Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.
Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.
Gene Test for Dosage of Warfarin Is Rebuffed
http://www.nytimes.com/2009/05/05/health/05thinner.html?_r=1&partner=rss&emc=rss
By ANDREW POLLACK
In a setback for the fledgling field of personalized medicine, Medicare has decided not to pay for genetic tests intended to help doctors determine the best dose of the blood thinner warfarin for a particular patient.
In a proposed decision posted on its Web site Monday, the Centers for Medicare and Medicaid Services said that there was not enough evidence that use of the tests improved patients’ health.
But the agency said it would pay for the tests as part of clinical trials to gather such evidence.
The warfarin response tests, which cost $50 to $500, look at variations in two specific genes in a patient. They are among a group of new tests that seek to tailor medical treatments based on a patient’s genetic makeup. Such tests might help tell which drug would be best for a particular person, or whether a patient might be susceptible to dangerous side effects.
As many as one million or more Medicare patients a year start therapy with the drug, which is used to prevent life-threatening blood clots.
But determining the proper dose of warfarin is notoriously tricky. Even a slight change in dosage can mean the difference between too little, which would not be effective in preventing blood clots, and too much, which can cause dangerous internal bleeding. Tens of thousands of people end up in the hospital each year with complications from warfarin, which is also sold under the brand name Coumadin.
But Medicare said there was little evidence that use of the genetic test led to better outcomes for patients compared with the existing procedure, in which doctors estimate an initial dose based on a patient’s age, weight and other factors. Then they test the blood’s clotting propensity every few days and adjust the dose accordingly.
Some studies have shown that using the genetic test might allow the proper dose to be achieved more quickly. But Medicare said there was little evidence that doing so translated into a lower risk of blood clots or hemorrhages. Conclusions about health outcomes, it said, “seem to us premature, even though they are intuitively appealing.”
Medicare’s proposed decision will be open for public comment for the next month.
Edward Abrahams, executive director of the Personalized Medicine Coalition, which advocates such genetic testing, said the expensive clinical trials required by Medicare might be unreasonable for diagnostic tests.
Several diagnostic companies, including Nanosphere, Osmetech and ParagonDx, sell warfarin genetic tests to hospitals and other laboratories. Some labs offer their own tests.
The decision was “not a complete pushback,” said Bill Moffitt, Nanosphere’s chief executive, pointing to Medicare’s willingness to pay to help generate evidence of the tests’ usefulness.
Kathy Hudson, director of the Genetics and Public Policy Center at Johns Hopkins University, agreed with Medicare’s decision. “We should pay for what works,” she said.
Medical societies were divided on the issue. And the Food and Drug Administration recommends, but does not require, a genetic test for patients starting on warfarin.
Critics say that there are various practical problems with the warfarin genetic tests.
The test results often do not come back fast enough to influence the initial dose. And simply knowing which variants of the two genes a patient has does not automatically tell the doctor what dose to give. That depends on other factors as well.
Moreover, use of the genetic tests does not eliminate the need to periodically test the patient’s blood-clotting propensity.
Teva Pharmaceutical eyes more acquisitions -CFO
http://www.reuters.com/article/marketsNews/idINL565608420090505?rpc=44
May 5 (Reuters) - Teva Pharmaceutical Industries (TEVA.O: Quote, Profile, Research, Stock Buzz), the world's biggest generic drugmaker, is in the market for more acquisitions following its purchase of rival Barr, Teva Chief Financial Officer Eyal Desheh said on Tuesday.
Desheh told Reuters, following the release of first-quarter results, that the first quarter was expected to be the weakest this year for launches of new products.
"The fourth quarter is supposed to be the most actice in new launches and in between we expect improvement from one quarter to the next," he said.
Desheh also said Teva (TEVA.TA: Quote, Profile, Research, Stock Buzz) was seeing only marginal impact from the global economic slowdown, and this was being offset by customers seeking generic drugs that are cheaper than branded products.
