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We continue to suffer from an enormously undervalued stock which I believe is the result of a few shareholders who for some reason are not invested in the long-term growth of the company.
Yeah that's easy for an european like me. LoL
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http://www.bloomberg.com/news/2012-08-07/pfizer-agrees-to-settle-foreign-bribery-case-with-u-s-.html
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http://www.reuters.com/article/2012/08/07/us-pfizer-settlement-idUSBRE8760WM20120807
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Great, thank you very much!
Maybe the last hour to buy extremely cheap.
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Pfizer & Supreme Court
Supreme Court dismisses Pfizer's appeal in patent infringement case
Grau & Angulo
Miguel Gil
Spain
February 4 2013
The Supreme Court recently dismissed Pfizer's appeal in a patent infringement case regarding the besylate salt of amlodipine (commercialized by Pfizer as NORVAS). The judgment, which was issued on January 3 2013, was served on the parties on January 14 2013.
In 2005 Pfizer sued Bexal and Uso Racional for alleged infringement of the Spanish part of European Patent 244.944 ('EP'944'). This patent claimed a certain process for the manufacture of the besylate salt of amlodipine. The defendants argued that they did not use the process claimed in Pfizer's patent, but rather a process by the Polish company Adamed, which fell outside the scope of Pfizer's patent. The Adamed process is disclosed and claimed in a European patent owned by that company (European Patent 993.447).
The main discrepancy of the litigation was whether the Adamed process of manufacturing amlodipine besylate fell within the scope of Pfizer's patent EP'944 under the doctrine of equivalents.
In the first instance judgment, issued by Barcelona Commercial Court No 3 on July 31 2008, the infringement action was upheld and Bexal and Uso Racional were sentenced to pay damages of more than €4.5 million. Pfizer requested provisional enforcement of the judgment and the defendants paid the above sum.
However, on February 24 2010 the Barcelona Court of Appeal upheld the appeal filed by Bexal and Uso Racional. The court concluded that the Adamed process fell outside the scope of Pfizer's patent even under the doctrine of equivalents, and thus it dismissed Pfizer's infringement action and revoked the first instance decision. Bexal and Uso Racional then claimed and obtained reimbursement of the damages that they had been obliged to pay in 2008, plus interest.
Pfizer appealed the second instance judgment before the Supreme Court, based on the following grounds:
An ordinary cassation appeal – appeals before the Supreme Court are admissible only on certain exceptional grounds, which are specifically contemplated in the Civil Procedure Act. One of these exceptional grounds is that the appealed judgment applied a legal provision that has been in force for less than five years, provided that there is no previously consolidated Supreme Court case law on legal provisions with similar content. Pfizer argued that the judgment of the Barcelona Court of Appeal infringed the wording of Article 69.1 of the European Patent Convention and its Protocol of Interpretation (in force since December 2007).
An extraordinary appeal for procedural infringement – Pfizer argued that the judgment of the Barcelona Court of Appeal infringed the rules on burden of proof and that the court had assessed the expert evidence on file in a wrong and illogical manner. The Supreme Court can decide on this kind of procedural appeal only if the ordinary cassation appeal is admissible as such.
Bexal and Uso Racional filed an opposition to these appeals, arguing first that the ordinary cassation appeal was inadmissible. In this regard, they explained that Pfizer's infringement action was filed in 2005, whereas the current wording of Article 69.1 of the European Patent Convention and its protocol entered into force in December 2007, and therefore they were not applicable to the case. Moreover, neither Pfizer nor the first and second instance judgments mentioned these provisions. Thus, Bexal and Uso Racional argued that it was simply untrue that the judgment of the Barcelona Court of Appeal had applied rules which entered into force less than five years ago.
The Supreme Court upheld this argument and dismissed Pfizer's cassation appeal on the grounds of inadmissibility. In addition, as argued by Bexal and Uso Racional, the Supreme Court sated that there was previous case law on the doctrine of equivalents, and therefore the requirements of the Civil Procedure Act were not met. In light of this, the Supreme Court concluded that Pfizer's allegation regarding the application of the current wording of Article 69.1 of the European Patent Convention and its protocol was just an excuse for the appeal to be admitted. With the ordinary cassation appeal being inadmissible, the extraordinary appeal for procedural infringement was also dismissed.
For further information on this topic please contact Miguel Gil at Grau & Angulo by telephone (+34 93 202 34 56), fax (+34 93 240 53 83) or email (m.gil@gba-ip.com).
This article was first published by the International Law Office, a premium online legal update service for major companies and law firms worldwide. Register for a free subscription.
http://www.lexology.com/library/detail.aspx?g=63c2d6af-ca88-4c75-8dc6-74e88511eebe
Bought another 100000 shares for 0,015!
ATDF 0.015 100000 11:29
Real-Time Level 2 Quote Montage
MPID
Bid Price
Size
Date/Time
ATDF 0.015 100000 11:29
MERQ 0.014 10000 10:43
DLNY 0.0137 10000 02/08
CANT 0.013 10000 07:40
ETRF 0.011 10000 10:46
LAFC 0.01 10000 01/07
UBSS 0.0061 60000 09:30
NITE 0.005 28000 10:17
VERT 0.005 10000 02/01
PUMA 0.003 10000 08:30
CDEL 0.0003 10000 09:09
MAXM 0.0001 10000 12/06
PERT 0.0001 10000 02/08
CSTI 0.0001 10000 09:30
VFIN U 11/09
GUGS U 01/04
RAFF U 08:15
MPID
Ask Price
Size
Date/Time
MERQ 0.016 10000 10:36
ETRF 0.0176 12500 10:44
PERT 0.0178 15400 09:30
NITE 0.0191 10000 02/08
CANT 0.0191 10000 07:40
DLNY 0.02 10000 02/04
VERT 0.025 40000 09:30
CSTI 0.04 400000 09:30
PUMA 0.04 10000 08:30
LAFC 0.08 10000 01/07
CDEL 0.243 2500 09:09
UBSS 0.60 100000 09:30
ATDF 1.00 220 11:29
MAXM 200000.00 1 04/11
VFIN U 11/09
GUGS U 01/04
RAFF U 08:15
Look for the trades now!
I bought shares and they declared my shares as a sell volume.
That's not the same thing!
That's true! I thought it's an error or something else.
Most of my trades, several hundred thousand shares, showed as a sell but it was a buy!
They used NITE in my case! I believe the short volume was changed several times but I'm not sure about that.
SEC should step in and investigate...
IMO
Maybe the FBI should take a look behind the trades again.
IMO
Pfizer Joins Our Top Ten Disgorgement List
By Richard L. Cassin | Wednesday, August 8, 2012 at 8:02AM
We haven't had to update our list of corporate FCPA cases with the biggest disgorgements since March 2011. But now we do, thanks to Pfizer.
In its settlement yesterday, it paid $15 million in criminal penalties to the DOJ, and $45.2 million in disgorgement and pre-judgment interest to the SEC.
That lands Pfizer sixth on the top ten disgorgement list. Dropping off the list is GE and its 2010 settlement, when it disgorged $22.5 million.
(We're lumping together Pfizer and its subsidiary, Wyeth; the SEC and Shearman & Sterling also count related companies as one enforcement action. And we're including pre-judgment interest on the disgorgement, as we've always done).
As a reminder, disgorgement -- giving up profit derived from bribe-tainted sales -- was never mentioned when the FCPA was first debated and adopted in 1977, nor when Congress amended the law in 1988 or 1998. In fact, as of 1977, the SEC had barely used disgorgement in any type of securities enforcement actions, and 27 years passed before disgorgement popped up in an FCPA case.
That was in 2004 when ABB Ltd disgorged $5.9 million to settle civil antibribery, books-and-records, and internal-controls offenses. Since then the SEC has used disgorgement in about three quarters of its FCPA-related enforcement actions.
Pfizer, by the way, doesn't make our overall top ten list of FCPA settlements. Those include both criminal and civil penalties. Pfizer's overall settlement was about $60 million; the current tenth-ranked settlement is Panalpina's at $81.8 million.
Here are the SEC's current top ten FCPA-related corporate disgorgements (including prejudgment interest):
1. Siemens $350 million in 2008
2. KBR $177 million in 2009
3. Snamprogetti $125 million in 2010
4. Technip $98 million in 2010
5. Daimler $91.4 million in 2010
6. Pfizer $45.2 million in 2012
7. Alcatel-Lucent $45 million in 2010
8. Chevron $25 million in 2007
9. Pride $23.5 million in 2010
10. Baker Hughes $23 million in 2007
For comparison, here's our current list of the top ten FCPA enforcement actions of all time.
http://www.fcpablog.com/blog/2012/8/8/pfizer-joins-our-top-ten-disgorgement-list.html
Pfizer, Wyeth Pay $60 Million In Settlement
By Richard L. Cassin | Tuesday, August 7, 2012 at 12:32PM
A subsidiary of Pfizer Inc. agreed with the DOJ today to pay a $15 million criminal penalty to resolve FCPA violations in Bulgaria, Croatia, Kazakhstan, and Russia.
Pfizer also agreed with the SEC to pay $26.3 million in disgorgement of profits and pre-judgment interest to settle civil charges. And Wyeth LLC, acquired by Pfizer three years ago, separately agreed to pay $18.8 million to the SEC in disgorgement and pre-judgement interest.
The DOJ gave the subsidiary, Pfizer H.C.P., a two-year deferred prosecution agreement. It charged the company in a two-count information with conspiracy and violations of the FCPA for improper payments to government officials, including publicly-employed regulators and health care professionals. The information and the deferred prosecution agreement were filed today in federal court in the District of Columbia.
The DOJ said Pfizer helped 'U.S. authorities in ongoing FCPA investigations of other companies and individuals.'
Other pharmas known to be facing FCPA investigations include AstraZeneca, Baxter International, Bio-Rad Laboratories, Bristol-Meyers Squibb, Covidien, Eli Lilly, GlaxoSmithKline, Merck, Sciclone Pharmaceuticals, Talecris Biotherapeutics, and Teva.
Pfizer's employees and agents paid bribes in Bulgaria, China, Croatia, Czech Republic, Italy, Kazakhstan, Russia, and Serbia, the SEC said. Improper payments went to foreign officials 'to obtain regulatory and formulary approvals, sales, and increased prescriptions for the company’s pharmaceutical products.'
Pfizer's people tried to conceal the bribery, the SEC said, by improperly recording the transactions in accounting records as legitimate expenses for promotional activities, marketing, training, travel and entertainment, clinical trials, freight, conferences, and advertising.
In addition to the $15 million criminal penalty paid to the DOJ, Pfizer disgorged to the SEC $16,032,676 in net profits and prejudgment interest of $10,307,268 for a total of $26,339,944. Wyeth disgorged $17,217,831 in net profits and prejudgment interest of $1,658,793, for a total of $18,876,624.
'Pfizer took short cuts to boost its business in several Eurasian countries,' the DOJ said, 'bribing government officials . . . . to the tune of millions of dollars.'
Pfizer today said: 'The actions which led to this resolution were disappointing, but the openness and speed with which Pfizer voluntarily disclosed and addressed them reflects our true culture and the real value we place on integrity and meeting commitments.'
In 2009, Pfizer paid $2.3 billion in civil and criminal penalties to U.S. enforcement agencies for unlawful prescription drug promotions.
________________
The DOJ's August 7, 2012 release is here.
The SEC's news release is here.
The SEC's Litigation Release No. 22438 and Accounting and Auditing Enforcement Release No. 3399 (both dated August 8, 2012) for U.S. Securities and Exchange Commission vs. Pfizer Inc., Civil Action No. 1:12-cv-01303 (D.D.C.) (filed Aug. 7, 2012) and U.S. Securities and Exchange Commission vs. Wyeth LLC, Civil Action No. 1:12-cv-01304 (D.D.C.) (filed Aug. 7, 2012) are here.
The SEC's civil complaint againt Pfizer can be downloaded here.
The SEC's civil complaint against Wyeth can be downloaded here.
http://www.fcpablog.com/blog/2012/8/7/pfizer-wyeth-pay-60-million-in-settlement.html
Who shorts this stock?
Pfizer proved with ponezumab and bapineuzumab (Phase 2 trial again) that Intellect Neurosciences technology works.
Intellect Neuroscience provide the next generation AMD/Alzheimer drug developed by Lonza (leader in ADC development and production).
IMO
Dramatic rise in Alzheimer's victims expected
Experts say the nation faces a financial and health care crisis as the number of patients with the incurable disease soars.
By Bruce Kennedy
Startling statistics suggest the country may be blindsided by a major health and financial crisis over the next several decades as baby boomers become more vulnerable to Alzheimer’s disease.
A new study published in the journal Neurology says the number of people with Alzheimer’s is expected to triple over the next 40 years to about 13.8 million by 2050, with about half of that group age 85 and older.
The Alzheimer’s Association estimates the costs for care related to the disease at $200 billion last year, according to The Los Angeles Times, with $140 billion of that paid by Medicare and Medicaid. The group says that by 2050, that cost will soar to $1 trillion annually.
