What is the difference between Amlexanox and GW-0742?

Amlexanox: 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 aphtho... GW-0742: GW-0742 is a synthetic small-molecule PPARδ (PPAR-beta/delta) agonist developed by GlaxoSmithKline as a phenoxyacetic-acid/thiazole derivative—not a peptide or hormone. It exhibits ~1000-fold selectiv...

What does the research say about Amlexanox vs GW-0742?

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, circulati… GW-0742: No human efficacy or safety data exist; the only identified human exposure is a single 15 mg oral dose administered to volunteers solely to characterize urinary metabolites for an anti-doping detection assay—a bioanalytical study yielding no therapeutic or safety information. Preclinical rodent findings include: oral GW-0742 (30 mg/kg/day × 3 weeks…

Amlexanox vs GW-0742

Q: Can you stack Amlexanox and GW-0742?

Amlexanox (metabolic) and GW-0742 (metabolic) are in the same category and may have overlapping mechanisms — researchers should review both profiles carefully before combining. Consult a licensed provider before combining any compounds.

Head-to-head comparison of Amlexanox and GW-0742 — mechanism, side effects, legal status, and pricing.

Amlexanox

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.

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GW-0742

GW-0742 is a synthetic small-molecule PPARδ (PPAR-beta/delta) agonist developed by GlaxoSmithKline as a phenoxyacetic-acid/thiazole derivative—not a peptide or hormone. It exhibits ~1000-fold selectivity for human PPARδ (EC50 = 1.1 nM) over PPARα and PPARγ. Never advanced past preclinical development, GW-0742 has no approved human therapeutic use and no registered clinical trials. It is prohibited at all times under WADA as a member of the banned PPARδ-agonist class (Hormone and Metabolic Modulators), though not individually named on the list.

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Amlexanox

GW-0742

Category

Metabolic

Legal Status

Research Only

Mechanism

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.

GW-0742 is a high-affinity, highly selective agonist of human PPARδ (EC50 = 1.1 nM for hPPARδ transactivation vs ~1.1 µM for hPPARα and ~2 µM for hPPARγ), conferring ~1000-fold selectivity for PPARδ over the other PPAR subtypes. Upon activation, PPARδ heterodimerizes with RXR and binds PPAR-response elements (PPREs) to alter transcription of genes governing fatty-acid oxidation, glucose utilization, and inflammatory signaling. In mice, however, GW-0742-induced hepatomegaly, hepatic/skeletal-muscle peroxisome proliferation, and skeletal myopathy were shown to be predominantly mediated by off-target PPARα cross-activation rather than PPARδ—a mechanism-based toxicity concern at animal-study exposures.

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

Where Researchers Are Buying

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COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower

Amlexanox

Best $/mg

$0.026/mg

Kimera ChemsC

1 trusted vendor listing

Compare all 1 vendor

GW-0742

Best $/mg

$0.058/mg

Kimera ChemsC

1 trusted vendor listing

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Lab Verification

COA corpus from Disclosed Labs — independently tested batches only.

Amlexanox

COAs

99.6%

Avg purity

Labs

Full testing data

GW-0742

COAs

99.6%

Avg purity

Labs

Full testing data

Amlexanox 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.

Key references

GW-0742 Research Summary

No human efficacy or safety data exist; the only identified human exposure is a single 15 mg oral dose administered to volunteers solely to characterize urinary metabolites for an anti-doping detection assay—a bioanalytical study yielding no therapeutic or safety information. Preclinical rodent findings include: oral GW-0742 (30 mg/kg/day × 3 weeks) reduced right ventricular hypertrophy and systolic pressure in rats with chronic hypoxia-induced pulmonary hypertension but did not prevent pulmonary vascular remodeling; intraperitoneal GW-0742 (0.1 mg/kg) improved survival and reduced intestinal injury, leukocyte activation, cytokines, and apoptosis markers in a mouse gut ischemia/reperfusion model; and GW-0742 ameliorated hepatic steatosis, ER stress, and lung inflammation in various mouse models. Critically, mouse studies also demonstrated hepatomegaly, hepatic/skeletal-muscle peroxisome proliferation, and skeletal myopathy driven predominantly by off-target PPARα cross-activation, indicating mechanism-based toxicity risk.

Can you stack Amlexanox and GW-0742?

Amlexanox and GW-0742 are both in the Metabolic category and may have overlapping mechanisms. Researchers should review both profiles carefully, understand the mechanisms of action, and monitor the relevant biomarkers when combining compounds in the same class. As always, consult a licensed healthcare provider before making any decisions about combining research compounds.

Other comparisons

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This platform provides informational tools only, not medical advice. This comparison is for educational purposes only. Consult a licensed provider.