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Or maybe they have the China market in mind? China has a population of 1.4 billion people and their wealth to middle-class is estimated at around 500 million. Chinese are hypochondriacs so they spend money on their health, second only to their children. This, and maybe India could be a huge market for RCPI for their health supplement version (and drug version) of anatabine citrate. BTW, GNC has stores in China, Hong Kong, Macau, New Zeland, Australia, and Taiwan. Or maybe this is the 'proof' they need to claim it is an 'anti-inflammatory'. Previously the FDA said they could make no such claim. Too bad it has taken so long to get here.
Rock Creek Pharmaceuticals Reports Human Proof of Principle Study of Lead Compound Demonstrating Inhibition of Inflammatory Markers In White Blood Cells
Jul 1, 2015
News Release:
"SARASOTA, Fla., July 1, 2015 /PRNewswire/ -- Rock Creek Pharmaceuticals, Inc., (NASDAQ: RCPI), a drug development company focused on chronic inflammatory disease and neurologic disorders, announced today the results of a human proof of principle study with anatabine citrate, the Company's lead compound. Results from the study show that a single oral dose of anatabine citrate can significantly inhibit the activation of inflammatory proteins in the blood of human subjects. The Company is developing this compound in a Phase 1 clinical trial under a Medicines and Healthcare Products Regulatory Agency (MHRA) regulatory protocol in the United Kingdom.
Rock Creek Pharmaceuticals
New Zealand Study
In December of 2014, the Company received a New Zealand Ministry of Health Ethics Committee approval to conduct a single-site, single dose, open-label human study, entitled "Determination of the Blood Pharmacodynamic Effects following a Single Dose of Oral Anatabine Citrate in Normal, Healthy Volunteers."
The primary objective of the study was to determine whether a single dose of orally administered anatabine citrate could reduce the activation of inflammatory proteins in human white blood cells. Blood samples were taken from ten healthy human subjects, collected before and after oral administration of anatabine citrate. The blood samples were immediately challenged with lipopolysaccharide (LPS), a well-known potent stimulator of inflammation. The blood samples were then evaluated to measure the activation of two proteins, NF-kB and STAT3, which are known to be central to inflammation. The study compared the amount of LPS-induced activation of NF-kB and STAT3 in the white blood cells before and after the administration of anatabine citrate. Activated NF-kB and STAT3 protein levels were measured by two different, well-established molecular biology methods.
Data analysis showed that there were statistically significant (p<0.05) reductions in LPS stimulated levels of both NF-kB and STAT3 in human white blood cells after a single oral dose of anatabine citrate. These data are consistent with several peer reviewed scientific papers showing that anatabine can reduce NF-kB and STAT3 activation in animal models of inflammatory diseases, as well as in several human cell lines as shown by in vitro studies. Additionally, evaluation of safety data showed that anatabine citrate was well tolerated by the study participants and there were no safety concerns.
Ryan Lanier, PhD, Rock Creek Pharmaceuticals' Chief Scientific Officer remarked, "This is the first time that anatabine citrate taken orally by human subjects has been shown to oppose the activation of these known inflammatory proteins in white blood cells. The data are entirely consistent with our proposed mechanism of action of anatabine citrate which forms the basis for our advancement of this compound into clinical trials for human inflammatory diseases."
About Anatabine Citrate:
Rock Creek Pharmaceuticals' Anatabine Citrate is a small molecule, cholinergic agonist which exhibits anti-inflammatory pharmacological characteristics, distinct from other anti-inflammatory drugs available such as biologics, steroids and non-steroidal anti-inflammatories. The Company has sponsored extensive pre-clinical (in vitro and in vivo) studies resulting in peer reviewed and published scientific journal articles, covering models of Multiple Sclerosis, Alzheimer's Disease, and Auto-Immune Thyroiditis. All these studies demonstrated the anti-inflammatory effects of Anatabine Citrate. In addition, the Company's compilation of human exposure, safety and tolerability data, derived primarily from human clinical studies and post-marketing data collection of the previously marketed nutraceutical product, has provided important insights for clinical development.
About Rock Creek Pharmaceuticals, Inc.:
Rock Creek Pharmaceuticals, Inc. is an emerging drug development company focused on the discovery, development and commercialization of new drugs, formulations and compounds that provide therapies for chronic inflammatory disease, neurologic disorders and behavioral health.
For more information, visit: http://www.rockcreekpharmaceuticals.com
Forward Looking Statements:
Certain statements contained in this release constitute forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Such statements include, but are not limited to statements identified by words such as "believes," "expects," "anticipates," "estimates," "intends," "plans," "targets," "projects" and similar expressions. The statements in this release are based upon the current beliefs and expectations of our company's management and are subject to significant risks and uncertainties. Actual results may differ from those set forth in the forward-looking statements. Numerous factors could cause or contribute to such differences, including, but not limited to, failure to obtain sufficient capital resources to fund our development program and operations, results of clinical trials and/or other studies, the challenges inherent in new product development initiatives, including the continued development and approval of anti-inflammatory drug candidates, the effect of any competitive products, our ability to license and protect our intellectual property, our significant payables, our ability to raise additional capital in the future that is necessary to maintain our business, changes in government policy and/or regulation, potential litigation by or against us, any governmental review of our products or practices, pending litigation matters, as well as other risks discussed from time to time in our filings with the Securities and Exchange Commission, including, without limitation, our annual report on Form 10-K for the fiscal year ended December 31, 2014 filed on March 12, 2015. We undertake no duty to update any forward-looking statement or any information contained in this press release or in other public disclosures at any time.
CONTACT:
Stephanie Carrington
Investors
Integrated Corporate Relations, Inc. (ICR): Redefining Strategic Communications
685 Third Avenue, 2nd Floor,
New York, NY 10017
(646) 277-1282
stephanie.carrington@icrinc.com
Ted Jenkins
Vice President, Corporate Strategy and Development,
Rock Creek Pharmaceuticals
2040 Whitfield Avenue, Suite 300
Sarasota, FL 34243
Direct: 941-251-0488
tjenkins@rockcreekpharmaceuticals.com
Logo - http://photos.prnewswire.com/prnh/20150617/223737LOGO
SOURCE Rock Creek Pharmaceuticals, Inc."
Keystone Symposia-NF-kappaB and MAP Kinase Signaling in Inflammation, March 13-17,2016 (Molecular and Cellular Biology)
Topics:
NF-kappaB Signaling in Cancer
Regulation of the Ubiquitin System by Deubiquitylases and Phosphorylation
NF-kappaB Signaling in Immunity
Role of Ubiquitylation in Control of Autophagy
Ubiquitination-Dependent Modulation of NF-kappaB Signaling I (Joint)
Transcriptional Regulation in Inflammation
Large Machines
NLR Signaling to NF-kappaB and IRF
Ubiquitylation and Human Disease
MAP Kinase Signaling in Inflammation
Structural Analysis of E3 Ligases and DUBs
Therapeutic Targeting of Inflammation
Small Molecules and Therapeutics
Ubiquitin-Dependent Modulation of NF-kappaB Signaling II (Joint)
Meeting Wrap-Up: Outcomes and Future Directions
Draft agenda at:
http://www.keystonesymposia.org/16X4
Booming | The latest on preventing Alzheimer's in the Courier Journal, Anita Curpier, June 25, 2015
Excerpts:
"The immune system attacks structures that are altered in some way, changing their appearance and making it seem like they are a foreign invader. This occurs with atherosclerosis (clogging of the arteries with cholesterol and other debris), the underlying cause of the vast majority of heart attacks.
The process begins when cholesterol from LDL (the bad kind of cholesterol) finds its way into the arterial wall where it is altered. In response, white blood cells of the immune system known as macrophages invade the artery wall and start to gobble up the cholesterol. This causes a cascade of immune responses that attracts more macrophages to the area, resulting in inflammation and damage to the artery that over time reduces the diameter, interfering with blood flow.