The unexpectedly large number of Alzheimer’s patients “will place a huge burden on society, disabling more people who develop the disease, challenging their caregivers, and straining medical and social safety nets,” said study co-author Jennifer Weuve, an assistant professor of medicine at the Rush Institute for Healthy Aging at Rush University Medical Center in Chicago.
One in eight older Americans is living with the mentally debilitating and incurable disease. And the Alzheimer’s Association says more than 15 million Americans provide unpaid care, valued at $210 billion, for persons with Alzheimer’s and other dementias.
"These projections are based on assumptions that we don't have a cure at this point, and people may be living longer going forward,” Dallas Anderson of the National Institute on Aging, part of the National Institutes of Health, told Reuters.
The search for the cure, meanwhile, is underway. The National Alzheimer’s Project Act was signed into law by President Obama in early 2011 -- and the president’s fiscal year 2013 budget proposal includes $100 million in additional funding for Alzheimer’s research, caregiver support, awareness, education and outreach.
But so far, the pharmaceutical companies have had no breakthroughs when it comes to a drug that might do anything more than treat the symptoms of Alzheimer’s. Firms like Pfizer (PFE -0.39%), Johnson & Johnson (JNJ +0.47%) and Eli Lilly (LLY +0.28%) have all reported failures over the last year or so in their search for Alzheimer’s treatments.
Craig Ritchie, an Alzheimer's researcher at Imperial College in London, told the Independent that the global recession is forcing many of those companies to streamline their neuroscience departments. “One can understand why,” he said last year. “But it is hugely disappointing because there is massive unmet need.”
http://money.msn.com/now/post.aspx?post=bdfa927b-cdf1-4f24-8f7e-bdd59fbc0d2d
BioMedReports: How would you characterize the mood among Alzheimer's researchers after the phase 3 results for Bapineuzumab and Solanezumab?
Dr. Daniel G. Chain, Ph.D.: Obviously, people were very disappointed by the results from the two sets of major Alzheimer's Phase 3 trials, but there were also glimmers of light that renewed hope and even strengthened the prevailing belief that beta amyloid (Aß) plays a central and causative role in the pathogenesis of Alzheimer's disease. Few now doubt that immunotherapy represents a realistic path forward pending improvements in drug design and the way we conduct clinical trials. Ely Lilly's drug solanezumab showed modest improvement in clinical outcomes when data was pooled from two clinical trials. The drug is to be further tested in a third phase 3 trial by the company and two independent trials conducted by leading academic groups. While bapineuzumab failed to show clinical benefit, the use of biomarkers clearly demonstrated the drug had engaged the target, reduced the amount of plaque and slowed neurodegeneration based upon the decrease in the amount of tau protein measured in the cerebral spinal fluid (CSF). Unfortunately, the drug also caused a significant incidence of vasogenic edema and microhemorrhages, especially in patients that carried the APOE4 gene. A Phase 2 trial is ongoing using a subcutaneous formulation that may avoid these side effects. There is a feeling of optimism among researchers that next generation drugs will have an improved probability of success because of the lessons we have learned from these results and other important recent developments in the field. I experienced this first-hand when I was invited as a Distinguished Speaker to the 6th Annual Alzheimer's Drug Discovery Summit in December and had the opportunity to listen to foremost leaders in the field including academic researchers and industry experts.
Among the themes that have become prevalent is that there is a compelling case for early intervention in the treatment of the disease in which relevant biochemical and neuropathological changes in the brain start many years -- in some case two decades or more -- before symptoms occur! Moreover, the rate of change is far greater before the appearance of symptoms such that the stage we commonly refer to as "Mild," is in fact relatively far advanced, reflecting significant damage to the brain, which is probably beyond repair.
http://finance.yahoo.com/news/novel-alzheimers-therapeutics-developer-says-130724320.html
FDA May Relax Guidlines on Early-Stage Alzheimer’s Trials
By Michelle Fay Cortez - Feb 7, 2013 5:09 PM GMT+0100
The lack of definitive biological markers for the earliest stages of Alzheimer’s disease has made it impossible to enroll patients in drug-research trials, U.S. regulators said, slowing development of new treatments.
The methods for trials were established in 1984 and cover patients with full-blown dementia who suffer both cognitive and functional limitations, the Food and Drug Administration said in a statement today. The agency is proposing to relax guidelines for early-stage Alzheimer’s drug trials by letting researchers show that a medication slows the cognitive decline, rather than improvement in both cognitive and functional deterioration.
People in the earliest stages of Alzheimer’s don’t always have functional limitations such as problems getting dressed, bathing and taking care of their own daily needs. For this group of people, showing that a medication slows the cognitive decline may be enough to win regulatory approval, the FDA said.
After an approval, companies would have to conduct larger, longer studies to show the improvement in mental function translates into improved health, the FDA said.
The draft document is subject to a 60-day comment period and could change based upon the input the FDA receives.
To contact the reporter on this story: Michelle Fay Cortez in Minneapolis at mcortez@bloomberg.net
http://www.bloomberg.com/news/2013-02-07/fda-may-relax-guidlines-on-early-stage-alzheimer-s-trials.html
FDA outlines path to test Alzheimer's drugs earlier
By Julie Steenhuysen
CHICAGO | Thu Feb 7, 2013 8:29pm EST
(Reuters) - Proposed U.S. guidelines may make it easier for drug companies to test Alzheimer's treatments in people at an earlier stage, when scientists think they may have the best shot at working.
The draft guidance document, issued on Thursday by the U.S. Food and Drug Administration, reflects changes in scientists' understanding of Alzheimer's. They now believe the disease begins at least a decade before symptoms appear.
"The scientific community and the FDA believe that it is critical to identify and study patients with very early Alzheimer's disease before there is too much irreversible injury to the brain," said Dr. Russell Katz, director of the Division of Neurology Products in the FDA's Center for Drug Evaluation and Research.
Current Alzheimer's drugs treat symptoms, but none has been proven to interrupt the steady destructive course of Alzheimer's that robs sufferers of their memories and independence.
"I think this will be hugely useful to the pharmaceutical industry," said Dr. Paul Aisen of the University of California, San Diego, and director of the Alzheimer's Disease Cooperative Study, a joint effort between the university and the National Institute on Aging focused on identifying the earliest signs of Alzheimer's.
Aisen said the draft document will help companies design clinical trials to test drugs in people before dementia strikes, such as prodromal disease, a precursor to Alzheimer's in which mild cognitive changes have occurred and there is some biomarker evidence, such as a brain scan, that suggests the changes are related to Alzheimer's disease.
The need for new treatments is great and growing. A study on Wednesday suggested that the number of Americans with Alzheimer's disease would triple to 13.8 million by 2050.
Drug companies have been working for years to develop so-called disease-modifying drugs, but so far, with little success.
Last summer, a promising drug called bapineuzumab being developed by Johnson & Johnson , Pfizer and Elan, failed to show a benefit in large trials of patients with mild to moderate Alzheimer's.
And a drug by Eli Lilly and Co known as solanezumab also failed to meet the main goals of two large trials in this same population. But the drug did appear to show a slight benefit in mild patients when results of both studies were pooled.
Researchers now plan to study Lilly's drug in patients with earlier-stage disease, including a trial known as the "A4" prevention study, which will study 1,000 volunteers aged 70 to 85 with pre-symptomatic disease, who have not yet developed significant memory problems.
The trial will be managed by the Alzheimer's Disease Cooperative Study under Aisen's direction.
Several other so-called prevention studies are testing drugs in people who are genetically predisposed to develop Alzheimer's at an early age. In one study, members of a large family in Colombia will test a drug from Roche Holding AG's Genentech unit known as crenezumab.
Maria Carrillo of the Alzheimer's Association, which has worked with the National Institute on Aging to develop new guidelines for identifying Alzheimer's at an earlier stage, said the proposed changes "open the door wider for those of us working on and thinking about prevention trials."
The FDA said the move is part of the government's efforts to respond to Alzheimer's as part of the National Alzheimer's Plan signed by President Obama last year. The plan aims to find an effective way to prevent or treat Alzheimer's by 2025.
http://www.reuters.com/article/2013/02/08/us-alzheimers-fda-idUSBRE91618N20130208
ILNS is heating up!
Thank you!
After a death cross in 2010 ILNS is in a long term downtrend but it seems to me to move sideways now.
I would like to ask you for your analysis.
IN-N01-OX2
• Humanized IgG4 Aß Mab conjugated to melatonin
• Conjugate expected to:
– Enhance Aß clearing capacity of Mab
– Deliver on-site neuroprotection of RPE cells against Aß and
other free radical sources
– Prevent off-target melatonin effects
• Therapeutic applications:
– Age-related macular degeneration
– Glaucoma
– Diabetic retinopathy
– Traumatic brain injury
– AD
• Lead optimization expected complete in 2012
– Internal activities plus LONZA (Visp, Switzerland)
• Partnering with Big Pharma anticipated in Phase 1 or earlier
http://content.stockpr.com/intellectns/media/d58aaf7b67c66fcf7837102deeddaa6a.pdf
N01-OX2 is a first-in-class ADC. It is a humanized monoclonal antibody specific for beta amyloid protein that is empowered to deliver on-site neuroprotection by its conjugation to melatonin. The goal of N01-OX2 is to reduce the oxidative stress that leads to cellular inflammation and damage. N01-OX2 is being developed for the treatment of age-related macular degeneration (AMD), the leading cause of blindness in people over the age of 55. AMD therapies generate $4 billion annually, even though the few approved treatments don't cure the disease and offer only modest improvements in vision for most patients. N01-OX2 also has potential applications for diabetic retinopathy, glaucoma, traumatic brain injury and Alzheimer’s disease.
http://www.intellectns.com/
Thank you for sharing!
http://otcshortreport.com/ILNS
Excellent!
ILNS will have two drugs in Phase 2 clinical trial in 2013, OX-1 and
bapineuzumab and we are close to out-licensing three drugs TAUC3, TOC-1, IN-N01. With Conjumab-A Dr. Chain could improve several other antibodies!
These are the facts and Investors should think about what's going on here!!
About 1.4m shares for 0.0165 and buying more.
Novel Alzheimer's Therapeutics Developer Says Investors Should Remain Undeterred Despite Disappointing Results From Major Phase 3 Trials
LOS ANGELES, CA--(Marketwire - Jan 30, 2013) - During his distinguished career, Dr. Daniel G. Chain, Ph.D. discovered various novel therapeutics to treat Alzheimer's disease which were licensed to multiple Big Pharma giants.
Dr. Chain trained as a Post-doctoral Research Fellow at the Center for Neurobiology and Behavior at Columbia University in New York. Dr. Chain obtained his B.Sc. in Biochemistry from the Institute of Biology in London and obtained his Ph.D. in Biochemistry from the Weizmann Institute of Science in Israel.
He currently serves as Chairman of Intellect Neurosciences, Inc. ( OTCQB : ILNS ), where he has also been Chief Executive Officer since October 2005.
In an exclusive interview with BioMedReports, Chain says that biotech investors should remain undeterred by the challenges currently being faced by those trying to find a cure for Alzheimer's disease and other age-related cognitive impairments.
BioMedReports: How would you characterize the mood among Alzheimer's researchers after the phase 3 results for Bapineuzumab and Solanezumab?
Dr. Daniel G. Chain, Ph.D.: Obviously, people were very disappointed by the results from the two sets of major Alzheimer's Phase 3 trials, but there were also glimmers of light that renewed hope and even strengthened the prevailing belief that beta amyloid (Aß) plays a central and causative role in the pathogenesis of Alzheimer's disease. Few now doubt that immunotherapy represents a realistic path forward pending improvements in drug design and the way we conduct clinical trials. Ely Lilly's drug solanezumab showed modest improvement in clinical outcomes when data was pooled from two clinical trials. The drug is to be further tested in a third phase 3 trial by the company and two independent trials conducted by leading academic groups. While bapineuzumab failed to show clinical benefit, the use of biomarkers clearly demonstrated the drug had engaged the target, reduced the amount of plaque and slowed neurodegeneration based upon the decrease in the amount of tau protein measured in the cerebral spinal fluid (CSF). Unfortunately, the drug also caused a significant incidence of vasogenic edema and microhemorrhages, especially in patients that carried the APOE4 gene. A Phase 2 trial is ongoing using a subcutaneous formulation that may avoid these side effects. There is a feeling of optimism among researchers that next generation drugs will have an improved probability of success because of the lessons we have learned from these results and other important recent developments in the field. I experienced this first-hand when I was invited as a Distinguished Speaker to the 6th Annual Alzheimer's Drug Discovery Summit in December and had the opportunity to listen to foremost leaders in the field including academic researchers and industry experts.
Among the themes that have become prevalent is that there is a compelling case for early intervention in the treatment of the disease in which relevant biochemical and neuropathological changes in the brain start many years -- in some case two decades or more -- before symptoms occur! Moreover, the rate of change is far greater before the appearance of symptoms such that the stage we commonly refer to as "Mild," is in fact relatively far advanced, reflecting significant damage to the brain, which is probably beyond repair.
Q: What are the main areas of progress in Alzheimer's research?
