By Thomas Reuters
- CHMP positive opinion supports Lucentis approval in EU for treatment in patients with visual impairment due to diabetic macular edema (DME)
- Pivotal data shows Lucentis provided rapid, superior and sustained vision gains compared to the current standard of care
- Diabetes-associated eye diseases such as DME are a leading cause of blindness in most developed countries in the working-age population
Basel, October 22, 2010 - Novartis has received a positive opinion from the Committee for Medicinal Products for Human Use (CHMP) for Lucentis(R) (ranibizumab) for the treatment of patients with visual impairment due to diabetic macular edema (DME), a leading cause of blindness in the working-age population in most developed countries.
"Lucentis was designed specifically for use in the eye, and its efficacy and safety have now been demonstrated in patients suffering loss of vision due to diabetic macular edema through a robust program of clinical trials," said David Epstein, Division Head of Novartis Pharmaceuticals.
The submission was supported by data from two Novartis-funded clinical trials, RESTORE and RESOLVE, which showed that Lucentis was superior in providing rapid and sustained visual acuity gain versus sham (dummy therapy) or laser therapy, the current standard of care. The RESTORE study showed patients treated with Lucentis alone or with Lucentis plus laser therapy achieved an average 5.9 letters and 5.5 letters gain in visual acuity at 12 months, respectively, compared to laser-treated patients as measured on a standard ETDRS eye chart.
The RESOLVE study showed that Lucentis-treated patients achieved an average 11.7 letters gain in visual acuity at 12 months compared to sham-treated patients, some of whom received laser treatment.
The pivotal data from RESTORE and RESOLVE are further supported by results of an independent US study conducted by the Diabetic Retinopathy Clinical Research Network (DRCR.net), showing that at one year nearly 50% of patients' eyes treated with Lucentis and laser therapy improved their visual acuity by 10 letters or more, compared to 28% with laser alone. In addition, the study demonstrated superior gains in visual acuity among Lucentis-treated patients up to two years.
Lucentis was generally well tolerated in clinical studies, either when given as monotherapy or when combined with laser treatment. Its safety profile was consistent with that previously reported in large controlled clinical trials, and in rigorous monitoring since Lucentis was first approved for wet age-related macular degeneration (AMD). Lucentis is currently licensed in more than 85 countries for the treatment of wet AMD.
Diabetic macular edema (DME) is a consequence of diabetic retinopathy - the most common diabetic eye complication, characterized by changes in the blood vessels of the retina - to the light-sensitive layer at the back of the eye. In patients with DME, leakage from these abnormal blood vessels occurs in the central portion of the retina, called the macula. Because this part of the eye is responsible for sharp central vision, DME can lead to significant visual impairment. Visual impairment due to DME affects approximately 1-3% of patients with diabetes, and DME is a leading cause of blindness in the working-age population in most developed countries.
Lucentis offers an entirely new pharmacological approach to treatment compared to the current standard of care for DME that involves the use of laser burns to stop the capillary leakage and to reduce swelling. Lucentis is an antibody fragment that is injected into the eye and acts by neutralizing vascular endothelial growth factor (VEGF), a protein that is known to increase vascular permeability, resulting in capillary leakage and macular edema in patients with diabetes.
Lucentis was developed by Genentech and Novartis. Genentech has the commercial rights to Lucentis in the United States where Lucentis is also approved for the treatment of macular edema following retinal vein occlusion (RVO). In addition, Genentech is conducting two Phase III studies, RISE and RIDE, in patients with diabetic macular edema. The results are expected in 2011. Novartis has exclusive rights in the rest of the world and plans to file in the European Union for approval of Lucentis for the treatment of visual impairment due to macular edema following RVO.
