A new therapeutic may be more effective against a variety of cancers–including colon, head and neck, mesothelioma, ovarian and pancreatic cancers–than previously thought.

Researchers from Buffalo, NY’s Roswell Park Cancer Institute (RPCI) injected a new formulation of a promising anti-cancer small chemical molecule–FL118–into human colon and head-and-neck tumors in animal models. They observed that the treatment was effective without relapse but was limited in that it could be delivered only by intraperitoneal (IP) administration, or injected into the body cavity. The study is slated to be published in the April 8 issue of the American Journal of Translational Research.

“This work represents a significant move forward,” Fengzhi Li, associate professor of oncology in RPCI’s Department of Pharmacology and Therapeutics and senior author on the study, said in a statement. “We’re targeting four of the most resilient and pervasive cancer survival mechanisms, and because the findings from preclinical testing have been so striking, we’re anxious to see FL118 tested in the clinical setting.”

IP injection is more often applied to animals rather than to humans, so producing the same results in humans will likely take additional work. However, the drug was more effective in controlling two types of cancer than a version reported in PLoS ONE.

FL118 is a targeted therapy that works by inhibiting the expression of four major cancer-survival gene products. The research suggests that FL118 could also treat mesothelioma, ovarian and pancreatic cancers, and potentially other solid tumors.

While the cause and progression of Alzheimer’s disease remains unknown, scientists widely accept that amyloid beta plaque buildup leads to cognitive dysfunction associated with the disease.

Now, researchers at the Max Planck Florida Institute for Neuroscience may have stumbled upon a potential cause of Alzheimer’s based on a newly discovered signaling pathway in cellular models of the disease. They found that the presence of the amyloid beta peptide triggers increased levels of a signaling protein, CentA1, and this protein appears to create cognitive dysfunction. The finding could open the door for new therapies to treat the debilitating disease.

The Institute, which opened in Jupiter, FL, in December 2012, is the first U.S. extension of the Munich, Germany-based Max Planck Society for the Advancement of Science.

Conducting tests on rat brain slices, researchers identified the signaling protein–called centaurin-α1, or CentA1–and measured its effects on neurons. They observed that the presence of amyloid beta triggered higher levels of CentA1, which seems to cause neuron dysfunction.

The researchers used RNA silencing to reduce the production of CentA1 in the rat brain samples, which caused the neurons exposed to amyloid beta to return to normal functioning–that is, the neurons no longer showed signs of Alzheimer’s–even though the amyloid beta was still present.

When they increased CentA1, a series of proteins was activated, and these proteins formed a signaling pathway from CentA1 to neuronal dysfunction. The researchers found that by inhibiting other proteins along the pathway, they were, in effect, able to “cure” the affected neurons. The research was published in the Journal of Neuroscience.

The scientists have already started to conduct studies in mouse models of Alzheimer’s disease.

In early trials conducted on mice they found the compound reduced by a third the number of ‘plaques’ on the brain, which are associated with the disease. The drug also doubled the number of new nerve cells in a particular region of the brain associated with memory. David Allsop, professor of neuroscience at Lancaster University, said he and colleagues were “highly encouraged” by the results, published in the journal PLoS ONE. He explained: “Many people who are mildly forgetful may go on to develop the disease because these senile plaques start forming years before any symptoms manifest themselves. “The ultimate aim is to give the drug at that stage to stop any more damage to the brain, before it’s too late.”

Researchers know that the ‘amyloid plaques’, as they are known, are associated with Alzheimer’s. However, there is debate about whether removing them significantly improves symptoms, or if by the time they are formed the damage is already done. Other drugs are being developed which attack the changes thought to lead to Alzheimer’s, at an early stage. The study was supported by the Alzheimer’s Research UK. Dr Eric Karran, director of research said: “These are promising early-stage results, and several years more work will be required to assess the potential of this approach.”

If Northwestern Medicine’s mouse studies come good, then in the future, doctors could treat lymphoma without toxic drugs with something as simple as minute particles of gold. These block the entry of HDL cholesterol and starve the cancer cells to death, according to new research in PNAS.

