Synthetic oil triheptanoin improves Rett syndrome, longevity

We know that, Triheptanoin is a triglyceride that is composed of three seven-carbon fatty acids. These odd-carbon fatty acids are able to provide anaplerotic substrates for the TCA cycle. Triheptanoin is used clinically in humans to treat inherited metabolic diseases, such aspyruvate carboxylase deficiency and carnitine palmitoyltransferase II deficiency. It also appears to increase the efficacy of the ketogenic diet as a treatment for epilepsy.

Now the research team used mice lacking the MeCP2 protein, which left them with severe Rett syndrome. In examining those mice, what stood out, according to Gabriele Ronnett, M.D., Ph.D., who led the research project at the Johns Hopkins University School of Medicine, was that they weighed the same as healthy mice but had large fat deposits accompanied by lower amounts of nonfat tissue, such as muscle. This suggested that calories were not being used to support normal tissue function but instead were being stored as fat.

This possibility led Ronnett and her research team to consider the role of mitochondria, which transform the building blocks of nutrients into a high-energy molecule, ATP. This molecule drives processes such as the building of muscle and the growth of nerve cells. Mitochondria use a series of biochemical reactions, collectively called the TCA cycle, to make this transformation possible. According to Susan Aja, Ph.D., a research associate and lead member of the research team, "If the components of the TCA cycle are low, nutrient building blocks are not processed well to create ATP. They are instead stored as fat."

Synthetic oil triheptanoin improves Rett syndrome, longevity

Akynzeo Approved for Side Effects of Chemotherapy

The combination drug Akynzeo [netupitant (left) and palonosetron (right)] has been approved by the U.S. Food and Drug Administration to treat nausea and vomiting among people undergoing chemotherapy, the agency said Friday in a news release.

Akynzeo contains a new anti-nausea drug, netupitant, and palonosetron, which was approved to treat nausea and vomiting in 2008.

The combination drug's effectiveness was evaluated in two clinical studies involving 1,720 people. The trials established that Akynzeo was more effective in preventing nausea and vomiting than palonosetron taken alone, the FDA said.

The most frequent side effects of the combination drug included headache, weakness, fatigue, indigestion and constipation.

Akynzeo is marketed and distributed by Eisai Inc. of Woodcliff Lake, N.J., under license from Switzerland-based Helsinn Healthcare.

Akynzeo Approved for Side Effects of Chemotherapy 

Harvoni Approved for Chronic Hepatitis C

In continuation of my update on  ledipasvir and sofosbuvir (Harvoni-combination pill) 

Harvoni, a daily pill that treats the most common form of hepatitis C, was approved by the U.S. Food and Drug Administration on Friday.

It's the first combination pill (ledipasvir and sofosbuvir) approved to treat the chronic infection, and the first medication that doesn't require that the antiviral drugs interferon or ribavirin be taken at the same time, the FDA said in a news release.

Both drugs in the combination pill interfere with the hepatitis C virus' ability to multiply. One of the drugs, sofosbuvir (Sovaldi) was approved in December 2013, while ledipasvir is a new antiviral, the agency said.

"With the development and approval of new treatments for hepatitis C virus, we are changing the treatment paradigm for Americans living with the disease," Dr. Edward Cox, director of the Office of Antimicrobial Products in the FDA's Center for Drug Evaluation and Research, said in the news release. "Until last year, the only available treatments for hepatitis C virus required administration with interferon and ribavirin. Now, patients and health care professionals have multiple treatment options, including a combination pill to help simplify treatment regimens."

One expert applauded Harvoni's approval.

"This is a giant step forward for people with [hepatitis C]. One pill, once daily, no interferon, no ribavirin and 94 to 99 percent cure! It moves the risk-benefit ratio needle way over toward benefit," said Dr. Douglas Dieterich, a professor of medicine in the division of liver diseases at The Mount Sinai Hospital in New York City.

However, price has been an issue with some of the new treatments for hepatitis C. For example, Sovaldi alone costs $1,000 a day and not all insurance companies cover the cost of treatment, experts have noted. Harvoni will cost $1,125 a pill, the Associated Press reported Friday.

