Dimebon Dimebolin Information Availability &#187; Alzheimer Disease

Pfizer, Medivation end development of potential Alzheimer’s treatment Dimebon

admin — Sat, 21 Jan 2012 12:26:49 +0000

TRENTON, N.J. — In a major setback for patients and doctors, drugmakers Pfizer Inc. and Medivation Inc. have halted development of a potential Alzheimer’s disease treatment after the drug for a second time yielded disappointing results in a late-stage clinical study.Dimebon was furthest along in testing among the experimental Alzheimer’s drugs being developed to try to stop or even reverse the course of the mind-robbing disease. Dimebon would have been the first such drug and specialists just a couple of years ago had hoped it would be on the market this year.

Pfizer, the world’s largest drugmaker by revenue, and Medivation said on Tuesday that Dimebon failed to significantly improve cognitive ability, as well as self-care and daily functions in patients with mild-to-moderate cases of the disease. The study involved about 1,000 patients who had Dimebon added to their ongoing treatment with Pfizer’s former blockbuster Alzheimer’s drug donepezil, or Aricept.

Aricept, jointly marketed by Pfizer and Japan’s Esai Co. Ltd. and once heavily advertised, had about $3.7 billion in sales in 2009. It lost U.S. patent protection in November 2010, and sales have since plunged.

Dimebon, known chemically as latrepirdine, would have been an even bigger blockbuster if it had panned out. The experimental drug looked promising after it kept Alzheimer’s symptoms from worsening for a year in an earlier patient study.

But Dimebon didn’t work as hoped in a late-stage trial in which patients took it for six months. After those results, announced in March 2010, the companies said they were continuing three other studies that could prove Dimebon helped patients in combination with other Alzheimer’s drugs or when used for a longer period.

Then last April Pfizer and Medivation said Dimebon also failed in another late-stage clinical trial, when it did not improve symptoms of the neurologic disorder Huntington’s Disease.

After the latest failure, New York-based Pfizer and Medivation, headquartered in San Francisco, said they are ending development of Dimebon, as well as their agreement to market the potential treatment.

Pfizer still has one Alzheimer’s treatment in late-stage testing, bapineuzamab, which it is jointly developing with Johnson & Johnson. It’s a biologic drug, grown in living cells rather than made by mixing chemicals, and works differently than Dimebon.

Alzheimer’s disease is the most common form of dementia, and drugmakers are trying to find a treatment that does more than temporarily ease the symptoms: memory problems, confusion, aggression and a general decline in ability to function, which together can hasten death. Many drugs have flopped in late-stage testing in recent years, including some that seemed to clear harmful plaque from afflicted brains.

The newest drug for Alzheimer’s symptoms, Namenda, was approved back in 2003.

Cases of Alzheimer’s disease are expected to triple by 2050, to around 106 million people worldwide. The disease strikes nearly a half million new patients a year, mainly as people hit their 70s or 80s.

In trading Tuesday, Pfizer shares rose 9 cents to $21.93, while Medivation stock dropped $1.82, or 3.3 percent, to $53.90.

http://www.washingtonpost.com/business/industries/pfizer-medivation-end-development-of-potential-alzheimers-treatment-dimebon/2012/01/17/gIQA91uF5P_story.html

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Sobering Statistics about Alzheimer’s Disease

admin — Thu, 22 Dec 2011 06:10:53 +0000

Each day, 1,232 people are diagnosed with Alzheimer’s disease.

Each week, 8,634 people are diagnosed with Alzheimer’s disease.

Every 70 seconds someone is diagnosed with Alzheimer’s disease….

Editor Note: For more statistics on Alzheimer’s disease see –

Alzheimer’s Disease Statistics

By the time you finish reading this article a few more people will be officially suffering from Alzheimer’s disease.

Here is a startling perspective.

It is not unusual for a person working on Wall Street (New York) to spend a total of three hours a day commuting to and from work. Many of these people live on Long Island, in Connecticut and New Jersey.

There are 180 minutes in three hours. There are 10,800 seconds in three hours.

