Amlexanox

Overview

Amlexanox is a non-peptide small-molecule 2-amino-chromeno[2,3-b]pyridine-3-carboxylic acid derivative (CAS 68302-57-8, MW 298.29 g/mol). Originally approved in 1996 as a topical oral paste for aphthous ulcers (FDA, now discontinued) and in Japan for allergic conditions, it was later characterized as a selective ATP-competitive inhibitor of the non-canonical IκB kinases TBK1 and IKKε. It is NOT approved for any metabolic, obesity, or performance indication; it is sold by research-chemical vendors labeled research-use-only and promoted off-label by biohacking outlets for fat loss. No validated human dose exists for metabolic applications.

Mechanism of Action

Two distinct mechanisms are documented. For its approved aphthous-ulcer indication, in vitro studies show amlexanox inhibits formation and release of inflammatory mediators (histamine, leukotrienes) from mast cells, neutrophils, and mononuclear cells, though the FDA label states the mechanism of ulcer healing is unknown. In preclinical metabolic research, amlexanox was identified as a selective ATP-competitive inhibitor of the non-canonical IκB kinases TBK1 and IKKε, which suppresses chronic low-grade inflammatory signaling implicated in obesity-linked insulin resistance.

Research Summary

In diet-induced obese and ob/ob mice, amlexanox treatment increased energy expenditure via thermogenesis, produced weight loss, improved insulin sensitivity, and decreased hepatic steatosis; these metabolic benefits require intact FGF21 signaling. In LDL-receptor-knockout mice on Western diet, amlexanox reduced triglycerides, cholesterol, circulating monocytes/eosinophils, macrophage plaque accumulation, and atherosclerotic lesion size. One randomized, double-blind, placebo-controlled proof-of-concept trial in 42 obese patients with type 2 diabetes and NAFLD showed statistically significant HbA1c and fructosamine reductions versus placebo, with a responder subgroup showing improved insulin sensitivity and reduced hepatic fat; rash occurred in several participants (two required biopsy). No obesity or diabetes indication has been approved by any regulator.

Vendors selling Amlexanox

Scored vendors carrying Amlexanox, ranked by trust grade. Grades are computed from indexed Certificates of Analysis. Full $/mg pricing is on the comparison page.

Prescribers who offer Amlexanox

3 prescribers in our directory work with Amlexanox, each confirmed from their own website. Peptides like Amlexanox require a prescription from a licensed provider.

Reported Side Effects

• Rash (occurred in several participants in the 2017 metabolic trial; two required biopsy)
• One serious adverse event (non-ST-elevation MI) occurred in a placebo-treated subject in the 2017 trial, not attributed to drug
• No validated long-term safety data for metabolic/obesity use
• Gray-market material identity and purity unverified
• No major systemic toxicity signal in FDA labeling for approved topical use

Compare Amlexanox with Others

Research References

• Amlexanox, CID 2161.
• Aphthasol (amlexanox oral paste) FDA package insert. 2002.
• An inhibitor of the protein kinases TBK1 and IKK-ε improves obesity-related metabolic dysfunctions in mice. 2013. PMID 23396211.
• Inhibition of IKKε and TBK1 Improves Glucose Control in a Subset of Patients with Type 2 Diabetes. 2017. PMID 28683283.

Frequently asked questions

Has Amlexanox been independently lab-tested?

Disclosed Labs has collected 1 Certificate of Analysis (COA) for Amlexanox from 1 independent testing lab. 1 vendor has submitted material for testing. Products average 99.6% tested purity across the corpus. Full testing data is available at https://www.disclosedlabs.com/peptides/amlexanox/testing.

Where can researchers source Amlexanox?

1 vendor with Disclosed Labs trust grades currently list Amlexanox, including Kimera Chems. Compare live prices and lab-verified COAs at https://www.disclosedlabs.com/prices/amlexanox.

Which prescribers offer Amlexanox with a prescription?

3 prescribers in the Disclosed Labs directory work with Amlexanox, each confirmed from their own website. Amlexanox requires a prescription from a licensed provider. Browse them at https://www.disclosedlabs.com/prescribers?peptide=Amlexanox.

How does Amlexanox work?

Two distinct mechanisms are documented. For its approved aphthous-ulcer indication, in vitro studies show amlexanox inhibits formation and release of inflammatory mediators (histamine, leukotrienes) from mast cells, neutrophils, and mononuclear cells, though the FDA label states the mechanism of ulcer healing is unknown. In preclinical metabolic research, amlexanox was identified as a selective ATP-competitive inhibitor of the non-canonical IκB kinases TBK1 and IKKε, which suppresses chronic low-grade inflammatory signaling implicated in obesity-linked insulin resistance.

What does the research say about Amlexanox?

In diet-induced obese and ob/ob mice, amlexanox treatment increased energy expenditure via thermogenesis, produced weight loss, improved insulin sensitivity, and decreased hepatic steatosis; these metabolic benefits require intact FGF21 signaling. In LDL-receptor-knockout mice on Western diet, amlexanox reduced triglycerides, cholesterol, circulating monocytes/eosinophils, macrophage plaque accumulation, and atherosclerotic lesion size. One randomized, double-blind, placebo-controlled proof-of-concept trial in 42 obese patients with type 2 diabetes and NAFLD showed statistically significant HbA1c and fructosamine reductions versus placebo, with a responder subgroup showing improved insulin sensitivity and reduced hepatic fat; rash occurred in several participants (two required biopsy). No obesity or diabetes indication has been approved by any regulator.