| Indication | For the treatment of elevated intraocular pressure in patients with ocular hypertension or open-angle glaucoma. |
| Pharmacodynamics | Used in the treatment of glaucoma, brinzolamide inhibits aqueous humor formation and reduces elevated intraocular pressure. Elevated intraocular pressure is a major risk factor in the pathogenesis of optic nerve damage and glaucomatous visual field loss. Brinzolamide can decrease intraocular pressure by approximately 16-19% in patients with elevated intraocular pressure. |
| Mechanism of action | Brinzolamide is a highly specific inhibitor of CA-II, which is the main CA isoenzyme involved in the secretion of aqueous humor. Inhibition of CA in the ciliary process of the eye slows the formation of bicarbonate, and reduces sodium and fluid transport. This results in a reduction in the rate of aqueous humor secretion and the intraocular pressure. Brinzolamide is absorbed systemically following topical ocular administration. Since it has a high affinity for CA-II, brinzolamide binds extensively to red blood cells, where CA-II is primarily found. As sufficient CA-II activity remains, adverse effects resulting from the systemic inhibition of CA by brinzolamide are not observed. The metabolite N-desethyl brinzolamide is also formed. This metabolite binds to CA and accumulates in red blood cells as well. In the presence of brinzolamide, the metabolite binds mainly to carbonic anhydrase I (CA-I). |
| Absorption | Absorbed into systemic circulation following topical ocular application |
| Volume of distribution | Not Available |
| Protein binding | Approximately 60%. |
| Metabolism | Ophthalmic |
| Route of elimination | Not Available |
| Half life | 111 days |
| Clearance | Not Available |
| Toxicity | Not Available |
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