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 sight. Show all posts
Showing posts with label sight. 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.
Monday, December 6, 2010
Drug Therapy To Cure Macular Degeneration
By Administration
Lucentis-is a drug therapy based on the cancer drug Avastin for wet macular degeneration. The treatment involves periodic injection of the drug directly into the eye. A higher percentage of those treated with Lucentis have shown improved vision than with any other treatment. Macugen-is another drug therapy for macular degeneration. It also involves periodic injections directly into the eye. It employs a molecule that attacks a protein involved with the growth of macular degeneration related blood vessels. macular degeneration treatment Vitamins and Minerals-are a treatment that is being used to treat dry macular degeneration. There is evidence to suggest that vitamins and minerals that have antioxidant properties will slow the progression of intermediate dry macular degeneration to the advanced form. The treatment typically involves large doses of Vitamin C, Vitamin E, Beta Carotene and Zinc Oxide.
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Lucentis-is a drug therapy based on the cancer drug Avastin for wet macular degeneration. The treatment involves periodic injection of the drug directly into the eye. A higher percentage of those treated with Lucentis have shown improved vision than with any other treatment. Macugen-is another drug therapy for macular degeneration. It also involves periodic injections directly into the eye. It employs a molecule that attacks a protein involved with the growth of macular degeneration related blood vessels. macular degeneration treatment Vitamins and Minerals-are a treatment that is being used to treat dry macular degeneration. There is evidence to suggest that vitamins and minerals that have antioxidant properties will slow the progression of intermediate dry macular degeneration to the advanced form. The treatment typically involves large doses of Vitamin C, Vitamin E, Beta Carotene and Zinc Oxide.
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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 30, 2010
Retinal Disease Highlights From the 2010 AAO Meeting
By Dr. Randall Wong
Many of us just returned from the largest ophthalmic “trade show” in the world. The American Academy of Ophthalmology convened in Chicago last week. This meeting was combined with the Middle East Africa Council of Ophthalmology (MEACO). Perhaps 40 K attended the meeting.
I also attended the 2 day retinal subspecialty meeting which preceded the larger AAO meeting. Thus, I had 5 days to expand my knowledge.
Most of the congress was focused on technology, especially electronic medical records. Few discoveries were revealed. This may be for two reasons: there is nothing really new going on right now, and/or, the Internet allows such rapid sharing of information, that it is impossible to “wow” anyone at this meeting. Probably both are true.
With regard to retinal disease, my particular specialty, there is little new, but lots to be excited about.
Avastin and Lucentis continue to be the mainstays of treatment for wet macular degeneration. There is evidence that the two drugs are similar in clinical efficacy…a notion I support. It is likely that these types of drugs will be delivered with a sustained release system, thus, obviating the need for repeated intraocular injections.
Ozurdex is now indicated for the treatment of uveitis. It was originally FDA approved for the treatment of RVO only. By itself, not earth-shattering, but does make sense clinically. Sustained release steroids for chronic intraocular inflammation. Sounds much better.
The highlight of the meeting is the potential for Iluvien to be FDA approved soon. Iluvien is similar to Ozurdex in that both are injectable intraocular sustained release systems. Iluvien will be a sustained release system that delivers intraocular steroids for the treatment of diabetic macular edema. While this is a particularly promising development for patients with diabetic retinopathy, this has larger implications for eye treatment overall.
What Does This Mean? Illuvien is likely to be the second FDA approved intraocular drug delivery system. This will be a significant endorsement of drug delivery to the eye. We are entering a new era of pharmaceutical therapeutics; sustained release inside the eye. For now, we are focused on retinal disease. But soon, very soon, devices will emerge promising better therapeutics for almost any eye condition.
Just think, glaucoma may be treated by such a device.
Many of us just returned from the largest ophthalmic “trade show” in the world. The American Academy of Ophthalmology convened in Chicago last week. This meeting was combined with the Middle East Africa Council of Ophthalmology (MEACO). Perhaps 40 K attended the meeting.
I also attended the 2 day retinal subspecialty meeting which preceded the larger AAO meeting. Thus, I had 5 days to expand my knowledge.
Most of the congress was focused on technology, especially electronic medical records. Few discoveries were revealed. This may be for two reasons: there is nothing really new going on right now, and/or, the Internet allows such rapid sharing of information, that it is impossible to “wow” anyone at this meeting. Probably both are true.
With regard to retinal disease, my particular specialty, there is little new, but lots to be excited about.
Avastin and Lucentis continue to be the mainstays of treatment for wet macular degeneration. There is evidence that the two drugs are similar in clinical efficacy…a notion I support. It is likely that these types of drugs will be delivered with a sustained release system, thus, obviating the need for repeated intraocular injections.
Ozurdex is now indicated for the treatment of uveitis. It was originally FDA approved for the treatment of RVO only. By itself, not earth-shattering, but does make sense clinically. Sustained release steroids for chronic intraocular inflammation. Sounds much better.