Dr. Daniel G. Chain: The development of sensitive brain imaging techniques such as structural MRI to measure brain atrophy, FDG-PET to measure glucose metabolism, and PET amyloid imaging agents represent some of the most important recent advances in the field laying the foundation for studies such as by the Alzheimer's Disease Neuroimaging Initiative (ADNI) and Dominantly Inherited Alzheimer's Network (DIAN) that provided extremely valuable information regarding the sequence of changes preceding and leading to AD. In fact, these studies led to a new way to think about the disease in which presymptomatic AD is just as much a disease state as symptomatic disease.
Q: Describe the main programs at Intellect Neurosciences.
Dr. Daniel G. Chain: Intellect has four main programs underway at the moment: CONJUMAB-A, TAUC3, TOC-1 and RVO3.
We are pioneering the use of antibody-drug conjugates and bi-specific vaccines for the treatment and prevention of multifactorial neurodegenerative conditions such as Alzheimer's disease, Huntington's disease and age-related macular degeneration. Increasingly we hear researchers emphasizing the need to target more than one disease component where, for example, Aß, tau protein and oxidative stress act in concert and synergistically causing irreversible damage to nerve cells. The use of combination therapies may even allow intervention after symptoms have begun in contrast to monotherapies, targeting only Aß, for example. However, regulators are averse to the idea of combining two independent investigational drugs before testing each one singly in human clinical trials and demonstrating clinical benefit. That issue is circumvented by the use of antibody drug conjugates in which two different molecules are combined chemically into a single entity as is the case with our CONJUMAB platform.
I am excited about the therapeutic potential of CONJUMAB-A, our lead preclinical program which I believe offers important advantages to other Aß antibodies currently in clinical development. All the other antibodies e.g. solanezumab, bapineuzumab, gantenerumab and crenzeumab are designed for a single purpose, namely to clear Aß from the brain. None of these antibodies act on secondary neurotoxic mechanisms such as oxidative stress which causes most of the damage from Aß. By contrast, CONJUMAB-A, an antibody drug conjugate, is empowered with additional neuroprotective properties to alleviate the damage while also potentially enhancing the clearance of Aß. In principle our approach could be applied to improve many different types of antibodies including those that previously disappointed in clinical trials. However, we are currently focused on optimizing CONJUMAB-A using our own antibody IN-N01 which targets the N-terminus of Aß. We believe IN-N01 to be superior to bapineuzumab because of its reduced potential to cause inflammation which results from our reengineering of the originally produced IG1 class antibody into an IgG4 class antibody. We believe this safety feature is particularly important for antibodies that bind Aß aggregates and not just soluble single monomeric Aß. Among several potential indications, we have decided to focus on age related macular degeneration (AMD) for proof of concept studies since AMD and AD share several similarities while the eye offers less challenge for delivering the drug.
Over the past two years, Intellect has established its position as a leader in tau immunotherapy using funds from our deal with ViroPharma to support new patent filings by the company, in-license new technologies and initiate an important collaboration with leading Alzheimer's research groups led by Dr. Frank LaFerla and Dr. Kim Green at the University of California, Irvine. Tau immunotherapy is rapidly gaining traction in the Alzheimer's field and has potential applications for many orphan indications as well, such as frontotemporal dementia. However, in contrast to other approaches that have targeted tangles, Intellect is targeting the earliest steps in tau pathology focused on two different pathogenic forms, a truncated form known as delta tau and an aggregated from known as oligomeric tau -- each of which occurs before filaments leading to tangle formation. Over the next several months we expect to generate important in vivo data in relation to the two monoclonal antibodies, TauC3 and TOC-1, that we acquired from Northwestern University under an exclusive license agreement.
Finally, we continue our development of our RECALL-VAX platform focusing on a bi-specific chimeric peptide vaccine approach that targets both Aß and delta tau in a flu-shot like vaccine approach. Vaccines against multiple antigens have precedent so this is another approach for combination therapies. Disease-modification itself is becoming less attractive as an approach for treating Alzheimer's disease for two main reasons. First, as evidenced by the Phase 3 clinical trials results, patients who are symptomatic probably have disease that is too far advanced to benefit significantly from treatments that slow the degenerative process. Second, treating very early stage or presymptomatic patients will be extremely expensive and prove too costly a burden for healthcare systems. An article by scientists from the Karolinska Institute in Sweden, published in the October issue of Current Alzheimer's Research, indicated the economic cost of treatment with a chronically and frequently administered disease-modifying drug would outweigh the cost of palliative care, including full-time nursing care of patients with advanced disease. This economic model leads one to conclude that a vaccination given on an annual or semi-annual basis may be the only economically feasible approach to prevent and manage Alzheimer's disease. Therefore, a vaccine such as RV03 being developed by Intellect Neurosciences offers a promising prophylactic approach that could potentially be administered to tens of millions of people around the world. Although still at an early stage, we are confident about our ability to produce a high value asset.
Q: Do you feel confident regarding Intellect's pipeline?
Dr. Daniel G. Chain: We are very confident in the science behind our pipeline, and are encouraged by the interest shown in our programs by several global pharmaceutical companies some of which have already signed confidentiality agreements. In addition, many independent papers have been published recently that support many of our hypotheses for the development of these assets. Further, we are beginning to see encouraging early stage results that we hope to share soon regarding each of our pipeline programs.
Q: What challenges do you face?
Dr. Daniel G. Chain: The biggest challenge is the funding needed to support our R&D activities and also to grow and maintain our substantial global patent portfolio, which is the heart of Intellect's business model. We need to dispel the skepticism that pervades among many stakeholders in the pharmaceutical industry resulting from previous disappointments in the AD field, or at least separate ourselves from it.
One of Intellect's strengths is its diversified portfolio, which provides us "multiple shots on goal." We are extremely cost-efficient as the result of effective outsourcing R&D to highly specialized contract research organizations. Even so, as a small company, maintaining adequate funding to continue all of our programs concurrently is quite challenging. We are currently in talks with potential licensing and co-marketing partners to help maintain the pace of our research, but in this environment, we are facing the same challenges as all other companies of our relative size. We, therefore, have to choose which programs to push forward at any given moment, which often disrupts the momentum of other programs, all based upon the funding we receive and the goals of potential partners who continue nevertheless to show considerable interest and have expressed an eagerness to see validation in preclinical models.
Q: Do you have anything you wish to add?
Dr. Daniel G. Chain: It is imperative that the company and its investors remain undeterred by the challenges currently being faced both by the industry and within Intellect itself. Intellect has continued to grow and develop new strategies to continue on regardless of what the market has done. We wish to communicate to our current and potential investors that significant advances have been made in the Alzheimer's area and express our confidence in our ability to prevail where others have failed. While one set of compounds for which we hold licenses has met with challenges, that is not the entirety of Intellect Neurosciences. Intellect has never relied solely on one program to sustain it, and we have continuously executed on our plans to license our programs, and anticipate being able to do so again as we generate new data and advance our earlier-stage programs through proof of concept.
The full version of this report can be found here:
http://www.biomedreports.com/20130130120929/novel-therapeutics-developer-says-investors-should-remain-undeterred-despite-resutls-from-major-alzheimers-phase-3-trials.html
Healthcare investors and Biotech traders interested in accessing BioMedReports' new complete database of clinical trials and upcoming FDA and world-wide regulatory decisions which can be used to make more profitable trades and see upcoming catalysts can go to: http://biomedreports.com/fdacal.html
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No details from Lonza today:
http://www.lonza.com/about-lonza/media-center/news/2013/130124-fyr-2012-e.aspx
LONZA shareholders are not satisfied with the performance of the directors, they may remove the directors or refuse to re-elect them. We may be see the LONZA deal details on thursday.
Article in german language:
Lonza-Präsident Soiron bangt um sein Amt
Lonza-Verwaltungsratspräsident Rolf Soiron bangt um sein Amt.
Die Lonza nimmt den Widerstand von unzufriedenen Aktionären vorweg und plant offenbar, mehrere Verwaltungsräte auszuwechseln. Lonza-Präsident Rolf Soiron könnte an der Generalversammlung gar abgewählt werden.
Im April vergangenen Jahres sagte Lonza-Präsident Rolf Soiron auf die Frage zur Zukunft des Werkes Visp, dass es zwar weniger Stellen geben wird, an Massenentlassungen denke aber niemand. Ein Satz, welcher den Lonza-Präsidenten viel Glaubwürdigkeit gekostet hat, strich der Chemikonzert doch ein halbes Jahr später im Wallis 400 Arbeitsplätze. Mit seiner Beschwichtigung wog er die Mitarbeitenden in falscher Sicherheit, und bei den Investoren sorgte er für Stirnrunzeln, schliesslich hatte er kurz zuvor ein grosses Sparprogramm angekündigt, so die «NZZ am Sonntag».
Mehr zum Thema:
Weniger Entlassungen als angekündigt
Gehörte der Basler jahrelang unangefochten zum Kreis der Schweizer Wirtschaftskapitäne, muss er heute kämpfen. Wie die Zeitung weiter schreibt, steht seine Wiederwahl bei Lonza auf der Kippe – und sein Ruf als Manager auf dem Spiel. Ein erster Putschversuch gegten Soiron war an der letzten Generalversammlung gescheitert.
Investoren erachten deshalb einen Angriff auf Soiron für gut möglich. Noch halten sich die Fonds bedeckt: Sie warten ab. Sollte Lonza am Donnerstag ein enttäuschendes Jahresergebnis vorlegen, ist Soirons Sitz in Gefahr. Da sind sich Beobachter einig, so die «NZZ am Sonntag». Das Unternehmen möchte ein neuerliches Kräftemessen mit unzufriedenen Aktionären unbedingt vermeiden. Lonza habe vor, mehrere Verwaltungsräte zu ersetzen, erklären zwei Quellen aus dem Umfeld des Gremiums unabhängig voneinander. Abgelöst werden sollen langjährige Mitglieder, sei zu hören. Ein Firmensprecher wollte nicht kommentieren, ob der Generalversammlung vom 9. April Rochaden vorgeschlagen werden, berichtet die «NZZ am Sonntag» weiter.
In der Konzernleitung rumore es ebenfalls. Nicht einmal den Topmanagern sei klar, wo es strategisch hingehen soll, verlautet aus deren Umfeld. Sie seien verunsichert, Abgänge auf den obersten Führungsstufen könnten in nächster Zeit nicht ausgeschlossen werden.
http://www.1815.ch/wallis/aktuell/lonza-praesident-soiron-bangt-um-sein-amt-90027.html
http://www.lonza.com/about-lonza/knowledge-center/events/corporate/full-year-result-2012.aspx
LONZA Full Year Results 2012; Date: 24 January 2013
Location:
City: Basel
Country: Switzerland
http://www.lonza.com/about-lonza/knowledge-center/events/corporate/full-year-result-2012.aspx
My sentiments exactly!
Aes-103 alias 5-hmf (Blockbuster drug) [Needle]
Robert Swift - Aesrx Patent:
http://patentscope.wipo.int/search/en/WO2011146471
Aesrx - Angel Investors [Haystack]:
http://www.xconomy.com/boston/2011/12/14/aesrx-navigates-valley-of-death-to-get-sickle-cell-drug-into-trials/
http://m.bizjournals.com/boston/blog/mass-high-tech/2012/09/aesrx-takes-in-525k-in-debt-financing.html?r=full
Lonza will produce Roche's breast cancer Blockbuster-ADC T-DM1.
News from Switzerland (in german):
http://www.1815.ch/wallis/aktuell/roche-bestaetigt-auftrag-fuer-lonza-visp---88327.html
...and the products licensed under ANTISENILIN platform
Removing Impediments Towards Management Of Sickle Cell Disorder
By EDITH NNAJI (NAN)
Last updated: 01/01/2013
SICKEL cell, a genetic blood disorder, decreases the functions of the cells of the human body and subjects the patients to various complications.
Medical experts have aggressively viewed the disorder as a challenge to medical practice because it shortens life.
For instance in the U.S, prior to the discovery of more effective management of the disorder, the average life expectancy of persons with this condition was estimated at 42 years in males and 48 years in females.
Of course, life expectancy in the developing nations including Nigeria will be lower for such patience if the U.S, with its awareness on the dangers of the sickness, coupled with advanced technology, could only record this feat.
Even with the prevailing better management of the disease, medical report indicates that patients can only live into their 50s or more.
With this grim drag on human existence and the World Health Organisation’s (WHO) report in 2006 that Nigeria is one of the countries with the highest number of people with sickle cell, health experts have raised concerns on the provision of efficient management of the disease.
The analysis of the report indicates that the annual figure for Africa in 2006 was 200,000 while Nigeria accounted for 150,000 children with the disorder.
Also, medical findings show that 30 per cent of Nigerians are carriers and the prevalence rate was put at 20 per 1,000 births. This is alarming and the stakeholders in the health sector are resolute to address the challenge.
So in 1998, a drug, Niprisan, was developed at the Nigerian National Institute for Pharmaceutical Research and Development (NIPRD) under the U.S. patent.
