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Micro dosing botox - https://www.yahoo.com/lifestyle/microdosing-botox-trend-spiking-york-150036973.html
Microdosing had a big year. From Silicon Valley execs to A-list comedians, it seems that everyone had an opinion on the supposedly life-altering benefits of extreme moderation in 2019. But it’s not just tiny doses of THC or psychedelics making headlines: The just-a-little-bit approach is trending in beauty, too.
“Micro-Botox” is an injectable technique in which itty-bitty amounts of a neuromodulator (like Botox Cosmetic, Dysport, or Xeomin) are used to tighten pores and tame oil and sweat production, in addition to providing more natural-looking line reduction. According to top dermatologists in Los Angeles and New York, the procedure is a rising star in doctors’ offices everywhere, where it’s also nicknamed baby Botox, microtox, mesobotox, or skin Botox.
Of course, there are nuances to the burgeoning trend — and, as with any injectable, there are still risks, so studying up is the best jumping-off point. So, what does it really mean to microdose Botox, and what do you need to know before you book an appointment? We checked in with the experts to answer all our burning questions, below.
What is micro-Botox?
“Micro-Botox refers to the injection of multiple small doses of Botox into the skin,” says Chaneve Jeanniton, MD, board-certified oculofacial plastic surgeon and founder of Brooklyn Face & Eye in New York. ”It’s injected superficially and therefore only targets the skin, where oil production, facial flushing, and acne occur. But it differs from conventional Botox as it does not iron out wrinkles caused by muscle contractions.” That’s right: Botox injected at the top layer of the skin works to control oil and redness while making pores appear smaller, which could mean fewer breakouts, but won’t stamp out wrinkles.
Perhaps the biggest caveat is that, because this treatment goes by many names, it can mean different things for different injectors. Where one doctor might stick to subdermal injections just at the surface level of the skin for a patient who wants to reduce sweat (similar to an armpit injection) or oil, another might go a little deeper to also lightly paralyze the muscle for added fine-line reduction. Like all parts of dermatology, it’s not an exact science, so it’s very important to ask questions, do your research, and ultimately make sure you and your injector are on the same page about your goals.
For Karyn Grossman, MD, a board-certified L.A. cosmetic dermatologist with a celebrity following, micro-Botox means just barely entering the muscle to soften, but not paralyze, the patient’s expression. “You can inject neuromodulator in different amounts in similar places [to a traditional Botox injection], but place it higher in the skin,” she says of her technique. Her main objective is to avoid the “frozen” look at all costs, which is where micro-Botox often comes in handy. “Frozen is not youthful,” she adds.
Vanessa Lee, RN, founder and in-demand injector at L.A.’s The Things We Do, falls somewhere in the middle. She says that she likes to “just barely kiss” the muscle with the Botox for a slight smoothing effect. “It doesn’t take away fine lines by any means, but it is a significant change in the skin,” she says, noting that the softened look results in a “did she or didn’t she?” effect that’s very natural-looking — fresh, not frozen.
How long does it last?
Just like Botox applied in the traditional way (injected into the muscle), micro-Botox lasts up to three or four months; however, there are some potential long-term benefits when mixed with H.A. filler.
Should you mix micro-Botox with other injectables?
Cocktailing or layering Botox with hyaluronic acid dermal filler isn’t just common — our experts say that the technique is actually more valuable than the sum of its parts. “You get a synergistic effect when you decrease muscle contraction and put a little stretch [on the skin] with fillers,” Dr. Grossman says, noting that this is believed to be one way to prompt your body to make more collagen, a building block of youthful skin that tapers off as we age.
“My favorite cocktail for this treatment is Botox, hyaluronic acid filler, and vitamin C,” Dr. Jeanniton says. “It results in smooth, plump, glowing skin. I will often also add PRP to the mixture for a truly sublime result.”
What should I look for in an injector?
Necessary qualifications vary by state, but Dr. Grossman says that finding a skilled injector is very important, on top of checking out their qualifications. “Intradermal injecting is a more difficult skill to learn than the subdermal,” she says. “It’s a precision thing.” Pick someone who lacks skill, she says, and you could put yourself at risk.
So, what are the risks?
“After treatment, minor swelling and redness and the possibility of slight bruising are expected, similar to regular Botox injections,” says Dr. Jeanniton. Adding in H.A. filler? Uneven texture is also a possibility, says Dr Grossman, who adds that while occlusions — which is what happens if an injector accidentally enters a vein — are rare, they can occur whenever injecting into vascular areas, even the skin. “There’s never no risk,” Dr. Grossman says.
Then, there are longterm risks. “One risk is weakening of muscles on the face, which can interfere with facial expressions,” says Joshua Zeichner, MD, board-certified dermatologist and director of cosmetic and clinical research in dermatology at New York’s Mount Sinai Hospital. Dr. Grossman agrees, noting that muscles of the face can eventually atrophy, which means that restraint is important if this is something you plan on maintaining.
Who’s a good candidate?
Essentially, anyone who is looking for any of the aforementioned benefits is a candidate, but Lee says those with dry skin should avoid the treatment or risk making skin drier due to decreased oil and sweat.
Is micro-Botox more popular than regular Botox?
Our experts say that, while it hasn’t usurped traditional Botox injection techniques, the trend shows no signs of slowing. “As issues like excess oil production are a relatively unmet need, I do think that micro-Botox will continue to gain popularity,” says Dr. Zeichner.
Different iterations of the treatment are also taking off. At Lee’s L.A. practice, injectors administer Botox mixed with H.A. filler via a microinfusion punch, which is basically a microneedling device that lightly punches the concoction into the skin using gold-plated .6mm needles. She says patients love it for both the immediate results and the longterm microneedling benefits.
How much does it cost?
It depends on where you live and the experience of your injector, but expect to pay in the ballpark of $500.
Does it hurt?
Dr. Grossman notes that, the closer the injection is to the surface of the skin, the more painful it is. Plus, since the product needs to be properly diffused, many injections are necessary. “It may be uncomfortable, as many pinches are given to the skin,” Dr. Zeichner says. Dr. Jeanniton adds that “a needle could be inserted anywhere from 50 to 100 times over the face compared to 5 to 20 times for traditional Botox injections,” so numbing cream is commonly applied before the treatment.
Like what you see? How about some more R29 goodness, right here?
Biotech in China
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A scientist in a biobank.
China’s largest biobank at Zhangjiang High-Tech Park, Shanghai.Credit: Imaginechina/REX/Shutterstock
Timing can make a big difference in a career. Is it worthwhile to stay longer in a comfortable job or is it the right moment to strike out for a new challenge? Similarly, timing can make all the difference when deciding to enter a developing market like China.
Just a decade ago, when China-born scientists with overseas experience began returning to the country, lured by their homeland’s fast growth and growing financial means, they found a drug industry dominated by generics. Undeterred, they got busy building the infrastructure for an industry capable of drug discovery and development, buoyed by substantial government support and a thriving economy.
Part of Career guide: China
Today, biotech specialists arriving in China find an industry at a turning point, with many key elements in place for innovation: a university system churning out doctorates and strong basic research, substantial financial backing from both the private and public sectors, regulations that are becoming globally harmonized and a vibrant group of entrepreneurial leaders with ambitions for China and abroad.
They also find a country facing significant unmet medical needs — particularly in cancer, neurology and diabetes — and a rapidly ageing population. Although China is the world’s second largest pharmaceutical market after the United States, some of the most effective modern medicines are not on sale. For example, of the 42 cancer drugs approved globally in the past five years, only four are available in China. But this is set to change. Recent regulatory changes will bring imported drugs to China more quickly, and local biotechs are racing to develop domestic — and, they hope, global — blockbuster drugs. For academics and entrepreneurs, it is an ideal time to build on the biotech investments of the past, says Lan Huang, chief executive of New York-based BeyondSpring Pharmaceuticals, which is running drug trials in China.
A hunger for science
It only took two visits to Shanghai’s Zhangjiang Hi-Tech Park to convince Greg Scott to set up a life-science consulting business there, amid a hotbed of drug research and development (R&D) companies. He founded ChinaBio in 2007, and encourages others to consider a move to China. “Do it! It is a great experience,” he says. “If I was helping someone plan their career, China has to be a part of it as the number one drug market outside the United States.”
It is not just entrepreneurs and multinational drug company employees; many academic and staff scientists also find working in China a stimulating career move. Ray Stevens, a chemist renowned for determining the crystal structures of the body’s receptors, which are important for identifying drug targets, can recall the exact moment he decided to trade sunny California for Shanghai, uprooting his school-age children and wife. Like many academics, he had visited China several times, but it was not until 2009, after delivering a talk on membrane proteins to colleagues in the neighbouring city of Suzhou, that he decided to make the move.
“One of the big attractions was the energy and excitement the students had for science. It won me over,” Stevens says. After he had finished his talk, “a group of students came up to the podium to ask questions. They kept asking questions as I made my way to the bathroom and even followed me in. I was amazed; they were so hungry. It was the moment I decided to spend my sabbatical in China”.