Lymphoma cells have a “hunger” for the lipoprotein HDL-cholesterol. They have more HDL receptors on their surface than normal cells, and are dependent on HDL-C for their growth. The synthetic nanoparticles have a spongy surface and a gold core and mimic HDL-C. They are taken up by the lymphoma cell, where they absorb the existing cholesterol and block the entry of more cholesterol. This cuts off the cell’s nutrient source.

In the lab, the gold nanoparticles killed cultured B-cell lymphoma cells, and slowed the growth of B-cell lymphoma tumors in mice, without affecting healthy cells. The particles have also been tested in lymphoma as a delivery system for cancer chemotherapies, but early studies showed that they were effective without the cytotoxic payload.

The particle was originally developed as a potential treatment for heart disease, as C Shad Thaxton explains: “At first I was heavily focused on developing nanoparticles that could remove cholesterol from cells, especially those involved in heart disease. The lymphoma work has broadened this focus to how the HDL nanoparticles impact both the removal and uptake of cholesterol by cells. We discovered the particles are multi-taskers.”

Stem cell-based therapeutics are a fast-growing area of early-stage biotech research, targeting diseases from amyotrophic lateral sclerosis and Duchenne muscular dystrophy to cancer and HIV, supporting regenerative medicine, and even potentially making the deaf hear again. Stem cells can also be used in drug screening, as they can give early signs of the effects of drugs on the whole body.

However, all of this requires a stable, reliable and plentiful supply of stem cells, and current methods can be expensive and prone to contamination.

A team of researchers at the University of Edinburgh in the U.K. has created a gel-based scaffold that acts as a framework. The cells cling to it and multiply, and then drop off as the gel cools, almost like ripe fruit.

Dr. Paul de Sousa, of the University of Edinburgh’s Scottish Centre for Regenerative Medicine, said: “This development could greatly enhance automated production of embryonic stem cells, which would improve the efficiency and reduce the cost of stem cell manufacturing. We are also looking into whether this work could help develop pluripotent stem cells induced from adult cells.”

Breakthroughs like this are going to be vital to the move toward stem cell therapies, enabling preclinical and clinical stages of R&D, and allowing the large-scale production of therapies once they are approved

Preclinical studies have raised a potential red flag on anti-VEGF therapies, suggesting that increasingly aggressive use in eye disease could trip off side effects and even cause long-term damage.

When the researchers blocked VEGF-A in mice, they found changes to the ciliary body, which produces aqueous humor (the fluid that fills the front portion of the eye), linked with falling intraocular pressure. The research was published in Investigative Ophthalmology & Visual Science (IOVS).

A number of companies are developing VEGF-A inhibitors for eye disease or have launched them onto the market, for example Allergan and Molecular Partner’s ($AGN) MP0260 in preclinical development for wet age-related macular degeneration (AMD), or Bayer and Regeneron‘s Eylea (VEGF Trap-Eye; aflibercept) and OSI Pharmaceuticals/Pfizer’s ($PFE) Macugen (pegaptanib), both approved for wet AMD. Other indications include diabetic macular edema and retinopathy of prematurity.

While these effects on the ciliary body or associated adverse events haven’t been seen in clinical trials or current use, the researchers are concerned that moves towards continuous delivery of the inhibitors–or the use of more potent inhibitors–could increase the risk, and suggest that these findings should perhaps change the direction of research.

“I am hoping that revealing the possible negative side effects of VEGF inhibition in the eye will motivate research into new ways to block edema and blood vessel growth in the eye that does not require continuous inhibition of intraocular VEGF,” said Patricia D’Amore of Schepens Eye Research Institute/Massachusetts Eye and Ear.

Totally blind mice have had their sight restored by injections of light-sensing cells into the eye, UK researchers report.

The team in Oxford said their studies closely resemble the treatments that would be needed in people with degenerative eye disease.Similar results have already been achieved with night-blind mice. Experts said the field was advancing rapidly, but there were still questions about the quality of vision restored. Patients with retinitis pigmentosa gradually lose light-sensing cells from the retina and can become blind.

The research team, at the University of Oxford, used mice with a complete lack of light-sensing photoreceptor cells in their retinas. The mice were unable to tell the difference between light and dark.

