Human cells may not be unlike electric batteries. They from time to time have small energy retailers or can’t hold vigor. Micro Present-day Stimulation Remedy provides your cells with all the “energy” it takes, similar in order to recharging a new battery. Studies in addition have shown this MCS Remedy increases microcirculatory circulation, increases ATP concentrations plus stimulates amino acidity and source of nourishment concentrations directly into cells.
Every located cell inside body has a power charge. It is theorized that a part of what creates macular degeneration is usually a loss with the energy source inside cell, or losing the electrical charge. As being a flashlight will not likely work without getting a charged battery pack, the photoreceptors inside retina will not likely function not having an energy source. MCS Remedy is shown to increase the energy source within your cell.
This Macular Degeneration Foundation identified in starting pre-clinical trials by groundbreaking ophthalmologists plus researchers this micro present-day stimulation therapy can boost visual acuity, sharpness plus color perception in 68 percentage of individuals with dry out macular weakening and 58 percent of those with your wet kind. Reports from Russia advocate similar benefits.
A review published by way of Dr. Merrell J. Allen plus Dr. Leland N. Michael eligible Nutritional By using supplements, Electrical Excitement and Age Related Macular Degeneration showed this 60 percentage of individuals showed much better in visible acuity following combining micro present-day stimulation therapy and natural supplementation.
Drs. Leeway Halloran plus August L. Viewer studied 25 individuals declared with generally untreatable vision diseases including macular weakening, retinitis pigmentosa, CMV-retinitis, plus diabetic retinopathy. The individuals were handled with combining micro present-day stimulation therapy and natural supplementation. Overall final results showed outstanding increase with visual job in visible acuity in many and plainly established your safety with the combination of MCS therapy and natural supplementation.
Showing posts with label optics. Show all posts
Showing posts with label optics. Show all posts
Friday, January 28, 2011
Sunday, January 23, 2011
Sustained-release implants on track for retinal vascular disease treatment
by:Elias Reichel
KAANAPALI, Hawaii — Sustained-release corticosteroids will play a significant role in retinal vascular disease, but the current implants still need improvements, one presenter here said.
"It is important to realize [steroids] will have a continued role in our treatment of diseases. They may also serve for adjunctive [therapies] like stem cell treatments and [instances] where transplantation or immunoreactions may occur," Elias Reichel, MD, who discussed outcomes using Ozurdex (dexamethasone intravitreal implant, Allergan) and Iluvien (fluocinolone acetonide intravitreal implant, Alimera), said at Retina 2011. "So, having a better delivery system for corticosteroids is very useful for many of the diseases we are seeing in our offices."
Challenges include needing to achieve and maintain clinically effective concentrations in the vitreous over time while maximizing efficacy and minimizing adverse effects, Dr. Reichel said.
As part of a 6-month study, the dexamethasone implant demonstrated 2- to 3-month peak efficacy, had a low incidence of IOP issues and conferred a cataract progression of approximately 5%. Additionally, 45% of the patients gained three lines of visual acuity, Dr. Reichel said.
The U.S. Food and Drug Administration has approved the device for all retinal venous obstructive disease.
The fluocinolone implant is now part of a 36-month study and has demonstrated efficacy to at least 30 months. Between 30% and 40% of patients gained at least three lines of visual acuity. However, the device has a moderately higher risk of IOP issues and a cataract progression rate of 50%, according to Dr. Reichel.
The device has received a complete response letter from the FDA.
"Current formulations that we have are good but can be better," Dr. Reichel said. "We really have to look at longer duration and this reduced risk trade-off."
* Disclosure: Dr. Reichel is a consultant to Alimera and Allergan.
KAANAPALI, Hawaii — Sustained-release corticosteroids will play a significant role in retinal vascular disease, but the current implants still need improvements, one presenter here said.
"It is important to realize [steroids] will have a continued role in our treatment of diseases. They may also serve for adjunctive [therapies] like stem cell treatments and [instances] where transplantation or immunoreactions may occur," Elias Reichel, MD, who discussed outcomes using Ozurdex (dexamethasone intravitreal implant, Allergan) and Iluvien (fluocinolone acetonide intravitreal implant, Alimera), said at Retina 2011. "So, having a better delivery system for corticosteroids is very useful for many of the diseases we are seeing in our offices."
Challenges include needing to achieve and maintain clinically effective concentrations in the vitreous over time while maximizing efficacy and minimizing adverse effects, Dr. Reichel said.
As part of a 6-month study, the dexamethasone implant demonstrated 2- to 3-month peak efficacy, had a low incidence of IOP issues and conferred a cataract progression of approximately 5%. Additionally, 45% of the patients gained three lines of visual acuity, Dr. Reichel said.
The U.S. Food and Drug Administration has approved the device for all retinal venous obstructive disease.
The fluocinolone implant is now part of a 36-month study and has demonstrated efficacy to at least 30 months. Between 30% and 40% of patients gained at least three lines of visual acuity. However, the device has a moderately higher risk of IOP issues and a cataract progression rate of 50%, according to Dr. Reichel.
The device has received a complete response letter from the FDA.
"Current formulations that we have are good but can be better," Dr. Reichel said. "We really have to look at longer duration and this reduced risk trade-off."
* Disclosure: Dr. Reichel is a consultant to Alimera and Allergan.
Sunday, January 2, 2011
Genetic Testing for AMD is here Today
By; Diana Shechtman OD FAAO & Steven Ferrucci OD FAAO
Age-Related macular degeneration (AMD) is a progressive disease and the leading cause of vision loss among the elderly, affecting central vision required for daily activities such as driving and reading. There are a number of factors affecting AMD, such as advanced age, smoking, UV exposure, overall health (that contribute to high blood pressure, obesity, diet) and family history. Many factors may be modified and yet others like genetics cannot. Although AMD may seem to be hereditary in some families and not others, genetics have been shown to contribute significantly to the disease. Multiple twin and sibling studies have collaborated to the familial nature of the disease. First-degree relatives of patients with AMD are at a significantly increased risk for the disease. Furthermore, large epidemiological studies have suggested a strong genetic risk factor for AMD. In fact, the risk of developing AMD increases 4 fold among patients with a positive family history. In 2005 a breakthrough occurred in the area of genetic research and AMD; Klein and associates discovered a strong link between AMD and certain genetic variants. Similarly, numerous other genes have been implicated in AMD, which may increase the risk of AMD up to 70%.
Until recently there was no test to help determined patient’s inherited risk for AMD. Today, Macula Risk (ArcticDX, Toronto, Ontario) is a genetic test specifically designed to determine genetic predisposition to AMD and vision loss attributed to the more advanced stage of the disease.
Macula Risk genetic test separates individuals into one of 5 macula risk (MR) categories, with MR 3 through 5 representing an increased risk for the more advance stage of the disease. This accounts for approximately 20% of the general population. MR1 has less than a 5% risk of the advanced stage of the disease, while MR 5 carries greater than 55% risk. These results can aid the doctor in devising a specific management plan and follow-up protocol in order to reassure early intervention to prevent vision loss.
The test only requires a simple in-office cheek swab, which is sent directly to the genetic lab. The report includes test results and written genetic support information (including access to genetic counseling). Macula Risk genetic testing is covered by most insurance providers, including Medicare, as long as the specific diagnosis (ICD-9) are identified by the doctor. The prognostic genetic test is intended for patients who have a diagnosis of early or intermediate AMD. Thus, the “at risk patient,” would have to pay a fee for the test.
Despite our best efforts and new treatment options available today, many people are still losing vision from AMD. New advancements in the area of AMD are becoming an integral part in preventing future visual deterioration. AMD is affected by both environmental and genetic factors that interact with one another to determine prevalence and progression of the disease. Furthermore, at this time we do not know all of the genes linked to AMD. Hence, genetic testing in the area of AMD is only a risk indicator and cannot predict “without a shadow of a doubt,” which patients will and which will not develop the disease. However, this test provides a genetic profile screening to help identify those at risk as well as aids in tailoring a distinct management approach for those with the disease. With various researches devoted to treatment options for AMD, genetic testing in the area of AMD is at the frontier of providing crucial information.
REFERENCES
1. Swaroop, Branham KE, Chen W, Abecasis G. Genetic susceptibility to age-related macular degeneration: a paradigm for dissecting complex disease traits. Hum Mol Genet 2007; 16: 174-82.
2. Klein ML, Mauldin WM, Stoumbos VD. Heredity and age-related macular degeneration. Observations in monozygotic twins. Arch Ophthalmol. 1994; 112: 932-7.
3. Meyers SM, Greene T, Gutman FA. A twin study of age-related macular degeneration. Am J Ophthalmol. 1995; 120: 757-66.
4. Heiba IM, Elston RC, Klein BE, et al. Sibling correlations and segregation analysis of age-related maculopathy: The Beaver Dam Eye Study. Genet Epidemiol. 1994; 11: 51-67.
5. Klaver CC, Wolfs RC, Assink JJ, et al. Genetic risk of age-related maculopathy. Population-based familial aggregation study. Arch Ophthalmol. 1998; 116: 1646-51.
6. Seddon JM, Ajani UA, Mitchell BD. Familial aggregation of age-related maculopathy. Am J Ophthalmol. 1997; 123: 199-206.
7. Klein RJ, Zeiss C, Chew EY, et al. Complement Factor H Polymorphism in Age-Related Macular Degeneration. Science 2005; 308: 385-389.
8. Seddon JM, Reynolds R, Maller J, Fagerness JA, Daly MJ, Rosner B. Prediction model for prevalence and incidence of advanced age-related macular degeneration based on genetic, demographic, and environmental variables. Invest Ophthalmol Vis Sci 2009; 50 (65): 2044-53.
