Dorzoptik (dorzolamide) eye drops solution 20 mg/ml. 5 ml. bottle dropper №1


Manufacturer: Croatia

The sensitivity to dorzolamidu and to any of the components of the drug was improved. Nirkov’s deficiency is severe (creatine clearance is less than 30 ml/XB). Hyperchloremic acidosis.



Dorzoptik Composition
active substance: dorzolamide;

1 ml 20 mg dorzolamide as dorzolamide hydrochloride;

Dorzoptik excipients: mannitol (E 421) hydroxyethyl cellulose; sodium, dihydrate; sodium benzalkonium hydroxide chloride, solution 50%; water for injections.

Dorzoptik Dosage form
Eye drops, solution.

Basic physical and chemical properties: transparent, colorless, somewhat viscous liquid.

Pharmacotherapeutic group
Antiglaucoma agents for topical use. Carbonic anhydrase inhibitors. Dorzolamide. ATX code S01E C03.

Dorzolamide is a topical carbonic anhydrase inhibitor in the form of eye drops. Carbonic anhydrase is an enzyme found in many tissues of the body (including the tissues of the eye), which is involved in the hydration of carbon dioxide and dehydration of carbonic acid. In humans, this enzyme is represented by various isoenzymes, the most active of which is carbonic anhydrase II, primarily found in erythrocytes, and then in cells of other tissues. Inhibition of carbonic anhydrase of the ciliary body of the eye leads to a decrease in the secretion of intraocular fluid (mainly due to a decrease in the formation of bicarbonate ions with a subsequent decrease in the transport of sodium ions and fluid).

After topical application, the drug reduces intraocular pressure, regardless of whether it is associated with an increase in glaucoma.

Dorzolamide reduces intraocular pressure without the development of side effects characteristic of miotics, such as night blindness, accommodation spasm, pupil constriction.

When applied topically in the form of a 2% ophthalmic solution, dorzolamide reduces increased intraocular pressure, which is the main risk factor in the pathogenesis of optic nerve damage and glaucomatous deterioration of visual functions (loss of visual fields).

With oral administration, the effect of dorzolamide occurs after 60-90 minutes and lasts for 8-12 hours. Dorzolamide passes into the systemic circulation. In the case of continuous oral administration, dorzolamide accumulates in erythrocytes by selective binding to type II carbonic anhydrase. Plasma retains very low concentrations of this drug in free form.

Dorzolamide is metabolized to N-deseyl-dorzolamide, which inhibits carbonic anhydrase II less strongly, but at the same time inhibits the less active isoenzyme, carbonic anhydrase I. This metabolite accumulates in red bodies, where it mainly binds to carbonic anhydrase I.

Dorzolamide binds moderately to plasma proteins (about 33%). It is excreted in the urine both unchanged (80%) and in the form of metabolites (20%). Release from erythrocytes follows from non-linear kinetics, resulting in an initial rapid decline in concentration followed by a very slow withdrawal phase with an average elimination half-life of 4 months. In equilibrium, renal clearance is approximately 1.3 mg per day at a dose of 4 mg with a renal clearance of 90 ml / min.

When administered orally with dorzolamide to simulate the maximum systemic effect with its long-term topical application, a uniform concentration is achieved after 13 weeks. In a state of equilibrium, no drug was found in the blood plasma in free form or in the form of metabolites. The degree of inhibition of carbonic anhydrase in erythrocytes was lower than that required to obtain a pharmacological effect on the respiratory system or renal function.

In elderly patients with renal insufficiency (creatinine clearance 30-60 ml / min), higher concentrations of the metabolite in erythrocytes were found, but no significant differences in carbonic anhydrase inhibition and no significant clinical side effects were observed.

In contrast to oral administration, ophthalmic administration provides a localized effect at lower doses.

With intraconjunctival application, the enzyme activity of carbonic anhydrase is inhibited in the endothelial cells of the cornea, ciliary body, lenticular epithelial cells and the cornea within 1-8 hours after application. In the cornea and lenticular epithelial cells, enzyme activity is inhibited even 10 hours after instillation.

Dorzolamide is rapidly distributed into the tissues of the eye. Noticeable concentrations of dorzolamide appear in the bloodstream within 15 minutes after instillation (in the cornea, lacrimal fluid, iris, ciliary body) and reach a maximum level about 1 hour after application.

Treatment of increased eye pressure in patients with:

ocular hypertension;
open-angle glaucoma;
pseudoexfoliative glaucoma;
as adjunctive therapy to beta-blocker therapy or as monotherapy when beta-blocker therapy has not been successful or beta-blockers are contraindicated.

Hypersensitivity to dorzolamide or to any of the components of the drug.

Severe renal failure (creatinine clearance less than 30 ml / min).