Reconstruction

They injected “precursor” cells which will develop into the building blocks of a retina once inside the eye. Two weeks after the injections a retina had formed, according to the findings presented in the Proceedings of the National Academy of Sciences journal.Prof Robert MacLaren said: “We have recreated the whole structure, basically it’s the first proof that you can take a completely blind mouse, put the cells in and reconstruct the entire light-sensitive layer.”Previous studies have achieved similar results with mice that had a partially degenerated retina. Prof MacLaren said this was like “restoring a whole computer screen rather than repairing individual pixels”.The mice were tested to see if they fled being in a bright area, if their pupils constricted in response to light and had their brain scanned to see if visual information was being processed by the mind.

Vision

Prof Pete Coffee, from the Institute of Ophthalmology at University College London, said the findings were important as they looked at the “most clinically relevant and severe case” of blindness. ”This is probably what you would need to do to restore sight in a patient that has lost their vision,” he said. However, he said this and similar studies needed to show how good the recovered vision was as brain scans and tests of light sensitivity were not enough.He said: “Can they tell the difference between a nasty animal and something to eat?” Prof Robin Ali published research in the journal Nature showing that transplanting cells could restore vision in night-blind mice and then showed the same technique worked in a range of mice with degenerated retinas. He said: “These papers demonstrate that it is possible to transplant photoreceptor cells into a range of mice even with a severe level of degeneration. ”I think it’s great that another group is showing the utility of photoreceptor transplantation.”

Researchers are already trialling human embryonic stem cells, at Moorfields Eye Hospital, in patients with Stargardt’s disease. Early results suggest the technique is safe but reliable results will take several years. Retinal chips or bionic eyes are also being trialled in patients with retinitis pigmentosa.

Innovative Research has had several new references in publications over the past week. Below are just a few of the newest ones. Dont forget were constantly adding these to our website and to our reference only site

Label-free DNA Sensor for Detection of Bladder Cancer Biomarkers in Urine

Y Shin, AP Perera, MK Park – Sensors and Actuators B: Chemical, 2012

… St. Louis, MO). For urine experiments, normal human urine was purchased from
Innovative Research (Novi, MI) and stored at 4 °C until used. Other chemicals were
analytical reagent grade, and used as received. All samples …

Engineering Polypeptide Coatings to Augment Gene Transduction and< i> in vivo</i> Stability of Adenoviruses

ZK Jiang, SBS Koh, M Sato, IC Atanasov, M Johnson… – Journal of Controlled …, 2012

… Human serum (pooled from 10 donors) was purchased from Innovative Research, Inc., Novi,
MI. Ad or Ad-K60KP370 was applied to AML-12 cells in serum-free media or serum-free media
containing blood clotting factor, Factor X (FX), at physiological concentration (8 g/ml). …

Novel Inhibitors of Staphylococcus aureus Virulence Gene Expression and Biofilm

Y Ma, Y Xu, BD Yestrepsky, RJ Sorenson, M Chen – 2012

… Twenty цl of culture supernatant was added to 100 цl phosphate buffered saline (PBS), 10
цl human plasma (Innovative Research, Novi, MI), and10 цl S2403 (1 mg/ml) (Diapharma
group Inc., West Chester, OH) and incubated at 37uC for 2 hours. …

The foibles of the country’s real estate market are largely absent in biotech’s boomtown. Like pioneers rushing for gold, biotech and pharma outfits have swept into Cambridge, MA, and dismissed the hefty propriety costs in search of talent and technology that could lead to lucrative new drugs.

In a New York Times article, Biogen Idec ($BIIB) CEO George Scangos serves as a leading mover in the industry’s rush to Cambridge. After Scangos took the top job at Biogen in 2010, he quickly jettisoned his predecessor’s plan of keeping business folks and executives a half hour outside Boston in Weston, MA, while R&D stayed in Cambridge. And now Biogen is planning to ditch its HQ in sleepy Weston for a new $500 million facility under construction in the biotech hotbed of Cambridge.

Of course, Scangos has plenty of company. As the Times reports, the biotech industry’s growth is the leading factor in the whopping 3.4 million square feet of space at various stages of construction or planning in the city that sits across the Charles River from Boston.

Pfizer ($PFE) has been moving research and hundreds of employees to Cambridge as it exits facilities in Groton, CT, Sandwich, U.K., and elsewhere. Novartis, which houses its global R&D operation in Cambridge, is erecting two major buildings there at a cost of $600 million. The list goes on.

