Data Include Results from Phase 1 Studies with Monoclonal Antibody Targeting. Interleukin-9 (IL-9); Preclinical Data Provide Further Rationale for IL-9. Inhibition in Developing Potential Asthma Therapies
GAITHERSBURG, MD, USA | May 24, 2007 | MedImmune, Inc. (Nasdaq: MEDI) today announced the presentation of data highlighting recent progress within the company’s inflammatory disease pipeline, including results from two Phase 1 clinical studies with its monoclonal antibody (MAb) targeting IL-9 and preclinical data demonstrating a central role for IL-9 in the pathology of asthma. These data, along with preclinical results from other respiratory inflammation programs within MedImmune’s pipeline, were presented during the American Thoracic Society (ATS) 2007 International Conference, held May 18-23 in San Francisco, CA. Preclinical results were also presented this week at the 94th Annual Meeting of The American Association of Immunologists (AAI), held May 18-22 in Miami Beach, FL.
The IL-9 protein is implicated in a range of characteristic features of asthma, including increased airway inflammation, obstruction and hyperresponsiveness, mucin production and mast cell generation. Earlier preclinical study results have demonstrated that inhibition of IL-9 leads to decreased airway inflammation and hyperresponsiveness in animal models. The clinical results presented at ATS show that the anti-IL-9 MAb was well tolerated and support further study of the antibody in multiple-dose studies in patients with asthma.
"We are very encouraged by these clinical results, which provided the impetus for MedImmune to initiate a Phase 2 trial with our anti-IL-9 MAb and underscore our ongoing commitment to advancing potential treatments for respiratory inflammatory diseases," said Barbara White, M.D., vice president, clinical development, inflammatory disease. "Additionally, as we expand our body of knowledge about IL-9’s role in mast cell regulation, airway remodeling, and other functions involved in the onset of asthma symptoms, we believe these preclinical data provide further support for IL-9 inhibition as a potential therapeutic approach to treating patients with moderate to severe asthma."
Preclinical data presented at ATS suggest that IL-9 plays a critical and unique role in regulating mast cells, which are centrally important in allergic inflammation of the airways. Additional presented data provide insight to IL-9’s role in allergen-induced airway remodeling, a process involving structural changes that occur in conjunction with, or as a result of, chronic airway inflammation such as that seen in patients with asthma.
Data presented at ATS include:
–"Allergic Sensitization and Airway Inflammation in Response to Low Dose House Dust Mite Exposure After Influenza A Infection" (Publication Page A211, Poster Board #C61, presented in a poster session titled, "Inflammation and Host Defense," on Sunday, May 20 at 8:15 a.m.)
— "Proinflammatory Effects of Type 1 Interferon Exacerbate Primary RSV Disease in Susceptible NAB Mice" (Publication Page A210, Poster Board #C56, presented in a poster session titled, "Inflammation and Host Defense," on Sunday, May 20 at 8:15 a.m.)
— "Chitinase-Like Protein BRP-39 Mediates IL-13 Induced Airway Hyperresponsiveness (Publication Page A 253, Poster Board #508, presented in a poster session titled, "Mechanisms of Allergic Lung Inflammation, on Sunday, May 20 at 1:30 p.m.)
— "First In-Human Use of MEDI-528, a Monoclonal Antibody Against Interleukin-9" (Publication Page A483, Poster Board #F34, presented in a poster session titled, "Biologically Based Therapies for Asthma," on Monday, May 21 at 8:15 a.m.)
* "Distribution and Characterization of Lung Mast Cell Subtypes in COPD" (Publication Page A320, Poster Board #303, presented in a poster session titled, "Innate and Immune Mechanisms of Inflammation in Microbial Pathogenesis" on Monday, May 21 at 8:15 a.m.)
— "Occurrence of Mast Cells and Basophils in Central and Peripheral Airways of Patients with Mild Asthma" (Publication Page A455, Poster Board #D18, presented in a poster session titled, "Mast Cells," on Monday, May 21 at 8:15 a.m.)
–"Enzymatically Inactive Chitinase-Like Protein YKL-40 Promotes Macrophage Activation and Lung Inflammation" (Publication Page A471, Poster Board #D63, presented in a poster session titled, "Macrophages and Lymphocytes," on Monday, May 21 at 8:15 a.m.)
— "IL-33 Is a Potent Activator of Mast Cells" (Publication Page A456, Poster Board #D19, presented in a poster session titled, "Mast Cells," on Monday, May 21 at 8:15 a.m.)
