Verteporfin, a benzoporphyrin derivative monoacid ring A, is a photosensiti
sing drug for photodynamic therapy (PDT) activated by low-intensity, nonhea
t-generating light of 689nm wavelength. Activation generates cytotoxic oxyg
en free radicals.
The specificity and uptake of verteporfin for target cells with a high expr
ession of low density lipoprotein (LDL) receptors, such as tumour and neova
scular endothelial cells, is enhanced by the use of a liposomal formulation
and its rapid uptake by plasma LDL.
Verteporfin therapy (at light doses < 150 J/cm(2)) selectively damages neov
ascular endothelial cells leading to thrombus formation and specific occlus
ion of choroidal neovascular vessels in subfoveal lesions in patients with
age-related macular degeneration (AMD).
Repeated applications of verteporfin therapy 6 mg/m(2) improved or maintain
ed visual acuity in the majority of patients with some classic subfoveal ch
oroidal neovascularisation (CNV) secondary to AMD at I year's follow-up in
2 large multicentre, placebo-controlled, double-blind trials.
Furthermore, in a subgroup of these patients with predominantly classic CNV
secondary to AMD, there was a significantly more marked visual acuity (VA)
benefit with 67.3% of verteporfin-treated eyes experiencing less than a 15
-letter loss of VA versus 39.3% with placebo treatment.
Multiple applications of verteporfin therapy were well tolerated in patient
s with subfoveal CNV secondary to AMD. The most common adverse events were
visual disturbances, injection site reactions, photosensitivity reactions a
nd infusion-related back pain.