In general the burbs outside Boston offer cheaper digs than the city. Yet biopharma isn’t the insurance industry. It needs copious inventions to thrive. And the cost of real estate in Cambridge–which offers of smorgasbord of biotech talent and innovations–has become another cost of doing business for a bevy biotech and pharma outfits.

“It’s an amazing place to be,” Scangos told the Times. “The intellectual firepower that is in Cambridge, between Harvard and MIT and the number of companies, is quite remarkable.”

Don’t be fooled by the overflow of news on stock swings and megabucks involved in biotech; many people–and I would guess most–become enamored with this industry because of the promise of transforming scientific discoveries into new therapies.

Bank on 2013 being a year when real innovators in life sciences with bold ideas look like smart businesspeople, too.

It turns out that economies demand innovation from biotech. Healthcare payers have shown over and over again that incremental improvements or marginal benefits from new drugs won’t be rewarded. And we see companies like Moderna Therapeutics gaining investments with bold plans to revolutionize biotech.

You really never know whether companies like Moderna–which is using a messenger RNA platform to spur the body to produce its own therapeutic proteins–will ultimately succeed. Yet we see investors such as Flagship betting their futures on truly transformative technologies.

This is what has made companies like Biogen ($BIIB) and Genentech great.

The money problem continues

Don’t let the spate of recent venture rounds in the lead-up to Christmas fool you. The biotech industry has a money problem, and it’s not going to disappear in 2013.

For four years after the financial crisis in 2008, biotech didn’t do so badly on the venture front. Certainly there was no wild party in the venture suite, but the money flowed steadily enough to support startups and fuel clinical stage development–until the first half of this year.

After a weak start, the second quarter saw only $697 million in 90 deals, a 42% plunge compared to the same period the year before. The numbers picked up considerably in the third quarter, but not enough to replace the hundreds of millions that evaporated earlier in the year. The Russians have helped, providing Rusnano with hundreds of millions of dollars to sink into biotech companies. But new players can’t fill the void.

In an innovative industry like biotech, the absence of venture backing is a big deal. And without a new crop of drug developers to take the place of the companies that are being bought out or fail, there will be fewer deals to do in the future. And that means fewer promising drugs for Big Pharma to take up the pipeline.

Like every other industry, biotech is cyclical. But lean times get tiresome. They also threaten to do some lasting damage to the complex ecosystem that supports a diverse group of players.

Open R&D comes of age in 2013

When GlaxoSmithKline ($GSK) made its big announcement earlier this year that it will open up its data to qualified investigators, you could feel the industry flinch. Now look for some others to follow suit in a fashion that will make this trend all but unavoidable.

Big Pharma R&D has been hiding behind its elaborate Chinese walls for decades. If they were churning out a bunch of big new drugs every year, that could continue. But the whole system broke down, and not just because it became clear that too many big players liked to hide some discomforting information that patients and physicians needed to know about. The old way of developing drugs doesn’t work anymore, and in fashioning a new approach in a more open ecosystem, the walls will come tumbling down.

It’s not easy. First, the data has to be standardized so that investigators know how to work with it. TransCelerate can go a long way to managing the first halting steps in this direction. There will be holdouts, to be sure, but they’re not asking for much initially.

Once another Big Pharma company takes the data pledge, the rest of the boards are likely to find the pressure to open up unbearable. Managing the process will then become the focus rather than trying to avoid the inevitable.

Keep in mind, though, that there are limits to what you can do in the open. No one is going to simply hand over valuable IP to rivals. On the other hand, there’s never been a better time to take the pledge. Too many players have had to cover too many huge settlements for past misbehavior. Changing the industry’s reputation will require concrete actions. Simple promises to do better next time won’t cut it.

Eli Lilly will make major strategic changes

Eli Lilly ($LLY) CEO John Lechleiter knew that 2012 would not be a great one for his company, with the loss of patent exclusivity on Zyprexa hammering the Indianapolis-based drug giant’s bottom line. Yet Lilly failed to deliver a Phase III winner with solanezumab, among other late-stage setbacks.