In 2011, Stevens moved to China as a visiting professor. Just a year later, the president of ShanghaiTech University, Mianheng Jiang, came calling, offering the chance to set up his own institute. He now runs the iHuman Institute at ShanghaiTech, is a member of China’s Thousand Talents Plan and was in 2017 awarded a Magnolia Prize, an accolade given to foreigners who have contributed significantly to Shanghai’s development. He has also co-founded a biotech company, RuiYi, in Shanghai.
Building biotech
The passion for science that Stevens discovered did not spring up accidentally. It has been fostered by government support for biotechnology that has intensified over the past decade, creating a force attracting scientists and the entrepreneurially inclined to China. Of the 2 million returnees to China over the past 6 years, it is estimated 250,000 work in the life sciences. And, although many scientists making the move were born and raised in China and have a decade or more experience working in the West, non-Chinese speakers such as Stevens and Scott are coming and thriving here, too.
The push for innovation comes from the highest levels of government, with the biotech industry receiving special attention in not just one but three of the government’s latest five-year plans: the strategic blueprints that determine the country’s economic goals for the forthcoming half-decade. The latest plan, China’s thirteenth, stipulates that the biotechnology sector should exceed 4% of gross domestic product by 2020 and that there should be 10 to 20 life-science parks for biomedicine with an output surpassing 10 billion yuan (US$1.5?billion). China has more than 100 life-science parks dotted across the country; run by local governments, these hubs lure companies with tax breaks and subsidies. It is estimated that more than $100?billion has already been invested in the life-sciences sector by state, provincial or local governments in an effort to hit the five-year-plan targets.
The Thousand Talents Plan has been especially successful at recruiting life-science talent. “Since 2008, 7,000 returnees have been recruited across all disciplines,” says Dan Zhang, former secretary-general of the Thousand Talents programme and chief executive of Fountain Medical Development in Beijing, which helps companies to carry out clinical trials. “The life sciences committee for biotech is one of the largest groups in the programme. We’ve recruited more than 1,400 people, from both science and industry — including company founders, chief scientific officers or leading academics.”
Returnees, especially those recruited via the Thousand Talents Plan, have had a “huge impact” on the industry, says Zhang. He says that returnees are the force behind the majority of drug approvals in China, that they fill peer review committees and life-science faculties, and that many are made university deans of schools of pharmacy and medicine. Sheng Ding, for example, has split his time between a biomedical-research facility in California and Tsinghua University in Beijing as dean of the school of pharmaceutical sciences since 2015. The generous grants and prestige of a place on the Thousand Talents Plan or similar programmes can increase an applicant’s attractiveness to employers and enable them to command higher salaries.
Deep pockets
Since the global financial crisis, financing for biotechs in China has been on the rise, whereas the sector has taken a hit in the West. Chinese investors who are looking to diversify their portfolios away from property and manufacturing are encouraged by the growth prospects of the life sciences, given China’s unmet medical needs and ageing population. Chinese venture capital and private equity funds raised $45?billion for investment in the life sciences in the two and half years prior to June 2017, according to ChinaBio. So far, only $12?billion has been invested in the industry, with financiers on the hunt for good companies to invest in. Most of the cash is going towards financing innovative biotechs that are, in turn, hiring at a rapid pace (see ‘Three years’).
THREE YEARS
https://www.nature.com/articles/d41586-018-00542-3
I have been a little surprised that no question came up yesterday or in previous presentation by CFO about whether MNTA was developing their Humira biosimilar to be interchangable and Craig simply referred to it as a high quality biosimilar and interchangable status was never mentioned. Is there a reason they would not talk about that?
Thanks
Here is a different take on Alzheimers that has shown promise. Write up from "Aging" and podcast from "Stemtalk"
http://www.aging-us.com/article/100690
https://www.ihmc.us/stemtalk/episode-12/
in 2014 Angiomax did about 157 million in US sales in 4th qtr. How long does patent protection extend now? This would seem(assuming approval)like a large value driver for EGRX.
Given the coming earnings, cash flow and pipeline I bought more shares today.
mizuho - from yahoo finance
http://www.investors.com/news/technology/eagle-pharma-downgraded-on-challenging-hospital-environment/?ven=YahooCP&src=AURLLED&ven=yahoo
njectable-drug specialist Eagle Pharmaceuticals (EGRX) stock was down sharply Monday after it got a downgrade from Mizuho saying that its thesis had played out.
Eagle stock jumped 28% on June 10 when Teva Pharmaceutical Industries (TEVA) won a patent case against several generic drugmakers, including Pfizer's (PFE) Hospira unit and Sagent Pharmaceuticals (SGNT), that were trying to launch generic versions of its blood-cancer drug Treanda. In January, Teva and Eagle launched a low-volume, faster-acting version of Treanda called Bendeka, which it says it expects to replace Treanda on the market eventually.
Mizuho analyst Irina Koffler wrote in her research note that she expects the companies to retain market exclusivity for Bendeka until 2019, but she said other catalysts might be slow in coming.
"The Treanda/Bendeka switch is a genuine success story for Eagle, but its other hospital launches like Ryanodex and Docetaxel have been more challenging," Koffler wrote as she downgraded the stock to neutral from buy. "We are reminded that cost is still critical within this setting, and this insight has influenced our longer-term outlook on Bendeka and the rest of Eagle's portfolio."
Koffler noted that Eagle is preparing to file for approval of a version of Eli Lilly's (LLY) lung-cancer drug Alimta, which is altered in a way similar to Bendeka's reformulation of Treanda, but she doubted that it will be as lucrative as the Teva deal.
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"We are concerned about competition from other 505(b)(2) filers like Allergan (AGN), who has already launched this type of product in EU," she wrote. "For this reason, we think that replicating a Bendeka-like agreement could be challenging here."
Eagle turned its first annual profit last year, of 16 cents a share, which analysts expect to jump to $4.56 this year with the help of the Bendeka launch. The stock nonetheless has a single-digit Relative Strength Rating, and it was down 12% in afternoon trading on the stock market today, under 40.
What was his reasoning?
it does seem counter intuitive. If anyone has seen the report please post his reasoning.
Vale output
http://www.mineweb.com/mineweb/view/mineweb/en/page39?oid=149679&sn=Detail&pid=39
severe weather conditions, including heavy rains, impacted Vale first-quarter output, both in Brazil and Australia.
Vale declared force majeure on some iron ore sales contracts on January 11 following heavy rainfall, and subsequently lifted the declaration on January 23.
"The summer season in the Southern Hemisphere was extremely rainy, hitting Brazilian mining districts such as the Iron Quadrangle in the southeast and Carajas in the north of the country, where our iron ore operations are concentrated," Vale noted in its first-quarter 2012 production report issued Tuesday.
Vale's iron ore production reached 70 million metric tons in the first quarter of the year, a 2.2% decline from the 71.54 million metric tons reported during the same quarter of last year. Rainfall at Carajas was even heavier than last summer as precipitation levels were 57% higher than in Q1 2011, reaching a peak in January of this year.
The heavy rainfall forced Vale to declare force majeure on January 11 after the weather led to stoppages on mining and railroad operations affecting the company's Southeastern and Southern Systems.
Nevertheless, Vale's pellet production increased 1.4% from 12.52 million metric tons in the first quarter of last year to 12.7 million metric tons for the first quarter of this year.
Manganese ore output dropped 2.9% in the first quarter from 498,000 metric tons in the first-quarter 2011 to 484,000 metric tons.
The rainy season and geological problems in Australia caused some problems for coal production, which nevertheless rose 65.4% on a year-on-year basis from 1.42 million metric tons in Q1 2011 to 2.4 million metric tons for the first-quarter 2012. The ramp up of the Moatize coal project in Mozambique contributed substantially to production.
Vale's nickel production rose 7.5% during the first quarter of this year from 59,000 metric tons in first-quarter 2011 to 63,000 metric tons. "The performance of this quarter was influenced by weaker production at Voisey's Bay and Sorowako, which more than offset the increases at Sudbury, VNC and Onca Puma," the company said.
First-quarter copper production was up slightly from 70,000 metric tons in the first-quarter 2011 to 73,000 metric tons. A maintenance shutdown of the Sossego operations and the temporary stoppage of mining at Sudbury impacted first-quarter 2012 production.
Production downtime at Vale's Sudbury mining operations impacted Q1 2012 platinum and palladium production as platinum production declined 33.4% to 38,000 troy ounces and palladium output dropped 18.6% to 59,000 ounces. Gold production during the same period dropped 36.9% to 19,000 ounces while silver output stayed steady at 595,000 ounces.
Vale's potash production dropped 12% in the first quarter of the year from 134,000 metric tons in 1Q11 to 118,000 metric tons. "The output reduction was caused by the geological conditions of the [Taquari-Vassouras] mine," said Vale. "We are implementing improvements in the infrastructure and conducting maintenance works to deal with these issues."
What is ex dividend date for Vale's April Dividend?
Thanks
One thing that Shea said a couple of times at end was "now that we are in a royalty situation" My understanding is that they will not be until Amphastar would launch and they would hope to prevent or delay this with suit so it seemed an odd choice of words. any thoughts?
Can you describe what you think the terms a settlement might contain?
