Critical Care and Sleep Medicine

Rootstown, OH, United States

Critical Care and Sleep Medicine

Rootstown, OH, United States
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Sidney Braman, MD, Professor in the Pulmonary, Critical Care and Sleep Medicine Division of the Icahn School of Medicine at Mount Sinai – National Jewish Health Respiratory Institute and lead author of the study will present a poster presentation titled "Respiratory Failure that Develops During Hospitalization: A Comparison of Medical vs. Surgical Patients" (Abstract #A1895) from 11:15 am – 1:00 pm on Sunday, May 21 in a session on Critical Care: Outcomes in Respiratory Failure. James P. Lamberti, MD, Professor of Medicine at Virginia Commonwealth University Inova Campus and Medical Director of Respiratory Care Services at Inova Fairfax Hospital, will present a poster presentation titled "Medicare Patients Who Develop Respiratory Failure During Hospitalization Have Higher Mortality Compared to Medicare Patients Admitted with Respiratory Failure" (Abstract #A1893) from 11:15 am – 1:00 pm on Sunday, May 21 during the same session. "Respiratory compromise is a significant cause of morbidity and mortality, and we believe that the data scheduled for presentation at ATS 2017 provide an important foundation on which to expand our understanding of this serious condition and help develop effective intervention strategies that may improve patient care and outcomes," said Phillip Porte, Executive Director of RCI. About Respiratory Compromise Respiratory compromise, which includes respiratory distress, insufficiency, failure and arrest, can occur across numerous clinical scenarios. For example, respiratory compromise may appear post-operatively or may be drug-induced by the delivery of a sedative, opioid, or analgesic to patients who were not properly assessed or properly monitored. According to the U.S. Department of Health & Human Services, Agency for Healthcare Research and Quality, respiratory compromise is the third most rapidly increasing hospital inpatient cost in the United States, with $7.8 billion spent on respiratory compromise in U.S. hospitals in 2007. Respiratory compromise increases patient mortality rates by over 30 percent and hospital and ICU stays by almost 50 percent. RCI defines respiratory compromise as a state in which there is a high likelihood of decompensation into respiratory insufficiency, respiratory failure or death that could be prevented or mitigated through specific interventions (enhanced monitoring and/or therapies). About Respiratory Compromise Institute The Respiratory Compromise Institute brings together a broad-based coalition of organizations, companies, and individuals dedicated to reducing—and eventually eliminating—preventable adverse events and deaths due to respiratory compromise. iii Kelley SD, SA, Agarwal S, Parikh N, Erslon M, Morris P. Respiratory insufficiency, arrest and failure among medical patients on the general care floor. Crit Care Med. 2012;40(12):764. iv NAMDRC, National Association for Medical Direction of Respiratory Care. Reducing respiratory compromise and depression. PR Web. Available at http://www.prweb.com/pdfdownload/12615503.pdf. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/respiratory-compromise-institute-to-present-data-at-ats-2017-highlighting-high-incidence-of-respiratory-compromise-among-hospitalized-medicare-patients-300458857.html


The studies are the first retrospective analyses of mortality associated with respiratory failure based on Medicare administrative claims data for inpatient admissions to short-term acute care hospitals. The study was conducted for the time period between January 1, 2012 and December 31, 2014. Based on a review of the Medicare database of hospital admissions, an annual estimate of at least 111,020 Medicare beneficiaries suffer from respiratory compromise. The first study (Abstract #A1895) evaluated medical records for patients who developed respiratory failure after hospitalization for medical (n =16,653) or surgical (n =13,895) inpatient stays. The average age for the medical and surgical groups was 73.2 and 72.4 years of age, respectively. In-hospital mortality was greater for medical compared with surgical patients (32.7% vs. 25.1%, p < 0.0001). Mortality during the 30 days post-discharge was also greater for medical compared with surgical patients (15.3% vs. 9.8%, p < 0.0001). In both medical and surgical groups, hospital mortality was considerably worse when acute kidney failure occurred during the hospitalization (p <0.0001). While both groups had a high rate of intubation, medical patients had more non-invasive mechanical ventilation compared with surgical patients (33% vs. 14%, p < 0.001). The majority of patients in both groups showed evidence of a prior hospitalization within the year previous to the index admission used in this analysis. Medical patients were more likely to have been in a skilled nursing facility (26% vs. 16%, p < 0.001). "While these data verify that respiratory compromise is a significant safety issue in the hospital setting, particularly among this elderly population, we know that it can be identified in most cases and by doing so, acute respiratory failure may be prevented," said Sidney Braman, MD, Professor in the Pulmonary, Critical Care and Sleep Medicine Division of the Icahn School of Medicine at Mount Sinai – National Jewish Health Respiratory Institute and lead author of the study. "The results support the need for improved monitoring and intervention strategies to reduce the risk of respiratory compromise and improve outcomes." The other study (Abstract #A1893) compared Medicare patients who had hospital-acquired respiratory compromise (HARC) (n=16,653, average age 73.2 years) with patients who had respiratory failure diagnosed at the time of hospital admission (n = 18,503, average age = 70.8 years). In-hospital mortality was 32.7% in patients with HARC versus 27.8% in those patients with respiratory failure diagnosed at time of hospital admission (p < 0.0001). Mortality at 30 days post hospital discharge was also significantly different (HARC: 15.3% and respiratory failure at time of hospital admission: 12.9%, p = 0.0001). Patients with HARC had high rates of concomitant diseases (chronic heart failure (45%), hypertension (38%), atrial fibrillation (35%), acute kidney failure (36%), pneumonia (31%) and septicemia (26%). "This analysis shows that Medicare patients who are recognized as having respiratory failure after hospitalization have significantly higher mortality than patients diagnosed as having respiratory failure at time of hospital admission," said James P. Lamberti, MD, Professor of Medicine at Virginia Commonwealth University Inova Campus and Medical Director of Respiratory Care Services at Inova Fairfax Hospital. "The fact that 48% of patients who develop HARC either die in the hospital or within 30 days of hospital discharge