While these people are commuting to and from work each day, another 154 persons are diagnosed with Alzheimer’s.

_____________________________

Each day, 1,232 people are diagnosed with Alzheimer’s disease.

Each week, 8,634 people are diagnosed with Alzheimer’s disease.

_____________________________A recent Harris Interactive poll showed that more than 100 million Americans have been touched by Alzheimer’s. More than 33 million Americans are worried about Alzheimer’s disease.

Startling numbers.

Alzheimer’s disease is a death sentence. Brain death. A typical person takes from 5-20 years to die. It is not unusual for the disease to take more than a decade to kill someone.

When most people think about Alzheimer’s they think about a person losing their memory. Persons that know someone suffering from Alzheimer’s disease watch them lose their ability to brush their teeth, take a shower, put on their cloths, go to the bathroom, and eat.

They await the worse day of them all — the day the person suffering from Alzheimer’s won’t know them. Or anyone for that matter.

Alzheimer’s disease is sinister and ugly.

If you don’t know someone directly or indirectly that is suffering from Alzheimer’s you will soon. It might have happened while you were reading this article.

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Why Can’t I Buy Dimebon for Alzheimer’s?

admin — Thu, 17 Nov 2011 06:11:56 +0000

Why can’t, I, WE, buy Dimebon for Alzheimer’s disease?

TERMINATED. That is the word they used when the Dimebon clinical trial that my mother was enrolled in was abruptly canceled on May 7, 2010.

The termination was caused by the failure of the Dimebon Connection Study. My mother was not enrolled in the that study. But, because the study failed to produce the necessary results for potential FDA approval the rug was pulled from under our feet.

We weren’t the only ones. There were more than 2,000 patients enrolled in Dimebon clinical trials. This means at least 1,000 participants received Dimebon. The other participants received a placebo.

The study was not terminated due to any safety findings. Dimebon was well-tolerated in clinical trials.

Safety was not an issue. The problem was efficacy. In other words, the drug did not provide enough benefit to participants. From a statistical standpoint it did not stop memory loss. There was some benefits registered on the behavior scale.

Now to my point.

Dotty did benefit. While on Dimebon, she was more alert and her behavior was dramatically improved over what I had come to expect.

Keep in mind here, Dotty was diagnosed before entering the clinical trial as being in the moderate to severe stage of Alzheimer’s. She scored 14 on the MMSE. She also scored 16 during the trial.

I did ask the personnel at the clinical trial site if they thought that Dotty was showing any improvement. They told me yes. I asked how?

Here is an example. At the outset of the clinical trial they showed Dotty a picture of a fork. Then asked, what do you with this? She could not say or demonstrate how you use a fork. When they put a fork in her hand she could demonstrate what you do with a fork.

Later in the study, they did the same test over. Sure enough, Dotty looked at the picture of the fork and then demonstrated what you do with a fork.

By the way, by the point in the clinical trial I didn’t have to ask anyone anything. I saw with my own eyes, ears, and brains that Dotty was a different person.

How much better?

Hold on tight. Better than she had been in many years. Let me set this straight. I couldn’t tell if there was any improvement in Dotty’s memory, and if you would like to know the truth, I didn’t care.

What I did care about was that Dotty seemed to be more interested in living her life. She was a fuller, better person.

My point. I can accept memory loss. I don’t spend much time thinking about Dotty’s memory, or what she can or can’t remember. What I do care about is the look on Dotty’s face, and how she responds to activity.

Dotty clearly looked more there, and was clearly experiencing “more enjoyment”.

As my close friends know, I was “dancing on the ceiling”.

We are not the only one’s that saw benefits from Dimebon. There are several articles and stories on this website from other caregivers that were enrolled in the Dimebon clinical trials.

I know they want an answer to this question.

Why Can’t We Buy Dimebon in the United States?

The drug is safe. The drug has been used in Russia since 1983.