Pixantrone Now Available in Europe on a Named-Patient Basis
http://finance.yahoo.com/news/Pixantrone-Now-Available-in-prnews-15128644.html?.v=1
Cell Therapeutics and IDIS Partner to Accelerate Patient Access to Pixantrone through Program
SEATTLE, May 5 /PRNewswire-FirstCall/ -- Cell Therapeutics, Inc. (CTI) (Nasdaq and MTA: CTIC) today announced that pixantrone is now available on a named-patient basis in Europe. Pixantrone will be supplied by IDIS to healthcare professionals for the treatment of individual patients with aggressive non-Hodgkin's lymphoma (NHL) that has either relapsed after standard therapies or is refractory to them. We know of no therapy that has previously been shown to be effective treatment for such patients.
"CTI has worked hard to make pixantrone available in Europe at the prescriber's request as it provides an option for these difficult to treat aggressive NHL patients," noted Craig Philips, President of CTI. "We continue to work toward potential approval of pixantrone at the end of 2009 in the United States and expect to complete the submission of the New Drug Application to the Food & Drug Administration this quarter."
"Our experience with pixantrone has been positive with patients achieving a complete response where such a result was not achievable with other treatments," said Prof. Pier Luigi Zinzani, M.D., Institute of Hematology and Oncology, University of Bologna. "I am pleased that it is now available on a named-patient basis as it has the potential to address a significant unmet need in this heavily pretreated patient population."
A named-patient program is a compassionate use drug supply program under which physicians can legally supply investigational drugs to qualifying patients. Under a named-patient program, investigational drugs can be administered to patients who are suffering from serious illnesses prior to the drug being approved by the European Medicines Evaluation Agency. "Named-patient" distribution refers to the distribution or sale of a product to a specific healthcare professional for the treatment of an individual patient. In Europe, under the named-patient program the drug is most often purchased through the national health system.
Interesting to compare the restructuring charges to AMLN (13-$15M/200 jobs) and to DSCO ($0.6M/24 jobs).
Scientific Meeting Calendar
NOTE: ANYONE MAY UPDATE THIS FILE
Edits: Added - Renal Week, ACAAI, AHA, ASH
MAY 2009
American Association of Neurological Surgeons - AANS
May 2-6, 2009
San Diego, CA, USA
http://www.aans.org/
Association for Research in Vision and Ophthalmology - ARVO
May 3-7, 2009
Fort Lauderdale, FL, USA
http://www.arvo.org/eweb/startpage.aspx?site=AM2009
American Society of Hypertension - ASH
May 6-9, 2009
San Francisco, CA
http://www.ash-us.org/annual_meeting/future_dates.htm
American Association of Clinical Endocrinologists - AACE
May 13-17, 2009
Houston, Texas
http://www.aace.com/meetings/ams/2009/
American Psychiatric Association - APA
May 16-21, 2009
San Francisco
http://www.psych.org/Events/AnnualMeeting.aspx
American Conference for the Treatment of HIV - ACTHIV
May 15-17, 2009
Denver, Colorado, United States
http://www.acthiv.org/
American Thoracic Society - ATS
May 15-20, 2009
San Diego, California
http://www.thoracic.org/
European Human Genetics Conference
May 23-26, 2009
ACV, Vienna, Austria
http://www.eshg.org/eshg2009/
American Society for Clinical Oncology - ASCO
May 29-June 2, 2009
Orlando, Florida
http://www.asco.org
Digestive Disease Week - DDW
May 30-June 4, 2009
Chicago, IL
http://www.ddw.org/wmspage.cfm?parm1=605
JUNE 2009
American Diabetes Association - ADA
June 5-9, 2009
New Orleans, LA
http://professional.diabetes.org/Meetings_GeneralList.aspx
Endocrine Society - ENDO
June 10-13, 2009
Washington, DC
http://www.endo-society.org/endo/media.cfm
AUGUST 2009
International Congress of Respiratory Science - ICRS
August 9-13, 2009
Bonn, Germany
http://www.respiratory-science.org/
OCTOBER 2009
International Congress on Coronary Artery Disease - ICCAD
October 11 to 14, 2009
Prague, Czech Republic
http://www2.kenes.com/cad/pages/home.aspx
Society for Neuroscience - SFN
October 17-21, 2009
Chicago, USA
http://www.sfn.org/am2009/
World Diabetes Congress - IDF
October 18-22, 2009
Montreal, Canada
http://www.worlddiabetescongress.org/
American Society of Human Genetics - ASHG
October 20-24, 2009
Honolulu, Hawaii
http://www.ashg.org/2009meeting/
Renal Week 2009
October 27 November 1, 2009
San Diego, CA
http://asn-online.org/education%5Fand%5Fmeetings/renal%5Fweek/
American College of Chest Physicians - CHEST
October 31 - November 5, 2009
San Diego, California
http://www.chestnet.org/CHEST/program/about09.php
NOVEMBER 2009
American College of Allergy, Asthma & Immunology - ACAAI
November 5-11, 2009
Miami Beach, FL
http://www.acaai.org/Member/Annual_Meeting/Annual+Meeting.htm
American Heart Association - AHA
November 14-18, 2009
Orlando, Fl
http://scientificsessions.americanheart.org/portal/scientificsessions/ss/seeyounextyear2009
DECEMBER 2009
American Society of Hematology - ASH
December 5-8, 2009
New Orleans, LA
http://www.hematology.org/meetings/2009/index.cfm
--
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.