demonstrates the urgent need for further study of HARC. Since this study utilized Medicare administrative claims data, a prospective observation study is required to understand the time course and progression of respiratory compromise after hospital admission. Better clinical data will hopefully allow development of strategies for early identification and intervention in the continuum of respiratory compromise to respiratory failure within the hospital. Further study will also identify the role of palliative care in this group of patients with a very high risk of death." Phillip Porte, Executive Director of RCI, commented: "Collectively, the study results suggest the urgent need for further study of hospital acquired respiratory compromise, with a focus on early identification and preventative strategies to reduce respiratory compromise. While data on respiratory compromise are limited, these two studies help establish a foundation of the incidence among elderly patients in the hospital setting and provide a compelling call to action to improve our understanding to prevent and manage respiratory compromise to mitigate progression to more debilitating forms of respiratory dysfunction." Respiratory compromise, which includes respiratory distress, insufficiency, failure and arrest, can occur across numerous clinical scenarios. For example, respiratory compromise may appear post-operatively or may be drug-induced by the delivery of a sedative, opioid, or analgesic to patients who were not properly assessed or properly monitored. According to the U.S. Department of Health & Human Services, Agency for Healthcare Research and Quality, respiratory compromise is the third most rapidly increasing hospital inpatient cost in the United States, with $7.8 billion spent on respiratory compromise in U.S. hospitals in 2007. Respiratory compromise increases patient mortality rates by over 30 percent and hospital and ICU stays by almost 50 percent. RCI defines respiratory compromise as a state in which there is a high likelihood of decompensation into respiratory insufficiency, respiratory failure or death that could be prevented or mitigated through specific interventions (enhanced monitoring and/or therapies). The Respiratory Compromise Institute brings together a broad-based coalition of organizations, companies, and individuals dedicated to reducing—and eventually eliminating—preventable adverse events and deaths due to respiratory compromise. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/respiratory-compromise-institute-presents-data-underscoring-respiratory-compromise-as-a-leading-cause-of-mortality-in-hospitalized-medicare-patients-300460784.html


NESS ZIONA, Israel, May 24, 2017 (GLOBE NEWSWIRE) -- Kamada Ltd. (Nasdaq:KMDA) (TASE:KMDA.TA), a plasma-derived protein therapeutics company focused on orphan indications, today announced that a poster comprising updated data from the Company’s U.S. Phase 2 clinical trial of its proprietary inhaled Alpha-1 Antitrypsin (AAT) therapy for the treatment of Alpha-1 Antitrypsin Deficiency (AATD) was presented by Professor Mark Brantly, M.D., Vice Chair of Research, Department of Medicine, Chief Division of Pulmonary, Critical Care and Sleep Medicine, Professor of Medicine, Molecular Genetics and Microbiology at the University of Florida College of Medicine and Alpha One Foundation Research Professor, at the 2017 American Thoracic Society (ATS) International Conference, being held May 19-24 in Washington, D.C.  AATD is an orphan disease currently treated by intravenous AAT augmentation therapy. The U.S. Phase 2 clinical trial was a double-blind, placebo-controlled study evaluating the safety and efficacy of AAT by inhalation in 36 AATD patients. Patients were treated with Kamada’s AAT for inhalation (80 mg/day or 160 mg/day) or placebo via the eFlow® device for 12 weeks during the double-blind period. Primary efficacy measures included antigenic AAT levels and Anti-Neutrophil Elastase inhibitory (ANEC) levels in the lung, as well as additional anti-proteolytic and anti-inflammatory biomarkers. Following this double-blind period, eligible patients (total of 26) entered an additional 12-week open-label extension study with the active drug (160 mg/day) to further assess safety and tolerability.  Previously announced top-line data from this trial indicated that patients treated with Kamada’s inhaled AAT demonstrated a significant increase in endothelial lining fluid (ELF), AAT antigenic and ANEC levels compared to the placebo group. The updated data included in the poster presentation demonstrated that ELF-AAT, neutrophil elastase (NE)-AAT and ANEC complexes concentration significantly increased in subjects receiving the 80 mg and 160 mg doses, (median increase of 38.7 neutrophil migration (nM), p-value<0.0005 (80 mg/day, n=12), and median increase of 46.2 nM, p-value<0.002 (160 mg/day, n=10)).  This is a specific measure of the anti-proteolytic effect in the ELF and represents the amount of NE that was broken down by AAT.  The increase in levels of functional AAT was six times higher (160 mg per day) than is achievable with intravenous (IV) AAT.  In addition, ELF NE decreased significantly.  Also, the 80 mg data demonstrated a significant reduction in the percentage of neutrophils.  Finally, aerosolized M-specific AAT was detected in the plasma of all subjects receiving inhaled AAT, consistent with what was seen in the Phase 2/3 clinical trial of inhaled AAT conducted by Kamada in the EU. “Inhaled AAT significantly increases functional AAT levels in the ELF versus placebo and versus what can be achieved with IV AAT,” said Naveh Tov, M.D., Ph.D., Kamada’s Vice President, Clinical Development and Medical Director for Pulmonary Diseases.  “Inhaled AAT also restores protease anti-protease homeostasis and reduces the percentage of neutrophils and NE concentration in the lower respiratory tract of AAT deficient individuals.  Finally, detection of normal M-specific AAT in the plasma of study subjects indicates that inhaled AAT passed from the alveolar compartment and the interstitial space.  Collectively, we believe that these findings, as well as the previously announced top-line data from this trial, and the clinically significant results of our European Phase 2/3 study, support the use of inhaled AAT for the treatment of AATD.” “The positive updated data from this clinical trial build on the previously obtained compelling top-line results,” said Professor Brantly, the Primary Investigator of the clinical trial.  “These most recent encouraging results further support the use of inhaled AAT as a safe and effective treatment for AATD.  I continue to be excited about the prospect of conducting a pivotal clinical trial in the U.S. to further evaluate inhaled AAT in the clinic.” “We are currently discussing a regulatory pathway in the U.S. for the Company’s inhaled AAT with the U.S. Food and Drug Administration,” said Amir London, Kamada’s Chief Executive Officer.  “We expect to have an approved Investigational New Drug Application to conduct a pivotal Phase 3 study prior to the end of the year, which would allow us to initiate the clinical study in the U.S. in 2018.  In Europe, we anticipate a regulatory decision from the European Medicines Agency in regards to our inhaled AAT for the treatment of AATD in the second half of 2017.” The poster presented at the ATS meeting was titled, “A7677 - Inhaled Alpha-1-Antitrypsin (AAT) Restores Lower Respiratory Tract Protease- Anti-Protease Homeostasis and Reduces Inflammation in Alpha-1 Antitrypsin Deficient Individuals: A Phase 2 Clinical Study Using Inhaled Kamada-API”. About eFlow® Technology and PARI Pharma The Company’s inhaled AAT therapy is delivered by an investigational eFlow® Nebulizer System developed by PARI Pharma and optimized specifically for Kamada. The optimized device uses eFlow Technology to enable highly efficient aerosolization of medication via a vibrating, perforated membrane that includes thousands of laser-drilled holes. Compared with other nebulization technologies, eFlow Technology produces aerosols with a very high density of active drug, a precisely defined droplet size and a high proportion of respirable droplets delivered in the shortest possible period of time. Combined with its quiet mode of operation, small size, light weight and battery use, eFlow Technology reduces the burden of taking daily, inhaled treatments. About Kamada Kamada Ltd. is focused on plasma-derived protein therapeutics for orphan indications, and has a commercial product portfolio and a robust late-stage product pipeline. The Company uses its proprietary platform technology and know-how for the extraction and purification of proteins from human plasma to produce Alpha-1 Antitrypsin (AAT) in a highly-purified, liquid form, as well as other plasma-derived Immune globulins.  AAT is a protein derived from human plasma with known and newly-discovered therapeutic roles given its immunomodulatory, anti-inflammatory, tissue-protective and antimicrobial properties. The Company’s flagship product is GLASSIA®, the first and only liquid, ready-to-use, intravenous plasma-derived AAT product approved by the U.S. Food and Drug Administration. Kamada markets GLASSIA® in the U.S. through a strategic partnership with Baxalta (now part of Shire plc) and in other counties through local distributors.  In addition to GLASSIA®, Kamada has a product line of seven other pharmaceutical products administered by injection or infusion, that are marketed through distributors in more than 15 countries, including Israel, Russia, Brazil, India and other countries in Latin America and Asia. Kamada has five late-stage plasma-derived protein products in development, including an inhaled formulation of AAT for the treatment of AAT deficiency for which a MAA was submitted to the EMA after completing a pivotal Phase 2/3 clinical trials in Europe.  Kamada has also completed its Phase 2 clinical trials in the U.S for the treatment of AAT deficiency with inhaled AAT. In addition, Kamada's intravenous AAT is in development for other indications such as type-1 diabetes, GvHD and prevention of lung transplant rejection. Kamada also leverages its expertise and presence in the plasma-derived protein therapeutics market by distributing more than 10 complementary products in Israel that are manufactured by third parties. This release includes forward-looking statements within the meaning of Section 27A of the U.S. Securities Act of 1933, as amended, Section 21E of the U.S. Securities Exchange Act of 1934, as amended, and the safe harbor provisions of the U.S. Private Securities Litigation Reform Act of 1995.  Forward-looking statements are statements that are not historical facts, such as statements regarding assumptions and results related to financial results forecast, commercial results, timing and results of clinical trials and EMA and U.S. FDA submissions and authorizations.  Forward-looking statements are based on Kamada’s current knowledge and its present beliefs and expectations regarding possible future events and are subject to risks, uncertainties and assumptions.  Actual results and the timing of events could differ materially from those anticipated in these forward-looking statements as a result of several factors including, but not limited to, unexpected results of clinical trials, delays or denial in the U.S. FDA or the EMA approval process, additional competition in the AATD market or further regulatory delays.  The forward-looking statements made herein speak only as of the date of this announcement and Kamada undertakes no obligation to update publicly such forward-looking statements to reflect subsequent events or circumstances, except as otherwise required by law.


NESS ZIONA, Israel, May 24, 2017 (GLOBE NEWSWIRE) -- Kamada Ltd. (Nasdaq:KMDA) (TASE:KMDA.TA), a plasma-derived protein therapeutics company focused on orphan indications, today announced that a poster comprising updated data from the Company’s U.S. Phase 2 clinical trial of its proprietary inhaled Alpha-1 Antitrypsin (AAT) therapy for the treatment of Alpha-1 Antitrypsin Deficiency (AATD) was presented by Professor Mark Brantly, M.D., Vice Chair of Research, Department of Medicine, Chief Division of Pulmonary, Critical Care and Sleep Medicine, Professor of Medicine, Molecular Genetics and Microbiology at the University of Florida College of Medicine and Alpha One Foundation Research Professor, at the 2017 American Thoracic Society (ATS) International Conference, being held May 19-24 in Washington, D.C.  AATD is an orphan disease currently treated by intravenous AAT augmentation therapy. The U.S. Phase 2 clinical trial was a double-blind, placebo-controlled study evaluating the safety and efficacy of AAT by inhalation in 36 AATD patients. Patients were treated with Kamada’s AAT for inhalation (80 mg/day or 160 mg/day) or placebo via the eFlow® device for 12 weeks during the double-blind period. Primary efficacy measures included antigenic AAT levels and Anti-Neutrophil Elastase inhibitory (ANEC) levels in the lung, as well as additional anti-proteolytic and anti-inflammatory biomarkers. Following this double-blind period, eligible patients (total of 26) entered an additional 12-week open-label extension study with the active drug (160 mg/day) to further assess safety and tolerability.  Previously announced top-line data from this trial indicated that patients treated with Kamada’s inhaled AAT demonstrated a significant increase in endothelial lining fluid (ELF), AAT antigenic and ANEC levels compared to the placebo group. The updated data included in the poster presentation demonstrated that ELF-AAT, neutrophil elastase (NE)-AAT and ANEC complexes concentration significantly increased in subjects receiving the 80 mg and 160 mg doses, (median increase of 38.7 neutrophil migration (nM), p-value<0.0005 (80 mg/day, n=12), and median increase of 46.2 nM, p-value<0.002 (160 mg/day, n=10)).  