And, Dimebon was proven to be safe in the clinical trials.

http://www.alzheimersreadingroom.com/2011/11/why-cant-i-buy-dimebon-for-alzheimers.html

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Alzheimer’s Association statement on negative Phase III trial results for latrepirdine (Dimebon)

admin — Tue, 09 Aug 2011 15:15:39 +0000

“The Alzheimer’s Association is disappointed to learn of the negative results from the Phase III clinical trial of latrepirdine (Dimebon),” said William Thies, Ph.D., Alzheimer’s Association chief medical and scientific officer. “People with Alzheimer’s, their families and caregivers desperately need more and better treatment options for this devastating, fatal brain disease.”

Nonetheless, the Alzheimer’s Association remains optimistic about the future prospects for better Alzheimer treatments and prevention strategies. Several dozen other compounds are in the pipeline for Alzheimer’s disease. We remain encouraged by the fact that drugs in the pipeline for Alzheimer’s attack the disease from a variety of angles.

“The population is aging, and we need to make significant advances soon in the treatment and prevention of Alzheimer’s. It is an overwhelming epidemic, already claiming millions of individuals, and it is on track to deplete our healthcare resources and devastate Medicare,” Thies said. “The current level of federal research funding for Alzheimer’s is unacceptable considering the many millions of people this disease affects and the huge financial impact on our economy and society. And, these numbers will grow exponentially with the aging of our population.”

According to the Association, in order to get better diagnosis, treatments and prevention for Alzheimer’s, we must address two important issues:

(1) We must address the chronic underinvestment in research to ultimately solve the Alzheimer crisis. We need to get more Alzheimer drugs in the pipeline. To do this, we must increase the research investment in Alzheimer’s to levels similar to other leading causes of death, such as cancer and heart disease. Only then will we have the chance to see the same type of progress — such as declining death rates, and viable lifestyle-based prevention strategies — and stop this epidemic. If we do not invest now, the cost of Alzheimer’s disease to taxpayers in Medicare and Medicaid costs will be $20 trillion dollars over the next 40 years — equal to 25 economic stimulus bills.

(2) In addition to increasing funding, it is imperative that people volunteer for Alzheimer clinical trials. Later this year, at the Alzheimer’s Association 2010 International Conference on Alzheimer’s Disease (ICAD), the Association is planning to launch a first of its kind tool to help match people with Alzheimer’s and caregivers with Alzheimer clinical trials.

Next week, the Alzheimer’s Association is bringing together advocates from across the country at the Alzheimer’s Action Summit to encourage legislators to increase funding for Alzheimer’s disease. Join us in Washington, D.C. or take action virtually at alz.org.

The Alzheimer’s Association
The Alzheimer’s Association is the leading voluntary health organization in Alzheimer care, support and research. Our mission is to eliminate Alzheimer’s disease through the advancement of research; to provide and enhance care and support for all affected; and to reduce the risk of dementia through the promotion of brain health. Our vision is a world without Alzheimer’s.

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Amyloid Theory in Alzheimer's Takes Another Hit

admin — Thu, 21 Oct 2010 07:33:54 +0000

Clinical trials of a drug aimed at reducing beta-amyloid plaque accumulation in Alzheimer’s disease have been stopped because of lack of efficacy, striking another blow against the amyloid theory of the disease.

Eli Lilly announced that it was halting development of a drug called semagacestat, an inhibitor of the gamma-secretase enzyme that produces beta-amyloid protein, after preliminary results from two large placebo-controlled trials indicated no benefit from the treatment.

“It did not slow disease progression and was associated with worsening of clinical measures of cognition and the ability to perform activities of daily living,” according to a Lilly press release.

The trials had a total of more than 2,600 participants with mild to moderate Alzheimer’s disease. Patients receiving the drug showed greater declines in these measures than did those in the placebo groups.

Lilly said it had instructed site investigators to stop dosing patients as soon as possible but to continue following participants for at least six months to collect cognitive function scores and safety data.

“These additional follow-up visits will help to answer a number of important questions, including whether the differences between patients who received semagacestat and those who received placebo will continue after semagacestat has been discontinued,” the company indicated.