Hepatitis C causes inflammation of the liver, which could spark other problems including diminished liver function (cirrhosis), scarring, liver cancer or liver failure. Most infected people aren't aware that they carry the virus until liver damage has occurred, the agency said.

Some 3.2 million Americans are believed to be infected with hepatitis C, the FDA said.

Harvoni was evaluated in three clinical studies involving more than 1,500 people who either hadn't been treated previously or hadn't responded to prior treatment. The most common side effects were fatigue and headache.

Harvoni Approved for Chronic Hepatitis C  

FDA Approves Uceris (budesonide) Rectal Foam for Ulcerative Colitis

In continuation of my update on budesonide

Salix Pharmaceuticals, Ltd. announced that the Food and Drug Administration (FDA) has granted final approval for Uceris (budesonide) rectal foam for the induction of remission in patients with active mild-to-moderate distal ulcerative colitis (UC) extending up to 40cm from the anal verge. The foam is a rectally administered corticosteroid that overcomes treatment limitations associated with currently approved therapies which are often ineffective due to insufficient distribution of active drug to the distal colon. On September 15, 2014 the FDA tentatively approved Uceris rectal foam pending expiration of the 45-day waiting period described in section 505( c )(3)( C ) of the Federal Food, Drug and Cosmetic Act. The waiting period has expired and the FDA has granted Uceris rectal foam final approval as of October 7, 2014.

FDA Approves Uceris (budesonide) Rectal Foam for Ulcerative Colitis

Attacking type 2 diabetes from a new direction with encouraging results

Type 2 diabetes affects  an estimated   28  million  Americans  according  to  the  American  Diabetes association, but medications now  available  only  treat  symptoms,  not  the root  cause of the disease.    New research from Rutgers shows promising evidence that     a  modified form of a different drug, niclosamide     now used to eliminate    intestinal parasites   may       hold the key to battling the disease at its source.

Ref : http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.3699.html

Attacking type 2 diabetes from a new direction with encouraging results  

'Programmable' antibiotic harnesses an enzyme to attack drug-resistant microbes

Rockefeller University researchers colonized mouse skin with a mix of bacterial cells, some resistant to the antibiotic kanamycin. They made the resistant cells glow (left) and treated the mix with an enzyme that targeted and killed off most resistant cells (right).

Conventional antibiotics are indiscriminate about what they kill, a trait that can lead to complications for patients and can contribute to the growing problems of antibiotic resistance. But a a 'programmable' antibiotic would selectively target only the bad bugs, particularly those harboring antibiotic resistance genes, and leave beneficial microbes alone.

Researchers at Rockefeller University and their collaborators are working on a smarter antibiotic. And in research to be published October 5 in Nature Biotechnology, the team describes a 'programmable' antibiotic technique that selectively targets the bad bugs, particularly those harboring antibiotic resistance genes, while leaving other, more innocent microbes alone.

"In experiments, we succeeded in instructing a bacterial enzyme, known as Cas9, to target a particular DNA sequence and cut it up," says lead researcher Luciano Marraffini, head of the Laboratory of Bacteriology. "This selective approach leaves the healthy microbial community intact, and our experiments suggest that by doing so you can keep resistance in check and so prevent certain types of secondary infections, eliminating two serious hazards associated with treatment by classical antibiotics."

The new approach could, for instance, reduce the risk of C. diff, a severe infection of the colon, caused by the Clostridium difficile bacterium, that is associated with prolonged courses of harsh antibiotics and is a growing public health concern.

The Cas9 enzyme is part of a defense system that bacteria use to protect themselves against viruses. The team coopted this bacterial version of an immune system, known as a CRISPR (clustered regularly interspaced short palindromic repeats) system and turned it against some of the microbes. CRISPR systems contain unique genetic sequences called spacers that correspond to sequences in viruses. CRISPR-associated enzymes, including Cas9, use these spacer sequences as guides to identify and destroy viral invaders.

