Learn more about ways to help stop your macular degeneration by clicking on this sentence.
Avastin is the brand name for Bevaciumab a monoclonal antibody or an antibody that is an identical clone of a single parent cell. It was approved in 2004 by the FDA for use in the treatment of some cancers and is used as a first or second line treatment for patients.
As the first clinically available angiogenesis inhibitor the United States it inhibits new cancer cells by blocking the growth of blood vessels in pre-existing tumors. A solid, non-liquid, tumor needs to grow additional blood vessels to be able to reach a certain size.
With an angiostatic agent such as Avastin the growth of new blood vessels is slowed stopping the cancer from growing indefinitely. It is usually given every 14 days intravenously in the arm and can be used with other drugs in combination and with intravenous 5-fluorouracil-based chemotherapy.
Developed by Genentech (NYSE: DNA), a leading biotechnology corporation, it is marketed in the United States under the Genentech name and outside the US under Roche.
When it was originally available in 2004 it was only FDA approved for the treatment of many forms of small cell lung cancer and metastatic colon cancer. A metastatic cancer, in this case colon cancer, is a cancer that spreads from one part or organ to another non-adjacent part or organ.
In 2008 the FDA opened up the doors and allowed for the treatment of breast cancer. There are also clinical trials under way to use Avastin for the treatment of non-metastatic colon cancer, metastatic renal cell carcinoma, metastatic breast cancer, metastatic glioblastoma multiform, metastatic hormone-refractory prostate cancer, metastatic or unresectable locally advanced pancreatic cancer, and metastatic ovarian cancer.
Avastin is also currently being used off-label, the practice of prescribing drugs for a purpose outside the scope of the drug’s approved label, for the treatment of wet macular degeneration by some retinal specialists.
Wet macular degeneration or AMD is a condition that causes loss of vision from the growth of abnormal blood vessel choriocapillaries, through Bruch’s membrane. This eventually leads to blood and protein leaking below the macula, an oval spot near the middle of the retina in the human eye. With AMD rapid, often irreversible vision loss can occur through the leaking, bleeding and scaring of the blood vessels if left untreated.
Dr. Philip J Rosenfeld, MD, PhD of the Bascom Palmer Eye Institute conducted a study that showed positive results for the treatment of AMD with Avastin. According to Dr. Rosenfeld’s study Avastin improved vision in as little as one week for patients treated for AMD.
For AMD treatment Avastin is used in very low amounts by retinal specialists. They usually have a pharmacists transfer the drug from the original vile to a pre-filled needles containing single doses. The specialists will then usually treat the patient in their own office.
As with any drug it is always best to talk to your doctor or pharmacist before starting any treatment.
For more information go to www.maculardegenerationassociation.org
Friday, November 27, 2009
Monday, November 16, 2009
New treatment proves that Macular Degeneration can be cured
Micro Current Stimulation (MCS) which like acupuncture for the eyes. This procedure has proven results that will improved eye site from 20/100 to 20/60 and from 20/25 to 20/20. MD is the destruction of cells in the central part of the retina. A new revolutionary (MSC) treatment will reverse the disease. This treatment will re-generate the cells in the retina as it re-charges the cells and give them new life. This procedure increases the cells production of an energy chemical called ATP which creates new protein. Based on reports from patients this procedure has astonishing results.
For more information go to www.maculardegenerationassociation.org
For more information go to www.maculardegenerationassociation.org
Monday, November 9, 2009
Treatment for macular degeneration
By Emily Singer
Molecular Sunglasses for Macular Degeneration
Dampening a light-sensing reaction in the eye might slow a common cause of blindness.
Molecules designed to slow the production of toxic byproducts in the eye by making it less sensitive to light are now being tested in patients with macular degeneration, the leading cause of blindness in people age 50 and older. If successful, the compounds would provide a much needed therapy for the disease, which affects more than 15 million people in the United States.
In macular degeneration, cells in the center of the eye, called the macula, deteriorate. A handful of new treatments for the more severe form of the disease, known as wet AMD, have been approved in recent years. But no treatments are yet available for the dry form, which accounts for about 90 percent of cases. Some dry cases ultimately progress to the wet form, which accounts for a large part of AMD-related blindness. “If you can treat dry AMD, you can kill two birds with one stone,” both reducing early symptoms and preventing progression to the wet form, says Paul Sieving, director of the National Eye Institute, in Bethesda, MD.
While scientists are still trying to understand the causes of AMD–age is the biggest risk factor, with genetics and lifestyle factors also playing a role–a growing pool of evidence suggests that the build up of specific compounds in the eye can hasten the cellular damage that underlies the disease. These compounds accumulate in the photoreceptors–cells in the retina that detect light–during normal eye function as the light-sensitive pigments in these cells change conformation in response to photons.
One form of the photopigment, a derivative of vitamin A, is highly reactive and leaks into nearby tissue called the retinal pigment epithelium. “Over time we think these compounds are a burden for the retinal pigment epithelium, which is essential for the healthy function of the photoreceptors,” says Janet Sparrow, director of the Retinal Cell Biology Laboratory at Columbia University, in New York. “In age-related macular degeneration, particularly the dry form, these cells die, and the photoreceptors follow.”
