year or refer to the Certificate of Analysis.
Shelf Life: ≥12 months if stored properly.
Stock Solution Storage: 0 - 4 oC for 1 month or refer to the Certificate of Analysis.
Drug Formulation: To be determined
HS Tariff Code: 382200
How to use
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.
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.
- Reilly SM, et al. An inhibitor of the protein kinases TBK1 and IKK-e improves obesity-related metabolic dysfunctions in mice. Nat Med. 2013 Mar;19(3):313-21.
- Zhang Y, et al. AmLexanox Suppresses Osteoclastogenesis and Prevents Ovariectomy-Induced Bone Loss. Sci Rep. 2015 Sep 4;5:13575.
- Bell, J. AmLexanox for the treatment of recurrent aphthous ulcers. Clin Drug Investig, 2005. 25(9): p. 555-66.
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