Disclaimer
The foregoing release contains forward-looking statements that can be identified by terminology such as "recommended," "plans," or similar expressions, or by express or implied discussions regarding potential new indications or labeling for Lucentis or regarding potential future revenues from Lucentis. You should not place undue reliance on these statements. Such forward-looking statements reflect the current views of management regarding future events, and involve known and unknown risks, uncertainties and other factors that may cause actual results with Lucentis to be materially different from any future results, performance or achievements expressed or implied by such statements. There can be no guarantee that Lucentis will be submitted or approved for any additional indications or labeling in any market. Nor can there be any guarantee that Lucentis will achieve any particular levels of revenue in the future. In particular, management's expectations regarding Lucentis could be affected by, among other things, unexpected clinical trial results, including unexpected new clinical data and unexpected additional analysis of existing clinical data; unexpected regulatory actions or delays or government regulation generally; competition in general; government, industry and general public pricing pressures; the company's ability to obtain or maintain patent or other proprietary intellectual property protection; the impact that the foregoing factors could have on the values attributed to the Novartis Group's assets and liabilities as recorded in the Group's consolidated balance sheet, and other risks and factors referred to in Novartis AG's current Form 20-F on file with the US Securities and Exchange Commission. Should one or more of these risks or uncertainties materialize, or should underlying assumptions prove incorrect, actual results may vary materially from those anticipated, believed, estimated or expected. Novartis is providing the information in this press release as of this date and does not undertake any obligation to update any forward-looking statements contained in this press release as a result of new information, future events or otherwise.
Saturday, October 23, 2010
Sunday, October 17, 2010
Complement inhibition may be the future of dry AMD therapy
CHICAGO — Ongoing clinical trials exploring the use of complement inhibitors for treating nonexudative age-related macular degeneration offer promise for a disease state that has long been considered difficult to treat.
A number of recent studies have implicated the complement immune system in AMD. However, nonexudative AMD remains a "uniquely human disease," and, therefore, no animal model exists in which to prove potential therapeutic strategies, Philip J. Rosenfeld, MD, PhD, said here are Retina Subspecialty day preceding the joint meeting of the American Academy of Ophthalmology and the Middle East Africa Council of Ophthalmology.
As a result, Dr. Rosenfeld said, human trials will prove important in determining whether complement inhibition is of any real clinical benefit.
Several such trials are already underway. Alcon is currently investigating its POT-4 (AL-78898A) anti-C3 cyclic peptide in human trials. There is some evidence that POT-4 may also affect VEGF expression in the retina, Dr. Rosenfeld said.
Separately, Genetech/Roche has an anti-factor D (FCFD4514S) that inhibits the C3 and C5 alternative pathway convertases. Phase 1 studies have been successfully completed with that agent, Dr. Rosenfeld said.
Two separate C5 inhibitors are being studied: Eculizumab/Sollris (Alexion) and ARC1905, an anti-C5 aptamer (Ophthotech).
"One of the advantages is that while you block the downstream activated species, you preserve the more proximal species that are important for the clearance of bacteria, particularly the encapsulated organisms," Dr. Rosenfeld said.
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A number of recent studies have implicated the complement immune system in AMD. However, nonexudative AMD remains a "uniquely human disease," and, therefore, no animal model exists in which to prove potential therapeutic strategies, Philip J. Rosenfeld, MD, PhD, said here are Retina Subspecialty day preceding the joint meeting of the American Academy of Ophthalmology and the Middle East Africa Council of Ophthalmology.
As a result, Dr. Rosenfeld said, human trials will prove important in determining whether complement inhibition is of any real clinical benefit.
Several such trials are already underway. Alcon is currently investigating its POT-4 (AL-78898A) anti-C3 cyclic peptide in human trials. There is some evidence that POT-4 may also affect VEGF expression in the retina, Dr. Rosenfeld said.
Separately, Genetech/Roche has an anti-factor D (FCFD4514S) that inhibits the C3 and C5 alternative pathway convertases. Phase 1 studies have been successfully completed with that agent, Dr. Rosenfeld said.
Two separate C5 inhibitors are being studied: Eculizumab/Sollris (Alexion) and ARC1905, an anti-C5 aptamer (Ophthotech).