The two trials began in 2008; one was scheduled to run until June 2011 and the other until March 2012.

Lilly is also halting other, smaller, short-term studies of semagacestat.

The drug is the latest anti-amyloid agent to fail in late-stage, placebo-controlled trials, casting more doubt on whether this approach can ever work in established Alzheimer’s disease.

Negative clinical results have also been found for tarenflurbil, latrepirdine (Dimebon), and bapineuzumab, which target beta-amyloid protein production or the sticky plaques that form when soluble beta-amyloid changes shape to become fibrous and insoluble.

But development of bapineuzumab is continuing, with preliminary PET scan data indicating that the drug successfully breaks up amyloid plaques in Alzheimer’s patients as intended. Clinical results from the phase III study are now eagerly awaited in the Alzheimer’s community.

The Lilly trials of semagacestat also included PET scans to measure effects on plaque burden. The company’s announcement did not include those results; a Lilly spokesman said the PET data were still blinded and would not be available for analysis for at least six months.

Those data could be critical in determining whether beta-amyloid is a worthwhile target for Alzheimer’s drugs, as well as what went wrong with semagacestat specifically.

A finding that semagacestat treatment did reduce plaque accumulation, yet failed to show clinical benefit, might suggest that this approach will not work in patients with established symptoms.

But Samuel Gandy, MD, of Mount Sinai School of Medicine in New York City, told MedPage Today that it might only cast doubt on gamma-secretase as the specific target.

“There are new data suggesting that some of the gamma-secretase genes that cause familial Alzheimer’s also lower enzyme activity,” Gandy wrote in an e-mail.” This could be the explanation for the Lilly drug: i.e., that low gamma-secretase activity can be part of the disease and therefore using an inhibitor might be very challenging.”

He agreed that the PET data would be important in figuring out what happened.

“If the amyloid burden got worse, that means that low gamma-secretase activity can increase amyloid buildup like in familial AD. If the amyloid burden got better, that could suggest that some other gamma secretase substrate (e.g., Notch) was also inhibited and caused side effects,” Gandy said.

Lilly emphasized that it was not giving up yet on beta-amyloid as a target. The company is continuing development of an anti-amyloid monoclonal antibody, solanezumab, with two phase III trials now underway.

Dealing with Caregiver Stress

admin — Wed, 06 Oct 2010 13:57:11 +0000

Are you providing care at home to a loved one who suffers from a disease or other health problem? Or are you, perhaps, the primary contact for a loved one in hospital or a nursing home? Either of these roles can place extra demands on your time and energy, and may lead to additional stress in your life.

The following tips can help you manage this stress so you can provide the best possible support to the person dear to you.

Try to find out all you can about the specific disease or condition – Parkinson’s, Alzheimer disease, Huntington’s, Korea or other health problem. All these conditions have websites: Parkinson.ca, Alzheimer.mb.ca or huntingtonsociety.ca. By getting the facts, you can set realistic expectations for yourself about what you are capable of doing. It will also give you an idea of what to expect.
Get some help. You can consider joining a support group or speaking to a therapist. Talking and sharing with like minded individuals can decrease caregiver stress. A therapist can guide you on how to balance the care of your loved with taking care of yourself. Remember you can’t take care of another person if you are not well yourself.
Surround yourself with friends and build up a support network. You want to be around people who are positive; people who you can call on and possibly go for a walk or even shop with. We all have those amazing friends who celebrate in our successes and share our burdens. Surround yourself with these people.
Practice self-care: eat right, exercise and get enough sleep! How many times have we been told on TV or in magazines that walking, cycling, or going to a gym at least three times a week has numerous benefits and that getting eight hours’ sleep is more important than anything. It’s well documented that for every mile you run or walk you add another minute to your life. So leave the car at home and walk to the grocery store when you can, and turn the TV off and go to bed early. In addition, appreciate humour. A good laugh can lighten almost any burden. Finally, consider adding a few guilt-free breaks from caring to your schedule. This will help you avoid burn-out.
Simplify your lifestyle by letting go of less meaningful things to conserve your time and energy for what is more important. Accept that you may not be able to do the things you would normally. I have a magnet on my fridge which says: “So I’m not super Mom – Adjust”.
Choose how you react to situations: We all make choices every day. If an unexpected situation develops you can choose to get angry, cry, laugh it off or let it go. Your reaction is your choice. Keep in mind that you have no control over anyone else’s behaviour. The late comedian, George Carlin, once said: “If you can smile when things go wrong, you probably have someone in mind to blame.”
Start a journal. “Journaling” is an effective way to express your emotions. Putting pen to paper can help you see things more clearly and put them into perspective.