9. www.macularisk.com/en/physicians/order.html (accessed Dec. 14th , 2010)
Age-Related macular degeneration (AMD) is a progressive disease and the leading cause of vision loss among the elderly, affecting central vision required for daily activities such as driving and reading. There are a number of factors affecting AMD, such as advanced age, smoking, UV exposure, overall health (that contribute to high blood pressure, obesity, diet) and family history. Many factors may be modified and yet others like genetics cannot. Although AMD may seem to be hereditary in some families and not others, genetics have been shown to contribute significantly to the disease. Multiple twin and sibling studies have collaborated to the familial nature of the disease. First-degree relatives of patients with AMD are at a significantly increased risk for the disease. Furthermore, large epidemiological studies have suggested a strong genetic risk factor for AMD. In fact, the risk of developing AMD increases 4 fold among patients with a positive family history. In 2005 a breakthrough occurred in the area of genetic research and AMD; Klein and associates discovered a strong link between AMD and certain genetic variants. Similarly, numerous other genes have been implicated in AMD, which may increase the risk of AMD up to 70%.
Until recently there was no test to help determined patient’s inherited risk for AMD. Today, Macula Risk (ArcticDX, Toronto, Ontario) is a genetic test specifically designed to determine genetic predisposition to AMD and vision loss attributed to the more advanced stage of the disease.
Macula Risk genetic test separates individuals into one of 5 macula risk (MR) categories, with MR 3 through 5 representing an increased risk for the more advance stage of the disease. This accounts for approximately 20% of the general population. MR1 has less than a 5% risk of the advanced stage of the disease, while MR 5 carries greater than 55% risk. These results can aid the doctor in devising a specific management plan and follow-up protocol in order to reassure early intervention to prevent vision loss.
The test only requires a simple in-office cheek swab, which is sent directly to the genetic lab. The report includes test results and written genetic support information (including access to genetic counseling). Macula Risk genetic testing is covered by most insurance providers, including Medicare, as long as the specific diagnosis (ICD-9) are identified by the doctor. The prognostic genetic test is intended for patients who have a diagnosis of early or intermediate AMD. Thus, the “at risk patient,” would have to pay a fee for the test.
Despite our best efforts and new treatment options available today, many people are still losing vision from AMD. New advancements in the area of AMD are becoming an integral part in preventing future visual deterioration. AMD is affected by both environmental and genetic factors that interact with one another to determine prevalence and progression of the disease. Furthermore, at this time we do not know all of the genes linked to AMD. Hence, genetic testing in the area of AMD is only a risk indicator and cannot predict “without a shadow of a doubt,” which patients will and which will not develop the disease. However, this test provides a genetic profile screening to help identify those at risk as well as aids in tailoring a distinct management approach for those with the disease. With various researches devoted to treatment options for AMD, genetic testing in the area of AMD is at the frontier of providing crucial information.
REFERENCES
1. Swaroop, Branham KE, Chen W, Abecasis G. Genetic susceptibility to age-related macular degeneration: a paradigm for dissecting complex disease traits. Hum Mol Genet 2007; 16: 174-82.
2. Klein ML, Mauldin WM, Stoumbos VD. Heredity and age-related macular degeneration. Observations in monozygotic twins. Arch Ophthalmol. 1994; 112: 932-7.
3. Meyers SM, Greene T, Gutman FA. A twin study of age-related macular degeneration. Am J Ophthalmol. 1995; 120: 757-66.
4. Heiba IM, Elston RC, Klein BE, et al. Sibling correlations and segregation analysis of age-related maculopathy: The Beaver Dam Eye Study. Genet Epidemiol. 1994; 11: 51-67.
5. Klaver CC, Wolfs RC, Assink JJ, et al. Genetic risk of age-related maculopathy. Population-based familial aggregation study. Arch Ophthalmol. 1998; 116: 1646-51.
6. Seddon JM, Ajani UA, Mitchell BD. Familial aggregation of age-related maculopathy. Am J Ophthalmol. 1997; 123: 199-206.
7. Klein RJ, Zeiss C, Chew EY, et al. Complement Factor H Polymorphism in Age-Related Macular Degeneration. Science 2005; 308: 385-389.
8. Seddon JM, Reynolds R, Maller J, Fagerness JA, Daly MJ, Rosner B. Prediction model for prevalence and incidence of advanced age-related macular degeneration based on genetic, demographic, and environmental variables. Invest Ophthalmol Vis Sci 2009; 50 (65): 2044-53.
9. www.macularisk.com/en/physicians/order.html (accessed Dec. 14th , 2010)
Monday, December 20, 2010
New Investment to Boost Gene Therapy Development
National Neurovision Research Institute (NNRI), the Foundation Fighting Blindness’ clinical trial support organization, announced today that one of its key partners, biopharmaceutical company Oxford BioMedica, has established a collaboration with sanofi-aventis, a major international pharmaceutical company, to develop and commercialize gene therapy treatments for vision-robbing retinal degenerative diseases that affect tens of millions of people around the world.
The collaboration will significantly bolster the development of the following gene therapy products: StarGen™ for the treatment of Stargardt disease, a form of early-onset macular degeneration; UshStat™ for the treatment of Usher syndrome, the leading cause of deaf-blindness; and RetinoStat® for the treatment of age-related macular degeneration, the leading cause vision loss in people 55 and older in developed countries.
The development of treatments for these and other retinal degenerative diseases is a key goal of the National Neurovision Research Institute and is the basis for its partnership with Oxford BioMedica. In 2006, Paul and Diane Manning, with the National Neurovision Research Institute, established a partnership with Oxford BioMedica to advance gene therapies for these and other related retinal degenerative diseases.
“The investment from sanofi-aventis is a wonderful boost for the development of Oxford BioMedica’s gene therapy products and will greatly enhance our ability to move these emerging treatments into and through the clinical trial process,” says Stephen Rose, Ph.D., chief research officer, Foundation Fighting Blindness. “This collaboration affirms the great potential for gene therapy to treat and cure a number of retinal degenerative diseases including Stargardt disease and Usher syndrome that, as rare diseases, often do not receive the attention or investment necessary to bring about promising treatments.”
“An important goal of the Foundation, through NNRI, is to attract investment from large pharmaceutical companies for the development and production of treatments for inherited retinal disease,” says Morton Goldberg, M.D., chairman of the board of NNRI. “The NNRI-Oxford partnership is an excellent model of how NNRI collaborations can accelerate the translation of laboratory-based research into clinical trials, ultimately getting successful treatments for rare diseases like inherited retinal degenerations to the market and out to the people who need them.”
Based on the agreement, Oxford BioMedica will receive an upfront payment of $26 million and a further $24 million from sanofi-aventis over a three-year period.
The treatments will utilize Oxford BioMedica’s LentiVector® gene delivery technology to deliver healthy vision-saving genes to the retina. For more information on this technology, visit www.oxfordbiomedica.co.uk/
The collaboration will significantly bolster the development of the following gene therapy products: StarGen™ for the treatment of Stargardt disease, a form of early-onset macular degeneration; UshStat™ for the treatment of Usher syndrome, the leading cause of deaf-blindness; and RetinoStat® for the treatment of age-related macular degeneration, the leading cause vision loss in people 55 and older in developed countries.
The development of treatments for these and other retinal degenerative diseases is a key goal of the National Neurovision Research Institute and is the basis for its partnership with Oxford BioMedica. In 2006, Paul and Diane Manning, with the National Neurovision Research Institute, established a partnership with Oxford BioMedica to advance gene therapies for these and other related retinal degenerative diseases.
“The investment from sanofi-aventis is a wonderful boost for the development of Oxford BioMedica’s gene therapy products and will greatly enhance our ability to move these emerging treatments into and through the clinical trial process,” says Stephen Rose, Ph.D., chief research officer, Foundation Fighting Blindness. “This collaboration affirms the great potential for gene therapy to treat and cure a number of retinal degenerative diseases including Stargardt disease and Usher syndrome that, as rare diseases, often do not receive the attention or investment necessary to bring about promising treatments.”
“An important goal of the Foundation, through NNRI, is to attract investment from large pharmaceutical companies for the development and production of treatments for inherited retinal disease,” says Morton Goldberg, M.D., chairman of the board of NNRI. “The NNRI-Oxford partnership is an excellent model of how NNRI collaborations can accelerate the translation of laboratory-based research into clinical trials, ultimately getting successful treatments for rare diseases like inherited retinal degenerations to the market and out to the people who need them.”
Based on the agreement, Oxford BioMedica will receive an upfront payment of $26 million and a further $24 million from sanofi-aventis over a three-year period.
The treatments will utilize Oxford BioMedica’s LentiVector® gene delivery technology to deliver healthy vision-saving genes to the retina. For more information on this technology, visit www.oxfordbiomedica.co.uk/
Saturday, December 11, 2010
German company's retinal implant can restore vision
by: Retina Implant
Restoring vision to the blind is the sort of feat reserved for ancient religious texts and modern science fiction novels. But a company in Germany did just that with an eye implant.
Retina Implant AG is in the process of developing a sub-Retina Implant, designed to be inserted into the eye to treat back-of-the-eye disorders. A first clinical trial showed that the device can enable people suffering from a certain type of macular degeneration to see. The patients had retinitus pigmentosa, an inherited and incurable degenerative condition that causes tunnel vision and often, eventually, complete blindness. Retina Implant estimates that the condition affects about 200,000 people in the U.S. and Europe.
