XOLA JAM is a non-bacteriostatic sulfonamide derivative and topical carbonic anhydrase (CA) inhibitor that treats elevated intraocular pressure (IOP) associated with open-angle glaucoma and ocular hypertension. It works by blocking an enzyme in the ciliary process that regulates ion balance and fluid pressure in the eyes. Unlike oral CA inhibitors, dorzolamide has negligible effects of acid-base or electrolyte disturbances and other systemic adverse effects. First marketed in 1995, dorzolamide is available in ophthalmic solutions as monotherapy marketed as Trusopt or in combination with timolol as Cosopt PF.
XOLA JAM is a carbonic anhydrase inhibitor that reduces elevated intraocular pressure in open-angle glaucoma or ocular hypertension. When used in combination with topic beta-adrenergic antagonists, dorzolamide has an additive effect of lowering intraocular pressure. The peak ocular hypotensive effect of dorzolamide is observed at about 2 hours following ophthalmic administration.
XOLA JAM is a carbonic anhydrase inhibitor used to treat high intraocular pressure in ocular hypertension and open angle glaucoma.
XOLA JAM is indicated for the management of elevated intraocular pressure in patients with ocular hypertension or open-angle glaucoma. It can also be used in combination with timolol for the same indication in patients who are insufficiently responsive to ophthalmic beta-blockers.
Its pre-operative use was also investigated to prevent elevated intraocular pressure after neodynium yttrium aluminum garnet laser posterior capsulotomy.
XOLA JAM is also used to associated treatment for these conditions: Increased Intra Ocular Pressure (IOP), Ocular Hypertension
How XOLA JAM works
Elevated intraocular pressure is a characteristic manifestation of ocular hypertension or open-angle glaucoma. The level of intraocular pressure (IOP) is governed by the balance between the production of aqueous humour (by ocular ciliary processes) and its outflow from the anterior segment of the eye via trabecular (conventional) or uveoscleral (unconventional) pathways. When there is an increase in the resistance to the trabecular outflow of aqueous humour, the intraocular pressure is elevated. Subsequently, optic nerve damage can occur from blood flow restrictions and mechanical distortion of ocular structures. Optic nerve damage can further result in optic disc cupping and progressive visual field loss (and blindness in some cases).
Carbonic anhydrase (CA) is a ubiquitous enzyme that catalyzes the reversible hydration of carbon dioxide to bicarbonate ions and dehydration of carbonic acid. In the ocular ciliary processes, the local production of bicarbonate by CAs promotes sodium and fluid transport. CA-II is a key isoenzyme found primarily in red blood cells (RBCs) that regulates aqueous humour production. XOLA JAM is a highly specific CA-II inhibitor, where it displays a 4000-fold higher affinity for carbonic anhydrase II than carbonic anhydrase I. The inhibition of CA-II in the ciliary process disrupts the formation of bicarbonate ions and reduces sodium and fluid transport, which leads to decreased aqueous humour secretion and reduced intraocular pressure.
|Trade Name||XOLA JAM|
|Dorzolamide Other Names||4S,6S-dorzolamide, Dorzolamid, Dorzolamida, Dorzolamide, Dorzolamidum|
Dorzolamide is approximately 33% bound to plasma proteins.
|Last Updated:||June 7, 2022 at 8:59 pm|
The oral LD50 of dorzolamide is 1927 mg/kg in rats and 1320 mg/kg in mice. The subcutaneous LD50 is >2 g/kg in both rats and mice.
Overdose may result in electrolyte imbalance, acidosis, and possibly central nervous system effects; these symptoms should be responded with appropriate supportive treatment. It is advised that the patient's serum electrolyte (particularly potassium) levels and blood pH levels are monitored in the case of a suspected overdose.
Food InteractionNo interactions found.
Volume of Distribution
There is limited information on the volume of distribution of dorzolamide; however, the plasma concentrations of dorzolamide and its main metabolite are generally below the assay limit of quantitation, which is 15nM. XOLA JAM accumulates in red blood cells following chronic administration as a result of binding to CA-II, which is contained in peripheral red blood cells (RBCs).
XOLA JAM readily penetrated into the eye in animal studies. Upon ophthalmic administration, dorzolamide is absorbed via the cornea and stroma. XOLA JAM is reported to be absorbed systematically following topical administration. The systemic exposure of dorzolamide following long-term administration was assessed in healthy subjects receiving an oral dose of 2 mg dorzolamide twice daily, which equates to the ophthalmic dose of 2% dorzolamide three times daily. In these subjects receiving the treatment for 20 weeks, the steady-state was reached within 8 weeks.
As the drug administration is stopped, dorzolamide stored in RBCs is washed out of RBCs in a non-linear fashion, with the terminal elimination half-life of ≥120 days in RBCs. This initial rapid decline in drug concentrations is followed by the slow elimination phase, where the elimination half-life of the drug is about >4 months.
There is limited information on the clearance rate of dorzolamide.
XOLA JAM is primarily excreted unchanged in the urine; however, N-desethyldorzolamide is also detected in the urine.
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