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No, the correct flow chart is: if the 1st degree has a defined mutation then I will look for that specific mutation in the tested subject (man or woman), no need to look for CNV in case like that. However, when the family history strongly suggests that the breast cancer runs in the family and no mutation has been found in BRCA1/2 then I will look for CNV.
The main question is whether isolated DNA is markedly different from natural DNA. Judge Sweet thinks it is not. I think this will be overturned, but I don't count. Worse case MYGN, ROSG and others will have protection via patents such as method of use.
Thanks for clarifying. I didn't think nerispirdine is different from Fampridine, but if SNY is already recruiting for P3 investigators perhaps it is.
You're right, the same goes for man. However, I've made an even bigger mistake in post #msg-48837095. Can you see it?
We're on the same wavelength #msg-48467022.
There's nothing "obvious" about what the problem was
it was never a simple or obvious diagnosis
No need to imagine, DNA sequences are not patentable but I said I do believe the 101 can be overcome by the "isolated" (DNA) and this is a reasonable way to protect genomic know how especially as about 20% of the genome has been patented already.
Scientific Meeting Calendar
NOTE: ANYONE MAY UPDATE THIS FILE
Edits: Added Autoimmunity, APS, Stem Cells, ASM, ASGCT, ACR, ISTH, AUA.
APRIL 2010
European Congress on Clinical Microbiology and Infectious Diseases
- ASCMID
Vienna, Austria
April 10-13, 2010
http://www.escmid.org/
American Academy of Neurology - AAN
Toronto, Canada
April 10–17
http://www.aan.com/
National Kidney Foundation - NKF
Orlando, FL
April 13-17, 2010
http://www.kidney.org/news/meetings.cfm
European Association for the Study of the Liver - EASL
Vienna, Austria
April 14-18, 2010
http://www.easl.eu/
American Association for Cancer Research - AACR
Washington, D.C.
April 17-21, 2010
http://www.aacr.org/
World Vaccine Congress - WVCDC
Washington, D.C.
April 19-22, 2010
http://www.terrapinn.com/2010/wvcdc/index.stm
International Society for Heart and Lung Transplantation - ISHLT
Chicago, IL
April 21-24, 2010
http://www.ishlt.org/meetings/annualMeeting.asp
American Association of Clinical Endocrinologists - AACE
Boston, MA
April 21–25, 2010
http://www.aace.com/meetings/ams/2010/
International Conference on Antiviral Research - ICAR
San Francisco, CA
April 25-28, 2010
http://isar.phrm.cf.ac.uk/
European Lung Cancer Conference - ESMO
Geneva, Switzerland
April 28 - May 1, 2010
http://www.esmo.org/events/lung-2010-iaslc.html
MAY 2010
American Association of Neurological Surgeons - AANS
Philadelphia, PA
May 1-5, 2010
http://www.aans.org/
Digestive Disease Week - DDW
New Orleans, LA
May 1-5, 2010
http://www.ddw.org/
Society of Thoracic Surgeons - AATS
Toronto, ON, Canada
May 1-5, 2010
http://www.aats.org/annualmeeting/
Association for Research In Vision and Ophthalmology - ARVO
Fort Lauderdale, Fl
May 2 – 6, 2010
http://www.arvo.org/EWEB/startpage.aspx?site=am2010
World Congress on Osteoporosis - IOF
Florence, Italy
May 5-8, 2010
http://www.iofwco-ecceo10.org/
International Congress on Autoimmunity
Ljubljana, Slovenia
May 5-9, 2010
http://www2.kenes.com/auto2010/Pages/Home.aspx
American Pain Society - APS
Baltimore, MD
May 6-8, 2010
http://www.ampainsoc.org/
World Stem Cells & Regenerative Medicine Congress
London, UK
May 11-13, 2010
http://www.terrapinn.com/2010/stemcells/
The Heart Rhythm Society - HRS
Denver, CO
May 12-15, 2010
http://www.hrsonline.org/Sessions/
American Thoracic Society - ATS
New Orleans, LA
May 14-19, 2010
http://conference.thoracic.org/
American College of Obstreticians & Gynecologists - ACOG
San Francisco, CA
May 15-19, 2010
http://www.acog.org/
American College of Radiology - ACR
Washington, DC
May 15-19, 2010
http://www.acr.org/
American Society of Gene & Cell Therapy - ASGCT
Washington, DC
May 19-23, 2010
http://www.asgct.org/
International Society on Thrombosis & Haemostasis - ISTH
Cairo, Egypt
May 22-25, 2010
http://www.isth.org/
American Society for Microbiology - ASM
San Diego, CA
May 23-27, 2010
http://www.asm.org/
American Urological Association - AUA
San Francisco, CA
May 29 - June 3, 2010
http://www.auanet.org/content/homepage/homepage.cfm
JUNE 2010
European Society of Human Genetics - ESHG
Gothenburg, Sweden
June 12-15, 2010
https://www.eshg.org/
OCTOBER 2010
American Association for the Study of Liver Diseases - AASLD
Boston, Massachusetts
October 29 - November 2, 2010
http://www.aasld.org/
NOVEMBER 2010
American Society of Human Genetics - ASHG
Washington, DC
November 2-6, 2010
http://www.ashg.org/
----
Procedure for Updating Calendar
When adding or modifying entries, please follow these steps:
