Binzotim1%+0.5%

Treatment of elevated IOP in adult patients with open-angle glaucoma or ocular HTN for whom monotherapy provides insufficient IOP reduction.

Drugs for miotics and glaucoma

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).Like propranolol and nadolol, timolol competes with adrenergic neurotransmitters such as catecholamines for binding at beta(1)-adrenergic receptors in the heart and vascular smooth muscle and beta(2)-receptors in the bronchial and vascular smooth muscle. Beta(1)-receptor blockade results in a decrease in resting and exercise heart rate and cardiac output, a decrease in both systolic and diastolic blood pressure, and, possibly, a reduction in reflex orthostatic hypotension. Beta(2)-blockade results in an increase in peripheral vascular resistance. The exact mechanism whereby timolol reduces ocular pressure is still not known. The most likely action is by decreasing the secretion of aqueous humor.

1 drop into the affected eye(s) twice daily

1 drop into the affected eye(s) twice daily

Ketoconazole, itraconazole, clotrimazole, ritonavir, troleandromycin; oral Ca-channel blockers, guanethidine, β-blockers, antiarrhythmics, digitalis glycosides, parasympathomimetics; quinidine, cimetidine.

Bronchial asthma, severe COPD, sinus bradycardia, 2nd or 3rd degree AV block, overt cardiac failure, cardiogenic shock, severe allergic rhinitis, bronchial hyperreactivity, hyperchloraemic acidosis, severe renal impairment.

Dysgeusia, blurred vision, eye pain & irritation, foreign body sensation.

No data available

Control cardiac failure prior to therapy. History of severe cardiac & resp disease. Patients subject to hypoglycemia or labile insulin-dependent diabetes. May mask hyperthyroidism or worsen Prinzmetal's angina, severe peripheral & central circulatory disorders & hypotension. History of atopy or severe anaphylactic reaction to a variety of allergens. Avoid concomitant use of 2 local β-adrenergic blockers or 2 local carbonic anhydrase inhibitors. Close monitoring of IOP in patients with pseudoexfoliative or pigmentary glaucoma. Narrow-angle glaucoma. Monitor patients with compromised corneas eg, patients with DM or corneal dystrophies. Remove contact lenses prior to application; reinsert after 15 min. May impair ability to drive or operate machinery. Pregnancy. Childn <18 yr.

Store in cool and dry place

Drugs for miotics and glaucoma

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).Like propranolol and nadolol, timolol competes with adrenergic neurotransmitters such as catecholamines for binding at beta(1)-adrenergic receptors in the heart and vascular smooth muscle and beta(2)-receptors in the bronchial and vascular smooth muscle. Beta(1)-receptor blockade results in a decrease in resting and exercise heart rate and cardiac output, a decrease in both systolic and diastolic blood pressure, and, possibly, a reduction in reflex orthostatic hypotension. Beta(2)-blockade results in an increase in peripheral vascular resistance. The exact mechanism whereby timolol reduces ocular pressure is still not known. The most likely action is by decreasing the secretion of aqueous humor.

No data available