Savara Pharmaceuticals’ AeroVanc for Cystic Fibrosis Patients Achieves Positive Results in Phase I Clinical Trial

Austin, TX, April 26, 2012 – Savara Pharmaceuticals, an emerging specialty pharmaceutical company developing innovative pulmonary drugs for the treatment of serious and life-threatening conditions, today announced top-line data from its Phase Ia clinical study of the company’s AeroVanc inhaled antibiotic. AeroVanc (vancomycin hydrochloride inhalation powder) is a novel dry powder form of vancomycin in a capsule-based inhaler for the treatment of respiratory methicillin-resistant Staphylococcus aureus (MRSA) infections in patients with cystic fibrosis (CF).

The dose-escalating Phase Ia clinical trial examined the safety and pharmacokinetics of AeroVanc in healthy volunteers. Single-ascending doses of inhaled AeroVanc were compared to vancomycin administered intravenously. AeroVanc demonstrated a favorable pharmacokinetic profile with slow systemic absorption from the lungs, suggesting prolonged residence of the drug in the lung, the site of anti-MRSA action. AeroVanc was well tolerated at all dose levels, with only infrequent mild adverse events that resolved spontaneously.

“Respiratory MRSA infections are a growing concern for CF patients. Recent published evidence suggests that MRSA accelerates the decline in pulmonary function and shortens the life expectancy of CF patients,” said Bruce C. Marshall, MD, Vice President of Clinical Affairs, Cystic Fibrosis Foundation. “While inhaled antibiotics have been successfully used to control Pseudomonas aeruginosa infections in CF patients, there is no inhaled treatment available for MRSA infections. We are very interested in AeroVanc development, and hopeful AeroVanc will be a new treatment option for respiratory MRSA in CF patients.”

“AeroVanc has demonstrated excellent local tolerability and a favorable pharmacokinetic profile to effectively combat MRSA infections in this Phase I clinical trial,” said Robert Neville, Chief Executive Officer of Savara. “AeroVanc has the potential to make a significant impact on CF patients’ lives as the first approved inhaled treatment for pulmonary MRSA infections.”

Savara has recently completed enrollment for a Phase Ib clinical trial of AeroVanc evaluating tolerability and lung pharmacokinetics in CF patients. Results from this study are anticipated in the first half of 2012.

About AeroVanc
AeroVanc (vancomycin hydrochloride inhalation powder) is a proprietary inhaled dry powder form of vancomycin in a capsule-based device designed for convenient self-administration. Vancomycin administered by IV is the antibiotic of choice for the treatment of MRSA-related bronchopneumonia, however, IV administration, poor penetration into the lungs and systemic toxicities limit its use in a chronic setting. AeroVanc is being developed for the treatment of MRSA infections in cystic fibrosis patients. By delivering vancomycin directly to the site of infection, AeroVanc is expected to improve clinical efficacy and reduce systemic exposure.

About MRSA and Cystic Fibrosis
Cystic fibrosis is a genetic disease characterized by the prevalence of thick, sticky mucus produced in the lung, frequent lung infections and a resultant decline in pulmonary function. As the disease progresses, patients’ lungs are typically colonized with bacteria that are difficult to eradicate. In recent years, infections and colonization by MRSA have become increasingly common, with a prevalence of up to 30 percent of all cystic fibrosis patients. MRSA infections have been found to cause a decline in lung function and are associated with a significantly shortened life expectancy. Currently there is no approved inhaled treatment for MRSA infections in cystic fibrosis patients.

About Savara Pharmaceuticals
Savara Pharmaceuticals is an emerging specialty pharmaceutical company developing innovative pulmonary drugs for the treatment of serious and life-threatening conditions. The company’s lead product, AeroVanc (vancomycin hydrochloride inhalation powder), is a dry powder inhaled antibiotic for the treatment of methicillin-resistant Staphylococcus aureus (MRSA) infection in patients with cystic fibrosis.