This is a specific measure of the anti-proteolytic effect in the ELF and represents the amount of NE that was broken down by AAT.  The increase in levels of functional AAT was six times higher (160 mg per day) than is achievable with intravenous (IV) AAT.  In addition, ELF NE decreased significantly.  Also, the 80 mg data demonstrated a significant reduction in the percentage of neutrophils.  Finally, aerosolized M-specific AAT was detected in the plasma of all subjects receiving inhaled AAT, consistent with what was seen in the Phase 2/3 clinical trial of inhaled AAT conducted by Kamada in the EU. “Inhaled AAT significantly increases functional AAT levels in the ELF versus placebo and versus what can be achieved with IV AAT,” said Naveh Tov, M.D., Ph.D., Kamada’s Vice President, Clinical Development and Medical Director for Pulmonary Diseases.  “Inhaled AAT also restores protease anti-protease homeostasis and reduces the percentage of neutrophils and NE concentration in the lower respiratory tract of AAT deficient individuals.  Finally, detection of normal M-specific AAT in the plasma of study subjects indicates that inhaled AAT passed from the alveolar compartment and the interstitial space.  Collectively, we believe that these findings, as well as the previously announced top-line data from this trial, and the clinically significant results of our European Phase 2/3 study, support the use of inhaled AAT for the treatment of AATD.” “The positive updated data from this clinical trial build on the previously obtained compelling top-line results,” said Professor Brantly, the Primary Investigator of the clinical trial.  “These most recent encouraging results further support the use of inhaled AAT as a safe and effective treatment for AATD.  I continue to be excited about the prospect of conducting a pivotal clinical trial in the U.S. to further evaluate inhaled AAT in the clinic.” “We are currently discussing a regulatory pathway in the U.S. for the Company’s inhaled AAT with the U.S. Food and Drug Administration,” said Amir London, Kamada’s Chief Executive Officer.  “We expect to have an approved Investigational New Drug Application to conduct a pivotal Phase 3 study prior to the end of the year, which would allow us to initiate the clinical study in the U.S. in 2018.  In Europe, we anticipate a regulatory decision from the European Medicines Agency in regards to our inhaled AAT for the treatment of AATD in the second half of 2017.” The poster presented at the ATS meeting was titled, “A7677 - Inhaled Alpha-1-Antitrypsin (AAT) Restores Lower Respiratory Tract Protease- Anti-Protease Homeostasis and Reduces Inflammation in Alpha-1 Antitrypsin Deficient Individuals: A Phase 2 Clinical Study Using Inhaled Kamada-API”. About eFlow® Technology and PARI Pharma The Company’s inhaled AAT therapy is delivered by an investigational eFlow® Nebulizer System developed by PARI Pharma and optimized specifically for Kamada. The optimized device uses eFlow Technology to enable highly efficient aerosolization of medication via a vibrating, perforated membrane that includes thousands of laser-drilled holes. Compared with other nebulization technologies, eFlow Technology produces aerosols with a very high density of active drug, a precisely defined droplet size and a high proportion of respirable droplets delivered in the shortest possible period of time. Combined with its quiet mode of operation, small size, light weight and battery use, eFlow Technology reduces the burden of taking daily, inhaled treatments. About Kamada Kamada Ltd. is focused on plasma-derived protein therapeutics for orphan indications, and has a commercial product portfolio and a robust late-stage product pipeline. The Company uses its proprietary platform technology and know-how for the extraction and purification of proteins from human plasma to produce Alpha-1 Antitrypsin (AAT) in a highly-purified, liquid form, as well as other plasma-derived Immune globulins.  AAT is a protein derived from human plasma with known and newly-discovered therapeutic roles given its immunomodulatory, anti-inflammatory, tissue-protective and antimicrobial properties. The Company’s flagship product is GLASSIA®, the first and only liquid, ready-to-use, intravenous plasma-derived AAT product approved by the U.S. Food and Drug Administration. Kamada markets GLASSIA® in the U.S. through a strategic partnership with Baxalta (now part of Shire plc) and in other counties through local distributors.  In addition to GLASSIA®, Kamada has a product line of seven other pharmaceutical products administered by injection or infusion, that are marketed through distributors in more than 15 countries, including Israel, Russia, Brazil, India and other countries in Latin America and Asia. Kamada has five late-stage plasma-derived protein products in development, including an inhaled formulation of AAT for the treatment of AAT deficiency for which a MAA was submitted to the EMA after completing a pivotal Phase 2/3 clinical trials in Europe.  Kamada has also completed its Phase 2 clinical trials in the U.S for the treatment of AAT deficiency with inhaled AAT. In addition, Kamada's intravenous AAT is in development for other indications such as type-1 diabetes, GvHD and prevention of lung transplant rejection. Kamada also leverages its expertise and presence in the plasma-derived protein therapeutics market by distributing more than 10 complementary products in Israel that are manufactured by third parties. This release includes forward-looking statements within the meaning of Section 27A of the U.S. Securities Act of 1933, as amended, Section 21E of the U.S. Securities Exchange Act of 1934, as amended, and the safe harbor provisions of the U.S. Private Securities Litigation Reform Act of 1995.  Forward-looking statements are statements that are not historical facts, such as statements regarding assumptions and results related to financial results forecast, commercial results, timing and results of clinical trials and EMA and U.S. FDA submissions and authorizations.  Forward-looking statements are based on Kamada’s current knowledge and its present beliefs and expectations regarding possible future events and are subject to risks, uncertainties and assumptions.  Actual results and the timing of events could differ materially from those anticipated in these forward-looking statements as a result of several factors including, but not limited to, unexpected results of clinical trials, delays or denial in the U.S. FDA or the EMA approval process, additional competition in the AATD market or further regulatory delays.  The forward-looking statements made herein speak only as of the date of this announcement and Kamada undertakes no obligation to update publicly such forward-looking statements to reflect subsequent events or circumstances, except as otherwise required by law.