In August 2002, the American company Xechem International, acquired the exclusive world-wide rights to Niprisan and later renamed it Nicosan/Hemoxin which was launched in 2006 by former President Olusegun Obasanjo.
However, the production of Nicosan was stopped and in further response to the challenge of providing effective management for the disease, three institutions recently signed an agreement on production of sickle cell drug in Nigeria.
They are NIPRD, Nigeria Export Import Bank (NEXIM Bank) and the Federal Ministry of Health.
They are to rebrand and retain the name Nicosan for effective management of the disease.
According to medical experts, Nicosan, as a phytomedicine, appears to be safe and effective in reducing crises associated with severe pains over a six-month follow-up period.
The drug, produced with extracts from four botanical plants in Nigeria, does not cure sickle cell but reduces the frequency of crises.
With this somewhat relieving potency, it is worrisome that the necessary fund to sponsor the production has not been forthcoming.
According to Mr Robert Orya, the Managing Director of NEXIM, the bank has yet to release the seeded fund for the production of the drug.
“Within the first week of signing the agreement with the Federal Ministry of Health, we were bombarded with law suits and there are lots of outstanding legal issues.’’
“The suits stemmed from disagreements between foreign pharmaceutical companies and their Nigerian counterparts.
“NEXIM has always been committed because even for social reasons, a lot of Nigerians are suffering from sickle cell.
“We have a situation where parents come into the bank with their sick children and it evokes emotions even more than money,’’ he explained.
He explained further that the bank had syndicated more than N700 million in loans with some banks for the production of the drug in the country, adding that a loan recovery committee had also been set up.
Orya assured the public that as soon as a pending case in court was cleared, the production of the drug would begin.
Dr Mohammed Pate, the Minister of State for Health, said the production of the drug in Nigeria would be a relief to carriers.
“NIPRD has done well in terms of coming up with this and is being complemented by NEXIM Bank as well as other stakeholders to finance the production,’’ he said.
Prof. Karniyus Gamaniel, the Director-General of NIPRD, said the commercial production of Niprisan would have begun but for the legal action.
He said that the cost of the pilot production of Niprisan was N250 million for one year for 300, 000 patients.
Between the legal battle and the actual production of Niprisan, therefore, what are sickle cell patients saying?
Mrs Deborah Rotimi, a patient, said: “I am like any other child; this has always been my belief even as I will be 30 years by January 2013.
“Although I am a sickle cell carrier; the last health crisis I had was in 2005 and it was not an experience to remember.
I live every day of my life on drugs and I pray that one day government will start the production of the sickle cell drug to help the situation.’’
Mrs Veronica Osi, who has a son with sickle cell disorder, said if government could produce the drug at an affordable price; it would go a long way to help the carriers.
“My 18-year-old son has been with sickle cell disease from birth, we spend everything we have to make sure that he lives because we love him.
“Anytime he has crisis, I become ill more than him, seeing him going through blood transfusion and so many things is a terrible experience.
“We depend on God and the assurance by the doctors that the government would soon begin the production of a drug for its management. We hope that the drug will come and he will not die,’’ she said.
Dispute or no dispute, stakeholders hold the belief that government should take decisive measures at accelerating processes that will ensure the production of the drug as well as its availability and affordability to all sickle cell patients.
http://nigerianobservernews.com/01012013/features/features4.html
The Company’s product pipeline includes OX1(Phase II trial in the second half of 2013,up to $120 million in milestones, as well as a tiered royalty rate (with a cap in the “mid-teens”)), OX2, IN-N01, NO1-OX2 (ADC development by Lonza), TOC-1, tauC3, and the vaccines RV01, RV02, RV03.
Lonza to Expand Antibody Drug Conjugate (ADC) Manufacturing Capacity to Meet Growing Customer Demand
Basel, Switzerland, 8 January 2013 – Lonza today announced plans to invest CHF 14 million to expand Antibody Drug Conjugate (ADC) manufacturing capacity in Visp, Switzerland. Oncology therapeutics including ADCs represent one of the fastest growing segments of the pharma and biotech industry and the deployment of ADC targeted therapies has intensified in recent years.
Because cGMP manufacturing of ADCs presents unique challenges, facilities must be designed to handle both biological species and highly potent cytotoxic small molecule drugs. Lonza has been a pioneer in the manufacturing of ADCs since its initial investment in 2006 which established manufacturing suites for both small and large scale projects, dedicated Research & Development labs, and Quality Control facilities specifically for ADCs. Since 2010, Lonza has validated large scale manufacturing of platform technologies primarily utilized by ADC drug developers.
The expansion of the ADC facility will double the existing large-scale manufacturing capacity in Visp while allowing current operations to continue without interruption. It is the next step in bringing challenging new technologies to one of Lonza’s main sites. The capacity expansion, expected to be complete in the second quarter of 2014, has the potential to bring new job opportunities across all functions in Visp.
“We have witnessed significant growth in the ADC market in the past 24 months and this investment is necessary to continue to support the growing product demands from our customers” said Stefan Stoffel, Head of Lonza’s Chemical Manufacturing business unit. “Lonza Visp will continue to offer a fully integrated end-to-end development and manufacturing solution for ADCs, including the cytotoxic small molecules used in these products and all associated analytics. In addition, Lonza can support protein development and manufacturing via our global biologics development and manufacturing sites.”
Lonza’s continued investment to increase ADC capacity and highly trained personnel allows its customers to capitalize on the unique infrastructure of the Visp site and limit their own investment in the expertise, assets, and infrastructure required to work with these highly potent biological products in a highly regulated environment.
http://www.lonza.com/about-lonza/media-center/news/2013/130108-P2P-e.aspx
...and maybe a tauC3, TOC-1 license agreement
Age-related macular degeneration and cancer mortality in the atherosclerosis risk in communities study.
Cheung N, Shankar A, Klein R, Folsom AR, Couper DJ, Wong TY; Atherosclerosis Risk in Communities (ARIC) Study Investigators.
Centre for Eye Research Australia, University of Melbourne, Victoria, Australia.
Abstract
OBJECTIVE:
To examine the prospective association of early age-related macular degeneration (AMD) with cancer mortality.
METHODS:
A population-based cohort study of 10 029 persons aged 49 to 73 years free of cancer. The AMD signs were evaluated from retinal photographs taken in 1993 through 1995. Cancer mortality was determined from death records.
RESULTS:
There were 464 cases of early AMD. Over 10 years, there were 234 cancer deaths (71 lung cancer deaths). After controlling for age, sex, race, field center, education, smoking status, pack-years of smoking, body mass index (calculated as weight in kilograms divided by height in meters squared), and diabetes mellitus, early AMD was associated with cancer mortality (rate ratio [RR], 1.68; 95% confidence interval [CI], 1.03-2.73). This association was overall stronger in African American individuals (RR, 3.93; 95% CI, 1.67-9.22) than white individuals (RR, 1.28; 95% CI, 0.71-2.32) and for lung cancer deaths (RR, 2.14; 95% CI, 0.97-4.72) than non-lung cancer deaths (RR, 1.50; 95% CI, 0.81-2.78). In African American individuals, early AMD was associated with a 5-fold higher risk of lung cancer deaths (RR, 5.28; 95% CI, 1.52-18.40).
CONCLUSIONS:
Middle-aged African American individuals with early AMD may be at increased risk of dying of cancer, particularly lung cancer. This association was not present in white individuals and needs confirmation in other studies.
http://www.ncbi.nlm.nih.gov/pubmed/17846365
Lucentis nears final NICE nod for diabetes-related vision loss
New reimbursement comes as Novartis faces new AMD rival Eylea in U.K.
January 3, 2013 | By Tracy Staton
Novartis is one step closer to marketing Lucentis in a new group of patients. The National Institute for Health and Clinical Excellence officially changed its mind on the Swiss drugmaker's eye treatment, recommending the pricey injection for use in diabetics.
The NICE move comes as Lucentis faces new competition from Bayer's Eylea in age-related macular degeneration. Bayer launched the head-to-head competitor in December in the U.K.
To win the new recommendation in patients with diabetic macular edema, Novartis offered a discount--as yet undisclosed--off the usual £742-per-injection price (about $1,200).
Novartis ($NVS) has been fighting for Lucentis in the U.K., and not only at NICE. Faced with competition from Avastin, a Roche ($RHHBY) cancer drug used off-label to treat AMD, Novartis is jealously guarding its status as a government-approved choice. When one group of doctors in the NHS was found to be using Avastin rather than Lucentis, Novartis protested--and after offering a discount, won the day.
But now, here comes Eylea. Sold by Regeneron ($REGN) in the U.S., the new drug has proven a formidable competitor. In the U.S. AMD market, Eylea racked up 2012 sales far beyond original expectations. Bayer says Eylea is as effective as Lucentis, but needs to be injected less often. With Bayer sure to come on strong promoting Eylea, Novartis will no doubt be inspired to hit back with its own marketing for Lucentis' new use.
http://www.fiercepharma.com/story/lucentis-nears-final-nice-nod-diabetes-related-vision-loss/2013-01-03
Researchers say Alzheimer's studies must focus on abnormalities in patients' brains
BY PAUL HARASIM
LAS VEGAS REVIEW-JOURNAL
Posted: Dec. 13, 2012 | 12:43 a.m.
A normal human brain, what most of us carry around in our heads, is the size of a large grapefruit but looks like a large pinkish-gray walnut. Doctors who have held the organ say it feels soft and squishy.
For most of her 83 years, before she started exhibiting major symptoms of brain-killing Alzheimer's disease three years ago, Verna Kinersly's brain operated normally, which is to say, amazingly.
What scientists estimate as 20 million billion bits of information move around in a normal brain every second, which enabled her to think, move, see, hear, taste, smell, create and feel emotions.
Without her asking, her brain also stored memories, controlled every heartbeat, breath and blink. It also received and analyzed information, so as a young mother, when she saw her daughter falling face first out of a chair across the room, she knew just how fast she needed to run to save her.
Today, her diseased brain doesn't analyze situations well enough for her to safely walk across the street.
That so much of human life is often mysteriously controlled by something so small ---- within the normal 3-pound brain is more power than in any supercomputer ---- prompted Nobel laureate James Watson, co-discoverer of DNA's structure, to call the human brain "the most complex thing we have yet discovered in our universe."
No one still knows how the brain coordinates myriad processes and assimilates vast amounts of information to function as an integrated whole.
LOOKING FOR A BREAKTHROUGH
It's morning at the Cleveland Clinic Lou Ruvo Center for Brain Health, where director Dr. Jeffrey Cummings recently acquired medicine's most sophisticated brain imaging protocol for Alzheimer's, enabling researchers, for the first time, to detect the disorder at the earliest sign of memory problems. It's an advancement that could lead to accelerated treatment and development of drugs against the disease.
Jerry Kinersly, a retired banker with a scientific bent, sits inside the center with his wife and talks about how the complexity of the brain undoubtedly plays a role in the difficulty researchers have had in unlocking the baffling workings of Alzheimer's.
Kinersly, 83, says his wife, currently enrolled in a clinical trial, desperately wants to be part of a research breakthrough into the incurable disease, what most clinicians say is the only real hope for ameliorating the disorder's devastating human destruction.
About 5.4 million people in America have been diagnosed with Alzheimer's, and the number is expected to increase to 16 million by 2050. Alzheimer's Disease International estimates there are more than 35 million living worldwide with dementia, and that could increase to 115.4 million by 2050.
"It's not only terribly costly in human terms, but it can bankrupt the country," Kinersly says, noting that his wife, who is losing her speech to the disease, volunteered to be part of a clinical trial not only to help herself, but all of mankind. "I know helping mankind may sound corny, but that's how we feel. We believe finding answers to this disease are that important both on the human and economic front."
Experts project health care costs for the disease in the U.S. to hit $1.1 trillion in 2050.
While the National Institutes of Health spend annually $450 million on Alzheimer's research, cancer research totals more than $6 billion a year, heart disease $4 billion and HIV/AIDS $3 billion.
Given the devastation caused by Alzheimer's, the research funding allocation for the disease stuns Kinersly.
"It's kind of hard to believe," he says.
Larry Ruvo, one of the nation's top private fundraisers for brain research and the man who built the center in honor of his father, Lou, who died of Alzheimer's, puts it another way.
"The amount of funding we get to end this tsunami of a disease is disgraceful," he says. "It's time for people to stand up and say so to their elected representatives."
PLAQUES AND TANGLES
Like so many research trials with participants around the world, the one Verna Kinersly is in supports the still unproven but prevailing theory that the chief blame for driving the disease falls on the beta-amyloid protein, which forms sticky plaques and kills brain cells in sufferers.
Her 18-month trial treatment involves active immunization, using a type of vaccine that theoretically will trigger the body's immune defense against beta-amyloid.
The National Institutes of Health report that more than 50,000 volunteers, both with and without Alzheimer's, are urgently needed to participate in more than 175 trials and studies in the United States, 25 of them at the Ruvo Center. Dr. Kate Zhong, the center's senior director of clinical research and development, points out that is more than any other center has in the country.
Studies nationwide generally deal with possible causes and risk factors of Alzheimer's, as well as trials of drugs and behavior modifications aimed at treatment, prevention and improving diagnosis.