Global in-market sales of Azilect reached $55M in 1Q, a 50% increase over the comparable period in 2008.
DSCO has recently axed 24 employees from its commercial and corporate personnel.
http://finance.yahoo.com/news/Discovery-Labs-Reports-First-pz-15061812.html
CGRB - CB7630 (Abiraterone Acetate) started phase 3 trial in chemotherapy-naive castration-resistant prostate cancer patients.
http://finance.yahoo.com/news/Cougar-Biotechnology-bw-15066718.html?.v=1
Pharma: The 10 Most Promising New Drugs S&P Ratings compiles its list of the most promising late-stage drugs due out over the next two years
By Arthur Wong From Standard & Poor's RatingsDirect
http://www.businessweek.com/investor/content/may2009/pi2009051_087752.htm?chan=top+news_top+news+index+-+temp_investing
But shorter course of telapravir like in the 8+16 arm, might result in higher relapse rates.
Oral Cladribine's CLARITY trial
Both groups had fewer brain lesions than those in the placebo group and showed more than 30 percent reduction in the risk of disability progressing, compared with placebo, Merck said.
* lymphopenia that takes "weeeks to months" after discontinuation to resolve
Right you are! PROVE 1 and 2 didn't enroll cirrhotic patients, and as you've previously posted in #msg-37316151, it is an important and surprising finding. One expects that absorption of a PIs should varied significantly by fibrosis score in patients with advanced fibrosis/cirrhosis. This is important as this subgroup is among the hardest patients to treat.
FTY720 TRANSFORMS study
* NEW - 2 BREAST CANCERS IN FTY GROUP!! coincidence?
skin cancers increased
Nice call on Latisse, it sure looks like it is on a good track.
(you are a user, I presume?)
Antiplatelet Drugs: Improving the therapeutic window
http://www.nature.com/nrd/journal/v8/n5/full/nrd2886.html
By Erika Kennington, May 2009
Antiplatelet therapies are commonly used to lower the risk of heart attack and stroke caused by the formation of blood clots containing aggregated platelets over ruptured or denuded atherosclerotic plaques (atherothrombosis). However, such therapies also impair normal platelet function, and this can cause prolonged or even fatal bleeding. Now, a ligand-based design strategy targeting a G protein-coupled receptor (GPCR) on platelets has been used to identify a novel antiplatelet agent that does not prolong bleeding and which might be used in combination with existing agents to provide more effective antiplatelet therapy.
Platelet aggregation is regulated by multiple GPCRs, ligands for which include thromboxane A2 (TXA2) and ADP. Currently, the most widely used antiplatelet therapies are aspirin, which inhibits the production of TXA2, and clopidogrel, which antagonizes the P2Y12 ADP receptor. Another platelet GPCR — the EP3 receptor for the inflammatory mediator prostaglandin E2 (PGE2) — has also recently been identified as having a key role in atherothrombosis by Fabre and colleagues (see Further reading). PGE2 production is increased in inflamed atherosclerotic plaques, but the healthy arterial wall produces negligible amounts of PGE2, suggesting that antagonizing the platelet EP3 system might not have detrimental effects on normal platelet function, unlike aspirin and P2Y12 antagonists.