"One of the advantages is that while you block the downstream activated species, you preserve the more proximal species that are important for the clearance of bacteria, particularly the encapsulated organisms," Dr. Rosenfeld said.
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Sunday, October 10, 2010
Angiogenesis Discovery Points to Novel Therapy for Multiple Diseases
Tatiana Byzova, PhD, a faculty member in Lerner Research Institute's Department of Molecular Cardiology and Director of the Center for Angiogenesis Research, and colleagues have discovered a fundamental biological pathway in angiogenesis (formation of blood vessels), published online October 3, 2010 in Nature (DOI: 10.1038/nature09421). The significance of this discovery is summarized by Dr. Byzova, in that "it affects many biological processes - from wound healing to aging."
Some pathologies included in that spectrum are age-related macular degeneration, atherosclerosis, and rheumatoid arthritis, while their published data indicate a particularly notable role in cancer. The results of this advanced understanding point to an exciting new approach for novel therapies.
In 1989, a protein called vascular endothelial growth factor (VEGF) was identified as a trigger of angiogenesis. This discovery led Genentech to develop the first effective treatment for macular degeneration; related work contributed to the development of a drug to block VEGF function in cancer, essentially starving the tumor of the nutrients the blood would otherwise bring.
However, although many tumors respond to anti-VEGF treatment, most develop resistance to the therapy and continue to survive over time. One possible explanation is that VEGF is not the only trigger leading to angiogenesis. This is precisely what Dr. Byzova's team has found.
Dr. Byzova's research has identified a class of oxidized lipids that are abundantly present in highly vasculated tumors. Further interrogation parsed out the process through which these products induce new blood vessel formation. It appears that cells use a family of receptors previously known to recognize foreign products such as bacteria to sense and respond to the danger of oxidation. The results point to a novel therapy that may well be an alternate way to starve the tumors that have managed to survive despite VEGF inhibition. Through uncovering a potential way to get around tumor resistance to VEGF, Dr. Byzova's group has opened up new doors for developing treatments for cancer. The fundamental discovery also provides substantial insight for novel treatments for other diseases that involve inflammation, oxidative stress, and angiogenesis.
Overall, this foundational discovery of a novel mechanism of angiogenesis comes just one year after Dr. Byzova headed a study that pioneered the identification of a new genetic-based human disease, published in Nature Medicine.
Some pathologies included in that spectrum are age-related macular degeneration, atherosclerosis, and rheumatoid arthritis, while their published data indicate a particularly notable role in cancer. The results of this advanced understanding point to an exciting new approach for novel therapies.
In 1989, a protein called vascular endothelial growth factor (VEGF) was identified as a trigger of angiogenesis. This discovery led Genentech to develop the first effective treatment for macular degeneration; related work contributed to the development of a drug to block VEGF function in cancer, essentially starving the tumor of the nutrients the blood would otherwise bring.
However, although many tumors respond to anti-VEGF treatment, most develop resistance to the therapy and continue to survive over time. One possible explanation is that VEGF is not the only trigger leading to angiogenesis. This is precisely what Dr. Byzova's team has found.
Dr. Byzova's research has identified a class of oxidized lipids that are abundantly present in highly vasculated tumors. Further interrogation parsed out the process through which these products induce new blood vessel formation. It appears that cells use a family of receptors previously known to recognize foreign products such as bacteria to sense and respond to the danger of oxidation. The results point to a novel therapy that may well be an alternate way to starve the tumors that have managed to survive despite VEGF inhibition. Through uncovering a potential way to get around tumor resistance to VEGF, Dr. Byzova's group has opened up new doors for developing treatments for cancer. The fundamental discovery also provides substantial insight for novel treatments for other diseases that involve inflammation, oxidative stress, and angiogenesis.
Overall, this foundational discovery of a novel mechanism of angiogenesis comes just one year after Dr. Byzova headed a study that pioneered the identification of a new genetic-based human disease, published in Nature Medicine.