Thanks
Interesting article on statins - http://www.sciencedaily.com/releases/2008/07/080703113631.htm
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Statins Have Unexpected Effect On Pool Of Powerful Brain Cells
ScienceDaily (July 6, 2008) — Cholesterol-lowering drugs known as statins have a profound effect on an elite group of cells important to brain health as we age, scientists at the University of Rochester Medical Center have found. The new findings shed light on a long-debated potential role for statins in the area of dementia.
See also:
Health & Medicine
* Stem Cells
* Brain Tumor
* Cancer
Mind & Brain
* Multiple Sclerosis
* Dementia
* Brain Injury
Reference
* Encephalopathy
* Astrocyte
* Multi-infarct dementia
* Brain damage
Neuroscientists found that statins, one of the most widely prescribed classes of medication ever used, have an unexpected effect on brain cells. Researchers looked at the effects of statins on glial progenitor cells, which help the brain stay healthy by serving as a crucial reservoir of cells that the brain can customize depending on its needs. The team found that the compounds spur the cells, which are very similar to stem cells, to shed their flexibility and become one particular type of cell.
The new findings come at a time of increasing awareness among neurologists and cardiologists of the possible effects of statins on the brain. Several studies have set out to show that statins provide some protection against dementia, but the evidence has been inconclusive at best. Meanwhile, there is some debate among physicians about whether statins might actually boost the risk of dementia. The new research published in the July issue of the journal Glia by Steven Goldman, M.D., Ph.D., and first author Fraser Sim, Ph.D., provides direct evidence for an effect of statins on brain cells.
"There has been a great deal of discussion about a link between statins and dementia, but evidence either way has been scant," said Goldman, a neurologist who led the team. "This new data provides a basis for further exploration.
"These findings were made through experiments done in cell culture using human brain cells and exposing them to doses of statins used widely in patients. But this research was not done in people. There are a great number of questions that need to be explored further before anyone considers changing the way statins are used," Goldman added.
Goldman's team is recognized as a leader identifying and directing the molecular signals that direct the development of stem cells and their daughter cells, known as progenitor cells. In this study, Sim ran a genomic screen to see which genes are more active in these cells compared to other brain cells. Sim and Goldman found several related to cholesterol, including the enzyme HMG-CoA reductase, which is central to making cholesterol and is the main target of statins.
"It was quite surprising that the cholesterol-signaling pathways are so active in these cells," Goldman said. "Since such signaling is blocked with compounds used literally by millions of patients every day, we decided to take a closer look."
The team measured the effects of two widely used statins, simvastatin and pravastatin, on glial progenitor cells, which can become either astrocytes or oligodendrocytes. The team looked at progenitor cells from 16 patients who had brain tissue removed during surgery to treat epilepsy, tumors, or vascular problems.
Scientists found that both compounds, when used at doses that mimic those that patients take, spur glial progenitor cells to develop into oligodendrocytes. For example, in one experiment, they found about five times as many oligodendrocytes in cultures of human progenitor cells exposed to pravastatin compared to cultures not exposed to the substance. Similarly, they found that the number of progenitor cells was just about one-sixth the level in cultures exposed to simvastatin compared to cultures not exposed to the compound.
To understand the process, think of a baseball team raising a group of great young prospects. They run fast, they throw hard, they hit well. Most teams will tailor their players to the positions the team needs -- a few pitchers, for instance, and several batters. Any team that suddenly found itself with all pitchers or all hitters would be ill prepared to compete.
The Rochester team discovered that statins essentially push most of the raw talent in one direction.
Scientists don't really know the long-term effects of such a shift. Physicians are looking at statins as a possible treatment for multiple sclerosis, where the myelin coating that covers nerve cells in the central nervous system is damaged. Myelin is produced by oligodendrocytes -- so spurring the development of oligodendrocytes might provide one way to reduce or repair the damage seen in M.S.
But the body maintains a pool of uncommitted glial progenitor cells for a reason. The body normally turns to that reservoir of cells when it needs to repair damage from a variety of causes, such as an infection, hemorrhage, a serious blow to the head, or inflammation within the brain, such as in patients with multiple sclerosis. No one knows the consequences if such cells weren't available when needed, though increased cognitive impairment might be one possibility.
"These are the cells ready to respond if you have a region of the brain that is damaged due to trauma, or lack of blood flow like a mini-stroke," said Sim, assistant professor of Neurology. "Researchers need to look very carefully at what happens if these cells have been depleted prematurely."
Glial progenitor cells are distributed throughout the brain and, according to Sim, make up about 3 percent of our brain cells. While true stem cells that can become any type of cell are very rare in the brain, their progeny, progenitor cells, are much more plentiful. They are slightly more specialized than stem cells but can still develop into different cell types.
The work may be relevant to drugs commonly used by diabetics as well. That's because the team discovered that a signaling molecule called PPAR gamma is central to the effect of statins on glial progenitor cells. When PPAR gamma was blocked, the statins no longer had the effect. Since PPAR gamma is the main target of diabetes medications such as Avandia and Actos, which trigger the molecule, Goldman said it's likely that those medications have the same effect on progenitor cells. He also noted that many patients are on both diabetes drugs and statins, which could increase the effect.
"Our results suggest the need for awareness of the possible toxicities accruing to long-term statin use, and identify one such potential toxicity, the premature differentiation and attendant long-term depletion of oligodendrocyte progenitor cells of the adult brain," conclude the authors in their Glia paper.
Besides Sim and Goldman, other authors include medical student Jennifer Lang, technical associate Tracy Ali, Cornell scientist Neeta Roy, and neurosurgeons Edward Vates, M.D., and Webster Pilcher, M.D. The National Institute of Neurological Disorders and Stroke and the National Multiple Sclerosis Society funded the work.
Adapted from materials provided by University of Rochester Medical Center.
Dew-MNTA-When does standstill agreement with NVS expire. Thomas listed 7/25 but I thought you had said a few days ago it expired in 10 days. Thanks
Momenta Pharma (MNTA): Upgraded to Overweight from Underweight at Morgan Stanley
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April 28, 2008 9:00 AM EDT
From Notable Calls
Morgan Stanley is upgrading Momenta Pharma (NASDAQ: MNTA) to Overweight-V and increasing their target to $22. Firm believes the stars could be finally aligning for the FDA approval of MNTA/NVS’s M-Enox in 2008-09 as the only genericversion of SNY’s Lovenox (blood thinner), potentially leading to: 1) 40-50% share of the $1.5+ billion U.S. Lovenox market, 2) peak potential earnings of $3/sh and 3) a share price of $40+. The downside risk of a long delay or non-approval is that the stock returns to $6.
Why are they upgrading now? Firm believes that the heparin (a complex sugar) contamination crisis may have given MNTA the unique opportunity to prove to the FDA its proprietary technology for characterizing complex sugars. Last week’s Nature publication shows that MNTA worked with the FDA to identify the heparin contaminant. They view this work as a game changer, underestimated by the Street. In our opinion, the FDA is now more likely to view MNTA’s technology as sufficient to show that M-Enox is the same as Lovenox (also a complex sugar) — a key regulatory hurdle and one they feel competitors Teva and Amphastar cannot achieve.
Notablecalls: This is a game-changing upgrade for this stock. Morgan Stanley has been neg on MNTA for quiet some time (UW rating) and now they are saying the stock could do $35+ under bullish scenario.
I expect to see a 10%-15% upside move in MNTA today.
For more calls go to http://notablecalls.blogspot.com/
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Medicine From Milk: Gene Therapy Transforms Goats Into Pharmaceutical Factories
ScienceDaily (Feb. 1, 2008) — University of Pennsylvania researchers have used gene therapy to reduce the time it takes to breed large animals capable of producing therapeutic proteins in their milk, such as insulin or those that fight cancer. This represents a significant milestone in drug development, as current methods involve cloning, which takes more time and generally costs more.
--------------------------------------------------------------------------------
See also:
Health & Medicine
Gene Therapy
Genes
Prostate Cancer
Plants & Animals
Biotechnology
Cows, Sheep, Pigs
Life Sciences
Reference
Vector (biology)
Dairy cattle
Dairy product
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"Having an easier way to harness nature's power to produce large quantities of specific proteins in milk could increase the availability of drugs for people who could otherwise not afford these treatments," said Ina Dobrinski, one of the researchers on the study.
The study also is significant because it may also be a new way to eliminate diseases in future generations of animals, such as those used for livestock. Here's why: To get the goats to produce specific proteins, the researchers used radiation to kill a portion of a male goat's germ cells (the cells that produce sperm). Then they used a modified adeno-associated virus (a well studied and tolerated gene therapy vector) to insert a gene in the remaining cells. Once the new gene took hold in the germ cells, a predictable number of female offspring produced the desired protein in their milk.
The advance is immediately valuable for pharmaceutical development and biology research, but a similar approach could be used to bolster the food supply by eliminating genetic disorders in animals over several generations. It is also possible that once perfected, this technique could eliminate disease genes in humans over several generations, assuming ethical concerns can be resolved adequately.
This study is published in the February 2008 print edition of The FASEB Journal.