More than a century has passed since German physician Dr. Alois Alzheimer first described abnormal deposits of beta-amyloid protein plaques and tau protein tangles in the autopsied brain of a woman who suffered with dementia.
Now the most common form of dementia, Alzheimer's stands as the only cause of death among the top 10 in the U.S. without a means to prevent, cure or even slow its progression ---- a fact made less surprising by scientists admitting more was learned about the brain in the past 25 years of the 20th century, largely because of advances in techniques and imaging technology, than in all of previous human history. One out of eight people 65 and older ---- 13 percent ---- currently has Alzheimer's.
Both Cummings, one of the world's most renowned researchers, and William Thies, chief medical and scientific officer for the Alzheimer's Association, agree that there is good reason the abnormal deposits described by Alzheimer still garner the most attention by researchers: The brains of people with Alzheimer's disease are often riddled with plaques and tangles, which many scientists believe are linked to the development of the degenerative dementia.
The two methods being pursued to prevent the formation of plaques, where drug companies have spent the most money ---- billions ---- are vaccinations and drugs.
A string of experimental drugs designed to attack beta-amyloid have failed recently in clinical trials, leaving some drug company executives wondering whether they should cut research funding for plaque and boost funds for more research into tangles, which has had mixed results in the past. The work of Australian researcher Dr. Claude Wischik, who fervently believes tau is the cause of the disease, has served as a catalyst for many companies to invest hundreds of millions in drugs to stymie the protein. Wischik is awaiting the results of a clinical trial testing his causation theory.
Still, this spring U.S. officials said they would help fund a $100 million trial of the Roche pharmaceutical company's amyloid-targeted drug, crenezumab, in 300 people who are genetically predisposed to develop early onset Alzheimer's.
Research into both plaques and tangles, Cummings believes, needs to continue.
"We're getting closer to real answers," he says as he sits in an office full of charts and studies.
Use of an imaging protocol that enables researchers to detect the beta-amyloid brain plaque, for the first time, early in the disease process is under way at the Ruvo Center. Cummings believes anti-amyloid drug trials have failed because patients enrolled in studies had progressed too far in the disease for treatments to be effective. A trial testing the accuracy of the scanner agent in the new imaging protocol is taking place in Las Vegas.
While insurance companies don't cover the high cost of the test, Cummings believes the new imaging protocol will one day be widely used at the Ruvo Center and elsewhere to help make a concrete diagnosis. For now, he says it's a research tool that will get new clinical trial drugs to patients earlier.
The center also has an anti-amyloid trial studying the efficacy of Bexarotene, an anti-cancer drug that also has shown promise against Alzheimer's.
With several drugs failing to reduce the buildup of beta-amyloid plaques, it isn't surprising, Cummings says, that research branches out into other areas, including surgical procedures that might boost memory and reverse cognitive decline.
Earlier this month, researchers at Johns Hopkins Memory and Alzheimer's Treatment Center surgically implanted a pacemakerlike device into the brain of a second patient in the early stages of the disorder ---- a form of deep brain stimulation similar to that already used successfully on thousands of Parkinson's disease patients to reduce tremors and the need for medication.
Dr. Paul Rosenberg ¬- head of the Johns Hopkins study, which also will involve 40 patients at three other U.S. sites and one in Canada - says he is heartened by a preliminary Canadian study that found that low-voltage electrical charges delivered directly to the brain 130 times a second over 13 months showed sustained increases in a patient's glucose metabolism, an indicator of brain cell activity. Most Alzheimer's patients show decreases in glucose metabolism over the same time frame.
Of the six patients studied in Canada ---- those implanted do not feel the electrical current ---- tests showed that two individuals appeared to have better than expected cognitive function.
Cummings says his biggest concern about deep brain stimulation for Alzheimer's is that the disease is a widespread process in the brain, with the stimulation hitting only a localized area. It would be "very difficult to apply" such surgery to 5.4 million people with the disease, Cummings says, but he hopes making "drugs available to many people can be the way forward." If the surgery is positive in select patients, Cummings "would be delighted."
Both Cummings and Thies were excited last month by the findings of an English researcher who discovered a mutated gene, known as TREM2, that is suspected of interfering with the brain's ability to prevent the buildup of plaque.
It is only the second gene found to increase Alzheimer's in older people. The other, ApoEF, was discovered in 1993.
Both make a carrier of either gene three to five times more likely to increase the chances of developing Alzheimer's.
The discovery, Cummings says, can provide clues to how and why the disease progresses, as well as open the door to a possible new drug to strengthen the gene, perhaps allowing the brain's white blood cells to work.
PART OF AGING
Though in the distinct minority, there are researchers who believe that investigating the plaques and tangles in search of a cure for Alzheimer's disease is a mistake.
"Old age is probably not curable," Dr. Ming Chen said recently in a wide-ranging phone interview.
Chen, who heads a research group at the University of South Florida, suggests that "tremendous social pressures" have pushed scientists to target Alzheimer's as a curable disease. He says that as people live longer, Alzheimer's researchers have been driven by the fear of the societal devastation caused by increasing numbers of dementia sufferers.
To Chen, Alzheimer's appears an unfortunate part of aging for some people, just as some people suffer with osteoporosis and severe heart disease.
Writing in the December 2011 issue of the Journal of Alzheimer's Disease, Chen said researchers should de-emphasize the quest for a cure ---- he doesn't think there is a villainous pathogen ---- and instead search for effective prevention and treatment focusing on dementia as part of the aging process.
More studies, he said, should be done of interventions to strengthen or manipulate aging brain cells.
He stresses controlling risk factors, such as diabetes and hypertension, where studies have shown people are more vulnerable to developing Alzheimer's.
What seems to support Chen's position are study findings out of the University of California, San Francisco, in 2011. That report found that as many as half of Alzheimer's cases worldwide could be prevented through lifestyle changes and treatment of chronic conditions such as diabetes. Even a 25 percent reduction in the seven risk factors ---- depression, diabetes, smoking, obesity, sedentary lifestyles, midlife high blood pressure and low education - could prevent 3 million cases of Alzheimer's disease worldwide and nearly half a million in the U.S. alone, the study found.
Energizing the aging brain through social activities and educational opportunities can help fight off dementia, Chen says. He notes, too, that many older people live alone, hastening cognitive decline. The Alzheimer's Association estimates 800,000 individuals with the disease, or one in seven, live alone.
Cummings also believes in a "use it or lose it" doctrine for the brain. He says a laid-back retirement might literally cause people to lose their minds. Quitting the world of meaningful work for a retired life of lounging around with a TV remote might seem enticing, he says, but that passive lifestyle is increasingly seen by researchers as a high risk factor for Alzheimer's.
It is time, Cummings says, for the nation's top governmental leaders and public health officials to have a frank discussion about the implications of retirement and a disease for which age is unquestionably a risk factor.
"We have a social idea of what retirement consists of, and we need to re-examine that idea," he says. "The logical extension of the data we have on dementia is that a person who is still capable of working, who is mentally stimulated with a strong sense of purpose, is better off from the cognitive point of view continuing to engage in that position."
TIMING MATTERS
Early onset Alzheimer's, in which genes have proven to be a major factor, should be treated differently from the more common form of the disease, which often strikes people in their 60s and beyond, Chen says. About 5 percent of Alzheimer's patients get the disease before their 60s.
Chen says medical interventions still should be found to deal with the three acknowledged genes that carry mutations causing early onset Alzheimer's: APP, PSEN1 and PSEN2.
Cummings and Thies strongly disagree with Chen's contention that the older age Alzheimer's is a normal part of aging. While they acknowledge that there may well be multiple factors causing the condition, including genetics and lifestyle, they also believe researchers are zeroing in on slowing the molecular process at the heart of Alzheimer's.
It is also clear, Cummings says, that stem cell research might play a role in Alzheimer's treatment.
Scientists at the University of California, Irvine, have found that neural stem cells can rescue memory in mice genetically engineered to have advanced Alzheimer's, raising hopes of a potential treatment.
CLINICAL TRIALS
Neurologist Dr. Charles Bernick says he has been moved by the fact that hundreds of Southern Nevadans want to be part of clinical trials: "They know what they're testing probably won't help them, but they really do want to help others."
They are people who include 85-year-old Richard Parker, who power walks five miles a day and does 200 curls with 10-pound dumbbells. He was part of a study that tested a pill he took three times a day for his short-term memory problems. The pill turned out not to be effective, but he thinks the exercise is.
"We have a center in this town doing research dedicated to stopping Alzheimer's," he says. "Why wouldn't people want to support it? You might want to help yourself and other people as well."
Currently ongoing at the Ruvo Center is the first multisite clinical trial in the United States aimed at trying to identify Alzheimer's disease through an inexpensive blood test.
A successful trial could be a precursor to detecting the disease before memory loss occurs, a big step toward allowing earlier therapeutic interventions to halt or stabilize progression of the disease.
Another unique trial investigates the efficacy of a chair developed by the Israel-based company Neuronix. The chair combines mental exercise and transcranial magnetic stimulation in the hopes of improving brain function.
New drugs to be studied, some of which involve memory testing, blood tests and brain imaging, include:
¦ Takeda, an oral tablet designed to delay the onset of Alzheimer's.
¦ IGIV, an intravenous drug that could slow the progression of the disease.
¦ Biogen Idec, another intravenous drug study of a medication aimed at slowing disease progression.
¦ Avanir, testing of a drug that has shown early promise of treating agitation and other behavioral problems in Alzheimer's patients.
¦ Resveratrol, testing of an active ingredient in red wine, one found to have potential in slowing the disease.
Both Cummings and Thies say there is a greater sense of urgency among researchers since President Barack Obama signed the National Alzheimer's Project Act into law last year.
It calls for scientists to find a way to treat or prevent the disease by 2025, a goal some experts feel is too ambitious.
The five drugs currently approved by the FDA for treating the cognitive symptoms of Alzheimer's disease ---- Namenda, Razadyne, Exelon, Aricept and Cognex ---- hit the marketplace between 1993 and 2003.
In its attempt to see the 2025 goal is realized, the Obama administration plans to spend an additional $156 million over the next two years.
Philanthropist Ruvo calls it "far too little ... it makes no sense considering the devastation of the disease."
Contact reporter Paul Harasim at pharasim@ reviewjournal.com or 702-387-2908.
Lessening the toll Alzheimer's disease takes on patients, caregivers
What caregivers, researchers, policy makers and physicians recommend to better handle the rising storm of Alzheimer’s disease includes:
• Increase public awareness of the impact of the disease.
• Expand financial and service support to people with Alzheimer’s disease and family caregivers.
• Expand outreach to enhance health care providers’ knowledge of the disease.
• Increase research funding. Currently, Alzheimer’s research receives $450 million per year, compared with cancer, which gets $6 billion.
• Remove age barriers that keep people with younger-onset Alzheimer’s disease from receiving services that seniors can.
• Address sliding-fee scales for people with Alzheimer’s disease.
• Establish and fund a statewide information and referral system for those with Alzheimer’s and their families.
• Provide funding or incentives to encourage long-term care organizations to come to the area.
• Encourage training and education about the disease for all levels of hospital personnel as part of licensing.
• Encourage medical boards to provide continuing medical education regarding Alzheimer’s to primary care physicians.
• Provide and expand respite services for the family caregivers of Alzheimer’s patients.
• Explore use of volunteers to provide support to family caregivers by working with community- and faith-based groups.
• Encourage business community to create employee assistance programs that include training of caregivers.
• Develop a public awareness campaign that removes stigma of Alzheimer’s disease.
• Re-evaluate the effectiveness of medical home models for people with Alzheimer’s.
http://www.lvrj.com/health/researchers-say-alzheimer-s-studies-must-focus-on-abnormalities-in-patients-brains-183303051.html
Intellect Neurosciences and iNovacia Enter Research Service Agreement to Evaluate Lead Compounds for CONJUMAB-A Program
October 03, 2012 09:35 | Source: Intellect Neurosciences, Inc.
NEW YORK and STOCKHOLM, Oct. 3, 2012 (GLOBE NEWSWIRE) -- Intellect Neurosciences, Inc. (OTCBB:ILNS), a biopharmaceutical company engaged in the discovery and development of disease-modifying therapeutic agents for the treatment of proteinopathies, and iNovacia, leading experts in compound screening, announced today they have entered into a Research Service Agreement to evaluate preclinical compounds for the drug optimization and selection program for Intellect's antibody drug conjugate, CONJUMAB-A, which is being developed for age related macular degeneration (AMD).
CONJUMAB-A is anticipated to counter the neurotoxic effects of amyloid beta accumulation and to promote its clearance away from tissues where it causes damage. iNovacia will perform a series of in vitro tests to evaluate compounds, which are designed to allow Intellect to select the optimal drug candidate for further development.
