Table 1.
Authors | Study Design | Pertinent Results | Takeaways |
Gonzalez-Hilarion et al (2012) [12] | Utilized screening to determine small molecules which can act as
potential inhibitors. Administered to 3 derived cell lines with nonsense mutation and observed results. |
Determined an increase in nonsense containing mRNAs in treated
cells. Synthesis of full length, functional protein. Evidence that amlexanox rescues expression of nonsense-containing mRNAs. |
Amlexanox should be further investigated to determine its effect on diseases caused by nonsense mutations. Has effect on potential conditions such as cystic fibrosis. |
Oral et al (2017) [6] | Double-blind, placebo study of 42 obese patients with type 2 diabetes and nonalcoholic fatty liver disease (NAFLD). Length: 12 weeks | Patients administered amlexanox demonstrated improved insulin
sensitivity and hepatic steatosis. Increase in serum IL-6 levels at 2-4 weeks. |
Amlexanox to be further examined as a potential therapeutic for NAFLD and type 2 diabetes. |
Beyett et al (2018) [24] | Utilized both amlexanox and derived analogs to determine cellular effect on inflammation. | Determined that amlexanox likely inhibits kinases which affect chronic low-grade inflammation. | Amlexanox is promising therapeutic in treatment of type 2 diabetes and obesity through its presumed mechanism of action. |
He et al (2019) [3] | NAFLD mice models were established using 8-week-old mice, which were fed either high-fat diet (HFD) and/or lipopolysaccharide (LPS) diets. All HFD mice administered either amlexanox or vehicle for 18 weeks. HFD+LPS mice were administered either amlexanox or vehicle for the final 6 weeks. | Amlexanox improved insulin signaling in hepatocytes through inhibiting inflammation in hepatic stellate cells (HSCs). IKKe was detected only in HSCs and was not identified in hepatocytes. | Amlexanox has the potential to improve the insulin signaling pathway in hepatocytes, which further demonstrates promise as a future therapeutic for metabolic disease. |