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Slick JWillie-maybe we'll make an honest man out of him yet!
The trick is to keep him under oath...
You may have missed my point, which was that anatabloc should not be judged by its questionable introduction, but by its current potential. I agree that Biden also has a questionable past, but he has persevered to remain relevant.
His plagiarism was despicable, and his gaffs are cringeworthy, but he is a far cry from the self-serving slickness of JW.
You got me...I'm not a Republican. I'm glad it's all out in the open now...whew. lol
He reports the facts, or at least the info that is publicly available. Then he puts a humorous spin on it, ie., embellishment, exaggeration, parody, etc. I didn't learn anything new, nor did I sell based on his superficial assessment of the story. So no, he did not make up my mind for me. I wasn't happy anatabloc was the butt of his jokes, but I can appreciate and accept the humor from it.
There is nothing to defend in regards to the past. Anatabloc had a rudimentary initiation by a company/founder with a speckled history. It is a very humiliating piece of its origins, and it will continue to stigmatize the development until more credible studies are concluded. Unlike the ugly past, the legacy is far from over. Biden overcame the embarrassment of plagiarism, which plagued all his presidential runs, to become Vice President. My point is that it eventually matters not how it started, but how it finishes.
Life is not a fairy tale, and Anatabine is no exception. That is not to say it won't some day become a very beneficial medication. Mullen is a credible scientific leader who does validate the potential here. Is he fallable? Of course. Could anatabine falter? Of course. But there is a good indication that they are going to research the compound -- inside and out -- to determine if it has a place in medicine.
I completely disagree. He didn't twist anything. His description is basically what has been made public through a variety of reports/sources. Of course he embellished intentionally to put a comical spin, but smart people know that.
Twisting facts? That is the MO at Fox Newz...
Uh oh...not good. Jon Stewart just ridiculed Anatabloc, JW, and Maureen McDonnell, on the opening segment of The Daily Show. The most damning part was Maureen approaching Romney's wife about Abloc maybe curing her MS. This, folks, is why you don't make idiotic claims and recommendations on serious medical conditions without the expertise and advanced clinical evidence to back it up. If it is legitimate, time will tell. But telling it before its' time is absolutely foolish.
This situation is quite the fluke (from microwaving tobacco to anatabine), but as serendipity may have it, something good may come of it. But then again, who the hell knows.
Hopefully Colbert passes on the story...
Four charged with manipulating U.S. marijuana-related stocks
Reuters
16 hours ago
http://finance.yahoo.com/news/four-charged-manipulating-u-marijuana-214402268.html
By Jonathan Stempel
Aug 5 (Reuters) - U.S. authorities on Tuesday charged four stock promoters with civil fraud for manipulating the securities of marijuana-related and other microcap companies, and three were hit with criminal charges over their trades in a penny stock.
The U.S. Securities and Exchange Commission said Mikhail Galas, Alexander Hawatmeh, Christopher Mrowca and Tovy Pustovit made more than $2.5 million by buying six thinly traded stocks and then artificially driving up their prices through a so-called "pump-and-dump" scheme.
It said the defendants, all in their early- to mid-20s, conducted "matched" offsetting trades to create an appearance of growing demand and promoted the stocks with "blast" emails through websites such as Explosive Alerts and moneyrunnersgroup.com.
The SEC said two of the stocks were GrowLife Inc, which has said it provides soil, nutrients and other products to help cultivate plant-based medicines, and Hemp Inc, which has said it focuses on the industrial hemp industry but does not cultivate or market medical cannabis.
Galas, Hawatmeh and Mrowca were also charged criminally by the U.S. Department of Justice with conspiracy to commit securities fraud and conspiracy to launder monetary instruments in connection with one of the non-marijuana-related stocks, ISM International Inc.
Lawyers for the defendants could not immediately be located.
GrowLife and Hemp are not defendants in either case.
Galas, of Vancouver, Washington; Hawatmeh, of Salem, Oregon; and Mrowca, of Bradenton, Florida, have been arrested and are in federal custody, according to a spokeswoman for U.S. Attorney Jenny Durkan in Seattle, who announced the criminal charges.
Pustovit also lives in Vancouver, the SEC said.
In May, the SEC warned investors about possible scams involving marijuana-related investments, saying fraudsters often try to exploit new growth industries by manipulating stocks.
The cases are U.S. v. Mrowca et al, U.S. District Court, Western District of Washington, No. 14-mj-05172; and SEC v. Galas et al in the same court, No. 14-05621.
(Reporting by Jonathan Stempel in New York; Editing by Dan Grebler)
What a horrific 3 weeks for Rock Creek's shares, shedding almost 50% of its value since July 10th. I'm not sure how significantly the McDonnell trial is weighing into this slide, or if JW's testimony may prompt a flood of lawsuits against RCPI, but I would guess there is a correlation with the former, and an increased likelihood of the latter.
Another factor hurting shares, for sure, is the general market sell-off, which has also been significant in the past week (as has been the RCPI capitulation). But the greatest reason for the weakness, I think, is the FDA request for more info regarding the IND. That announcement came July 11th. On July 10th, the shares 63 cents. The stock has declined steadily since then.
Therefore, if the IND is eventually approved, which I believe is most certainly the case, I think the stock can easily jump to pre-July 11th levels.
Unfortunately, I bought more at .49 (as I said I would after the July 11th announcement, if it dropped 20%). I plan on buying additional shares under 40 cents early next week, and would like to sell the majority of those cheaper shares for a (hopefully) quick double or so, once the IND is (hopefully) allowed to proceed.
Ps. I'm encouraged by the announcement/progress on the European clinical trials. Definitely gives us more shots on goal.
Fwiw - The news release based on the result of that study, which was announced less than a year later:
Medigene achieves positive formulation study results for RhuDex® and announces phase II proof-of-concept study for the treatment of autoimmune diseases
http://www.medigene.com/presse-investoren/news/pressemitteilungen/medigene-achieves-positive-formulation-study-results-for-r
Positive results of clinical formulation study enable further clinical development with new, optimized formulation
Phase II proof-of-concept (PoC) study for autoimmune diseases in the indication primary biliary cirrhosis (PBC) planned to start by year-end 2012
PoC study builds basis for further development in rheumatoid arthritis
Martinsried/Munich, June 21, 2012. Medigene AG (Frankfurt, Prime Standard: MDG) announced today that the clinical formulation trial with RhuDex® achieved positive results and that the further clinical development of RhuDex® for the treatment of autoimmune diseases will continue with an optimized oral formulation. As the next development step, Medigene plans to initiate a phase II proof-of-concept study in primary biliary cirrhosis (PBC) before the end of 2012 to verify both the mechanism of action and the overall clinical profile of RhuDex® for the treatment of autoimmune diseases. The study results are expected to build a basis for the further development in rheumatoid arthritis.