The highlight of the meeting is the potential for Iluvien to be FDA approved soon. Iluvien is similar to Ozurdex in that both are injectable intraocular sustained release systems. Iluvien will be a sustained release system that delivers intraocular steroids for the treatment of diabetic macular edema. While this is a particularly promising development for patients with diabetic retinopathy, this has larger implications for eye treatment overall.
What Does This Mean? Illuvien is likely to be the second FDA approved intraocular drug delivery system. This will be a significant endorsement of drug delivery to the eye. We are entering a new era of pharmaceutical therapeutics; sustained release inside the eye. For now, we are focused on retinal disease. But soon, very soon, devices will emerge promising better therapeutics for almost any eye condition.
Just think, glaucoma may be treated by such a device.
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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Monday, October 4, 2010
Retinal Degeneration Can be Prevented with Nanotechnology Gene Therapy
Friday, 01 October 2010
Researchers from Tufts University published results from a study showing vision-saving gene therapy to the eyes can be delivered via nanotechnology. A protein called Glial Cell Line-Derived Neurtrophic Factor (GDNF) can protect the eyes from diseases of the retina, such as and retinitis pigmentosa.
The previous method for delivering genetic material with a virus had several problems and side effects. Although the study is in its infancy, and the results are temporary, mice injected with the GDNF carrying nanoparticle had a 3.9 to 7.7-fold reduction in damage to the retina. Seven days after treatment, the GDNF-nanoparticle treated mice had up to 39% better eyesight than mice in the control group.
Two weeks after the treatment, GDNF-nanoparticle-injected mice had nuclear layers of the retina that were almost 24 to over 39 percent thicker than control mice. However, after 14 days, these advantages seem to have vanished. According to Dr. Brett Katzen, "The idea of using gene therapy to help cure - or at least improve - the eyesight of patients with macular degeneration should be exciting to eye doctors everywhere. This is a great first step." The research shows an incredible potential for nanotechnology to develop an effective carrier for delivering gene therapy.
This therapy can then lead to a new generation of treatments for retinal diseases. Age-related macular degeneration is the leading cause of blindness in Americans over the age of 65.
Researchers from Tufts University published results from a study showing vision-saving gene therapy to the eyes can be delivered via nanotechnology. A protein called Glial Cell Line-Derived Neurtrophic Factor (GDNF) can protect the eyes from diseases of the retina, such as and retinitis pigmentosa.
The previous method for delivering genetic material with a virus had several problems and side effects. Although the study is in its infancy, and the results are temporary, mice injected with the GDNF carrying nanoparticle had a 3.9 to 7.7-fold reduction in damage to the retina. Seven days after treatment, the GDNF-nanoparticle treated mice had up to 39% better eyesight than mice in the control group.
Two weeks after the treatment, GDNF-nanoparticle-injected mice had nuclear layers of the retina that were almost 24 to over 39 percent thicker than control mice. However, after 14 days, these advantages seem to have vanished. According to Dr. Brett Katzen, "The idea of using gene therapy to help cure - or at least improve - the eyesight of patients with macular degeneration should be exciting to eye doctors everywhere. This is a great first step." The research shows an incredible potential for nanotechnology to develop an effective carrier for delivering gene therapy.
This therapy can then lead to a new generation of treatments for retinal diseases. Age-related macular degeneration is the leading cause of blindness in Americans over the age of 65.
Monday, September 13, 2010
Macular Degeneration and your eyesight
You have most probably heard of this very common condition that damages your eyesight as you age. Because this condition affects more elderly people it is often referred to as age-related macular degeneration. Unfortunately there is no cure available for this condition however there are treatments that can help. This blog outlines the latest in research and treatments regarding macular degeneration and aims to help you make the most out of your eyesight in the mean time.
Now macular degeneration as the name implies affects the macula, which is an area right at the back of the eye on a structure that detects light known as the retina. Your macula is the part of the retina that allows you to see things in great detail. In fact many birds have better maculas than us, as they need to see things in great detail from up in the air. The condition of macula degeneration implies that the macula is damaged and as this damage becomes more extensive your eyesight will be affected. There are two types of macula degeneration and they are known as the wet or the dry type, the most common of the two is ‘dry’ maculae degeneration. In this type you get little yellow patches that pop up around your macula and your vision slowly worsens. In ‘wet’ macula degeneration there are tiny blood vessels in the back of your eye that grow and then leak out blood and other fluid. This tends to make ones vision worse more quickly and you should note that dry degeneration can turn into the wet kind.
Those who present with this condition for the most part have difficulty reading, making out fine detail and even have trouble recognizing friends and families faces. After a few years of having this condition things that are in the middle of your vision will begin to look blurred and you may struggle to make things out. After a while the middle of your vision may just appear black and you often cant see anything in this area, this means that you will be unable to see things that are right in front of you. However your peripheral vision will not be affected.