Scientists believe that something similar may occur in the brain. Microglia, close relatives of macrophages, swarm around damaged areas of the brain, gobbling up cells damaged by Alzheimer's disease. Sounds good, but just like in the arterial walls, the microglia may get too feisty and stir up inflammation that damages surrounding brain cells that are healthy, accelerating the effects of Alzheimer's.
Anti-inflammatory drugs
One way to try to counteract inflammation is with NSAIDs (nonsteroidal anti-inflammatory drugs). For example, a low-dose aspirin can reduce inflammation and prevent spontaneous blood clotting. This has been quite popular, but more recently concerns about internal bleeding and other complications have caused doctors to be more cautious. As such, do not start taking NSAIDS regularly on your own without consulting your doctor.
Can NSAIDS help the brain? Hard to say at this point. Some research findings suggest that NSAIDs might be helpful as older folks who took them appeared to have a lower incidence of Alzheimer's. One study reported that the NSAID, naproxen, was effective. Other studies say no. There can be many explanations for inconsistent findings, like when the drugs are taken. If Alzheimer's already has a significant foothold, the drugs many not be helpful."
Article at:
http://www.courier-journal.com/
Weight loss, combined with vitamin D, reduces inflammation linked to cancer, chronic disease in 'Fred Hutch', June 24, 2015
My comments: BTW your Anatabloc has 40iu of D3
Excerpts:
"For the first time, researchers at Fred Hutchinson Cancer Research Center have found that weight loss, in combination with vitamin D supplementation, has a greater effect on reducing chronic inflammation than weight loss alone. Chronic inflammation is known to contribute to the development and progression of several diseases, including some cancers."
"At the end of the study, all of the participants had reduced levels of inflammation, regardless of whether they took vitamin D, “which highlights the importance of weight loss in reducing inflammation,” Duggan said. However, those who saw the most significant decline in markers of inflammation were those who took vitamin D and lost 5 to 10 percent of their baseline weight. These study participants had a 37 percent reduction in a pro-inflammatory cytokine called interleukin-6, or IL-6, as compared to those in the placebo group, who saw a 17.2 percent reduction in IL-6. The researchers found similar results among women in the vitamin D group who lost more than 10 percent of their starting weight. While IL-6 has normal functions in the body, elevated levels are associated with an increased risk of developing certain cancers and diabetes and may be implicated as a cause of depression, Duggan said.
“We were quite surprised to see that vitamin D had an effect on an inflammation biomarker only among women who lost at least 5 percent of their baseline weight,” Duggan said. “That suggests vitamin D can augment the effect of weight loss on inflammation.”"
Article at:
http://www.fredhutch.org/en/news/releases/2015/06/weight-loss-plus-vitamin-d-reduces-inflammation.html
In brains of mice, the key to Alzheimer's? in 'The Saint Augustine Register', June 20, 2015 BARBARA PETERS SMITH-SARASOTA HERALD-TRIBUNE
Excerpts:
"The laboratory mice that mimic some aspects of Alzheimer’s disease are a useful first step in exploring new therapies, scientists say, but drawing conclusions from this basic research is misleading.
One major distinction: The mice can be programmed to develop the telltale buildup of amyloid plaque in the brain — sticky accretions of beta amyloid proteins that are early markers of the disease. But they do not go on to show the tau protein pathology that accompanies later stages of the disease in human brains — toxic “tangles” of tau that are always present in full-blown Alzheimer’s.
It’s an important distinction, agrees Michael Mullan, a consultant and former CEO at The Roskamp Institute in Sarasota, which has sponsored Alzheimer’s research since 2003. Mullan and current CEO Fiona Crawford were part of a team of scientists who discovered in the early 1990s that the onset of Alzheimer’s was related to the brain’s accumulation of beta amyloid.
“We’re partially responsible” for the mouse-heimer’s confusion, Mullan says, “because we found the genetic errors.”
These engineered lab mice can be made to contract what might be considered a mild case of Alzheimer’s. “You don’t have to do too much to them to stop them getting it,” Mullan says. “It’s not a robust model of late-onset Alzheimer’s. You’re basically inducing Alzheimer’s in an otherwise healthy brain, and a young brain. We have about 300 drugs back there,” he adds, gesturing to the Roskamp labs, “that stop mice from getting Alzheimer’s. The real trick is translating that to human studies.”
Mullan believes this is already starting to happen. In March the biotech firm Biogen Idec announced early success in a clinical safety trial with 166 patients of an antibody that both removed amyloid plaque from brains and clearly slowed the progress of cognitive decline.
Even if Biogen Idec’s drug performs well in Phase 3 trials, researchers say, our understanding of Alzheimer’s is still at the toddler stage. Greicius emphasizes that while brain scans have helped fill in some blanks, there is still a great deal to be learned from studying donated brains of people who die of the disease.
And Mullan predicts that the path ahead will remain one of trial and error. “The way these things usually play out is that when you have a new treatment for something, it’s a big step forward,” he says. “Then what you see over a period of three or four years are the people who don’t do well. And then those people become a target for new approaches. And then we’ll find out: Does the antibody itself stop working over a period of time? But that’s how science works — those small steps.”"
Article at:
http://staugustine.com/news/2015-06-20/brains-mice-key-alzheimers#.VYc-4_lVhHw
Latest RCPI Presentation: "Investor Presentation", June 2015
Highlights:
PhaseI clinical trial underway-data expected 3Q 2015
Potential Therapeutic Applications:
Autoimmune Diseases
Inflammation
Alzheimer’s Disease
Autoimmune Thyroiditis: Human Study
Preclinical Model of Multiple Sclerosis
Anatabine Citrate: Psoriasis Indication
Anatabine Citrate: Regulatory Strategy
Phase 1 underway in EU-Study Completion expected in Third Quarter/2015
Investigational New Drug Application (IND) filed with US FDA -On Clinical Hold, Company plans to respond to FDA in context of overall strategy and ongoing acquisition of preclinical and human clinical data
Initial Clinical Targets: Psoriasis & Osteoarthritis
•Dermatology (Psoriasis)
•Arthritic Conditions(Osteoarthritis)
•Inflammatory Bowel Disorders(Ulcerative Colitis, Crohn’s)
• Auto-Immune Disorders(Thyroiditis)
•CNS(Alzheimer’s, Multiple Sclerosis)
Intellectual Property-Anatabine Citrate
Novel Compound-US Patent 8,557,999
Method of Anatabine synthesis
Six pending US and foreign patents pending for “use” of Anatabine, its isomers and derivatives for inflammatory conditions
Presentation at:
http://investors.rockcreekpharmaceuticals.com/index.php?s=19&item=19
From the Sept 30, 2014 RCPI Quarterly Report:
"On March 12, 2014, the Company entered into a series of equity and financing transactions that resulted in gross cash proceeds to it of approximately $9.3 million and cash availability under a credit facility of approximately $5.8 million, for total available funds of $15.1 million. Under one of its transactions, holders of previously held warrants with strike prices ranging from $1.50 to $2.00 agreed to immediately exercise an aggregate of 4.2 million warrants at a reduced strike price of $1.00 per share. The investors also were issued new warrants for an equal number of shares that have a term of seven years and a strike price of $1.00 per share. This transaction resulted in proceeds of approximately $4.2 million. Under another transaction, the Company sold 5.1 million shares with matching warrants to purchase another 5.1 million shares to other investors at a purchase price of $1.00 for each share and its matching warrant. This transaction resulted in proceeds to us of $5.1 million. Finally, the Company entered into a credit facility with another investor under which that investor agreed to loan it up to $5.8 million. The credit facility provides for an interest rate of 3% on any funds drawn by the Company. It also provides the lender with the option to convert any loan amount into a unit consisting of a share of the Company’s common stock and a matching seven-year warrant at a conversion price of $1.00 per unit."
