Clearcure

Uses

No FDA- or EMA-approved therapeutic indications on its own.

Naphazoline is a sympathomimetic vasoconstrictor used for the symptomatic relief of redness and itching of the eye, and nasal congestion.

Naphazoline is indicated for use as OTC eyedrops for ocular vasoconstriction or as a nasal preparation for nasal congestion.

Clearcure is also used to associated treatment for these conditions: Acne, Asthenopia, Ocular Irritation, Skin Mycoses, Eye discomfort, Skin disinfection, Irrigation of the ocular surface therapyBacterial Conjunctivitis, Blepharoconjunctivitis, Conjunctivitis, Conjunctivitis allergic, Dacryocystitis, Dacryostenosis, Dermatitis, Eczematous of the Eyelid, Eye Pain, Eye redness, Iritis, Lacrimation, Nasal Allergies, Nasal Congestion, Noninfective conjunctivitis, Otitis Media (OM), Photophobia, Foreign body sensation in eye, Ocular bacterial infections, Ocular vasoconstriction

How Clearcure works

Information regarding the mechanism of action of boric acid in mediating its antibacterial or antifungal actions is limited. Boric acid inhibits biofilm formation and hyphal transformation of Candida albicans, which are critical virulence factors . In addition, arrest of fungal growth was observed with the treatment of boric acid .

Naphazoline is a vasoconstrictor that functions by stimulating alpha adrenergic receptors in arterioles leading to decreased congestion at the site of administration.

Naphazoline causes the release of norepinephrine in sympathetic nerves. Norepinephrine binds to alpha adrenergic receptors and causes vasoconstriction. Naphazoline is also a mild beta adrenergic receptor agonist, which can cause rebound vasodilation after the alpha adrenergic stimulation has ended. Naphazoline's release of norepinephrine also triggers a negative feedback loop which decreases production of norepinephrine, which can lead to rhinitis medicamentosa after long term use when naphazoline is stopped.

Toxicity

Acute oral LD50 is 2660 mg/kg in rat . Individuals are likely to be exposed to boric acid from industrial manufacturing or processing. Local tissue injury from boric acid exposure is likely due to caustic effects. Systemic effects from boric acid poisoning usually occur from multiple exposures over a period of days and involve gastrointestinal, dermal, CNS, and renal manifestations. Gastrointestinal toxicity include persistent nausea, vomiting, diarrhea, epigastric pain, hematemesis, and blue-green discoloration of the feces and vomit . Following the onset of GI symptoms, a characteristic intense generalized erythroderma follows . Management of mild to moderate toxicity should be supportive. In case of severe toxicity, dialysis may be required in addition to supportive treatment.

In high doses or when ingested, naphazoline can lead to central nervous system depression (which can progress to coma and death), hypothermia, bradycardia, and death. This effect is especially pronounced in children under 6 years.

Long term use of naphazoline can lead to rhinitis medicamentosa once naphazoline is stopped. This condition is a result of norepinephrine release by naphazoline triggering a negative feedback loop.

Safety and effectiveness in children under 12 has not been established. Studies in elderly patients have yet to be performed. Risk in pregnancy, breast feeding, and on overall fertility have not been established, though pregnant and breast feeding patients should consider the risk and benefit before starting naphazoline treatment.

Volume of Distribution

Volume of distribution ranges from 0.17 to 0.5 L/kg in humans, where large amounts of boric acid are localized in brain, liver, and kidney .

Distribution data for naphazoline are scarce but imidazoline compounds are distributed throughout the body, and can cross the blood-brain barrier.

Elimination Route

Boric acid is well absorbed from the gastrointestinal tract, open wounds, and serous cavities but displays limited absorption in intact skin . Following intraperitoneal injection in mice, the peak concentration was reached in about 1.0-1.5 hr in the brain whereas the value was 0.5 hr in other tissues .

Absorption data for naphazoline are scarce but imidazoline compounds in general are weakly basic and lipophilic, with high bioavailability from the gastrointestinal tract.

Half Life

According to human cases of poisoning, the elimination half-life of boric acid ranges from 13 to 24 hours .

Half life has not been determined but effects last for 4 to 8 hours. Other imidazoline compounds have half lives varying from 2 to 12 hours.

Clearance

A case report of acute boric acid poisoning following oral ingestion of 21 g of boric acid presents the total body clearance of 0.99 L/h before hemodialysis .

Clearance data for naphazoline is unavailable.

Elimination Route

Regardless the route of administration, boric acid predominantly undergoes rapid renal excretion of >90% of total administered dose as unchanged form. Small amounts are also excreted into sweat, saliva, and feces. Following administration as ointment, urinary excretion of boric acid accounted for only 1% of the administered dose .

Imidazoline compounds undergo some hepatic metabolism but a large fraction of the dose may be excreted unchanged in the urine. Urinary excretion is higher with more acidic urine.

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