In 2013, expect the chief executive to pull the trigger on some major deals to give investors faith in the future of the company.

Lechleiter has made it clear that he’s not interested in megamergers, and this stance probably won’t change because the industry has figured out the economic hitches of such deals. However, the company will need to aggressively pursue the type of bolt-on acquisitions that have been the toast of pharma chiefs around the world.

Lilly has a fairly robust pipeline of diabetes drugs, with promising candidates such as dulaglutide and an ongoing alliance with Boehringer Ingelheim. But the company has shown weakness in one of the core areas of its business and pipeline, the central nervous system (CNS). If ever, solanezumab won’t be a factor for Lilly for years. And it ditched a Phase III effort for pomaglumetad methionil in schizophrenia.

Look for Lechleiter to show that Lilly can be a future leader in the CNS arena with a significant deal. What choice does he have, really?

Hep C race reaches finish line

In pursuit of cures for a serious liver disease, biopharma outfits cranked out one huge news event after another this year from their hepatitis C programs. The major drivers have been the snowballing problem of hep C in the aging population and the success of all-oral therapies that could wipe out the virus relatively quickly without need of interferon.

In 2012, Gilead Sciences ($GILD) led the race for such therapies with cocktails built around its candidate sofosbuvir, which it picked up in the monster buyout of Pharmasset ($VRUS) for $11 billion. Next year we’ll see Gilead build its lead in this race, which includes rivals such as Abbott/AbbVie, Bristol-Myers Squibb ($BMY) and a pack of other wily developers.

Gilead aims to seek FDA approval of sofosbuvir next year, and the Foster City, CA-based drugmaker is in position to become the first company with an all-oral regimen against hep C on the market. Timing is hugely important in this race, because millions of patients in the U.S. and abroad are expected to jump at the chance to get rapid cures once all-oral regimens become available.

Yet hep C comes in multiple variants, with distributions of each varying from country to country. Bristol-Myers understands this as well as anyone, and the New York-based drug giant aims to be the first to market with an all-oral combo in Japan. In fact, expect many companies to seize opportunities to develop and commercialize new hep C therapies in geographies other than the U.S.

This is a potential $20 billion market, and companies will seek many different paths to grab their share of it

The investment cash has been flowing into biotechnology this week. This morning Nuron Biotech joined the parade, announcing an $80 million deal designed to boost its work expanding a portfolio of vaccines while pushing ahead on a late-stage development program for multiple sclerosis. Just days ago the Exton, PA-based Nuron bagged Meningitec, which guards against meningitis, sepsis and pneumonia, from Pfizer ($PFE). Now HealthCare Royalty Partners II has agreed to invest $30 million in the company with an additional $50 million for a royalty pact based on sales of its vaccines.

Nuron has been pursuing an unorthodox strategy for a biotech. It’s been building a market for vaccines–a strategy that also included the acquisition of Pfizer’s neglected Hib vaccine last year–while developing a pipeline of new chemical entities. Its most advanced program is built around NU100, a recombinant human interferon beta-1b product in a late-stage study for multiple sclerosis.

Nuron launched the Phase III for NU1001 a little more than a year ago, with plans to recruit 500 MS patients in 125 sites across Europe and Asia. The product is designed to make interferon–a product associated with a laundry list of side effects–more tolerable for patients. Interferon beta is the most frequently used treatment for relapsing-remitting MS.

“We are confident that Nuron can build the infrastructure to expand Meningitec’s market in Europe while capitalizing on new markets with unvaccinated and under-vaccinated populations,” Gregory B. Brown, M.D., the founding managing director of HC Royalty, said in a release. “In the company’s pipeline, lead candidate NU100, for example, is a proprietary human interferon beta-1b, which is in a Phase III clinical trial for multiple sclerosis, and may improve long-term clinical efficacy, tolerability and safety for patients currently requiring therapy with interferon.”

In its release HealthCare Royalty Partners said that it had invested more than $2 billion in 40 royalty agreements over the past decade.

Actelion might have a shot at breaking into the market for new oral drugs against immune-related disorders. The Swiss biotech ($ATLN) scored positive efficacy data from a midstage trial with patients suffering from plaque psoriasis on its candidate ponesimod. And the company intends to follow up the results in planned late-stage trials.