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Pharmaceutical company Pharmaxis (ASX: PXS) is pleased to announce it has received Marketing Authorisation for Bronchitol from the European Commission. The licence allows the new cystic fibrosis treatment to be made available to patients aged 18 and over throughout the European Union.

Pharmaxis CEO Dr Alan Robertson said, “This is a very significant event, which means that patients living with cystic fibrosis in Europe will now be able to receive the proven clinical benefits of Bronchitol.” Bronchitol will be made available across 29 European countries at an average ex‐factory price of approximately 20‐25 Euros per day. CF patients in Germany and the UK, where there is no requirement for pricing and reimbursement approval before launch, will be first to benefit from Bronchitol. These two countries make up 40% of the European market by value. Pharmaxis expects stock to be available for sale in Europe by mid May ahead of the official launch of the product, which will take place at the European Cystic Fibrosis Symposium in Dublin from 6th ‐ 9th June 2012. Bronchitol has been developed to help clear the airways of people with the world’s most common, life limiting genetic disease, cystic fibrosis. In two large Phase 3 clinical trials, Bronchitol improved mucus clearance, improved lung function and reduced infectious episodes when patients were treated for 6 months.

Dr Robertson said, “We have built considerable momentum around Bronchitol in recent months with the German and UK sales teams fully recruited. The CF centres have been introduced to Pharmaxis and information on local treatment practices has been collected. “Pharmaxis has now secured three drug approvals in the world’s largest pharmaceutical markets. This is a credit not only to the company but also the investigators and patients throughout the world who have taken part in our clinical programs,” Dr Robertson said.

Bronchitol is approved for marketing in Australia and has been recommended for listing on Australia’s Pharmaceutical Benefits Scheme.

Parents Organize Cystic Fibrosis Fundraiser

 BILLINGS – It is a genetic illness that strikes at least 30,000 children across the U.S., and a local couple is hoping their fundraising walk in July will help find a cure, not just for countless cystic fibrosis patients but for their own son as well.

When Alex Glass was born, he immediately required surgery.

“My lower intestine clogged, so the doctors said we have to get that out,” said Alex.

“His small intestines have ruptured twice, and he was full of meconium, it was pressing his organs up,” said Alex’s father, Rob.

Alex had meconium Ileus, which required surgery. Doctors who treated Alex, however, knew that this is the first sign of cystic fibrosis and told Rob.

“(He) came in and see us and talked with us about cystic fibrosis, and said ‘you know, kids that have meconium Ileus, about 10% of those end up being CF kids,” said Rob.

Tests were run, and the results confirmed the fears: Alex had cystic fibrosis. The genetic disorder most commonly affects the lungs, but can affect many other internal organs as well such as the liver, pancreas, and the intestines. It is invariably fatal, but modern medical technologies have lengthened the lifespan of those affected by CF.

“It’s the most lonely, terrible feeling you can imagine. It was really, really tough, you don’t know who to turn to,” said Rob, recounting the moment he heard the news, barely able to hold back his emotions.

Alex found out about his condition when he was five years old, and currently manages his condition with medical treatment as well as a variety of medications. However, Alex still discovers that he has to face some challenges that his peers are exempt from.

“It’s just the coughs that irritate me,” said Alex, coughing.

“He’s missed 47 days of school so far this year between doctor’s appointments and actually being physically sick,” said Rob.

As mentioned earlier, CF patients are now living longer lives. In the 50s, kids with the condition were not expected to live past their first birthday. Currently, CF patients can expect median survival age into the 30s. Still, that is not good enough for a concerned father like Rob.

“I’ve heard for years that cystic fibrosis is going to be the next disease that they find a cure for. The last one was smallpox,” said Rob, who is organizing a fundraiser walk in July to raise awareness and research funds for the Cystic Fibrosis Foundation. The walk is planned to be held at ZooMontana in July.

Until a cure is found, however, hope is getting the Glass family through each and every day.