"For thousands of years, people have domesticated cows and goats to make milk, butter and cheese. And for thousands of years dairy products have been used as folk remedies for practically every human illness. Most have been completely ineffective." said Gerald Weissmann, MD, editor-in-chief of The FASEB Journal. "So it is reassuring that modern science would find a way to use the milk we drink to yield of drugs that actually work."
Adapted from materials provided by Federation of American Societies for Experimental Biology, via EurekAlert!, a service of AAAS.
Quite a bit of clinical data. Type cyberknife in search field.
http://www.redjournal.org/search/results
Transgenic goat milk could prevent diarrhea in developing world
http://www.nutraingredients.com/news/science.asp
By staff reporter
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04/08/2006 - Milk produced by transgenic goats is seen to shore up protective intestinal bacteria against illness, thanks to the antibacterial action of an enzyme found in human breast milk; if the findings hold true for humans it could help prevent death from diarrheal illness in the developing world.
In a new study to be published in the August issue of Transgenic Research (reference unavailable at time of publication), researchers from UC Davis report positive results in milk from goats bred to carry the gene for human lysozyme on the intestinal health of young goats and pigs.
They hope that their findings, said to “underscore the potential for using biotechnology to improve the healthfulness of the milk of dairy animals by introducing the beneficial properties of human milk into dairy animals,” could one day be used to protect children against diarrheal illness.
The goats whose milk was used in the study were bred eight years ago using gene-transfer technology, as part of a long-standing effort by researchers to find a way of enriching cow's or goats milk with beneficial compounds found in human breast milk.
Lysozyme is understood to be one of the most beneficial components contributing to the well-being of breast-fed infants, thanks to its inhibitory effect on growth of bacteria that cause intestinal infections by destroying the bacterial cell wall, combined with encouraging the growth of beneficial bacteria.
However natural goats milk contains only 0.06 per cent the amount of lysozyme as human milk, meaning that children who, for whatever reason, receive goats milk instead of human milk, may be missing out on an important booster in early life.
“This goat's milk represents one of the first transgenic food products that has the potential to really benefit human health,” said co-leader of the study Professor Jim Murray.
Although cow's milk is the most commonly consumed milk in the West, on a worldwide basis goat's milk is believed to be drunk by more. Since more than 2 million children a year die of diarrheal illness, it is hoped that this breakthrough could offer protection to some of the goat milk-drinkers among them.
Murray and co-researcher Elizabeth Maga suggest that the transgenic procedure could be used to produce powdered milk enriched with lysozyme – and even whole goat herds for developing nations.
Even though human studies have not yet been conducted, their optimism is based on results in pigs, which are often used as a research model by virtue of having a digestive system similar to humans'. Kid goats were also used, so that the effects of the milk could also be observed on ruminants with multi-chamber stomachs.
The pigs fed milk from the transgenic goats were seen to have lower levels of coliform bacteria in the small intestine – including few E coli, some strains of which can cause serious illness – when compared to a control group of pigs fed normal goats milk.
The goats fed the transgenic goat milk, however, displayed higher levels of coliform bacteria and similar levels of E Coli compared to the control goats.
“Although the effects were different in the goats than in the pigs, the study demonstrates clearly that the consumption of pasteurized goat's milk containing human lysozyme can impact the bacterial makeup of the digestive tract in two distinct models,” said Maga.
The researchers are recommending larger, more in-depth studies to examine other possible benefits, and also project that the technology could prove even more beneficial if applied to cow's milk, since cows produce a greater volume of milk.
It was that imclone has droped patent application for EGFR drugs with radiation after objections from YMI and that amgen is going ahead with there chemo trial in combination with there EGFR so this would be the test of imclone patent regarding EGFR in combo with chemo.
Do you consider eniluracil a long shot because of history of failed trials. Part of the attraction for me of ADH is the simplicity of there argument for why there approach should work. It is suprising to me that GSK did not think of this.
Thanks, Scott
Way OT - I am looking to hedge my portfolio using options or preferably shorting a few stocks. I tried to short OSTK today but shares unavailable for shorting. I know I could short the BBH but would prefer specific companies. Not neccessarily biotech. I am asking here as I know Dew was short DNA and advice and comments here have always been sensible. Thanks
OT but interesting - WHAT GERMS DON'T KNOW CAN'T HURT YOU
CHICAGO RESEARCHERS TEST A NOVEL STRATEGY TO FIGHT KILLER BACTERIA THAT ARE IMMUNE TO ANTIBIOTICS
By Lee Scheier, a Chicago freelance writer and a frequent contributor to the Magazine
Published November 14, 2004
When Christopher Reeve died last month of a bacterial infection, he was surrounded by doctors who were powerless to prevent the lethal microbes from overwhelming his body's defenses. The death of the quadriplegic film star, whose disease took root in the pressure sores he got from sitting in a wheelchair, drew renewed attention to the tens of thousands of hospital patients and others who each year succumb to a runaway bacteria attack.
The problem is increasingly alarming because of bacteria's well-known ability to develop resistance to even the most up-to-date antibiotics. Although many patients contract infections they didn't come into the hospital with, many also bring along germs that have been living peacefully inside them for their entire lives and which suddenly flare up. These patients often die because no drugs work against the microorganisms.
But continually inventing new antibiotics isn't the answer, says Dr. John Alverdy, a gastroenterological surgeon and researcher at the University of Chicago. Instead of trying to kill bacteria, Alverdy is developing an approach that, in effect, makes them feel safe and content inside their human host. If they don't sense a need or opportunity to attack, he reasons, they remain happy campers and no infection occurs.
"I don't want to kill bugs," asserts Alverdy, whose goal is to find drugs that blind the bacteria to signals that the person is ill and vulnerable to attack. "In essence, the bacteria become ignorant of how sick the host really is," he says.
Alverdy has long been on a mission to deal with such bacteria, but his efforts intensified in February 1998 on reading a letter to the Tribune from Jill Cunniff of Highland Park. She had written about the death of her 7-year-old son, Danny, from an infection while being treated for leukemia.
"Many children will die from the secondary infections that they will contract while they are immunosuppressed during chemotherapy," Cunniff wrote. "My 7-year old son was technically in remission [from leukemia] when he died from a fungal infection contracted in the hospital. . . ."
Alverdy was deeply moved by her account and later read it to an audience of physicians and grant coordinators at the National Institutes of Health in Bethesda, Md. "I told them that this was the human face of all the statistics we cite," he recalls. "I told them that we gave this kid all the antibiotics in the world and it didn't work, which is why we have to find alternative ways to treat these lethal infections."
He put the letter on the wall of his Chicago office in clear view of his desk and telephoned Cunniff. "He told me that my letter powerfully described the terrible problem of death from hospital-induced infections that he was working on," she says. "The doctors gave Danny amphotericin and vancomycin. The bottom line is that the antibiotics didn't help."
Eight months after his plea to NIH, Alverdy received a $1 million grant to study how pathogens turn virulent. The research led to his strategy for treating infections without antibiotics.
The seriousness of the problem can hardly be overstated. According to the Centers for Disease Control and Prevention, each year nearly 2 million patients in the U.S. get an infection while hospitalized, and about 90,000 die as a result.
"Antibiotic resistance is a ticking time bomb," says Dr. Abigail Salyers, professor of microbiology at the University of Illinois at Urbana-Champaign. She notes that not only are many bacteria and fungi becoming resistant to antibiotics, but the pharmaceutical industry has cut back or eliminated antibiotic drug discovery programs because they are not highly profitable.
According to a report of the American Society of Microbiologists, the driving force in the development of antibiotic resistance is widespread overuse of the drugs. More than 90 percent of strains of one form of bacteria, Staphylococcus aureus, have become resistant to penicillin and other antibiotics.
A similar problem exists with the most deadly pathogen of all, Pseudomonas aeruginosa, the one that's getting Alverdy's attention. It is antibiotic-resistant, extremely quick to act and metabolically diverse; that is, it can grow anyplace it finds one of the vast array of nutrients it can subsist on. It is found almost everywhere, including drinking fountains, faucets, streams, moist soil and the surface of vegetables.
"The average person is exposed to Pseudomonas aeruginosa every day," says Dr. Alan Hauser, assistant professor of microbiology and immunology at Northwestern University.
An estimated 70 percent of those infected with it die. It claims the lives of 60 percent of patients in burn units, 50 percent of AIDS patients and most of those with cystic fibrosis. Alverdy reasoned that he should start with this most wanton of killers. "If I could defeat the worst [form of bacteria], then I could apply that template of discovery to defeat many of the others," he says.
Those include germs like the ones that cause bacterial pneumonia and are now 20 percent resistant to penicillin. In some cases, says Salyers, half the bacteria of a particular species are resistant to at least one antibiotic. "What's at stake," she says, "is the possible loss of the effective use of antibiotics. This would be the first time in history that a cure was actually lost."
Alverdy argues that killer bacteria are innately benign and only turn virulent when they sense the host's tissue defenses are weakened, threatening their environment-the intestines, in the case of Pseudomonas aeruginosa.