The researchers were able to direct Cas9 at targets of their choosing by engineering spacer sequences to match bacterial genes then inserting these sequences into a cell along with the Cas9 gene. The cell's own machinery then turns on the system. Depending on the location of the target in a bacterial cell, Cas9 may kill the cell or it may eradicate the target gene. In some cases, a treatment may prevent a cell from acquiring resistance, they found.

"We previously showed that if Cas9 is programmed with a target from a bacterial genome, it will kill the bacteria. Building on that work, we selected guide sequences that enabled us to selectively kill a particular strain of microbe from within a mixed population," says first author David Bikard, a former Rockefeller postdoc who is now at the Pasteur Institute in Paris.

'Programmable' antibiotic harnesses an enzyme to attack drug-resistant microbes 

FDA Grants Amgen Priority Review Designation For Ivabradine For The Treatment Of Chronic Heart Failure

Amgen announced the U.S. Food and Drug Administration (FDA) has granted priority review designation for ivabradine for the treatment of chronic heart failure (HF). Ivabradine is an oral drug that inhibits the I_f current ("funny" current) in the sinoatrial node, the body's cardiac pacemaker.  Ivabradine works to slow the heart rate without negative effects on myocardial contractility or ventricular repolarization.  Heart failure is a common condition that affects approximately 26 million worldwide, including approximately 5.1 million people in the U.S. 

FDA Grants Amgen Priority Review Designation For Ivabradine For The Treatment Of Chronic Heart Failure

New class of compounds protect brain cells from traumatic brain injury

A new class of compounds has now been shown to protect brain cells from the type of damage caused by blast-mediated traumatic brain injury (TBI). Mice that were treated with these compounds 24-36 hours after experiencing TBI from a blast injury were protected from the harmful effects of TBI, including problems with learning, memory, and movement.

Traumatic brain injury caused by blast injury has emerged as a common health problem among U.S. servicemen and women, with an estimated 10 to 20 percent of the more than 2 million U.S. soldiers deployed in Iraq or Afghanistan having experienced TBI. The condition is associated with many neurological complications, including cognitive and motor decline, as well as acquisition of psychiatric symptoms like anxiety and depression, and brain tissue abnormalities that resemble Alzheimer's disease.

"The lack of neuroprotective treatments for traumatic brain injury is a serious problem in our society," says Andrew Pieper, M.D., Ph.D., senior study author and associate professor of psychiatry, neurology, and radiation oncology at the University of Iowa Carver College of Medicine. "Everyone involved in this work is motivated to find a way to offer hope for patients, which today include both military personnel and civilians, by establishing a basis for a new treatment to combat the deleterious neuropsychiatric outcomes after blast injury."

It is known that TBI, as well as certain neurodegenerative diseases, damages axons - the tendril-like fibers that sprout from brains cells (neurons) and form the connections called synapses. In TBI, axon damage is followed by death of the neuron. The new study, published Sept. 11 in the journal Cell Reports, shows that a group of compounds, called the P7C3 series, blocks axon damage and preserves normal brain function following TBI.

Pieper led the team of scientists that discovered the P7C3 compound several years ago at UT Southwestern Medical Center. Subsequent studies showed that the root compound and its active analogs protect newborn neurons from cell death and also protect mature neurons in animal models of neurodegenerative diseases, including Parkinson's disease and amyotrophic lateral sclerosis (ALS).

The researchers have also previously shown efficacy of P7C3 molecules in brain injury due to concussion, and plan to investigate whether these compound might be applicable in stroke as well, given that there appear to be common factors mediating neuronal cell death in these conditions.
Ref : http://www.cell.com/cell/abstract/S0092-8674(10)00672-0

New class of compounds protect brain cells from traumatic brain injury

Synthesis produces new fungus-derived antibiotic

A fortuitous collaboration has led to the total synthesis of a recently discovered natural antibiotic. The laboratory recreation of a fungus-derived antibiotic, viridicatumtoxin B, may someday help bolster the fight against bacteria that evolve resistance to treatments in hospitals and clinics around the world.