The 326-patient study nailed its primary goal, with 46% of patients on a 20-mg dose of the oral compound achieving at least a 75% improvement on an index to rate the severity of the skin disease at 16 weeks. Also, 48.1% of patients reached the same goal on a 40-mg dose. Those numbers trumped the 13.4% improvement in patients on placebo.

Actelion appears to have notched another R&D victory with ponesimod, building on the impressive late-stage study results earlier this year with macitentan in patients with pulmonary arterial hypertension (PAH). Macitentan is under FDA review and holds the key to Actelion’s future in the competitive market for drugs against PAH, for which its aging blockbuster Tracleer is used.

The biotech faces plenty of competition in the psoriasis arena too. Ponesimod–a selective S1P1 modulator–has now produced positive efficacy results in midstage trials with psoriasis and multiple sclerosis patients. (The market for MS pills has already stoked a rivalry among Novartis ($NVS), Sanofi ($SNY) and Biogen Idec ($BIIB).) Amgen ($AMGN), however, has shown better evidence of efficacy in a midstage trial for its injected drug brodalumab in psoriasis patients, Vontobel analysis Andrew Weiss noted, as quoted by Reuters.

“However, a strength of Actelion’s compound is the oral route of administration,” Weiss pointed out in the Reuters report.

On the safety front ponesimod’s profile was similar to results from a midstage study in MS patients, according to the company. The most common side effects in the psoriasis study were shortness of breath and increased liver enzymes classified as “asymptomatic.”

Actelion has had one of the largest R&D budgets among global biotechs as CEO Jean-Paul Clozel has invested big in broadening the scope of the business beyond Tracleer. He made a point to note in the company’s release this morning that ponesimod came from his company’s discovery work and seems to have a shot at treating multiple immune disorders.

“Actelion will rapidly move forward with the preparation of the pivotal program and discussions with health authorities for the psoriasis indication,” Clozel said in a statement

The startup biotech Blend Therapeutics rang in 2012 with seed cash and will now close out the year with a fresh injection of $16 million in B-round bucks budgeted to take this startup–one of the latest from the prolific scientist Robert Langer–right to the threshold of clinical development. The biotech has also secured the talents of biotech vet Mark Iwicki at the helm, whose 23 years in the business includes a stint as CEO of Sunovion.

The new injection of cash, will allow the developer to double its staff from 10 to about 20 next year. Most of those new employees will go straight to work on two preclinical drug programs, with a novel “mono-functional” platinum cancer drug on track to complete IND enabling work.

Watertown, MA-based Blend has a trio of notable scientific backers in Cambridge, MA. Along with Langer, there’s his longtime associate Omid Farokhzad, an associate professor at Harvard Medical School, as well as MIT’s Stephen Lippard, whose work at MIT has been heavily concentrated on platinum anticancer therapies. He’s been exploring new nanomolecular constructs that can improve the therapeutic punch of platinum drugs.

The lead program helps illustrate the approach. Iwicki notes that previous platinum drugs bind to DNA at two points, which can trigger resistance to the drug. Their mono-functional drug binds at one point, avoiding that trap while delivering the potent treatment in a nanoparticle delivery vehicle that can leave healthy tissue alone while concentrating the therapeutic, a new molecular entity, where it’s needed–a big trend in cancer drug development.

Blend’s plan is to “build a better platinum drug,” says Iwicki, “and use nanoengineering to improve it.” And there’s plenty of potential for combination therapies with the technology, he adds, which has also helped garner attention from potential partners.

NanoDimension led the round with participation from existing investors Flagship Ventures and New Enterprise Associates. Langer has relied on a number of early-stage investors to launch a string of biotech companies, including Selecta (a 2011 Fierce 15 company) and Bind Biosciences (a 2008 Fierce 15 company).

San Diego-based Fate Therapeutics, which focuses on the discovery and development of adult stem cell modulators, has announced that its Wnt protein therapeutic program, in development for use in skeletal muscle regeneration, has moved several steps closer to its goal.

After dealing with manufacture, formulation and delivery issues, Fate now has a selection of candidate proteins and has validated their therapeutic potential in a number of preclinical animal models. Naturally occurring proteins in the Wnt family are involved in stem cell fate and tissue development and repair.