Dr. Frank Mathias, CEO of Medigene AG, comments: "Medigene has developed a logical and integrated non-clinical and clinical program for RhuDex®. We have a new, optimized formulation for this candidate and now want to prove the clinical relevance of RhuDex®'s mode of action as quickly as possible. The PBC indication offers an extremely useful and rapid way to achieve this goal. The results will be highly valuable for the further development of RhuDex® in the treatment of rheumatoid arthritis."
The objective of the clinical formulation trial was to develop an optimized oral formulation of the active substance suitable for the treatment of chronic diseases. All endpoints of the study were met. The new formulation is characterized by an optimized pharmacokinetic profile, excellent tolerability and a reduction of dose units. Based on the results of this study, RhuDex® will now be administered in a formulation based on Gelucire. This excipient is a known lipid-based compound belonging to the group of excipients "generally regarded as safe" (GRAS), and is used in marketed drug formulations.
With the new formulation, Medigene plans to initiate a phase II clinical proof-of-concept study with RhuDex® for the treatment of autoimmune diseases. Medigene will conduct this study in the indication of primary biliary cirrhosis (PBC), allowing the company to generate widely accepted clinical data on relevant disease parameter modification after only three months of treatment. In addition, patients with PBC do not receive explicit immunomodulating baseline therapy, as is the case, for example, in the treatment of rheumatoid arthritis. Thus, this patient group is suitable to preliminarily confirm that RhuDex®, due to its specific mode of action, does not adversely affect the ability to mount a spontaneous inflammatory reaction. Therefore, this clinical study is an important step for the further development of RhuDex® in the treatment of rheumatoid arthritis.
In parallel to the planned initiation of this proof-of-concept study, Medigene has initiated additional regulatory non-clinical studies to enable the necessary chronic treatment of patients with autoimmune diseases. Also, non-clinical studies are being conducted to integrate additional translational aspects into clinical development.
About RhuDex®: Medigene is developing RhuDex® as an oral, disease-modifying drug for the treatment of autoimmune diseases such as rheumatoid arthritis. RhuDex® is a CD80 antagonist that blocks undesired T-cell activation and thus has an immunomodulating and anti-inflammatory effect. Therefore, this drug candidate can be classified with the group of "Disease-Modifying Antirheumatic Drugs" (DMARDs). In a phase IIa trial in 29 patients in the indication rheumatoid arthritis, RhuDex® showed initial signs of biological activity.
About RhuDex® RapidFACT(TM) formulation study: During the recently completed clinical formulation study, variations of a RhuDex® formulation were given subsequently in single dose applications to ten healthy volunteers. Due to the innovative RapidFACT(TM) (Rapid Formulation Development and Clinical Testing) study design, variants of formulations could be tested and evaluated for their tolerability and pharmacokinetic profile over a short period of time, since the respective formulation variant was produced immediately prior to dosing.
All formulations investigated showed an excellent tolerability profile. The final formulation demonstrates the most advantageous prolongation of plasma absorption and elimination phases to achieve steady compound plasma levels with repeat daily dosing. Due to the highly flexible study design, additional preliminary data on the effect of concomitant food intake ("food effect") and on dose proportionality have also been obtained.
About Primary Biliary Cirrhosis (PBC): The autoimmune disease PBC is a chronic liver disease that initially affects the bile ducts. The bile ducts are progressively destroyed by inflammatory processes, causing biliary stasis and build-up of bile in the liver. Liver tissue is destroyed and replaced by connective tissue, liver cirrhosis develops. As in rheumatoid arthritis, the activation of T cells via a CD28-CD80 interaction has been described as involved in the pathogenesis of PBC, a process that is to be inhibited by RhuDex® treatment.
About Rheumatoid Arthritis: Rheumatoid arthritis is the most common inflammatory arthropathy worldwide. More than 0.5 - 1% of the world's population is affected by this chronic disease, which leads to pain, deformity, restricted mobility, and often stiffening of the joints. The body's own connective tissue (e.g., articular cartilage) is attacked and damaged by the individual's immune system. For this reason, rheumatoid arthritis is considered to be an autoimmune disease.
Medigene AG is a publicly listed (Frankfurt: MDG, prime standard) biotechnology company headquartered in Martinsried/Munich, Germany. Medigene focuses on clinical research and development of novel drugs against cancer and autoimmune diseases. Medigene is the first German biotech company to have revenues from marketed products, which are distributed by partner companies. It has two drug candidates in clinical trials and is developing an innovative vaccine technology. For more information, please visit www.medigene.com.
Here is a news release of a similar deal Quotient Clinical signed in 2011 with Medigene, a German pharmaceutical company:
Quotient Announces New RapidFACT Program With MediGene
http://www.lifescienceleader.com/doc/quotient-announces-new-rapidfact-program-with-medigene-0001
June 24, 2011
Quotient Clinical, a business unit of Quotient Bioresearch (Quotient), today announced an agreement with MediGene AG (MediGene), the German biotechnology company, to undertake a RapidFACT™ formulation development and clinical testing program on RhuDex®, subject to ethical and Medicines and Healthcare products Regulatory Agency (MHRA) approval. Rhudex® is a new potential first-in-class treatment for rheumatoid arthritis and other inflammatory disorders.
Quotient Clinical’s RapidFACT service exploits its tightly integrated GMP manufacturing and clinical testing processes and facilities to enable the rapid clinical evaluation of new drug formulations. Compared to conventional development processes, RapidFACT enables shortening of project timelines, and a reduction of ~90 per cent in API consumption, which combine to deliver significant cost savings. MediGene will use the drug formulation selected in this program as the basis for the further clinical development of RhuDex®.
Mark Egerton, MD Quotient Clinical, commented: “We are delighted to be working with MediGene to advance RhuDex® to the next stage of clinical development. RhuDex® targets a novel mechanism and has the potential to become a new first-in-class therapy for rheumatoid arthritis. RapidFACT has now been employed across a wide selection of development projects, and we have secured strong data to validate the time and cost savings benefits that can be delivered to development project teams”.
For more information on Quotient Clinical, please call UK +44 (0)115 974 9000, USA – 1-800-769-3518, email clinical@quotientbioresearch.com or visit www.quotientbioresearch.com/clinical.
About Quotient Clinical
Quotient Clinical is a leading provider of early development services. Its Translational Pharmaceutics™ platform offers a unique and streamlined process to reduce the time from First-in-Human studies to Proof-of-Concept by integrating flexible drug product manufacture into clinical trials.
Drug product formulations can be efficiently optimised for downstream development using the RapidFACT™ service (Rapid Formulation development And Clinical Testing) in a process that significantly shortens timelines and saves significant money.
14C clinical studies can be provided as a fully integrated service using the flexible Synthesis-to-Clinic™ platform. Synthesis-to-Clinic enables all the processes involving 14C drug products, from synthesis of the 14C labelled drug molecule through to conduct of human clinical trials, to be undertaken with a single vendor and a single project manager throughout, delivering significant time and cost savings.