There are things that you can do to cope with this condition as well as medicines that can help. Your doctor may teach you how to make better use of your peripheral vision and tell you that using bright lighting in your home will help you see better. You may also need to make text on the computer screen bigger and use magnifying glasses when reading a book. Most of the medical treatments are aimed at the treatment of wet macular degeneration and in fact there are not many effective treatments for the dry variety. Laser therapy can be used to stop the macular degeneration from getting worse in the sense that these lasers burn away those yellow patches that form around the macular early in the disease course. Also there is no need to worry as laser therapy is not painful and is quite quick, however the evidence supporting this form of treatment is not great at this stage. In fact some research suggests that laser treatment can cause new blood vessels to from on the back of the eye that can make your sight worse.
Mineral and vitamin supplements may be useful in slowing down or stopping macula degeneration from occurring. You should take zinc, vitamin E and C as well as beta-carotene. Remember here that you will need to take them for a long time and in high doses to be affective and remember that these are not without their side effects. Some people find that they have problems with passing urine, others complain of stomach pains and some people notice that their skin turns a little yellow. If this is that case with you then you should stop taking the tablets and visit your doctor.
Wet macular degeneration can be treated with photodynamic laser surgery whereby a dye that is sensitive to light is injected into your bloodstream and then a laser is shone into your eye. The dye that was injected into the blood helps the laser to destroy all of those leaky blood vessels that are damaging your eye. This method has mixed reviews on effectiveness and one should have a good discussion with their doctor regarding the risks and benefits of this procedure before having it done.
There is another type of laser that can be used to destroy the blood vessels in the eye that leak, but this is only affective in a few people with very severe disease. There is a chance with this procedure that the blood vessels will grow back anyway and the laser can sometimes damage the eye. Radiotherapy is another option but lacks suitable research to say whether or not it works and we always worry that radiation may damage other parts of the eye.
There is an injection that you can have in your eyeball called pegaptanib, however for obvious reasons not many people like the idea of this if they can help it. Also you have to have two injections every month and the evidence is not great that it works wonders, although there are some convincing studies. There is another injection called ranibizumab that you get in your eyeball and this also does not have great results but is indicated in people with wet macular degeneration that is getting worse.
So the most important thing is what will happen to you and in this case the outcome is not fantastic. Over many years your vision will gradually get worse and it will be much worse in the centre of your vision than in the peripheries and you are unlikely to go completely blind. Unfortunately we don’t know how quickly things will turn bad and each patient is different, but most people manage to get around even with severe disease as they are able to use their peripheral vision much more effectively.
Now macular degeneration as the name implies affects the macula, which is an area right at the back of the eye on a structure that detects light known as the retina. Your macula is the part of the retina that allows you to see things in great detail. In fact many birds have better maculas than us, as they need to see things in great detail from up in the air. The condition of macula degeneration implies that the macula is damaged and as this damage becomes more extensive your eyesight will be affected. There are two types of macula degeneration and they are known as the wet or the dry type, the most common of the two is ‘dry’ maculae degeneration. In this type you get little yellow patches that pop up around your macula and your vision slowly worsens. In ‘wet’ macula degeneration there are tiny blood vessels in the back of your eye that grow and then leak out blood and other fluid. This tends to make ones vision worse more quickly and you should note that dry degeneration can turn into the wet kind.
Those who present with this condition for the most part have difficulty reading, making out fine detail and even have trouble recognizing friends and families faces. After a few years of having this condition things that are in the middle of your vision will begin to look blurred and you may struggle to make things out. After a while the middle of your vision may just appear black and you often cant see anything in this area, this means that you will be unable to see things that are right in front of you. However your peripheral vision will not be affected.
There are things that you can do to cope with this condition as well as medicines that can help. Your doctor may teach you how to make better use of your peripheral vision and tell you that using bright lighting in your home will help you see better. You may also need to make text on the computer screen bigger and use magnifying glasses when reading a book. Most of the medical treatments are aimed at the treatment of wet macular degeneration and in fact there are not many effective treatments for the dry variety. Laser therapy can be used to stop the macular degeneration from getting worse in the sense that these lasers burn away those yellow patches that form around the macular early in the disease course. Also there is no need to worry as laser therapy is not painful and is quite quick, however the evidence supporting this form of treatment is not great at this stage. In fact some research suggests that laser treatment can cause new blood vessels to from on the back of the eye that can make your sight worse.
Mineral and vitamin supplements may be useful in slowing down or stopping macula degeneration from occurring. You should take zinc, vitamin E and C as well as beta-carotene. Remember here that you will need to take them for a long time and in high doses to be affective and remember that these are not without their side effects. Some people find that they have problems with passing urine, others complain of stomach pains and some people notice that their skin turns a little yellow. If this is that case with you then you should stop taking the tablets and visit your doctor.
