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I was kind of hoping you got BiolineRX’s BL-1040 (I'm a share holder ), but I guess you were doing too well (this one enrolls the worst cases).
Alimta approved for front-line NSCLC maintenance:
http://finance.yahoo.com/news/FDA-approves-new-use-for-apf-1267180136.html?x=0&.v=1
Take it easy, there's plenty of time.
"The results of the long-term, 5-year study of Lantus versus NPH insulin on progression of retinopathy in patients with type 2 diabetes, published on-line in Diabetologia, showed similar effects on retinopathy and overall safety in the two treatment groups,"
http://www.reuters.com/article/rbssHealthcareNews/idUSL610092120090706
FDA tries to speed access to Protalix Gaucher drug
http://www.reuters.com/article/marketsNews/idINN0624836120090706?rpc=44
* FDA asks Protalix to speed access to Gaucher drug
* FDA says Protalix drug meets expanded access criteria
* FDA action to offset likely shortages of Genzyme drug
BOSTON, July 6 (Reuters) - Biotechnology company Protalix BioTherapeutics Inc (PLX.A: Quote, Profile, Research, Stock Buzz) said on Monday it has been approached by the U.S. Food and Drug Administration to expand access to its experimental drug for Gaucher disease to help offset likely shortages of an alternative drug make by Genzyme Corp (GENZ.O: Quote, Profile, Research, Stock Buzz).
Genzyme, which makes Cerezyme, the world's leading treatment for Gaucher disease, a rare but serious disorder, recently announced it would shut down its plant in Boston after a virus halted production of Cerezyme and Fabrazyme, its treatment for Fabry disease.
Protalix said the FDA has asked the company to consider submitting a treatment protocol that would allow use of its experimental treatment prGCD under an expanded access program. Under this program, a treatment protocol may be submitted for a drug that has not yet been approved but is in development for a serious disease for which no other therapy is available.
The company said it is discussing the parameters of a proposed treatment protocol which would allow an increased number of patients with Gaucher disease to have access to prGCD, which is in late-stage development.
Protalix said the FDA indicated it believes the company's development program for prGCD satisfies the regulatory criteria required to supply prGCD for expanded access.
Genzyme has said it expects its Boston plant will be on line in late July, with shortages of Cerezyme expected to hit in August. Shortages of Fabrazyme will likely start to be seen in September or October.
Cerezyme is Genzyme's biggest selling product and one of the world's most expensive drugs. Cerezyme and Fabrazyme represented about 37 percent of the company's 2008 revenue of $4.6 billion.
Great news and get well, Dovi!
BioLineRx signed a deal for BL-1040 with Ikaria Holdings Inc.
Upfront only $7M but payment will get to $285M with milestones, royalties will be 11-15%.
NVO’s Victoza (a/k/a liraglutide) officially approved in the EU.
http://www.novonordisk.com/press/sea/sea.asp?sShowNewsItemGUID=fef45783-0017-45f7-8185-ad751bad7019&sShowLanguageCode=en-GB
Good read for you Dubi, so you won't get too bored when you're back :)
Novel consortium to address shortfall in innovative medicines for psychiatric disorders
http://www.nature.com/nrd/journal/v8/n7/full/nrd2939.html
One of the first projects to be selected for funding under the European Innovative Medicines Initiative will address the challenges of developing drugs to treat schizophrenia and depression.
By Bethan Hughes
On 18 May 2009, the European Commission announced the first 15 projects of the Innovative Medicines Initiative (IMI) that have been selected to address research bottlenecks in drug development (see Nature Rev. Drug Discov. 7, 110; 2008). Three projects aim to improve predictions of drug safety, one will use pharmaco-epidemiology methods to monitor the benefits and risks of medicines, four will create training programmes and seven will address drug development challenges in six therapeutic areas.
As soon as the finer details of the contract negotiations are complete — for example, reaching agreements on intellectual property generated by each consortium — the successful projects will share 110 million euros from the European Commission and 136 million euros provided in kind by the pharmaceutical industry over 5 years.
These IMI projects are unique because, for the first time, they each bring together a wide range of pharmaceutical companies to work with an academic consortium (that could also include small- and medium-sized enterprises and patient organizations). "Many companies already have collaborations with academic consortia, so that is not new," says Tine B. Stensbøl, Divisional Director of Discovery Pharmacology Research at the pharmaceutical company Lundbeck in Denmark, and the European Federation of Pharmaceutical Industries and Associations (EFPIA) coordinator for one of the selected consortia called NEWMEDS (Novel Methods Leading to New Medications in Depression and Schizophrenia). "But what is new is that we have so many EFPIA partners joining forces and working with one academic consortium," she says.
Overall, NEWMEDS aims to address the major need for improved treatments for depression and schizophrenia. "Enormous amounts of money have been invested by industry, as well as by academia, but the outcome has been very limited," says Mihály Hajós, Associate Research Fellow at the Neuroscience Department, Pfizer Global R&D, Connecticut, USA, whose team is participating in NEWMEDS. "We need to have this collaboration between academic groups and industry to make innovative progress," he adds.
The main focus of NEWMEDS, says Stensbøl, will be on schizophrenia. "We plan to divide our project into three clusters: one, to develop better animal models; two, to generate translational technology that could help provide early indicators of efficacy, such as functional magnetic resonance imaging; and three, to develop tools to improve patient stratification."
A key advantage of NEWMEDS will be the possibility to pool clinical data and samples from several pharmaceutical companies in a novel way. "We can sit together as scientists across companies in a pre-competitive environment and openly discuss how to use different technologies and models to get useful information from the enormous data sets that we have," says Stensbøl.
A large percentage of the clinical data from patients with schizophrenia, that will be available to NEWMEDS, will come from development programmes in which the compounds were initially evaluated using animal models based on the standard 'dopamine hypothesis' of schizophrenia. This might make it more likely that such compounds will have activities similar to existing therapies, rather than representing therapeutic breakthroughs, explains Andreas Meyer-Lindenberg, Director of the Central Institute of Mental Health in Mannheim, Germany.
"One perceived cause of the lack of truly innovative therapies for schizophrenia is that we tried to figure out how the first-generation antipsychotics — which were essentially found by serendipity — worked, and then used animal models based on that understanding to screen new compounds. Arguably, this has contributed to every approved antipsychotic so far also having dopamine D2 receptor-blocking activity: we have been looking under the lamp post for the keys because that's where the light shines," he says.
Stensbøl still considers that the clinical data collected could be valuable, however. "There's no reason not to believe that the dopamine system has, at least for some patients, an impact on schizophrenia. We need to learn from that and dissect those data in greater detail. Rather than just throwing them away, I think we can gain a lot by using novel technology to look beyond the biology that we have focused on for many years," she says.
Nevertheless, it is widely agreed that new animal models are needed to aid the development of novel therapies. According to Professor Shitij Kapur, Head of Schizophrenia, Imaging and Therapeutics at the Institute of Psychiatry, Kings College, London, UK, there are two major unmet needs in the treatment of schizophrenia. The first is to control positive symptoms, such as hallucinations and delusions, in the long term, because some patients either do not respond to treatment, or respond initially but cannot be maintained on therapy. The second is to develop therapies that effectively address the negative symptoms (such as social withdrawal and apathy) and cognitive deficits.