As part of the process, Rice organic chemist K.C. Nicolaou and structural biologist Yousif Shamoo and their colleagues created and tested a number of variants of viridicatumtoxin B that could lead to the simplified synthesis of a new generation of more effective antibiotics.

The work reported this month in the Journal of the American Chemical Society (JACS) focused on a tetracycline discovered in 2008 by scientists who isolated small amounts from penicillium fungi. The yield wasn't nearly enough for extensive testing, but it provided a basis for the discoverers to analyze its structure through magnetic resonance imaging, Nicolaou said.

"We're inspired by molecules that are biologically active and have the potential to become medicines one day," he said.

The new discovery belongs to a class of antibiotics known as tetracyclines for their distinctive molecular structure. They proved potent  in  initial tests on
Gram-positive bacteria, so named for a staining technique to mark bacteria that are more susceptible to antibiotics than their Gram-negative counterparts.

The first tetracyclines, discovered in the late 1940s, ushered in a new class of
powerful antibacterial agents to treat high-mortality diseases,    among  them
anthrax and plague as well as such bacterial infections as chlamydia, syphilis
and Lyme disease.

To find new weapons, especially  against  "superbugs" that resist nearly all antibiotics, synthetic chemists pursue the complex  process  of  mimicking the
structures of effective natural molecules as they build drug candidates atom by atom.

"Tetracyclines are widespread antibiotics today, but bacteria are building resistance to a lot of them," Nicolaou said. "This new tetracycline is not plentiful in nature, so the only way we can make it available to study by biologists for its potential in medicine is to synthesize it in the laboratory."

Ref : http://pubs.acs.org/doi/abs/10.1021/ja506472u

Synthesis produces new fungus-derived antibiotic 

High-dose fluticasone effective against eosinophilic esophagitis, study shows...

I continuation of y update on Fluticasone..

Results from a clinical trial show that high doses of the corticosteroid fluticasone propionate safely and effectively induce remission in many people with eosinophilic esophagitis (EoE), a chronic inflammatory disease of the esophagus characterized by high levels of white blood cells called eosinophils. However, some trial participants did not respond to fluticasone even after six months of high-dose treatments, providing evidence that certain people with EoE are steroid-resistant. By analyzing gene expression -- the degree to which certain genes are turned on or off -- in esophageal tissues, the scientists identified a cluster of genes that may help predict steroid responsiveness.

Ref :Read more

High-dose fluticasone effective against eosinophilic esophagitis, study shows

Bowel cancer breakthrough may benefit thousands of patients

Researchers at Queen's University have made a significant breakthrough that may benefit
patients with bowel cancer. 

Dr Sandra van Schaeybroeck and her team have discovered how two genes cause bowel cancer cells to become resistant to treatments used against the disease. The research, which was funded by Cancer Research UK, was published this month in the international journal CellReports.

The activity of the two genes, called MEK and MET, was uncovered when the researchers looked at all the different pathways and interactions taking place in bowel cancer cells.

Dr van Schaeybroeck and her group found that these bowel cancers switch on a survival mechanism when they are treated with drugs that target faulty MEK genes. But when the researchers added drugs that also block the MET gene, the bowel cancer cells died.

The team are now testing a new approach to target these two genes in the most aggressive forms of bowel cancer in a European Commission funded clinical trial that is being led by Dr van Schaeybroeck.

Bowel cancer breakthrough may benefit thousands of patients

FDA Approves Zontivity to Reduce the Risk of Heart Attacks and Stroke

The U.S. Food and Drug Administration  approved Zontivity (vorapaxar) tablets to reduce the risk of heart attack, stroke, cardiovascular death, and need for procedures to restore the blood flow to the heart in patients with a previous heart attack or blockages in the arteries to the legs.

Zontivity is the first in a new class of drug, called a protease-activated receptor-1 (PAR-1) antagonist. It is an anti-platelet agent, designed to decrease the tendency of platelets to clump together to form a blood clot. By decreasing the formation of blood clots, Zontivity decreases the risk of heart attack and stroke.