— "A Central Role for IL-9 in Regulating Mast Cell Progenitor Trafficking and Lung Inflammation After Allergen Challenge" (Publication Page A798, Poster Board #910, presented in a poster session titled, "Cytokine and Chemokine Regulation of Lung Inflammation," on Tuesday, May 22 at 1:30 p.m.)
— "Central Role of IL-9 in Allergen-Induced Airway Remodeling" (Publication Page A798, Poster Board #913, presented in a poster session titled, "Cytokine and Chemokine Regulation of Lung Inflammation" on Tuesday, May 22 at 1:30 p.m.)
— "Antibody Responses in Primary RSV Bronchiolitis Are T-Lymphocyte Independent" (Publication Page A761, presented in a poster session titled, "Modeling RSV Infection and Host Response," on Tuesday, May 22 at 3 p.m.)
— "Modeling the Interaction Between Aeroallergens and the Immune System In Vivo" (Publication Page A929, Poster Board #G92, presented in a poster session titled, "Modulation of Immunologic Inflammation in Animal Models" on Wednesday, May 23 at 8:15 a.m.)
Preclinical results from several of MedImmune’s inflammation biology programs were also presented at the AAI meeting, including new information about the role High Mobility Group Box Protein 1 (HMGB1) may play in inflammatory disorders.
"As we advance our pipeline of innovative product candidates targeting inflammatory diseases, we are particularly focused on the role of B cells in autoimmunity," said Anthony J. Coyle, Ph.D., vice president, research and development, and head, inflammation and autoimmunity research. "These data provide new insight into the mechanisms by which the pro-inflammatory protein HMGB1, implicated in the activation of B cells, may contribute to the pathology of a range of disorders such as joint inflammation and sepsis."
Data presented at AAI include:
— "Regulation of TLR9 dependent DNA Immune complex mediated cell activation by High Mobility Group Box Protein 1 (HMGB1) and Receptor for Advanced Glycation End products (RAGE)," J. Immunol., Apr 2007; 178: 128.35.
–"Targeting different isoforms of HMGB1 leads to different beneficial effects in preclinical models of sepsis and joint inflammation," J. Immunol., Apr 2007; 178: 100.6.
— Genomic-based high throughput screening and identification of small molecule inhibitors targeting interferon-alpha signaling pathways," J. Immunol., Apr 2007; 178: 131.17.
— "Fc dependent mechanisms are necessary for ADCC and effective depletion of murine B cells by humanized anti-CD19 MAb," J. Immunol., Apr 2007; 178: 131.27.
About IL-9 and Asthma
As mentioned above, IL-9 has been associated with symptoms of asthma. It is one of at least 29 naturally occurring interleukins in the human body. MedImmune is conducting research to evaluate the potential to use MAbs targeting IL-9 to treat or prevent symptomatic, moderate-to-severe, persistent asthma.
Asthma is a chronic disease of the airways that may cause wheezing, breathlessness, chest tightness and coughing. According to the U.S. Centers for Disease Control and Prevention (CDC), more than 20 million Americans reported having asthma in 2001, including more than six million children. In 2000, the CDC reported that there were more than 10 million asthma-related outpatient visits to private physician offices and hospital clinics (nearly 5 million of these involved children under 18). The National Institutes of Health (NIH) have estimated asthma-related healthcare costs in the U.S. at $14 billion annually.
About HMGB1
HMGB1, a pro-inflammatory protein secreted by different cell types, is part of the body’s response to trauma and infection. HMGB1 is expressed at high levels beginning 12 to 72 hours after an injury, which is about the time inflammation-associated tissue damage begins. Because of the timing and duration of expression of HMGB1, it may be an important factor in the sequence of events that result in severe tissue damage following injury or during chronic inflammation.
About MedImmune, Inc.
MedImmune strives to provide better medicines to patients, new medical options for physicians, rewarding careers to employees, and increased value to shareholders. Dedicated to advancing science and medicine to help people live better lives, the company is focused on the areas of infectious diseases, cancer and inflammatory diseases. With more than 2,500 employees worldwide, MedImmune is headquartered in Maryland. For more information, visit the company’s website at http://www.medimmune.com.
This announcement may contain, in addition to historical information, certain forward-looking statements that involve risks and uncertainties, in particular, related to the research and development of antibodies targeting Il-9. Such statements reflect management’s current views and are based on certain assumptions about the success of this program. Actual results could differ materially from those currently anticipated as a result of a number of factors, including risks and uncertainties discussed in MedImmune’s filings with the SEC. MedImmune is developing IL-9-related product candidates for potential future marketing. There can be no assurance that such development efforts will succeed, that such products will receive required regulatory clearance or that, even if such regulatory clearance were received, such products would ultimately achieve commercial success.