With a strong customer base across the United States, Europe and Japan, the goal of Quotient Clinical is to provide a unique and comprehensive range of early development services to pharmaceutical and biotechnology customers.
Quotient Clinical is a business unit of Quotient Bioresearch.
About Quotient Bioresearch
Quotient Bioresearch is a leading provider of early stage and specialist drug development services to pharmaceutical, biotechnology and medical device clients worldwide. The company offers a unique range of drug development service through its three business units – Chemistry and Metabolism, Bioanalytical Sciences and Clinical. Quotient has grown rapidly in the past three years through a combination of both acquisition-led and organic growth.
For further information: www.quotientbioresearch.com
About MediGene
MediGene AG is a publicly listed (Frankfurt: MDG, prime standard) biotechnology company headquartered in Martinsried/Munich, Germany. MediGene is the first German biotech company to have revenues from marketed drugs. It has various drug candidates in clinical development and possesses innovative platform technologies. MediGene focuses on clinical research and development of novel drugs against cancer and autoimmune diseases.
Here is a 2010 article from the CEO of Quotient Clinical, RCPI's new contractor:
February 9, 2010
Using Translational Pharmaceutics To Enhance Drug Development
http://www.lifescienceleader.com/doc/using-translational-pharmaceutics-to-enhance-drug-development-0001
By Mark Egerton
An effective drug product must deliver a new chemical entity (NCE) to the right place, at the right time, at the right concentration, for its beneficial effect to be expressed. The goal of the early development team is to deliver a drug candidate that is suitable for full commercial development, where nomination of the candidate is supported by a data package demonstrating some proof of safety and tolerability and proof of efficacy — albeit in a relatively small number of subjects. The project team must also recommend a drug product (e.g. formulation, dose strength) that will become the medicine that is available in the marketplace. For oral medicines, the competitive nature of the pharmaceutical industry inevitably means that a once or twice daily dosing regimen is key to success.
Oral drug products used in FIH (first in human) studies are often relatively simple (e.g. API in solution, suspension, or capsule). In most early development projects, the NCE must be transitioned into a more suitable form (e.g. formulated API in capsule or tablet) that can deliver reliable and reproducible exposure to enable the proof-of-concept study and subsequent progression into later development. NCEs currently emerging from the industry’s R&D pipeline, however, are often characterized with poor solubility and permeability, presenting significant challenges to optimization.
Conventional approaches to optimizing a drug product typically focus on a range of in vitro formulation systems which are screened in one or more preclinical in vivo models prior to selecting a small number of lead prototypes for testing in humans. The industry’s perseverance with this approach is surprising given its limitations. Translation of bioavailability between preclinical species and humans is poor, and the process is linear and “rigid” such that, if the formulations tested in the clinic fail to meet the target criteria, the project must retrench to the in vitro/preclinical phase. Since one cycle of this process can take up to 18 months and cost more than $1.5 million, the time and financial penalties on the development project are significant.
A NEW PARADIGM
Translational pharmaceutics offers a new development paradigm in which the screening and selection of candidate drug products is driven on the basis of human data. A technology platform that integrates formulation development, GMP drug product manufacturing, and clinical testing enables drug products to be manufactured and dosed in a clinical study within time frames as short as 24 hours. Furthermore, the clinical data obtained from one candidate drug product can inform the real-time manufacture and dosing of the next candidate within a 10- to 14-day cycle time.
The ability to respond to human data is maintained by the use of flexible clinical protocols and the incorporation of “design space” concepts into regulatory submissions, which secure preapproval to test a range of variable formulation compositions (as opposed to discrete predefined systems). There is no requirement for any in vivo preclinical screening of formulations. This innovative strategy ensures that all selection decisions are based upon human data, increasing the chances of success and the precision of the drug product that is finally selected.
Performance metrics from projects undertaken to date demonstrate that the time required to deliver an optimized drug product can be, at least, halved compared with the conventional process. The quantity of API consumed in this process is also reduced by 90% to 95% — delivering another significant benefit to the development project. Since this approach can be applied to all types of oral dosage forms, including solutions/suspension and solids, immediate release, and modified release, and can encompass all types of formulation technology, we anticipate that translational pharmaceutics will deliver a broad impact on overall development efficiency of oral medicines.
Dr. Mark Egerton is CEO of Quotient Clinical and has more than 20 years of experience in the pharma and biotech industries. He has worked in a range of organizations from large multinational pharma companies to private venture-funded biotech firms. He has a Ph.D. in biochemistry, and he began his pharmaceutical R&D career at Sandoz (now Novartis) in Switzerland and then Zeneca (now AstraZeneca) in the UK.
Another (older) story offering a little insight into the relationship between TRGT and RJ Reynolds:
Big Pharma's new drug has a twisted history
By Dr. Allan Spreen on 11/09/2011
What's the difference between Big Pharma and Big Tobacco?
Not much, if you ask me.
They have the same repugnant ethical standards. They both get away with murder. And as of late, they even share the same research lab. I call it the kill-two-humans-with-one-stone strategy. And I wish I were joking.
Here's how it all began...
Big Pharma and Big Tobacco share the same bed
You see, back in the 1950s U.S. researchers began testing on a high blood pressure drug called mecamylamine. The drug didn't do much to lower blood pressure. So what the heck, they gave it to children with Tourette's syndrome.
(Don't ask me why they gave it to kids with Tourette's.)
Of course, mecamylamine didn't help the Tourette's symptoms. But researchers did notice that the children who took mecamylamine had a slight improvement in their depression symptoms.
Now, jump forward to the mid-1980s. (This is where Big Pharma comes in.)
In the mid-1980s, R.J. Reynolds Tobacco Company spent lots of money to develop "safer" cigarettes. A man named Donald deBethizy ran the R&D department. Specifically, he oversaw research into the effects of nicotine on the body.
Over many years, RJR scientists learned a lot about the body's nicotine receptors. For instance, when your body's nicotinic receptors get over stimulated, you're prone to depression.
The RJR scientists started tinkering with other compounds that could affect nicotinic receptors. They wanted to find something that would give you all the benefits of nicotine (such as increased alertness) without the negative effects of cigarettes.
That's when RJR researchers stumbled across the hypertension drug from the 1950s. That drug, the researchers discovered, relaxes your brain's nicotinic receptors. Because of this, they believed they had a new depression blockbuster on their hands.
The RJR scientists started to pour all their energies into mecamylamine research. They soon spun off from RJR to form a subsidiary called Targacept. And in 2000, they broke off entirely from Big Tobacco with $30.4 million in venture capitol money.
And guess what Targacept is now developing?