1. Copy the complete text from the old calendar.
2. Make your additions or modifications, inserting any new items in chronological order.
3. Near the top of the message, give a very brief description of your changes (e.g. “Edits: Added entry for AASLD”).
4. Post the updated calendar in a new message as a reply to the message with the old calendar.
I've read Judge Sweet’s decision (got the PDF as well and can forward to Roy if he wishes to upload to his site). Not a patent lawyer but think there's a good chance a higher court will reverse it as I do believe the 101 can be overcome by the "isolated".
Did you mean Sanofi Aventis teriflunomide?
ROSG's patent strategy taken towards the USPTO is working alright as few of its patents were issued and allowed. Courts on the other hand are a different story. The genetic patent landscape is evolving: judge Sweet has recently invalidated both MYGN's patents on BRCA1/2 genes, the composition claims and the method claims under 35 USC 101. For the composition claims, he found that the claimed isolated DNA is not “markedly different” from native DNA. I believe it should be identical for RNA, although no judge has said so. However, isolated sequences are not easy to obtain and higher court might reverse it. If not, ROSG's IP protection may not be as strong as they think i.e. claims covering miRNAs sequences may be vulnerable and the patent protection will relay on claims covering uses of miRNAs as diagnostic biomarkers and therapeutic targets.
I'm not watching them very closely these days, last time I've met with them was Oct 08.
It won't be long before Teva will make an acquisition in South America and Brazil looks like the top target. Sanofi is ahead of Teva there as it already bought the largest generics company - Medley. I think the Chinese market is probably still too fragmented to be a current top priority target for Teva, and they are waiting for regulatory changes to make a move.
Assuming your friend is not eligible for surgical resection or liver transplant, s/he may still be (if there are no extrahepatic metastases), a candidate for liver-directed therapy (such as TACE) that shrinks the tumor*. Unfortunately, systemic therapy will probably be needed anyway and Nexavar (400mg bid or qd depending on tolerability) would be the drug of choice (again if liver function is no worse than Child Pugh A,B7-8).
There are number of targeted therapies in late-stage clinical trials for HCC and many in earlier stage, I will add about those later if you wish.
* Docs here use Nexavar in conjunction with local therapy and even earlier if the patient can afford it.
Teva's CFO indicated that Teva is a minor player in those two countries for a reason: there are many local generic companies there that produce cheap low quality generics. Teva is waiting for regulatory changes to make it adequate for them. Teva has almost no presence in Brazil but they intend to penetrate to this market since regulatory environment is changing there.
“Emerging markets”
During investor meeting last Jan, Teva's CFO Eyal Deshe talked about Brazil, Russia, Mexico, and Turkey as global targets for Teva and mentioned India and China as the less interesting ones for this aspect.
FDA Panel Recommends Approval of New Oxycodone Formulation
http://www.medpagetoday.com/Neurology/PainManagement/16132
Acurox panel is next on April 22.
Weird voting indeed.