To respond to these challenges, much research is needed to understand the underlying pathophysiology of the disease. Currently, says Kapur, the best clues are coming from genetics. Meyer-Lindenberg agrees: "Schizophrenia is overwhelmingly heritable, and genes are the majority of the cause. Even in depression, close to 40% of the disease risk is due to genetics," he notes.
Genome-wide association studies have identified single nucleotide polymorphisms associated with a risk of developing schizophrenia, but so far the relative risk has not been sufficient to strongly justify the development of diagnostic tests or simple animal models based on these variants. This raises the question of which genes to base animal models on. "We don't have the luxury of going after 25 candidates," says Kapur. "Fortunately, a number of copy number variations (CNVs) have now been reliably replicated in schizophrenia that increase the risk 10–15 times, so that is very hopeful. Not all patients have the same CNVs, however, but they might provide clues about pathways involved in the disease biology," he adds.
These genetic variants are also providing important research avenues for human clinical studies. "You can select people based on their genotype as healthy volunteers and know that their brain systems are biased by the genetic variant in a way that leads to its role in schizophrenia [this is known as an intermediate phenotype or endophenotype]. Then you have a much better sample in which to test new drugs in the volunteer phase," says Meyer-Lindenberg.
"This could help us to determine early signs of effectiveness of a drug treatment," says Hajós. "Once we are sure that an endophenotype has impacted animals and humans in the same way, we can evaluate if it is beneficial for a patient. Then we will have the proof of concept needed to say that it is a target we could invest in and hope that patients will benefit."
A greater knowledge of endophenotypes may also improve our understanding of the complexity of the disease. "What is becoming overwhelmingly apparent is that these disorders are very likely to arise from the inheritance of multiple susceptibility genes, and quite possibly protective genes, that interact with each other and the environment — which could include the intra-uterine environment — to produce a very complex phenotype. Currently we use the overall term 'schizophrenia', but we are almost certainly talking about a heterogeneous group of disorders that have different pathophysiologies," says Husseini K. Manji, Global Therapeutic Area Head, Neuroscience R&D, Johnson & Johnson, New Jersey, USA, who thinks that an underappreciation of the complexity of the condition has contributed to lack of progress so far.
Manji's view, and the way he thinks the field is going, is to deconstruct the illness into component parts and develop animal models that do not have to recapitulate the whole syndrome. "If we are able to map symptoms associated with specific brain circuits, and understand the synapses, connectivity and synchronous response characteristics of neuronal ensembles in those circuits, this will lead to the possibility of identifying completely novel targets. Then we can tailor drugs to those targets to address circuitry and synaptic aspects that will hopefully lead to changes in overall symptoms," he says.
This change in approach to drug development for psychiatric disorders like schizophrenia would require acceptance from regulatory agencies. "I do think that there is an increased recognition among key stakeholders that, in order to really make progress in this arena, there needs to be an increased focus on the subcomponents of the illness," says Manji, adding that optimal treatment of schizophrenia in the future is going to require a multipronged approach. "As we progress with better identification of genes, advanced imaging technology, and good biomarkers, we will be poised to do much more."
On 2 patent cases relevant to Teva
Obviousness on the basis of chemical similarity
http://www.nature.com/nrd/journal/v8/n7/full/nrd2928.html#US-Court-reverses-policy-on-obviousness-of-gene-patents
Medicinal chemistry often involves making modifications to previously identified lead compounds to improve biological activity or physicochemical properties. However, to be patentable, a compound must be non-obvious in the context of prior art. So, how can it be shown whether or not it was obvious to get from one structure to another? The US Court Of Appeals for the Federal Circuit (CAFC) has recently ruled in two cases that consider this issue.
The first case was between Wyeth and Altana Pharma, and the generics company Teva. Wyeth is exclusive licensee of a patent (US4,758,579) that protects the proton pump inhibitor Protonix (pantoprazole). Teva asserted that Protonix was obvious in light of an earlierAltana patent and literature articles. The structure of Protonix is very similar to that of a compound (known as compound 12) that is described in the earlier Altana patent, but with a different substitution on the pyridine ring.
To establish obviousness in situations that involve new chemical compounds, a reason or motivation can be identified that would have led a chemist to select and modify a known compound in a particular manner to achieve the claimed compound. So, working in this framework, would it have been obvious to choose compound 12 as a lead compound, and then obvious to make the substitution?
Altana and Wyeth argued that one would not have selected compound 12 over the other approx90 compounds in the prior art, and suggested that a new compound would only be obvious if the prior art pointed to a single compound for further development efforts. But the Court disagreed, considering that compound 12 was a "natural choice", and that it was one of the more potent compounds described in the earlier patent. Moreover, the Court rejected Altana and Wyeth's 'single-compound' argument, as it would have imposed a "rigid test" in determining obviousness.
In addition, it was felt that, on the basis of literature references, one would have known what the pKa (the acid dissociation constant) should be to achieve optimal stability of the compound in the body, and it was known that this pKa value could be achieved by the substitution of a methoxy group (as contained in compound 12) for a methyl group on the carbon atom at the 3 position of the pyridine ring to arrive at Protonix. On the basis of this and other findings, the Court therefore denied Altana and Wyeth's injunction to prevent Teva selling its generic drug before the expiration of the '579 patent.
The second case centred on Procter and Gamble's osteoporosis drug Actonel (risedronate), which is protected by patent US5,583,122. Teva argued that structural similarities between Actonel and a compound — 2-pyr EHDP — that was disclosed in an expired Procter and Gamble patent rendered the claims of the '122 patent obvious.
Actonel and 2-pyr EHDP are bisphosphonates and are positional isomers of one another — that is, they contain the same atoms oriented in different ways. Both contain a hydroxy-ethane-diphosphonate group; in Actonel, this is connected to carbon 3 of the pyridine ring, whereas in 2-pyr EHDP, it is connected to carbon 2 of the pyridine ring.
Proctor and Gamble had conducted experiments with hundreds of bisphosphonate compounds but could not predict the properties, such as efficacy or toxicity, of new compounds on the basis of the compound structure. So, because the properties of bisphosphonates were unpredictable, and the advantageous properties of Actonel were not expected, the Court held that the patent was not obvious.
From Nature Patent watch on the Protonix patent case:
http://www.nature.com/nrd/journal/v8/n7/full/nrd2928.html#US-Court-reverses-policy-on-obviousness-of-gene-patents
Obviousness on the basis of chemical similarity
Medicinal chemistry often involves making modifications to previously identified lead compounds to improve biological activity or physicochemical properties. However, to be patentable, a compound must be non-obvious in the context of prior art. So, how can it be shown whether or not it was obvious to get from one structure to another? The US Court Of Appeals for the Federal Circuit (CAFC) has recently ruled in two cases that consider this issue.