While this reaction is vital for sight, researchers believe that slowing the cycle in the subset of photoreceptors responsible for night vision, known as rods, could slow damage without having a large impact on daytime vision. (Preliminary results suggest it can affect dark-adaptation–when our eyes adjust to low-light conditions.) “During the daytime, the rods are spinning like crazy, wasting vitamin A for no good use,” says Ryo Kubota, an ophthalmologist and founder of Acucela, a Seattle-based startup that is developing treatments for macular degeneration. “It’s like a CCD camera pointed at the sun.”
One compound developed by Acucela that is in clinical trials inhibits the enzyme that converts the photopigment in photoreceptors from one form to another. This process happens only in the eye, allowing the drug to be administered systemically without affecting other tissue, says Kubota. The company has finished initial safety testing in humans and plans to begin a clinical trial assessing the compound’s effectiveness in patients with late-stage dry macular degeneration in a few weeks. Kubota also aims to test the compound in diabetic retinopathy and Stargardt disease, a rare, genetically inherited form of macular degeneration.
A second drug that acts by a slightly different mechanism is being evaluated for macular degeneration by Sirion Therapeutics, a Florida-based pharmaceutical company. The compound is a synthetic vitamin A derivative that is thought to reduce toxin buildup by binding to one of the proteins involved in the reaction. According to preliminary results from tests of the drug in patients with late-stage dry macular degeneration, it can slow the scarring that is characteristic of the disease by 45 percent. However, scientists won’t know if the results are statistically significant until completion of the study next year. Because no treatments have been approved for dry AMD, the U.S. Food and Drug Administration has fast-tracked the drug, speeding the review process.
For more information go to www.maculardegenerationassociation.org
Molecular Sunglasses for Macular Degeneration
Dampening a light-sensing reaction in the eye might slow a common cause of blindness.
Molecules designed to slow the production of toxic byproducts in the eye by making it less sensitive to light are now being tested in patients with macular degeneration, the leading cause of blindness in people age 50 and older. If successful, the compounds would provide a much needed therapy for the disease, which affects more than 15 million people in the United States.
In macular degeneration, cells in the center of the eye, called the macula, deteriorate. A handful of new treatments for the more severe form of the disease, known as wet AMD, have been approved in recent years. But no treatments are yet available for the dry form, which accounts for about 90 percent of cases. Some dry cases ultimately progress to the wet form, which accounts for a large part of AMD-related blindness. “If you can treat dry AMD, you can kill two birds with one stone,” both reducing early symptoms and preventing progression to the wet form, says Paul Sieving, director of the National Eye Institute, in Bethesda, MD.
While scientists are still trying to understand the causes of AMD–age is the biggest risk factor, with genetics and lifestyle factors also playing a role–a growing pool of evidence suggests that the build up of specific compounds in the eye can hasten the cellular damage that underlies the disease. These compounds accumulate in the photoreceptors–cells in the retina that detect light–during normal eye function as the light-sensitive pigments in these cells change conformation in response to photons.
One form of the photopigment, a derivative of vitamin A, is highly reactive and leaks into nearby tissue called the retinal pigment epithelium. “Over time we think these compounds are a burden for the retinal pigment epithelium, which is essential for the healthy function of the photoreceptors,” says Janet Sparrow, director of the Retinal Cell Biology Laboratory at Columbia University, in New York. “In age-related macular degeneration, particularly the dry form, these cells die, and the photoreceptors follow.”
While this reaction is vital for sight, researchers believe that slowing the cycle in the subset of photoreceptors responsible for night vision, known as rods, could slow damage without having a large impact on daytime vision. (Preliminary results suggest it can affect dark-adaptation–when our eyes adjust to low-light conditions.) “During the daytime, the rods are spinning like crazy, wasting vitamin A for no good use,” says Ryo Kubota, an ophthalmologist and founder of Acucela, a Seattle-based startup that is developing treatments for macular degeneration. “It’s like a CCD camera pointed at the sun.”
One compound developed by Acucela that is in clinical trials inhibits the enzyme that converts the photopigment in photoreceptors from one form to another. This process happens only in the eye, allowing the drug to be administered systemically without affecting other tissue, says Kubota. The company has finished initial safety testing in humans and plans to begin a clinical trial assessing the compound’s effectiveness in patients with late-stage dry macular degeneration in a few weeks. Kubota also aims to test the compound in diabetic retinopathy and Stargardt disease, a rare, genetically inherited form of macular degeneration.
A second drug that acts by a slightly different mechanism is being evaluated for macular degeneration by Sirion Therapeutics, a Florida-based pharmaceutical company. The compound is a synthetic vitamin A derivative that is thought to reduce toxin buildup by binding to one of the proteins involved in the reaction. According to preliminary results from tests of the drug in patients with late-stage dry macular degeneration, it can slow the scarring that is characteristic of the disease by 45 percent. However, scientists won’t know if the results are statistically significant until completion of the study next year. Because no treatments have been approved for dry AMD, the U.S. Food and Drug Administration has fast-tracked the drug, speeding the review process.
For more information go to www.maculardegenerationassociation.org
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