"When the host is traumatized, bacteria like Pseudomonas aeruginosa are like rats leaving a sinking ship," says Dr. James Shapiro, professor of genetics at the U of C and an expert on bacterial behavior. "It makes sense for bacteria in a dying host to escape" by killing the host with its lethal toxins.
Based on pioneering research by Shapiro showing that bacteria are social organisms that can communicate with each other, Alverdy and his partner, Dr. Eugene Chang, professor of medicine at the University of Chicago, developed a compound that interferes with those communications.
In a recent study, they induced stress in laboratory mice and then introduced Pseudomonas aeruginosa directly into their intestines. All the mice died of the resulting infection, called gut-derived sepsis. However, when Alverdy and Chang treated the mice with their compound, a form of polyethylene glycol, the mice were completely protected. Amazingly, a virulent attack was prevented though not a single bacterium was killed.
Chang explains that the high-molecular-weight polyethylene glycol they used acts as an artificial mucus. A non-toxic polymer, it coats the bacteria and intestines and blocks the signals the microbes would otherwise send each other to mass for war and release lethal toxins. The study was recently published in the journal "Gastroenterology."
Alverdy first used the polyethylene glycol formulation on five patients who were dying of gut-derived sepsis when he worked at Chicago's Michael Reese Hospital.
"One of the patients was an 18-year-old girl who had had her appendix removed and was in the ICU," says Alverdy. "She was dying, her family was sobbing, yet there was no infection to be found anywhere. The only evidence was how sick she was. So I figured the bacteria must be in her intestines. I flushed 10 liters of polyethylene glycol through her intestines and she got better within 18 hours. So did the four other patients." All five survived.
Alverdy believes his study shows that the strategy of foiling bacterial communication holds more promise than using antibiotic drugs to fight an attack after it starts.
"Drug companies have spent billions of dollars trying to manipulate inflammation after it is initiated and have universally failed," says Alverdy. "Why not interdict before it occurs?"
Antibiotic treatment merely creates a never-ending, escalating arms race between medical researchers and bacteria, he says. And the bacteria always stay one step ahead of advances by quickly generating a genetic defense against the drugs. "Because generations of bacteria have faced multiple attempts at their elimination," he notes, "they have evolved the means to perpetually develop and refine their virulence capabilities."
Able to divide every 20 minutes, a bacterial cell could produce 5 billion progeny cells in just under 11 hours. "In the short term, we may be more clever than the bugs," says Alverdy, "but in the long term, they are more clever than we are . . . . We are just starting to understand how clever they are about changes in our biochemistry."
Shapiro agrees: "Bacteria are small, but they're not stupid," he says, noting that bacteria are very sophisticated in their information processing. "Every time a bacterium divides, tens of millions of biochemical processes have to be coordinated and controlled. The bacterial cell is the ultimate, just-in-time production facility."
This cell-to-cell communication is what allows Pseudomonas aeruginosa to make decisions about whether to assemble and secrete lethal toxins, Shapiro's research shows. "A single bacterium would not take on a host," he says. "They can sense their population density. When they sense how many of their own group are around and realize that the numbers are sufficient to kill the host, they attack."
Because the introduction of polyethylene glycol renders the bacteria unable to sense a cataclysmic change in their environment, they don't secrete the signaling molecules and don't mass for battle.
The polyethylene glycol also works by keeping the bacteria further away from the intestinal wall than usual. "Without physical contact it is rare for infection to occur," says Alverdy.
Dr. Dara Frank, professor of microbiology and molecular genetics at the Medical College of Wisconsin, is researching ways to disrupt the system that bacteria use to pump out toxins and deliver them to the cells. She says Alverdy's work is impressive, with solid data. "I think he's asking really big questions. We know that the signaling molecules are expressed in humans, particularly in cystic fibrosis patients. I think the signaling molecules are a good target to go after."
Hauser says an advantage of treatment with polyethylene glycol is that it is non-toxic and would likely be safe in a clinical trial.
"Approaches like Alverdy's have the potential to lead to interventions that could dramatically enhance our ability to prevent or treat these hospital-acquired infections," Hauser says.
On average, we have 500 to 700 species of bacteria living in or on our bodies, 3 trillion in all. A newborn baby has no "flora," a term used to describe the full array of microbes that inhabit our intestines and other structures. But around the 7th to 10th day the baby acquires all the flora it will have for the rest of its life from the environment.
The trillions of bacteria live in our intestines, sharing a kind of peaceful coexistence. But certain stresses, like surgical trauma, send signals that can cause bacteria to become virulent.
And a hospital intensive-care unit "is a strange new world for the bacteria," Alverdy says. "It's as though the bacteria is saying, 'I've been in your body for 50 years, and now I'm in an intensive care unit. They're attacking you with drugs. They won't let you eat, won't let you poop. They put the food in your veins so I have to go into your bloodstream to eat.' "
Although the bacteria have been alerted to the fact that the host is diseased and vulnerable, they have no reason to attack until the severity of the illness and the harshness of the therapies converge to create an alarming change in the bacterial environment. At that point they sense that the host has become a liability and signal each other to ascertain if there are enough of them to invade, inflame or kill the host. If the numbers are sufficient, they launch an assault.
Conversely, says Alverdy, when patients in the ICU are fed again, taken off morphine and begin to have bowel movements, the infection disappears. This, he believes, is because the bacteria sense that the host's health is improving.
Bacteria know that their survival is dependent on their host's survival, says Alverdy. "Organisms have a history of jumping to new hosts to survive, having moved, historically, from crops into cows and into man. A bacteria that kills its [sick] host has the chance that a bird will eat the carcass and ingest it, giving it a new lease on life."
Alverdy, Chang and others have formed a company in an effort to continue their research. "We have just had an offer in the millions of dollars for the licensing rights to high molecular weight [polyethylene glycol]," says Alverdy. They are awaiting approval from the FDA to begin human clinical trials. The first two populations that will undergo the trials are bone marrow transplant patients and children at risk for a type of colitis.
"If Danny [Cunniff] could have survived to get past point A and get a bone marrow transplant, he might be alive today," says his mother. "What's the point of treating cancer if the infections take you out of the treatment plan?"
She currently participates in an Internet support group with about 300 other parents. "Almost every parent in my support group who had a child [with] cancer that required an immunosuppression regimen lost that child to infections. Every kid that gets a bone marrow transplant, it's the same worry. It's the opportunistic pathogens that will kill you."
Copyright © 2004, Chicago Tribune
NEOP- I have been hesitant to post on this as I do not relly know enough about management of company but valuation looks compelling to me. I became interestedin this co after Rodman presentation (still available). Dutton also has report and co reported earnings today and will hold conf. call at 11 this morning (eastern time). Company has market cap of 27-30 million (trades on bulletin board) and will have two phase 3 trials next year underway. I could write a lot more but info is presented better than I could at Rodman or Dutton.
BPA "Yes, I found it troubling that the middle dose works better than both the low and high doses. The overall data package for LibiGel was therefore somewhat disappointing and not fully consistent with the bluster in the prior press release. Is this consistent with your view?"
"P.S. I am holding my shares but have not bought more"
Yes,also my view. I did talk to the woman from BPA (did not catch her name)who was on call yesterday and she did say that P+G trials were similar with middle dose working and high and low dose ineffective. No explanation on science of it though.
Dew, during BPA call toward end of Q+A someone asked about statistical significance of 75 and 300mcg dose. Answer was yes against baseline but not against placebo. Middle dose of 150mcg was quite effective but am curious what you think about this. Thanks
Tea found to fight Alzheimer's enzym
26/10/2004 - Drinking tea could help improve memory and may also slow the development of Alzheimer’s disease, suggests new research from the UK.
Laboratory tests by a team at the University of Newcastle found that tea, and particularly green tea, inhibits the activity of the same enzymes in the brain currently targeted by drugs for Alzheimer’s disease.
The researchers are hoping to develop a medicinal tea as an alternative treatment to slow memory loss in Alzheimer’s sufferers, estimated to include around 10 million people worldwide, and rising.
Lead researcher Dr Ed Okello said: “Although there is no cure for Alzheimer’s, tea could potentially be another weapon in the armoury which is used to treat this disease and slow down its development.”
“Our findings are particularly exciting as tea is already a very popular drink, it is inexpensive, and there do not seem to be any adverse side effects when it is consumed. Still, we expect it will be several years until we are able to produce anything marketable.”
Dr Okello added that the findings suggested tea could boost the memory of everyday drinkers too.
The researchers from Newcastle University’s Medicinal Plant Research Centre found both green and black tea inhibited the activity of the enzyme acetylcholinesterase (AChE), which breaks down the chemical messenger or neurotransmitter, acetylcholine. Alzheimer’s is characterised by a drop in acetylcholine.
Green tea and black tea also hinder the activity of the enzyme butyrylcholinesterase (BuChE), which has been discovered in protein deposits found on the brain of patients with Alzheimer’s.
Green tea went one step further in that it obstructed the activity of beta-secretase, which plays a role in the production of protein deposits in the brain that are associated with Alzheimer’s disease. Scientists also found that it continued to have its inhibitive effect for a week, whereas black tea’s enzyme-inhibiting properties lasted for only one day.