The first case was between Wyeth and Altana Pharma, and the generics company Teva. Wyeth is exclusive licensee of a patent (US4,758,579) that protects the proton pump inhibitor Protonix (pantoprazole). Teva asserted that Protonix was obvious in light of an earlierAltana patent and literature articles. The structure of Protonix is very similar to that of a compound (known as compound 12) that is described in the earlier Altana patent, but with a different substitution on the pyridine ring.
To establish obviousness in situations that involve new chemical compounds, a reason or motivation can be identified that would have led a chemist to select and modify a known compound in a particular manner to achieve the claimed compound. So, working in this framework, would it have been obvious to choose compound 12 as a lead compound, and then obvious to make the substitution?
Altana and Wyeth argued that one would not have selected compound 12 over the other approx90 compounds in the prior art, and suggested that a new compound would only be obvious if the prior art pointed to a single compound for further development efforts. But the Court disagreed, considering that compound 12 was a "natural choice", and that it was one of the more potent compounds described in the earlier patent. Moreover, the Court rejected Altana and Wyeth's 'single-compound' argument, as it would have imposed a "rigid test" in determining obviousness.
In addition, it was felt that, on the basis of literature references, one would have known what the pKa (the acid dissociation constant) should be to achieve optimal stability of the compound in the body, and it was known that this pKa value could be achieved by the substitution of a methoxy group (as contained in compound 12) for a methyl group on the carbon atom at the 3 position of the pyridine ring to arrive at Protonix. On the basis of this and other findings, the Court therefore denied Altana and Wyeth's injunction to prevent Teva selling its generic drug before the expiration of the '579 patent.
Will D-Mab Be Better Than Zometa in Prostate Cancer?
I think it will for a couple of reasons:
The level of bone turnover is the highest in prostate cancer and since denosumab strongly inhibits osteoclasts, which are the main driver for SREs there, I'd expect it to be efficient in preventing SREs in this setting. One more point is - D-mab should also delay/reduce bony metastasis for the same reason (plus prostate cancer cells primarily metastasize to the bone), and if so, it is going to be a touchdown (big unmet need and Zometa has not been shown to prevent the formation of bony metastases). Other parameters like safety and subQ vs infusion might also help.
I'm quite sure denosumab will be non inferior to Zometa and optimistic it will even be superior.
Amiodarone is not approved for AF by the FDA but it is the most commonly used drug (especially in patients with left ventricular hypertrophy, because of its potency (why do you suppose they bothered doing a head-to head Multaq vs Amiodarone trial?). In fact, it is so effective that I doubt it will be matched by any of the newer agents. But it has a lot of side effects that limit its potential and make Multaq a safer choice.
[OT] Matt Taibbi on how Goldman Sachs has engineered every major market manipulation since the Great Depression
The Great American Bubble Machine
http://www.rollingstone.com/politics/story/28816321/the_great_american_bubble_machine
Two points on Multaq:
1. In the DIONOSYS (head-to-head vs Amiodarone) trial - Multaq showed to be less effective at suppressing AF but safer.
2. Multaq is contraindicated in patients with severe heart failure (class IV and II-III). It can be used in patients with AF/AFL and no or stable heart failure.
So, Multaq is likely to compete and in time replace Amiodarone because of the safety advantages, imo.
Contact: Jules Asher
NIMHpress@nih.gov
301-443-4536
NIH/National Institute of Mental Health
Schizophrenia and bipolar disorder share genetic roots
Chromosomal hotspot of immunity/gene expression regulation implicated
A trio of genome-wide studies – collectively the largest to date – has pinpointed a vast array of genetic variation that cumulatively may account for at least one third of the genetic risk for schizophrenia. One of the studies traced schizophrenia and bipolar disorder, in part, to the same chromosomal neighborhoods.
"These new results recommend a fresh look at our diagnostic categories," said Thomas R. Insel, M.D., director of the National Institute of Mental Health (NIMH), part of the National Institutes of Health. "If some of the same genetic risks underlie schizophrenia and bipolar disorder, perhaps these disorders originate from some common vulnerability in brain development."
Three schizophrenia genetics research consortia, each funded in part by NIMH, report separately on their genome-wide association studies online July 1, 2009, in the journal Nature. However, the SGENE, International Schizophrenia (ISC) and Molecular Genetics of Schizophrenia (MGS) consortia shared their results – making possible meta-analyses of a combined sample totaling 8,014 cases and 19,090 controls.
All three studies implicate an area of Chromosome 6 (6p22.1), which is known to harbor genes involved in immunity and controlling how and when genes turn on and off. This hotspot of association might help to explain how environmental factors affect risk for schizophrenia. For example, there are hints of autoimmune involvement in schizophrenia, such as evidence that offspring of mothers with influenza while pregnant have a higher risk of developing the illness.
"Our study was unique in employing a new way of detecting the molecular signatures of genetic variations with very small effects on potential schizophrenia risk," explained Pamela Sklar, M.D., Ph.D., of Harvard University and the Stanley Center for Psychiatric Research, who co-led the ISC team with Harvard's Shaun Purcell, Ph.D.
"Individually, these common variants' effects do not all rise to statistical significance, but cumulatively they play a major role, accounting for at least one third – and probably much more – of disease risk," said Purcell.
Among sites showing the strongest associations with schizophrenia was a suspect area on Chromosome 22 and more than 450 variations in the suspect area on Chromosome 6. Statistical simulations confirmed that the findings could not have been accounted for by a handful of common gene variants with large effect or just rare variants. This involvement of many common gene variants suggests that schizophrenia in different people might ultimately be traceable to distinct disease processes, say the researchers.
"There was substantial overlap in the genetic risk for schizophrenia and bipolar disorder that was specific to mental disorders," added Sklar. "We saw no association between the suspect gene variants and half a dozen common non-psychiatric disorders."
Still, most of the genetic contribution to schizophrenia, which is estimated to be at least 70 percent heritable, remains unknown.
"Until this discovery, we could explain just a few percent of this contribution; now we have more than 30 percent accounted for," said Thomas Lehner, Ph.D., MPH, chief of NIMH's Genomics Research Branch. "The new findings tell us that many of these secrets have been hidden in complex neural networks, providing hints about where to look for the still elusive – and substantial – remaining genetic contribution."
The MGS consortium pinpointed an association between schizophrenia and genes in the Chromosome 6 region that code for cellular components that control when genes turn on and off. For example, one of the strongest associations was seen in the vicinity of genes for proteins called histones that slap a molecular clamp on a gene's turning on in response to the environment. Genetically rooted variation in the functioning of such regulatory mechanisms could help to explain the environmental component repeatedly implicated in schizophrenia risk.
The MGS study also found an association between schizophrenia and a genetic variation on Chromosome 1 (1p22.1) which has been implicated in multiple sclerosis, an autoimmune disorder.