Monday, October 4, 2010
Retinal Degeneration Can be Prevented with Nanotechnology Gene Therapy
Friday, 01 October 2010
Researchers from Tufts University published results from a study showing vision-saving gene therapy to the eyes can be delivered via nanotechnology. A protein called Glial Cell Line-Derived Neurtrophic Factor (GDNF) can protect the eyes from diseases of the retina, such as and retinitis pigmentosa.
The previous method for delivering genetic material with a virus had several problems and side effects. Although the study is in its infancy, and the results are temporary, mice injected with the GDNF carrying nanoparticle had a 3.9 to 7.7-fold reduction in damage to the retina. Seven days after treatment, the GDNF-nanoparticle treated mice had up to 39% better eyesight than mice in the control group.
Two weeks after the treatment, GDNF-nanoparticle-injected mice had nuclear layers of the retina that were almost 24 to over 39 percent thicker than control mice. However, after 14 days, these advantages seem to have vanished. According to Dr. Brett Katzen, "The idea of using gene therapy to help cure - or at least improve - the eyesight of patients with macular degeneration should be exciting to eye doctors everywhere. This is a great first step." The research shows an incredible potential for nanotechnology to develop an effective carrier for delivering gene therapy.
This therapy can then lead to a new generation of treatments for retinal diseases. Age-related macular degeneration is the leading cause of blindness in Americans over the age of 65.
Researchers from Tufts University published results from a study showing vision-saving gene therapy to the eyes can be delivered via nanotechnology. A protein called Glial Cell Line-Derived Neurtrophic Factor (GDNF) can protect the eyes from diseases of the retina, such as and retinitis pigmentosa.
The previous method for delivering genetic material with a virus had several problems and side effects. Although the study is in its infancy, and the results are temporary, mice injected with the GDNF carrying nanoparticle had a 3.9 to 7.7-fold reduction in damage to the retina. Seven days after treatment, the GDNF-nanoparticle treated mice had up to 39% better eyesight than mice in the control group.
Two weeks after the treatment, GDNF-nanoparticle-injected mice had nuclear layers of the retina that were almost 24 to over 39 percent thicker than control mice. However, after 14 days, these advantages seem to have vanished. According to Dr. Brett Katzen, "The idea of using gene therapy to help cure - or at least improve - the eyesight of patients with macular degeneration should be exciting to eye doctors everywhere. This is a great first step." The research shows an incredible potential for nanotechnology to develop an effective carrier for delivering gene therapy.
This therapy can then lead to a new generation of treatments for retinal diseases. Age-related macular degeneration is the leading cause of blindness in Americans over the age of 65.
Saturday, September 18, 2010
Glaucoma eye drops showing some effect against Macular Degeneration
by Dr. Edward Paul
Eye redness was the clue that something was happening to Celia Ramirez's vision. Although she wasn't having trouble driving or doing other tasks, her children urged her to have a checkup. It turned out she was in the early stages of age-related macular degeneration (AMD), a disease that attacks a person's central field of vision.
Mrs. Ramirez, who lives in the Rio Grande Valley, had surgery that successfully controlled her eye pressure, but her central vision continued to degrade.Eye specialist William Sponsel, Ph.D., associate professor and director of research at the Department of Ophthalmology at the University of Texas Health Science Center at San Antonio (UTHSC).Found a treatment with a new combination of drugs.
The miracle is the carbon dioxide, which is crucial for vision. The healthy eye produces enough carbon dioxide to dilate blood vessels around the retina and maintain proper blood flow. The ailing eye does not produce enough. This holds important implications for the treatment of patients with blinding eye diseases such as AMD and glaucoma, which are marked by diminished circulation of blood in the back of the eye. Eye pressure also is a conventional barometer of eye health.
About 60 of 65 patients have seen their vision improve while receiving treatment at UTHSC's teaching hospital, University Hospital. "The patients are receiving combination drug therapy, including agents that trick the eye into retaining more of its carbon dioxide," Dr. Sponsel said. "We have patients with glaucoma and no AMD, patients with AMD and no glaucoma, and patients with both disorders. All appear to demonstrate benefit in the central visual area, regardless of the cause of that visual loss."