In 1995, the company’s founder and current board member Dr. Eberhart Zrenner said that implanting a chip inside the eye was as far-fetched as using the space shuttle to get to an adjacent star in the Milky Way. But Dr. Zrenner, who is also chairman of the University of Tuebingen Eye Hospital in Germany, didn’t give up. Ten years later the company launched its first human trial. At the time, Retina Implant also began talking to venture capital firms in Europe, but the technology was deemed too risky. It wasn’t until a wealthy businessman, who was personally interested because he had relatives who suffered from vision loss, that the company found significant outside investment.
Retina Implant isn’t the only group working on bionic-eye-like projects, but it seems to have a jump on the competition. Scientists at the Mass. Institute of Technology are also conducting clinical trials with their own version of a sub-Retina Implant, but don’t anticipate implanting their device in humans until 2013. Sylmar, Calif.-based Second Site Medical Products Inc. is developing a device for sufferers of retinitus pigmentosa, but that’s an epi-retinal prosthesis used in conjunction with an external camera attached to eyewear.
Retina Implant’s product sits underneath the retina ’directly replacing light receptors lost in macular degeneration,’ according to the company. Its most advanced and studied sub-Retina Implant is a 3mm-by-3mm microchip with an array of approximately 1,500 photosensitive electrodes. Electrical power for the device is provided inductively through transmitter coils attached to the skin.
In November, the company published results (PDF) from the first in-human clinical trial that proved the device can work in the Proceedings of the Royal Society B, a peer-reviewed academic journal. The company’s research with 11 human subjects showed that people who had been completely blind had regained up to two percent of their vision. enough to recognize letters in a newspaper headlines and see utensils before them when seated at a table. That number may seem insignificant ’ but it’s impossible to calculate the value a blind person places on seeing again, no matter how dimly.
In October, Retina Implant announced that it would increase its manufacturing footprint 25-fold (PDF).
Retina Implant is in the process of commencing a larger, 60-patient clinical trial in several sites across Europe. In this trial, the subjects will have the option to keep the implant permanently. In the first trial, the chips were all removed after four months except for one patient who lobbied the government to allow him to keep the device because his outcomes were so positive. To date, no complications have been reported, according to the company.
Retina Implant believes its device can win CE Mark approval in the European Union as soon as the end of 2011, but it does not have yet have definite plans for entering the U.S. market.
MassDevice recently spoke with Retina Implant CEO Walter Wrobel about the difficulties of developing such a technically advanced medical device and his company’s efforts to prove the device’s effectiveness enough to get it to market.
Restoring vision to the blind is the sort of feat reserved for ancient religious texts and modern science fiction novels. But a company in Germany did just that with an eye implant.
Retina Implant AG is in the process of developing a sub-Retina Implant, designed to be inserted into the eye to treat back-of-the-eye disorders. A first clinical trial showed that the device can enable people suffering from a certain type of macular degeneration to see. The patients had retinitus pigmentosa, an inherited and incurable degenerative condition that causes tunnel vision and often, eventually, complete blindness. Retina Implant estimates that the condition affects about 200,000 people in the U.S. and Europe.
In 1995, the company’s founder and current board member Dr. Eberhart Zrenner said that implanting a chip inside the eye was as far-fetched as using the space shuttle to get to an adjacent star in the Milky Way. But Dr. Zrenner, who is also chairman of the University of Tuebingen Eye Hospital in Germany, didn’t give up. Ten years later the company launched its first human trial. At the time, Retina Implant also began talking to venture capital firms in Europe, but the technology was deemed too risky. It wasn’t until a wealthy businessman, who was personally interested because he had relatives who suffered from vision loss, that the company found significant outside investment.
Retina Implant isn’t the only group working on bionic-eye-like projects, but it seems to have a jump on the competition. Scientists at the Mass. Institute of Technology are also conducting clinical trials with their own version of a sub-Retina Implant, but don’t anticipate implanting their device in humans until 2013. Sylmar, Calif.-based Second Site Medical Products Inc. is developing a device for sufferers of retinitus pigmentosa, but that’s an epi-retinal prosthesis used in conjunction with an external camera attached to eyewear.
Retina Implant’s product sits underneath the retina ’directly replacing light receptors lost in macular degeneration,’ according to the company. Its most advanced and studied sub-Retina Implant is a 3mm-by-3mm microchip with an array of approximately 1,500 photosensitive electrodes. Electrical power for the device is provided inductively through transmitter coils attached to the skin.
In November, the company published results (PDF) from the first in-human clinical trial that proved the device can work in the Proceedings of the Royal Society B, a peer-reviewed academic journal. The company’s research with 11 human subjects showed that people who had been completely blind had regained up to two percent of their vision. enough to recognize letters in a newspaper headlines and see utensils before them when seated at a table. That number may seem insignificant ’ but it’s impossible to calculate the value a blind person places on seeing again, no matter how dimly.
In October, Retina Implant announced that it would increase its manufacturing footprint 25-fold (PDF).
Retina Implant is in the process of commencing a larger, 60-patient clinical trial in several sites across Europe. In this trial, the subjects will have the option to keep the implant permanently. In the first trial, the chips were all removed after four months except for one patient who lobbied the government to allow him to keep the device because his outcomes were so positive. To date, no complications have been reported, according to the company.
Retina Implant believes its device can win CE Mark approval in the European Union as soon as the end of 2011, but it does not have yet have definite plans for entering the U.S. market.
MassDevice recently spoke with Retina Implant CEO Walter Wrobel about the difficulties of developing such a technically advanced medical device and his company’s efforts to prove the device’s effectiveness enough to get it to market.
Sunday, November 28, 2010
Melatonin for Macular Degeneration?
By Cathy Wong, Alternative Medicine Guide
Melatonin may help treat age-related macular degeneration, according to a recent report. A leading cause of blindness in the United States, age-related macular degeneration develops when certain cells in the retina deteriorate and gradually destroy your central vision.
A hormone with antioxidant effects, melatonin may help stop shortening of telomeres (chromosomal structures that become shorter over time due to factors like aging, inflammation, and damage caused by free radicals). By preventing telomere-shortening in the cells of the retina, the report suggests, melatonin may help preserve eyesight and slow the progression of age-related macular degeneration.
While melatonin shows promise as a natural remedy for age-related macular degeneration, it's too soon to recommend melatonin supplements for this condition. For help in protecting your eyesight as you age, wear UV-protective lenses when outdoors in the daylight and consider upping your intake of foods rich in lutein (such as leafy green vegetables, green beans, and mango).
As always please check with your doctor before starting/ or changing any medications or supplements.
Melatonin may help treat age-related macular degeneration, according to a recent report. A leading cause of blindness in the United States, age-related macular degeneration develops when certain cells in the retina deteriorate and gradually destroy your central vision.
A hormone with antioxidant effects, melatonin may help stop shortening of telomeres (chromosomal structures that become shorter over time due to factors like aging, inflammation, and damage caused by free radicals). By preventing telomere-shortening in the cells of the retina, the report suggests, melatonin may help preserve eyesight and slow the progression of age-related macular degeneration.
While melatonin shows promise as a natural remedy for age-related macular degeneration, it's too soon to recommend melatonin supplements for this condition. For help in protecting your eyesight as you age, wear UV-protective lenses when outdoors in the daylight and consider upping your intake of foods rich in lutein (such as leafy green vegetables, green beans, and mango).
As always please check with your doctor before starting/ or changing any medications or supplements.
Monday, November 22, 2010
Acceleron's ACE-041 Demonstrates Clinical Efficacy
By Acceleron
CAMBRIDGE, Mass – November 19, 2010 – Acceleron Pharma, Inc., a biopharmaceutical company developing novel protein therapeutics that regulate the growth and development of tissues and cells, including muscle, bone, red blood cells, and vasculature, today announced the presentation of interim results from the first-in-human clinical study of ACE-041 in patients with advanced cancer at the 22nd EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics in Berlin, Germany. The presentation was given by Professor Sunil Sharma, the Jon and Karen Huntsman Presidential Professor of Cancer Research at the Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah.
“It has been very encouraging to see so many signals of efficacy in this trial, in particular because these are end-stage cancer patients,” said Dr. Sunil Sharma. “It is also important to note that while we have demonstrated significant activity with ACE-041 monotherapy in this study, we might expect to see even more efficacy in future studies with ACE-041 used in combination with other therapies.”
“The clinical activity and safety profile of ACE-041 confirms our understanding that the ALK1 pathway plays a fundamental and distinct role compared to the VEGF-axis in tumor angiogenesis,” said Dr. Matthew Sherman, M.D., Chief Medical Officer at Acceleron Pharma. “This has significant implications because nearly all patients treated with VEGF inhibitors eventually either fail therapy or develop resistance to these drugs. There is a tremendous need for novel therapies that go beyond VEGF to target the tumor blood supply.”
In a phase 1, first-in-human clinical study, patients with advanced-stage tumors were treated with multiple ascending doses of ACE-041, to evaluate the safety and pharmacokinetics of ACE-041. This study also explored antitumor activity of ACE-041.
Summary of interim findings presented:
· ACE-041 subcutaneously (SC) injected once every three weeks (q3w) is generally well-tolerated · Common side effects include mild or moderate peripheral edema, fatigue, nausea, headache, anorexia, and anemia. A single case of Grade 3 congestive heart failure was reported · Toxicities commonly associated with VEGF inhibition (hypertension, proteinuria, or bleeding) have not been observed · ACE-041 pharmacokinetics support dosing every 3 weeks · One patient with refractory head and neck cancer achieved a partial response and three patients had prolonged disease stabilization · Rapid reduction in tumor metabolic activity observed in several patients, measured by FDG-PET imaging · An expanded cohort study is ongoing at the dose level intended for Phase 2 studies,
ACE-041 is being developed for the treatment of advanced cancer and age-related macular degeneration (AMD).