“I pretty much want to be like Shakespeare, writing plays,” said Alex, when asked about what he wants to be when he grows up.

“I’m hopeful. We’re really hopeful,” said Rob, when asked about the future in general.

To learn more about the walk, and for registration information, click on Connections.

Computer-designed molecules point to new therapy for cystic fibrosis

By developing software that uses 3-D models of proteins involved in cystic fibrosis, a team of scientists at Duke University has identified several new molecules that may ease the symptoms of the disease.
Computer algorithms created by the team predict how well a given molecular structure will block a basic protein-protein interaction known to occur in cystic fibrosis. To test the predictions, the scientists synthesized the molecules and measured how well they attached to one of the proteins in that interaction. The team then placed the best molecule into human cells with the cystic fibrosis mutation in a laboratory dish and found that their new drug blocked the protein-protein interaction and increased the cells’ ability to balance salt and water levels.
The results, which appear in the April 19 Public Library of Science Computational Biology journal, suggest that computers could make drug design for cystic fibrosis faster.
“We have known the genetic cause of cystic fibrosis since 1985. Now, by understanding its biology and chemistry, we can design and create targeted drugs to correct for the genetic flaw,” said Bruce Donald, a Duke computer scientist and biochemist who led the study.
Cystic fibrosis, or CF, is a childhood disease causing the lungs and pancreas to fill with mucus, making it hard to breathe and absorb nutrients from food. The mucus builds in the organs as the levels of salt and water in the cells become unbalanced because of a defective protein.
That protein, called CFTR, the cystic fibrosis transmembrane conductance regulator, regulates salt and water in the cell. In CF, it is defective because the genes that generate it are mutated. CFTRs are routinely rounded up for recycling in the cell by a protein called CAL that binds to CFTR and hauls it away. But defective CFTR proteins in cystic fibrosis patients send a signal that they are faulty, making their recycling rate much higher.
Currently, no treatments exist to target the genetic mutations that cause cystic fibrosis. Scientists have discovered molecules that target CFTRs’ defects, such as incorrect folding and fast recycling, and there are a few molecules that help correct how CFTR folds or slow down the CAL recycling truck. These molecules help keep copies of CFTR functioning in the cell membrane to maintain some balance between salt and water levels.
Donald and his graduate student Kyle Roberts thought that computer algorithms based on the structure of CAL and similar proteins could quickly generate several dozen more molecules for slowing recycling by CAL and increase the pool of potential cystic fibrosis treatments.
“Research shows that you only need a fraction of normal CFTR activity to alleviate cystic fibrosis symptoms, so keeping CFTR in the membrane by using our inhibitors could have a significant therapeutic effect,” said Roberts, first author of the new study.
Donald and Roberts’ algorithms searched several thousand potential inhibitors and ranked them based on how strongly it predicted each would bind with CAL. In collaboration with researchers at Dartmouth and in Germany, the scientists synthesized 11 of the highest-ranked sequences and used fluorescent light to measure each molecule’s attachment to CAL.
The results show that many of the algorithm-generated molecules attach more strongly to CAL than the connection between CAL and CFTR in nature. The best computer-generated molecules also bind more efficiently to CAL than any previously reported inhibitor.
In a culture of human cells with the cystic fibrosis mutation, the best algorithm-generated inhibitor increased CFTR activity by 12 percent. Donald said the new molecule could be used in combination with another molecule, which corrects how CFTR proteins fold and raises CFTR’s activity by 15 percent. The two molecules should work together and could increase CFTR’s activity by about 27 percent, he said.
He cautioned that it could be several years before patients with the disease could use the new molecular combination as treatment because the molecules have not yet been tested in patients with the disease. The team has made its software freely available, Donald said, so the computer-design approach could quicken the pace at which molecules and resulting cystic fibrosis therapies are developed.

The study was funded by the National Institutes of Health.