Incidence of Alzheimer’s disease is expected to rise fast with ageing populations but there is currently no cure. Drugs are available to slow the development of the disease by hindering the activity of AchE and others are being developed which scientists hope will inhibit the activity of BuChE and beta-secretase. But many of those currently available, such as donepezil, have unpleasant side effects and the medical profession is keen to find alternatives.
Professor Clive Ballard, director of research at the UK-based Alzheimer’s Society, noted that the research builds on previous evidence that suggests that green tea may be beneficial due to antioxidant properties.
"Certainly the effect on the cholinesterase enzyme (the target of current anti-dementia drugs such as Aricept) and beta-secretase (an enzyme which is important in the build up of plaques) is very exciting and requires further investigation," he said.
The findings, published in the journal Phytotherapy Research (18, pp624-627), are the latest in a long line of results pointing to tea’s disease-fighting potential. It is also being widely researched for its anti-cancer activity and benefits for heart health.
The Newcastle researchers are seeking funding to carry out further tests on green tea. They need to find out exactly which components of green tea inhibit the activity of the enzymes AChE, BuChE and beta-secretase.
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Statins: A Risky Step? (Ivanhoe Exclusive)
By Stacie Overton, Ivanhoe Health Correspondent
ORLANDO, Fla. (Ivanhoe Newswire) -- Those "miracle" pills that lower your cholesterol may, in fact, be doing more harm than good. At least one researcher is out to determine if statins pose more risks than benefits.
Beatrice Golomb, M.D., Ph.D., from the University of California, San Diego, is involved in an NIH-funded study of 1,000 subjects who have been randomized to receive statins or placebo. The study will look at the effect these drugs have on cognitive function. Another study she's involved in will examine all adverse events caused by the drugs.
The research comes during a time when statins are now being questioned by doctors and patients alike. Dr. Golomb says, "From the reports that come into us, people are experiencing severe muscle weakness, which is also linked to cognitive problems." Those cognitive problems include everything from the inability to recall names or balance a checkbook to forgetting whole episodes. The concern, says Dr. Golomb, is that statins haven't been adequately studied for their harmful effects. She tells Ivanhoe: "We're really interested in the balance of risks and benefits of these drugs. There are lots and lots of people looking at the benefit side. There are so few people evaluating the [risk] side. You can bet that the $20 billion a year in statin drug company revenue is going to make sure that any promising lead looking at potential benefits will be followed."
Statins are not the only drugs that have been questioned. In fact, Dr. Golomb says one-fifth of drugs released to the market will ultimately be withdrawn or have major black box warnings. She says, "A full one-half of the problems that lead to those endpoints won't be identified for over seven years after the drug is released." A recent example of this is the drug Phen-Fen. Dr. Golomb says: "That was a drug given to huge numbers of people for a number of years before a problem was identified. And it wasn't even identified by any of the mechanisms that are in place to try to identify the adverse effects. It was identified by the keen perception of one physician -- a radiologist who happened to notice a lot of the patients that she was seeing heart abnormalities in had listed these medications on their medication list."
Dr. Golomb says statins need further study to fully uncover the true risks in all subgroups of people. She says: "[Statins] clearly benefit middle-aged men with heart disease or [middle-aged men] at risk of heart disease. But they've never been shown to benefit women or the elderly." She says an average 55-year-old woman on statins with no family history of heart disease will not live any longer as a result of taking a statin.
This article was reported by Ivanhoe.com, who offers Medical Alerts by e-mail every day of the week. To subscribe, go to: http://www.ivanhoe.com/newsalert/.
SOURCE: Ivanhoe interview with Beatrice Golomb, M.D., Ph.D., University of California, San Diego, October 19, 2004
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CLEVELAND, Ohio, Oct 19 (Reuters) - Statins are the world's best-selling drugs, taken by millions to reduce the risk of heart attack by lowering cholesterol levels, but many people who could benefit are not using them and many who do take them get no such benefit, a leading cardiologist said on Tuesday.
Clinical trials have consistently shown that statins reduce the incidence of heart attack by about a third, but a majority of people taking the drugs don't receive this benefit from them, Dr. Eric Topol, head of cardiovascular medicine at the Cleveland Clinic, told Reuters in an interview.
"We just don't know who they are," he said.
Many people who are taking statins should not be on the drugs, while many who are not taking them should be, he said.
"They are misappropriated," Topol said of statins, which must be prescribed. "It's chaos," he added.
Topol said doctors too often focus on reducing patients' low-density lipoprotein, or LDL, the so-called bad cholesterol blamed for clogging arteries and causing heart attacks and strokes.
"Everything tells us it's not the LDL, it's the inflammation process. This LDL-centric thinking is wrong," Topol said.
Blood levels of bad cholesterol are just one factor among many that lead to cardiovascular disease, he said.
The majority of people who have lowered their LDL cholesterol with statins have not reduced their risk of heart attack or stroke, nor do they have better survival rates, Topol said.
The anti-inflammatory properties of statins may be the reason why the drugs seem to be beneficial for other diseases unrelated to cardiovascular disease, he said.
Recent studies suggest statins help bone healing and reduce mild cognitive impairment, the precursor to Alzheimer's disease.
Topol predicted that one day medicines will be matched to individuals' genetic makeup. One such test being developed by the Cleveland Clinic focuses on the five or more genes associated with cardiovascular disease, he said.
Statins are taken by an estimated 13 million Americans, and are sold by AstraZeneca (AZN.L: Quote, Profile, Research) , Pfizer Inc. (PFE.N: Quote, Profile, Research) , Merck (MRK.N: Quote, Profile, Research) , Bristol-Myers Squibb (BMY.N: Quote, Profile, Research) , and Novartis AG (NOVN.VX: Quote, Profile, Research) .
© Reuters 2004. All Rights Reserved.
Prana giving quite a good presentation on alzheimers right now.
http://www.pranabio.com.
No, do not know which drugs they mean. If I find out I will post. Here is another article of interest.
VEGF contributes to asthma development
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04/10/2004 - Scientists at Yale University in the US have discovered the vascular endothelial growth factor (VEGF) plays an important role in the development of the disease and raises the possibility of new asthma drugs that block VEGF receptors and signalling pathways.
In this new approach to asthma, the scientists discovered that when VEGF is expressed in the lungs of genetically engineered transgenic mice, asthma-like alterations developed. VEGF is normally associated with the growth of new blood vessels in the lung and other organs.
Previous studies showed that people with allergies and asthma have an excess of T-helper type 2 cells (TH2). Elias and his team found that when VEGF is produced, the TH2 response is increased.
Jack Elias, principal investigator of this study said: "In humans with asthma, there is an increased level of VEGF, so we mimicked this condition in mice by over expressing VEGF in their lungs."
"In additon to growing new blood vessels, many other features of asthma were also seen in these mice. We observed mucous formation, airway fibrosis and asthma-like pulmonary function abnormalities. We also found that if you block VEGF, you block the asthma-like manifestations in other mouse asthma models."
A high percentage of people with asthma have allergies suggesting a higher tendency to become allergic to exposed particles and antigens. Normal individuals become tolerant to the same agents, instead of becoming allergic, a process that has yet to be understood.
"We found this tolerance is broken in the genetically-engineered transgenic mice, suggesting that the VEGF-induced break in tolerance contributes to the allergic sensitisation of asthmatic patients," Elias said.
Elias and his team are currently examining how VEGF works at the cellular and molecular level. These latest findings add to the growing body of research from Elias's lab that has advanced knowledge of asthma, a rapidly increasing chronic lung condition, which affects 150 million patients worldwide and 40 million in the US.
Asthma is a highly prevalent chronic disease estimated to cost at least $13 billion in the US alone each year. In the UK, there are four times as many people with asthma than with diabetes. The number of patients with asthma in the seven largest pharmaceutical markets is set to rise from 51.4 million in 2003 to 62.4 million in 2013, stimulating greater demand for cost-effective asthma therapies.
Datamonitor estimates that the market for asthma and chronic obstructive pulmonary disease (COPD) products will reach $18 billion by 2011.
The research appears in a report in the journal Nature Medicine.
OT - Alzheimers
Alzheimer's breakthrough 'excites' scientists
Leigh Dayton, Science writer
30sep04
SCIENTISTS may have identified a trigger and a treatment for the mental ravages of Alzheimer's disease after a series of remarkable experiments by Australian and US researchers.
Until now, no external cause of the frightening brain disorder has been found, and existing therapies only slow the progression to dementia and death.
"It's a very exciting finding," admitted team leader Ralph Martins, a molecular biologist with Edith Cowan University and the Sir James McCusker Alzheimer's Disease Research Unit at Hollywood Private Hospital in Perth.
University of Melbourne Alzheimer's expert Colin Masters agreed. "This could be a major finding with important implications," he commented.
Earlier this month, Alzheimer's Australia estimated that the disease affected 162,300 people and at least 1million relatives and carers. By 2020, Alzheimer's will hit almost 300,000 Australians.
Women are more at risk of the disease, known to run in families.