To investigate this possibility, Singh et al. used a ligand-based design strategy to synthesize EP3 receptor antagonists. Following detailed structure–activity relationship studies, one compound (DG-041) was selected for further evaluation. DG-041 showed >1,000-fold selectivity for EP3 receptors in radioligand displacement assays against other PGE2 receptors, whereas it was inactive against a range of other GPCRs. Furthermore, it blocked the PGE2-mediated inhibition of cAMP production and inhibited the platelet aggregation response in both rat and human plasma.
The authors then compared the in vivo effects of DG-041 on platelet function and bleeding time with those of the P2Y12 antagonist clopidogrel. DG-041 completely inhibited platelet aggregation with no concurrent increase in bleeding time (even at high doses), indicating that EP3 blockade has a negligible effect on bleeding. Conversely, the minimum effective dose of clopidogrel required to inhibit platelet aggregation significantly increased bleeding time. Furthermore, PGE2 restored the aggregation response, indicating that the efficacy of P2Y12 antagonists is limited in the context of inflamed plaque.
Finally, as initial clinical trials of DG-041 are likely to require co-administration with current antiplatelet drugs, the effects of combining EP3 and P2Y12 antagonists were investigated. Adding DG-041 suppressed the PGE2 facilitation of platelet aggregation seen with clopidogrel alone and did not increase bleeding time, suggesting that co-administration of EP3 and P2Y12 antagonists could represent a superior antiplatelet therapy.
ORIGINAL RESEARCH PAPER
1. Singh, J. et al. Antagonists of the EP3 receptor for prostaglandin E2 are novel antiplatelet agents that do not prolong bleeding. ACS Chem. Biol. 4, 115–126 (2009)
The anticoagulants market
http://www.nature.com/nrd/journal/v8/n5/full/nrd2851.html
By Irena Melnikova1, May 2009
Thrombosis — localized blood clot formation — is a leading cause of morbidity and mortality associated with arterial diseases, such as myocardial infarction and stroke, and venous thromboembolic (VTE) disorders, including deep vein thrombosis and pulmonary embolism1. VTE is the third leading cause of cardiovascular-related death, after myocardial infarction and stroke, and is one of the leading causes of death in patients with cancer.
Antithrombotic drugs, including anticoagulants, antiplatelet agents and direct thrombolytics, are used for both the prevention and the acute treatment of thrombosis1 (Table 1). Anticoagulants target elements of the coagulation cascade (Fig. 1) and are typically used for short- and long-term management of thrombotic disorders of both the arterial and venous systems. The most common use of anticoagulation is for stroke prevention in patients with atrial fibrillation (Table 1).
Current anticoagulants
Vitamin K antagonists and heparins have dominated the anticoagulant market for over half a century. Warfarin inhibits the vitamin K-dependent activation of several clotting factors (Fig. 1) and is the most commonly prescribed anticoagulant. Until recently, it was the only orally bioavailable agent of this kind and it remains the only approved drug for long-term anticoagulation therapy. Use of warfarin in patients with atrial fibrillation reduces the incidence of stroke by 64%. Despite proven efficacy, warfarin carries the risk of serious or fatal bleeding, has an unpredictable pharmacokinetic profile, is subject to drug–drug interactions and is affected by an individual's genetic make-up and diet, making it hard to dose. Various generic vitamin K antagonists overall generated global sales of over US$700 million in 2008 (Ref. 2).