NESS ZIONA, Israel, May 24, 2017 (GLOBE NEWSWIRE) -- Kamada Ltd. (Nasdaq:KMDA) (TASE:KMDA.TA), a plasma-derived protein therapeutics company focused on orphan indications, today announced that a poster comprising updated data from the Company’s U.S. Phase 2 clinical trial of its proprietary inhaled Alpha-1 Antitrypsin (AAT) therapy for the treatment of Alpha-1 Antitrypsin Deficiency (AATD) was presented by Professor Mark Brantly, M.D., Vice Chair of Research, Department of Medicine, Chief Division of Pulmonary, Critical Care and Sleep Medicine, Professor of Medicine, Molecular Genetics and Microbiology at the University of Florida College of Medicine and Alpha One Foundation Research Professor, at the 2017 American Thoracic Society (ATS) International Conference, being held May 19-24 in Washington, D.C.  AATD is an orphan disease currently treated by intravenous AAT augmentation therapy. The U.S. Phase 2 clinical trial was a double-blind, placebo-controlled study evaluating the safety and efficacy of AAT by inhalation in 36 AATD patients. Patients were treated with Kamada’s AAT for inhalation (80 mg/day or 160 mg/day) or placebo via the eFlow® device for 12 weeks during the double-blind period. Primary efficacy measures included antigenic AAT levels and Anti-Neutrophil Elastase inhibitory (ANEC) levels in the lung, as well as additional anti-proteolytic and anti-inflammatory biomarkers. Following this double-blind period, eligible patients (total of 26) entered an additional 12-week open-label extension study with the active drug (160 mg/day) to further assess safety and tolerability.  Previously announced top-line data from this trial indicated that patients treated with Kamada’s inhaled AAT demonstrated a significant increase in endothelial lining fluid (ELF), AAT antigenic and ANEC levels compared to the placebo group. The updated data included in the poster presentation demonstrated that ELF-AAT, neutrophil elastase (NE)-AAT and ANEC complexes concentration significantly increased in subjects receiving the 80 mg and 160 mg doses, (median increase of 38.7 neutrophil migration (nM), p-value<0.0005 (80 mg/day, n=12), and median increase of 46.2 nM, p-value<0.002 (160 mg/day, n=10)).  This is a specific measure of the anti-proteolytic effect in the ELF and represents the amount of NE that was broken down by AAT.  The increase in levels of functional AAT was six times higher (160 mg per day) than is achievable with intravenous (IV) AAT.  In addition, ELF NE decreased significantly.  Also, the 80 mg data demonstrated a significant reduction in the percentage of neutrophils.  Finally, aerosolized M-specific AAT was detected in the plasma of all subjects receiving inhaled AAT, consistent with what was seen in the Phase 2/3 clinical trial of inhaled AAT conducted by Kamada in the EU. “Inhaled AAT significantly increases functional AAT levels in the ELF versus placebo and versus what can be achieved with IV AAT,” said Naveh Tov, M.D., Ph.D., Kamada’s Vice President, Clinical Development and Medical Director for Pulmonary Diseases.  “Inhaled AAT also restores protease anti-protease homeostasis and reduces the percentage of neutrophils and NE concentration in the lower respiratory tract of AAT deficient individuals.  Finally, detection of normal M-specific AAT in the plasma of study subjects indicates that inhaled AAT passed from the alveolar compartment and the interstitial space.  Collectively, we believe that these findings, as well as the previously announced top-line data from this trial, and the clinically significant results of our European Phase 2/3 study, support the use of inhaled AAT for the treatment of AATD.” “The positive updated data from this clinical trial build on the previously obtained compelling top-line results,” said Professor Brantly, the Primary Investigator of the clinical trial.  “These most recent encouraging results further support the use of inhaled AAT as a safe and effective treatment for AATD.  I continue to be excited about the prospect of conducting a pivotal clinical trial in the U.S. to further evaluate inhaled AAT in the clinic.” “We are currently discussing a regulatory pathway in the U.S. for the Company’s inhaled AAT with the U.S. Food and Drug Administration,” said Amir London, Kamada’s Chief Executive Officer.  “We expect to have an approved Investigational New Drug Application to conduct a pivotal Phase 3 study prior to the end of the year, which would allow us to initiate the clinical study in the U.S. in 2018.  In Europe, we anticipate a regulatory decision from the European Medicines Agency in regards to our inhaled AAT for the treatment of AATD in the second half of 2017.” The poster presented at the ATS meeting was titled, “A7677 - Inhaled Alpha-1-Antitrypsin (AAT) Restores Lower Respiratory Tract Protease- Anti-Protease Homeostasis and Reduces Inflammation in Alpha-1 Antitrypsin Deficient Individuals: A Phase 2 Clinical Study Using Inhaled Kamada-API”. About eFlow® Technology and PARI Pharma The Company’s inhaled AAT therapy is delivered by an investigational eFlow® Nebulizer System developed by PARI Pharma and optimized specifically for Kamada. The optimized device uses eFlow Technology to enable highly efficient aerosolization of medication via a vibrating, perforated membrane that includes thousands of laser-drilled holes. Compared with other nebulization technologies, eFlow Technology produces aerosols with a very high density of active drug, a precisely defined droplet size and a high proportion of respirable droplets delivered in the shortest possible period of time. Combined with its quiet mode of operation, small size, light weight and battery use, eFlow Technology reduces the burden of taking daily, inhaled treatments. About Kamada Kamada Ltd. is focused on plasma-derived protein therapeutics for orphan indications, and has a commercial product portfolio and a robust late-stage product pipeline. The Company uses its proprietary platform technology and know-how for the extraction and purification of proteins from human plasma to produce Alpha-1 Antitrypsin (AAT) in a highly-purified, liquid form, as well as other plasma-derived Immune globulins.  AAT is a protein derived from human plasma with known and newly-discovered therapeutic roles given its immunomodulatory, anti-inflammatory, tissue-protective and antimicrobial properties. The Company’s flagship product is GLASSIA®, the first and only liquid, ready-to-use, intravenous plasma-derived AAT product approved by the U.S. Food and Drug Administration. Kamada markets GLASSIA® in the U.S. through a strategic partnership with Baxalta (now part of Shire plc) and in other counties through local distributors.  