Some of the views expressed in the following notes on newly approved products should be regarded as preliminary, as there may have been limited published data at the time of publication, and little experience in Australia of their safety or efficacy. However, the Editorial Executive Committee believes that comments made in good faith at an early stage may still be of value. Before new drugs are prescribed, the Committee believes it is important that more detailed information is obtained from the manufacturer's approved product information, a drug information centre or some other appropriate source.
vials containing 15 mg/0.5 mL suspension
Approved indication: macular degeneration
Australian Medicines Handbook section 11.7
Most people with age-related macular degeneration have the non-exudative (dry) form. The exudative (wet) form is less common, but is more likely to cause blindness. Blood vessels grow through defects in the basement membrane of the retina then leak. This leakage causes loss of vision and scarring. The vessels can be treated with photocoagulation or, in patients with classical subfoveal choroidal neovascularisation, photodynamic therapy with verteporfin.
As the exudative form involves neovascularisation, it is possible that inhibiting angiogenesis will stop the disease progressing. Anecortave acetate is a molecule, structurally related to cortisol, which inhibits the proteases needed for blood vessel growth. Injecting the depot formulation through a cannula into the posterior juxtascleral area can stabilise the condition for several months. If indicated, the injection can be repeated six months later.
A clinical trial randomised 128 patients to receive anecortave (3 mg, 15 mg or 30 mg) or a placebo. Most of these patients with wet age-related macular degeneration had predominantly classic lesions. After six months there was a significant difference in the size of the lesions in patients given 15 mg anecortave. Although this difference was not statistically significant after 12 months, there was a significant difference in visual acuity. Patients given 15 mg anecortave were more likely to have stable vision and less likely to have severe loss of vision than patients given placebo. Efficacy seems greater in the patients with predominantly classic lesions.1 The advantage of anecortave over placebo remained for those patients still in the study after 24 months.2
During the study approximately 41% of patients dropped out, mainly because of disease progression.1 Adverse events reported during clinical trials include eye pain, hyperaemia, cataract, reduced intraocular pressure and ptosis.
The product information contains summary data from phase II trials comparing anecortave with verteporfin and photodynamic therapy. One trial gave patients anecortave or placebo 5-8 days after photodynamic therapy with verteporfin. Anecortave did not have a statistically significant advantage over placebo. The other trial has now been published. It randomised 263 patients with predominantly classic lesions to receive anecortave and 267 to receive photodynamic therapy with verteporfin. After 12 months, 45% of the anecortave group and 49% of the photodynamic therapy group had lost less than three lines of vision on the trial's visual acuity chart. Although the trial was designed to show that anecortave was not inferior, non-inferiority could not be confirmed.3
The Transparency Score () is explained in New drugs: transparency', Vol 37 No 1, Aust Prescr 2014;37:27.
- The Anecortave Acetate Clinical Study Group. Anecortave acetate as monotherapy for treatment of subfoveal neovascularization in age-related macular degeneration. Ophthalmology 2003;110:2372-85.
- Schmidt-Erfurth U, Michels S, Michels R, Aue A. Anecortave acetate for the treatment of subfoveal choroidal neovascularization secondary to age-related macular degeneration. Eur J Ophthalmol 2005;15:482-5.
- Slakter JS, Bochow T, D'Amico DJ, Marks B, Jerdan J, Sullivan EK. Anecortave acetate (15 milligrams) versus photodynamic therapy for treatment of subfoveal neovascularization in age-related macular degeneration. Ophthalmology 2006;113:3-13.