"CONJUMAB-A will be a first-in-class drug compound intended to address an important unmet need in AMD, which is the leading cause of blindness in people over the age of 55. We believe the antibody drug conjugate will show improved efficacy compared to the naked amyloid beta antibodies currently in clinical development for AMD. iNovacia has significant expertise in compound screening, including assay development, and we are confident in their ability to conduct these important studies and deliver data in a timely manner," said Daniel Chain, Ph.D., chairman and CEO of Intellect. "Based on recent discussions with global pharmaceutical companies that have expressed interest in the CONJUMAB-A program, we foresee near-term opportunities for potential partnership."
"We look forward to our inaugural collaboration with the team at Intellect Neurosciences, with the hope that we might continue to work together on future compounds," said Dr. Thomas Olin, CEO of iNovacia. "We have established a successful track record with several pharmaceutical and biotechnology customers in the United States and in Europe and are anxious to provide value to Intellect as well."
About CONJUMAB-A
The CONJUMAB platform empowers monoclonal antibodies targeting amyloidogenic proteins with additional neuroprotective properties by combining them chemically with a small molecule, such as an antioxidant. CONJUMAB-A, the first compound from this platform, is a monoclonal antibody specific for beta amyloid conjugated to melatonin, which is recognized as a potent antioxidant. Beta amyloid, when it accumulates in the retina of the eye, causes damage by oxidative stress. The conjugate is anticipated to increase the therapeutic window for melatonin to protect retinal epithelial cells, promote clearance of beta-amyloid away from sites of damage, and avoid potential off-target side effects. CONJUMAB-A also may have potential applications for diabetic retinopathy, glaucoma, traumatic brain injury, and Alzheimer's disease.
About Intellect Neurosciences
Intellect Neurosciences, Inc., develops innovative approaches aimed at arresting or preventing Alzheimer's disease and other neurodegenerative diseases, with a specific focus on proteinopathies. Intellect's pipeline includes therapeutic vaccines, antibodies and neuroprotective antibody drug conjugates.
For more information, please visit www.intellectns.com.
The Intellect Neurosciences, Inc. logo is available at http://www.globenewswire.com/newsroom/prs/?pkgid=14741
About iNovacia
iNovacia provides high-throughput screening (HTS), fragment-based screening (FBS) and other drug discovery services to translate targets into validated leads for pharmaceutical and biotech companies. Enabled by a proprietary 300,000 compound library of highest international standard, unique biophysical tools for characterization of mode-of-action and structure-activity relationships, iNovacia mitigates technical risk, minimizes lead-time and optimizes quality of drug discovery projects. iNovacia is a wholly owned subsidiary of Kancera AB (Nasdaq OMX Stockholm First North, KAN).
Safe Harbor Statement Regarding Forward--Looking Statements:
The statements in this release and oral statements made by representatives of Intellect Neurosciences relating to matters that are not historical facts (including, without limitation, those regarding future performance or financial results, the timing or potential outcomes of research collaborations or clinical trials, any market that might develop for any of Intellect's product candidates and the sufficiency of Intellect's cash and other capital resources) are forward--looking statements that involve risks and uncertainties, including, but not limited to, the likelihood that actual performance or results could materially differ, that future research will prove successful, the likelihood that any product in the research pipeline will receive regulatory approval in the United States or abroad, or Intellect's ability to fund such efforts with or without partners. Intellect undertakes no obligation to update any of these statements. Readers are cautioned not to place undue reliance on these forward--looking statements, which speak only as to the date hereof. Accordingly, any forward-looking statements should be read in conjunction with the additional risks and uncertainties detailed in Intellect's filings with the Securities and Exchange Commission, including those factors discussed under the caption "Risk Factors" in Intellect's Annual Report on Form 10-K (file no. 333--128226), filed on October 13, 2011, and in our Quarterly Report on Form 10-Q for the quarterly period ended March 31, 2012, which was filed on May 14, 2012.
Contact for Intellect Neurosciences:
Jules Abraham
Principal
JQA Partners, LLC
917-885-7378
jabraham@jqapartners.com
http://globenewswire.com/news-release/2012/10/03/494869/10007130/en/Intellect-Neurosciences-and-iNovacia-Enter-Research-Service-Agreement-to-Evaluate-Lead-Compounds-for-CONJUMAB-A-Program.html
Swedish Cancer Drug Firm Kancera Acquires Stockholm-Based CRO iNovacia
Feb 18, 2011
Swedish cancer drug firm Kancera is taking over Stokholm-based iNovacia, which provides drug discovery services to the biotech and pharma industries. iNovacia will become Kancera’s CRO arm.
iNovacia offers a range of services for both synthetic and biomolecules, spanning assay development and lead optimization, to medicinal and computational chemistry, ADME profiling, fragment-based NMR screening, and protein-protein/ligand interaction studies. The firm has a strategic alliance in place with new Jersey-based Provid Pharmaceuticals to serve the U.S. market and with Moscow-based Asinex for the development of chemical screening libraries.
iNovacia and Kancera already have links. iNovacia was spun out from Pharmacia and Biovitrum's drug development unit back in 2006. The firm subsequently established partnerships with the Cancer Centre Karolinska and Sprint Bioscience, which specializes in structure-based pharmaceutical design. Then, just last year iNovacia and Sprint Bioscience together with the Karolinska Institute and a group of private investors founded Kancera with a starting pipeline of two anticancer projects.
The two projects still form the backbone of Kancera’s R&D operations. The PFKFB3 program for solid tumors is currently at the lead-optimization stage. An ROR-1 program for leukemia therapy is expected to yield a clinical candidate in 2013.
PFKFB3 is one of four variants of the phosphofructokinase 2 enzyme. This variant has been shown to be highly up-regulated in the absence of oxygen and is overexpressed and overactivated in many types of human cancer, the firm points out. Kancera's project builds on the hypothesis that specific inhibition of PFKFB3 will lead to a reduction in metabolism and cell growth in oxygen-deficient cancer environments.
The firm expects blocking PFKFB3 will effectively starve and weaken the tumor cells, reducing their resistance to radiotherapy and chemotherapy. Last month Kancera and its partner Sprint reported solving the 3- dimensional crystal structure of a novel chemical class in complex with the target enzyme PFKFB3.
The leukemia program is focused on developing either antibody or small molecule inhibitors of the growth factor ROR-1 as a means to prompting leukemic cells to commit cellular suicide. Kancera says its work has already led to several classes of synthetic compounds that are effective against ROR-1.
In January the firm also announced it had identified compounds that kill chronic lymphocytic leukemia cells 25 times more selectively than cytostatic drugs currently used for treating the disease. Kancera is in addition looking to expand its pipeline such that it has at least four projects running at various phases of the preclinical phase in parallel with new drug discovery efforts. It aims to give priority to projects that could yield drug candidates within 3–5 years from start.
http://www.genengnews.com/gen-news-highlights/swedish-cancer-drug-firm-kancera-acquires-stockholm-based-cro-inovacia/81244707/
Dan Shochat, Ph.D.
Vice President
Dan Shochat, Ph.D. has more than 28 years of experience in the biotechnology industry and is a pioneer in the antibody development arena. Prior to joining Intellect, he served as vice president of nonclinical development at KaloBios Therapeutics. Prior, he was among the first employees of Immunomedics Inc., Newark, NJ where he served as group director, product R&D. Dr. Shochat is the inventor of several technologies, including that of the approved in vivo tumor-imaging agent CEA-Scan; Mylotarg - the first approved antibody-cytotoxic drug conjugate; and the design, process and formulation for the commercial radiolabeling of the B1 antibody at a 55 Curie scale. The lead product from this work was Bexxar, a radioiodinated antibody for the treatment of Non-Hodgkin's Lymphoma that was approved by the FDA on June 2003. He is co-founder of Celscia Therapeutics Inc. - a therapeutic antibodies development company - which merged with KaloBios Therapeutics in January 2004.
From 2001 to 2007 Dr. Shochat was a member of the Technical Advisory Committee to the Board of Directors of the Australian Nuclear Science and Technology Organization. He also serves as consultant and member of scientific advisory boards of several biopharmaceutical companies and venture capital funds.
Dr. Shochat earned B.Sc. in Zoology and Physiology (1965) and M.Sc. in Physiology (1968) from the Hebrew University of Jerusalem, Israel and Ph.D. in Biochemistry and Protein Chemistry (1976) from LSU Medical Center, New Orleans, LA. He was a post-doctoral fellow in the Department of Biochemistry (1975-1978) and Sr. Research Associate at the Division of Experimental Pathology (1978-1983), the University of Kentucky Medical Center, Lexington, KY. In 1983 he participated in founding the Center for Molecular Medicine and Immunology at the University of Medicine and Dentistry of New Jersey, Newark, NJ, where he was an Associate Member until he joint Immunomedics, Inc. in 1984. From 1986-1992 Dr. Shochat served successively as visiting lecturer and adjunct professor at the Chemistry Department of Rutgers University Graduate School (Newark, NJ campus).
http://www.intellectns.com/company-info/management-team
Bexxar (tositumomab)
Bexxar (tositumomab) refers most often to the Bexxar therapeutic regimen, a type of radioimmunotherapy: Unlike traditional chemotherapy (and much likeZevalin), Bexxar combines the powerful anti-cancer effects of radiation ("radio-") with the targeted, precision action of a monoclonal antibody ("immuno")1.
Tositumomab is a monoclonal antibody that, like rituximab (Rituxan) and ibritumomab tiuxetan (Zevalin), targets the CD20 protein found on the surface of B lymphocytes.
What it's effective for and why
The Bexxar therapeutic regimen has proven to be effective in treating indolent, CD20 positive B-cell non-Hodgkin's lymphomas. It has been FDA approved since 2003 for the treatment of follicular lymphoma when the disease isrefractory to rituximab and when it has relapsed following a prior regimen of chemotherapy2. Bexxar works as a combination of two closely related monoclonal antibodies: tositumomab seeks out and finds B lymphocytes (identifying them by the protein CD20), then using the iodine 131 to kill the cell with targeted radiation.
The Bexxar therapeutic regimen features two steps, the dosimetric step, and the therapeutic step. The dosimetric step involves only an infusion of tositumomab. It is followed, 7-14 days later, by the therapeutic step: once again, the patient receives an infusion of tositumomab, but this time it is followed by an additional smaller dose of tositumomab that is attached to the radioactive isotope Iodine-131. This step delivers approximately 75 cGy of radiation to the body.
Side effects: Overview3
In general, Bexxar produces side effects similar to many other drugs: nausea, vomiting, stomach, back or neck pain, diarrhea, loss of appetite, mouth sores, headaches, and hair loss to name a few. More severe side effects that have been reported include chest pain, constipation, brittle nails, hoarse voice, or a puffy face. It is important to remind the reader that not everyone receiving the drug will develop these side effects.
Additionally, some patients given the Bexxar injection have gone on to develop other cancers, notably leukemia, skin cancer, myelodysplastic syndrome (MDS) or other cancers.
http://bexxar.cancertreatment.net/
Lonza to make antibody conjugates for preclinical trials
By Gareth MacDonald+
01-Oct-2012
Lonza to make preclinical trial supplies of an antibody-drug conjugate (ADC) at its facility in Visp, Switzerland
Lonza will use its facility in Visp, Switzerland to make preclinical trial supplies of an antibody-drug conjugate (ADC) being developed by Intellect Neurosciences.
The candidate drug in question - IN-NO1-OX2 or Conjumab-A - combines one of Intellect’s beta amyloid protein targeting Antisenilin antibodies with a small molecule neuroprotective compound.
Under the contract, Switzerland-based Lonza will combine the core antibody with various neuroprotective compounds from its own library for further assessment by Intellect and several unnamed ‘specialised' contract research organisations (CROs).
Work on the project has already begun according to Stefan Stoffel, Lonza head of chemical manufacturing operations, who said: "We have already generated a detailed road map for the optimisation and manufacture of Conjumab-A, and are excited to be associated with this entirely novel and promising application for antibody-drug conjugates."
ADC development
The decision to develop and produce the candidate ADCs in Visp fits with plans Lonza outlined in August when it said making more high-tech, high-value pharmaceutical products and ingredients at the plant was key to increasing its competitiveness.
At the time recently appointed COO Beat In-Albon – who was called in to handle the ‘Visp Challenge ’ – said: “The focus will be on process production, process optimisation as well as the introduction of higher margin, new technology products.”
While it is hard to say how significant the Intellect contract is for Lonza – no financial terms were disclosed – the deal does underline the interest top tier contract manufacturing organisations (CMOs) have in ADC development and manufacture.
In recent years Lonza, SAFC, Goodwin Biotechnology and Piramal have invested in this type of manufacturing , while – in July – French firm Novasep invested €3m to add ADC production capacity at its plant in Le Mans.
http://www.in-pharmatechnologist.com/Processing/Lonza-to-make-antibody-conjugates-for-preclinical-trials
Pipeline activities:
Tue, Oct 16, 2012 9:35 AM EDT
Our antibody-drug conjugate platform, CONJUMAB, provides potential development of two independent antibody-based products from the same starting material, our compound, IN-N01. Our recent agreement with Lonza, with whom we signed a letter of intent, was an important step in the development of our first ADC, CONJUMAB-A. We are excited to have reached a point at which Lonza is now manufacturing the preclinical materials for the drug optimization and drug selection program, and look forward to testing these compounds in the near future. With sufficient financial resources, we could reasonably expect to file two INDs within two years, one for CONJUMAB-A initially focused on age-related macular degeneration and a second for IN-N01 for a second indication such as familial Alzheimer's disease or traumatic brain injury, both of which could qualify as orphan diseases.