Report at:
http://app.quotemedia.com/data/downloadFiling?webmasterId=101533&ref=9891585&type=HTML&symbol=RCPI&companyName=Rock+Creek+Pharmaceuticals+Inc&formType=10-Q&dateFiled=2014-11-10&cik=0000776008
It was my impression from the message board that the investor in question for the line of credit was J.W.---It could be that I am wrong, but that's the source
Could it be that this is to replace the line of credit they had with J.W.? With the squabble they are having with J.W., maybe he cancelled their credit card.
On the positive side, let's hope the 'revelation' is near. The 'revelation' must be dramatic and strong. Having said that, this continues to be one of a 'thousand cuts' that makes retail investors become cynical. Certainly these 'private' offerings seem to have the slant that they wouldn't invest millions unless they saw (greedy) opportunity and the end of the tunnel. This isn't the first time, insiders or 'institutional investors' have bought into RCPI and lost. What bothers me at this point are the following:
1. If Anatabine Citrate is so great like so many of us think it is, why hasn't any outside Big Pharma shown any interest? With presentations at professional conferences, seems like no one is interested (financially). (that we know of)
2. If Anatabine Citrate has the potential most of us feel it has, why does the management keep nickle and diming funding to keep it alive for the next 6 months to a year. (driving the stock even lower) Why don't they do like others and go with a HUGE IPO in the magnitude of several million dollars? Other small biotech seem to be able to do this with much less to offer.
3. More and more interest in 'chronic inflammation' is making it's way into the public eye but no one has yet to declare decisively that this is the 'holy grail' to solving many of the aging diseases that afflict we humans.
When and if a 'profound' announcement is made that will cause the stock to significantly rise and put doubters to rest, we have only two choices: hang on for that great day or capitulate and move on. I'm of the opinion that in some near future, breaktrhoughs will come with proof of performance for compounds like Anatabine Citrate, the big question is whether RCPI will be chosen when that day comes?
Alternate explanation for memory loss:
"Subject: THIS EXPLANATION WORKS FOR ME!
Brains of older people are slow because they know so much. People do not decline mentally with age, it just takes them longer to recall facts because they have more information stored in their brains, scientists believe.
Much like a computer struggles as the hard drive becomes more full, so humans also take longer to access information, it has been suggested.
Researchers say this slowing down is not the same as cognitive decline. The human brain works slower in old age, said Dr. Michael Ramscar, but only because we have stored more information over time. The brains of older people do not get weak. On the contrary, they simply know more, but just may not be able to access the information....
Also, older people often go to another room to get something and when they get there, they stand there wondering what they came for. It is NOT a memory problem, it is nature's way of making older people do more exercise.
SO THERE!! "
From an anonymous email source:
?????
Furred-up arteries. Diabetes. Eye disease. Dementia. Depression. Why doctors now believe they could all be triggered by one SILENT KILLER in The Daily Mail, June 15, 2015
Excerpts:
" From diabetes to atherosclerosis, the eye condition age-related macular degeneration and even dementia, inflammation may be the silent killer that links them all."
"'Even diseases which we have traditionally thought of as degenerative, such as dementia, are turning out to have a major inflammatory component,' says Professor Paul Morgan, an immunologist at Cardiff University."
"Generally speaking, inflammation is a good thing. It's likely that people who could mount a strong inflammatory response would have been at an evolutionary advantage, as they'd have been more likely to survive long enough to reproduce. The trouble only comes if the inflammation isn't switched off and becomes chronic and more widespread.
If inflammation does stay switched on, then the risk of 'friendly-fire' elsewhere in the body starts to outweigh the benefits
Studies have suggested that this kind of chronic, low-grade inflammation - a kind of smouldering fire in our cells and tissues - is more common in rich Western populations than in more traditional societies.
With this kind of low-grade inflammation, you probably won't realise you have it, though doctors can measure inflammation by looking at levels of a substance called C-reactive protein (CRP) in the blood.
'If you take regular blood samples from people living in America or the UK, you find a lot of people who have no apparent infection but who have a fixed raised level of CRP for no apparent reason,' says Professor Rook.
That's a marked difference from, for example, indigenous populations living in the Ecuadorian Amazon, as a recent study in the American Journal of Human Biology suggested."
"The cause of chronic inflammation is up for debate. Professor Rook suspects it's down to a change in our relationship with so-called 'old friends' - bacteria and parasites that we've lived with peacefully for much of human history.
Now that we're living cleaner lives, our immune systems are no longer receiving the same input they would have done during the first two to three years of life, and so are more likely to unleash inflammation at the slightest stimulus. It's a similar theory to the rise in allergies and auto-immune disease: the body overreacts to even minor threats. But there may be other explanations, too, such as rising levels of obesity.
Fat cells release some of the same inflammatory substances that are produced in response to infection and injury, and people with a higher body mass index have higher levels of inflammatory markers.
Then there's the fact we're all living longer lives, meaning there's more time for inflammation in response to everyday wear and tear to accumulate. 'Often it's very hard to pin down a single thing as the trigger for chronic inflammation,' says Professor Morgan. 'Probably, in most people, it is a combination of things that provides the initial trigger.'
Once established, though, that smouldering fire can have multiple effects. Take type 2 diabetes: for several decades, scientists have noticed higher levels of inflammation in patients with the condition.
Damage brought about by everyday exposure to stressors such as chemicals and bacteria triggers inflammation and tissue damage (file photo)
+3
Damage brought about by everyday exposure to stressors such as chemicals and bacteria triggers inflammation and tissue damage (file photo)
It is now thought inflammatory chemicals released by fat cells (many people with type 2 are overweight) make tissues less sensitive to the effects of insulin, resulting in raised blood sugar levels, and these can promote yet more inflammation. Fat on your belly, and which can wrap around your organs - visceral fat - is thought to be the biggest culprit.
It's a similar story with age-related macular degeneration (AMD), a leading cause of blindness in older people which is caused by damage to the macula, the area of the eye responsible for central vision. Here, damage brought about by everyday exposure to stressors such as chemicals and bacteria triggers inflammation and tissue damage."
"There's a growing consensus that inflammation elsewhere in the body can also affect the brain - possibly resulting in diseases, such as dementia, as well as depression and schizophrenia.
e now know this isn't strictly true. In fact, inflammatory chemicals can get into the brain and, once there, they activate resident immune cells called microglia, which produce more inflammatory substances as a result.
'That leads to increasing levels of toxic molecules within the brain, while levels of other chemicals, such as serotonin (important for regulating mood), decrease,' says Golam Khandaker, a psychiatrist at Cambridge University. 'This is very relevant for something like depression, where the problem is feeling low in mood and not being able to think straight.'
Here, too, anti-inflammatory drugs could help. For instance, a 2012 study found that a daily aspirin reduced the risk of depression by 40 per cent in elderly men with a history of the condition - although more research is needed.
What if you're healthy but are worried you might have undiagnosed inflammation that could be boosting your risk of future disease?"
Article at:
http://www.dailymail.co.uk/health/article-3125357/Furred-arteries-Diabetes-Eye-disease-Dementia-Depression-doctors-believe-triggered-one-SILENT-KILLER.html
International Alzheimer's prevention study expands in 13WMAZ article, June 16, 2015
Excerpts:
"A five-year, international study into the genetic roots of the country's sixth-leading killer is expanding. The TOMMORROW study, which is going on in about 50 locations in North America, Europe and Australia, tests a drug — one used to control diabetes — to see whether it could prevent, or at least delay, the onset of Alzheimer's disease"
""It's about delaying the onset of Alzheimer's rather than treating the symptoms" after a diagnosis, he said."
"Participants must be ages 65-83, have no signs of Alzheimer's and carry a set of genetic mutations that are believed to put them at risk for Alzheimer's — something that a blood test at Quest will determine."