NASCAR driver Denny Hamlin gives $150,000 to Children’s Hospital of Richmond at VCU

Denny HamlinRICHMOND, Va. (WTVR) – NASCAR driver and Chesterfield native Denny Hamlin announced Wednesday his foundation, the Denny Hamlin Foundation, would give $150,000 to Children’s Hospital of Richmond at VCU and the Cystic Fibrosis Foundation.

The money will pay for cystic fibrosis research and clinical trials in Richmond.

“This is a big day for the Denny Hamlin Foundation,” Hamlin said in a statement. “It is exactly what I envisioned the foundation doing when I started it five years ago, and we’ve worked hard to get to a point where we can give this kind of gift.”

Cystic Fibrosis is a genetic disease that affects about 30,000 children and adults in the United States and about 70,000 worldwide, according to a statement from the hospital. There is no cure for the disease.

“This generous donation will help accelerate our ability to bring these therapies to our patients, and the newly established Denny Hamlin Foundation Summer Scholars program will help us train the next generation of CF research scientists,” said Bruce Rubin, M.D., professor and chair of the VCU Department of Pediatrics and physician-in-chief of Children’s Hospital of Richmond at VCU.

Hamlin, whose cousin has the disease, organized The Denny Hamlin Short Track Showdown to raise money for his foundation. The race is April 26 at Richmond International Raceway. [Click here for more details]

Hamlin said money raised from the race will benefit the Children’s Hospital of Richmond and other programs.

Read woman’s amazing battle against cystic fibrosis

Sophie Longton who has cystic fibrosis.Photo Ben Parsons

WHEN Sophie Longton was just eight years old doctors told her she may not live to see her 20th birthday.

Sophie was given the devastating news she was suffering from Cystic Fibrosis – a disease which has no cure.

The condition is the most common life-threatening illness in the UK and to many it would seem like a death sentence.

But for Sophie, of Woodhead Road, Read, it has given her a thirst for life that has seen her become an ambassador for the CF Trust, address politicians at the Labour Party Conference and interview leading genome scientists for BBC’s Horizon programme.

The former Clitheroe Royal Grammar School Sixth Form pupil, who is now 25, campaigns to raise awareness of Cystic Fibrosis and gives talks on the condition to organisations from Padiham Rotary Club to multi-national pharmaceutical giant GlaxoSmithKline.

Sophie said: “I tell people – can you imagine waking up every day and coughing up thick green mucus? Can you imagine taking 30 tablets and doing two hours of treatment every single day? Can you imagine knowing that unless a cure is found, your life will be cut short by Cystic Fibrosis?

“This is how it affects my life and this is what I have to do.”

Sophie, an academic mentor at Mount Carmel High School, Accrington, admits every day is a battle with the disease.

The inherited condition means her lungs are affected by mucus which causes chest infections and can leave lasting damage. Cystic Fibrosis also affects the digestive system and Sophie has developed pancreatitis which leaves her with severe pain.

Sophie has had to undergo two hours of physio every morning since she was eight to clear mucus from her lungs as well as a daily cocktail of medicine.

“It is a big change of lifestyle. I was eight when I was diagnosed. It was a huge shock. Every single day from that day to this I have done two hours of physio.

“It is not something I enjoy. I feel sick, I cough up blood and sometimes I’m sick because I cough so much. But I have no choice. I have got to get through those days.”

Exercise has played a huge part in keeping Sophie’s lungs functioning. She started running aged eight, became a champion cross-country and netball captain at school and still goes jogging every evening after work.

Many people think a life-limiting illness would limit someone’s life – but not Sophie – she lives life to the full.

“I try to never let it stop me doing anything,” she said. “It actually makes me do more as I want to get more out of life.

“It gives me a zest for life and it has opened up some amazing opportunities for me.”

She became an ambassador for the CF Trust at 16. The position has meant she travels around the country giving talks on her experiences of Cystic Fibrosis.

A YouTube video Sophie made as she underwent intensive anti-biotics treatment for a chest infection went viral around the world with more than 150,000 hits.