Today at the ComBio 2004 meeting in Perth, Professor Martins and his colleagues will present new findings showing that if a normal age-related hormonal process "overshoots", it causes the build-up of brain-clogging substances called amyloid-beta proteins.
These proteins are known to kill brain cells and cause dementia.
However, Professor Martins said yesterday that "by chance" two existing drugs - one used to treat prostate cancer and another that boosts female fertility - could slow or even halt the destruction because they interfere with the protein-boosting process.
Two years ago, scientists with North Carolina-based Voyager Pharmaceuticals found some evidence that elevated levels of a hormone called gonadotropin were linked with dementia.
Excited by the result, Professor Martins and colleagues at the Research Unit, Edith Cowan and the University of Western Australia studied 1000 Perth women over the age of 70, not taking hormone replacement therapy. Surprisingly, they found no link between mental decline and the women's varying levels of the sex hormone oestrogen.
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transgenic fish - Fish to help stem severe bleeding
Scientists have used GM fish to produce a blood clotting agent
A fish could be used to produce a treatment for people with haemophilia and gunshot wounds, scientists believe.
Researchers have already made a blood clotting agent, known as factor VII, from genetically modified tilapia, a freshwater fish farmed for food.
As well as being used to treat a rare form of haemophilia, factor VII can also be used to stem internal bleeding.
The research is being carried out by the University of Southampton and US experts, the New Scientist reports.
Factor VII is already produced using hamster cells but the cost of a single injection can be as high as £6,000.
It is used to treat a rare form of haemophilia, sometimes known as Alexander's disease, and for people with the more common haemophilia A and B who reject traditional forms of treatment.
Soldiers
But the protein has also been used by soldiers to stem bleeding caused by accidents and gunshot wounds.
Professor Norman Maclean of the University of Southampton, who led the research, told BBC News Online he was hoping to produce the protein for about a tenth of the current price.
The project, which is being run in conjunction with the Florida bio-tech firm AquaGene, has produced the protein by adding a human gene to the fish, which then excretes the factor VII into its blood.
The protein is then removed from the blood and transferred into humans.
He said: "It works by forming clots when someone has internal bleeding.
"The form of haemophilia it could treat is quite rare so I think the largest benefit will come from treating crash victims and people with gunshot wounds who have severe internal bleeding."
Prof Maclean said he also believed fish could be used to treat other diseases.
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15/07/2004 - Researchers at Johns Hopkins University have produced evidence that may help support a new entrant to the eye health market - sulphoraphane, an indirect antioxidant found in broccoli and broccoli sprouts.
Sulphoraphane protected eye cells from damage caused by UV light, which can lead to the increasingly common condition macular degeneration, reported the researchers in the 13 July issue of the Proceedings of the National Academy of Sciences (vol 101, no 28, pp 10446-10451).
Epithelial cells in the eyes are very sensitive to damage caused by the oxidants generated by light exposure. The eye has a number of antioxidant functions to reduce damage to the retina, but as people age, the eye becomes less efficient at removing oxidants. This is believed to be a major cause of age-related macular degeneration, the leading cause of blindness among the elderly. It affects an estimated 30 million people worldwide but this number is expected to double by 2030.
Professor Paul Talalay and Xiangqun Gao at the Laboratory for Molecular Pharmacology at Johns Hopkins Medical School divided human adult retinal pigment epithelial cells into two groups, treating one with sulphoraphane for a 24-hour period. The other acted as control.
Exposing the cells to UV light afterwards, survival in the sulphoraphane group was much higher, Dr Gao told NutraIngredients, and this protection was dose-dependent, increasing with the amount of sulforaphane provided.
The researchers have yet to demonstrate the same effect in people, proceeding first with a study on mice. And they are a long way from making any inroads into the eye health market, an area with typically low consumer awareness of the association between diet and eye health.
However Dr Gao noted that sulphoraphane could have significant benefits over the category leader, lutein. This ingredient was worth $24.5 million in Europe in 2003, with forecast growth of 12 per cent, according to Frost & Sullivan. Sulphoraphane's advantages have much to do with the mechanism behind its action in the body.
Sulphoraphane glucosinolate (SGS) plays a role in boosting the body’s natural Phase 2 enzyme antioxidant defense systems and functions as a powerful indirect antioxidant detoxifying carcinogens before they can damage cells. Typical direct antioxidant molecules, such as vitamins C and E, scavenge one free radical or other oxidant molecule at a time. Once a direct antioxidant molecule binds to a free radical molecule, rendering it harmless, the antioxidant is consumed and is no longer active.
“Antioxidants react with free radicals directly and once they have reacted, they have to be regenerated. But sulphoraphane does not work directly on free radicals. Instead, it up-regulates or boosts the defence system, letting the body itself fight free radicals.”
This mechanism has two advantages, according to Dr Gao.
“It means that the compound not only protects eyes but also every part of the body. It also lasts longer in the body, for between four to five days in the cells,” he said.
More than 125 scientific papers have been published on sulphoraphane, broccoli and broccoli sprouts, with many of them focusing on sulphoraphane’s anti-cancer activity. It also appears to kill bacteria in the stomach that leads to ulcers and stomach cancer.
In a recent study, Dr Bernhard Juurlink at the University of Saskatchewan showed that feeding broccoli sprouts to rats prevented high blood pressure, heart disease and stroke.
Broccoli sprouts, three-day-old broccoli plants, have been found to provide 20 times the concentration of sulphoraphane glucosinolate as found in adult broccoli. Broccoli sprouts are being marketed by a company set up by the John Hopkins team in Baltimore, called Brassica Protection Products, which offers patented concentrated forms of the sprouts.
They are sold in the US, Japan and New Zealand as a vegetable, and the company is looking for partners for use of the ingredient in other applications.
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(OT)Telik presentation- Telk's presentation today at Needham confererence one of the best I have heard for clarity and impressive data.
more on CJC -
"Weighing up the biotech risks
Duncan Stewart
Financial Post
Thursday, April 15, 2004
Biotech investing is risky. The firms can have no revenue and seek approval based on a limited series of clinical trials. The rewards from a successful treatment can be enormous: Canadian stocks Conjuchem and TLC The Laser Center are up 3700% and 780%, respectively, in the past year, just on hopes of successful treatments.
I think that the chances of success for each company are substantially different. The data from both sets of clinical trials look encouraging, but I believe that there exists an additional source of risk for TLC that is much less severe for Conjuchem.
Investors in the health-care sector have always known that different disease indications have different risk profiles, but in a research comment published last Wednesday, Philippa Flint, of RBC Capital Markets, attempted a more systematic look at clinical trial risk. She stated that drugs for diseases where there are "clearly defined clinical endpoints and regulators familiar with other compounds that have been successful in clinical trials" have a lower risk profile. But a new treatment that is the first in class or with unclear endpoints is much riskier. Although her report did not explicitly mention it as a factor, I believe that clinical trials where either the disease or the mechanisms of action of the drug are not well understood also are much riskier.
Conjuchem is testing a more durable version of GLP-1 (Glucagon-like Peptide) in Type II diabetes. Scientists have long understood how GLP-1 fits into the insulin pathway and how it could control blood sugar levels with minimal risk of hypoglycemia. But the naked peptide is broken down in the bloodstream far too rapidly to be a useful therapy. For Conjuchem to get FDA approval, it has to go through the usual clinical trial hoops. But diabetes is a well-studied disease, with many alternative treatments having been submitted to the regulators over past decades. The endpoints are clear. Further, there are a host of markers that allow drug developers to monitor how effective its drug is. One can measure blood sugar levels upon waking or after a specified meal, or even better, blood marker HbA1c is a reliable indicator of average blood glucose levels over the last 90 days.
When Conjuchem came out with interim data Monday, it was able to demonstrate that its drug was able to reduce average glucose levels, body weight and HbA1c levels, all with high statistical significance. Since the drug has only been administered for a month, and it is a three-month trial, an optimist could hope the cuts would get better over the course of the trial.
Many bad things could still happen but, based on the data and the markers we have seen so far, an investor could have a fairly high level of confidence that the longer trial data will continue to be positive, that it will lead to a Phase III trial and then to an FDA approval. There are no guarantees, but the clinical risk is as low as it gets.
While TLC is mainly known for its laser eye correction business, much of the recent run up in price has come from the potential to treat dry Age-Related Macular Degeneration (AMD) using a proprietary blood filtering technology. Dry AMD is the leading cause of blindness in the elderly but there is no treatment available today. While scientists know that the disease is always accompanied by deposits on the retina called drusen, the precise mechanism of action is not understood.
The TLC treatment removes various compounds from the blood (some of which are found in drusen) and although the substances build up again, it is hoped that the temporarily lower levels cause the ongoing deterioration of vision to slow, halt or even reverse. Small-scale trials have proven encouraging. But I believe the clinical risk is fairly high. The FDA has never approved a treatment for dry AMD, so TLC will be blazing a path. While plasma levels of various compounds can be measured, there is no clear scientific link between those levels and the progression of the disease ... there are no markers to indicate probability of success for dry AMD. TLC's treatment will either work, or it won't. If it does the stock will keep going up, but if not, the risk to investors is significant.