Wet macular degeneration can be treated with photodynamic laser surgery whereby a dye that is sensitive to light is injected into your bloodstream and then a laser is shone into your eye. The dye that was injected into the blood helps the laser to destroy all of those leaky blood vessels that are damaging your eye. This method has mixed reviews on effectiveness and one should have a good discussion with their doctor regarding the risks and benefits of this procedure before having it done.
There is another type of laser that can be used to destroy the blood vessels in the eye that leak, but this is only affective in a few people with very severe disease. There is a chance with this procedure that the blood vessels will grow back anyway and the laser can sometimes damage the eye. Radiotherapy is another option but lacks suitable research to say whether or not it works and we always worry that radiation may damage other parts of the eye.
There is an injection that you can have in your eyeball called pegaptanib, however for obvious reasons not many people like the idea of this if they can help it. Also you have to have two injections every month and the evidence is not great that it works wonders, although there are some convincing studies. There is another injection called ranibizumab that you get in your eyeball and this also does not have great results but is indicated in people with wet macular degeneration that is getting worse.
So the most important thing is what will happen to you and in this case the outcome is not fantastic. Over many years your vision will gradually get worse and it will be much worse in the centre of your vision than in the peripheries and you are unlikely to go completely blind. Unfortunately we don’t know how quickly things will turn bad and each patient is different, but most people manage to get around even with severe disease as they are able to use their peripheral vision much more effectively.
Wednesday, September 1, 2010
FDA grants pSivida, Alimera expedited review for macular degeneration therapy
FDA grants pSivida, Alimera expedited review for macular degeneration therapy
August 31, 2010 by MassDevice staff
pSivida Corp. and Alimera Sciences win priority review status for their Iluvien drug/device combination, designed to treat diabetic macular degeneration.
PSDV, ALIM logos
The Food & Drug Administration put pSivida Corp. (NSDQ:PSDV) and Alimera Sciences Inc. (NSDQ:ALIM) on the fast track, granting an expedited review for their drug/device combination designed to treat diabetic macular edema.
Watertown, Mass.-based pSivida and Alpharetta, Ga.-based Alimera filed a new drug application with the FDA in June for Iluvien, a sustained release drug delivery system that delivers flucocinolone acetonide, a steroid, for the treatment of DME.
The federal watchdog agency granted priority review status to the application, moving the goal for finishing the review from 10 months back to six months.
That means a response could drop during the fourth quarter, pSivida president and CEO Dr. Paul Ashton said in prepared remarks, adding that FDA approval would trigger a $25 million milestone payment from Alimera.
The milestone payment wouldn't be the first time Alimera ponied up for pSivida. Its $72 million IPO in April triggered the repayment of a $15 million loan and $225,000 in interest. The companies are seeking European approval for Iluvien. If it makes it to market, pSivida will collect 20 percent of the net profits.
The FDA has already cleared a pair of pSivida products: Retisert, for the treatment of posterior uveitis, and Vitrasert for the treatment of AIDS-related cytomegalovirus retinitis. Both are licensed to Bausch & Lomb Inc. The company is also developing other ophthalmic products with Pfizer Inc. (NYSE:PFE), its largest shareholder, and has products of its own in the pipeline outside of ophthalmology, according to a press release.
*
August 31, 2010 by MassDevice staff
pSivida Corp. and Alimera Sciences win priority review status for their Iluvien drug/device combination, designed to treat diabetic macular degeneration.
PSDV, ALIM logos
The Food & Drug Administration put pSivida Corp. (NSDQ:PSDV) and Alimera Sciences Inc. (NSDQ:ALIM) on the fast track, granting an expedited review for their drug/device combination designed to treat diabetic macular edema.
Watertown, Mass.-based pSivida and Alpharetta, Ga.-based Alimera filed a new drug application with the FDA in June for Iluvien, a sustained release drug delivery system that delivers flucocinolone acetonide, a steroid, for the treatment of DME.
The federal watchdog agency granted priority review status to the application, moving the goal for finishing the review from 10 months back to six months.
That means a response could drop during the fourth quarter, pSivida president and CEO Dr. Paul Ashton said in prepared remarks, adding that FDA approval would trigger a $25 million milestone payment from Alimera.
The milestone payment wouldn't be the first time Alimera ponied up for pSivida. Its $72 million IPO in April triggered the repayment of a $15 million loan and $225,000 in interest. The companies are seeking European approval for Iluvien. If it makes it to market, pSivida will collect 20 percent of the net profits.
The FDA has already cleared a pair of pSivida products: Retisert, for the treatment of posterior uveitis, and Vitrasert for the treatment of AIDS-related cytomegalovirus retinitis. Both are licensed to Bausch & Lomb Inc. The company is also developing other ophthalmic products with Pfizer Inc. (NYSE:PFE), its largest shareholder, and has products of its own in the pipeline outside of ophthalmology, according to a press release.