Heparins interact with various factors of the coagulation cascade (Fig. 1) and are used for short-term prophylaxis of thrombosis. Heparins are injectable, which limits their use to an in-patient setting or for short-term (not more than 2 weeks) VTE prophylaxis. In the case of unfractionated heparins, additional complications include monitoring and dose adjustment requirements and the risk of heparin-induced thrombocytopoenia (HIT), which develops in 3% of patients. HIT leads to thrombosis and increased mortality. The incidence of HIT is substantially reduced with low molecular weight heparins (LMWHs). The most widely prescribed LMWH, enoxaparin (Lovenox; Sanofi–Aventis), is the leading drug for the prophylaxis of VTE and is also used in acute coronary syndromes. It is the best-selling anticoagulant on the market, with global sales of approximately $4 billion in 2008. However, over the next 5 years, the market share of enoxaparin is expected to decline owing to generic competition and the introduction of new oral anticoagulants.
The large market opportunity and knowledge of the shortcomings of current anticoagulants resulted in increased interest in new agents that would be at least as effective as those currently available, but with an improved safety profile (specifically, reduced risk of bleeding) and greater ease of use (oral agents, especially in a chronic setting).
Direct thrombin inhibitors
Thrombin, or factor IIa, catalyses the production of fibrin (Fig. 1) and is involved in other coagulation-related reactions, making it an attractive therapeutic target.
Parenteral direct thrombin inhibitors (DTIs) currently on the market are primarily used in patients undergoing percutaneous coronary intervention (PCI) and in patients with or at risk for HIT. In the United States, bivalirudin (Angiomax; Medicines Company) has become a dominant anticoagulant used in PCI. Improved patient outcomes drive its widespread use. Patients treated with bivalirudin show a reduction in severe bleeding of up to 59% and a reduction in 1 year mortality of up to 47% compared with those treated with a combination of heparin and a platelet glycoprotein IIb and IIIa inhibitor3. Bivalirudin goes off-patent in 2010 (unless a patent extension is granted), after which its market share is expected to be eroded by generic competition.
The first approved oral DTI, ximelagatran (Exanta; AstraZeneca), was withdrawn from the market in 2006 owing to its link to liver toxicity. Last year, a second oral DTI, dabigatran (Pradaxa; Boehringer Ingelheim) gained approval in the European Union and Canada for prevention of VTE following joint-replacement surgery2; a filing for US approval is expected in 2009. However, the biggest market opportunity for dabigatran (or indeed for any oral anticoagulant) lies in stroke prevention in patients with atrial fibrillation. Phase III trial results in atrial fibrillation are expected in 2009. Given its large lead in development (about 3 years ahead of competition), dabigatran could become a dominant player in this setting, ending the era of warfarin and rapidly achieving a blockbuster status.
Factor Xa inhibitors
Factor Xa is a coagulation factor that is essential for the formation of thrombin (Fig. 1). Several oral factor Xa inhibitors are in late stages of development: rivaroxaban (Xarelto; Bayer/Johnson&Johnson), apixaban (Bristol–Myers Squibb/Pfizer) and edoxaban (Daiichi Sankyo).
Market indicators
Rivaroxaban was approved for the prevention of VTE post joint-replacement surgery in the European Union and Canada last year. In Phase III studies, rivaroxaban demonstrated a reduced rate of deep vein thrombosis, pulmonary embolism and all-cause mortality versus enoxaparin (9.6% versus 18.9%) without an increased risk of bleeding4. A new drug application (NDA) for this indication is under review by the US Food and Drug Administration. Phase III trials in stroke prevention due to atrial fibrillation are ongoing.
An NDA for apixaban for VTE prophylaxis after orthopaedic surgery was originally planned for 2009. However, apixaban missed a primary end point of non-inferiority to enoxaparin in the Phase III ADVANCE-1 trial. Despite this setback, development of apixaban for this indication continues in ADVANCE-2 and -3 trials. In addition to VTE prophylaxis, apixaban is in Phase III trials for stroke prevention due to atrial fibrillation and in Phase II studies in acute coronary syndromes.
Daiichi Sankyo's strategy for edoxaban is to seek approval in the largest market segment — atrial fibrillation — right from the start. A pivotal Phase III programme was initiated at the end of 2008. However, the company also plans to pursue indications such as VTE and acute coronary syndromes at a later stage.