She was chosen to feature on the BBC’s Horizon programme “Miracle Cure? A Decade of the Human Genome” about the future of treatments.

She said: “It gave me such an insight into making a documentary. Meeting and interviewing the scientists was amazing. They are the people at the forefront of the research.

“They have been researching for 10 years and spent £30m. They are testing it on 130 patients who inhale the gene therapy treatment every month for a year. The fault copy of the genes is replaced by the healthy copy. Then they will analyse the results.”

It has given her fresh hope of a cure after many false dawns and Sophie is determined to stay fighting fit for the day scientists make that vital breakthrough.

“I cannot benefit from anything unless I keep myself well. The more physio and exercise and treatment I get the better I feel. My hard work has been paying off because my lung function is the best it has been.”

But for now Sophie will keep on campaigning and raising awareness of CF. She is days away from moving to Australia where she hopes to volunteer for the Cystic Fibrosis organisation in Perth.

Her friend Tamsin is running the London Marathon to raise money for CF and Sophie is urging people to sponsor her at

Big Advance against Cystic Fibrosis

TEHRAN (FNA)- Stem cell researchers have taken a critical step in making possible the discovery in the relatively near future of a drug to control cystic fibrosis (CF), a fatal lung disease that claims hundreds of lives each year, with 1,000 new cases diagnosed annually. 

Beginning with the skin cells of patients with CF, Jayaraj Rajagopal, MD, and colleagues at Massachusetts General Hospital (MGH) first created induced pluripotent stem (iPS) cells, and then used those cells to create human disease-specific functioning lung epithelium, the tissue that lines the airways and is the site of the most lethal aspect of CF, where the genes cause irreversible lung disease and inexorable respiratory failure.

That tissue, which researchers now can grow in unlimited quantities in the laboratory, contains the delta-508 mutation, the gene responsible for about 70 percent of all CF cases and 90 percent of the ones in the United States. The tissue also contains the G551D mutation, a gene that is involved in about 2 percent of CF cases and the one cause of the disease for which there is now a drug.

The work is featured on the cover of this month’s Cell Stem Cell journal. Postdoctoral fellow Hongmei Mou, PhD, is first author on the paper, and Rajagopal is the senior author.

Mou credits learning the underlying developmental biology in mice as the key to making tremendous progress in only two years. “I was able to apply these lessons to the iPS cell systems,” she said. “I was pleasantly surprised the research went so fast, and it makes me excited to think important things are within reach. It opens up the door to identifying new small molecules [drugs] to treat lung disease.”

Doug Melton, PhD, co-director of the Harvard Stem Cell Institute, said, “This work makes it possible to produce millions of cells for drug screening, and for the first time human patients’ cells can be used as the target.” Melton, who is also co-chair of Harvard’s inter-School Department of Stem Cell and Regenerative Biology and is the Xander University Professor, added, “I would expect to see rapid progress in this area now that human cells, the very cells that are defective in the disease, can be used for screening.”

Rajagopal said, “The key to our success was the ecosystem of the Harvard Stem Cell Institute and MGH. HSCI investigators pioneered the strategies we used, helped us at the bench, and gave us advice on how to combine our knowledge of lung development with their exciting new platforms. Indeed, we also enjoyed a wonderful collaboration with Darrell Kotton’s lab at Boston University that was able to convert mouse cells into lung tissue. These interactions really helped fuel us ahead.”

The epithelial tissue created by Rajagopal and his colleagues at the MGH Center for Regenerative Medicine also provides researchers with the same cells that are involved in a number of common lung conditions, including asthma, lung cancer, and chronic bronchitis, and may hasten the development of new insights and treatments into those conditions as well.

“We’re not talking about a cure for CF; we’re talking about a drug that hits the major problem in the disease. This is the enabling technology that will allow that to happen in a matter of years,” said Rajagopal, a Harvard Medical School assistant professor of Medicine.