*
Monday, August 23, 2010
Gene therapy can correct inherited retinal eye diseases
Researchers at the American Academy of Ophthalmology have found that Leber’s congenital Amaurosis (LCA), a very severe form of retinal disease
can be improved with the help of gene therapy.
Not only that, but the improvements were also found to be stable for two years.
Gene Therapy Can Correct Retinal Eye Diseases: LCA can be diagnosed in children at a very early age, sometimes even at infancy.
The main symptoms
of LCA are severity in vision loss and nystagmus(involuntary eye movement). By the time a person reaches his thirties or forties LCA develops into blindness.
* The impact of gene therapy could mainly be observed in children. The visual acuity and light sensitivity was tremendous in these children.
* Not only in children, researchers were also able to observe improvement in adults.
The Research and Theory: LCA is due to the mutations caused in any of the 13 genes in our body. Researchers were studying a Type 2 LCA which is due to mutation in the RPE65 gene.
* The doctors injected a normal functioning RPE65 gene which was joined with a virus into the sub-retinal space upon performing a surgery.
* The altered virus places the normally functioning RPE65 gene into the diseased cells and modifies the defective enzymes.
* After 2 weeks from the date of surgery, doctors observed that the patients reported an improvement in vision even in dim light.
* There were a few patients who also said that their visual acuity improved.
* A few even experienced massive improvement in nystagmus.
* The most encouraging result was that none of the patients experienced adverse effects.
Gene therapy does not improve sight on a permanent basis. But, gene therapy can correct inherited retinal eye diseases and help people restore sight.
People who undergo gene therapy need not be classified as blind any more. Researchers are trying hard to implement this technique in a safer way in younger children.
can be improved with the help of gene therapy.
Not only that, but the improvements were also found to be stable for two years.
Gene Therapy Can Correct Retinal Eye Diseases: LCA can be diagnosed in children at a very early age, sometimes even at infancy.
The main symptoms
of LCA are severity in vision loss and nystagmus(involuntary eye movement). By the time a person reaches his thirties or forties LCA develops into blindness.
* The impact of gene therapy could mainly be observed in children. The visual acuity and light sensitivity was tremendous in these children.
* Not only in children, researchers were also able to observe improvement in adults.
The Research and Theory: LCA is due to the mutations caused in any of the 13 genes in our body. Researchers were studying a Type 2 LCA which is due to mutation in the RPE65 gene.
* The doctors injected a normal functioning RPE65 gene which was joined with a virus into the sub-retinal space upon performing a surgery.
* The altered virus places the normally functioning RPE65 gene into the diseased cells and modifies the defective enzymes.
* After 2 weeks from the date of surgery, doctors observed that the patients reported an improvement in vision even in dim light.
* There were a few patients who also said that their visual acuity improved.
* A few even experienced massive improvement in nystagmus.
* The most encouraging result was that none of the patients experienced adverse effects.
Gene therapy does not improve sight on a permanent basis. But, gene therapy can correct inherited retinal eye diseases and help people restore sight.
People who undergo gene therapy need not be classified as blind any more. Researchers are trying hard to implement this technique in a safer way in younger children.
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 27, 2010
Medicine from Moss to produce human protien
Diabetics use human insulin produced in bacteria in order to treat their metabolic disorder. Many other genetically engineered proteins are also on the advance. They are being used for diagnosis as well as for therapy.
Whereas insulin used to be extracted from slaughterhouse waste, today it is produced genetically in bacteria. However, more complex proteins have to be synthesised in more complex organisms. This takes place mostly in bioreactors using animal cell lines. Biotechnologist Prof. Ralf Reski from Freiburg, Germany, has developed the moss Physcomitrella patens into a safe and inexpensive alternative supplier of medicine.
His group has now, under Dr. Eva Decker, for the first time succeeded in producing a human protein in a moss bioreactor, which has been assigned the "orphan drug" status by the respective EU authorities. This means the development and approval of such medication receive particular support from the authorities. In many people the amount of this protein decreases with old age - with severe consequences. Eva Decker explains: "With the complement factor H we have produced a protein in moss that otherwise occurs only in blood and is important for the immune system. Not enough of this protein in older people is the main cause of blindness for 50 million people worldwide. This age-related macular degeneration (AMD) is a problem, particularly in industrialised countries."
Biochemists from the Freiburg Centre for Systems Biology under Dr. Andreas Schlosser were able to show with the help of high-performance mass spectrometers that the human factor H engineered into and produced by moss was a complete protein. Infection biologists headed by Prof. Peter F. Zipfel from the Hans-Knöll-Institute in Jena, Germany, were able to prove in biological assays that factor H from moss is fully functional. "Currently factor H is not available in pharmacies, so treatment for AMD with this protein is not possible. To date recombinant production of factor H was barely feasible. I am convinced that for the first time the moss bioreactor is a promising option", says Peter Zipfel.