If a patient fails an anti-TNF agent (there are 5 in the market), doc can either put him on a different anti-TNF agent or switch to a non anti-TNF agent (Actemra, Orencia, Rituxan). Among the latter class (Simponi and Cimzia mentioned in the Sermo Event Report are both anti-TNFs), Orencia has the better efficacy/safety profile and a broader label. BMY also conducts a phase III head-to-head vs. Humira trial to compete in 1st line RA:
http://clinicaltrials.gov/ct2/show/NCT00929864?term=NCT00929864&rank=1
LLY’s 5,464,826 “use” patent will probably not hold but the compound patent expires on November 15, 2010, so I assume Teva thinks the compound patent is strong and the risk is not worth if they can get a "clean" launch on Nov. 2010. Anyway Teva has to give 3 months notice to LLY before.
Sanofi settles with Sandoz, Teva on Eloxatin patent
Generic drug makers to stop selling their versions in June
http://www.reuters.com/article/idCNLDE63002M20100401?rpc=44
Do you know how effective Allopurinol is in gout?
And the gout flares in the higher dose groups seems odd to me but maybe its too small an n?
Apotex sues FDA to block Teva's H-W exclusivity for Cozaar/Hyzaar:
Apotex is saying that the patent expired because Merck? didn't pay fees to the USPTO therefore, Teva should not have exclusivity. I think they can only delay Teva from launching with exclusivity.
The FDA is questioning CEPH’s data on the co-primary endpoint called Patient Global Impression of Severity, which is subjective. This would seem to be a case where an SPA would have been helpful.
I find it quite surprising that Judge Sweet did not wait for the Supreme Court ruling in Bilski.
I personally see no rationale for allowing a composition of matter patent for a gene though.
Regarding Judge Sweet’s decision on the USPTO’s motion for judgment on the pleadings, re Myriad Genetics’ BRCA patents:
Bear in mind that MYGN still has other 'method of use' patents covering the test, which were not invalidated. MYGN will appeal in circuit court and litigation will take few more years. As noted by Peter, Supreme Court ruling in Bilsky case might change the view.
Robbie, there was nothing new or material. Talked about (known) Gaucher data (emphasized bone issue I've mentioned here #msg-46558730) and the PRX-105 program currently enrolling 10 healthy volunteers:
http://clinicaltrials.gov/ct2/show/NCT01093859?term=PRX-105&rank=1
Happy Easter and Passover to you and yours.
I expect Lorcaserin to face the FDA’s Endocrinologic and Metabolic Drug Advisory Committee as well.
I didn't catch the talk but I think it was mainly about PRX-105. If there was anything material beyond what's in #msg-47914149, I'll find out and post on Sun.
Not to mention it [Zevalin] works better and is recommended over rituxan.
Great minds consider psychiatric syndroms
The Future of Psychiatric Research: Genomes and Neural Circuits
http://www.sciencemag.org/cgi/content/summary/327/5973/1580
Huda Akil et al., Science 26 March 2010
The burden of neuropsychiatric illnesses is enormous. These conditions, which include schizophrenia, mood disorders, and autism, affect thought, emotions, and a person’s very sense of self. Together, they are the leading cause of disability in North America and Europe and constitute 40% of all years lost to disability. In the United States, the cost in lost earnings due to psychiatric disease is estimated conservatively to be $200 billion per year ( 1). The burden to individuals, families, and society is all the more tragic because these illnesses typically begin early in life, are lifelong, and damage the affected individuals’ self-perception, productivity, and ability to relate to others.
Unfortunately, there have been no major breakthroughs in the treatment of schizophrenia in the last 50 years and no major breakthroughs in the treatment of depression in the last 20 years ( 2). Over the last few decades, drug treatments have emerged that help a subset of these patients ( 3), but a sizable proportion are resistant to all currently available treatments. This heterogeneity points to the complexity of the underlying biology and underscores the urgent need for a more sophisticated understanding of the causes of these illnesses.
Psychiatric disorders present a unique challenge, even relative to other brain disorders, such as Alzheimer’s, Huntington’s, or Parkinson’s diseases, because for psychiatric disorders we know much less about underlying genetic, molecular, and cellular causes or even the primary anatomical sites of the brain defects. This frustrating lack of progress requires us to confront the complexity of the brain, especially in the context of higher-order functions, such as cognition and mood. This calls for a new perspective and a combination of novel tools and analytical methods.