Fate’s FT301 program includes a number of proprietary Wnt7a-based protein therapeutics that are in development for the regeneration of skeletal muscle by modulating stem cells. In August, Fate snagged $9.2 million of equity financing, but the specific programs that this will support have not been disclosed.

The company also said it has strengthened its advisory team by adding K. Christopher Garcia of Stanford University School of Medicine, the researcher who published the first molecular structure of a Wnt protein.

While Alzheimer’s disease immunotherapies have been able to prevent the tangles of amyloid beta (Aβ) protein deposits developing in the brain, Eli Lilly ($LLY) has gone a step further. According to a paper in the Cell Press journal Neuron, one of the pharma company’s antibodies has cleared existing plaques in a mouse model of Alzheimer’s disease.

Studies show that previous antibodies against Aβ in mice have been able to reduce or stop the buildup of the Aβ plaques. However, the same antibodies given to mice that already have plaques in their brains seem to set off severe side effects, including small bleeds in the brain known as microhemorrhages.

The researchers at Lilly have created a tweaked antibody that targets just the insoluble Aβ that makes up the plaques rather than the circulating soluble form of the protein. In mice given shots of the plaque-specific antibody, their Aβ tangles were cleared with no side effects. However, the mice that had the less-specific version of the antibody had no clearance of plaque and bleeding in their brains, perhaps because the antibodies were saturated with the free-floating form and so couldn’t target the insoluble form.

“The data suggest that an antibody that binds to only insoluble amyloid beta is likely critical for plaque removal without the associated adverse event of microhemorrhage. These findings have important implications for current and future development of antibodies for the treatment of Alzheimer’s disease,” first author Ronald DeMattos of Lilly said in a statement.

This may be behind the failure of Pfizer ($PFE) and Johnson & Johnson’s ($JNJ) Phase III Alzheimer’s drug, which targets both soluble and insoluble Aβ, and which was scrapped in August after its results fell short.

Despite many years of research, Alzheimer’s disease is still somewhat of a mystery, with therapeutics on the market only dealing with symptoms rather than slowing, stopping or even reversing the course of the disease, the real goal. Amyloid plaques appear to develop up to 10 years before symptoms appear, so tying together a biomarker that can detect the disease in its early stage with a therapeutic that may be able to halt and reverse the plaque development before it does any long-lasting harm would be the holy grail.

Innovative Research sells antibodies. We sell antibodies, and proteins as well, some of those are amyloid beta products. Other than that Innovative Research of course sell high quality material to reputable companies. You MIGHT already know that, you might know that because this is at the end of nearly every blog article.

Swedish drug developer Kancera says it has slowed the growth of pancreatic cancer tumors in preclinical animal trials with its first-generation PFKFB3 inhibitors.

The drug initially failed to work in an animal study involving human colon cancer, according to the company.

By blocking PFKFB3, the idea is to reduce the metabolism of the cancer tumors and starve its energy/food supply. PFKFB3 is believed to support cancer growth because it enables production of glucose, which cancer craves. Kancera claims that the drug generated a 20% reduction in pancreatic cancer tumor growth versus placebo treatment. That may not sound like a lot, but as the company notes, patients diagnosed with pancreatic cancer have a less than 2% survival rate 5 years after the diagnosis. And so Kancera insists that the initial promise PFKFB inhibitors show in reducing pancreatic cancer growth is license to proceed

“That PFKFB inhibitors alone can reduce the growth of pancreatic cancer is very encouraging,” CEO Thomas Olin said in a statement.

Kancera’s initial results are encouraging but they’re a long way from human trials. Coming next will be a bid to improve the drug properties of the company’s PFKFB inhibitors and test how well they work to combat tumor growth combined with standard pancreatic cancer therapy.

Kancera isn’t the only company targeting PFKFB3, whose full name is 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3. Advanced Cancer Therapeutics is developing a possible brain cancer treatment with the same enzyme target in mind.

Innovative Research had nothing to do with this…..but we could have. Innovative Research offers high quality cancer serum, and plasma as well as brand new proteins and antibodies to specifically target the immune system. By providing cytokines and interleukins, Innovative Research hopes that the research community and laboratories all around the world will continue to provide results driven research.