Like other drugs that inhibit blood clotting, Zontivity increases the risk of bleeding, including life-threatening and fatal bleeding. Bleeding is the most commonly reported adverse reaction in people taking Zontivity. The drug’s prescribing information (label) includes a Boxed Warning to alert health care professionals about this risk.

Zontivity must not be used in people who have had a stroke, transient ischemic attack (TIA), or bleeding in the head, because the risk of bleeding in the head is too great.

“In patients who have had a heart attack or who have peripheral arterial disease, this drug will lower the risk of heart attack, stroke, and cardiovascular death. In the study that supported the drug’s approval, Zontivity lowered this risk from 9.5 percent to 7.9 percent over a 3-year period – about 0.5 percent per year,” said Ellis Unger, M.D., director of the Office of Drug Evaluation I in the FDA’s Center for Drug Evaluation and Research.

FDA Approves Zontivity to Reduce the Risk of Heart Attacks and Stroke

Promising discovery in fight against antibiotic-resistant bacteria .....

Researchers at  the  University  of British  Columbia  have identified a small molecule  that prevents  bacteria from forming into biofilms, a frequent cause of infections. The anti-biofilm peptide works on a range of bacteria including many that cannot be treated by antibiotics...

Hancock and his colleagues found that the peptide known as 1018  consisting of just 12 amino acids, the building blocks of protein  destroyed biofilms and prevented them from forming.

Bacteria are generally separated into two classes, Gram-positives and Gram-negatives, and the differences in their cell wall structures make them susceptible to different antibiotics. 1018 worked on both classes of bacteria as well as several major antibiotic-resistant pathogens, including Pseudomonas aeruginosa, E. coli and MRSA.

"Antibiotics are the most successful medicine on the planet. The lack of effective antibiotics would lead to profound difficulties with major surgeries, some chemotherapy treatments, transplants, and even minor injuries," says Hancock. "Our strategy represents a significant advance in the search for new agents that specifically target bacterial biofilms."

Promising discovery in fight against antibiotic-resistant bacteria 

Researchers identify drugs to slow progression of idiopathic pulmonary fibrosis

Researchers in separate clinical trials found two drugs slow the progression of idiopathic pulmonary fibrosis, a fatal lung disease with no effective treatment or cure, and for which there is currently no therapy approved by the Food and Drug Administration.

Paul W. Noble, MD, chair of the Department of Medicine at Cedars-Sinai and director of the Women's Guild Lung Institute, is the senior author of the multicenter study that found that the investigational drug pirfenidone significantly slowed the loss of lung function and reduced the risk of death. Pirfenidone was developed by InterMune Inc. and in 2011 was approved by the European Union for the treatment of idiopa Studies Published In New England Journal Of Medicine Identify Promising Drug Therapies For Fatal Lung Disease thic pulmonary fibrosis.

The findings of the ASCEND drug trial are published online by the New England Journal of Medicine and are being presented this week at the International Conference of the American Thoracic Society in San Diego. "What we discovered about the anti-inflammatory and anti-fibrotic properties of pirfenidone offers help and encouragement to so many patients suffering from this relentless disease that robs them of breath and life," said Noble.

Researchers identify drugs to slow progression of idiopathic pulmonary fibrosis

New drug offers promising possibility for treating adults with periodontitis

University of Pennsylvania researchers have been searching for ways to prevent, half and reverse periodontitis. In a report published in the Journal of Immunology, they describe a promising new target: a component of the immune system called complement. Treating monkeys with a complement inhibitor successfully prevented the inflammation and bone loss that is associated with periodontitis, making this a promising drug for treating humans with the disease.

George Hajishengallis, a professor in the School of Dental Medicine's Department of Microbiology, was the senior author on the paper, collaborating with co-senior author John Lambris, the Dr. Ralph and Sallie Weaver Professor of Research Medicine in the Department of Pathology and Laboratory Medicine in the Perelman School of Medicine. Their collaborators included Tomoki Maekawa, Toshiharu Abe, Evlambia Hajishengallis and Kavita B. Hosur of Penn Dental Medicine and Robert A. DeAngelis and Daniel Ricklin of Penn Medicine.