"Our study results spotlight the importance not only of genes, but also the little-known DNA sequences between genes that control their expression," said Pablo Gejman, M.D., of the NorthShore University HealthSystem Research Institute, of Evanston, ILL, who led the MGS consortium team. "Advances in biotechnology, statistics, population genetics, and psychiatry, in combination with the ability to recruit large samples, made the new findings possible."
The SGENE consortium study pinpointed a site of variation in the suspect Chromosome 6 region that could implicate processes related to immunity and infection. It also found significant evidence of association with variation on Chromosomes 11 and 18 that could help account for the thinking and memory deficits of schizophrenia.
The new findings could eventually lead to multi-gene signatures or biomarkers for severe mental disorders. As more is learned about the implicated gene pathways, it may be possible to sort out what's shared by, or unique to, schizophrenia and bipolar disorder, the researchers say.
Contact: Bruce Goldman
goldmanb@stanford.edu
650-725-2106
Stanford University Medical Center
Schizophrenia linked for first time to chromosome region in study led by Stanford scientists
STANFORD, Calif. — Stanford University School of Medicine scientists have played a major role in an international effort that has shown, for the first time, that modern genetic technologies can solve the riddle of how gene variations lead to schizophrenia.
Researchers at Stanford and 14 other institutions carried out a study of common DNA variations throughout the genome, and then combined forces with two independent studies to complete a pooled analysis of 27,000 individuals. The largest genetic differences between the study participants with and without schizophrenia were found on a stretch of chromosome 6 containing numerous genes associated with immune response (and some with other roles). This raises the possibility that immune function plays a role in schizophrenia.
Stanford's Jianxin Shi, PhD, and Douglas Levinson, MD, are first and second authors of one of three linked papers to be published online together in Nature on July 1. Their paper reports on the Molecular Genetics of Schizophrenia Project. This undertaking implicated a region of the human genome not previously suspected as a risk factor for schizophrenia. That finding was bolstered by another of the simultaneously published papers, which showed an even stronger association when the number of subjects was increased to almost 48,000, and identified significant association in two additional genes. The third paper shows that there are likely to be many common gene variations, perhaps hundreds or more, that have small effects in the risk of schizophrenia.
Taken together, "the papers present the first highly significant findings of gene regions associated with schizophrenia risk," said Levinson, professor of psychiatry and behavioral sciences, director of that department's Program on the Genetics of Brain Function, and the Walter E. Nichols, MD, Professor in the School of Medicine.
It is already known that schizophrenia — which strikes close to one in every 100 people — has a very strong genetic component, probably accounting for at least 80 percent of risk for this disease. However, unlike sickle-cell anemia or Huntington's disease, in which a defect at a single genetic location is responsible, most cases of schizophrenia are believed to involve interactions among a multitude of genes, with a variant of any single gene contributing only a tiny bit to a person's risk.
"That makes it hard to tease out, in a statistically significant way, any of these schizophrenia-associated genes," said Levinson. But it is feasible with very large numbers of subjects, he said. Finding genes involved in a multigenic trait can, at least in theory, be accomplished by means of so-called genome-wide association studies, in which DNA variations are measured in two large groups of people, one with a common pathology and the other without it.
To achieve the needed sample size, data from three independent studies were pooled and analyzed in a special way that corrected for differences in how those disparate studies were designed and run. Such a methodology is called a meta-analysis. Shi, a research scientist in Levinson's laboratory, designed and performed the meta-analysis on the resulting pooled-subject group, some 8,000 individuals with schizophrenia and 19,000 normal controls of European ancestry. (Restricting the study population to people of similar ancestry excludes numerous non-disease-related genetic differences that would otherwise be observed, Shi said.)
In 1999, when Levinson and Shi's study began, genomic technologies were nowhere near as advanced as they are today. But the recent hybridization of Silicon Valley-style microelectronics with biotechnology-bred DNA assay techniques has resulted in powerful new microarrays capable of scanning entire genomes for tiny variations called "single base-pair polymorphisms," or SNPs.
A DNA base pair is effectively the genome's smallest possible accounting unit — the penny, as it were, of genetic variation. As a simplified analogy, think of your genetic inheritance as a stack of 3 billion pennies, with each coin bearing one of four mint marks. If you set two such stacks (representing two individuals' genomes) side by side and compare two adjacent pennies' mint marks at any given height, they'll usually be the same. We're all descendants of a common ancestor, so the similarities in our genomic sequences shouldn't surprise anyone.
But evolution happens. Every few hundred "pennies" or so, you will observe a divergence, or SNP — one chemical "mint mark" on this genome, another on that one. With the human genome being so huge, this comes to something like 10 million SNPs, of which about a million occur with frequencies of at least 5 percent.
Using commercially available "SNP chips" designed to detect those more-common variants, the investigators looked for differences between the DNA of people with schizophrenia versus the DNA of those without the disease. The scientists required that such differences achieve "genome-wide statistical significance." Here's why: If you flip a million coins, one at a time, you're going to see all kinds of seemingly miraculous events — say, 15 heads in a row — that may seem significant but are typical when you toss even a perfectly balanced coin so many times.
Shi's job was to devise analytical techniques to determine whether the "finding" of a SNP's greater likelihood among schizophrenics was real or spurious. The genomic region on chromosome 6 survived this rigorous statistical test.
"These findings show that our genetic methods are working, and that the genetic underpinnings of schizophrenia can be understood," said Levinson. "Similar methods have produced critical new discoveries in many other common diseases, once very large numbers of people could be studied. Now we see that the same approach works for psychiatric disorders like schizophrenia."
Painkiller Dosage: It's J&J vs. Wyeth
http://www.businessweek.com/technology/content/jul2009/tc2009071_125516.htm
The suggested FDA curb on acetaminophen dosage has set the two companies battling over the relative safety of rival classes of analgesics
By Arlene Weintraub
When an advisory panel to the Food & Drug Administration suggested on June 30 that dosing restrictions be imposed on the popular painkiller acetaminophen, the agency set the stage for a war between two consumer-product stalwarts. On one side is Johnson & Johnson (JNJ), maker of the most famous acetaminophen product, Tylenol. On the other is Wyeth (WYE), which makes Advil, a member of the competing class of painkillers known as non-steroidal anti-inflammatories (NSAIDS). What they're battling over is public perception—and both have a decided interest in coming out on top.
The panel recommended that the maximum dose of acetaminophen be reduced from 1,000 milligrams to 650 milligrams. The 1,000 mg. version, tantamount to what's found in over-the-counter Extra Strength Tylenol, would be made into a prescription product. The recommendation was prompted by concerns that too much acetaminophen can cause liver damage. Overdoses are responsible for 56,000 emergency room visits a year, the FDA estimates. Panel members were particularly concerned about combination products that contain, say, acetaminophen and antihistamines, for fear that consumers would take those along with Tylenol, or another product like it, causing an inadvertent overdose.
J&J's McNeil Consumer Healthcare unit went on the attack, expressing in a written statement its disapproval of the panel's advice. "McNeil Consumer Healthcare believes that this recommendation is likely to lead to more serious adverse events as consumers shift to other over-the-counter products such as non-steroidal anti-inflammatory drugs (NSAIDS) in search of pain relief," the statement said. It went on to point out that, unlike NSAIDS and other competitors, acetaminophen doesn't cause "adverse events, such as stomach discomfort and bleeding."