"Participants are tested for mutations in the apolipoprotein E gene, or APOE-e, which is associated with an increased number of clumps of proteins known as amyloid and tau. These protein clumps, in turn, have been linked to to Alzheimer's. Researchers also are interested in the gene known as TOMM40, which is believed to interact with APOE-e.
Participants who carry that gene combination will be given either the experimental drug compound pioglitazone or a placebo. Pioglitazone, also known as Actos, is commonly prescribed to help control blood sugar in Type 2 diabetes.
For years, scientists have linked high blood sugar with a greater risk of dementia. Controlling blood sugar may slow a toxic buildup of those proteins."
Article at:
http://www.13wmaz.com/story/news/health/2015/06/15/international-alzheimers-prevention-study-expands/71264946/
Alzheimer's biotech vTv Therapeutics files for a $173 million IPO
By Renaissance Capital in Nasdaq News Release, June 16, 2015,
Excerpts:
"vTv Therapeutics, a biotech developing treatments for Alzheimer's and type 2 diabetes, filed on Monday with the SEC to raise up to $173 million in an initial public offering. The company's lead product candidate, azeliragon for Alzheimer's disease, is enrolling for a Phase 3 trial, the results of which are expected to be released in mid-2018. Its Executive Chairman, Jeffrey Kindler, was the CEO of Pfizer from 2006 to 2010.
vTv is a newly formed entity that will combine the operations of TransTech Pharma (formed in 1998) and High Point Pharmaceuticals (formed by TransTech in 2008). The predecessors have raised more than $500 million through private placements and collaborations with Novo Nordisk, Merck, Boehringher Ingelheim, Pfizer (2006-2011) and Forest Laboratories. The company is now majority owned by Ronald Perelman's MacAndrews.
The High Point, NC-based company, which was founded in 1998 and booked $2 million in sales for the 12 months ended March 31, 2015, plans to list on the NASDAQ under the symbol VTVT. Piper Jaffray and Stifel are the joint bookrunners on the deal. No pricing terms were disclosed."
News Release at:
http://www.nasdaq.com/article/alzheimers-biotech-vtv-therapeutics-files-for-a-173-million-ipo-cm487323
Anti-Amyloid Treatment in Asymptomatic Alzheimer’s A4 study is a landmark public-private partnership, funded by the National Institute on Aging/NIH, Eli Lilly and Company, and several philanthropic organizations. The A4 trial is coordinated by the Alzheimer’s Disease Cooperative Study, located at the University of California, San Diego."
A4 website at:
http://a4study.org./
"The research involves monthly infusions — an hour of IV injection of the anti-amyloid plaque drug solanezumab"
Santa Cruz Dementia article at:
http://www.santacruzsentinel.com/health/20150615/drug-trials-may-be-key-to-understanding-alzheimers
Interesting discourse on the FDA 'lost' process:
Congressional Hearing To Remove Roadblocks to Ampligen Approval at FDA
By Cort Johnson on February 5, 2015
Letter to Congress:
"Subject: Request for Hearing on ME/CFS treatment denial I am writing to you on behalf of one million patients in the US and 17 million more worldwide that are disabled and suffering from Myalgic Encephalomeylitis, (poorly identified as Chronic Fatigue Syndrome), ME/CFS. We are writing to request that you conduct a hearing to examine the denial of access to treatment for this disease by the FDA. One drug over the course of 20 + years has demonstrated that it can improve the lives of a significant proportion of the patients suffering from this life-robbing illness, and yet we are still denied access to the drug. We believe that a hearing and or independent adjudication is the only path to justice. Below are a few of the critical issues that must be addressed: 1) The experts in the field and the FDA advisory panel say it is safe for approval. Dr. Janet Woodcock, Director of the Center for Drug Evaluation and Research and members of the current Rheumatology Division agreed at a meeting with experts, patients and the drug company that safety was not the issue; but are simply unclear on efficacy. 2) The FDA has stated that this is a serious, life-threatening and complex illness. The FDA has the regulatory authority to provide expanded access via approval with conditions. Experts with decades of experience with the disease and the drug are willing work with the FDA to design the conditional studies. The drug manufacturer has offered to implement an extensive REMS (Risk Evaluation and Mitigation Strategy) program that would educate physicians, patients, and pharmacists on the diagnosing and treating ME/CFS and the safe and appropriate use of the drug. 3) The drug has been used in patients for more than 20 years and over 100,000 doses. Experts agree that they have seen improvement in approximately 40% of the patients using the drug. 4) Seven hundred patients provided testimony at the FDA advisory meeting for this drug’s approval. Four thousand signed a petition requesting the drug be approved. That was in 2012. Patients have been suffering for decades at a cost of $22 billion a year. 5) The small bio-tech company is the only company that recognized the severe nature of this disease has been shuffled through five FDA divisions, with each division applying new and different standards and requirements for approval. After the denial, the FDA lead reviewer admitted at a public meeting she did not understand the disease. 6) FDA’s appeals process is highly flawed. A top regulatory law firm, Hyman Phelps, stated in presentation that any company utilizing this path would require deep pockets and years without necessarily any hope of approval.
Read more: Congressional Hearing To Remove Roadblocks to Ampligen Approval at FDA http://www.cortjohnson.org/blog/2015/02/05/congressional-hearing-ampligen-roadblocks-fda-called/
Re Amarin FDA Lawsuit:
Article in Reuters News Daily, Tuesday, June 9, 2015:
Excerpts:
"The U.S. Food and Drug Administration, responding to a lawsuit filed by Amarin Corp over information the company wants to disseminate for its fish oil drug, said it had no objection to Amarin sharing the data with healthcare providers.
The FDA’s letter to Amarin, dated June 8 and filed with a U.S. District Court judge in New York, appears to undercut the lawsuit, saying the small drugmaker should have come to the agency with its concerns “as other pharmaceutical companies sometimes do” before filing a complaint against it in court."
Article at:
http://newsdaily.com/2015/06/fda-undercuts-amarin-lawsuit-on-fish-oil-drug-information/
Congressional House of Representatives 400 page 'out of the box' thinking re FDA, drugs, and unmet needs: "To accelerate the discovery, development, and delivery of 21st century cures, and for other purposes. "
See at:
http://energycommerce.house.gov/sites/republicans.energycommerce.house.gov/files/114/Analysis/Cures/20150127-Cures-Discussion-Document.pdf
FDA, Woodcock, Clinical Trials, etal:
Woodcock-calls-to-cut-clinical-costs-via-new-efficiencies
GAO critical of FDA’s clinical trial oversight
US FDA working to make clinical trials less wasteful
Focus on funding FDA overseas clinical trial policing, says ACRO
FDA plans QbD for clinical trials to cut industry & regulatory monitoring costs
See for articles:
http://www.outsourcing-pharma.com/Clinical-Development/FDA-s-Woodcock-calls-to-cut-clinical-costs-via-new-efficiencies
You are correct. Most people think of clinical trials as phases 1,2, and 3, where phase 1 deals with safety, phase 2 deals with preliminary efficacy/safety, and phase 3 deals with large patient population efficacy/safety. To quote their press release: "The trial consists of three parts, with Part Two being optional. The objectives of Parts One and Two are to evaluate the safety, tolerability, and pharmacokinetic (PK) profiles of various modified and immediate release formulations of anatabine citrate in healthy adult subjects, and to identify an optimal formulation for multiple day dosing in Part Three. Exploratory pharmacodynamic (PD) outcome measures are also being assessed."