Market outlook
The anticoagulant market is projected to grow from around $6 billion in 2008 to over $9 billion in 2014 (Fig. 2). The growth will be driven by demographics of the ageing population and increased incidence of cardiovascular disease, but mainly by the approval of new agents that will offer substantial improvements over the current standards of care. The availability of oral anticoagulants is poised to have the greatest effect on the atrial fibrillation-related stroke prevention segment of the market, in which the use of warfarin is expected to become obsolete (Fig. 2).
AGN - Latisse did well at $12.3M for Q1.
And here comes the day after black box for all Botulinum toxin products:
http://www.fda.gov/bbs/topics/NEWS/2009/NEW02005.html
Dunno, but I have one for you: what rates were disclosed by Vertex for the first time in this year's EASL?
The criteria in PROVE 1 was different - patients not achieving RVR in PROVE 1 were automatically counted as treatment failures in the 12+12 arm and received 48 weeks of total therapy. In PROVE 2, non RVR patients were allowed to stop treatment at 24 weeks so non RVR patients were counted.
Genetic variant impairs communication within the brain
http://www.eurekalert.org/pub_releases/2009-04/uob-gvi043009.php
Possible consequences: Schizophrenia or manic depression
For some time now it has been known that certain hereditary factors enhance the risk of schizophrenia or a manic-depressive disorder. However, just how this occurs had remained obscure. Researchers at the Zentralinstitut für Seelische Gesundheit in Mannheim, Heidelberg University and Bonn University are now able to answer this question, at least for one common genetic variant: this impairs the interoperation of certain regions of the brain. The study is to appear on 1st May in the prestigious scientific journal Science. It will also be suited to provide fresh stimuli for the search for cures.
The scientists examined test persons with whom a certain genetic trait had undergone a characteristic mutation. A year ago, a research team had demonstrated that this mutation was, amongst other things, associated with an enhanced risk of schizophrenia. In addition to this, people carrying this variant were more susceptible to a bipolar malady also known as a manic-depressive disorder. In the present case, however, our results were based on examinations of 115 healthy subjects.
"At this point, no-one had the slightest idea of what effect the genetic variant we had observed might have on the brain", declares Professor Dr. Andreas Meyer-Lindenberg. The director of the Zentralinstitut für Seelische Gesundheit was the initiator of the study. "We examined our test subjects in magnetic resonance tomographs, which reveal how the various areas of the brain interoperate".
Result: persons suffering from this high-risk genetic variant exhibited a change in the communication between their dorsolateral prefrontal cortex (DLPFC) and other regions of their brains. The DLPFC plays an active role in the working memory and diverse "higher" cerebral functions. It comprises a right-hand and a left-hand fraction, and it was the communication between these two halves which had become impaired. In contrast to this, the link between the DLPFC and the hippocampus, a further region of the brain of importance for the memory, was improved. Both these noteworthy phenomena had already been shown to exist in patients suffering from schizophrenia.
Moreover, carriers of this high-risk gene also displayed an enhanced linkage between the amygdala and a number of other cerebral regions. The amygdala, also known as the "almond", plays an active role in the manner in which we cope with our emotions. "Which is why we have related this phenomenon to the bipolar impairment, which is, as we know, characterised by erratic mood swings", Professor Dr. Dr. Henrik Walter of Bonn University explains.
Over 100 years ago, the German psychiatrist Carl Wernicke had already suspected that schizophrenia might be attributable to impaired interoperation between different regions of the brain. The new study, employing an innovative combination of modern genetics and cerebral imaging, has confirmed this suspicion.
The mutated gene contains the building plan for a protein whose precise function is still not clear. Diverse study groups worldwide are currently engaged in finding answer to this question – amongst other reasons, because this could provide approaches to novel treatments. "It is impressive that using modern methods we are able to trace such subtle genetic effects in the living brain", says Professor Dr. Peter Kirsch, head of the Study Group for Cerebral Imaging in Mannheim. Carriers of this variant, incidentally, must not be worried that they are destined to suffer from schizophrenia or bipolar impairment. "This genetic variant plays only a minor role in these disorders", says Dr. Christine Esslinger from the Zentralinstitut für Seelische Gesundheit reassuringly. Other factors must at all events become involved before a disorder such as this breaks out.