Dire Warnings
J&J consultant Dr. Kenneth Rothman, who spoke to panel members at the FDA confab, warned that if acetaminophen restrictions caused 30% of patients to switch to NSAIDS, the result could be 5,000 deaths per year from stomach bleeding and other complications. Responded Wyeth in a statement: "The dire predictions being made about the hypothetical health consequences of patients switching from OTC acetaminophen to an OTC NSAID as a result of acetaminophen restrictions are contradicted by actual real world experience."
Why do these companies care so much? Even though Tylenol and Advil went generic long ago, the brand equity they provide is still vital to both companies. Tylenol is one of the best-known brands in J&J's consumer-products basket, which has provided a major cushion in a rough economy. While J&J's prescription-drug and medical-device units have stagnated of late, its consumer business has been growing about 10% year-over-year. Consumer products accounted for $16 billion of the company's $64 billion in sales last year. (The company does not break out Tylenol sales.)
J&J's consistent leadership on drugstore shelves has helped its stock weather the recession better than that of some of its pure-play competitors: J&J's stock has fallen only 3% this year, while consumer giant Procter & Gamble (PG) has dropped 14%, and prescription drugmaker Pfizer has lost 13%.
Pfizer is now trying to be less of a pure play, which is why it announced in January that it would buy Wyeth for $68 billion. Advil is one of the crown jewels in that purchase, with sales of $673 million in 2008. In 2006, Wyeth introduced Advil PM, a direct competitor to the similarly named Tylenol PM. Both pain drugs contain a sleep medication. Sales of Advil PM rose a remarkable 17% in 2008, after Wyeth advertised the drug heavily on television. Advil PM was the fastest growing product for Wyeth Consumer Healthcare, the unit that accounted for 12% of the company's $22.8 billion in sales last year.
Vicodin and Percocet
The FDA panel also voted in favor of recalling prescription drugs containing acetaminophen, such as Abbott Laboratories' (ABT) Vicodin and Endo Pharmaceuticals' (ENDP) Percocet. The branded versions and their generic counterparts were prescribed 124 million times last year, making them the most popular class of prescription drug on the market. Sales totaled $1.4 billion.
In a press conference after the panel vote, FDA officials didn't indicate whether they would go so far as to remove products from the market. But they did say they detected strong support for lowering dosages on both the prescription and over-the-counter versions of acetaminophen and for beefing up cautionary language on labels. Such actions would be in keeping with a raft of safety measures the agency has imposed on popular consumer products lately.
In a statement to BusinessWeek, the FDA says it has been paying more attention to products after they hit the market in reponse to pressure from Congress. "We have increased our communications to the public about drug safety issues using a variety of vehicles," including medication guides and boxed warnings, the agency said. "The goal of this program is to ensure that patients and prescribers have the most up-to-date information to inform decisions about appropriate use of drugs in individual patients."
Weintraub is a senior writer for BusinessWeek's Science & Technology department.
While you were away from your PC:
End of the road for that scam - Biolite finally admits today that the trial was a failure and ditches the drug (the stock lost some 30%).
FDA Approves Multaq(R) for Patients with Atrial Fibrillation or Atrial Flutter
http://finance.yahoo.com/news/FDA-Approves-MultaqR-for-prnews-2537930297.html?x=0&.v=1
As expected:
FDA denies to approve King, Acura's pain drug
http://www.reuters.com/article/marketsNews/idESBNG17874420090702?rpc=44
Teva's biosimilar version of somatropin - Tev-Tropin is on the market since 2005 and hardly gained any market share presumably due to lack of AB rating and bad administration system. This should solve the latter problem:
Teva, Antares get FDA nod for needle-free device
http://www.reuters.com/article/marketsNews/idINBNG33649420090629?rpc=44
* Needle-free device to administer human growth hormone
* Antares shares rise as much as 58 pct (Adds analyst comments, updates share movement)
By Anand Basu
BANGALORE, June 29 (Reuters) - Teva Pharmaceutical Industries Ltd (TEVA.TA: Quote, Profile, Research, Stock Buzz) (TEVA.O: Quote, Profile, Research, Stock Buzz) said U.S. health regulators approved its partner Antares Pharma Inc's (AIS.A: Quote, Profile, Research, Stock Buzz) needle-free injector device to administer the Israeli company's human growth hormone.
"This is an important validation of the Teva partnership, which is the primary driver of our valuation and excitement about Antares stock," Ladenburg Thalmann analyst Matthew Kaplan said by phone.
Shares of Antares rose as much as 58 percent to a new year high of $1.14, before paring some gains to trade up at $1.02 in morning trade Monday on the American Stock Exchange.
Teva, the world's largest generic drug maker, and Antares filed a supplemental new drug application last year to use the needle-free device to administer Tev-Tropin, a human growth hormone.
Human growth hormone is a protein, given by injection, that is commonly used to treat children with growth hormone deficiency.
Kaplan, who rates Antares a "buy" with a $2 price target, said he expects it to receive about $10 million annually in the form of royalties from sales of Tev-Tropin and of the device, Tev-Tropin Tjet injector system.
He expects Teva to derive about $100 million annually from sales of the products.
The market for human growth hormone in the United States is about $1 billion, Teva said, citing industry estimates.
"This is the first of five products that are partnered with Teva to gain approval. We expect additional approval of possibly two additional partnered products in 2010, and another in 2011 and the fifth in 2012," Kaplan said.
The two companies have entered into several agreements, under which Antares is developing injection systems for administration of some Teva's drugs.
Shares of Teva were almost flat at $48.46 Monday on Nasdaq.
Biomedreports.com against TheStreet.Com’s biomedical columnist Adam Feuerstein:
http://biomedreports.com/index.php?option=com_content&view=article&id=1683&Itemid=83
Takeda’s Diabetes Drug Alogliptin Rejected by FDA
http://www.bloomberg.com/apps/news?pid=20601101&sid=aFC11q4WMIRs
By Kanoko Matsuyama
June 27 (Bloomberg) -- Takeda Pharmaceutical Co., Asia’s biggest drugmaker, failed to gain U.S. regulatory approval to market its new diabetes drug alogliptin because of insufficient data.
The U.S. Food and Drug Administration issued a so-called complete-response letter saying the company must provide more data on cardiovascular risks, Osaka-based Takeda said today in a statement.
The rejection is a blow to Takeda President Yasuchika Hasegawa’s plan for alogliptin to serve as a new revenue generator when its top seller, diabetes treatment Actos, loses patent protection in 2011.
“We expect to resubmit the application in about two years,” Takeda spokesman Hisashi Tokinoya said by telephone today. “We’re still negotiating the design of the test with the FDA and hope to reach agreement in the near future.”
At least eight analysts, including Mitsuya Sakurai of CLSA Ltd. in Tokyo, had anticipated the delay of alogliptin, a drug for Type 2 diabetes.