In addition to GLASSIA®, Kamada has a product line of seven other pharmaceutical products administered by injection or infusion, that are marketed through distributors in more than 15 countries, including Israel, Russia, Brazil, India and other countries in Latin America and Asia. Kamada has five late-stage plasma-derived protein products in development, including an inhaled formulation of AAT for the treatment of AAT deficiency for which a MAA was submitted to the EMA after completing a pivotal Phase 2/3 clinical trials in Europe.  Kamada has also completed its Phase 2 clinical trials in the U.S for the treatment of AAT deficiency with inhaled AAT. In addition, Kamada's intravenous AAT is in development for other indications such as type-1 diabetes, GvHD and prevention of lung transplant rejection. Kamada also leverages its expertise and presence in the plasma-derived protein therapeutics market by distributing more than 10 complementary products in Israel that are manufactured by third parties. This release includes forward-looking statements within the meaning of Section 27A of the U.S. Securities Act of 1933, as amended, Section 21E of the U.S. Securities Exchange Act of 1934, as amended, and the safe harbor provisions of the U.S. Private Securities Litigation Reform Act of 1995.  Forward-looking statements are statements that are not historical facts, such as statements regarding assumptions and results related to financial results forecast, commercial results, timing and results of clinical trials and EMA and U.S. FDA submissions and authorizations.  Forward-looking statements are based on Kamada’s current knowledge and its present beliefs and expectations regarding possible future events and are subject to risks, uncertainties and assumptions.  Actual results and the timing of events could differ materially from those anticipated in these forward-looking statements as a result of several factors including, but not limited to, unexpected results of clinical trials, delays or denial in the U.S. FDA or the EMA approval process, additional competition in the AATD market or further regulatory delays.  The forward-looking statements made herein speak only as of the date of this announcement and Kamada undertakes no obligation to update publicly such forward-looking statements to reflect subsequent events or circumstances, except as otherwise required by law.


NESS ZIONA, Israel, May 24, 2017 (GLOBE NEWSWIRE) -- Kamada Ltd. (Nasdaq:KMDA) (TASE:KMDA.TA), a plasma-derived protein therapeutics company focused on orphan indications, today announced that a poster comprising updated data from the Company’s U.S. Phase 2 clinical trial of its proprietary inhaled Alpha-1 Antitrypsin (AAT) therapy for the treatment of Alpha-1 Antitrypsin Deficiency (AATD) was presented by Professor Mark Brantly, M.D., Vice Chair of Research, Department of Medicine, Chief Division of Pulmonary, Critical Care and Sleep Medicine, Professor of Medicine, Molecular Genetics and Microbiology at the University of Florida College of Medicine and Alpha One Foundation Research Professor, at the 2017 American Thoracic Society (ATS) International Conference, being held May 19-24 in Washington, D.C.  AATD is an orphan disease currently treated by intravenous AAT augmentation therapy. The U.S. Phase 2 clinical trial was a double-blind, placebo-controlled study evaluating the safety and efficacy of AAT by inhalation in 36 AATD patients. Patients were treated with Kamada’s AAT for inhalation (80 mg/day or 160 mg/day) or placebo via the eFlow® device for 12 weeks during the double-blind period. Primary efficacy measures included antigenic AAT levels and Anti-Neutrophil Elastase inhibitory (ANEC) levels in the lung, as well as additional anti-proteolytic and anti-inflammatory biomarkers. Following this double-blind period, eligible patients (total of 26) entered an additional 12-week open-label extension study with the active drug (160 mg/day) to further assess safety and tolerability.  Previously announced top-line data from this trial indicated that patients treated with Kamada’s inhaled AAT demonstrated a significant increase in endothelial lining fluid (ELF), AAT antigenic and ANEC levels compared to the placebo group. The updated data included in the poster presentation demonstrated that ELF-AAT, neutrophil elastase (NE)-AAT and ANEC complexes concentration significantly increased in subjects receiving the 80 mg and 160 mg doses, (median increase of 38.7 neutrophil migration (nM), p-value<0.0005 (80 mg/day, n=12), and median increase of 46.2 nM, p-value<0.002 (160 mg/day, n=10)).  This is a specific measure of the anti-proteolytic effect in the ELF and represents the amount of NE that was broken down by AAT.  The increase in levels of functional AAT was six times higher (160 mg per day) than is achievable with intravenous (IV) AAT.  In addition, ELF NE decreased significantly.  Also, the 80 mg data demonstrated a significant reduction in the percentage of neutrophils.  Finally, aerosolized M-specific AAT was detected in the plasma of all subjects receiving inhaled AAT, consistent with what was seen in the Phase 2/3 clinical trial of inhaled AAT conducted by Kamada in the EU. “Inhaled AAT significantly increases functional AAT levels in the ELF versus placebo and versus what can be achieved with IV AAT,” said Naveh Tov, M.D., Ph.D., Kamada’s Vice President, Clinical Development and Medical Director for Pulmonary Diseases.  “Inhaled AAT also restores protease anti-protease homeostasis and reduces the percentage of neutrophils and NE concentration in the lower respiratory tract of AAT deficient individuals.  Finally, detection of normal M-specific AAT in the plasma of study subjects indicates that inhaled AAT passed from the alveolar compartment and the interstitial space.  Collectively, we believe that these findings, as well as the previously announced top-line data from this trial, and the clinically significant results of our European Phase 2/3 study, support the use of inhaled AAT for the treatment of AATD.” “The positive updated data from this clinical trial build on the previously obtained compelling top-line results,” said Professor Brantly, the Primary Investigator of the clinical trial.  “These most recent encouraging results further support the use of inhaled AAT as a safe and effective treatment for AATD.  I continue to be excited about the prospect of conducting a pivotal clinical trial in the U.S. to further evaluate inhaled AAT in the clinic.” “We are currently discussing a regulatory pathway in the U.S. for the Company’s inhaled AAT with the U.S. Food and Drug Administration,” said Amir London, Kamada’s Chief Executive Officer.  “We expect to have an approved Investigational New Drug Application to conduct a pivotal Phase 3 study prior to the end of the year, which would allow us to initiate the clinical study in the U.S. in 2018.  