This work was supported by the German Federal Ministry of Education and Research (BMBF), the Freiburg Initiative for Systems Biology and the Cluster of Excellence BIOSS.
Dr. Annette Büttner-Mainik, first author of the publication, was a Kekulé scholarship holder from the endowment fund of the German Chemical Industry (FCI).
The title of the original publication is: Annette Büttner-Mainik, Juliana Parsons, Hanna Jérôme, Andrea Hartmann, Stephanie Lamer, Andreas Schaaf, Andreas Schlosser, Peter F. Zipfel, Ralf Reski, Eva L. Decker (2010): Production of biologically active recombinant human Factor H in Physcomitrella. Plant Biotechnology Journal, doi: 10.1111/j.1467-7652.2010.00552.x.
"It will take a while before medication produced in moss is available in pharmacies", says Ralf Reski, member of the Innovation Think Tank of the governor of Baden-Wuerttemberg. "We are further optimising the moss bioreactor using methods from Systems Biology and Synthetic Biology. However, the implementation of clinical studies and the setting up of industrial production is long-winded and expensive; this is the task of industry and not of university research."
Whereas insulin used to be extracted from slaughterhouse waste, today it is produced genetically in bacteria. However, more complex proteins have to be synthesised in more complex organisms. This takes place mostly in bioreactors using animal cell lines. Biotechnologist Prof. Ralf Reski from Freiburg, Germany, has developed the moss Physcomitrella patens into a safe and inexpensive alternative supplier of medicine.
His group has now, under Dr. Eva Decker, for the first time succeeded in producing a human protein in a moss bioreactor, which has been assigned the "orphan drug" status by the respective EU authorities. This means the development and approval of such medication receive particular support from the authorities. In many people the amount of this protein decreases with old age - with severe consequences. Eva Decker explains: "With the complement factor H we have produced a protein in moss that otherwise occurs only in blood and is important for the immune system. Not enough of this protein in older people is the main cause of blindness for 50 million people worldwide. This age-related macular degeneration (AMD) is a problem, particularly in industrialised countries."
Biochemists from the Freiburg Centre for Systems Biology under Dr. Andreas Schlosser were able to show with the help of high-performance mass spectrometers that the human factor H engineered into and produced by moss was a complete protein. Infection biologists headed by Prof. Peter F. Zipfel from the Hans-Knöll-Institute in Jena, Germany, were able to prove in biological assays that factor H from moss is fully functional. "Currently factor H is not available in pharmacies, so treatment for AMD with this protein is not possible. To date recombinant production of factor H was barely feasible. I am convinced that for the first time the moss bioreactor is a promising option", says Peter Zipfel.
This work was supported by the German Federal Ministry of Education and Research (BMBF), the Freiburg Initiative for Systems Biology and the Cluster of Excellence BIOSS.
Dr. Annette Büttner-Mainik, first author of the publication, was a Kekulé scholarship holder from the endowment fund of the German Chemical Industry (FCI).
The title of the original publication is: Annette Büttner-Mainik, Juliana Parsons, Hanna Jérôme, Andrea Hartmann, Stephanie Lamer, Andreas Schaaf, Andreas Schlosser, Peter F. Zipfel, Ralf Reski, Eva L. Decker (2010): Production of biologically active recombinant human Factor H in Physcomitrella. Plant Biotechnology Journal, doi: 10.1111/j.1467-7652.2010.00552.x.
"It will take a while before medication produced in moss is available in pharmacies", says Ralf Reski, member of the Innovation Think Tank of the governor of Baden-Wuerttemberg. "We are further optimising the moss bioreactor using methods from Systems Biology and Synthetic Biology. However, the implementation of clinical studies and the setting up of industrial production is long-winded and expensive; this is the task of industry and not of university research."
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.
Thursday, June 10, 2010
Ann Arbor Pharma Firm Testing Zinc For Alzheimer's Treatment
Ann Arbor-based Adeona Pharmaceuticals Inc. (AMEX: AEN) Monday announced the completion of 50 percnet enrollment in Part 2 of its clinical study, "A Prospective, Randomized, Double Blind Trial of a Novel Oral Zinc Cysteine Preparation in Alzheimer's Disease (CopperProof-2)."
The CopperProof-2 study represents the first controlled clinical study of oral zinc cysteine for the dietary management of Alzheimer's disease and mild cognitive impairment.
Part 2 of the CopperProof-2 study is designed as a 60-subject comparator study. Subjects are randomized on a 50:50 basis to receive either Zinthionein ZC or matching placebo. After 3 and 6 months on clinical trial material, serum measurements of zinc and copper are taken, and any changes in cognitive function using standard clinical tests used in Alzheimer's disease and mild cognitive impairment are recorded.