About ACE-041
ACE-041 is a recombinant receptor fusion protein that inhibits angiogenesis by preventing BMP9 and BMP10, members of the TGFβ protein superfamily, from interacting with activin receptor-like kinase 1 (ALK1), a receptor that is found on proliferating endothelial cells. ACE-041 inhibits ALK1 signaling, which is required for the development of mature, functional capillary networks. In animal studies, treatment with ACE-041 inhibits tumor angiogenesis and growth and ocular neoangiogenesis. In a clinical study of patients with advanced, refractory solid tumors, treatment with ACE-041 was generally well-tolerated and antitumor activity was observed, resulting in tumor shrinkage and stabilization of disease. ACE-041 is being developed for the treatment of advanced-stage cancer and age-related macular degeneration (AMD).
About Acceleron Pharma
Acceleron is a privately-held biopharmaceutical company committed to discover, develop, manufacture and commercialize novel biotherapeutics that modulate the growth of red blood cells, bone, muscle, fat and the vasculature to treat musculoskeletal, metabolic and cancer-related diseases. Acceleron’s scientific approach takes advantage of its unique insight into the regenerative powers of the TGF-β superfamily of proteins. Acceleron utilizes proven biotherapeutic technologies and capitalizes on the company’s internal GMP manufacturing capability to rapidly and efficiently advance its therapeutic programs. The investors in Acceleron include Advanced Technology Ventures, Alkermes, Bessemer Ventures, Celgene, Flagship Ventures, MPM BioEquities, OrbiMed Advisors, Polaris Ventures, QVT Financial, Sutter Hill Ventures and Venrock. For further information on Acceleron Pharma.
CAMBRIDGE, Mass – November 19, 2010 – Acceleron Pharma, Inc., a biopharmaceutical company developing novel protein therapeutics that regulate the growth and development of tissues and cells, including muscle, bone, red blood cells, and vasculature, today announced the presentation of interim results from the first-in-human clinical study of ACE-041 in patients with advanced cancer at the 22nd EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics in Berlin, Germany. The presentation was given by Professor Sunil Sharma, the Jon and Karen Huntsman Presidential Professor of Cancer Research at the Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah.
“It has been very encouraging to see so many signals of efficacy in this trial, in particular because these are end-stage cancer patients,” said Dr. Sunil Sharma. “It is also important to note that while we have demonstrated significant activity with ACE-041 monotherapy in this study, we might expect to see even more efficacy in future studies with ACE-041 used in combination with other therapies.”
“The clinical activity and safety profile of ACE-041 confirms our understanding that the ALK1 pathway plays a fundamental and distinct role compared to the VEGF-axis in tumor angiogenesis,” said Dr. Matthew Sherman, M.D., Chief Medical Officer at Acceleron Pharma. “This has significant implications because nearly all patients treated with VEGF inhibitors eventually either fail therapy or develop resistance to these drugs. There is a tremendous need for novel therapies that go beyond VEGF to target the tumor blood supply.”
In a phase 1, first-in-human clinical study, patients with advanced-stage tumors were treated with multiple ascending doses of ACE-041, to evaluate the safety and pharmacokinetics of ACE-041. This study also explored antitumor activity of ACE-041.
Summary of interim findings presented:
· ACE-041 subcutaneously (SC) injected once every three weeks (q3w) is generally well-tolerated · Common side effects include mild or moderate peripheral edema, fatigue, nausea, headache, anorexia, and anemia. A single case of Grade 3 congestive heart failure was reported · Toxicities commonly associated with VEGF inhibition (hypertension, proteinuria, or bleeding) have not been observed · ACE-041 pharmacokinetics support dosing every 3 weeks · One patient with refractory head and neck cancer achieved a partial response and three patients had prolonged disease stabilization · Rapid reduction in tumor metabolic activity observed in several patients, measured by FDG-PET imaging · An expanded cohort study is ongoing at the dose level intended for Phase 2 studies,
ACE-041 is being developed for the treatment of advanced cancer and age-related macular degeneration (AMD).
About ACE-041
ACE-041 is a recombinant receptor fusion protein that inhibits angiogenesis by preventing BMP9 and BMP10, members of the TGFβ protein superfamily, from interacting with activin receptor-like kinase 1 (ALK1), a receptor that is found on proliferating endothelial cells. ACE-041 inhibits ALK1 signaling, which is required for the development of mature, functional capillary networks. In animal studies, treatment with ACE-041 inhibits tumor angiogenesis and growth and ocular neoangiogenesis. In a clinical study of patients with advanced, refractory solid tumors, treatment with ACE-041 was generally well-tolerated and antitumor activity was observed, resulting in tumor shrinkage and stabilization of disease. ACE-041 is being developed for the treatment of advanced-stage cancer and age-related macular degeneration (AMD).
About Acceleron Pharma
Acceleron is a privately-held biopharmaceutical company committed to discover, develop, manufacture and commercialize novel biotherapeutics that modulate the growth of red blood cells, bone, muscle, fat and the vasculature to treat musculoskeletal, metabolic and cancer-related diseases. Acceleron’s scientific approach takes advantage of its unique insight into the regenerative powers of the TGF-β superfamily of proteins. Acceleron utilizes proven biotherapeutic technologies and capitalizes on the company’s internal GMP manufacturing capability to rapidly and efficiently advance its therapeutic programs. The investors in Acceleron include Advanced Technology Ventures, Alkermes, Bessemer Ventures, Celgene, Flagship Ventures, MPM BioEquities, OrbiMed Advisors, Polaris Ventures, QVT Financial, Sutter Hill Ventures and Venrock. For further information on Acceleron Pharma.
Monday, November 15, 2010
Macular Degeneration Treatments/Therapies Breakthroughs
by Isobel Washington
Macular degeneration is an eye condition characterized by the deterioration of the macula, which is the central "lens-like" part of the eye's retina responsible for sharp central vision. Affecting central vision and often leading to vision loss, macular degeneration has had limited treatment options. Recently, there have been some breakthroughs to help patients retain vision.
Significance
Macular degeneration is the leading cause of vision loss and blindness among Americans age 65 and older. Vision loss from this condition is a growing problem, since this age demographic represents an increasingly larger percentage of the U. S. population.
Function
Treatments for macular degeneration work to preserve vision ability at the time of treatment, and slow the progression of the disease (it's a progressive disease that affects vision over time). Treatment cannot restore vision that is already lost through the disease. There is no cure or treatment to stop the progression of macular degeneration, there are ways to preserve and prolong current vision.
Eye Injections
Lucentis and Macugen are FDA-approved ocular injection treatments, and are highly effective for preserving vision and inhibiting macular degeneration symptoms, according to AllAboutVision.com. A 2005 study on Lucentis demonstrated success rate of 95 percent for improving and sustaining vision in macular degeneration patients.
Laser Treatment
Laser technology is now used to destroy the abnormal, leaky blood vessels that cause vision loss in macular degeneration patients. The National Eye Institute points out, however, that while this treatment may be effective for preventing vision loss, it is also comes with the risk of destroying healthy tissue that surrounds the treatment area.
Photodynamic Therapy
This method uses special light treatment to activate an injected drug, verteporfin, in the blood vessels, so that it destroys the new, abnormal blood vessels being hyper-produced in the eye (those that cause vision impairment or loss). The National Eye Institute reports that this light-activation method slows vision loss, but doesn't stop it.
Investigational Treatments
Investigational treatments for macular degeneration, in various stages of research and FDA clinical studies, include Avastin, a cancer treatment drug. As of 2009, the National Eye Institute reports that no available treatment provides a cure for macular degeneration, and that vision loss may result, despite treatment.
About the Author
Isobel Washington has been a freelance journalist since 2007. Washington's work first surfaced in Europe, where she served as a restaurant critic and journalist for "LifeStyles" magazine. Her love of travel and culture inspired her first novel, which is currently underway. Washington has a 10-year career in marketing communication and holds a Bachelor of Science degree.
Macular degeneration is an eye condition characterized by the deterioration of the macula, which is the central "lens-like" part of the eye's retina responsible for sharp central vision. Affecting central vision and often leading to vision loss, macular degeneration has had limited treatment options. Recently, there have been some breakthroughs to help patients retain vision.
Significance
Macular degeneration is the leading cause of vision loss and blindness among Americans age 65 and older. Vision loss from this condition is a growing problem, since this age demographic represents an increasingly larger percentage of the U. S. population.
Function
Treatments for macular degeneration work to preserve vision ability at the time of treatment, and slow the progression of the disease (it's a progressive disease that affects vision over time). Treatment cannot restore vision that is already lost through the disease. There is no cure or treatment to stop the progression of macular degeneration, there are ways to preserve and prolong current vision.
Eye Injections
Lucentis and Macugen are FDA-approved ocular injection treatments, and are highly effective for preserving vision and inhibiting macular degeneration symptoms, according to AllAboutVision.com. A 2005 study on Lucentis demonstrated success rate of 95 percent for improving and sustaining vision in macular degeneration patients.
Laser Treatment
Laser technology is now used to destroy the abnormal, leaky blood vessels that cause vision loss in macular degeneration patients. The National Eye Institute points out, however, that while this treatment may be effective for preventing vision loss, it is also comes with the risk of destroying healthy tissue that surrounds the treatment area.