Again it's the pharma vocabulary that kinda throws those of us that aren't familiar with it. According to Wikipedia: "Pharmacokinetics, sometimes abbreviated as PK (from Ancient Greek pharmakon "drug" and kinetikos "moving, putting in motion"; see chemical kinetics), is a branch of pharmacology dedicated to determining the fate of substances administered externally to a living organism. The substances of interest include pharmaceutical agents, hormones, nutrients, and toxins. It attempts to discover the fate of a drug from the moment that it is administered up to the point at which it is completely eliminated from the body. Pharmacokinetics describes how the body affects a specific drug after administration through the mechanisms of absorption and distribution, as well as the chemical changes of the substance in the body (e.g. by metabolic enzymes such as cytochrome P450 or glucuronosyltransferase enzymes), and the effects and routes of excretion of the metabolites of the drug.[1] Pharmacokinetic properties of drugs may be affected by elements such as the site of administration and the dose of administered drug. These may affect the absorption rate.[2] Pharmacokinetics is often studied in conjunction with pharmacodynamics, the study of a drug's pharmacological effect on the body."
Having said that, it would appear that RCPI is doing more than others in their phase 1 clinical trials---it almost looks like they are trying to do a version of phase 1 and 2 all in phase 1.
Best Stocks Under $5: Rock Creek Pharmaceuticals (RCPI) recommendation at 'Investor Place, Ethan Roberts, InvestorPlace Contributor, 6/12/15 Closing Price: $2.82 (+41%)
Recommendation:
"Rock Creek Pharmaceuticals (RCPI) is a Sarasota, Florida-based pharmaceutical company that is focusing on developing treatments for inflammatory, neurological and behavioral disorders.
This week RCPI announced the completion of Phase I of its clinical trials for Anatabloc, an anti-inflammatory supplement molecular whose active ingredient is antabine citrate, which is found in various vegetables. The supplement had no adverse events or safety concerns reported on human subjects.
The company has previously had difficulty getting Food and Drug Administration approval for an anatabine citrate supplement. The testing is being conducted is in the United Kingdom.
Rock Creek expects to begin Part 2 of its study in the third quarter."
Recommendation at:
http://investorplace.com/2015/06/5-best-stocks-week-aoi-rcpi-seed-axn-dskx/#.VX7QtflVhHx
New drug can clear all psoriasis symptoms in World Pharma News, 11 JUNE 2015
Excerpts:
"A University of Manchester led trial of a new psoriasis drug has resulted in 40 percent of people showing a complete clearance of psoriatic plaques after 12 weeks of treatment and over 90 percent showing improvement. The research tested 2,500 people with psoriasis. Half were given a new drug - ixekizumab - either once every two or four weeks. The other half were given a placebo or a widely used drug for psoriasis called etanercept.
The ixekizumab groups showed quick and extensive improvements in their condition, outperforming the groups on placebo or etanercept. Around half of these patients showed improvement as early as week four of the trial and up to 71% had shown a high level of improvement, as measured using a scale called the Psoriasis Area and Severity Index, by week 12."
"Ixekizumab is a monoclonal antibody - a cloned antibody - which neutralises the inflammatory effects of an interleukin (IL) a protein in the skin which carries signals to cells - known as (IL)-17A. This protein is increasingly becoming recognised as one of the causes of the characteristic red, scaly plaques of psoriasis which affect around 2% of people in the UK."
Article at:
http://www.worldpharmanews.com/research/3108-new-drug-can-clear-all-psoriasis-symptoms
Nuts May Reduce Risk Of Death From Multiple Causes, Study Finds in 'Forbes', Alice G Walton, 6/11/2015
Excerpts:
"It turned out that people who regularly ate nuts had a reduced risk of death from all of the causes included in the analysis – about 23% reduce risk, compared to people who didn’t eat nuts. And while most studies in the past have been interested in the links between nuts and cardiovascular disease, the current study found the benefit also applied to death from other diseases including cancer, stroke, diabetes, respiratory, and neurodegenerative diseases. The reduction in risk of developing neurodegenerative disease like Alzheimer’s was robust: for someone who ate 10 or more grams of nuts per day, it was about 45% less than someone who ate none."
Article at:
http://www.forbes.com/sites/alicegwalton/2015/06/11/nuts-reduce-risk-of-death-from-any-cause-study-finds/?ss=pharma-healthcare
FDA: Drug Companies Routinely Hide The Reasons Their Drugs Are Rejected From Investors in 'Forbes', Matthew Herper, 6/12/2015
Excerpts:
"Seven times between August 11, 2008, and June 27, 2013, the Food and Drug Administration declined to approve a new medicine, in part, because patients were more likely to die when taking the drug than in a control group. Yet only one of those companies told investors – and the public – about that concern.
That’s perhaps the most shocking detail from a sweeping FDA analysis, published in the new issue of the British Medical Journal, of what pharmaceutical companies tell the world when the agency rejects a drug. The conclusion: at best, the industry’s communications about rejections are insufficient and misleading. At worst, they sound close to outright lies – and investors faced with an FDA rejection should never believe anything that executives have to say unless those executives make public the full text of the rejection letter – something that, in the time span of this analysis, no company has done."
Complete article at:
http://www.forbes.com/sites/matthewherper/2015/06/12/fda-drug-companies-routinely-hide-the-reasons-their-drugs-are-rejected-from-investors/?ss=pharma-healthcare
Coming up Boston 2015 12th World Congress on Inflammation, August 8-15, 2015
Tentative symposiums:
"SYMPOSIUM 1: Innate Memory and Programming in Acute and Chronic Inflammation
SYMPOSIUM 2: Mechanisms Underlying Microbiome-Mediated Inflammation
SYMPOSIUM 3: Disease Modication in Osteoarthritis: Myth or Reality?
SYMPOSIUM 4: The ‘Eicosanoid Storm’
SYMPOSIUM 5: Cytokines and Inflammation – Sponsored by ICIS
SYMPOSIUM 6: Novel Biologics Therapies for Immune and Inflammatory Disorders – Sponsored by SCIL-AUS
SYMPOSIUM 7: New Therapeutic Strategies for Respiratory Diseases – Sponsored by ERS
SYMPOSIUM 8: The Neutrophil: An Old Dog with New Tricks – Sponsored by GREMI
SYMPOSIUM 9: Ocular Inflammation. Translation Focused – Sponsored by Ora, Inc.
SYMPOSIUM 10: Glucocorticoids in the Regulation of Inflammatory Response – Sponsored by Italian Inflammation Group
SYMPOSIUM 11: A Role for Epigenetics in Inflammatory Disease: Spotlight on Monocytes and Macrophages
SYMPOSIUM 12: Next Generation Kinase Inhibitors – Sponsored by BIRA-UK
SYMPOSIUM 13: miRNAs in Inflammation
SYMPOSIUM 14: Mucosal Immunity: Hot Topics in IBD
SYMPOSIUM 15: Inhibitory Receptor/Immune Checkpoints/Immunotherapeutics – Sponsored by IRA-USA
SYMPOSIUM 16: Mechanisms of Fibrosis
SYMPOSIUM 17: Therapeutics with Localized Action – Optimal Ways to Treat Tissue Inflammation
SYMPOSIUM 18: Ion Channels and Inflammation – Sponsored by IRN-Canada
SYMPOSIUM 19: Harnessing Novel Resolution Mechanisms to Control Inflammation
SYMPOSIUM 20: Skeletal Muscle Inflammation
SYMPOSIUM 21: Regulation of Inflammation in Tissues by Costimulatory and Coinhibitory Pathways
SYMPOSIUM 22: Atopic Dermatitis, Psoriasis and IL-4/IL-17 Biology
SYMPOSIUM 23: Defining Sub-Phenotypes in Chronic Respiratory Diseases to Improve Drug Development and
Disease Management
SYMPOSIUM 24: Biological and Non-Biological Therapies of Autoimmune Diseases – Sponsored by JSIR-Japan
SYMPOSIUM 25: Complement Targeted Therapies - Is There Light at the End of the Tunnel?