Conjuchem and TLC are targeting potential gold mines of large and growing markets and are running good FDA clinical trial programs. But at the end of the day, TLC investors are taking a bigger risk.
Duncan Stewart is a partner and fund manager at Tera Capital Corp. and may hold positions in the companies named.
© National Post 2004"
CJC comments from Canada -ConjuChem stock jumps 13% on test results
LEONARD ZEHR
gam
Better-than-expected test results with a potential breakthrough drug to treat Type 2 diabetes sent ConjuChem Inc.'s stock price to a 13-per-cent gain in hectic trading yesterday.
"We believe the stock has more room for appreciation," Orion Securities analyst Joe Walewicz said in a report. He initiated coverage of ConjuChem with an "overweight" recommendation and 12-month target price of $18.
On the Toronto Stock Exchange, ConjuChem rose $1.69 to $14.17, putting it within striking distance of its 52-week high of $14.97.
The Montreal-based drug developer said that based on interim Phase II results, normal glucose or a "therapeutically meaningful improvement" was achieved in 80 per cent of diabetic patients after receiving its DAC:GLP-1 drug for 28 days.
Moreover, 27 per cent of patients reached the target HbA1c level of 7 per cent or less.
HbA1c is a 90-day measure of the amount of hemoglobin in the bloodstream that has bound to glucose and is the standard measurement in diabetes management.
The company said the drug also showed a statistically significant reduction of 0.8 per cent in HbA1c, which analysts said wasn't expected at this stage of the trial.
Regulators would look for at least a 0.7-per-cent reduction in HbA1c in a final Phase III trial, analysts say.
ConjuChem president and chief executive officer Jacques Lapointe said the company hadn't planned to report HbA1c reductions because 28 days wasn't considered to be enough time to get reliable data.
"The fact that such strong reductions were achieved under the circumstances, with such a high level of statistical significance, could not be ignored," he said.
"We came to the conclusion that this information was material and should be publicly disclosed."
The drug also produced statistically significant reductions in body weight of patients and average fasting glucose levels, without any notable adverse side-effects.
"We are becoming more convinced with each piece of clinical news that DAC:GLP-1 is a commercially viable anti-diabetes drug," Sprott Securities analyst David Dean said in a report.
He rates the stock as a "buy," with a 12-month target price of $21.50.
The interim results prompted Dundee Securities analyst David Martin to raise his 12-month target price to $18 from $16, citing reduced risk.
In a new report, he said the efficacy of DAC:GLP-1 was competitive with Amylin Pharmaceutical Inc.'s Exenatide, and slightly better on some measures.
Among other things, Mr. Martin said patient responses were achieved with once-daily dosing of DAC:GLP-1, compared with twice-daily dosing of Exenatide, a synthetic version of an animal version of GLP-1, which has completed clinical testing.
"By midyear, we expect further differentiation of DAC:GLP-1 on the basis of dosing convenience," he said.
"When final three-month data are reported for all 196 patients, we expect most will be adequately maintained with dosing every two days or longer."
- ConjuChem Reports Positive Interim Phase II DAC(TM):GLP-1 Results
Monday April 12, 4:00 pm ET
- Statistically significant data in key efficacy parameters -
MONTREAL, April 12 /CNW/ - ConjuChem Inc. (TSX:CJC - News) today announced interim results from its ongoing monotherapy Phase II clinical trial that is evaluating the Company's proprietary compound DAC(TM):GLP-1 to treat Type 2 Diabetes.
"All of the data available from patients who have completed the first 28 days therapy in this study substantiates the results seen in our Phase I/II multi-dose trial with a much larger population of patients that more closely resemble typical patients with Type 2 diabetes," said Dr. Jean Paul Castaigne, Chief Scientific Officer and Vice President of ConjuChem. "In particular, to observe a 0.8% reduction of HbA1c (A1c) after only a month of monotherapy with DAC(TM):GLP-1 is very encouraging."
Trial Design/Patient Profile
This Phase II monotherapy trial began in October 2003 and has been designed to assess the compound's effectiveness in reducing glucose levels as measured by multiple parameters including A1c after three months of treatment and to assist in determining the optimum subcutaneous dosage regimen for this drug. The study will also evaluate the drug's impact on weight control. This international trial has centers in the United States, Canada and Europe.
Inclusion in the study required each patient to have an A1c level greater than 7.5%. The vast majority of these patients were on one or two oral anti- diabetic medications and in need of further medical intervention. The trial has now completed enrolment at 196 patients, all of whom were washed out of all oral medications for 15 days prior to receiving DAC(TM):GLP-1. The male to female ratio is 60/40, the mean age for the study population is 58 (+/-) 10 years and the mean duration of disease is 5.9 (+/-) 3.3 years. The mean A1c level at the time of inclusion in the study was 8.7 (+/-) 0.9% with an average basal fasting glucose level of 11.2 (+/-) 2.5 mmol/l. Both of these values are significantly higher than those recorded in the preceding Phase I/II multi- dose trial and reflect the more severely diseased patient profile of this monotherapy Phase II trial.
The trial has two principle stages. Stage one (titration stage) entailed each patient receiving, for 28 days, escalating daily doses of DAC(TM):GLP-1 in a monotherapy protocol to safely build a targeted plasma concentration of the drug in a patient. After this initial 28 day period, each patient is subsequently randomized into one of five dosing cohorts (administration once a day, three times a week, twice a week, once a week, no treatment) in the 60-day second stage of the trial (maintenance stage). The data reported on today only addresses results from the titration stage of the trial.
Preliminary Results
From a safety perspective, the results to date are entirely consistent with the results from the Company's Phase I/II multi-dose trial. The compound has been well tolerated with no serious adverse events reported. Specifically, there has been no injection site irritation, no modification of blood pressure and no immune reaction. Consistent with side-effects seen with the GLP-1 class of compound, some mild to moderate transient nausea and vomiting was observed. However, treatment guidelines were developed that, in almost all cases, effectively controlled these side-effects.
From an efficacy perspective, of the 100 patients that have completed the titration stage of the protocol, an analysis of the interim data available to date from more than 80 patients reveals the following results:
- A highly statistically significant reduction of A1c levels was
observed at this early stage of analysis (mean of 0.8%, p value
(equal sign) 0.001); Glucose normalization or a therapeutically
meaningful improvement as measured by A1c levels achieved in 80% of
the patients; furthermore 27% of patients have reached the target of
7.0% or less. A1c reflects the previous three months average plasma
glucose level. As such, the full impact of a drug's reduction on
glucose as measured by A1c is best analyzed after a three month
course of therapy;
- A highly statistically significant reduction in body weight (mean of
2.3 kg (5.1 lbs.), p value (equal sign) 0.001);
- A highly statistically significant reduction in the average mean
daily glucose level (mean of 26%, p value (equal sign) 0.001);
- A highly statistically significant reduction in average fasting
glucose level (mean of 24%, p value (equal sign) 0.001);
The Company anticipates reporting the main results from this study including data from the five maintenance dose cohorts around mid-year.
The Company will be hosting a conference call to discuss these results on Tuesday, April 13, 2004 at 8:30 a.m. EST. The call will be audio-cast live and archived for 90 days at www.financialdisclosure.ca and www.conjuchem.com.
About GLP-1
GLP-1, the body's most potent insulinotropic hormone is a naturally occurring 36 amino acid peptide. GLP-1 has been shown to normalize blood glucose levels by a) stimulating insulin secretion and lowering glucagons secretion in a glucose-dependent manner; b) delaying gastric emptying; c) induces Beta cell proliferation; d) restores Beta cell sensitivity to glucose; and e) increases peripheral sensitivity to insulin (glycogen synthesis). Moreover, GLP-1 appears to have a very attractive safety profile, with a low probability of inducing hypoglycemia. However, the half-life of native GLP-1, without the benefit of DAC(TM) Technology, is only about 5 minutes, as it is simultaneously degraded by serum enzymes and cleared through renal excretion.
About ConjuChem
ConjuChem, the albumin bioconjugation company, is developing long-acting therapeutic compounds based on bioconjugation platform technologies. When applied to peptides, the Company's systemic DAC(TM) Technology enables the creation of new drugs with significantly enhanced therapeutic properties as compared to the original peptide. The Company is developing compounds to treat various disorders including diabetes, HIV/AIDS, human growth deficiencies and congestive heart failure.
Detailed descriptions of the Company, DAC(TM) Technology and ConjuChem's product pipeline can be viewed on the Company's web page www.conjuchem.com.
http://www.newswire.ca/en/releases/orgDisplay.cgi?okey=13617
For further information
Lennie Ryer, Vice President, Chief Financial Officer, ConjuChem Inc., (514) 844-5558 ext. 224, ryer@conjuchem.com
Michael Polonsky, Investor Relations, (416) 815-0700 ext. 231, (416) 815-0080, mpolonsky@equicomgroup.com
--------------------------------------------------------------------------------
Source: ConjuChem Inc.
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OT CJC - Interim results for phase 2 diabetes trial
CJC has scheduled a conference call for 8:30 on Tuesday morning:
http://www.financialdisclosure.ca