Disruption of Neural Circuits
Illnesses such as schizophrenia, autism, and mood disorders are likely the result of disruptions of neural circuits, the functional ensembles of brain cells that thought, feelings, and behavior. A defect in the development, anatomical structure, functional integration, or dynamics of such a circuit can lead to a constellation of symptoms. Given the complexity of neural circuits, there are many possible ways to disrupt them ( 4). Thousands of genes are involved in regulating neural development and function. It is not surprising, therefore, that disturbances in the structure and function of one or several of these genes can lead to broad and complex neuropsychiatric phenotypes. This complexity explains the high prevalence of neuropsychiatric disorders. It also indicates that many genetic mutations, epigenetic changes, and other cellular and morphological brain lesions can converge on disturbing a given brain circuit and result in shared clinical manifestations (e.g., delusions and hallucinations) that lead to the same clinical diagnosis (e.g., schizophrenia). Thus, starting from a diagnosis and searching broadly for genetic causes that are commonly shared across all affected individuals is not likely to succeed, because a great deal of biological heterogeneity lies at the basis of circuit dysfunction.
This does not mean, however, that these diseases are not genetically based and transmitted, nor does it suggest that the search for genetic causes will be fruitless. Indeed, ample evidence demonstrates the heritability of these disorders. For example, there is much greater concordance of diseased states in identical twins versus fraternal twins. In autism, in as many as 80% of families of identical twins, both display autistic features if one is affected ( 5). Concordance of schizophrenia is estimated to be ~50% in identical twins, as opposed to ~5 to 10% in fraternal twins ( 6, 7). In some persons, nongenetic factors—such as intrauterine infection, malnutrition, or stress—may also be required to trigger the illness ( 8). Because of these complexities, most of the genes involved in the major psychiatric illnesses have not yet been identified, and animal models for them are limited.
Recent studies indicate that for many patients, psychiatric illnesses are due to genetic vulnerabilities that are shared by affected members of a given family, but vary across families, such that a given family has a unique, or “private,” mutational profile ( 9). It is therefore critical to focus on approaches that can detect private mutations and will take into account the genetic and neurobiological heterogeneity of psychiatric disorders.
Genomics and Circuit Analysis
What is the best strategy for unraveling the biological causes of psychiatric illnesses? We suggest that their solution will require the integration of two general approaches that have matured dramatically in the last 3 years: Genomics and Circuit Analysis
Genomics is the combination of largescale sequencing with systematic computational analysis of genomes. In the last 2 years, sequencing the human genome has become significantly faster and much less expensive. This makes it feasible to sequence the complete genome of many afflicted individuals to discover the genetic bases of these disorders within subjects and families. It is no longer necessary to target specific genes or chromosomal regions based on preconceived notions about the nature of the genetic defect. This approach has already proven useful in the analysis of X-linked mental retardation ( 10). New insight into the complex genetic basis of psychiatric disease comes from recent analysis of gene copy number variants present in patients with autism, schizophrenia, and bipolar disorder ( 11). Some of these mutations are absent from either parent’s DNA, which suggests that they are de novo mutations. Many deleted or amplified DNA segments contain genes needed primarily for the functioning of nerve cells, not for cells in other tissues. Most of the neural genes thus far identified as mutant have been observed only once, which suggests that the total number of genes whose disruption can result in the severe mental illnesses is at least several hundred. Mutations in many different genes have the potential to cause the neural circuit malfunction of psychiatric illness. It is therefore critical that computational biologists be engaged in analyzing the results of this sequencing effort in order to ascertain the contribution of the observed variants or allelic combinations to the disease in the general population.
Circuit analysis is the study of the structure, function, and dysregulation of relevant neural circuits. We are now beginning to identify the possible locations of aberrant circuitry in some diseases, including depression, which is associated with hyperactivity in the subgenual cingulate region (Brodmann area 25) of the prefrontal cortex ( 12); anxiety states, where there is hyperactivity in the amygdala ( 13); and obsessive-compulsive disorder, where there is an abnormality in the striatum ( 14). We need biological markers for the disruptions in neural circuitry involved in mental disorders in order to fully elucidate the anatomical basis of each illness, to provide more objective diagnoses, and to follow responses to treatment.