The Health Science Center is the first medical center to initiate this combination therapy for patients with central visual loss, Dr. Sponsel said. Considerable research yielded the conclusions that now help patients. "You don't expect these patients to get better, you expect them to get worse," he said. "We have seen dramatic results that bode well for treatment of these disorders in the future."
The researchers measure patients' sensitivity to light on visual function tests. An increase of 10 points represents more than a million-fold increase in actual visual acuity. Mrs. Ramirez's vision in the macula -- the central visual area that enables perception of letters and colors -- was scored as virtually zero on early tests. After the recent treatment, her score is now 24.
The miracle agents are called "carbonic anhydrase inhibitors" (CAI's). Given as eye drops, CAI's reach the back of the eye rapidly and slow the clearance of carbon dioxide while increasing the supply of nutrients. They help dilate blood vessels within and behind the retina, which is the structure that receives, processes and transmits visual images relayed from the brain.
Dr. Sponsel pursued this line of research in an intriguing way -- after discovering that adults who hyperventilated and rapidly blew off their body's carbon dioxide showed decreased vision, eye pressure and circulation in the back of the eye. He was treating subjects one week with a CAI called dorzolamide and the next week with placebo eye drops. During hyperventilation, the subjects on dorzolamide maintained good light sensitivity in their central field of vision, while the same subjects during placebo treatment showed central visual loss. Dr. Sponsel holds two U.S. patents on this work. One valuable aspect of the research is that it proves increased eye pressure is not necessarily the definitive indicator of eye vessel disease.
Eye redness was the clue that something was happening to Celia Ramirez's vision. Although she wasn't having trouble driving or doing other tasks, her children urged her to have a checkup. It turned out she was in the early stages of age-related macular degeneration (AMD), a disease that attacks a person's central field of vision.
Mrs. Ramirez, who lives in the Rio Grande Valley, had surgery that successfully controlled her eye pressure, but her central vision continued to degrade.Eye specialist William Sponsel, Ph.D., associate professor and director of research at the Department of Ophthalmology at the University of Texas Health Science Center at San Antonio (UTHSC).Found a treatment with a new combination of drugs.
The miracle is the carbon dioxide, which is crucial for vision. The healthy eye produces enough carbon dioxide to dilate blood vessels around the retina and maintain proper blood flow. The ailing eye does not produce enough. This holds important implications for the treatment of patients with blinding eye diseases such as AMD and glaucoma, which are marked by diminished circulation of blood in the back of the eye. Eye pressure also is a conventional barometer of eye health.
About 60 of 65 patients have seen their vision improve while receiving treatment at UTHSC's teaching hospital, University Hospital. "The patients are receiving combination drug therapy, including agents that trick the eye into retaining more of its carbon dioxide," Dr. Sponsel said. "We have patients with glaucoma and no AMD, patients with AMD and no glaucoma, and patients with both disorders. All appear to demonstrate benefit in the central visual area, regardless of the cause of that visual loss."
The Health Science Center is the first medical center to initiate this combination therapy for patients with central visual loss, Dr. Sponsel said. Considerable research yielded the conclusions that now help patients. "You don't expect these patients to get better, you expect them to get worse," he said. "We have seen dramatic results that bode well for treatment of these disorders in the future."
The researchers measure patients' sensitivity to light on visual function tests. An increase of 10 points represents more than a million-fold increase in actual visual acuity. Mrs. Ramirez's vision in the macula -- the central visual area that enables perception of letters and colors -- was scored as virtually zero on early tests. After the recent treatment, her score is now 24.
The miracle agents are called "carbonic anhydrase inhibitors" (CAI's). Given as eye drops, CAI's reach the back of the eye rapidly and slow the clearance of carbon dioxide while increasing the supply of nutrients. They help dilate blood vessels within and behind the retina, which is the structure that receives, processes and transmits visual images relayed from the brain.
