| Indication | For the treatment of postoperative inflammation following ocular surgery and in the treatment of anterior uveitis. |
| Pharmacodynamics | Rimexolone is a glucocorticoid corticosteroid for systemic use. Corticosteroids suppress the inflammatory response to a variety of inciting agents of a mechanical, chemical, or immunological nature. They inhibit edema, cellular infiltration, capillary dilatation, fibroblastic proliferation, deposition of collagen and scar formation associated with inflammation. |
| Mechanism of action | Rimexolone is a glucocorticoid receptor agonist. The antiinflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition of arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. By binding to the glucocorticoid receptor, this drug ultimately leads to changes in genetic transcription involving the lipocortins and prostaglandins. |
| Absorption | Systemically absorbed. |
| Volume of distribution | Not Available |
| Protein binding | Not Available |
| Metabolism | Undergoes extensive metabolism. Following intravenous administration of radiolabeled rimexolone in rats, more than 80% of the dose was excreted in the feces as rimexolone and metabolites. Metabolites have been shown to be either less active than rimexolone or inactive in human glucocorticoid receptor binding assays. |
| Route of elimination | Following IV administration of radio-labelled rimexolone to rats, greater than 80% of the dose is excreted via the feces as rimexolone and metabolites. |
| Half life | The serum half-life of rimexolone could not be reliably estimated due to the large number of samples below the quantitation limit of the assay (80 pg/mL). However, based on the time required to reach steady-state, the half-life appears to be short (1-2 hours). |
| Clearance | Not Available |
| Toxicity | Symptoms of overdose include retinal toxicity, glaucoma, and subcapsular cataract. |