Macular Degeneration Treatments

Are you, a parent, or a grandparent suffering from the early stages of Age Related Macula Degeneration (ARMD)? Perhaps you or one of your loved ones has suffered from advancing ARMD.

You may have already been treated with focal laser photocoagulation or newer Macular Degeneration Treatments like Photodynamic Therapy (PDT) with Verteporfin or Intravitreal Anti-Vascular Endothelial Growth Factor (VEGF) drug therapy.

Giant steps forward are being taken in combating, or even completely curing, this potentially devastating Eye Disease with Experimental Macular Degeneration Treatments for ARMD.

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What are some of the Experimental Macular Degeneration Treatments?

Macular Degeneration Experimental Treatments can be divided into several categories:Genetically driven in which you may one day receive customized medical therapy based on your own unique genetic make-up.

  • VEGF inhibition

  • Alternative Therapies

    • Experimental Macular Degeneration Treatments primarily focus on the destruction of Choroidal Neovascular Membranes (CNVMs), which is a sign of Wet ARMD. The ideal treatment of the future will be able to arrest the disease at a stage before CNVMs develop; i.e., when it is Dry ARMD.

    To this end, researchers are testing better diagnostic procedures with predictive value (to predict who is more likely to develop significant visual loss), studying supplements to slow down the damaging effects on the macula, and analyzing better portable and home technology you can use to monitor any worsening of your ARMD.

    What genetic advancements are contributing to the Experimental Macular Degeneration Treatments?

    A significant genetic breakthrough in ARMD research happened in 2005 when multiple independent researchers discovered that one particular gene is strongly associated with the development of ARMD. This gene is called Compliment Factor H (CFH).

    This particular gene produces a protein that helps mediate inflammation by a primitive pathway referred to as the complement system, which is part of the body’s natural defense immune system. This gene is located at the region of chromosome 1q32.

    The complement system has three distinct pathways, each one exhibiting a similar terminal sequence that activates the cell-killing “membrane attack complex” (MAC). The MAC is one of the primary ways in which the immune system fights against foreign invaders.

    As lethal as the MAC is to foreign invaders like viruses, fungi, bacteria or other cells, MAC can also have a negative collateral effect on your good cells and tissues, causing damage or even cell death.

    Studies have revealed that ARMD develops as a result of a complement system regulation deficiency. Investigators discovered that drusen (the classic sign of ARMD-yellow spots in the Macula) contain nearly all of the proteins that make up the complement system as well as components of the MAC.

    External factors also play a role in regulating the complement system such as:

    Smoking: The risk of developing ARMD is over 2 times greater for current and former smokers than for those who have never smoked. Of risk factors that are self-imposed, smoking has been shown consistently to be associated with disease.

    Diet and nutrition may play an important part in ARMD and in maintaining eye health. Higher body mass index also appears to be mostly associated with early or ARMD progression.

    Other potential causes:

  • Serum cholesterol levels

  • Cataract surgery

  • Cardiovascular disease

  • Hypertension

  • Sunlight exposure

    • Non-modifiable risk factors have been reported to influence ARMD as well:

  • Age

  • Gender

  • Family History

  • Infectious agents

    • Since 2005, several other genes were identified as associated with ARMD and verified in subsequent studies. It is the combination of genetics and these risk factors, while not completely understood, that leads to a greater risk for ARMD development.

    Armed with these genetic advancements, scientists set out to develop new drug therapies for dry ARMD that specifically target regulation of the complement system.

    Examples of Experimental Macular Degeneration Treatments based on this concept include:

  • Eculizumab (Soliris, Alexion Pharmaceuticals): This drug is already FDA approved to treat a particularly severe form of hemolytic anemia. In its current form, this drug is administered as an intravenous infusion. This drug is being studied for its effectiveness at halting the progression of Dry ARMD to Wet ARMD.

  • ARC 1905 (Ophthotech) is another potent drug being studied. This drug inhibits both a phase in the complement system and MAC activities. It is currently being investigated in two different studies. In one study, ARC 1905 is being used in combination with Lucentis in patients with Wet ARMD. A separate study initiated in 2009 is investigating the use of ARC 1905 in patients with Dry ARMD.