Dr. Sponsel pursued this line of research in an intriguing way -- after discovering that adults who hyperventilated and rapidly blew off their body's carbon dioxide showed decreased vision, eye pressure and circulation in the back of the eye. He was treating subjects one week with a CAI called dorzolamide and the next week with placebo eye drops. During hyperventilation, the subjects on dorzolamide maintained good light sensitivity in their central field of vision, while the same subjects during placebo treatment showed central visual loss. Dr. Sponsel holds two U.S. patents on this work. One valuable aspect of the research is that it proves increased eye pressure is not necessarily the definitive indicator of eye vessel disease.
Monday, September 13, 2010
Macular Degeneration and your eyesight
You have most probably heard of this very common condition that damages your eyesight as you age. Because this condition affects more elderly people it is often referred to as age-related macular degeneration. Unfortunately there is no cure available for this condition however there are treatments that can help. This blog outlines the latest in research and treatments regarding macular degeneration and aims to help you make the most out of your eyesight in the mean time.
Now macular degeneration as the name implies affects the macula, which is an area right at the back of the eye on a structure that detects light known as the retina. Your macula is the part of the retina that allows you to see things in great detail. In fact many birds have better maculas than us, as they need to see things in great detail from up in the air. The condition of macula degeneration implies that the macula is damaged and as this damage becomes more extensive your eyesight will be affected. There are two types of macula degeneration and they are known as the wet or the dry type, the most common of the two is ‘dry’ maculae degeneration. In this type you get little yellow patches that pop up around your macula and your vision slowly worsens. In ‘wet’ macula degeneration there are tiny blood vessels in the back of your eye that grow and then leak out blood and other fluid. This tends to make ones vision worse more quickly and you should note that dry degeneration can turn into the wet kind.
Those who present with this condition for the most part have difficulty reading, making out fine detail and even have trouble recognizing friends and families faces. After a few years of having this condition things that are in the middle of your vision will begin to look blurred and you may struggle to make things out. After a while the middle of your vision may just appear black and you often cant see anything in this area, this means that you will be unable to see things that are right in front of you. However your peripheral vision will not be affected.
There are things that you can do to cope with this condition as well as medicines that can help. Your doctor may teach you how to make better use of your peripheral vision and tell you that using bright lighting in your home will help you see better. You may also need to make text on the computer screen bigger and use magnifying glasses when reading a book. Most of the medical treatments are aimed at the treatment of wet macular degeneration and in fact there are not many effective treatments for the dry variety. Laser therapy can be used to stop the macular degeneration from getting worse in the sense that these lasers burn away those yellow patches that form around the macular early in the disease course. Also there is no need to worry as laser therapy is not painful and is quite quick, however the evidence supporting this form of treatment is not great at this stage. In fact some research suggests that laser treatment can cause new blood vessels to from on the back of the eye that can make your sight worse.
Mineral and vitamin supplements may be useful in slowing down or stopping macula degeneration from occurring. You should take zinc, vitamin E and C as well as beta-carotene. Remember here that you will need to take them for a long time and in high doses to be affective and remember that these are not without their side effects. Some people find that they have problems with passing urine, others complain of stomach pains and some people notice that their skin turns a little yellow. If this is that case with you then you should stop taking the tablets and visit your doctor.
Wet macular degeneration can be treated with photodynamic laser surgery whereby a dye that is sensitive to light is injected into your bloodstream and then a laser is shone into your eye. The dye that was injected into the blood helps the laser to destroy all of those leaky blood vessels that are damaging your eye. This method has mixed reviews on effectiveness and one should have a good discussion with their doctor regarding the risks and benefits of this procedure before having it done.
There is another type of laser that can be used to destroy the blood vessels in the eye that leak, but this is only affective in a few people with very severe disease. There is a chance with this procedure that the blood vessels will grow back anyway and the laser can sometimes damage the eye. Radiotherapy is another option but lacks suitable research to say whether or not it works and we always worry that radiation may damage other parts of the eye.