SYMPOSIUM 26: Regenerative Medicine and Stem Cells in Inflammation
SYMPOSIUM 27: iNKT Cells – Mediators at the Interface of Inflammation and Immunity
SYMPOSIUM 28: Infection and Inflammation – Sponsored by BIS-Brazil
SYMPOSIUM 29: Biomarkers in Inflammation: Focus on Rheumatoid Arthritis
SYMPOSIUM 30: SLE: Current Therapeutic Landscape and Future Promises
SYMPOSIUM 31: New Visions in Ocular Therapy
SYMPOSIUM 32: Tregs in Human Autoimmunity
SYMPOSIUM 33: Gaseous Mediators as the Basis for Novel Anti-Inflammatory Drugs – Sponsored by IRN-Canada
SYMPOSIUM 34: Therapeutic Pathways in Inflammation: New Faces of Old Friends – Sponsored by RIS-Russian
SYMPOSIUM 35: Clinical Developments in Fibrosis
SYMPOSIUM 36: Novel Therapies in RA
SYMPOSIUM 37: Novel Targets and/or Novel Therapies – Sponsored by Celgene
SYMPOSIUM 38: Cardiovascular Inflammation
SYMPOSIUM 39: Predictive Toxicology
SYMPOSIUM 40: Translational Medicine
SYMPOSIUM 41: Innate Lymphoid Cells"
Website at:
http://inflammation2015.org/2015/HOME.aspx
Catabasis Pharmaceuticals to Present the Design of MoveDMD a Phase 1/2 Trial for its Product Candidate CAT-1004 for the Treatment of Duchenne Muscular Dystrophy at Parent Project Muscular Dystrophy’s Annual Connect Conference, Catabasis Pharmaceuticals, 12 Jun 15
Excerpts:
"CAT-1004 is an oral small-molecule that inhibits activated NF-kB a protein that coordinates cellular response to muscular damage stress and inflammation and plays an important role in muscle health. In skeletal muscle activated NF-kB drives muscle degeneration and suppresses muscle regeneration. In animal models of DMD CAT-1004 inhibited activated NF-kB reduced muscle inflammation and degeneration and increased muscle regeneration. In Phase 1 clinical trials CAT-1004 inhibited activated NF-kB and was well tolerated with no observed safety concerns. Catabasis Pharmaceuticals expects to initiate enrollment of a Phase 1/2 clinical trial of CAT-1004 for the treatment of DMD known as the MoveDMD trial in June 2015."
Article at:
http://www.pharmiweb.com/PressReleases/pressrel.asp?ROW_ID=117398#.VXtd5vlVhHw
Vitamin E Research Ramps Up in Nutritional Outlook, Melissa Kvidahl June 12, 2015
Excerpts:
"The review of multiple studies, published in Advances in Nutrition and led by vitamin E expert Maret Traber, revealed that inadequate vitamin E is associated with increased infection, anemia, stunting of growth, and poor outcomes during pregnancy for both infant and mother, and neurological disorders and muscle deterioration in children with an overt deficiency. On the other hand, increased vitamin E concentrations at birth were associated with improved cognitive function by age two. The nutrient was also found to possibly slow Alzheimer’s progression, increase cognitive function, and even reduce risk of dementia by 47%."
Article at:
http://www.nutritionaloutlook.com/1506/VitaminEResearch
Researchers Boost Body’s Inflammation-Reduction Mechanism to Combat Obesity-Fueled Disease in 'Endo Nurse', June 12, 2015
Excerpts:
"Researchers at University of California, San Diego School of Medicine and University College Dublin (UCD) have found that augmenting a naturally occurring molecule in the body can help protect against obesity-related diseases by reducing inflammation in the fat tissues. The study, published June 4 in the journal Cell Metabolism, focused on liver and kidney diseases, but the researchers believe it could lead to a new therapeutic approach for a variety of obesity-fueled conditions.
“This is a new way of reducing inflammation and protecting organs, using a compound that’s already produced by the body," said co-senior author Kumar Sharma, MD, a professor of medicine and director of the Center for Renal Translational Medicine at UC San Diego School of Medicine. “Essentially, we’re boosting the body’s natural response for reducing inflammation and showing the benefit in obesity-driven diseases."
Catherine Godson, PhD, co-senior author and director of the UCD Diabetes Complications Research Centre in UCD School of Medicine and UCD Conway Institute, said the study’s findings demonstrate the value and potential impact of fundamental research.
“Drawing on collaborative expertise in synthetic chemistry, molecular biology and translational medicine, the team has produced findings with significant potential to reduce inflammation, a critical driver of the devastating consequences of obesity-related diseases," she said."
"Borgeson said that a family of lipids, known as specialized pro-resolving mediators (SPMs), are the body’s natural shut-off mechanism for inflammation. “The process of telling the white blood cells to ‘calm down, you don’t have to be inflamed anymore’ is called inflammatory resolution and that’s what the SPMs induce."
In the study, the research team focused on an SPM called lipoxin A4, which has previously been found to reduce inflammation in kidney disease caused by ureteral obstruction. Working with an obese mouse model, the researchers gave the mice a synthetic version of lipoxin A4 to boost the amount of the natural substance already in their systems. The results showed significant disease improvement, primarily by affecting fat tissue."
Article at:
http://www.endonurse.com/news/2015/06/researchers-boost-body-s-inflammation-reduction-m.aspx
Corbus Pharmaceuticals Announces FDA Orphan Drug Designation for Resunab(TM) for the Treatment of Systemic Sclerosis (Scleroderma) in 'CNN Money', June 12, 2015
Excerpts:
"Corbus Pharmaceuticals Holdings, Inc. (NASDAQ: CRBP) ("Corbus" or the "Company"), a clinical stage drug development company targeting rare, chronic, and serious inflammatory and fibrotic diseases, announced today that the U.S. Food and Drug Administration ("FDA") has granted Corbus' lead drug candidate Resunab™ Orphan Drug Designation for the treatment of systemic sclerosis.
Systemic sclerosis is a chronic, serious, life-threatening inflammatory disease causing fibrosis of skin and internal organs, affecting predominately women in mid-life. Systemic sclerosis is associated with severe morbidity and high mortality. There are currently no FDA-approved drug therapies for systemic sclerosis.
"We are very pleased to receive FDA Orphan Drug Designation for Resunab in systemic sclerosis. This is an important regulatory milestone for the company and a significant step forward in our clinical development of Resunab targeting this rare disease associated with such a critical unmet need for safe and effective therapeutics," stated Yuval Cohen, Ph.D., Chief Executive Officer of the Company. "Based on its novel mechanism of action of triggering the inflammatory resolution pathway, we believe Resunab has the potential to become an important therapy for systemic sclerosis patients as well as other diseases in which chronic inflammation and fibrosis persist."
Resunab is a novel synthetic oral drug that has the potential to treat chronic inflammation and fibrosis. Pre-clinical and Phase 1 studies have shown Resunab to have a favorable safety, tolerability and pharmacokinetic profile. The FDA has already cleared the Corbus' investigational new drug application ("IND") for systemic sclerosis and the Company is preparing to commence Phase 2 studies.
The FDA Orphan Drug Designation program provides a special status to drugs and biologics intended to treat, diagnose or prevent so-called orphan diseases and disorders that affect fewer than 200,000 people in the U.S. This designation provides for a seven-year marketing exclusivity period against competition, as well as certain incentives, including federal grants, tax credits and a waiver of PDUFA filing fees."
Article at:
http://money.cnn.com/news/newsfeeds/articles/marketwire/1200803.htm
Is Lilly on the verge of an Alzheimer's turnaround? in 'Fierce Biotech', Damian Garde, June 12, 2015
Excerpts:
"Some early-stage success for Biogen ($BIIB) has inaugurated something of a second honeymoon for a class of investigational Alzheimer's disease treatments, and some investors believe Eli Lilly ($LLY), maker of a similar therapy, could be poised to reverse its bleak fortunes in the field.