Yes, they gave up on the "safe" cigarettes. Now, they're in the "safe" drug business. They acquired the rights to mecamylamine and its name. Now, they call it TC-5214.
In fact...
TC-5214 already made it through some early-phase clinical trials. As a result, stock prices for Targacept more than tripled in value at one point.
At this stage in the game, Targacept's future depends on the performance of TC-5214 in five late-stage clinical trials. If it does well, experts expect Targacept's stocks to skyrocket by 100 to 200 percent. In addition, you can pretty much guarantee the FDA will approve TC-5214 for depression.
Why TC-5214 should really scare you
Without a doubt, TC-5214 has a checkered history at best. But you want to know what should really scare you the most about this new drug?
It could be about as dangerous as they come.
You see, most new depression drugs on the market increase serotonin. But TC-5214 is different. It works just like the old high blood pressure from the 1950s. It modulates nicotinic receptors.
And guess which other drug on the market works this way too?
(I'll give you a clue...it's only potentially one of the most dangerous drugs on the market today! And no, that's not just me being paranoid again. Even TIME magazine lists this as the #1 prescription drug linked to violence on the market. And it works in a similar way to TC-5214.)
TC-5214 targets the same receptors as dangerous drug
If you hadn't already guessed, TC-5214 works just like Chantix (the smoking cessation drug). They both target your body's nicotinic receptors. Specifically, both drugs curb the activity of a chemical messenger called acetylcholine in the brain.
Ah, but the trustworthy developers (remember them!?) say TC-5214 is much safer than Chantix.
Yeah, riiiight. I believe that.
Research links Chantix to increased risk for violence, heart attack, and suicidal thoughts. I expect TC-5214 will run into the same problems.
Nevertheless, AstraZeneca jumped on board with Targacept in 2009. They will pay as much as $1.24 billion for the rights to TC-5214 if it passes snuff.
(Excuse the pun.)
Unfortunately, I think it will and someday soon, you'll see Chantix's evil twin on the shelves as an anti-depressant.
Targacept plans to announce the results of the phase III trial by the end of the year. I'll keep you posted on the results.
Nationally acclaimed as America’s “Nutrition Physician,” Dr. Spreen has been helping people stay healthy and disease-free as a private doctor, published author, and noted researcher.
In addition to his role as a Senior Member of the prestigious Health Sciences Institute Advisory Panel in Baltimore, MD, Dr. Spreen also coaches diving at the international and Olympic levels. NorthStar Nutritionals is proud to have Dr. Spreen as our Chief Research Advisor.
Dr. Spreen also writes the Guide to Good Health.
Here is the story from a couple weeks ago involving TRGT cancelling their mid-stage AD study:
Targacept ends Alzheimer's drug trial after mid-stage failure
Reuters
http://finance.yahoo.com/news/targacept-ends-alzheimers-drug-trial-204039165.html
July 14 (Reuters) - Targacept Inc said it was ending a mid-stage trial on its Alzheimer's drug as it did not show superiority over standard medication, sending its shares down as much as 19.8 percent.
The drug, TC-1734, which was being tested against Pfizer Inc's donepezil, had earlier failed another mid-stage trial conducted by partner AstraZeneca Plc.
"Based on (today's) results, we do not intend to invest in further development of TC-1734," Targacept Chief Executive Stephen Hill said.
UK-based AstraZeneca returned rights to the drug in March but the companies continue to co-develop another Alzheimer's drug, AZD1446.
The latest failure marks another setback to Targacept's already thinning pipeline. In September, the company discontinued the development of its schizophrenia drug, TC-5619 after it failed a mid-stage study.
(Reporting By Amrutha Penumudi; Editing by Don Sebastian)
Rock Creek needs capital, and Targacept (trgt) needs a drug. These two struggling companies have what the other needs: Rock Creek has an arguably promising compound, and Targacept has almost $100 million in cash. Targacept too, was born from tobacco (RJ Reynolds), as their novel drugs also target the nicotinic receptors. Here is their latest failure:
Press Release
http://www.targacept.com/newsroom/index.cfm?nid=Targacept%20to%20Discontinue%20TC-5214%20Overactive%20Bladder%20Program&newsyear=2014
Targacept to Discontinue TC-5214 Overactive Bladder Program
July 28, 2014
Targacept, Inc. (NASDAQ: TRGT), a clinical-stage biopharmaceutical company advancing NNR Therapeutics™, today announced top-line results from a Phase 2b clinical trial of TC-5214 as a treatment for overactive bladder (OAB). In the trial, the high dose of TC-5214 demonstrated mixed results on the co-primary endpoints by providing a statistically significant reduction in micturition frequency (p=0.033) and an improvement that did not reach statistical significance on episodes of urinary incontinence (p=0.379) per 24 hours, after 12 weeks of treatment. As a consequence of these results, Targacept is discontinuing further development of TC-5214 in OAB.
In this trial, TC-5214 was considered generally safe and well tolerated. However, there was a placebo corrected 15.1% rate of constipation and a 5.9% rate of urinary tract infection in the high dose group. Analyses of the full dataset from the trial are ongoing and Targacept plans to publish more detailed results.
“Although TC-5214 provided dose-dependent efficacy on several endpoints during the course of treatment, the results were not compelling enough to justify the compound’s continued development in overactive bladder,” said Dr. Stephen A. Hill, Targacept’s President and Chief Executive Officer. “Assessing these results together with our previous clinical trial outcomes, including data from our most recent trials in schizophrenia and Alzheimer’s disease, it is clear that modulation of nicotinic receptors can result in biological effects. However, these effects do not appear to predict new treatments with a meaningful improvement over the current standard of care for the indications studied. Targacept would like to thank the many patients, investigators, study site personnel and operational team members who contributed to making this a well-executed trial.”
Dr. Hill continued, “As part of our scenario planning over the past twelve months, we have considered a broad range of options for the optimal use of our resources, including the pursuit of non-nicotinic opportunities. In the coming months, Targacept will be continuing to carefully evaluate those portfolio options that we believe have the potential both to make a significant difference in patients’ lives and provide meaningful upside for our stakeholders. We will be holding a conference call in conjunction with our quarterly earnings release on August 6, 2014.”
About the Trial
The Phase 2b study was a double blind, placebo controlled, randomized, parallel group trial conducted at 119 sites in the United States and involved 768 randomized patients with OAB. The study’s co-primary endpoints were change in micturition frequency per 24 hours and change in urinary incontinence episodes per 24 hours, in each case from baseline to 12 weeks. The trial included a three- or five-week screening period, followed by a 12-week treatment period during which patients received either one of three doses of TC-5214 (0.5mg, 1mg or 2mg) or placebo twice daily, randomized in a ratio of 2:1:1:1 (placebo, low dose, mid dose, high dose), with a two-week follow-up period.
About Targacept
Targacept is dedicated to building health and restoring independence for patients. For more information, please visit www.targacept.com.