Earlier work by the Penn team had shown that the periodontal bacterium Porphyromonas gingivalis can hamper the ability of immune cells to clear infection, allowing P. gingivalisand other bacteria to flourish and inflame the gum tissue.

"P. gingivalis has many mechanisms to escape killing by the immune system, but getting rid of inflammation altogether is not good for them because they 'feed' off of it," Hajishengallis said. "So P. gingivalis helps suppress the immune system in a way that creates a hospitable environment for the other bacteria."

The researchers wanted to find out which component of the complement system might be involved in contributing to and maintaining inflammation in the disease. Their experiments focused on the third component of complement, C3, which occupies a central position in signaling cascades that trigger inflammation and activation of the innate immune system.

New drug offers promising possibility for treating adults with periodontitis

Screen of existing drugs finds compounds active against MERS coronavirus

Clinicians treating patients suffering from Middle East respiratory syndrome (MERS) currently have no drugs specifically targeted to the MERS coronavirus (MERS-CoV), a virus first detected in humans in 2012 that has since caused 614 laboratory-confirmed infections, including 181 that were fatal, according to the World Health Organization. The case count escalated sharply in the spring of this year, and the first cases in the United States were announced in early May. To address the urgent need for therapies, researchers supported by the National Institutes of Health screened a set of 290 compounds already approved by the U.S. Food and Drug Administration or far advanced in clinical development for other indications to determine if any might also show potential for working against MERS-CoV.

Screen of existing drugs finds compounds active against MERS coronavirus  

New anticancer compound discovered

A team of research scientists from VTT Technical Research Centre of Finland, the University of Turku and the University of Eastern Finland has discovered a previously unknown Cent-1 molecule that kills cancer cells. Their research also shows that new cancer drug candidates can be identified faster and at lower cost by using computer-assisted and cell-based screening of compounds.

Ref: http://mct.aacrjournals.org/content/13/5/1054

New anticancer compound discovered 

Compound reverses symptoms of Alzheimer's disease in mice

"It reversed learning and memory deficits and brain inflammation in mice that are genetically engineered to model Alzheimer's disease," Farr said. "Our current findings suggest that the compound, which is called antisense oligonucleotide (OL-1), is a potential treatment for Alzheimer's disease."

Farr cautioned that the experiment was conducted in a mouse model. Like any drug, before an antisense compound could be tested in human clinical trials, toxicity tests need to be completed.

Antisense is a strand of molecules that bind to messenger RNA, launching a cascade of cellular events that turns off a certain gene.

In this case, OL-1 blocks the translation of RNA, which triggers a process that keeps excess amyloid beta protein from being produced. The specific antisense significantly decreased the over expression of a substance called amyloid beta protein precursor, which normalized the amount of amyloid beta protein in the body. Excess amyloid beta protein is believed to be partially responsible for the formation of plaque in
the brain of patients who have Alzheimer's disease.

Scientists tested OL-1 in a type of mouse that overexpresses a mutant form of the human amyloid beta precursor gene. Previously they had tested the substance in a mouse model that has a natural mutation causing it to overproduce mouse amyloid beta. Like people who have Alzheimer's disease, both types of mice have age-related impairments in learning and memory, elevated levels of amyloid beta protein that stay in the brain and increased inflammation and oxidative damage to the hippocampus  the part of the brain responsible for learning and memory.

"To be effective in humans, OL-1 would need to be effective at suppressing production of human amyloid beta protein," Farr said.

Scientists compared the mice that were genetically engineered to overproduce human amyloid beta protein with a wild strain, which served as the control. All of the wild strain received random antisense, while about half of the genetically engineered mice received random antisense and half received OL-1. 

The mice were given a series of tests designed to measure memory, learning and appropriate behavior, such as going through a maze, exploring an unfamiliar location and recognizing an object. 

Scientists found that learning and memory improved in the genetically engineered mice that received OL-1 compared to the genetically engineered mice that received random antisense. Learning and memory were the same among genetically engineered mice that received OL-1 and wild mice that received random antisense.