Photodynamic Therapy
This method uses special light treatment to activate an injected drug, verteporfin, in the blood vessels, so that it destroys the new, abnormal blood vessels being hyper-produced in the eye (those that cause vision impairment or loss). The National Eye Institute reports that this light-activation method slows vision loss, but doesn't stop it.
Investigational Treatments
Investigational treatments for macular degeneration, in various stages of research and FDA clinical studies, include Avastin, a cancer treatment drug. As of 2009, the National Eye Institute reports that no available treatment provides a cure for macular degeneration, and that vision loss may result, despite treatment.
About the Author
Isobel Washington has been a freelance journalist since 2007. Washington's work first surfaced in Europe, where she served as a restaurant critic and journalist for "LifeStyles" magazine. Her love of travel and culture inspired her first novel, which is currently underway. Washington has a 10-year career in marketing communication and holds a Bachelor of Science degree.
Thursday, November 4, 2010
Qualifing Theraputic Discovery Project Program
by GEN news
Over the last couple of days, companies have been reporting on awards received under the Qualifying Therapeutic Discovery Project program. The IRS in conjunction with the Department of Health and Human Services, approved applications for projects that showed significant potential to produce new and cost-saving therapies, support jobs, and increase U.S. competitiveness.
Under the program, a total amount of $1 billion was allocated for credits and grants with a $5 million limit per each eligible applicant. The full list of companies receiving these awards can be found at http://bit.ly/b3VxSp.
Here are details for a few more companies:
Acceleron Pharma received five grants totaling $1,222,396.25: ACE-031 for Duchenne muscular dystrophy, ACE-536 for myelodysplastic syndrome, ACE-435, ACE-011 for anemia, and ACE-041 for advanced solid tumors, multiple myeloma, and age-related macular degeneration.
Aestus Therapeutics received one grant of $244,000: chronic neuropathic pain drug development.
BioCryst Pharmaceuticals received five grants totaling $1,064,297.89: four grants of $244,479.25 each were given to peramivir for influenza, BCX4208 for gout, forodesine for CLL and CTCL, and JAK inhibitor programs in psoriasis, ankylosing spondylitis, and multiple sclerosis. One grant of $86,380.89 was awarded to BCX4161 for hereditary angiodema.
Biodel received five grants totaling $1,222,396.25: Linjeta, VIAtab, smart basal, glucagon, and glargine.
Cardium Therapeutics received one grant of $244,479.25: Generx for advanced coronary artery disease.
Celsion received one grant of $244,479.25: Thermodox for primary liver cancer and recurrent chest wall breast cancer.
Cerus received two grants totaling $488,958.50: Intercept Blood System for platelets and red blood cells.
Charleston Laboratories received one grant of $244,479.25: CL-108 for moderate-to-severe pain.
CorMedix received two grants totaling $488,959.50: Neutrolin and Deferiprone.
Curis received two grants totaling $488,958.50: CUDC-101 and pipeline small molecules for cancer treatment.
Derma Sciences received one grant of $244,479.25: DSC127 for tissue repair.
Dicerna Pharmaceuticals received two grants totaling $488,958.50: Dicer Substrate Technology and DsiRNA molecules for the treatment of cancer.
DNA Medicine Institute received a grant of $222,999: Universal Blood Sensor.
Enzon Pharmaceuticals received five grants totaling $1,222,396.25: PEG-SN38, mRNA antagonist for HIF-1 alpha, Survivin, Androgen Receptor, and HER3.
Etubics received one grant of $244,479.25: CEA-expressing adenovirus as a colon cancer therapeutic vaccine.
GTx received five grants totaling $1,222,396.25: ALK inhibition therapy, Toremifene 20 mg, Ostarine, GTx-758, Toremifene 80 mg, which are all being developed for cancer and cancer supportive care.
Health Discovery received a grant of $244,479.25: SVM and RFE-SVM technology.
Icagen received three grants totaling $733,000: Selective sodium channel drugs to treat chronic pain, KCNQ agonists for epilepsy and pain, and TRPA1 drugs for inflammatory pain.
Inviragen received two grants totaling $488,958.50: Vaccines against dengue and chikungunya viruses.
InVivo Therapeutics received a grant of $244,000: biocompatible polymer scaffolding device designed for implantation into a lesion to treat acute open-wound SCI.
Light Sciences Oncology received two grants totaling $488,958.50: Aptocine for treatment of primary and secondary liver tumors and benign prostatic hyperplasia.
Lipocine received four grants totaling $977,917: hormone replacement therapy, high-risk pregnancy support, oral treatment of progressive glioblastoma multiforme, and opioid-resistant cough in advanced cancer patients.
Molecular Detection received a grant of $244,479.25: Detect-Ready panel that detects carriers of MRSA and related pathogens.
Neoprobe received a grant of $244,479.25: Lymphoseek.
Omeros received eight grants of uneven amounts totaling $1,723,086.51: PDE7 for Parkinson disease; addiction treatment; therapies for osteoarthritis and the protection of articular cartilage; drugs to treat pain, inflammation, and spasm of the urinary tract; MASP-2 MoAb for traumatic injury; medications for schizophrenia; intracameral OMS302 to maintain intraoperative mydriasis and reduce pain and inflammation; and products to improve function and reduce pain after arthroscopic surgery.
OncoMed Pharmaceuticals received five grants totaling $1,222,396.25: OMP-21M18, OMP-59R5, novel antibodies, Wnt pathway inhibitors, and drugs targeting the Wnt pathway in cancer stem cells, all for the treatment of cancer.
PolyMedix received two cash grants totaling $488,958.50: PMX-30063 for acute bacterial skin and skin structure infections (ABSSSI) caused by Staph and PMX-60056 in percutaneous coronary intervention patients.
pSivida received two cash grants totaling $488,958.50: research on new generations of the company’s drug delivery technologies targeting ophthalmic diseases.
Quanterix received three grants totaling $733,437.75: Diagnostics developed on the Single Molecule Array (SiMoA) for prostate cancer, Alzheimer disease, and Crohn disease.
Regulus Therapeutics received two cash grants totaling $488,958.50: miRNA therapeutics for HCV and fibrosis.
Sangamo BioSciences received four grants totaling $977,917: SB-509 for diabetic peripheral neuropathy, SB-509 for amyotrophic lateral sclerosis, SB-728-T for human immunodeficiency virus/acquired immunodeficiency syndrome, and SB-313-xTZ for recurrent or refractory glioblastoma multiforme.
Sea Lane Biotechnologies received six grants totaling $1.5 million: Surrobody™ therapeutic candidates and influenza antibodies.
Soligenix received a grant of $244,479.25: orBec in acute gastrointestinal graft vs. host disease.
Somaxon Pharmaceuticals received a grant of $244,479.25: Silenor.
Spectrum Pharmaceuticals received four grants totaling $977,917: RenaZorb for hyperphosphatemia in patients with chronic kidney disease and anticancer agents Zevalin, Apaziquone, and Belinostat.
Spherix received two grants totaling $469,478.50: triglycerides.
StemCells received four grants totaling $977,917: HuCNS-SC for diseases and disorders affecting the brain, the spinal cord, and the eye as well as hLEC human liver engrafting cells.
Synergenz BioScience received one grant of $94,836: Respiragene, a genetic-based test for lung cancer predisposition.
Telik received five grants totaling $1,222,396.25: Telintra in severe chronic neutropenia, Telcyta for refractory lymphoma and multiple myeloma, Telintra in low-to-intermediate-1 risk myelodysplastic syndrome, Telintra and Revlimid in myelodysplastic syndrome, and aurora and VEGFR kinase inhibitors for the treatment of cancer.
Threshold Pharmaceuticals received two grants totaling $488,958.50: TH-302 for the treatment of cancer, and the company’s hypoxia-activated prodrug technology platform for drug discovery.
Xoft received two grants totaling $469,478.50: electronic brachytherapy for the treatment of breast cancer and gynecological cancers.
Zalicus receive a grant of $244,479.25: Synavive for immunoinflammatory diseases.
Ziopharm Oncology received three grants totaling $733,437.75: Indibulin, Palifosfamide, and Darinaparsin, all for the treatment of cancer.
Over the last couple of days, companies have been reporting on awards received under the Qualifying Therapeutic Discovery Project program. The IRS in conjunction with the Department of Health and Human Services, approved applications for projects that showed significant potential to produce new and cost-saving therapies, support jobs, and increase U.S. competitiveness.
Under the program, a total amount of $1 billion was allocated for credits and grants with a $5 million limit per each eligible applicant. The full list of companies receiving these awards can be found at http://bit.ly/b3VxSp.
Here are details for a few more companies:
Acceleron Pharma received five grants totaling $1,222,396.25: ACE-031 for Duchenne muscular dystrophy, ACE-536 for myelodysplastic syndrome, ACE-435, ACE-011 for anemia, and ACE-041 for advanced solid tumors, multiple myeloma, and age-related macular degeneration.
Aestus Therapeutics received one grant of $244,000: chronic neuropathic pain drug development.
BioCryst Pharmaceuticals received five grants totaling $1,064,297.89: four grants of $244,479.25 each were given to peramivir for influenza, BCX4208 for gout, forodesine for CLL and CTCL, and JAK inhibitor programs in psoriasis, ankylosing spondylitis, and multiple sclerosis. One grant of $86,380.89 was awarded to BCX4161 for hereditary angiodema.
Biodel received five grants totaling $1,222,396.25: Linjeta, VIAtab, smart basal, glucagon, and glargine.