Patent news:
We remain determined to secure our ANTISENILIN patents still under review by the USPTO and hopeful that this can be accomplished over the next few months. The demonstration using biomarkers that bapineuzumab reduces amyloid plaque and neurodegeneration in the brain of Alzheimer's patients provides compelling new evidence in support of the ANTISENILIN platform technology. Similarly, we plan to continue with the appeal process that we initiated in February to overcome the challenge to our patents in Europe.
We were disappointed by the failure of one of our global pharmaceutical licensees to pay the $2 million milestone payment triggered by the issuance of our patent by the USPTO on May 8, 2012 eventually leaving us no option except to pursue our claim in the courts. The action of our licensee in this regard is unconscionable and, in my opinion at least, an affront to the pharmaceutical industry that desperately needs to foster rather than thwart innovation at a time that global pharmaceutical companies are substantially reducing their internal R&D and relying more and more on companies such as Intellect Neurosciences to provide the next generations of high value therapeutics. The community at large should be aghast that a small company such as ours needs to divert attention and limited resources from its critically important mission of developing disease modifying therapies for Alzheimer's and other serious neurological diseases.
http://finance.yahoo.com/news/intellect-neurosciences-issues-letter-shareholders-133500792.html
Intellect Neurosciences Announces New Findings Supporting Its Tau Oligomer Selective TOC-1 Monoclonal Antibody for the Treatment of Alzheimer's Disease
By GlobeNewswire, November 06, 2012, 09:35:00 AM EDT
NEW YORK, Nov. 6, 2012 (GLOBE NEWSWIRE) -- Intellect Neurosciences, Inc. (OTCBB:ILNS), a biopharmaceutical company engaged in the discovery and development of disease-modifying therapeutic agents for the treatment of Alzheimer's and other neurological diseases, announced today scientists at Northwestern University have published new findings on its tau oligomer selective TOC-1 monoclonal antibody. These new data explain a phenomenon concerning the role of aggregated oligomeric tau as an inhibitor of fast axonal transport (FAT). FAT is the mechanism by which newly synthesized membrane and other proteins made in the nerve cell body essential for neuronal membrane function and maintenance are provided to the synapse.
The paper, titled, "Tau oligomers and tau toxicity in neurodegenerative disease," was written by Lester Binder, Ph.D., the Abbott Laboratories, Duane and Susan Burnham Research Professor of Genetic and Molecular Medicine, at Northwestern University. It appeared in the recent edition of Biochemistry Society Transactions.
"The inhibition of FAT requires a small stretch of amino acids termed phosphatase-activation domain, or PAD. Using a PAD-specific antibody, TNT1 and Tau oligomer selective antibody TOC-1, Dr. Binder's research group was able to demonstrate the PAD is more exposed in oligomeric tau leading to dissociation of the microtubules in diseased neurons. This leads to an increase in FAT inhibition and represents an early event in AD pathogenesis. These findings support our belief, shared by several global pharmaceutical companies with whom we are in discussions, that TOC-1 has important therapeutic potential," stated Daniel Chain, PhD, chairman and CEO of Intellect.
Intellect previously obtained development and commercialization rights to TOC-1 under an exclusive license agreement with Northwestern University and plans to develop it for the treatment of Alzheimer's disease (AD) and other tauopathies.
Dr. Chain will speak about Intellect's TOC-1 program at the International Drug Discovery Science and Technology (IDDST) conference November 8-10 in Nanjing, China.
Intellect Neurosciences, Inc. develops innovative approaches aimed at arresting or preventing Alzheimer's disease and other neurodegenerative diseases especially focused on proteinopathies. Intellect's pipeline includes therapeutic vaccines, antibodies and neuroprotective antibody drug conjugates. For more information, please visit www.intellectns.com.
The Intellect Neurosciences, Inc. logo is available at http://www.globenewswire.com/newsroom/prs/?pkgid=14741
Safe Harbor Statement Regarding Forward-Looking Statements:
The statements in this release and oral statements made by representatives of Intellect Neurosciences relating to matters that are not historical facts (including, without limitation, those regarding future performance or financial results, the timing or potential outcomes of research collaborations or clinical trials, any market that might develop for any of Intellect's product candidates and the sufficiency of Intellect's cash and other capital resources) are forward-looking statements that involve risks and uncertainties, including, but not limited to, the likelihood that actual performance or results could materially differ, that future research will prove successful, the likelihood that any product in the research pipeline will receive regulatory approval in the United States or abroad, or Intellect's ability to fund such efforts with or without partners. Intellect undertakes no obligation to update any of these statements. Readers are cautioned not to place undue reliance on these forward-looking statements, which speak only as to the date hereof. Accordingly, any forward-looking statements should be read in conjunction with the additional risks and uncertainties detailed in Intellect's filings with the Securities and Exchange Commission, including those factors discussed under the caption "Risk Factors" in Intellect's Annual Report on Form 10-K (file no. 333--128226), filed on October 15, 2012.
CONTACT: Jules AbrahamJQA Partners, LLCjabraham@Jqapartners.com
http://www.nasdaq.com/article/intellect-neurosciences-announces-new-findings-supporting-its-tau-oligomer-selective-toc-1-monoclonal-antibody-for-the-treatment-of-alzheimers-disease-20121106-00803#.UOaT-W9FVHk
Daniel Chain Sues Pfizer for $2M
Posted in: Articles, biotechnology, neurological | October 17, 2012 at 6:32 am
Intellect Neurosciences has filed a breach of contract suit against Pfizer Inc. for failing to make a $2 million milestone payment for rights to its Alzheimer’s disease technology.
Intellect Neurosciences was founded by CEO Daniel Chain, who laid the groundwork for the technology in dispute with Pfizer during his tenure at Mindset, a Jerusalem-based startup.
Intellect contends that the licensing fee was triggered when the U.S. Patent and Trademark Office issued the company a patent on May 8 that covers its Antisenilin monoclonal antibody platform technology for the treatment and prevention of Alzheimer’s disease.
“It’s a distressing situation for us, a small company, to go head-to-head with a major company,” Intellect Neurosciences Chairman and CEO Daniel Chain said in a report to The Pink Sheet. The milestone payment “was clear, black and white in the agreement.”
Intellect Neurosciences’ patent discloses therapeutic antibodies to treat or delay onset of Alzheimer’s disease. The antibodies bind to both ends of the beta amyloid protein without binding to the amyloid precursor protein.
Following the recent American Neurology Association annual meeting, Chain posted an Oct. 9 personal perspective on the conference on the company’s homepage. “As the dust settles after the initial disappointing results from four major Alzheimer’s Phase III trials,” he concludes, the ANA “offered glimmers of light that renewed hope. The presenters and expert panelists conveyed a strong sense that Intellect is correct in its belief beta amyloid (Aß) plays a central and causative role in the pathogenesis of Alzheimer’s disease and that immunotherapy represents a realistic path forward. The next-generation drugs will have an improved probability of success because of the lessons we have learned.”
http://www.bioisrael.com/daniel-chain-sues-pfizer-for-2m
The last weeks to buy cheap, if Dr. Chain already signed an agreement (Conjumab-A,TOC-1, Recall-Vax, etc.), before 10-Q is out!
CAD106
October 15, 2012
In another step away from cancer therapeutic vaccines, CAD106, a vaccine co-developed by Novartis ($NVS) and Cytos that targets the amyloid ß peptide, has shown early hints of immune responses in a clinical trial in people with Alzheimer' s disease.
This vaccine could have potential to slow the development of the disease and fill a major unmet medical need. The World Health Organization says dementia is the fastest-growing global health epidemic and there is no treatment available that alters the course of the disease.
CAD106 targets a fragment of the harmful form of the beta amyloid peptide, the main component of the plaques found in the brains of people with Alzheimer's disease. In the Karolinska Institutet study, people with mild-to-moderate Alzheimer's developed protective antibodies against beta amyloid without any side effects, and the researchers want to carry out larger trials.
According to the company and the Karolinska Institutet, these are the first results to show a positive effect of an active vaccine against Alzheimer's. Development of the first vaccine against beta amyloid, Elan's AN1792, had to be discontinued as it triggered meningoencephalitis (inflammation of the brain and the membranes around the brain), but there were no signs of that in the CAD106 trial.
The agreement between Novartis and Cytos goes back to 2001, and covers a collaboration to develop therapeutic vaccines for the treatment of allergies, rheumatoid arthritis, and chronic nervous system disorders.
Read more: CAD106 - FierceVaccines http://www.fiercevaccines.com/special-reports/cad106#ixzz2GulhZgIo
Subscribe: http://www.fiercevaccines.com/signup?sourceform=Viral-Tynt-FierceVaccines-FierceVaccines
http://www.fiercevaccines.com/special-reports/cad106
Early steps toward an Alzheimer’s vaccine
POSTED JUNE 12, 2012, 12:24 PM
Heidi Godman, Executive Editor, Harvard Health Letter
Some encouraging Alzheimer’s news from Sweden: a vaccine called CAD106 appears to be safe and ramps up the body’s immune system against a protein likely involved in Alzheimer’s. The hope is that this vaccine will slow the progression of Alzheimer’s disease, and possibly even stop it.
The vaccine is designed to activate the body’s immune system against beta amyloid, a protein fragment that forms deposits called amyloid plaques between nerve cells in the brain. While it’s unclear if beta amyloid plaques cause Alzheimer’s or are a result of it, scientists do know that the plaques are an important biomarker of the disease. Some researchers believe that beta amyloid plaques interfere with communication between nerve cells or somehow inhibit processes needed to keep brain cells alive.
“Twenty-five years ago,” says Dr. Anthony L. Komaroff, professor of medicine at Harvard Medical School, “we knew very little about what caused Alzheimer’s disease and therefore how it might be prevented and treated. A lot of people were hopeless. We knew that we could see certain microscopic abnormalities in the brains of people with Alzheimer’s disease, called plaques and tangles. And we knew some of the chemicals inside the plaques and tangles. But we didn’t know if they caused the disease, and whether targeting them would help people with the disease.”
This vaccine work may help answer those questions.
Safety first
In the vaccine study, published online in Lancet Neurology, researchers from the Karolinska Institute gave 58 men and women with mild-to-moderate Alzheimer’s disease injections of CAD106 or a placebo and followed them for three years. Three-quarters of those who received CAD106 developed antibodies against beta amyloid protein. Virtually all of them—including those getting the placebo—reported one or more side effects, ranging from inflammation of the nose and throat to headache, muscle pain, and fatigue.
None, though, developed meningoencephalitis, an inflammation of brain tissue. That’s important because a trial of an earlier vaccine called AN1792 was abruptly stopped when 6% of those getting the vaccine developed meningoencephalitis. That vaccine apparently triggered a response among certain white blood cells that wound up attacking healthy brain tissue. CAD106, in comparison, targets only the beta amyloid proteins.
The next step in the development of CAD106 is a larger clinical trial to confirm the vaccine’s safety and to see if it is effective at slowing the relentless progression of Alzheimer’s disease.
“It’s much too early to say whether this particular vaccine will prove to be a valuable treatment in Alzheimer’s disease,” Dr. Komaroff says. “Nevertheless, in contrast to 25 years ago, today there is a lot of evidence that beta amyloid is one important cause of Alzheimer’s disease, and that targeting beta amyloid with drugs and vaccines may bring benefits. Because of biomedical research, today we have real reason for hope.”
Several other Alzheimer’s vaccines that target the beta amyloid protein are also being tested in clinical trials. Another effort moving forward includes an insulin-based nasal spray, which has shown promise in repairing damaged brain tissue involved in memory and cognition. The Obama administration’s National Alzheimer’s Plan, which was released last month, calls for $7.9 million in funding for this spray.
http://www.health.harvard.edu/blog/early-steps-toward-an-alzheimers-vaccine-201206124878
Safety, tolerability, and antibody response of active Aß immunotherapy with CAD106 in patients with Alzheimer's disease: randomised, double-blind, placebo-controlled, first-in-human study.
Winblad B, Andreasen N, Minthon L, Floesser A, Imbert G, Dumortier T, Maguire RP, Blennow K, Lundmark J, Staufenbiel M, Orgogozo JM, Graf A.
Source
Karolinska Institutet Alzheimer Disease Research Centre and Clinical Trial Unit, Geriatric Clinic, Karolinska University Hospital, Huddinge, Sweden. bengt.winblad@ki.se
Abstract
BACKGROUND:
Immunotherapy targeting the amyloid ß (Aß) peptide is a potential strategy to slow the progression of Alzheimer's disease. We aimed to assess the safety and tolerability of CAD106, a novel active Aß immunotherapy for patients with Alzheimer's disease, designed to induce N-terminal Aß-specific antibodies without an Aß-specific T-cell response.