There is an injection that you can have in your eyeball called pegaptanib, however for obvious reasons not many people like the idea of this if they can help it. Also you have to have two injections every month and the evidence is not great that it works wonders, although there are some convincing studies. There is another injection called ranibizumab that you get in your eyeball and this also does not have great results but is indicated in people with wet macular degeneration that is getting worse.
So the most important thing is what will happen to you and in this case the outcome is not fantastic. Over many years your vision will gradually get worse and it will be much worse in the centre of your vision than in the peripheries and you are unlikely to go completely blind. Unfortunately we don’t know how quickly things will turn bad and each patient is different, but most people manage to get around even with severe disease as they are able to use their peripheral vision much more effectively.
Now macular degeneration as the name implies affects the macula, which is an area right at the back of the eye on a structure that detects light known as the retina. Your macula is the part of the retina that allows you to see things in great detail. In fact many birds have better maculas than us, as they need to see things in great detail from up in the air. The condition of macula degeneration implies that the macula is damaged and as this damage becomes more extensive your eyesight will be affected. There are two types of macula degeneration and they are known as the wet or the dry type, the most common of the two is ‘dry’ maculae degeneration. In this type you get little yellow patches that pop up around your macula and your vision slowly worsens. In ‘wet’ macula degeneration there are tiny blood vessels in the back of your eye that grow and then leak out blood and other fluid. This tends to make ones vision worse more quickly and you should note that dry degeneration can turn into the wet kind.
Those who present with this condition for the most part have difficulty reading, making out fine detail and even have trouble recognizing friends and families faces. After a few years of having this condition things that are in the middle of your vision will begin to look blurred and you may struggle to make things out. After a while the middle of your vision may just appear black and you often cant see anything in this area, this means that you will be unable to see things that are right in front of you. However your peripheral vision will not be affected.
There are things that you can do to cope with this condition as well as medicines that can help. Your doctor may teach you how to make better use of your peripheral vision and tell you that using bright lighting in your home will help you see better. You may also need to make text on the computer screen bigger and use magnifying glasses when reading a book. Most of the medical treatments are aimed at the treatment of wet macular degeneration and in fact there are not many effective treatments for the dry variety. Laser therapy can be used to stop the macular degeneration from getting worse in the sense that these lasers burn away those yellow patches that form around the macular early in the disease course. Also there is no need to worry as laser therapy is not painful and is quite quick, however the evidence supporting this form of treatment is not great at this stage. In fact some research suggests that laser treatment can cause new blood vessels to from on the back of the eye that can make your sight worse.
Mineral and vitamin supplements may be useful in slowing down or stopping macula degeneration from occurring. You should take zinc, vitamin E and C as well as beta-carotene. Remember here that you will need to take them for a long time and in high doses to be affective and remember that these are not without their side effects. Some people find that they have problems with passing urine, others complain of stomach pains and some people notice that their skin turns a little yellow. If this is that case with you then you should stop taking the tablets and visit your doctor.
Wet macular degeneration can be treated with photodynamic laser surgery whereby a dye that is sensitive to light is injected into your bloodstream and then a laser is shone into your eye. The dye that was injected into the blood helps the laser to destroy all of those leaky blood vessels that are damaging your eye. This method has mixed reviews on effectiveness and one should have a good discussion with their doctor regarding the risks and benefits of this procedure before having it done.
There is another type of laser that can be used to destroy the blood vessels in the eye that leak, but this is only affective in a few people with very severe disease. There is a chance with this procedure that the blood vessels will grow back anyway and the laser can sometimes damage the eye. Radiotherapy is another option but lacks suitable research to say whether or not it works and we always worry that radiation may damage other parts of the eye.
There is an injection that you can have in your eyeball called pegaptanib, however for obvious reasons not many people like the idea of this if they can help it. Also you have to have two injections every month and the evidence is not great that it works wonders, although there are some convincing studies. There is another injection called ranibizumab that you get in your eyeball and this also does not have great results but is indicated in people with wet macular degeneration that is getting worse.