Cardium Therapeutics received one grant of $244,479.25: Generx for advanced coronary artery disease.
Celsion received one grant of $244,479.25: Thermodox for primary liver cancer and recurrent chest wall breast cancer.
Cerus received two grants totaling $488,958.50: Intercept Blood System for platelets and red blood cells.
Charleston Laboratories received one grant of $244,479.25: CL-108 for moderate-to-severe pain.
CorMedix received two grants totaling $488,959.50: Neutrolin and Deferiprone.
Curis received two grants totaling $488,958.50: CUDC-101 and pipeline small molecules for cancer treatment.
Derma Sciences received one grant of $244,479.25: DSC127 for tissue repair.
Dicerna Pharmaceuticals received two grants totaling $488,958.50: Dicer Substrate Technology and DsiRNA molecules for the treatment of cancer.
DNA Medicine Institute received a grant of $222,999: Universal Blood Sensor.
Enzon Pharmaceuticals received five grants totaling $1,222,396.25: PEG-SN38, mRNA antagonist for HIF-1 alpha, Survivin, Androgen Receptor, and HER3.
Etubics received one grant of $244,479.25: CEA-expressing adenovirus as a colon cancer therapeutic vaccine.
GTx received five grants totaling $1,222,396.25: ALK inhibition therapy, Toremifene 20 mg, Ostarine, GTx-758, Toremifene 80 mg, which are all being developed for cancer and cancer supportive care.
Health Discovery received a grant of $244,479.25: SVM and RFE-SVM technology.
Icagen received three grants totaling $733,000: Selective sodium channel drugs to treat chronic pain, KCNQ agonists for epilepsy and pain, and TRPA1 drugs for inflammatory pain.
Inviragen received two grants totaling $488,958.50: Vaccines against dengue and chikungunya viruses.
InVivo Therapeutics received a grant of $244,000: biocompatible polymer scaffolding device designed for implantation into a lesion to treat acute open-wound SCI.
Light Sciences Oncology received two grants totaling $488,958.50: Aptocine for treatment of primary and secondary liver tumors and benign prostatic hyperplasia.
Lipocine received four grants totaling $977,917: hormone replacement therapy, high-risk pregnancy support, oral treatment of progressive glioblastoma multiforme, and opioid-resistant cough in advanced cancer patients.
Molecular Detection received a grant of $244,479.25: Detect-Ready panel that detects carriers of MRSA and related pathogens.
Neoprobe received a grant of $244,479.25: Lymphoseek.
Omeros received eight grants of uneven amounts totaling $1,723,086.51: PDE7 for Parkinson disease; addiction treatment; therapies for osteoarthritis and the protection of articular cartilage; drugs to treat pain, inflammation, and spasm of the urinary tract; MASP-2 MoAb for traumatic injury; medications for schizophrenia; intracameral OMS302 to maintain intraoperative mydriasis and reduce pain and inflammation; and products to improve function and reduce pain after arthroscopic surgery.
OncoMed Pharmaceuticals received five grants totaling $1,222,396.25: OMP-21M18, OMP-59R5, novel antibodies, Wnt pathway inhibitors, and drugs targeting the Wnt pathway in cancer stem cells, all for the treatment of cancer.
PolyMedix received two cash grants totaling $488,958.50: PMX-30063 for acute bacterial skin and skin structure infections (ABSSSI) caused by Staph and PMX-60056 in percutaneous coronary intervention patients.
pSivida received two cash grants totaling $488,958.50: research on new generations of the company’s drug delivery technologies targeting ophthalmic diseases.
Quanterix received three grants totaling $733,437.75: Diagnostics developed on the Single Molecule Array (SiMoA) for prostate cancer, Alzheimer disease, and Crohn disease.
Regulus Therapeutics received two cash grants totaling $488,958.50: miRNA therapeutics for HCV and fibrosis.
Sangamo BioSciences received four grants totaling $977,917: SB-509 for diabetic peripheral neuropathy, SB-509 for amyotrophic lateral sclerosis, SB-728-T for human immunodeficiency virus/acquired immunodeficiency syndrome, and SB-313-xTZ for recurrent or refractory glioblastoma multiforme.
Sea Lane Biotechnologies received six grants totaling $1.5 million: Surrobody™ therapeutic candidates and influenza antibodies.
Soligenix received a grant of $244,479.25: orBec in acute gastrointestinal graft vs. host disease.
Somaxon Pharmaceuticals received a grant of $244,479.25: Silenor.
Spectrum Pharmaceuticals received four grants totaling $977,917: RenaZorb for hyperphosphatemia in patients with chronic kidney disease and anticancer agents Zevalin, Apaziquone, and Belinostat.
Spherix received two grants totaling $469,478.50: triglycerides.
StemCells received four grants totaling $977,917: HuCNS-SC for diseases and disorders affecting the brain, the spinal cord, and the eye as well as hLEC human liver engrafting cells.
Synergenz BioScience received one grant of $94,836: Respiragene, a genetic-based test for lung cancer predisposition.
Telik received five grants totaling $1,222,396.25: Telintra in severe chronic neutropenia, Telcyta for refractory lymphoma and multiple myeloma, Telintra in low-to-intermediate-1 risk myelodysplastic syndrome, Telintra and Revlimid in myelodysplastic syndrome, and aurora and VEGFR kinase inhibitors for the treatment of cancer.
Threshold Pharmaceuticals received two grants totaling $488,958.50: TH-302 for the treatment of cancer, and the company’s hypoxia-activated prodrug technology platform for drug discovery.
Xoft received two grants totaling $469,478.50: electronic brachytherapy for the treatment of breast cancer and gynecological cancers.
Zalicus receive a grant of $244,479.25: Synavive for immunoinflammatory diseases.
Ziopharm Oncology received three grants totaling $733,437.75: Indibulin, Palifosfamide, and Darinaparsin, all for the treatment of cancer.
Saturday, October 23, 2010
Novartis therapy Lucentis recommended for approval in EU to treat Diabetic Macular Edema
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.
- 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.
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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Wednesday, August 18, 2010
Drug Research could lead to AMD therapy
By Adrian Galbreth
New drug research may pave the way for more effective treatments of age-related macular degeneration - the leading cause of blindness in the western world.
Those are the claims being made by researchers at Tufts University School of Medicine, who say that a protein known as galectin-3 promotes the growth of new blood vessels, and that targeting the protein can "significantly reduce" angiogenesis.
The findings have been published in the Journal of Experimental Medicine and may lead to treatments for diseases caused by excessive angiogenesis, which include AMD, said Dr Noorjahan Panjwani, who led the project.
She explained: "Our study shows that galectin-3 protein binds to glycans of specific cell-adhesion proteins to activate the signaling pathways that bring about angiogenesis. This improved understanding may provide a more targeted approach to preventing harmful angiogenesis."
Meanwhile, another team of researchers at Tufts have found that that non-viral gene therapy can delay the onset of some forms of eye disease and offer hope to retinal degeneration sufferers.ADNFCR-1853-ID-800028486-ADNFCR
New drug research may pave the way for more effective treatments of age-related macular degeneration - the leading cause of blindness in the western world.
Those are the claims being made by researchers at Tufts University School of Medicine, who say that a protein known as galectin-3 promotes the growth of new blood vessels, and that targeting the protein can "significantly reduce" angiogenesis.
The findings have been published in the Journal of Experimental Medicine and may lead to treatments for diseases caused by excessive angiogenesis, which include AMD, said Dr Noorjahan Panjwani, who led the project.
She explained: "Our study shows that galectin-3 protein binds to glycans of specific cell-adhesion proteins to activate the signaling pathways that bring about angiogenesis. This improved understanding may provide a more targeted approach to preventing harmful angiogenesis."
Meanwhile, another team of researchers at Tufts have found that that non-viral gene therapy can delay the onset of some forms of eye disease and offer hope to retinal degeneration sufferers.ADNFCR-1853-ID-800028486-ADNFCR
Tuesday, July 20, 2010
Stem Cell Transplants Stalled Blindness in Rats
Researchers say putting nerve stem cells from StemCells Inc near the retinas of rats with a form of macular degeneration helped keep the disease from advancing to blindness for several months.Nerve stem cell transplants may help slow the progression of macular degeneration, the most common cause of blindness in the developed world, U.S. researchers said on Monday.
They said putting nerve stem cells from StemCells Inc near the retinas of rats with a form of macular degeneration helped keep the disease from advancing to blindness for several months.
"These cells improve the chemical environment in the back of the eye," said Ray Lund of the Casey Eye Institute at Oregon Health & Science University in Portland, whose findings were presented at the Society for Neuroscience meeting in Chicago.
Lund said the mechanism is not clear, but he suspects that when immature nerve cells are placed near the retina, they produce growth factors that protect the cells from damage by the disease.
"It's basically a chemical pump that is sitting in the right place and producing the right things," Lund said in a telephone interview.
Where normally animals with eye disease lost their vision by three months old, rats that got the transplants kept their vision for at least seven months, he said.
"There is no evidence that they (the transplanted cells) do any damage," Lund said, adding that the animals do not develop tumors, a key worry for stem cell transplants.
The findings raise hope for use of the treatment in humans with a range of diseases in which the retina become damaged, including age-related macular degeneration or AMD, which affects nearly 30 million people worldwide, including 15 million Americans.
People with AMD lose central vision when delicate light-sensing cells of the macula, a region at the center of the retina, become damaged.
In the rats, the researchers transplanted immature nerve cells into the space near the retina. Lund said the same could be done in people with retinal disease.