In Europe, we anticipate a regulatory decision from the European Medicines Agency in regards to our inhaled AAT for the treatment of AATD in the second half of 2017.” The poster presented at the ATS meeting was titled, “A7677 - Inhaled Alpha-1-Antitrypsin (AAT) Restores Lower Respiratory Tract Protease- Anti-Protease Homeostasis and Reduces Inflammation in Alpha-1 Antitrypsin Deficient Individuals: A Phase 2 Clinical Study Using Inhaled Kamada-API”. About eFlow® Technology and PARI Pharma The Company’s inhaled AAT therapy is delivered by an investigational eFlow® Nebulizer System developed by PARI Pharma and optimized specifically for Kamada. The optimized device uses eFlow Technology to enable highly efficient aerosolization of medication via a vibrating, perforated membrane that includes thousands of laser-drilled holes. Compared with other nebulization technologies, eFlow Technology produces aerosols with a very high density of active drug, a precisely defined droplet size and a high proportion of respirable droplets delivered in the shortest possible period of time. Combined with its quiet mode of operation, small size, light weight and battery use, eFlow Technology reduces the burden of taking daily, inhaled treatments. About Kamada Kamada Ltd. is focused on plasma-derived protein therapeutics for orphan indications, and has a commercial product portfolio and a robust late-stage product pipeline. The Company uses its proprietary platform technology and know-how for the extraction and purification of proteins from human plasma to produce Alpha-1 Antitrypsin (AAT) in a highly-purified, liquid form, as well as other plasma-derived Immune globulins.  AAT is a protein derived from human plasma with known and newly-discovered therapeutic roles given its immunomodulatory, anti-inflammatory, tissue-protective and antimicrobial properties. The Company’s flagship product is GLASSIA®, the first and only liquid, ready-to-use, intravenous plasma-derived AAT product approved by the U.S. Food and Drug Administration. Kamada markets GLASSIA® in the U.S. through a strategic partnership with Baxalta (now part of Shire plc) and in other counties through local distributors.  In addition to GLASSIA®, Kamada has a product line of seven other pharmaceutical products administered by injection or infusion, that are marketed through distributors in more than 15 countries, including Israel, Russia, Brazil, India and other countries in Latin America and Asia. Kamada has five late-stage plasma-derived protein products in development, including an inhaled formulation of AAT for the treatment of AAT deficiency for which a MAA was submitted to the EMA after completing a pivotal Phase 2/3 clinical trials in Europe.  Kamada has also completed its Phase 2 clinical trials in the U.S for the treatment of AAT deficiency with inhaled AAT. In addition, Kamada's intravenous AAT is in development for other indications such as type-1 diabetes, GvHD and prevention of lung transplant rejection. Kamada also leverages its expertise and presence in the plasma-derived protein therapeutics market by distributing more than 10 complementary products in Israel that are manufactured by third parties. This release includes forward-looking statements within the meaning of Section 27A of the U.S. Securities Act of 1933, as amended, Section 21E of the U.S. Securities Exchange Act of 1934, as amended, and the safe harbor provisions of the U.S. Private Securities Litigation Reform Act of 1995.  Forward-looking statements are statements that are not historical facts, such as statements regarding assumptions and results related to financial results forecast, commercial results, timing and results of clinical trials and EMA and U.S. FDA submissions and authorizations.  Forward-looking statements are based on Kamada’s current knowledge and its present beliefs and expectations regarding possible future events and are subject to risks, uncertainties and assumptions.  Actual results and the timing of events could differ materially from those anticipated in these forward-looking statements as a result of several factors including, but not limited to, unexpected results of clinical trials, delays or denial in the U.S. FDA or the EMA approval process, additional competition in the AATD market or further regulatory delays.  The forward-looking statements made herein speak only as of the date of this announcement and Kamada undertakes no obligation to update publicly such forward-looking statements to reflect subsequent events or circumstances, except as otherwise required by law.


NESS ZIONA, Israel, May 24, 2017 (GLOBE NEWSWIRE) -- Kamada Ltd. (Nasdaq:KMDA) (TASE:KMDA.TA), a plasma-derived protein therapeutics company focused on orphan indications, today announced that a poster comprising updated data from the Company’s U.S. Phase 2 clinical trial of its proprietary inhaled Alpha-1 Antitrypsin (AAT) therapy for the treatment of Alpha-1 Antitrypsin Deficiency (AATD) was presented by Professor Mark Brantly, M.D., Vice Chair of Research, Department of Medicine, Chief Division of Pulmonary, Critical Care and Sleep Medicine, Professor of Medicine, Molecular Genetics and Microbiology at the University of Florida College of Medicine and Alpha One Foundation Research Professor, at the 2017 American Thoracic Society (ATS) International Conference, being held May 19-24 in Washington, D.C.  AATD is an orphan disease currently treated by intravenous AAT augmentation therapy. The U.S. Phase 2 clinical trial was a double-blind, placebo-controlled study evaluating the safety and efficacy of AAT by inhalation in 36 AATD patients. Patients were treated with Kamada’s AAT for inhalation (80 mg/day or 160 mg/day) or placebo via the eFlow® device for 12 weeks during the double-blind period. Primary efficacy measures included antigenic AAT levels and Anti-Neutrophil Elastase inhibitory (ANEC) levels in the lung, as well as additional anti-proteolytic and anti-inflammatory biomarkers. Following this double-blind period, eligible patients (total of 26) entered an additional 12-week open-label extension study with the active drug (160 mg/day) to further assess safety and tolerability.  Previously announced top-line data from this trial indicated that patients treated with Kamada’s inhaled AAT demonstrated a significant increase in endothelial lining fluid (ELF), AAT antigenic and ANEC levels compared to the placebo group. The updated data included in the poster presentation demonstrated that ELF-AAT, neutrophil elastase (NE)-AAT and ANEC complexes concentration significantly increased in subjects receiving the 80 mg and 160 mg doses, (median increase of 38.7 neutrophil migration (nM), p-value<0.0005 (80 mg/day, n=12), and median increase of 46.2 nM, p-value<0.002 (160 mg/day, n=10)).  This is a specific measure of the anti-proteolytic effect in the ELF and represents the amount of NE that was broken down by AAT.  