Fortunately, there have been parallel advances in the development of a variety of powerful new methods for selectively analyzing neural circuitry, which allow the delineation of the brain-wide neuroanatomical connectivity patterns in normal experimental animals, in animal models of psychiatric illnesses, and in people. One example is the introduction of noninvasive ways to selectively activate or shut off specific neurons in a given circuit of a behaving animal using optical methods ( 15). Also effective for selectively turning neurons on or off are ligand-gated protein variants with customized binding sites, such as the Drosophila allostatin receptor and the G1 protein–coupled receptor (16). Neither of these techniques can be readily used in humans. However, other very recent technical advances include methods for tracing neural connections in humans using diffusion tensor imaging ( 17) (see the figure on page 1580); approaches to the analysis of gene expression and epigenetic modifications in animal and human brains ( 18, 19); and tools for studying cellular and circuit dynamics in the brain, including multiphoton imaging and calcium imaging coupled to creative electrophysiological strategies ( 20).
Because genes responsible for Huntington’s disease, Rett syndrome, Fragile X, and early-onset Alzheimer’s disease have been discovered, it has been possible to express these genes in mouse models and to learn a great deal about the mechanisms of pathogenesis. As new genetic variants are discovered for psychiatric disorders, it will be possible to introduce these mutations into mouse models to simulate the human disorder, providing badly needed insights into the pathogenesis of these disorders. The impact of these mutant genes on circuit development, structure, function, and pathogenesis can now be studied using the innovative approaches described above. The convergence of findings from multiple animal models with the critical mutations will help to identify the central features of circuit dysregulation that are shared regardless of the initial genetic defect. It is these shared features that are likely to underlie the human disease that is being modeled. This understanding will also allow us to devise new treatment strategies that target either specific defects or their final common path and can reset circuit function in spite of the heterogeneity of the genetic causes of its malfunction.
An International Project Now is the time to initiate an effort that relies on the combined power of these two critical sets of tools. One component of this effort would aim to provide the world of medical neuroscience, over the next decade, with the personal genomes of many patients who have been afflicted with severe psychiatric diseases, especially those with the clearest evidence for a genetic contribution, along with appropriate controls. The effort would begin by focusing on autism, schizophrenia, and bipolar disease, but would eventually include the study of other severe psychiatric disorders, especially major depression. For schizophrenia and bipolar disorder, thousands of DNA samples from carefully evaluated patients and their families are already available and thousands more are being collected.
A parallel component of this effort is tackling the study of neural circuitry, in animal models and in human subjects, to allow functional insights into the way that these altered genes can disrupt circuit formation, function, and dynamics. The neuroscience technologies described above tend to exist in highly specialized settings. Significant intellectual, technical, and financial investments are needed to refine them, to establish them broadly, and to integrate them with each other and with genetic analysis, so as to provide the tool kits needed by the scientific community.
Soon the cost of sequencing and analyzing single personal genomes will be in the $5000 to $10,000 range. Assuming that the inherent complexity of neural circuitry disease demands that we need to consider 100,000 personal genomes, we would need only a billion dollars over the next 10 years to do so. A similar figure for tackling neural circuitry would allow functional insights into these genes and inform us about how these genes can malfunction and cause disease. Two hundred million dollars a year, the sum of monies that will be needed, is a very small price to pay to reduce or eliminate the awful misery and burden to society caused by mental illness.