METHODS:
We did a phase 1, double-blind, placebo-controlled, 52-week study in two centres in Sweden. Participants, aged 50-80 years, with mild-to-moderate Alzheimer's disease were entered into one of two cohorts according to time of study entry and then randomly allocated (by use of a computer-generated randomisation sequence) to receive either CAD106 or placebo (4:1; cohort one received CAD106 50 µg or placebo, cohort two received CAD106 150 µg or placebo). Each patient received three subcutaneous injections. All patients, caregivers, and investigators were masked to treatment allocation throughout the study. Primary objectives were to assess the safety and tolerability of CAD106 and to identify the Aß-specific antibody response. Safety assessment was done by recording of all adverse events, assessment of MRI scans, physical and neurological examinations, vital signs, electrocardiography, electroencephalography, and laboratory analysis of blood and CSF. Patients with Aß-IgG serum titres higher than 16 units at least once during the study were classified as responders. This study is registered with ClinicalTrials.gov, number NCT00411580.
FINDINGS:
Between August, 2005, and March, 2007, we randomly allocated 31 patients into cohort one (24 patients to CAD106 treatment and seven to placebo) and 27 patients into cohort two (22 patients to CAD106 treatment and five to placebo). 56 of 58 patients reported adverse events. In cohort one, nasopharyngitis was the most commonly reported adverse event (10 of 24 CAD106-treated patients). In cohort two, injection site erythema was the most commonly reported adverse event (14 of 22 CAD106-treated patients). Overall, nine patients reported serious adverse events--none was thought to be related to the study drug. We recorded no clinical or subclinical cases of meningoencephalitis. 16 of 24 (67%) CAD106-treated patients in cohort one and 18 of 22 (82%) in cohort two developed Aß antibody response meeting pre-specified responder threshold. One of 12 placebo-treated patients (8%) had Aß-IgG concentrations that qualified them as a responder.
INTERPRETATION:
Our findings suggest that CAD106 has a favourable safety profile and acceptable antibody response in patients with Alzheimer's disease. Larger trials with additional dose investigations are needed to confirm the safety and establish the efficacy of CAD106.
FUNDING:
Novartis Pharma AG.
http://www.ncbi.nlm.nih.gov/pubmed/22677258
The Only Economically Sustainable Approach to Treat Alzheimer’s Disease may be through Next-Generation Vaccines
Jan 1 2013
Disease-modification is becoming less attractive as an approach for treating Alzheimer’s disease for two main reasons. First, as evidenced by recent Phase 3 clinical trials results, patients who are symptomatic probably have disease that is too far advanced to benefit significantly from treatments that slow the degenerative process. Second, treating very early stage or presymptomatic patients will be extremely expensive and prove too costly a burden for healthcare systems. An article by scientists from the Karolinska Institute in Sweden, published in the October issue of Current Alzheimer’s Research, indicated the economic cost of treatment with a chronically and frequently administered disease-modifying drug would outweigh the cost of palliative care, including full-time nursing care of patients with advanced disease. This economic model leads one to conclude that a vaccination given on an annual or semi-annual basis may be the only economically feasible approach to prevent and manage Alzheimer’s disease.
This idea generated significant interest and discussion when I introduced the topic at the 6th Annual Alzheimer’s Drug Discovery Summit in Philadelphia last month. One of my goals was to raise awareness of recent developments, including our own, that I believe could ultimately result in a safe and effective vaccine, which when administered to tens of millions of people around the world, could delay or prevent the onset of symptomatic Alzheimer’s disease. I started by reminding the audience of how the vaccine field evolved, beginning with the remarkable demonstration that “inoculation” of an Alzheimer’s mouse model with aggregated human beta amyloid protein (Aß) resulted in dramatic reduction of amyloid plaque in the brain. These data, first reported by scientists from Elan Pharmaceuticals in 1999, were the first in vivo demonstrations that antibodies against Aß can reduce plaque, confirming my predictions for the ANTISENILIN antibodies two years prior.
Unfortunately, the initial excitement regarding active immunotherapy was short-lived because of several ill-conceived choices made with the first Alzheimer’s vaccine tested in humans, AN1792. The trial was terminated after just two inoculations of the vaccine because of acute brain inflammation in several patients enrolled in the Phase 2 clinical trial. For a while, it seemed that Alzheimer’s immunotherapy was dead in the water. However, this initial failure was gradually shown to be largely the result of an autoimmune response against Aß, which can be easily avoided by removing the harmful C-terminus portion of Aß containing T-cell epitopes. The impact of this change is reflected by several successful safety trials involving second-generation vaccine candidates.
The AN1792 trial has since influenced the development of immunotherapy approaches. I wonder if progress may have been accelerated were it not for the AN1792 debacle. For example, there has been a major shift in focus from active immunotherapy to passive immunotherapy. This shift was based on the rationale that administering externally-generated antibodies is probably safer than stimulating an immune response in patients. However, passive immunotherapy was found to have its own significant safety issues, especially with antibodies that bind plaque with high affinity. On the other hand, second-generation vaccines currently in clinical development appear to have overcome the problems encountered with AN1792 and show no evidence of vasogenic edema or microhemorrhages. The different safety profiles between passive and active immunization strategies are likely related to the slower build-up of antibodies from active immunization. This change in approach avoids the rapid dissolution of pre-existing plaque that results when a bolus injection of externally administered antibody causes toxic fragments to be released back into circulation. This may be less of an issue if treatment is initiated before plaques form or using subcutaneous instead of intravenous administration as is being tested with bapineuzumab.
Table 1 (Information from www.clinicaltrials.gov)
Table 1 above summarizes three ongoing Phase 2 clinical trials to evaluate second-generation vaccines: CAD016 sponsored by Novartis in collaboration with Cytos, ACC-001 sponsored by Janssen Alzheimer’s immunotherapy R&D in collaboration with Pfizer, and AD02 sponsored by Affiris in collaboration with Glaxo. The three vaccines each contain a short-fragment corresponding to a portion of Aß adjacent to the N-terminus. In the case of AD02, the peptide is comprised of an artificial sequence of amino acids that mimics the structure of the N-terminus to produce a “mimotope.” The advantages of using short peptides (whether natural or artificial) are first to avoid incorporating potentially harmful T-cell epitopes that could cause an autoimmune response and second, to guarantee the antibodies generated in response to the vaccine only bind Aß not the amyloid precursor protein (APP) thereby reducing the potential for adverse off-target side-effects. However, the use of small peptides also poses challenges, especially regarding the ability to mount a robust and sustained antibody response even in the presence of a strong adjuvant. In CAD106 and ACC-001, several copies of the short peptides are linked to a much larger immunostimulatory molecule, a viral like particle in the case of CAD106 and a mutant form of diphtheria toxin in the case of ACC-001.
In each case, the larger molecules provide the necessary T-cell response to obtain an immune response. However, the disadvantage is a reduced concentration of active peptide per vaccine dose. The Phase 1 results with CAD106 were encouraging because they showed most vaccinated patients mounted an immune response, however, these responses appeared fairly transient, suggesting patients failed to obtain a sustained immune response. This could result in CAD106 needing to be administered repeatedly thereby losing the cost advantage of vaccination.
Intellect Neurosciences’ RECALL-VAX technology platform aims to overcome this challenge. In our vaccine candidate, a similar fragment of Aß is joined with a small bacterial T-cell epitope comprised of tetanus toxoid, thus assuring a higher molar concentration of the Ab peptide per vaccine dose. A second advantage rests in the fact most people have been inoculated against tetanus toxoid, allowing this new vaccine to recall a memory imprint that exists in the immune system, thereby improving the patient’s immunity against Alzheimer’s. Consequently, we believe RECALL-VAX has the best chance of developing a robust and sustained immune response in elderly patients whose immune systems are generally weakened by age. Intellect Neurosciences has been granted numerous patents in relation to RECALL-VAX, including in 26 European countries, Japan and the United States.
There is a growing sentiment among Alzheimer’s researchers that Aß monotherapy may be ineffective to treat the disease or stop it in its tracks for several reasons: First, the degree to which Aß levels need to be reduced to delay onset or slow progression is unknown. Secondly, Aß therapies are unlikely to improve function or plasticity of damaged but surviving nerve cells. Thirdly, other mechanisms are important, especially tau pathology, which acts synergistically with Aß in Alzheimer’s, causing irreversible damage to nerve cells.
This notion led to our collaboration with Dr. Frank LaFerla, Chancellor's Professor and Chair, Neurobiology and Behavior School of Biological Sciences, Director, Institute for Memory Impairments and Neurological Disorders and his team, and our collaboration with Dr. Kim Green at the University of California, Irvine, to evaluate a number of vaccine candidates based on the RECALL-VAX approach including, RV03, a first-in class bispecific vaccine targeting both Aß and ? tau, a particularly pathogenic form of the protein that precedes neurofibrillary tangle formation. Our combined research is focused on developing the first dual vaccine against these two important therapeutic targets to prevent the irreversible damage and death of nerve cells caused by these two proteins.
One hopes the improved safety profile of candidates currently in clinical development will stimulate interest in the vaccine approach and importantly lead to the type of investment needed to progress development of next-generation drugs, such as RV03, which has the potential to be a game-changer in the prophylaxis and management of Alzheimer’s disease.
I ended the talk with my favorite quote from the great 19th century French chemist and bacteriologist, Louis Pasteur (1822-1895), who first coined the word “vaccine”: “Through perseverance in one field of investigation, one succeeds in acquiring what I call the instinct of truth.” Pasteur’s determination to stay the course led to his creation of the first vaccines for rabies and anthrax and laid the foundations for the manufacture of many other vaccines saving millions of lives. We can learn from his example as we continue with our important mission to create a world without Alzheimer's disease.
In the meantime, I wish you a very happy, healthy and prosperous New Year.
-Daniel Chain, Ph.D., Chairman and CEO, Intellect Neurosciences, Inc.
http://www.intellectns.com/blog
Intellect Neurosciences CEO Daniel Chain Provides Conference Highlights of Alzheimer's Drug Development Summit in Neurotech Insights Magazine
NEW YORK, Jan. 2, 2013 (GLOBE NEWSWIRE) -- Intellect Neurosciences, Inc. (OTCBB:ILNS) announces Dr. Daniel G. Chain, Chairman and CEO, provided conference highlights from the December 11-12 Alzheimer's Drug Development Summit in Neurotech Insights magazine. Dr. Chain was a Distinguished Speaker at the conference.
In addition to Dr. Chain's presentation, titled "Recent Advancements in Vaccine Development for AD Prophylaxis and Management," which reviewed the challenges associated with the development of a safe and effective Alzheimer's vaccine and described the rationale in support of Intellect's ground-breaking approach, Dr. Chain provided overviews of the major talks of the conference. His overview concluded with an analysis of the way the federal government has failed to address the cost of development for new treatments for Alzheimer's disease.
In the article, Dr. Chain commented, "I fully concur with the Neurotechnology Industry Association's (NIO) belief that the solution to the problem of prevalence of neurological disease and the public health burden it presents lies in creating new market exclusivity for sponsors of novel disease-modifying therapeutics that are targeted to neurodegenerative disease, especially AD. The rationale of the NIO initiative follows that of the 1983 Orphan Drug Act, which has since spurred development of new medicines for hundreds of orphan diseases that, otherwise, would not have been addressable given the small market size. A guaranteed market exclusivity period of ten years would be sufficient to tilt the cost-benefit consideration toward continuing drug development for neurodegenerative diseases."
About Intellect Neurosciences
Intellect Neurosciences, Inc., develops innovative approaches aimed at arresting or preventing Alzheimer's disease and other neurodegenerative diseases, with a specific focus on proteinopathies. Intellect's pipeline includes therapeutic vaccines, antibodies and neuroprotective antibody drug conjugates. For more information, please visit www.intellectns.com.
The Intellect Neurosciences, Inc. logo is available at http://www.globenewswire.com/newsroom/prs/?pkgid=14741
Safe Harbor Statement Regarding Forward-Looking Statements:
The statements in this release and oral statements made by representatives of Intellect Neurosciences relating to matters that are not historical facts (including, without limitation, those regarding future performance or financial results, the timing or potential outcomes of research collaborations or clinical trials, any market that might develop for any of Intellect's product candidates and the sufficiency of Intellect's cash and other capital resources) are forward-looking statements that involve risks and uncertainties, including, but not limited to, the likelihood that actual performance or results could materially differ, that future research will prove successful, the likelihood that any product in the research pipeline will receive regulatory approval in the United States or abroad, or Intellect's ability to fund such efforts with or without partners. Intellect undertakes no obligation to update any of these statements. Readers are cautioned not to place undue reliance on these forward-looking statements, which speak only as to the date hereof. Accordingly, any forward-looking statements should be read in conjunction with the additional risks and uncertainties detailed in Intellect's filings with the Securities and Exchange Commission, including those discussed in Intellect's Quarterly Report on Form 10-Q (file no. 333-128226), filed on November 20, 2012 and the risk factors discussed under the caption "Risk Factors" in Intellect's Annual Report on Form 10-K (file no. 333-128226), filed on October 15, 2012.
Jules Abraham
JQA Partners, LLC
917-885-7378
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