So the most important thing is what will happen to you and in this case the outcome is not fantastic. Over many years your vision will gradually get worse and it will be much worse in the centre of your vision than in the peripheries and you are unlikely to go completely blind. Unfortunately we don’t know how quickly things will turn bad and each patient is different, but most people manage to get around even with severe disease as they are able to use their peripheral vision much more effectively.
Wednesday, September 1, 2010
FDA grants pSivida, Alimera expedited review for macular degeneration therapy
FDA grants pSivida, Alimera expedited review for macular degeneration therapy
August 31, 2010 by MassDevice staff
pSivida Corp. and Alimera Sciences win priority review status for their Iluvien drug/device combination, designed to treat diabetic macular degeneration.
PSDV, ALIM logos
The Food & Drug Administration put pSivida Corp. (NSDQ:PSDV) and Alimera Sciences Inc. (NSDQ:ALIM) on the fast track, granting an expedited review for their drug/device combination designed to treat diabetic macular edema.
Watertown, Mass.-based pSivida and Alpharetta, Ga.-based Alimera filed a new drug application with the FDA in June for Iluvien, a sustained release drug delivery system that delivers flucocinolone acetonide, a steroid, for the treatment of DME.
The federal watchdog agency granted priority review status to the application, moving the goal for finishing the review from 10 months back to six months.
That means a response could drop during the fourth quarter, pSivida president and CEO Dr. Paul Ashton said in prepared remarks, adding that FDA approval would trigger a $25 million milestone payment from Alimera.
The milestone payment wouldn't be the first time Alimera ponied up for pSivida. Its $72 million IPO in April triggered the repayment of a $15 million loan and $225,000 in interest. The companies are seeking European approval for Iluvien. If it makes it to market, pSivida will collect 20 percent of the net profits.
The FDA has already cleared a pair of pSivida products: Retisert, for the treatment of posterior uveitis, and Vitrasert for the treatment of AIDS-related cytomegalovirus retinitis. Both are licensed to Bausch & Lomb Inc. The company is also developing other ophthalmic products with Pfizer Inc. (NYSE:PFE), its largest shareholder, and has products of its own in the pipeline outside of ophthalmology, according to a press release.
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August 31, 2010 by MassDevice staff
pSivida Corp. and Alimera Sciences win priority review status for their Iluvien drug/device combination, designed to treat diabetic macular degeneration.
PSDV, ALIM logos
The Food & Drug Administration put pSivida Corp. (NSDQ:PSDV) and Alimera Sciences Inc. (NSDQ:ALIM) on the fast track, granting an expedited review for their drug/device combination designed to treat diabetic macular edema.
Watertown, Mass.-based pSivida and Alpharetta, Ga.-based Alimera filed a new drug application with the FDA in June for Iluvien, a sustained release drug delivery system that delivers flucocinolone acetonide, a steroid, for the treatment of DME.
The federal watchdog agency granted priority review status to the application, moving the goal for finishing the review from 10 months back to six months.
That means a response could drop during the fourth quarter, pSivida president and CEO Dr. Paul Ashton said in prepared remarks, adding that FDA approval would trigger a $25 million milestone payment from Alimera.
The milestone payment wouldn't be the first time Alimera ponied up for pSivida. Its $72 million IPO in April triggered the repayment of a $15 million loan and $225,000 in interest. The companies are seeking European approval for Iluvien. If it makes it to market, pSivida will collect 20 percent of the net profits.
The FDA has already cleared a pair of pSivida products: Retisert, for the treatment of posterior uveitis, and Vitrasert for the treatment of AIDS-related cytomegalovirus retinitis. Both are licensed to Bausch & Lomb Inc. The company is also developing other ophthalmic products with Pfizer Inc. (NYSE:PFE), its largest shareholder, and has products of its own in the pipeline outside of ophthalmology, according to a press release.
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