References
1. W. W. Eaton et al., Epidemiol. Rev. 30, 1 (2008).
2. J. A. Lieberman et al., Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) Investigators, N. Engl.
J. Med. 353, 1209 (2005).
3. G. Gartlehner et al., Ann. Intern. Med. 149, 734 (2008).
4. H. Jaaro-Peled et al., Trends Neurosci. 32, 485 (2009).
5. A. Bailey et al., Psychol. Med. 25, 63 (1995).
6. I. I. Gottesman, Schizophrenia Genesis: The Origins of Madness (W. H. Freeman, New York, 1991).
7. P. F. Sullivan, K. S. Kendler, M. C. Neale, Arch. Gen. Psychiatry 60, 1187 (2003).
8. E. L. Messias, C. Y. Chen, W. W. Eaton, Psychiatr. Clin. North Am. 30, 323 (2007).
9. J. M. McClellan, E. Susser, M.-C. King, Br. J. Psychiatry 190, 194 (2007).
10. P. S. Tarpey et al., Nat. Genet. 41, 535 (2009).
11. E. H. Cook Jr., S. W. Scherer, Nature 455, 919 (2008).
12. H. S. Mayberg et al., Neuron 45, 651 (2005).
13. S. G. Shah, H. Klumpp, M. Angstadt, P. J. Nathan, K. L. Phan, J. Psychiatry Neurosci. 34, 296 (2009).
14. L. R. Baxter Jr. et al., Arch. Gen. Psychiatry 49, 681 (1992).
15. A. Berndt, O. Yizhar, L. A. Gunaydin, P. Hegemann, K. Deisseroth, Nat. Neurosci. 12, 229 (2009).
16. E. M. Tan et al., Neuron 51, 157 (2006).
17. D. Le Bihan et al., J. Magn. Reson. Imaging 13, 534 (2001).
18. R. Bernard et al., J. Neurosci. Methods 178, 46 (2009).
19. M. Fagiolini, C. L. Jensen, F. A. Champagne, Curr. Opin. Neurobiol. 19, 207 (2009).
20. J. N. MacLean, B. O. Watson, G. B. Aaron, R. Yuste, Neuron 48, 811 (2005).
Jamie Oliver's Food Revolution comes to America. First episode tonight on ABC. Trailer:
http://videos.nymag.com/video/Jamie-Olivers-Food-Revolution-T#c=2B8KJ02H9XV5BBDH&t=Jamie%20Oliver's%20Food%20Revolution%20Trailer
GENZ still not doing very well with their manufacturing issues and the stock is down over 6% today:
Genzyme Announces FDA Enforcement Action Regarding Allston Plant
http://www.businesswire.com/portal/site/genzyme/index.jsp?ndmViewId=news_view&ndmConfigId=1019673&newsId=20100324005866&newsLang=en
BUSINESS WIRE)--Genzyme Corporation (NASDAQ: GENZ) announced today that the FDA notified the company yesterday afternoon that, while the agency recognizes Genzyme’s efforts, it intends to take enforcement action to ensure that products manufactured at the plant are made in compliance with good manufacturing practice regulations. The FDA enforcement action will likely result in a consent decree, under which a third party would inspect and review the plant’s operation for an extended period and certify compliance with FDA regulations. Under a consent decree, Genzyme also would be required to make payments to the government and could incur other costs.
Based on its initial communication with the agency and the medical need for patients, Genzyme expects that shipments of Cerezyme® (imiglucerase for injection) and Fabrazyme® (agalsidase beta), which are manufactured in Allston, will continue uninterrupted during the period of the enforcement action. In addition, Genzyme expects that shipments of Myozyme® (alglucosidase alfa) produced at the 160-L scale, which is filled and finished in Allston, will continue uninterrupted. Genzyme also fills and finishes Thyrogen® (thyrotropin alfa for injection) at the Allston plant and intends to discuss with the agency the company’s view that there is also a patient need for uninterrupted supply of this product. The discussions with the FDA are expected to occur over the next several weeks.
Genzyme will work cooperatively with the FDA to restore the agency’s confidence in its ability to operate the Allston plant at the highest standards, building on the progress it has made over the past year to address the manufacturing deficiencies at the Allston plant. This progress includes:
* Retaining a leading quality assurance advisory firm to help develop a comprehensive strategy and risk mitigation plan. More than 30 expert consultants from this firm are currently working at the Allston plant or at other Genzyme manufacturing facilities.
* Naming a new site head and reorganizing and strengthening the management team at the facility.
* Hiring two highly regarded industry veterans to serve as President of Global Manufacturing and Corporate Operations and Senior Vice President of Global Product Quality.
ChemGenex Shares Plunge After Panel Ruling on Drug
http://www.bloomberg.com/apps/news?pid=20601081&sid=as8Z_yuL37hw
Teva's latest trials are one small and few months long trial :
http://clinicaltrials.gov/ct2/show/NCT00947752?term=teva+song&rank=1
and one large and long:
http://clinicaltrials.gov/ct2/show/NCT01067521?term=teva+gala&rank=1
What will the FDA ask for? I'm guessing something in between - few hundred patients and couple of years long.
Roy was right on my GTCB call, I thought it would be approved eventually but it was approved 1st round.
On Copaxone - another question is how will the MS market change by the time a generic version gets approved?
Roy, I've heard the Israeli Nobel Laureate winner in chemistry - Aaron Ciechanover said similar things on Copaxone. He may be part of Teva's propaganda, I have no way of telling but he does know a thing or two on the issue.
Sure I was wrong, plenty of times and may be wrong on this one. Time will tel how the FDA will act.