None of us can totally eliminate stress from our lives. We need some stress to help us accomplish tasks and even to motivate us. The important thing is to remember to deal with this stress in a positive and healthy way. You will probably find that as you manage, and hopefully reduce, your caregiver stress , your energy, motivation and strength will increase. This in turn will help you to be more effective in caring for your loved one.

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Keeping brains working

admin — Wed, 29 Sep 2010 08:18:11 +0000

Alzheimer’s disease remains a difficult target as companies follow a variety of paths in search of treatments

Millions of dollars — much of it pouring into the Bay Area — is translating into cutting-edge research and potential drugs to tackle Alzheimer’s disease.

Yet despite breakthroughs in South San Francisco and Palo Alto and drug candidates under study in San Francisco, Novato and Berkeley, there still is no way to halt the mind-crippling disease.

The exact cause of Alzheimer’s remains elusive. What’s more, especially after a number of high-profile failures of once-promising drugs, scientists still aren’t sure if drugs now in development target Alzheimer’s triggers or its by-products.

“This is a multi-cause disease,” said Lennart Mucke, director of the neurological institute within the J. David Gladstone Institutes in San Francisco, “and we need more of an attack.”

The reality is grim: It could be five or 10 years — ormore — before science finds a drug or a combination of drugs to slow or halt the disease, let alone wipe it out.

As baby boomers grow older and live longer, today’s roster of 5.3 million Alzheimer’s patients will double by 2030 andcontinue to strip even the sharpest minds of their memories and dignity.

Basic research funding from the federal government, meanwhile, remains low for Alzheimer’s. That has narrowed the pipeline of potential new drugs, advocates say, as a tidal wave of new Alzheimer’s cases nears.

“These are sobering, challenging times,” said Bill Fisher, CEO of the Alzheimer’s Association of Northern California/Northern Nevada. “We need to realize we’re in this for the long haul and take heart for the increase in knowledge.”

No single answer

Yet baby boomers are big business in sickness and health, and the growing number of Alzheimer’s patients represents a staggering opportunity for drug developers. Biopharmaceutical industry players — ranging from giants like South San Francisco-based Genentech Inc. and Pfizer Inc. to smaller Plexxikon Inc. of Berkeley and BioMarin Pharmaceutical Inc. of Novato — are working on potential Alzheimer’s drugs.

Four FDA-approved medicines are used to treat Alzheimer’s symptoms — Pfizer’s Aricept, Novartis’ Exelon, Janssen Ortho’s Reminyl and Forest Laboratories’ Namenda — but none are proven to stop or reverse the disease.

Other drugs, notably Dimebon from San Francisco’s Medivation Inc. and, last month, semagacestat at Eli Lilly and Co., have failed in late-stage trials aimed at becoming the first new Alzheimer’s treatment in close to a decade.

Much of the research has tracked amyloid beta, clumps of proteins found in the brain of Alzheimer’s patients as well as some who haven’t developed the disease. Amyloid seems to act as a coolant for the brain, but too much can throw the process out of whack and cause neurons to commit suicide.

Janssen Alzheimer Immunotherapy, an Irish company with its R&D base in South San Francisco, has a Phase III drug that targets amyloid beta.

But amyloid starts to build up as much as 10 years before Alzheimer’s symptoms appear. By the time the disease is diagnosed — with patients becoming more irritable and irrational as their spouses, friends and children are increasingly unrecognizable to them — the neuronal loss already is substantial.