Forward-Looking Statements
This press release includes “forward-looking statements” made under the provisions of the Private Securities Litigation Reform Act of 1995. Forward-looking statements include statements, other than statements of historical fact, regarding without limitation: Targacept’s plans, expectations or future operations, financial position, revenues, costs or expenses. Actual results, performance or experience may differ materially from those expressed or implied by any forward-looking statement as a result of various important factors. Risks and uncertainties that Targacept faces are described in greater detail under the heading “Risk Factors” in Targacept’s most recent Annual Report on Form 10-K and in other filings that it makes with the Securities and Exchange Commission. As a result of the risks and uncertainties, the results or events indicated by the forward-looking statements may not occur. Targacept cautions you not to place undue reliance on any forward-looking statement.
In addition, any forward-looking statement in this press release represents Targacept’s views only as of the date of this press release and should not be relied upon as representing its views as of any subsequent date. Targacept disclaims any obligation to update any forward-looking statement, except as required by applicable law.
NNR Therapeutics™ and Building Health, Restoring Independence® are trademarks or service marks of Targacept, Inc. Any other service marks, trademarks and trade names appearing in this press release are the properties of their respective owners.
Contact:
Alan Musso, SVP, Finance and Administration and CFO
Targacept, Inc.
Telephone: 336.480.2186
Email: alan.musso@targacept.com
My reply was mostly in jest -- a topical segue if you will -- but I guess it hit a nerve. You make some good points Dino, however, there is an inherent contradiction in your statement, as well as other facets you did not consider.
Mark Cuban is an influential billionare, and his views are a direct representation of himself as a shareholder. So, if he is, or is interested in becoming a shareholder in a company using or considering these tax loopholes, your own words indicate a company should more deeply consider moving offshore.
The other layer that should not be ignored, is a company's loyalty and support to their employees. These are the individuals that allow a company to prosper, or not. They must be careful not to alienate them. So perhaps the off-shore nonsense is short-term thinking, and closing of these loopholes would render all that transitioning a foolish waste of time and resources. The inversion approach is nothing but a fancy scheme, a clever tactic, which was conceived by the politicians with their own personal gain in mind (with the help of these industry/corporate lobbies, no doubt).
Let's face it, the middle-class is being exploited and diminished, while the income disparity between the grossly rich and everyone else grows. These corporate maneuvers have a lot to do with this phenomenon.
You answered your own question.
Inflammation in Midlife May Presage Cognitive Decline
http://www.alzforum.org/news/research-news/inflammation-midlife-may-presage-cognitive-decline
11 Jul 2014
Neuroinflammation goes hand in hand with dementia, but it remains unclear which comes first. Epidemiologic research reported in the July 2 Neurology now links elevated peripheral cytokines in midlife to later cognitive decline, strengthening the case that inflammation may contribute to neurodegeneration. Researchers led by Archana Singh-Manoux at INSERM, Paris, retrospectively analyzed data from more than 5,200 cognitively healthy participants in a longitudinal study, and found that those with the highest plasma levels of the inflammatory protein IL-6 had the lowest cognitive scores at baseline and also experienced the steepest drop in mental abilities over the next 10 years. Although the effect size was modest, it nonetheless accelerated age-related cognitive decline by about four years, the authors calculated.
Holly Soares at Bristol-Myers Squibb, Wallingford, New Jersey, called the data intriguing. “It is consistent with the literature showing there are blood-based signatures that flag people who are progressing to dementia. The next step would be a prospective study to see how robust this finding is,” she told Alzforum. Soares was not involved in the research.
In elderly populations, high plasma levels of several inflammatory proteins associate with an increased risk of developing Alzheimer’s disease or vascular dementia (see, e.g., Engelhart et al., 2004; Tan et al., 2007). Few studies have looked at midlife, however, leaving it unclear whether inflammation represents a cause of dementia or merely an early symptom. A Dutch study hinted at the former, reporting that middle-aged children of AD patients, who have higher risk for the disease, had elevated levels of several cytokines (see van Exel et al., 2009).
To look more closely at middle-aged populations, Singh-Manoux and colleagues turned to the U.K. Whitehall II study. Participants were former London office workers, predominantly white, male, and well-educated, with an average age of 56 at baseline. The authors focused on two inflammatory proteins that have been consistently linked to dementia risk: the cytokine interleukin-6 (IL-6) and C-reactive protein (CRP), which is released by the liver in response to inflammation. The authors averaged plasma levels from two measurements taken a few years apart to arrive at baseline values, thus lessening the effect of any aberrant readings from temporary challenges to the immune system, such as infections. At baseline, participants at the highest third of IL-6 levels scored modestly worse on tests of reasoning and verbal fluency. Although the difference only amounted to approximately one-tenth of the baseline standard deviation in this population, it equaled an acceleration in age-related cognitive decline of about two years, the authors claim.
Over the next 10 years, the cognitive performance of all participants dropped by about one-third of the baseline standard deviation. Those with the highest IL-6 again fared worse than their peers in reasoning tests, with their losses corresponding to an additional two years of cognitive aging, for a total difference of four years. In addition, this group was almost twice as likely as peers to experience a drop of three points or more on the Mini-Mental Status Examination. However, people with high IL-6 did fine on short-term memory tests. Because speech and reasoning problems commonly occur in vascular dementia, whereas memory loss better characterizes AD, the data support other studies that have linked inflammatory markers more strongly to vascular dementia than AD, the authors note (see Schmidt et al., 2002; Sundelöf et al., 2009).
Although participants with high CRP levels showed a trend toward lower baseline cognition and faster decline, it was not significant after adjusting for confounding factors such as age, sex, and education. In an accompanying editorial, Mario Di Napoli at San Camillo de Lellis General Hospital, Rieti, Italy, and Jeremy Silverman at Icahn School of Medicine, Mount Sinai, New York, point out that IL-6 directly affects processes such as lipid metabolism that might contribute to cognitive decline, whereas CRP is activated downstream of IL-6 and thus may not become a factor until later in life. Some neuroimaging studies show that IL-6 associates more closely with brain volume loss than does CRP (see Jefferson et al., 2007; Fornage et al., 2008; Satizabal et al., 2012).