Also a physician trained as a pulmonologist, the specialty that treats CF patients, Rajagopal said, “When we talk about research and advances, donors and patients ask: ‘When? How soon?’ And we usually hesitate to answer. But we now have every single piece we need for the final push. So I have every hope that we’ll have a therapy in a matter of years.”

Cystic fibrosis, which used to claim its victims in infancy or early childhood, has evolved into a killer of those in their 30s because treatments of the infections that characterize the disease have improved. But despite those advances, there has been little progress in treating the underlying condition that affects the vast majority of patients: a defect in a single gene that interferes with the fluid balance in the surface layers of the airways and leads to a thickening of mucus, difficulty breathing and repeated infections and hospitalizations.

The discovery and recent FDA approval of the drug Ivacaftor, which corrects the G551D defect seen in about 2 percent of CF patients, has served as a proof of concept to demonstrate that the disease can be attacked with a conventional molecular treatment. In fact, Ivacaftor was found by screening thousands of drugs on a far less than ideal cell line. In the end, many drugs that functioned well on this cell line proved ineffective when used on genuine human airway tissue.

Genuine human airway tissue is the gold standard prior to drugs being tested clinically, but it has been extremely difficult to obtain the tissue from patients, and when it could be obtained, the tissue rarely survived long in the lab — all of which created a major bottleneck in screening for a therapy. But by creating iPS cells that contain the entire genome of a CF patient and directing those cells to develop into lung progenitor cells, which then develop into epithelium, the group appears to have solved this key problem.

Rajagopal, who did his own postdoctoral fellowship in Melton’s laboratory during the first half of the past decade after completing his training in pulmonary medicine, said that having both the G551D and 508 genes in the epithelial tissue provides a way to prove that the tissue will be effective in testing drugs against CF.

“We’ve created the perfect cell line to show that the drug out there that works against G551D mutation works in this system, and then we’re in business to screen for a drug against delta 508,” he said. “We’ll know soon that the cell line works. We know it makes bonafide airway epithelium, and we’ll have the proof of principle that the tissue responds properly to the only known drug. We think this is the near-ideal tissue platform to find a drug for the majority of CF.”

Rajagopal’s lab has created numerous other cell lines to further show that a CF drug that works in one patient should work in others and to see whether this will be an area that allows a more personalized approach to medicine.

How Does Cystic Fibrosis Express Itself?

Meconium ileus associated with cystic fibrosis symptoms share genes.


The same disease can have different symptoms in different people. For cystic fibrosis, researchers are beginning to understand why it affects people in different ways.

Cystic fibrosis is a genetic disease that can affect the lungs, liver or pancreas each with their own set of varying symptoms.

Researchers isolated several genes that were associated with severe intestinal blockage. These genes could be the target of future treatments for cystic fibrosis.

The study was led by Dr. Lisa Strug from The Hospital for Sick Children and the University of Toronto. Researchers analyzed the genetic data of 4,000 cystic fibrosis patients from the International Consortium in Gene Modifiers of Cystic Fibrosis.

The data revealed that several genes associated with meconium ileus could be associated with how cystic fibrosis expresses itself in different organs.

Cystic fibrosis occurs because of a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR), a protein that regulates chloride transport. Meconium ileus occurs in newborns where stool becomes too thick and causes a blockage in the small intestine.

Genes associated with meconium ileus may affect other diseases in organs that are affected by cystic fibrosis. According to the study, 15 percent of cystic fibrosis patients had meconium ileus as newborns.

Because cystic fibrosis is caused by a genetic mutation, researchers believe it is important to understand how different genes interact with the mutated CFTR. Different genes may affect the behavior of cystic fibrosis and researchers hope to target those genes for treatment.

Understanding the role genes play in cystic fibrosis can lead to treatment tailored to the individual and their specific cystic fibrosis symptoms. Future studies can target the genes associated with meconium ileus and see how it affects cystic fibrosis symptom development. 

