Currently Enrolling Trials
Visudyne (verteporfin for injection) is a photoenhancer. The drug is a blood-vessel-blocking photoreactive dye that gets injected into the arm of the patient. The dye moves to the blood vessels that are responsible for the loss of sight and is then activated by shining a non-burning beam of light into the eye. The treatment prevents the growth of the destructive blood vessels without hurting the surrounding tissues.
Visudyne is specifically indicated for the treatment of patients with predominantly classic subfoveal choroidal neovascularization due to age-related macular degeneration, pathologic myopia or presumed ocular histoplasmosis.
The dosage and administration is as follows:
- Recommended Dose: 6 mg/m body surface area.
- Reconstitution: Reconstitute each vial of Visudyne with 7 mL of Sterile Water for Injection to provide 7.5 mL containing 2 mg/mL of verteporfin. Reconstituted Visudyne must be protected from light and used within 4 hours.
- Dilution: Dilute desired dose of reconstituted Visudyne with 5% Dextrose for Injection to a total infusion volume of 30 mL.
- Infusion: Administer intravenously over 10 minutes at a rate of 3 mL/minute, using an appropriate syringe pump and in-line filter.
- Light Administration: The recommended light dose is 50 J/cm of neovascular lesion administered at an intensity of 600 mW/cm . The wavelength of the laser light should be 689±3 nm. This light dose is administered over 83 seconds, starting 15 minutes after the start of the Visudyne infusion
Adverse effects associated with the use of Visudyne may include, but are not limited to, the following:
- injection site reactions
- visual disturbance
Mechanism of Action
Visudyne therapy is a two-stage process requiring administration of both verteporfin for injection and nonthermal red light.
Verteporfin is transported in the plasma primarily by lipoproteins. Once verteporfin is activated by light in the presence of oxygen, highly reactive, short-lived singlet oxygen and reactive oxygen radicals are generated. Light activation of verteporfin results in local damage to neovascular endothelium, resulting in vessel occlusion. Damaged endothelium is known to release procoagulant and vasoactive factors through the lipo-oxygenase (leukotriene) and cyclo-oxygenase (eicosanoids such as thromboxane) pathways, resulting in platelet aggregation, fibrin clot formation and vasoconstriction. Verteporfin appears to somewhat preferentially accumulate in neovasculature, including choroidal neocovasculature. However, animal models indicate that the drug is also present in the retina. Therefore, there may be collateral damage to retinal structures following photoactivation including the retinal pigmented epithelium and outer nuclear layer of the retina. The temporary occlusion of choroidal neovascularization (CNV) following Visudyne therapy has been confirmed in humans by flourescein angiography.
Clinical Trial Results
Two placebo-controlled studies were conducted for 609 patients with age-related macular degeneration. At the end of the one-year treatment period, the group treated with Visudyne had statistically better visual acuity than did those who had placebo treatment. 60% of Visudyne-treated patients had stable vision over the year, versus the 45% of placebo-treated patients who had stable vision.