Commentators agreed that more research is needed to tease out the effect inflammation might have on the brain. Soares wondered whether these markers associate specifically with dementia, or rather might be general risk factors for many neurodegenerative diseases. Sid O’Bryant at the University of North Texas Health Science Center, Fort Worth, noted that he would like to see a follow-up study looking at a panel of inflammatory markers. Researchers also noted that because plasma cytokine levels fluctuate greatly, these molecules probably would be poor biomarkers. “Measurement of IL-6 in midlife is highly unlikely to be useful in clinical practice on an individual level,” Di Napoli and Silverman concluded.—Madolyn Bowman Rogers
Heart-Healthy Fatty Acids May Stave Off ALS
http://www.alzforum.org/news/research-news/heart-healthy-fatty-acids-may-stave-als
18 Jul 2014
The benefit to cardiovascular health offers one reason to chow down on foods loaded with omega-3 fatty acids. A paper in the July 14 JAMA Neurology online adds another: The same chemicals pare down a person’s risk of developing amyotrophic lateral sclerosis. Researchers at the Harvard School of Public Health determined that among a massive sample of one million people, those who ate the most omega-3-rich foods—such as salmon, flaxseed, and walnuts—had two-thirds the risk of developing ALS later on than those who ate the least. This retrospective, observational study cannot determine cause and effect, cautioned first author Kathryn Fitzgerald. She suspects that these unsaturated fatty acids, which form part of cell membranes in the brain, could protect neurons against oxidative stress or inflammation.
“The result is persuasive and consistent with earlier studies,” commented Michael Swash of the Royal London Hospital in an editorial accompanying the publication (Veldink et al., 2007; Okamoto et al., 2007). Unlike that previous work, which examined people’s diets after they were diagnosed with ALS, the current study analyzed data collected before any subject came down with the disease.
Despite finding that diet helps, eating more omega-3s would be unlikely to make much difference for people at high risk for ALS due to familial mutations, said Joseph Quinn of the Oregon Health and Science University in Portland, who was not involved in the study. Anne-Marie Wills of Massachusetts General Hospital in Boston suggested that since the incidence of ALS is so low compared with cardiovascular disease, healthy people should focus more on eating a heart-healthy diet (see full comment below).
Alzheimer’s researchers have been researching these fats for a long time. In a randomized, placebo-controlled clinical trial, introducing omega-3 fatty acids after diagnosis failed to improve symptoms in people Alzheimer’s disease (see Nov 2010 news story), and this "should make us skeptical about using omega-3 fatty acids to treat ALS," Wills said. Quinn said the picture for AD prevention remains incomplete. One study found people who dined on fish weekly were less likely to develop Alzheimer’s (see Jul 2003 news story).
Because inflammation and oxidative stress have been implicated in ALS, Fitzgerald, senior author Alberto Ascherio, and colleagues suspected that omega-3s might do some good. Fortunately, the data to answer their question was available. They obtained dietary and disease information from five longitudinal, prospective studies: the National Institutes of Health-American Association of Retired Persons Diet and Health Study, the Cancer Prevention Study II Nutrition Cohort, the Health Professionals Follow-Up Study, the Multiethnic Cohort Study, and the Nurses’ Health Study. Together, these cohorts included more than one million participants. Of those, nearly 1,000 developed ALS over the data collection periods of eight to 24 years, depending on the cohort.
The studies provided Fitzgerald with data on omega-3 fatty acid intake, based on food questionnaires the subjects filled out. She divided the participants into five quintiles, from those who savored the most omega-3s to those who ate the least. Those in the highest quintile had a 34 percent lower risk of developing ALS than those in the lowest. Intake of other kinds of fats did not influence ALS risk. While a thin physique has been associated with ALS (see May 2011 news story and O’Reilly et al., 2013), Fitzgerald found the omega-3 benefit held true even if she controlled for body mass index.
Mouse studies would be the obvious next step, Quinn said, and in fact one such experiment has already been done. Researchers attempted to treat ALS model mice with omega-3 fatty acids and found the disease course sped up, instead of slowing down (Yip et al., 2013). That might be because the researchers used seafood-derived fatty acids, while Fitzgerald observed plant-made versions were most beneficial, Wills speculated.
“This big-data study suggests that at least 20 percent of the U.S. population may be at risk for ALS due to inadequate omega-3 intake … It seems doubtful that any protection involves an ALS-specific mechanism, but more likely a general neuroprotective or anti-inflammatory mechanism,” Greg Cole of the University of California, Los Angeles, commented in an email to Alzforum. Cole was not part of the study group, but he has studied the role of such fatty acids in AD. “The study lacks measurement of blood levels of omega-3 but dietary questionnaires are reasonably well-validated,” he said. Fitzgerald said she hopes to examine how blood biomarkers for fatty acids correlate to ALS incidence in a follow-up study. Wills said that proving the fatty acid benefit experimentally would be difficult. “Unfortunately, deciding whether it would be helpful to increase [omega-3 fatty acid] intake if you carry an ALS mutation would require a very large and long clinical trial,” she wrote.—Amber Dance.
The request was not a search for answers, but rather, an appeal for discussion. None of us know what the hold-up is, possibly including mgmt.
The depth of discussion on each new company event would correlate directly to the level and breadth of expertise and knowledge present among the participants of this board. Unfortunately, this board appears to lack that level of sophistication. While I do not myself embody a high degree of knowledge regarding biotech operations or the FDA, I: do have some experience as an investor; am opened-minded to logical possibilities; and, can discern that quality in other posters who are gracious enough to share their insight without bias or an ulterior motive. I also can admit when I'm wrong (eventually,lol).
As far as the Friday-night-under-the-rug sweeping, it definitely is not good news. It doesn't take much common sense or experience to understand that. However, I don't think it is game-changing either. It isn't a safety issue for sure. My guess is that it has something to do with what I mentioned here (#msg-100362488):
You can't have bias without 'BS'. Nice to here an objective analysis from you as it relates to good ole Cortex. There truly is a first for everything. Good luck in your future endeavours--as long as they are rooted in clear-headed fairness.
Thank you, ohibbs, for your straightforward and thorough reply. I'll respond in more detail when I'm not trying to type on a stupid smartphone.
Uncertainty courtesy of the FDA, and a tactical trick by announcing Friday after hours. Welcome to biotech.
Any idea what the FDA is expecting from STSI, Anatabloc the supplement, or anatabine the drug?
Inflammasomes Spread from Cell to Cell
http://www.alzforum.org/news/research-news/inflammasomes-spread-cell-cell
30 Jun 2014
Scientists may have discovered a new immune signaling mechanism. Back-to-back papers in the June 22 Nature Immunology report that inflammasomes, multiprotein complexes previously thought to be strictly intracellular, function outside the cell. Two independent groups of scientists, one led by Pablo Pelegrín, Clinical University Hospital Virgen de la Arrixaca, Murcia, Spain, the other led by Eicke Latz, University of Bonn, Germany, found that activating inflammasomes caused their release from macrophages, whereupon they continued to provoke inflammation in the extracellular milieu. Furthermore, when engulfed by neighboring macrophages, these particles triggered an inflammatory cascade in those cells.
“Now we can broaden the inflammasome repertoire to include acting as extracellular signals," Pelegrín told Alzforum. Scientists debate how important these new mechanisms are for health and disease. Given that Aß has been shown to activate inflammasomes (see Dec 2012 news story), the findings might be relevant for Alzheimer's and potentially other neurodegenerative disorders.