Dr. Stephen Huhn, head of the Central Nervous System research program at StemCells Inc, said the cells are adult neural stem cells. He said they are multipotent, meaning they can morph into different types of nerve cells.
The company has already tested the treatment in a study of six patients with Batten's disease, a fatal inherited disorder of the nervous system.
"Having a cell that has already entered clinical testing that has been well tolerated at very high doses in the brain gives us a lot of confidence about exploring the same type of strategy in the eye," Huhn said.
Huhn said he thinks the cells may be especially well suited for use in the retina, brain and spinal cord, which are less likely to reject the cells than other parts of the body.
Ultimately, he said the hope is to develop a treatment for the dry form of macular degeneration, which affects around 90 percent of patients diagnosed with AMD. No treatments are available for this form of the disease.
Huhn said treating this form of the disease may prevent some people from developing wet AMD, in which tiny new blood vessels grow between the retina and the back of the eye.
This form of the disease can be treated with modern drugs like Lucentis, from Novartis and Roche's Genentech, and Pfizer's Macugen.
They said putting nerve stem cells from StemCells Inc near the retinas of rats with a form of macular degeneration helped keep the disease from advancing to blindness for several months.
"These cells improve the chemical environment in the back of the eye," said Ray Lund of the Casey Eye Institute at Oregon Health & Science University in Portland, whose findings were presented at the Society for Neuroscience meeting in Chicago.
Lund said the mechanism is not clear, but he suspects that when immature nerve cells are placed near the retina, they produce growth factors that protect the cells from damage by the disease.
"It's basically a chemical pump that is sitting in the right place and producing the right things," Lund said in a telephone interview.
Where normally animals with eye disease lost their vision by three months old, rats that got the transplants kept their vision for at least seven months, he said.
"There is no evidence that they (the transplanted cells) do any damage," Lund said, adding that the animals do not develop tumors, a key worry for stem cell transplants.
The findings raise hope for use of the treatment in humans with a range of diseases in which the retina become damaged, including age-related macular degeneration or AMD, which affects nearly 30 million people worldwide, including 15 million Americans.
People with AMD lose central vision when delicate light-sensing cells of the macula, a region at the center of the retina, become damaged.
In the rats, the researchers transplanted immature nerve cells into the space near the retina. Lund said the same could be done in people with retinal disease.
Dr. Stephen Huhn, head of the Central Nervous System research program at StemCells Inc, said the cells are adult neural stem cells. He said they are multipotent, meaning they can morph into different types of nerve cells.
The company has already tested the treatment in a study of six patients with Batten's disease, a fatal inherited disorder of the nervous system.
"Having a cell that has already entered clinical testing that has been well tolerated at very high doses in the brain gives us a lot of confidence about exploring the same type of strategy in the eye," Huhn said.
Huhn said he thinks the cells may be especially well suited for use in the retina, brain and spinal cord, which are less likely to reject the cells than other parts of the body.
Ultimately, he said the hope is to develop a treatment for the dry form of macular degeneration, which affects around 90 percent of patients diagnosed with AMD. No treatments are available for this form of the disease.
Huhn said treating this form of the disease may prevent some people from developing wet AMD, in which tiny new blood vessels grow between the retina and the back of the eye.
This form of the disease can be treated with modern drugs like Lucentis, from Novartis and Roche's Genentech, and Pfizer's Macugen.
Wednesday, June 30, 2010
Stem cell Therapy to Benefit Blind
Submitted by Jayden Roberts on Tue, 06/29/2010
Italian researchers have reported that about 12 people have regained their sight in a successful experiment conducted with some partly blind and severe eye damage suffering people. This was revealed in a study published online in the New England Journal of Medicine.
This is a remarkable success that will encourage the cell-therapy, which is done by transplanting cells from one’s own body to other parts. It has been claimed that the treatment has proved winning in 82 of 107 eyes. Also, it was partially complete in 14 others eyes. The benefits of the treatment are expected to last till 10 years after the process.
It is also noticeable that one man, who had been blind for more than five decades, have also completely restored his visual capacity. Appreciating the success, Ophthalmologist Ivan Schwab of the University of California praised and congratulated the team.
If the stem cell transplants become popular and are implemented even more, they can also prove helpful for the people who are affected by chemical burns on their corneas from heavy-duty cleansers and other chemicals. This will be a great help for people who have to suffer eyesight loss due to such mishaps.
However, the stem cell approach is not capable to treat optic nerve or macular degeneration, which is caused due to the damage in retina, as the treatment requires a few healthy tissues that can be transplanted.
Italian researchers have reported that about 12 people have regained their sight in a successful experiment conducted with some partly blind and severe eye damage suffering people. This was revealed in a study published online in the New England Journal of Medicine.
This is a remarkable success that will encourage the cell-therapy, which is done by transplanting cells from one’s own body to other parts. It has been claimed that the treatment has proved winning in 82 of 107 eyes. Also, it was partially complete in 14 others eyes. The benefits of the treatment are expected to last till 10 years after the process.
It is also noticeable that one man, who had been blind for more than five decades, have also completely restored his visual capacity. Appreciating the success, Ophthalmologist Ivan Schwab of the University of California praised and congratulated the team.
If the stem cell transplants become popular and are implemented even more, they can also prove helpful for the people who are affected by chemical burns on their corneas from heavy-duty cleansers and other chemicals. This will be a great help for people who have to suffer eyesight loss due to such mishaps.
However, the stem cell approach is not capable to treat optic nerve or macular degeneration, which is caused due to the damage in retina, as the treatment requires a few healthy tissues that can be transplanted.
Sunday, May 10, 2009
Foundation Fighting Blindness’ National Neurovision Research Institute Heralds Collaboration for Gene Therapy Advancements
Foundation Fighting Blindness’ National Neurovision Research Institute Heralds Collaboration for Gene Therapy Advancements
OWINGS MILLS, Md.--(BUSINESS WIRE)--The National Neurovision Research Institute (NNRI), the Foundation Fighting Blindness’ clinical trial support organization, announced today that one of its key partners, biopharmaceutical company Oxford BioMedica, has established a collaboration with sanofi-aventis, a major international pharmaceutical company, to develop and commercialize gene therapy treatments for vision-robbing retinal degenerative diseases that affect tens of millions of people around the world.
The collaboration will significantly bolster the development of the following gene therapy products: StarGen™ for the treatment of Stargardt disease, a form of early-onset macular degeneration; UshStat™ for the treatment of Usher syndrome, the leading cause of deaf-blindness; RetinoStat® for the treatment of age-related macular degeneration, the leading cause vision loss in people 55 and older in developed countries; and EncorStat™ for corneal graft rejection.
The development of treatments for these and other retinal degenerative diseases is a key goal of the National Neurovision Research Institute and is the basis for its partnership with Oxford BioMedica. In 2006, Paul and Diane Manning, with the National Neurovision Research Institute, established a partnership with Oxford BioMedica to advance gene therapies for these and other related retinal degenerative diseases.
“The investment from sanofi-aventis is a wonderful boost for the development of Oxford BioMedica’s gene therapy products and will greatly enhance our ability to move these emerging treatments into and through the clinical trial process,” says Stephen Rose, Ph.D., chief research officer, Foundation Fighting Blindness. “This collaboration affirms the great potential for gene therapy to treat and cure a number of retinal degenerative diseases including Stargardt disease and Usher syndrome that, as rare diseases, often do not receive the attention or investment necessary to bring about promising treatments.”
“An important goal of the Foundation, through NNRI, is to attract investment from large pharmaceutical companies for the development and production of treatments for inherited retinal disease,” says Morton Goldberg, M.D., chairman of the board of NNRI. “The NNRI-Oxford partnership is an excellent model of how NNRI collaborations can accelerate the translation of laboratory-based research into clinical trials, ultimately getting successful treatments for rare diseases like inherited retinal degenerations to the market and out to the people who need them.”
Based on the agreement, Oxford BioMedica will receive approximately €43 million ($56 million) from sanofi-aventis over a three-year period. Oxford BioMedica is eligible to receive additional fees if development efforts are successful.
The treatments will utilize Oxford BioMedica’s LentiVector® gene delivery technology to deliver healthy vision-saving genes to the retina.
About Foundation Fighting Blindness
The Foundation Fighting Blindness is the largest source of non-governmental funding for retinal degenerative disease research in the world. The urgent mission of the Foundation Fighting Blindness is to drive the research that will provide preventions, treatments and cures for people affected by retinitis pigmentosa, macular degeneration, Usher syndrome, and the entire spectrum of retinal degenerative diseases. The Foundation has invested over $140 million to provide seed money for scientific research of diseases of the retina, which cause blindness. Further information is available at www.FightBlindness.org.
About National Neurovision Research Institute (NNRI)
NNRI is a recently-established non-profit support organization of the Foundation Fighting Blindness (FFB), the leading non-government funding source for inherited orphan retinal degeneration research. The mission of NNRI is to accelerate the translation of laboratory based research into clinical trials for treatments and cures of retinal degenerative diseases. It is a medical research institute that obtains support from government agencies, corporations and private foundations. It may also receive royalties or licensing fees from the drug discovery processes and commercialization of new therapies. Further information is available at www.nnri.info.
OWINGS MILLS, Md.--(BUSINESS WIRE)--The National Neurovision Research Institute (NNRI), the Foundation Fighting Blindness’ clinical trial support organization, announced today that one of its key partners, biopharmaceutical company Oxford BioMedica, has established a collaboration with sanofi-aventis, a major international pharmaceutical company, to develop and commercialize gene therapy treatments for vision-robbing retinal degenerative diseases that affect tens of millions of people around the world.