Funding was provided by the Canadian Institutes of Health Research, Cystic Fibrosis Canada, the Cystic Fibrosis Foundation, the University of Toronto McLaughlin Centre, Genome Canada, the Ontario Research Fund, the National Institutes of Health and SickKids Foundation, and the Natural Sciences and Engineering Research Council of Canada

This study was published in the April edition of Nature Genetics.

5 Year-Old Harutyun: This Future Soldier Suffers From Cystic Fibrosis

Harutyun Sukiasyan is an active five year-old who wants to be a soldier when he grows up. The boy also suffers from CF (Cystic fibrosis).  Most kids so diagnosed in Armenia don’t make it past the age of twenty.

It is a genetic disease affecting most critically the lungs, and also the pancreas, liver, and intestine. It is characterized by abnormal transport of chloride and sodium across the epithelium tissue, leading to thick, viscous secretions.

In 1959, the median age of survival of children with cystic fibrosis in the U.S. was six months. Now, it is 37.4 years. In Canada, median survival increased from 24 years in 1982 to 47.7 in 2007.

Harutyun, his mother Svetlana and sister Srbuhie live with relatives in the #2 Section of Nork, Yerevan. Svetlana is divorced.

Eight people live in a damp one room apartment. Harutyun sleeps on the floor next to his mom.

The little boy’s coughing spells have gotten worse of late and his loss of sensitivity has increased.

Srbuhie is also sick. Svetlana has placed her in the care of a boarding school so that the girl can be properly fed and have a bed to sleep in. Srbuhie visits the family on the weekend.

Svetlana told me that Harutyun first started manifesting symptoms of the disease at the age of six months. At first, doctors couldn’t make a proper diagnosis.

It was only months later that doctors in Armenia diagnosed MS and told the mother that the disease was curable and wasn’t life threatening.

According to Wikipedia – While there are no cures for cystic fibrosis there are several treatment methods. The management of cystic fibrosis has improved significantly over the past 70 years. While infants born with cystic fibrosis 70 years ago would have been unlikely to live beyond their first year, infants today are likely to live well into adulthood. Recent advances in the treatment of cystic fibrosis have meant that an individual with cystic fibrosis can live a fuller life less encumbered by their condition.

Svetlana had to wait another three years before the health authorities registered the boy as “disabled”. (In Armenian – hashmandam. There are various degrees of disability in Armenia with each allowing for various pensions and treatment payments.)

She says that her son was never prescribed any medication for three years. Now he receives Creon and some vitamins.

(Creon contains digestive enzymes and is used to improve food digestion in people who cannot digest food properly)

“The last time Harutyun got the drug was in January. But the medication had already expired. I threw it in the garbage. In February, the polyclinic gave us the drug but it was the wrong dosage. I had to cut it up,” says the mother.

If he doesn’t take the drug before eating, he will throw up the food two or three minutes later.

Family physician Marina Gasparyan at the #14 Polyclinic in Yerevan says that the drug hadn’t expired, but does admit that the wrong dosage had been given afterwards.

Gasparyan says that they are doing all they can to assist, allocating drugs and vitamins.

The nebulizer Harutyun was using to take the drugs no longer works. The family can’t afford to purchase a new one.

All eight people survive on the 50,000 AMD ($129) pension of Svetlana’s mother.

Harutyun’s disability pension is only enough to buy some rice and macaroni. The boy has asked for some fruit for the past week, but Svetlana can’t afford any.

“I just don’t know how long my boy can live in these conditions. He’s not getting the nutrition he needs and the apartment makes matters worse. My priority is to get him out of here somehow and to provide sufficient meals,” said Svetlana.

She’s worked in stores and cafes as a clerk and waitress. But the jobs don’t last long.

When her employer finds out that she’s a single mom with a sick child, they fire her. They just don’t want the hassle.

As we were leaving, Harutyun turned and told us to visit him in the hospital.

“We don’t have a home of our own,” the little boy remarked.