Go Forth and Multiply.
Inflammasome specks (green) move from inside (asterisk) the cell (red) near the nucleus (blue), to the edge (arrow), then to the outside (arrowhead), where they instigate more inflammation. Image courtesy of Baroja-Mazo et al. Nature Immunology.
Found in myeloid immune cells such as macrophages and brain glia, inflammasomes comprise complexes of proteins activated by a variety of extracellular signals to cause inflammation (for a review, see Schroder and Tschopp, 2010). The best-studied inflammasome is called nod-like receptor (NLR) family, pyrin domain-containing 3 type inflammasome, or NLRP3. When it senses a problem, such as reactive oxygen species or Aß, NLRP3 oligomerizes and triggers assembly of a protein complex that goes by the long-winded name of apoptosis-associated speck-like protein containing a caspase-recruitment domain, or ASC. ASC bundles, called ASC specks, convert immature caspase-1 to its mature form, which in turn activates inflammatory interleukins IL-1ß and IL-18. These then stream from the cell to attract neutrophils and monocytes. This process causes inflammatory-related cell death, called pyroptosis.
Both groups noticed inflammasome material in the extracellular space and wondered if it might play additional roles there.
Pelegrín, with co-first authors Alberto Baroja-Mazo and Fatima Martín-Sánchez, found that macrophages taken from mouse bone marrow spewed NLRP3 and ASC complexes into the extracellular space within 10 to 30 minutes of activation (see image above). Once outside, these particles processed and activated pro-caspase-1 and pro-IL-1ß, which had also been released from the macrophage. These ASC specks were taken up by nearby macrophages, which then activated their own caspase-1, triggering release of more IL-1ß. This whole process seemed to work in vivo, too. When injected into the peritoneum of wild-type mice, ASC specks raised the amount of extracellular IL-1ß found there and recruited more white blood cells to the injection site.
Pelegrín’s group examined this process with various mutant forms of NLRP3. Some of these mutations have been linked to cryopyrin-associated periodic syndromes (CAPS), a type of autoinflammatory disorder. In cells with the D303N substitution, NLRP3 spontaneously aggregated. Outside the cells, this mutation caused ASCs to oligomerize into specks, which macrophages then engulfed, perpetuating an inflammatory cascade.
Latz and colleagues found something very similar. Using fluorescent antibody staining, first author Bernardo Franklin saw that after pyroptosis, ASC specks built up outside human monocytes. The ASC specks recruited and activated both caspase-1 and IL-1ß in the extracellular space. Macrophages then ingested these specks, causing their lysosomes to swell and leak, activating their own inflammasomes and causing endogenous ASC to aggregate, forming more specks. The researchers likened this cell-to-cell spread of ASC specks to the “seeding” activity of prion-like proteins.
To check for a similar process in vivo, Latz and his group injected fluorescently labeled ASC specks into the skin of mice and watched for the recruitment of neutrophils. Compared to plain fluorescent beads, the ASC specks attracted more of the immune cells, suggesting they caused the release of more IL-1ß, which attracts neutrophils. Injecting Pseudomonas bacteria into the mice’s footpads also promoted the appearance of ASC specks outside cells.
Could these findings be relevant to human disease? Pelegrín found that ASC specks were more abundant in the serum of people diagnosed with CAPS than in serum from healthy controls. Similarly, Latz’s group found extracellular ASC specks accumulating in the lungs of patients with chronic obstructive pulmonary disease, an inflammatory lung disorder that might be related to inflammasomes.
It is unclear what these findings mean for neurodegenerative diseases, said Pelegrín. He is studying how this process could relate to AD and related disorders by using animal models. Latz plans to do the same. Charles Dinarello, University of Colorado School of Medicine, Aurora, thinks this process could occur in the brain where it may contribute to Alzheimer’s and other neurodegenerative disorders. Seth Masters, Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia, believes this process could provide a drug target. “Therapies could be designed to shut down this amplification of inflammation,” he wrote in an email.
Dave Morgan, University of South Florida, Tampa, was less convinced that extracellular specks contribute to neurodegenerative diseases. While there is some evidence that Aß activates inflammasomes, Morgan doubts it is enough to generate ASC specks. “I suspect that activation of ASC specks is too severe to be a major participant in slow, progressive neurodegenerative diseases,” he said. On the other hand, it could be part of the secondary damage that follows stroke or severe brain trauma. In general, this is likely another way that the immune system cranks up its positive feedback system, and a possible target for therapeutic intervention for some forms of inflammation, Morgan said.
How is this process quenched after immune cells have successfully neutralized a threat? Pelegrín is studying that now.—Gwyneth Dickey Zakaib
It's also about $1.5m, which, for them, is a paltry amount.
I don't understand your reaction.
Stay tuned for the future unveiling of the alternative meaning of MoA...
Slide 14 would fall into the category of "pretty pictures". I have no idea what they are trying to convey with that one, other than describing the activity of different receptors within the cell membrane. My original point was to clarify the target audience of the presentation, which given the title of the file, is a no-brainer.
In-licensing not boilerplate? lol.
Without money to get very far with their own candidate in myriad indications, how likely is it that they buy rights to another drug at an affordable price with a high possibility of success?
So...are they just going to stack the molecules on each other and compress them?
Sure...that's the lifeblood of microcap biotech.
Systemic inflammation has negative effects on cognitive function in populations with dementia
(Note:This comes from the Nilvad Newsletter, an online publication monitoring the progress of Archer's Ph3 drug for Alzheimer's disease)
http://nilvad.newsweaver.com/InternalStudyNewsletter/18cfzm3khsf?a=1&p=34834365&t=21611585
by Colm Cunningham,
Delirium Basic Research Group, Trinity College Dublin colm.cunningham@tcd.ie
Colm Cunningham is a Wellcome Trust Senior Research Fellow in Neuroscience, with a strong interest in neuroinflammation. Research in his laboratory, in the Trinity College institute of Neuroscience, Trinity College Dublin, is dedicated to the development of animal models with which to study delirium during dementia and to examine its long-term consequences.
Delirium is a profound and serious acute neuropsychiatric syndrome that is especially prevalent in the elderly and demented population and is frequently triggered by acute systemic inflammation. It is now clear that delirium can accelerate cognitive decline in Alzheimer’s disease (Fong et al., 2009) and increases the risk for dementia generally (Davis et al., 2012). Over the last several years Dr Cunningham’s work, and that of collaborators and others in the field, has demonstrated that systemic inflammation has negative consequences for those with prior neurodegenerative disease. He has used animal models to show that a single systemic challenge with bacterial endotoxin can produce acute cognitive dysfunction, mimicking aspects of delirium, as well as driving progression of underlying disease (Cunningham, 2011). Among the key findings in this work is the observation that microglia (brain macrophages) are “primed” by neurodegenerative pathology to produce exaggerated responses to subsequent inflammatory insults (Perry et al., 2007), which may help us to understand how systemic inflammatory events produce CNS inflammation that is selectively amplified in those areas with prior brain pathology. Collectively these studies suggest that systemic inflammation leads to acute cognitive changes including delirium, and that even upon recovery from this acute event, patients may not recover their original baseline cognitive function (figure 1).