The completion of 50 percent enrollment follows Adeona's April 14 announcement of positive results from Part 1 of the CopperProof-2 study. Part 1 demonstrated a substantially lower incidence of adverse effects in Alzheimer's disease and mild cognitive impairment subjects (33 percent versus 100 percent) in favor of Zinthionein ZC (containing 150 mg of elemental zinc acetate and 100 mg of cysteine) compared to Galzin (containing either 50 mg or 100 mg of elemental zinc as zinc acetate).
Zinthionein ZC also demonstrated superior serum zinc bioavailability in Alzheimer's disease and mild cognitive impairment subjects compared to both the 50 mg and 100 mg dose levels of Galzin.
"Having pioneered the use of oral zinc therapy in dry age-related macular degeneration, which has now become the standard of care, I believe that Adeona's once-daily, high bioavailability, well-tolerated oral zinc cysteine formulation has the potential to ameliorate the sub-clinical zinc deficiency in Alzheimer's and mild cognitive impairment subjects and substantially grow current markets for oral zinc-based therapies," said David Newsome, M.D., Adeona's senior vice president for research and development.
Added Adeona CEO James S. Kuo, M.D.: "We are pleased to have reached this enrollment milestone on a timely basis and within budget. Along with the recently announced Meda collaboration for flupirtine's development and completion of 50 percent enrollment in the Trimesta multiple sclerosis clinical trial, it represents one of several major transformational changes taking place at the company in the past few months."
Observations by Adeona scientists and other scientists of sub-clinical zinc deficiency in Alzheimer's disease patients plus a body of published literature that chronic elevated copper exposure contributes to the progression of Alzheimer's disease and mild cognitive impairment prompted the present CopperProof-2 clinical study.
Alzheimer's disease can affect the entire brain but it is particularly associated with loss of tissue in the hippocampus, the area in the brain responsible for several functions including short-term memory retention and processing. The hippocampus has one of the highest concentrations of zinc in the brain. Hippocampal zinc is thought to play a role in hundreds of protective enzymes and other systems, including those that detoxify amyloid beta, an abnormally folded peptide that accumulates in aging and is a biomarker for Alzheimer's disease. When cerebrospinal fluid zinc is low, levels of the particularly toxic beta amyloid 42 are elevated.
Hippocampal zinc serves as a neurotransmitter, and also modulates a specific neuroreceptor. If the neuroexcitation goes uncontrolled, there is a derangement of brain tissue function, and possibly neuronal death. By elevating cerebrospinal fluid zinc, the receptor excitation may be better controlled, improving tissue function and thereby acute cognition and tissue survival, as may have been seen in the 1992 study. NMDA-receptor antagonists now available for Alzheimer's, including Namenda and Axura, annually sell an estimated $2.6 billion.
Zinthionein ZC is a once-daily, gastroretentive, sustained-release, oral tablet formulation of zinc and cysteine. Zinc, an essential nutrient, participates as a necessary factor in the activity of over 200 enzymes and the DNA binding capacity of over 400 nuclear regulatory elements. Zinc may also directly participate in antioxidant protection by reducing the susceptibility of sulfhydril groups to damage by oxidative free radicals. Cysteine is an amino acid that has potent anti-oxidant properties and is a necessary component of the copper-zinc-binding protein, metallothionein.
Zinthionein ZC was invented and developed by Adeona scientists to achieve the convenience of once-daily dosing, high oral bioavailability and to minimize gastrointestinal side effects associated with other commercially available, oral zinc products. All of Zinthionein ZC's constituents have GRAS (Generally Regarded as Safe) status. Adeona is developing Zinthionein ZC as a prescription medical food for the dietary management of Alzheimer's disease and mild cognitive impairment. Zinthionein ZC is protected by multiple U.S. and international pending patent applications held by Adeona.
Adeona is a pharmaceutical company developing new medicines for serious central nervous systems diseases. Adeona's primary strategy is to in-license clinical-stage drug candidates that have already demonstrated a certain level of clinical efficacy and develop them to an inflection point in valuation resulting in a significant development and marketing collaboration.
Its other drugs include Trimesta (estriol) is an investigational oral drug for the treatment of relapsing remitting multiple sclerosis, currently in clinical trials, and Effirma (flupirtine), a centrally-acting investigational oral drug for the treatment of fibromyalgia syndrome. Adeona has entered into a potential $17.5 million corporate partnership with Meda AB. As part of the agreement, Meda will assume all future development costs while Adeona is entitled to receive milestone payments and royalties.
The CopperProof-2 study represents the first controlled clinical study of oral zinc cysteine for the dietary management of Alzheimer's disease and mild cognitive impairment.