“The likelihood of Takeda winning approval is only about 5 percent,” Sakurai said by telephone on June 22. The analyst, who rates the stock “outperform,” expects the drug to be ready for sale during the quarter ending June 2013.
Takeda rose 0.8 percent to 3,790 yesterday on the Tokyo Stock Exchange. The stock has fallen 18 percent this year, against an 11 percent gain by the Nikkei 225 Stock Average.
‘Insufficient’ Data
The FDA told Takeda in March clinical data on alogliptin was “insufficient” based on new guidelines on diabetes treatments and cardiovascular risks released in December. Takeda had applied to the FDA to sell alogliptin, or SYR-322, as a once-daily treatment a year earlier in December 2007.
“SYR-322 is the most important drug development agenda for Takeda,” Tokinoya said. “We expect to lose patent protection on Actos, and with the decision by the FDA it’s difficult to have the drug in time for the patent expiration.’’
Proposed treatments for Type 2 diabetes should follow new testing standards to rule out an “unacceptable increase” in heart problems, according to the FDA’s guidance. The recommendations apply to all experimental diabetes drugs, even if studies are in progress or the medicine has been submitted for approval, the FDA said.
24 Million Patients
In the U.S., 24 million people, or 7.8 percent of the population, have diabetes, according to the American Diabetes Association’s Web site. Cardiovascular disease and stroke are the most life-threatening consequences of diabetes, the association said.
Diabetes is caused by the body’s inability to use or produce the hormone insulin. It can lead to heart disease, kidney failure, blindness or amputations. Most people have the Type 2 form linked to being overweight or inactive.
Takeda said on June 4 it delayed submitting an application to seek European approval for alogliptin by at least two years as it conducts additional patient studies on the drug’s efficacy. The company plans to file with European regulators in 2012.
If approved, alogliptin would compete with Merck & Co.’s Januvia as well as saxagliptin from Bristol-Myers Squibb Co. and AstraZeneca Plc. Saxagliptin is under review by the FDA, which will decide by July 30 whether to approve the pill, Bristol- Myers and Astrazeneca said April 23.
All three drugs are in a new class of diabetes treatments known as DPP4 inhibitors that spur the pancreas to produce more insulin and signal the liver to make less glucose, or blood sugar.
Actos generated 387 billion yen ($4 billion), or 25 percent, of Takeda’s revenue last year. Chesney projected global sales of alogliptin at 10 billion yen in 2013.
Lantus and association with an increased cancer risk -
The four studies are described and commented on in greater detail in the webcast on the EASD website:
http://webcast.easd.org/press/glargine/glargine.htm
D-Pharm plans TASE IPO on eve of Phase III trials
http://www.globes.co.il/serveen/globes/docview.asp?did=1000475791&fid=942
The company is making a $15 million rights issue as a preliminary step.
Gali Weinreb 29 Jun 09 09:53
D-Pharm, which is developing a treatment for stroke, is about to make a $15 million rights issue. This is a preliminary step towards a flotation on the Tel Aviv Stock Exchange, for which the company has already filed a shelf prospectus. The company seeks to ensure that it will have sufficient funds to complete Phase III clinical trials of its drug and gain US Food and Drugs Administration approval, or at least to reach intermediate results.
Shares of Clal Biotechnology, which owns 41% of D-Pharm, rose 6% on the announcement yesterday. The cost of the clinical trials will be in the region of $20-30 million, so that is presumably the kind of sum the company aims to raise in total.
Besides Clal Biotechnology, other large shareholders in D-Pharm are venture capital firm Pitango and IHCV. Sources inform "Globes" that most of the shareholders wish to take up their rights.
D-Pharm was founded in 1994 by Dr. Alex Kozak, who serves as president and CEO of the company. It has two products in its pipeline, with the stroke treatment clearly the leading one. Stroke is one of the most widespread medical conditions, and one of the most expensive for health systems to deal with. At present, there are no good treatments, and the market is worth billions of dollars.
The Novo Nordisk work from 2000 determined mitogenic potencies of insulin analogs only in one cancerous cell type - human osteosarcoma cells. I am aware of at least one other, more recent work, of independent scientists (Weinstein et. al., 2009) that looked at several cell lines. See abstract and results which are summarized in the table below.
http://www.ncbi.nlm.nih.gov/pubmed/19145584
So the question may be: are some insulin analogues more stimulatory for cancer behavior (in already transformed cells).
Sanofi Drug Cancer Risk Should Be Studied, Group Says
http://www.bloomberg.com/apps/news?pid=20601202&sid=aQxIxuyphsg0
By Phil Serafino and Albertina Torsoli
June 26 (Bloomberg) -- Sanofi-Aventis SA’s Lantus diabetes drug was linked to an increased risk of cancer in studies in Germany and Sweden, according to the European Association for the Study of Diabetes, which issued an “urgent” call for further research into the connection.
While patients should continue to take Lantus, they may want to consider alternatives, the group said in an e-mailed statement. The studies are published in the group’s journal, Diabetologia. Paris-based Sanofi said the research wasn’t conclusive and it stood behind the safety of Lantus.
A German study of about 127,000 insulin-treated patients in an insurance database showed a “statistically significant link between patients who had used Lantus insulin and those who had been diagnosed with cancer,” according to the statement. The study didn’t consider Levemir, an insulin produced by Novo Nordisk A/S, the group said.
Sanofi shares slumped 12 percent over the past two days, knocking 7.7 billion euros ($10.8 billion) off its market value, on concern that a study would show increased cancer risks. Lantus is Sanofi’s third-biggest-selling drug and helped first- quarter earnings beat analyst estimates.
After the German study, research was done using patient databases in Sweden, Scotland and the U.K., the association said. The Swedish study found that patients on Lantus alone had twice the risk of breast cancer than patients on insulins other than Lantus, the group said. The Scottish study showed a non- significant increased risk of breast cancer, while the U.K. study found no link between Lantus and cancer, the group said.
Edwin Gale, a professor of diabetic medicine at the University of Bristol and editor of Diabetologia, and Ulf Smith, president of the diabetes group, said in the statement that the studies had limitations, so further research is needed. Smith is a researcher at the Lundberg Laboratory for Diabetes Research at Göteborg University in Sweden.
“We believe people are entitled to know that use of Lantus insulin might be associated with greater risk, but this must also be balanced against the possibility that we might be causing unnecessary alarm by raising these concerns,” they said.
The diabetes research group has given its findings to the European Medicines Agency, the European Union’s drug regulator, and to Sanofi. While a clinical trial would be the best way to confirm the existence of a link to cancer, “such a trial would be slow, unfeasible and unethical,” Smith and Gale said.
“A large combined analysis of the best available databases worldwide is the best way forward, and EASD and Sanofi-Aventis are pledged to carry this investigation forward until we have either confirmed these preliminary observations or, more hopefully, finally put them to rest,” the researchers said in the statement.