The collaboration will significantly bolster the development of the following gene therapy products: StarGen™ for the treatment of Stargardt disease, a form of early-onset macular degeneration; UshStat™ for the treatment of Usher syndrome, the leading cause of deaf-blindness; RetinoStat® for the treatment of age-related macular degeneration, the leading cause vision loss in people 55 and older in developed countries; and EncorStat™ for corneal graft rejection.
The development of treatments for these and other retinal degenerative diseases is a key goal of the National Neurovision Research Institute and is the basis for its partnership with Oxford BioMedica. In 2006, Paul and Diane Manning, with the National Neurovision Research Institute, established a partnership with Oxford BioMedica to advance gene therapies for these and other related retinal degenerative diseases.
“The investment from sanofi-aventis is a wonderful boost for the development of Oxford BioMedica’s gene therapy products and will greatly enhance our ability to move these emerging treatments into and through the clinical trial process,” says Stephen Rose, Ph.D., chief research officer, Foundation Fighting Blindness. “This collaboration affirms the great potential for gene therapy to treat and cure a number of retinal degenerative diseases including Stargardt disease and Usher syndrome that, as rare diseases, often do not receive the attention or investment necessary to bring about promising treatments.”
“An important goal of the Foundation, through NNRI, is to attract investment from large pharmaceutical companies for the development and production of treatments for inherited retinal disease,” says Morton Goldberg, M.D., chairman of the board of NNRI. “The NNRI-Oxford partnership is an excellent model of how NNRI collaborations can accelerate the translation of laboratory-based research into clinical trials, ultimately getting successful treatments for rare diseases like inherited retinal degenerations to the market and out to the people who need them.”
Based on the agreement, Oxford BioMedica will receive approximately €43 million ($56 million) from sanofi-aventis over a three-year period. Oxford BioMedica is eligible to receive additional fees if development efforts are successful.
The treatments will utilize Oxford BioMedica’s LentiVector® gene delivery technology to deliver healthy vision-saving genes to the retina.
About Foundation Fighting Blindness
The Foundation Fighting Blindness is the largest source of non-governmental funding for retinal degenerative disease research in the world. The urgent mission of the Foundation Fighting Blindness is to drive the research that will provide preventions, treatments and cures for people affected by retinitis pigmentosa, macular degeneration, Usher syndrome, and the entire spectrum of retinal degenerative diseases. The Foundation has invested over $140 million to provide seed money for scientific research of diseases of the retina, which cause blindness. Further information is available at www.FightBlindness.org.
About National Neurovision Research Institute (NNRI)
NNRI is a recently-established non-profit support organization of the Foundation Fighting Blindness (FFB), the leading non-government funding source for inherited orphan retinal degeneration research. The mission of NNRI is to accelerate the translation of laboratory based research into clinical trials for treatments and cures of retinal degenerative diseases. It is a medical research institute that obtains support from government agencies, corporations and private foundations. It may also receive royalties or licensing fees from the drug discovery processes and commercialization of new therapies. Further information is available at www.nnri.info.
Sunday, April 19, 2009
Vigorous Exercise May Help Prevent Vision Loss
Vigorous exercise may help prevent vision loss, according to a pair of studies from the U.S. Department of Energy's Lawrence Berkeley National Laboratory. The studies tracked approximately 31,000 runners for more than seven years, and found that running reduced the risk of both cataracts and age-related macular degeneration.
The research, which is among the first to suggest that vigorous exercise may help prevent vision loss, offers hope for people seeking to fend off the onset of eye disease.
"In addition to obtaining regular eye exams, people can take a more active role in preserving their vision," says Paul Williams, an epidemiologist in Berkeley Lab's Life Sciences Division who conducted the research. "The studies suggest that people can perhaps lessen their risk for cataracts and macular degeneration by taking part in a fitness regimen that includes vigorous exercise."
A cataract, which is a cloudy opacity of the eye lens, is the leading cause of blindness. More than one-half of people in the U.S. over the age of 65 suffer from some form of cataracts. Macular degeneration, which is damage to the retina, is the leading cause of irreversible vision loss in older white Americans, affecting 28 percent of people aged 75 and older.
Macular degeneration gradually destroys sharp, central vision. Macular degeneration affects the macula, the part of the eye that allows you to see fine detail. The macula is located in the center of the retina, the light-sensitive tissue at the back of the eye. The retina instantly converts light, or an image, into electrical impulses. The retina then sends these impulses, or nerve signals, to the brain. Macular degeneration causes no pain.
The diseases have several known risk factors, such as sunlight exposure and diabetes in the case of cataracts, but few interventions. Now, it appears that vigorous cardiovascular exercise may be one way to derail the diseases.
To conduct the research, Williams analyzed data collected in the National Runners' Health Study, which he established in 1991 to determine the health benefits of running.
In this case, he followed approximately 29,000 male runners and 12,000 female runners for more than seven years. Of these people, 733 men reported being diagnosed with cataracts on a questionnaire filled out at the end of the study. Too few women reported cataracts to track.
Men who ran more than 5.7 miles per day had a 35 percent lower risk of developing cataracts than men who ran less than 1.4 miles per day. The study also analyzed men's 10-kilometer race performances, which is a good indicator of overall fitness. The fittest men boasted one-half the risk of developing cataracts compared to the least-fit men.
A second study found that running appeared to reduce the risk of macular degeneration. In the study, 152 men and women reported being diagnosed with the disease. Compared to people who ran less than 1.2 miles per day, people who averaged between 1.2 and 2.4 miles per day had a 19 percent lower risk for the disease, and people who ran more than 2.4 miles per day had between 42 percent and 54 percent lower risk of macular degeneration.
"These findings are compelling because of the large size of the study, and the fact that we are looking at something that is fairly well defined: vigorous exercise, as opposed to more moderate exercise," says Williams.
Most of the runners in the study exceeded the current public health recommendations for physical activity, which is at least 30 minutes of moderate-intensity activities such as brisk walking five days a week, or smaller doses of more vigorous exercise such as running. It is unclear whether people might also lower their risk for cataracts and age-related macular degeneration by walking.
"We know there are important health benefits to walking, including lowering heart disease risk," says Williams. "It is quite likely that the studies' results might apply to a lesser extent to smaller doses of more moderate exercise."
Williams also adds that further research is needed to explore why there is a link between vigorous exercise and a decreased risk for eye disease.
"We know some of the physiological benefits of exercise, and we know about the physiological background of these diseases, so we need to better understand where there's an overlap," says Williams.
The research, which is among the first to suggest that vigorous exercise may help prevent vision loss, offers hope for people seeking to fend off the onset of eye disease.
"In addition to obtaining regular eye exams, people can take a more active role in preserving their vision," says Paul Williams, an epidemiologist in Berkeley Lab's Life Sciences Division who conducted the research. "The studies suggest that people can perhaps lessen their risk for cataracts and macular degeneration by taking part in a fitness regimen that includes vigorous exercise."
A cataract, which is a cloudy opacity of the eye lens, is the leading cause of blindness. More than one-half of people in the U.S. over the age of 65 suffer from some form of cataracts. Macular degeneration, which is damage to the retina, is the leading cause of irreversible vision loss in older white Americans, affecting 28 percent of people aged 75 and older.
Macular degeneration gradually destroys sharp, central vision. Macular degeneration affects the macula, the part of the eye that allows you to see fine detail. The macula is located in the center of the retina, the light-sensitive tissue at the back of the eye. The retina instantly converts light, or an image, into electrical impulses. The retina then sends these impulses, or nerve signals, to the brain. Macular degeneration causes no pain.
The diseases have several known risk factors, such as sunlight exposure and diabetes in the case of cataracts, but few interventions. Now, it appears that vigorous cardiovascular exercise may be one way to derail the diseases.
To conduct the research, Williams analyzed data collected in the National Runners' Health Study, which he established in 1991 to determine the health benefits of running.
In this case, he followed approximately 29,000 male runners and 12,000 female runners for more than seven years. Of these people, 733 men reported being diagnosed with cataracts on a questionnaire filled out at the end of the study. Too few women reported cataracts to track.
Men who ran more than 5.7 miles per day had a 35 percent lower risk of developing cataracts than men who ran less than 1.4 miles per day. The study also analyzed men's 10-kilometer race performances, which is a good indicator of overall fitness. The fittest men boasted one-half the risk of developing cataracts compared to the least-fit men.
A second study found that running appeared to reduce the risk of macular degeneration. In the study, 152 men and women reported being diagnosed with the disease. Compared to people who ran less than 1.2 miles per day, people who averaged between 1.2 and 2.4 miles per day had a 19 percent lower risk for the disease, and people who ran more than 2.4 miles per day had between 42 percent and 54 percent lower risk of macular degeneration.
"These findings are compelling because of the large size of the study, and the fact that we are looking at something that is fairly well defined: vigorous exercise, as opposed to more moderate exercise," says Williams.
Most of the runners in the study exceeded the current public health recommendations for physical activity, which is at least 30 minutes of moderate-intensity activities such as brisk walking five days a week, or smaller doses of more vigorous exercise such as running. It is unclear whether people might also lower their risk for cataracts and age-related macular degeneration by walking.
"We know there are important health benefits to walking, including lowering heart disease risk," says Williams. "It is quite likely that the studies' results might apply to a lesser extent to smaller doses of more moderate exercise."
Williams also adds that further research is needed to explore why there is a link between vigorous exercise and a decreased risk for eye disease.
"We know some of the physiological benefits of exercise, and we know about the physiological background of these diseases, so we need to better understand where there's an overlap," says Williams.
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