Part 2 of the CopperProof-2 study is designed as a 60-subject comparator study. Subjects are randomized on a 50:50 basis to receive either Zinthionein ZC or matching placebo. After 3 and 6 months on clinical trial material, serum measurements of zinc and copper are taken, and any changes in cognitive function using standard clinical tests used in Alzheimer's disease and mild cognitive impairment are recorded.
The completion of 50 percent enrollment follows Adeona's April 14 announcement of positive results from Part 1 of the CopperProof-2 study. Part 1 demonstrated a substantially lower incidence of adverse effects in Alzheimer's disease and mild cognitive impairment subjects (33 percent versus 100 percent) in favor of Zinthionein ZC (containing 150 mg of elemental zinc acetate and 100 mg of cysteine) compared to Galzin (containing either 50 mg or 100 mg of elemental zinc as zinc acetate).
Zinthionein ZC also demonstrated superior serum zinc bioavailability in Alzheimer's disease and mild cognitive impairment subjects compared to both the 50 mg and 100 mg dose levels of Galzin.
"Having pioneered the use of oral zinc therapy in dry age-related macular degeneration, which has now become the standard of care, I believe that Adeona's once-daily, high bioavailability, well-tolerated oral zinc cysteine formulation has the potential to ameliorate the sub-clinical zinc deficiency in Alzheimer's and mild cognitive impairment subjects and substantially grow current markets for oral zinc-based therapies," said David Newsome, M.D., Adeona's senior vice president for research and development.
Added Adeona CEO James S. Kuo, M.D.: "We are pleased to have reached this enrollment milestone on a timely basis and within budget. Along with the recently announced Meda collaboration for flupirtine's development and completion of 50 percent enrollment in the Trimesta multiple sclerosis clinical trial, it represents one of several major transformational changes taking place at the company in the past few months."
Observations by Adeona scientists and other scientists of sub-clinical zinc deficiency in Alzheimer's disease patients plus a body of published literature that chronic elevated copper exposure contributes to the progression of Alzheimer's disease and mild cognitive impairment prompted the present CopperProof-2 clinical study.
Alzheimer's disease can affect the entire brain but it is particularly associated with loss of tissue in the hippocampus, the area in the brain responsible for several functions including short-term memory retention and processing. The hippocampus has one of the highest concentrations of zinc in the brain. Hippocampal zinc is thought to play a role in hundreds of protective enzymes and other systems, including those that detoxify amyloid beta, an abnormally folded peptide that accumulates in aging and is a biomarker for Alzheimer's disease. When cerebrospinal fluid zinc is low, levels of the particularly toxic beta amyloid 42 are elevated.
Hippocampal zinc serves as a neurotransmitter, and also modulates a specific neuroreceptor. If the neuroexcitation goes uncontrolled, there is a derangement of brain tissue function, and possibly neuronal death. By elevating cerebrospinal fluid zinc, the receptor excitation may be better controlled, improving tissue function and thereby acute cognition and tissue survival, as may have been seen in the 1992 study. NMDA-receptor antagonists now available for Alzheimer's, including Namenda and Axura, annually sell an estimated $2.6 billion.
Zinthionein ZC is a once-daily, gastroretentive, sustained-release, oral tablet formulation of zinc and cysteine. Zinc, an essential nutrient, participates as a necessary factor in the activity of over 200 enzymes and the DNA binding capacity of over 400 nuclear regulatory elements. Zinc may also directly participate in antioxidant protection by reducing the susceptibility of sulfhydril groups to damage by oxidative free radicals. Cysteine is an amino acid that has potent anti-oxidant properties and is a necessary component of the copper-zinc-binding protein, metallothionein.
Zinthionein ZC was invented and developed by Adeona scientists to achieve the convenience of once-daily dosing, high oral bioavailability and to minimize gastrointestinal side effects associated with other commercially available, oral zinc products. All of Zinthionein ZC's constituents have GRAS (Generally Regarded as Safe) status. Adeona is developing Zinthionein ZC as a prescription medical food for the dietary management of Alzheimer's disease and mild cognitive impairment. Zinthionein ZC is protected by multiple U.S. and international pending patent applications held by Adeona.
Adeona is a pharmaceutical company developing new medicines for serious central nervous systems diseases. Adeona's primary strategy is to in-license clinical-stage drug candidates that have already demonstrated a certain level of clinical efficacy and develop them to an inflection point in valuation resulting in a significant development and marketing collaboration.
Its other drugs include Trimesta (estriol) is an investigational oral drug for the treatment of relapsing remitting multiple sclerosis, currently in clinical trials, and Effirma (flupirtine), a centrally-acting investigational oral drug for the treatment of fibromyalgia syndrome. Adeona has entered into a potential $17.5 million corporate partnership with Meda AB. As part of the agreement, Meda will assume all future development costs while Adeona is entitled to receive milestone payments and royalties.
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