“Given the extensive clinical evidence covering over 70,000 patients and the results of post-marketing surveillance arising from 24 million patient-years of experience, Sanofi- Aventis stands behind the safety of Lantus,” Jean-Pierre Lehner, the Paris-based company’s chief medical officer, said in an e-mailed statement. “We consider that the results of these patient registries are not conclusive.”
Concern over Lantus was stoked by Ralph DeFronzo, a diabetes researcher at the University of Texas Health Science Center, on a June 11 conference call sponsored by Credit Suisse, UBS analysts said yesterday. He predicted an “earthquake” event that might prompt doctors to not “feel so comfortable with glargine” insulin, according to a transcript of the call. Glargine is a chemical name for Lantus. He didn’t provide details.
The stock dropped this week as word of the call spread among investors. Analysts at Morgan Stanley and JPMorgan Chase & Co. cut their rating on Sanofi today because of the talk of a study that highlighted the cancer risk.
Lantus is a long-acting, injectable form of insulin that is used to control the blood sugar level in diabetics, who have difficulty producing insulin naturally. The drug, approved for sale in the U.S. in 2000, was the first once-a-day form of insulin. An injection steadily releases insulin into the blood over 24 hours.
Diabetes affects 23.6 million people in the U.S., according to the American Diabetes Association.
Competing diabetes treatments include Byetta, marketed by Eli Lilly & Co. of Indianapolis and San Diego-based Amylin Pharmaceuticals Inc. DeFronzo was an investigator on a company- sponsored study of Byetta, also known as exenatide, which stimulates the body to produce more insulin. Amylin shares surged $1.10, or 8.7 percent, to $13.69 at 4 p.m. New York time in Nasdaq Stock Market trading.
‘Negative Headlines’
“Negative headlines from a publication in a major medical journal could substantially damage the Lantus franchise,” JPMorgan’s Hauber wrote in her report today before the European diabetes group’s announcement. “A worst-case scenario is difficult to quantify before seeing the data.”
Lantus was Sanofi’s fastest-growing drug last year, with sales up 28 percent from the previous year, the company said on Feb. 11. Lantus sales reached 2.45 billion euros ($3.45 billion) in 2008, or 9.9 percent of the company’s net pharmaceutical revenue.
The French drugmaker said in February 2008 it aimed to make the medicine the world’s top diabetes treatment by 2015, overtaking Takeda Pharmaceutical Co.’s Actos. Lantus, the world’s No. 1 insulin, takes second place to Actos in the $23 billion diabetes market.
Chief Executive Officer Chris Viehbacher, who joined Sanofi in December, has handled controversy over a diabetes treatment before. He was the public face of his former employer, GlaxoSmithKline Plc, in the debate over the Avandia diabetes drug, doing media interviews and speaking at regulatory hearings. Avandia lost sales after a report of heart risks in 2007.
Followed them in their previous life as BTGC (Israeli origin), since the negotiations to be acquired by TEVA back in 2003, via departure (after 20 years on the job), of the CEO Sim Fass in 2004, the next CEO - Christopher Clement, has resigned in Nov 2008 when the board actually took over, and Lee Simon (who was a former FDA Division director), is running the show since. So I won't be surprised if more management changes are going to take place as 4 of the old group already left (Fass, Clement, Hayden, and Horowitz) and the others may also leave.
Contact: Leslie Orr
Leslie_Orr@urmc.rochester.edu
585-275-5774
University of Rochester Medical Center
Controversial cancer stem cells offer new direction for treatment
In a review in Science, a University of Rochester Medical Center researcher sorts out the controversy and promise around a dangerous subtype of cancer cells, known as cancer stem cells, which seem capable of resisting many modern treatments.
The article proposes that this subpopulation of malignant cells may one day provide an important avenue for controlling cancer, especially if new treatments that target the cancer stem cell are developed and combined with traditional chemotherapy and/or radiation.
"The fact that these concepts are steadily making their way into the clinic is exciting, and suggests that the recent interest in cancer stem cells may yield beneficial outcomes in potentially unexpected ways," wrote co-authors Craig T. Jordan, Ph.D., professor of Medicine at URMC and director of the James P. Wilmot Cancer Center Translational Research for Hematologic Malignancies program; and Jeffrey Rosen, Ph.D., the C.C. Bell Professor of Molecular and Cellular Biology and Medicine at Baylor College of Medicine.
Cancer stem cells (CSCs) are a hot topic in the scientific community. First identified in 1994 in relation to acute myeloid leukemia, CSCs have now been identified in several solid tumors in mice as well. Scientists who study CSCs believe they have distinct properties from other cancer cells, and may be the first cells to undergo mutations.
Research from the past 10 years suggests that because CSCs may be the root of cancer, they also might provide a new opportunity for a treatment. Jordan and a group of collaborators, for example, are testing a new drug compound based on the feverfew plant that demonstrates great potential in the laboratory for causing leukemia CSCs to self destruct.
Another new approach, the authors said, is the use of chemical screens to search drug libraries for already approved agents that may target CSCs, or make resistant tumor cells more sensitive to chemotherapy and radiation.
Cancer stem cell biologists hypothesize that any treatment that targets the source of origin rather than simply killing all cells, healthy and malignant, would be an improvement over most conventional therapies.
Some scientists, however, are uncertain if CSCs have unique biological properties or any relevance to treatment, the authors noted. What is more likely to fuel cancer, other studies have found, are unfavorable factors in the neighboring cells surrounding the tumor, such as mutated genes, proteins that encourage cell growth, and a poor immune system, for instance.
The most challenging issue facing CSC biologists is that the number and type of cancer stem cells can vary from patient to patient. In some tumor samples, for example, CSCs are rare while in others they constitute a large portion of the tumor mass, the authors said.
To understand why CSCs are so variable, investigators are trying to determine what genes and pathways are responsible for activating cancers that have a poor prognosis, and whether these cancers also have a higher frequency of CSCs.
"Whether the cancer stem cell model is relevant to all cancers or not," they wrote, "it is clear that we need new approaches to target tumor cells that are resistant to current therapies and give rise to recurrence and treatment failure."
An unexpected benefit of so much attention on normal stem cells is that it has stimulated research in areas not previously the focus of cancer therapies, Jordan and Rosen said.
For example, pathways known to be important for normal stem cell self-renewal, such as the Wnt, Notch and Hedgehog(Hh) pathways, are now of increased interest due to their potential role in CSCs. The first clinical trial using an agent to block the Notch pathway in combination with chemotherapy for breast cancer has begun.
The authors conclude by spotlighting the pressing need for preclinical models to test appropriate doses and combinations of CSC therapies before they can move into human clinical trials.
Nice try, but in spite of what you guys think, it's not always about sex
BSX stock also goes up cause he will be replaced by Elliott - the former CEO of Zimmer.
Speculation on the potential association of Lantus with cancer
Sanofi Falls; UBS Cites Concerns on Lantus Safety
http://www.bloomberg.com/apps/news?pid=20601202&sid=adaAqTeByuTQ
By Trista Kelley and Albertina Torsoli
June 25 (Bloomberg) -- Sanofi-Aventis SA shares fell 4.6 percent in Paris trading after UBS AG said investors are concerned about the safety of the drugmaker’s Lantus diabetes treatment.