Figure 1
The Cunningham group is currently interrogating the mechanisms by which systemic inflammation acutely disrupts cognitive function and contributes to disease progression and these studies have lead to multiple collaborations with clinical colleagues investigating the role of particular pro-inflammatory cytokines in the development of delirium and the progression of dementia (Holmes et al., 2009; MacLullich et al., 2011). There is now a strong motivation to monitor the impact of such inflammatory insults in the NILVAD trial. Since this large multicentre trial will monitor patients with evolving Alzheimer type dementia for a period of 18 months, it is likely that a large number of patients will develop inflammatory events such as infections, surgeries or falls/injuries during this period, and such events may be associated with the development of delirium or other cognitive changes. As such, the occurrence of such events may have a significant impact on study outcomes in drug- and placebo-treated patients and capturing information about these events will be important both for the interpretation of variability in efficacy of nilvadipine and for the examination of the impact of nilvadipine on the consequences of such inflammatory exacerbations. In collaboration with Dr. Sean Kennelly, medical scientific advisor to the NILVAD project, it is now proposed that we capture such events via the adverse events checklist, through carer-informed reports at each visit, in particular noting unscheduled primary care or hospital visits, need for antibiotics, injuries, falls and other relevant inflammation-related ‘adverse events’. Since blood samples, and to a lesser degree CSF samples, will be collected at 4 times during the course of treatment, there are opportunities to assess biomarkers of inflammation and we will seek to do this. Such biomarker studies would facilitate the examination of inflammatory mediator association with these reported adverse events and the investigation of their relationship to the progression of disease in these patients.
It is becoming clear that acute and chronic co-morbidities can have a significant impact on the trajectory of dementia and, as such, the frequency and severity of these events in placebo- and drug-treated cohorts may have important implications for the trial. Our continuing animal model mechanistic studies will allow us to provide new data on key inflammatory pathways and to inform biomarker analysis as the trial progresses.
References
Cunningham, C. (2011) Systemic inflammation and delirium: important co-factors in the progression of dementia. Biochem Soc Trans, 39, 945-953.
Davis, D.H., Muniz Terrera, G., Keage, H., Rahkonen, T., Oinas, M., Matthews, F.E., Cunningham, C., Polvikoski, T., Sulkava, R., MacLullich, A.M. & Brayne, C. (2012) Delirium is a strong risk factor for dementia in the oldest-old: a population-based cohort study. Brain, 135, 2809-2816.
Fong, T.G., Jones, R.N., Shi, P., Marcantonio, E.R., Yap, L., Rudolph, J.L., Yang, F.M., Kiely, D.K. & Inouye, S.K. (2009) Delirium accelerates cognitive decline in Alzheimer disease. Neurology, 72, 1570-1575.
Holmes, C., Cunningham, C., Zotova, E., Woolford, J., Dean, C., Kerr, S., Culliford, D. & Perry, V.H. (2009) Systemic inflammation and disease progression in Alzheimer's disease. Neurology, 73, 768-774.
MacLullich, A.M., Edelshain, B.T., Hall, R.J., de Vries, A., Howie, S.E., Pearson, A., Middleton, S.D., Gillies, F., Armstrong, I.R., White, T.O., Cunningham, C., de Rooij, S.E. & van Munster, B.C. (2011) Cerebrospinal Fluid Interleukin-8 Levels Are Higher in People with Hip Fracture with Perioperative Delirium Than in Controls. J Am Geriatr Soc, 59, 1151-1153.
Perry, V.H., Cunningham, C. & Holmes, C. (2007) Systemic infections and inflammation affect chronic neurodegeneration. Nat Rev Immunol, 7, 161-167.
That is all boilerplate stuff from biotech companies.
Aspirin Cuts Pancreatic Cancer Risk by Half, Study Finds
http://www.bloomberg.com/news/2014-06-26/aspirin-cuts-pancreatic-cancer-risk-by-half-study-finds.html?cmpid=yhoo
By Nicole Ostrow Jun 26, 2014 12:05 AM ET
Regular aspirin use cut the risk of pancreatic cancer by half, according to a finding that adds one of the most lethal malignancies to the list of diseases the inexpensive pill may help fight.
Men and women who took low-dose, about 75 to 325 milligrams, of aspirin daily, usually to prevent heart disease, had a 48 percent lower risk of pancreatic cancer, according to research published today in Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research. Taking aspirin regularly for a decade cut the risk by 60 percent.
Studies have found that regular aspirin use reduces the risk for colon, esophageal, lung and prostate cancers, and the pill is often prescribed to lessen heart attack and stroke risk. About one in 60 adults will develop pancreatic cancer, which has a five-year survival rate of less than 5 percent, so finding ways to prevent the disease is “crucial,” said senior study author Harvey Risch.
“If people are already using low-dose aspirin for cardiovascular disease prevention, they can feel good that most likely it’s lowering their risk for pancreatic cancer,” said Risch, a professor of epidemiology at Yale University in New Haven, Connecticut, in a June 25 telephone interview. “For people whose doctors have told them through studying their family history of cancer or having done genetic testing have identified that they are at higher risk for pancreatic cancer, then using aspirin might be beneficial as part of a plan to try to lower their risk.”
46,000 Cases
Pancreatic cancer is the 10th most-common malignancy in the U.S., in terms of new cases each year, but the fourth highest in terms of deaths, the researchers said. This year, more than 46,000 new cases of the disease will be diagnosed and almost 40,000 people in the U.S. will die, according to the National Cancer Institute.
Risch said it’s unclear how aspirin works to lower pancreatic cancer risk as researchers are unsure how the cancer evolves. He said it could be that aspirin reduces cancer risk by lowering inflammation.
Still, today’s results don’t mean people should start taking aspirin to prevent pancreatic cancer as the medicine has side effects like gastrointestinal bleeding, he said.
The study involved patients from 30 hospitals in Connecticut, including 362 people with pancreatic cancer and 690 people who didn’t have the disease.
They found that both daily use of low-dose aspirin and daily use of regular aspirin, defined as a dose exceeding 325 milligrams, reduced pancreatic cancer risk. The findings were stronger in those taking the lower dose, Risch said.
The study also found that the longer a person took aspirin, the greater the protection against pancreatic cancer.
To contact the reporter on this story: Nicole Ostrow in New York at nostrow1@bloomberg.net
To contact the editors responsible for this story: Reg Gale at rgale5@bloomberg.net Angela Zimm, Drew Armstrong