  • JPE-1375 (Jerini AG): This small molecule targets a phase in the complement system that is believed to attract inflammatory cells. The goal of this treatment is to block inflammation associated with complement activation, but leave components that form the MAC alone. This, in turn, will prevent activation of other mediators, such as VEGF, and hence the development of CNVMs.

  • POT-4 (Potentia Pharmaceuticals/Alcon): This drug is currently being administered intravitreally (directly into the Vitreous of the eye) in clinical trials designed to evaluate its efficacy in patients with Geographic Atrophy.

  • TNX-234 (Tanox/Genentech) is a humanized antibody that is directed against a component of the complement system. It is being evaluated for safety in an intravitreal injection for patients with Geographic Atrophy.

    • There are other drugs being evaluated that target key factors beyond the complement system and are showing promise:

  • Copaxone (Glairamer Acetate injection, Teva Pharmaceuticals): This drug has already been proven safe for a different neurodegenerative disease, and its effectiveness is currently being evaluated in the prevention of Dry ARMD progression. Various delivery methods are being tested, including a weekly vaccination.

  • ACU-4429 (Acucela and Otsuka Pharmaceutical): This drug’s potential ability to slow the eyes’ visual cycle of light processing may result in the decreased creation of naturally toxic byproducts by the visual cycle. These byproducts may contribute to the development of ARMD. This drug is administered to patients as an oral, daily pill as opposed as by injection like many other treatments.

    • These genetic advances may one day pave the way for you to receive customized medical therapy based on your own unique genetic make-up.

    What VEGF Inhibition drugs are contributing to the Experimental Macular Degeneration Treatments ?

    Angiogenesis (or growth of new vessels created from pre-existing vasculature; otherwise known as neovascularization) is associated with several diseases such as cancer, ARMD, psoriasis, rheumatoid arthritis, and Diabetic Retinopathy. VEGF is a major molecular mediator of neovascularization and is present in CNVMs in Wet ARMD. Although the exact mechanism for disease progression of ARMD is not completely understood, it is increasing clear that VEGF plays an important role in the promotion of CNVMs and the vessel leakage that leads to loss of central vision.

    The VEGF Inhibition drugs that are in development employ one of several mechanisms of action to inhibit the VEGF functional pathway.

    Experimental Macular Degeneration Treatments using VEGF Inhibition include:

  • Aflibercept (VEGF Trap-Eye): This drug is a receptor decoy that targets VEGF with higher affinity than Lucentis and other currently available anti-VEGF therapies. It is being studied in clinical trials as an intravitreal injection. In other clinical trials it is being compared to Lucentis in order to assess its clinical applicability.

  • Bevasiranib (formerly Cand5, Acuity Pharmaceuticals): This is the first drug developed that works by RNA interference, the process by which small interfering RNA (siRNA) molecules inactivate messenger RNA, thereby suppressing RNA translation. RNA, or Ribonucleic acid, is a nucleic acid essential in building proteins.

    This drug is injected intravitreally and induces catalytic destruction of messenger RNA to silence gene expression, thereby targeting new production of VEGF. This drug has been studied in combination with other anti-VEGF treatments for additive positive effects.

    • What Alternative Therapies are contributing to the Experimental Macular Degeneration Treatments?

    Examples of Experimental Macular Degeneration Treatments that are Alternative Therapies include:

  • Anecortave acetate (Retaane): This drug can be administered as an injection and has been shown to be safe and well tolerated. However, it may a good option to be used in combination with other treatment for active CNVMs. It may also be an alternative therapeutic option before considering Intravitreal Anti-VEGF Therapy due to its less invasive character and lower risk profile.

  • Astaxanthin (AST): This is a carotenoid found in marine animals and vegetables that has been investigated for its effects on the developmental of experimental CNVMs in mice. Mice in this study had laser-induced CNVMs and were then treated with AST. The results were promising since the mice exhibited a significantly lower CNVMs volume as compared to those not treated with AST.

  • Radiation Therapy: This treatment may be a promising addition to Anti-VEGF Therapy for the control of CNVMs in ARMD. A drawback to this therapy is the risk of radiation to ocular tissue even though modern delivery systems permit relatively low dosages. Moreover, all of the advances in pharmaceuticals may make its role less important.

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