There have been “recent market questions on the safety of insulin analogues in undisclosed studies,” Gbola Amusa, an analyst at UBS AG in London, wrote in a report today. “In our discussions with physicians, we could not confirm any safety risk but did hear a number of long-established safety concerns, in particular that Lantus use may promote cancer.”
Sanofi is betting on Lantus, its third-biggest seller, to offset sales declines caused by generic competition to other drugs. Demand for the diabetes treatment helped first-quarter earnings beat analysts’ estimates, and Amusa said Lantus probably will make up about 33 percent of annual profit by 2013.
Data from clinical studies covering more than 70,000 patients as well as research since the drug went on the market “confirm the safety profile of Lantus,” Geoffroy Bessaud, a spokesman for Paris-based Sanofi, said by telephone. Lantus, approved for sale in the U.S. in 2000, was the first once-a-day form of insulin.
Sanofi shares dropped 2.13 euros to close at 44.45 euros in Paris, the steepest one-day decline since April 23.
‘Earthquake’ Event
Concern over Lantus was stoked by Ralph DeFronzo, a diabetes researcher at the University of Texas Health Science Center, on a June 11 conference call sponsored by Credit Suisse, Amusa said in a phone interview.
DeFronzo said he expected an “earthquake” event that might prompt doctors to not “feel so comfortable with glargine” insulin, according to the call’s transcript. Glargine is a chemical name for Lantus. Pressed for details, DeFronzo said, “Can’t tell you anything. So keep your ears open. It won’t take too long.”
Competing diabetes treatments include Byetta, marketed by Eli Lilly & Co. and Amylin Pharmaceuticals Inc. DeFronzo was an investigator on a company-sponsored study of Byetta. He didn’t return a call to his office in San Antonio.
UBS’s Amusa has a “sell” rating on Sanofi.
“We have to be careful not to taint a medicine which helps many patients, but if Sanofi have data we should see it,” said Kevin Scotcher, an analyst at Liberum Capital Ltd. in London. Sanofi’s Origin study, which is investigating the cardiovascular safety of Lantus, is likely to be completed in 2012, Bessaud said.
To be more precise, PLX's plant cell system has a reduced risk of viral contamination. (I believe we all agree that plant pathogen contamination mainly affect production efficiency, as the risk of transmission to humans is probably non-existent.)
Sanofi Plans to Overhaul Research and Development
http://www.bloomberg.com/apps/news?pid=20601202&sid=a_zeLU_9Dre4
By Albertina Torsoli
June 24 (Bloomberg) -- Sanofi-Aventis SA will announce a reorganization of its research and development operations in coming weeks, Chief Executive Officer Chris Viehbacher said.
“We have a number of things to address in terms of how we get our people to work together, how we can provide more latitude for creativity, how we can develop them scientifically and how we can encourage external collaboration, because there is a world of science out there,” Viehbacher told Reuters in an interview published today. Geoffroy Bessaud, a spokesman for Sanofi in Paris, confirmed the comments.
Viehbacher, who joined Sanofi from GlaxoSmithKline Plc in December, is overhauling the research effort after the obesity pill Acomplia, once Sanofi’s most promising new medicine, was rejected by regulators. The company also faces generic competition to drugs that make up about 20 percent of revenue.
In a letter to employees the week he joined, Viehbacher said that rethinking the organization and the management of Sanofi’s R&D teams was one of his priorities. On Feb. 11, he said the division, run by Marc Cluzel, would now show “lower spending internally” and “higher spending externally.”
“The company’s R&D track record is seen as weak,” Tero Weckroth, an analyst at Kepler Capital Markets in Zurich, wrote in a June 16 note to clients. “Discipline in R&D could increase value creation.”
Research Projects
The 49-year-old executive began his overhaul in April, when he announced Sanofi was dropping 14 of its 65 research projects and that more may be terminated in the coming months. He also started making acquisitions, including the April purchase of BiPar Sciences Inc. of Brisbane, California, seeking to fill up the company’s pipeline.
Sanofi will announce cost cuts on July 29, when it releases second-quarter results, Chief Financial Officer Jerome Contamine said on May 12, during the Bank of America and Merrill Lynch health-care conference in New York.
“We are working on various ways to reduce the costs,” Contamine said. In research, “we have reduced the portfolio, we have decided to open up the R&D to external R&D and it’s clear that we also will have to adapt the internal structure to this new shape of R&D,” Contamine said.
He said Sanofi was also studying cuts at its support functions.
Meeting Unions
Management is scheduled to meet with labor unions on June 30 and July 1 to discuss the reorganization, which may also extend to other businesses, Thierry Bodin, a representative of the CGT union at Sanofi, said in a phone interview. The drugmaker probably won’t say on those occasions how many jobs it plans to cut, he said.
Sanofi last year shed 927 jobs, mostly sales positions, in France. It may slash another 200 sales positions, La Tribune reported yesterday, citing an unidentified labor union representative.
“There is no certainty on that figure,” Bodin said.
Suspense is good, makes you sharper :)
Again, PLX's polyethylene bioreactors that can be used at room temperature, reduce costs of equipment and production but don't have much to do with risk of viral contamination.
Watson Wins Approval for Generic ‘Morning After’ Pill
http://www.bloomberg.com/apps/news?pid=20601202&sid=apyto.3Qk1UI
By Catherine Larkin
June 24 (Bloomberg) -- Watson Pharmaceuticals Inc. won U.S. approval to sell the first generic copy of Plan B, the emergency contraceptive made by Teva Pharmaceutical Industries Ltd.
The Watson medicine will be available by prescription only to women ages 17 and younger, according to a notice posted today on the Food and Drug Administration’s Web site. Teva, of Petah Tikva, Israel, has exclusive rights to an over-the-counter version of the pill for women ages 18 and older until Aug. 24, the FDA said.
Plan B, also known as “the morning after pill,” was approved in the U.S. for prescription use in 1999. After years of debate and urging by lawmakers, the drug was moved over the counter in 2006. Teva acquired Plan B with its purchase of Barr Pharmaceuticals Inc. in December. While Teva doesn’t disclose specific revenue for the product, spokeswoman Denise Bradley said in April that nonprescription use has doubled sales.
Generic drugs can cost 30 percent to 80 percent as much as the original drug, with prices falling more when there are more copies on the market. A one-time use package of Plan B costs $49.99 from Internet retailer Drugstore.com Inc. The medicine consists of two tablets of levonorgestrel taken 12 hours apart.
The FDA said April 22 that it wouldn’t stand in the way of a judge’s order to allow over-the-counter sales to 17-year-old women. Teva must formally apply with the agency to lower the age by one year, and the company continues to “work closely” with the FDA as it reviews the proposed change, Bradley said today.
Patty Eisenhaur, a spokeswoman for Corona, California-based Watson, didn’t immediately return a voice-mail message seeking comment.