In Mannheim, apart from Professor Meyer-Lindenberg, Dr. Christine Esslinger and Professor Kirsch, Professor Dr. Marcella Rietschel has also played a critical part in this study. In Bonn, the participation of Privatdozent Dr. Sven Cichon must be emphasised. The study has been supported by the Federal Ministry for Education and Research within the framework of the National Genome Research Network. The German Research Foundation (DFG) has also supported its work.
What ever happened to the midas touch?
Pity you couldn't sell after our last exchange.
CF101 failed (again) in phase IIb in RA. The stock will probably go down big time today.
Did GSK say if it is going to file an sNDA?
EASL Late-breaker posters
SE seen with both PIs - TMC435 (elevated bilirubin) and MK-7009 (vomiting) don't look good.
I remember 4:
Non-nuc polymerase inhibitor GS-9190
Caspase inhibitor GS-9450
NS4a with ACHN
Unnamed PI
Makes sense that ACOR's fast resubmission is a good sign. I'm optimistic about this.
GENZ's guidance for Cerezyme for 2009 $1.250M - $1.275M.
ACOR announced that it has resubmitted its NDA for Fampridine-SR.
Found that on Nov. 13, 2008, the USPTO declared interference between Wyeth's patent No. 7,291,347 for oral dosage of O-desmethylvenlafaxine succinate (Pristiq's active ingredient) and a patent application owned by Sepracor’s.
(sorry, no time to dig more, have a plane to catch)
Perhaps checking patients for blood calcitonin levels is a good place to start.
I told you at the time it is a good company with solid science (I do appreciate Pnina a lot) and that is still my view. However, this run up of the stock cannot be explained by the CF102 trial only. It is more likely that investors here believe (or know from a leak) that the confirmatory trial of CF101 went well. I tend to take some chips off the table considering the risk/reward of the stock. Will be interesting to see how it plays next week, do email me if you can, I might be able to check my gmail from time to time.
CF102 is a synthetic highly-selective agonist of the A3 adenosine receptor (A3AR), a Gi protein associated cell surface receptor, which is highly expressed on the surface of cancerous and inflammatory cells. Binding of CF102 to its target on cells, leads to apoptosis.
Are you still watching CanFite Dubi? The stock run from 50 to nearly 140 in less than 2 weeks (today it closed +18%). This came out today but the more important news regarding CF-101 are due soon.
Can-Fite set for liver cancer treatment study
http://www.globes.co.il/serveen/globes/docview.asp?did=1000442475&fid=942
The company intends to initially develop CF-102 for liver diseases, including cancer and hepatitis C.
Can-Fite BioPharma Ltd. (TASE:CFBI) has begun recruiting patients for the Phase I/II clinical trial of CF-102 treatment for liver cancer, after obtaining permission from the Ministry of Health and Rabin Medical Center (Beilinson Hospital) ethics committee.
The clinical trial will examine the safety and effectiveness of CF-102 on 40 patients at the Rabin Medical Center. Patients will receive increasing dosages of the drug during the trial period.
Can-Fite intends to initially develop CF-102 for liver diseases, including cancer and hepatitis C.
Liver cancer is one of the commonest forms of cancer worldwide, striking 450,000 new patients a year. It is especially prevalent among people suffering from hepatitis B and C, and alcoholics.
Can-Fite added that it expects in the coming weeks to announce the results of clinical trials for its drug, CF-101, for the treatment of rheumatoid arthritis and dry-eye syndrome (keratoconjunctivitis sicca). If the trials are successful, the company will begin Phase III trials of the drug for these indications.
Can-Fite's share jumped 11.2% in morning trading to NIS 1.30.
ISRG will probably lower the guidance.
As always, science offers what it can at a particular time. GWAS are excellent for identifying genes associated with diseases. However, as we now know too many genes contribute very little effect and it becomes medically impossible to deal with. Therefore, the next logical step is to deal with the entire genome. Since shortly we shall have technology for a $1000 genome, we may find better drug candidates and perhaps better disease markers. Now the trend is that genes show limited value, so scientists are looking at the proteome. But proteome is not the sole answer either and there will be more fascinating areas like epigenome imo.
...and thought that you wouldn't have a female in mind