Triamcinolone hexacetonide, an exogenous synthetic corticosteroid, is a highly potent glucocorticoid receptor (GR) agonist for the study of auto-reactive pericarditis and diabetic macular edema.

Triamcinolone hexacetonide exhibited significant protective effects in a chemically induced model of articular cartilage damage, and this effect was dose-dependent. Guinea pigs injected with the drug exhibited significantly reduced fibrosis and bone spur formation. Triamcinolone hexacetonide injected into the ipsilateral knee of rabbits after partial lateral meniscectomy and severance of the metatarsophalangeal ligament and fibular collateral ligament reduced chondrocyte cloning, cell loss, bone spur formation, and fibrosis. [1]
In addition, the half-life of commercially available Triamcinolone hexacetonide in the vitreous humor is twice as long as that of regular Triamcinolone hexacetonide. [2]
Localized application of Triamcinolone hexacetonide at the site of lingual nerve injury has been shown to produce beneficial changes such as reduced mechanical sensitivity and promotion of nerve regeneration. [3]