“The entire field is trying to come up with earlier diagnosis and earlier intervention,” said Stef Heylen, who heads Janssen AI’s research as chief medical officer. “If you could intervene early, the prospect for the patient could be better.”

Mucke’s lab at the Gladstone Institutes, for one, is trying to make the brain more resistant to the amyloid proteins that aren’t removed naturally. One way of doing that could be by lowering the amount of the protein tau, which would help the brain balance the increase in amyloid.

Gladstone is working with the University of California, San Francisco, including UCSF’s Memory and Aging Center, to make electroencephalography, or EEG, recordings to look for potential ties between epilepsy and Alzheimer’s.

Gladstone also is working with Merck & Co. on a possible drug to block the most detrimental effects of ApoE4, which is believed to be the main genetic risk factor for Alzheimer’s.

Eventually, Mucke and other scientists said, an effective Alzheimer’s treatment may be a cocktail of drugs like those used to combat HIV. Some drugs may limit amyloid beta, others may target ApoE4 or tau, and others may go after other mechanisms.

“There are often no single answers to complex problems,” Mucke said.

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Amyloid Theory in Alzheimer's Takes Another Hit

admin — Sun, 19 Sep 2010 03:54:20 +0000

The two trials began in 2008; one was scheduled to run until June 2011 and the other until March 2012.

Lilly is also halting other, smaller, short-term studies of semagacestat.

The drug is the latest anti-amyloid agent to fail in late-stage, placebo-controlled trials, casting more doubt on whether this approach can ever work in established Alzheimer’s disease.

Those data could be critical in determining whether beta-amyloid is a worthwhile target for Alzheimer’s drugs, as well as what went wrong with semagacestat specifically.

A finding that semagacestat treatment did reduce plaque accumulation, yet failed to show clinical benefit, might suggest that this approach will not work in patients with established symptoms.

But Samuel Gandy, MD, of Mount Sinai School of Medicine in New York City, told MedPage Today that it might only cast doubt on gamma-secretase as the specific target.

He agreed that the PET data would be important in figuring out what happened.

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Eli Lilly Halts Alzheimer's Drug Trial

admin — Thu, 16 Sep 2010 03:53:59 +0000

NDIANAPOLIS (TheStreet) — Eli Lilly(LLY) was forced to halt development of an experimental Alzheimer’s disease drug after an early look at results from two late-stage clinical trials determined the drug to be ineffective.

Lilly shares fell 2% to $34.75 in Tuesday’s pre-market trading on news of the setback for the Alzheimer’s drug semagacestat, one of two drugs being in the company’s pipeline that are in late-stage studies against the neuro-degenerative disease.

The failure of semagacestat will also heighten concerns about Lilly’s future growth given the looming loss of patent protection through 2014 on drugs that presently account for 60% of the company’s revenue.

Tuesday, Lilly said it would take a charge of 3-4 cents a share in the third quarter to account for the halting of the semagacestat clinical trials. The company reiterated 2010 guidance of $4.44 to $4.59 a share on a reported basis.

The two phase III clinical trials of semagacestat enrolled more than 2,600 patients with mild to moderate Alzheimer’s, randomizing them to treatment with semagacestat or a placebo. An interim analysis of the studies found that semagacestat-treated patients were performing worse on tests of cognition and ability to complete daily living tasks compared to patients treated with a placebo. In addition, semagacestat patients were at a higher risk for developing skin cancer.

Lilly said Tuesday that phase III trials involving the company’s other late-stage Alzheimer’s drug solanezumab are continuing. Both semagacestat and solanezumab are designed to reduce the levels of amyloid beta plaques, protein substances that attach to and destroy neurons in the brain. Amyloid beta is thought to one of the causes of Alzheimer’s.

Semagacestat works by inhibiting an enzyme, gamma secretase, which the body uses to form amyloid beta plaques.

Earlier this year, Pfizer(PFE) and Medivation(MDVN) said a phase III study of their Alzheimer’s drug Dimebon also failed, although additional clinical trials of that drug continue.