The increase in levels of functional AAT was six times higher (160 mg per day) than is achievable with intravenous (IV) AAT.  In addition, ELF NE decreased significantly.  Also, the 80 mg data demonstrated a significant reduction in the percentage of neutrophils.  Finally, aerosolized M-specific AAT was detected in the plasma of all subjects receiving inhaled AAT, consistent with what was seen in the Phase 2/3 clinical trial of inhaled AAT conducted by Kamada in the EU. “Inhaled AAT significantly increases functional AAT levels in the ELF versus placebo and versus what can be achieved with IV AAT,” said Naveh Tov, M.D., Ph.D., Kamada’s Vice President, Clinical Development and Medical Director for Pulmonary Diseases.  “Inhaled AAT also restores protease anti-protease homeostasis and reduces the percentage of neutrophils and NE concentration in the lower respiratory tract of AAT deficient individuals.  Finally, detection of normal M-specific AAT in the plasma of study subjects indicates that inhaled AAT passed from the alveolar compartment and the interstitial space.  Collectively, we believe that these findings, as well as the previously announced top-line data from this trial, and the clinically significant results of our European Phase 2/3 study, support the use of inhaled AAT for the treatment of AATD.” “The positive updated data from this clinical trial build on the previously obtained compelling top-line results,” said Professor Brantly, the Primary Investigator of the clinical trial.  “These most recent encouraging results further support the use of inhaled AAT as a safe and effective treatment for AATD.  I continue to be excited about the prospect of conducting a pivotal clinical trial in the U.S. to further evaluate inhaled AAT in the clinic.” “We are currently discussing a regulatory pathway in the U.S. for the Company’s inhaled AAT with the U.S. Food and Drug Administration,” said Amir London, Kamada’s Chief Executive Officer.  “We expect to have an approved Investigational New Drug Application to conduct a pivotal Phase 3 study prior to the end of the year, which would allow us to initiate the clinical study in the U.S. in 2018.  In Europe, we anticipate a regulatory decision from the European Medicines Agency in regards to our inhaled AAT for the treatment of AATD in the second half of 2017.” The poster presented at the ATS meeting was titled, “A7677 - Inhaled Alpha-1-Antitrypsin (AAT) Restores Lower Respiratory Tract Protease- Anti-Protease Homeostasis and Reduces Inflammation in Alpha-1 Antitrypsin Deficient Individuals: A Phase 2 Clinical Study Using Inhaled Kamada-API”. About eFlow® Technology and PARI Pharma The Company’s inhaled AAT therapy is delivered by an investigational eFlow® Nebulizer System developed by PARI Pharma and optimized specifically for Kamada. The optimized device uses eFlow Technology to enable highly efficient aerosolization of medication via a vibrating, perforated membrane that includes thousands of laser-drilled holes. Compared with other nebulization technologies, eFlow Technology produces aerosols with a very high density of active drug, a precisely defined droplet size and a high proportion of respirable droplets delivered in the shortest possible period of time. Combined with its quiet mode of operation, small size, light weight and battery use, eFlow Technology reduces the burden of taking daily, inhaled treatments. About Kamada Kamada Ltd. is focused on plasma-derived protein therapeutics for orphan indications, and has a commercial product portfolio and a robust late-stage product pipeline. The Company uses its proprietary platform technology and know-how for the extraction and purification of proteins from human plasma to produce Alpha-1 Antitrypsin (AAT) in a highly-purified, liquid form, as well as other plasma-derived Immune globulins.  AAT is a protein derived from human plasma with known and newly-discovered therapeutic roles given its immunomodulatory, anti-inflammatory, tissue-protective and antimicrobial properties. The Company’s flagship product is GLASSIA®, the first and only liquid, ready-to-use, intravenous plasma-derived AAT product approved by the U.S. Food and Drug Administration. Kamada markets GLASSIA® in the U.S. through a strategic partnership with Baxalta (now part of Shire plc) and in other counties through local distributors.  In addition to GLASSIA®, Kamada has a product line of seven other pharmaceutical products administered by injection or infusion, that are marketed through distributors in more than 15 countries, including Israel, Russia, Brazil, India and other countries in Latin America and Asia. Kamada has five late-stage plasma-derived protein products in development, including an inhaled formulation of AAT for the treatment of AAT deficiency for which a MAA was submitted to the EMA after completing a pivotal Phase 2/3 clinical trials in Europe.  Kamada has also completed its Phase 2 clinical trials in the U.S for the treatment of AAT deficiency with inhaled AAT. In addition, Kamada's intravenous AAT is in development for other indications such as type-1 diabetes, GvHD and prevention of lung transplant rejection. Kamada also leverages its expertise and presence in the plasma-derived protein therapeutics market by distributing more than 10 complementary products in Israel that are manufactured by third parties. This release includes forward-looking statements within the meaning of Section 27A of the U.S. Securities Act of 1933, as amended, Section 21E of the U.S. Securities Exchange Act of 1934, as amended, and the safe harbor provisions of the U.S. Private Securities Litigation Reform Act of 1995.  Forward-looking statements are statements that are not historical facts, such as statements regarding assumptions and results related to financial results forecast, commercial results, timing and results of clinical trials and EMA and U.S. FDA submissions and authorizations.  Forward-looking statements are based on Kamada’s current knowledge and its present beliefs and expectations regarding possible future events and are subject to risks, uncertainties and assumptions.  Actual results and the timing of events could differ materially from those anticipated in these forward-looking statements as a result of several factors including, but not limited to, unexpected results of clinical trials, delays or denial in the U.S. FDA or the EMA approval process, additional competition in the AATD market or further regulatory delays.  The forward-looking statements made herein speak only as of the date of this announcement and Kamada undertakes no obligation to update publicly such forward-looking statements to reflect subsequent events or circumstances, except as otherwise required by law.

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