The Indiana drugmaker has seen its shares rise more than 10% this week in the lead-up to Monday, when Lilly is expected to offer a peek at long-term results from a once-failed Alzheimer's therapy, Reuters reports.
The treatment, solanezumab, flamed out in two huge Phase III studies in 2012, failing to improve cognition and function compared to placebo. But, poring over the data, Lilly noted a positive effect on patients with mild forms of Alzheimer's, so the company extended the trials on those patients for another two years, gathering the data now set to see the light of day. Positive results in the open-label extension study would bode well for Lilly's ongoing, placebo-controlled Phase III trial on mild patients and, the thinking goes, inject new life into an antibody written off by many. Lilly's comeback plans for solanezumab have long been known to investors, and the sudden surge of optimism is likely tied to results from a study conducted by another company altogether."
Article at:
http://www.fiercebiotech.com/story/lilly-verge-alzheimers-turnaround/2015-06-12
Exclusive: Alzheimer's group may scrap early look at highly sought Lilly data, Ransdell Pierson, REUTERS, JUN. 12, 2015,
Excerpts:
"The Alzheimer's Association may not offer an early look at highly sought clinical trial data on an experimental drug from Eli Lilly and Co after news of the impending release led to a jump in the company's shares.
The influential patient group had been expected to post abstracts containing detailed trial findings on its website in the coming days, ahead of a conference planned for July in Washington, D.C."
"Shares of Lilly have jumped 7 percent this week, largely on Wall Street expectations that favorable long-term effectiveness data could emerge from the study of solanezumab, an injectable drug with potential to become the first approved treatment to delay progression of Alzheimer's."
Article at:
http://www.businessinsider.com/r-exclusive-alzheimers-group-may-scrap-early-look-at-highly-sought-lilly-data-2015-6
Alzheimer's Prevention Program: Keep Your Brain Healthy for the Rest of Your Life, Dr Gary Small MD UCLA, University of California Television (UCTV)
One hour video worth the watch. Focus on 'anti-inflammatory lifestyle'. Recognizes need more effective treatments/medicines. Emphasis on non-medical changes to ones lifestyle to improve cognition and better health. He covers the history of Alzheimers and non-genetic areas to improve brain health. He's pitching his book but his presentation probably gives away a lots of the info in his book. Well worth the hour to watch. Things you can do now while waiting for the magic bullet. You can almost see where something like anatabine citrate would fit in and supplement what we can't control by lifestyle changes.
Video at:
The bigger question is that several years ago, there was an application for Anatabine Citrate and it's application for use to mitigate or reduce chronic diseases, coronary disorders, and certain cancers. That doesn't seem to exist anymore. It was said that the PTO rejected it because Anatabine Citrate is a 'natural' compound and 'natural' compounds are not patentable. Now that the FDA declares Anatabine Citrate a drug and needs an approved NDI application before RCPI can pursue it's potential use and sales in the United States. For a drug, it needs to show safety and efficacy through various clinical trials with data approved by the FDA before RCPI can market and sell it. So, what's your take on all this??
OK, think I found it. The patent is for Anatabine Citrate. So it looks like RCPI has the patent for Anatabine Citrate as a supplement and various formulations. Whether this construes Anatabine Citrate as a drug, someone with more expertise needs to comment???
Abstract
Anatabine citrate and formulations containing anatabine citrate are useful for promoting health and well-being.
Claims
Anatabine citrate.
A composition comprising a salt of claim 1 and an acceptable pharmaceutical, dietary supplement or food grade carrier, excipient, or diluent.
The composition of claim 2 which is a solid dosage form.
The composition of claim 3 further comprising at least one selected from the group consisting of sodium citrate, dicalcium phosphate, starches, lactose, sucrose, glucose, mannitol, silicic acid, carboxymethylcellulose, alginates, gelatin, polyvinylpyrrolidone, sucrose, acacia, glycerol, agaragar, calcium carbonate, potato or tapioca starch, alginic acid, silicates, sodium carbonate, paraffin, quaternary ammonium compounds, cetyl alcohol, glycerol monostearate, kaolin, bentonite clay, talc, calcium stearate, magnesium stearate, solid polyethylene glycols, and sodium lauryl sulfate.
A controlled release formulation comprising a salt of claim 1 and a biodegradable polymer.
The controlled release formulation of claim 5 wherein the biodegradable polymer is selected from the group consisting of poly(orthoesters), poly(anhydrides), and combinations thereof.
An extended release formulation comprising a salt of claim 1 and a swellable polymer.
The extended release formulation of claim 7 wherein the swellable polymer is selected from the group consisting of poly(ethylene oxide), hydroxypropyl methylcellulose, and combinations thereof.
patent at:
https://www.lens.org/lens/patent/US_8557999_B2
I think you are incorrect. There are 4 patents listed including the systhesis one. I am asking about the latest one in October 2013.
Patents Issued to Rock Creek Pharmaceuticals, Inc.
In October 2013, the PTO issued a patent to Rock Creek covering anatabine citrate, the active component in the Anatabloc® product line.
U.S. Patent No. 8,557,999 10/15/2013 Anatabine Citrate Expiration date: 3/23/2030
In August 2012, the PTO issued a patent to Rock Creek for an anatabine citrate and yerba mate composition and uses thereof in assisting weight loss and curbing the urge for tobacco.
U.S. Patent No. 8,241,680 8/14/2012 Nutraceutical Product Containing Anatabine and Yerba Mate Expiration date: 7/30/2030
In June 2012 the PTO, issued a patent to Rock Creek for an improved method of synthesizing anatabine that facilitates large scale commercial production of high purity anatabine.
U.S. Patent No. 8,207,346 6/26/2012 Method of Synthesizing Anatabine Expiration date: 10/16/2030
In 2011 the PTO issued a design patent to Rock Creek for the 20-piece dispenser used for our CigRx® and Anatabloc® products.
U.S. Design Patent No. D639,178 6/07/2011 Dispenser Expiration date: 08/03/2024
Patent question---Does the latest anatabine patent, dated 10/15/2013, from the PTO give RCPI a patent on anatabine as a drug? Big answer regarding BigPharma interest in anatabine, if any.
http://rockcreekpharmaceuticals.com/html/patents.php
Chronic inflammation induces telomere dysfunction and accelerates ageing in mice in 'Nature Communication', Diana Jurk, Caroline Wilson, João F. Passos, Fiona Oakley, Clara Correia-Melo, Laura Greaves, Gabriele Saretzki, Chris Fox, Conor Lawless, Rhys Anderson, Graeme Hewitt, Sylvia LF Pender, Nicola Fullard, Glyn Nelson, Jelena Mann, Bart van de Sluis, Derek A. Mann & Thomas von Zglinicki, 24 June 2014
Abstract:
"Chronic inflammation is associated with normal and pathological ageing. Here we show that chronic, progressive low-grade inflammation induced by knockout of the nfkb1 subunit of the transcription factor NF-?B induces premature ageing in mice. We also show that these mice have reduced regeneration in liver and gut. nfkb1-/- fibroblasts exhibit aggravated cell senescence because of an enhanced autocrine and paracrine feedback through NF-?B, COX-2 and ROS, which stabilizes DNA damage. Preferential accumulation of telomere-dysfunctional senescent cells in nfkb1-/- tissues is blocked by anti-inflammatory or antioxidant treatment of mice, and this rescues tissue regenerative potential. Frequencies of senescent cells in liver and intestinal crypts quantitatively predict mean and maximum lifespan in both short- and long-lived mice cohorts. These data indicate that systemic chronic inflammation can accelerate ageing via ROS-mediated exacerbation of telomere dysfunction and cell senescence in the absence of any other genetic or environmental factor.