They also tested the effect of administering the drug through the central nervous system, so it crossed the blood brain barrier to enter the brain directly, and of giving it through a vein in the tail, so it circulated through the bloodstream in the body. They found where the drug was injected had little effect on learning and memory.

Ref http://iospress.metapress.com/content/px72758w0158103u/?issue=4&genre=article&spage=1005&issn=1387-2877&volume=40

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Compound
reverses symptoms of Alzheimer's disease in mice  

Scientists have found a potential cure for Ebola (Science Alert)

Ebola and related viruses cause hemorrhagic fever and death through organ failure, and can have a mortality rate of up to 90%, among the highest of any known human disease.  But researchers working in a high-contaminant biological laboratory maintained by USAMRIID at Fort Detrick in Maryland, US, may have found a potential cure.

The scientists have discovered a molecule, named BCX4430, (see structure) which looks a lot like the "A" that makes up DNA: adenosine. Adenosine is one of four base pairs in DNA, and is also used in the genomes of RNA-based viruses,  such as Ebola. But because BCX4430 looks so much like Adenosine, the scientists found that members of the Filoviridae virus family, such as Ebola, can accidentally use it as a building block when trying to grow inside our cells

  
In the study, the team gave Macaque monkeys effected with the deadly Marburg virus (a close relative to Ebola) two doses for BCX4430 a day  for 14 days.

The monkeys who weren't given any of the treatment were dead by day 12, whereas all but one monkey who was given BCX4430 survived, even if they only received treatment 48 hours after they were infected.

Luckily, only virus cells appear to be tricked into using BCX4430, and human and monkey cells do just fine with the molecule around. In vitro experiments
also suggest that BCX4430 could potentially be used against a wide range of
viruses, including SARS, influenza, measles and dengue.
It's too early to get excited just yet, with no human trials yet conducted. But the newly discovered molecule holds the greatest potential we've ever seen for curing these terrifying diseases.

http://www.nature.com/nature/journal/vaop/ncurrent/fig_tab/nature13027_F1.html

Scientists
have found a potential cure for Ebola (Science Alert)

Cancer drugs block dementia-linked brain inflammation, study finds

A class of drugs developed to treat immune-related conditions and cancer -- including one currently in clinical trials for glioblastoma and other tumors -- eliminates neural inflammation associated with dementia-linked diseases and brain injuries, according to UC Irvine researchers.

In their study, assistant professor of neurobiology & behavior Kim Green and colleagues discovered that the drugs, which can be delivered orally, eradicated microglia, the primary immune cells of the brain. These cells exacerbate many neural diseases, including Alzheimer's and Parkinson's, as well as brain injury.

"Because microglia are implicated in most brain disorders, we feel we've found a novel and broadly applicable therapeutic approach," Green said. "This study presents a new way to not just modulate inflammation in the brain but eliminate it completely, making this a breakthrough option for a range of neuroinflammatory diseases."

The researchers focused on the impact of a class of drugs called CSF1R inhibitors on microglial function. In mouse models, they learned that inhibition led to the removal of virtually all microglia from the adult central nervous system with no ill effects or deficits in behavior or cognition. Because these cells contribute to most brain diseases -- and can harm or kill neurons -- the ability to eradicate them is a powerful advance in the treatment of neuroinflammation-linked disorders.

Green said his group tested several selective CSF1R inhibitors that are under investigation as cancer treatments and immune system modulators. Of these compounds, they found the most effective to be a drug called PLX3397, created by Plexxikon Inc., a Berkeley, Calif.-based biotechnology company and member of the Daiichi Sankyo Group. PLX3397 is currently being evaluated in phase one and two clinical trials for multiple cancers, including glioblastoma, melanoma, breast cancer and leukemia.

Crucially, microglial elimination lasted only as long as treatment continued. Withdrawal of inhibitors produced a rapid repopulation of cells that then grew into new microglia, said Green, who's a member of UC Irvine's Institute for Memory Impairments and Neurological Disorders.

Ref : http://www.cell.com/neuron/abstract/S0896-6273(14)00171-8