Brands, Medical Use, Clinical Data
- Antineoplastic Agents
- Photosensitizing Agents
- Powder for solution to be mixed for injection (2mg verteporfin/mL reconstituted verteporfin)
Brands / Synonyms
Benzoporphyrin derivative; Visudyne; Visudyne
For the treatment of patients with predominantly classic subfoveal choroidal neovascularization due to age-related macular degeneration, pathologic myopia or presumed ocular histoplasmosis.
Verteporfin, otherwise known as benzoporphyrin derivative, is a medication used in conjunction with laser treatment to eliminate the abnormal blood vessels in the eye associated with conditions such as the wet form of macular degeneration. Verteporfin accumulates in these abnormal blood vessels and, when stimulated by nonthermal red light with a wavelength of 693 nm in the presence of oxygen, produces highly reactive short-lived singlet oxygen and other reactive oxygen radicals, resulting in local damage to the endothelium and blockage of the vessels.
Mechanism of Action
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 neovasculature. However, animal models indicate that the drug is also present in the retina.
Overdose of drug and/or light in the treated eye may result in nonperfusion of normal retinal vessels with the possibility of severe decrease in vision that could be permanent. An overdose of drug will also result in the prolongation of the period during which the patient remains photosensitive to bright light.
Biotrnasformation / Drug Metabolism
Metabolized to a small extent to its diacid metabolite by liver and plasma esterases. NADPH-dependent liver enzyme systems (including the cytochrome P450 isozymes) do not appear to play a role in the metabolism of verteporfin.
VISUDYNE is contraindicated for patients with porphyria or a known hypersensitivity to any component
of this preparation.
Drug interaction studies in humans have not been conducted with VISUDYNE. Verteporfin is rapidly
eliminated by the liver, mainly as unchanged drug. Metabolism is limited and occurs by liver and plasma esterases.
Microsomal cytochrome P450 does not appear to play a role in verteporfin metabolism.
Based on the mechanism of action of verteporfin, many drugs used concomitantly could influence the
effect of VISUDYNE therapy. Possible examples include the following: Calcium channel blockers, polymyxin B or
radiation therapy could enhance the rate of VISUDYNE uptake by the vascular endothelium. Other photosensitizing
agents (e.g., tetracyclines, sulfonamides, phenothiazines, sulfonylurea hypoglycemic agents, thiazide diuretics and
griseofulvin) could increase the potential for skin photosensitivity reactions. Compounds that quench active oxygen
species or scavenge radicals, such as dimethyl sulfoxide, b -carotene, ethanol, formate and
mannitol, would be expected to decrease VISUDYNE activity. Drugs that decrease clotting, vasoconstriction or platelet
aggregation, e.g., thromboxane A2 inhibitors, could also decrease the efficacy of VISUDYNE therapy.