Article at:
http://www.nature.com/ncomms/2014/140624/ncomms5172/full/ncomms5172.html
They knew 7 years ago: Is Chronic Inflammation the Key to Unlocking the Mysteries of Cancer? in Scientific American, Gary Stix, November 9, 2008
Excerpts:
"In the past 15 years, innate immunity has come into its own. Inflammation, its hallmark characteristic, has gained recognition as an underlying contributor to virtually every chronic disease—a list that, besides obvious culprits such as rheumatoid arthritis and Crohn’s disease, includes diabetes and depression, along with major killers such as heart disease and stroke. The possibility of a link with a third major killer—cancer—has received intensive scrutiny in this decade. “The connection between inflammation and cancer has moved to center stage in the research arena,” notes Robert A. Weinberg of the Massachusetts Institute of Technology’s Whitehead Institute for Biomedical Research, who has highlighted the changing emphasis in a revision of his leading textbook, The Biology of Cancer (Garland Science, 2006).
This transformation recognizes that the immune inflammatory state serves as a key mediator of the middle stages of tumor development. Cancer begins with a series of genetic changes that prompt a group of cells to overreplicate and then invade surrounding tissue, the point at which true malignancy begins. Eventually some tumor cells may break off and establish new growths (metastases) at distant sites. That much has been understood for a long time. But cancer biologists and immunologists have begun to realize that the progression from diseased tissue to full-blown invasive cancer often requires cells that normally participate in healing cuts and scrapes to be diverted to the environs of the premalignant tissue, where they are hijacked to become co-conspirators that aid and abet carcinogenesis. As some researchers have described the malignant state: genetic damage is the match that lights the fire, and inflammation is the fuel that feeds it."
"This new view implies that rooting out every last cancer cell in the body might not be necessary. Anti-inflammatory cancer therapy instead would prevent premalignant cells from turning fully cancerous or would impede an existing tumor from spreading to distant sites in the body. Cancer sufferers might then be able to survive, in the same way that new drugs have let HIV patients live longer. “I don’t think a cure is necessarily the goal. It doesn’t need to be,” comments Lisa M. Coussens, a cancer biologist at the University of California, San Francisco. “If you can manage the disease and live your natural life span, that’s a huge win.”"
"In the late 1990s Frances Balkwill of the Institute of Cancer at Queen Mary, University of London, had been doing research on a cytokine (a hormonelike immune signaling molecule) known as tumor necrosis factor (TNF), which was named for its ability to kill cancer cells when administered directly into a tumor at high levels. But when TNF lingers as a chronic, low-level presence in the tumor, it acts very differently. Balkwill’s lab turned off the TNF gene in mice so that the rodents could not produce the protein: to their surprise, the mice did not contract tumors. “That really put us as the cat among pigeons,” she recalls. “All the people who were working on TNF as an anticancer agent were horrified. This cytokine they thought was a treatment for cancer was actually working as an endogenous tumor promoter.”"
"Biologists have now been able to follow the inflammation link down to the level of individual signaling molecules, providing harder evidence for a connection to carcinogenesis. For example, nuclear factor-kappa B (NF-KB) is a complex of proteins that acts as a master switch for turning inflammation genes on and for controlling cell death. As biological pathways go, NF-KB’s is world-famous, having been discovered and patented for use in drug development by scientific stars that include Nobelists David Baltimore and Phillip A. Sharp and having subsequently become the object of multimillion-dollar patent litigation.
In 2004 Yinon Ben-Neriah and Eli Pikarsky of the Hebrew University of Jerusalem and their colleagues reported that mice engineered to develop hepatitis (which can cause liver cancer) contracted precancerous lesions that did not progress to full malignancy when NF-KB was curtailed through a genetic alteration or when the proinflammatory TNF signaling molecule was shut off. In the latter group, a neutralizing antibody blocked TNF and prevented it from binding to a receptor on the premalignant liver cells; loss of the receptor prevented the TNF from triggering a molecular cascade that turns on the NF-KB master switch. Blocking NF-KB prompted the precancerous liver cells to initiate apoptosis, or programmed cell death. In a related finding that year, Michael Karin and his collaborators at the University of California, San Diego, found that inhibiting NF-KB in mice engineered to develop colitis, which can lead to colon cancer, also promoted apoptosis. And shutting down the pathway in inflammatory cells, such as macrophages, deterred tumor development as well."
"The case for a role in metastasis is stronger—and recent studies lend credence to this hypothesis. Karin’s group reported in the April 5 Nature that inflammation, not genetic changes in cancer cells, spurs metastasis in mice engineered to acquire prostate cancer. The research suggests that a cytokine produced by inflammatory cells near a prostate tumor induces tumor cells to decrease production of a protein that blocks metastasis. This result, Karin notes, may explain the puzzling observation that cutting into tumors, such as for a prostate biopsy, sometimes seems to encourage metastasis. If he is correct, the inflammation generated by the intervention could be at fault. Around the same time, Pollard’s group reported in Cancer Research on a study in mice that observed that macrophages accompany breast tumor cells in their migration toward blood vessels that will transport them to remote sites, all the while sending chemical messages to their partners."
"Instead of just killing cancer cells—the goal of current drug therapies and radiation—new approaches may supplement existing drugs by slowing inflammation. Without the involvement of macrophages and other innate cells, the premalignant tissue would remain in check.
Cancer could, in essence, become a chronic disease akin to rheumatoid arthritis, another inflammatory condition. “Keep in mind almost no one dies of primary cancer,” says Raymond DuBois, provost of the University of Texas M. D. Anderson Cancer Center and a researcher of anti-inflammatory agents for cancer. “A patient almost always dies from a metastasis.”
A pharmaceutical against chronic inflammation represents a more alluring proposition than massacring malignant cells (and, unavoidably, healthy ones), a consequence of existing chemotherapies. Taken alone, such an agent might be benign enough to use every day as a preventive for high-risk patients."
"Still, it seems likely that a new generation of anti-inflammatory agents will join the chemotherapeutic arsenal. Chronic diseases—and their underlying inflammatory conditions—are hallmarks of an aging population. “We’re all a little bit overinflamed,” Pollard observes. Treating the smoldering embers that surround the tumor rather than just mutant cells could make cancer a disease we can live with."
Article at:
http://www.scientificamerican.com/article/chronic-inflammation-cancer/
Research finds link between chronic inflammation, tumor development in breast cancer, Published On: Jun 10 2015 05:05:36 PM EDT Updated On: Jun 10 2015 05:18:45 PM EDT
2 minute Video at:
http://www.local10.com/news/health/research-finds-link-between-chronic-inflammation-tumor-development-in-breast-cancer/33510556
Dementia Drug Developer Axovant Climbs After $315M IPO at ABC News,
Jun 11, 2015
Excerpts:
"Shares of Axovant Sciences nearly doubled in value after the dementia drug developer said its initial public offering raised $315 million, more than Axovant had expected.
The offering valued Axovant at around $1.4 billion, and the stock climbed $14.90, or 99 percent, to end its first trading day at $29.90. It peaked at $31.17. Several biotech companies have had sizeable IPOs this year and seen their shares jump, including Aduro Biotech Inc., which doubled in valued on its first day of trading after a $119 million IPO. Shares of BluePrint Medicines Corp. are up more than 80 percent since their debut in late April.
Axovant Sciences Ltd. expanded its offering to 21 million shares and said the offering priced at $15 a share, at the high end of its estimates. It plans to use proceeds to fund research and for general corporate purposes. The shares are trading under the symbol "AXON."
The company's main drug candidate is called RVT-101. Axovant is preparing to start late-stage trials of RVT-101 as a once-per-day treatment for dementia caused by Alzheimer's disease and also wants to study the drug as a treatment for other types of dementia. British drugmaker GlaxoSmithKline PLC previously studied the drug in 13 clinical trials, but sold it to Axovant in December in a relatively modest deal that included a $5 million upfront payment."
Article at:
http://abcnews.go.com/Business/wireStory/alzheimers-drug-developer-axovant-climbs-315m-ipo-31692244