Notice to Investors and Stockholders of MedImmune
This release is neither an offer to purchase nor a solicitation of an offer to sell shares of MedImmune. MedImmune stockholders are urged to read the relevant tender offer documents from AstraZeneca PLC that have been filed on May 3, 2007 because they contain important information that stockholders should consider before making any decision regarding tendering their shares. AstraZeneca has filed tender offer materials with the U.S. Securities and Exchange Commission, and MedImmune has also filed a Solicitation/Recommendation Statement on Schedule 14D-9 with respect to the offer. The tender offer materials (including an Offer to Purchase, a related Letter of Transmittal and certain other offer documents) and the Solicitation/Recommendation Statement contain important information, which should be read carefully before any decision is made with respect to the tender offer. The Offer to Purchase, the related Letter of Transmittal and certain other offer documents, as well as the Solicitation/Recommendation Statement, are available for free at the U.S. Securities and Exchange Commission’s web site at http://www.sec.gov, at AstraZeneca’s website at http://www.astrazeneca.com or at MedImmune’s website at http://www.medimmune.com.
SOURCE MedImmune, Inc.
Post Views: 166
Data Include Results from Phase 1 Studies with Monoclonal Antibody Targeting. Interleukin-9 (IL-9); Preclinical Data Provide Further Rationale for IL-9. Inhibition in Developing Potential Asthma Therapies
GAITHERSBURG, MD, USA | May 24, 2007 | MedImmune, Inc. (Nasdaq: MEDI) today announced the presentation of data highlighting recent progress within the company’s inflammatory disease pipeline, including results from two Phase 1 clinical studies with its monoclonal antibody (MAb) targeting IL-9 and preclinical data demonstrating a central role for IL-9 in the pathology of asthma. These data, along with preclinical results from other respiratory inflammation programs within MedImmune’s pipeline, were presented during the American Thoracic Society (ATS) 2007 International Conference, held May 18-23 in San Francisco, CA. Preclinical results were also presented this week at the 94th Annual Meeting of The American Association of Immunologists (AAI), held May 18-22 in Miami Beach, FL.
The IL-9 protein is implicated in a range of characteristic features of asthma, including increased airway inflammation, obstruction and hyperresponsiveness, mucin production and mast cell generation. Earlier preclinical study results have demonstrated that inhibition of IL-9 leads to decreased airway inflammation and hyperresponsiveness in animal models. The clinical results presented at ATS show that the anti-IL-9 MAb was well tolerated and support further study of the antibody in multiple-dose studies in patients with asthma.
"We are very encouraged by these clinical results, which provided the impetus for MedImmune to initiate a Phase 2 trial with our anti-IL-9 MAb and underscore our ongoing commitment to advancing potential treatments for respiratory inflammatory diseases," said Barbara White, M.D., vice president, clinical development, inflammatory disease. "Additionally, as we expand our body of knowledge about IL-9’s role in mast cell regulation, airway remodeling, and other functions involved in the onset of asthma symptoms, we believe these preclinical data provide further support for IL-9 inhibition as a potential therapeutic approach to treating patients with moderate to severe asthma."
Preclinical data presented at ATS suggest that IL-9 plays a critical and unique role in regulating mast cells, which are centrally important in allergic inflammation of the airways. Additional presented data provide insight to IL-9’s role in allergen-induced airway remodeling, a process involving structural changes that occur in conjunction with, or as a result of, chronic airway inflammation such as that seen in patients with asthma.
Data presented at ATS include:
–"Allergic Sensitization and Airway Inflammation in Response to Low Dose House Dust Mite Exposure After Influenza A Infection" (Publication Page A211, Poster Board #C61, presented in a poster session titled, "Inflammation and Host Defense," on Sunday, May 20 at 8:15 a.m.)
— "Proinflammatory Effects of Type 1 Interferon Exacerbate Primary RSV Disease in Susceptible NAB Mice" (Publication Page A210, Poster Board #C56, presented in a poster session titled, "Inflammation and Host Defense," on Sunday, May 20 at 8:15 a.m.)
— "Chitinase-Like Protein BRP-39 Mediates IL-13 Induced Airway Hyperresponsiveness (Publication Page A 253, Poster Board #508, presented in a poster session titled, "Mechanisms of Allergic Lung Inflammation, on Sunday, May 20 at 1:30 p.m.)
— "First In-Human Use of MEDI-528, a Monoclonal Antibody Against Interleukin-9" (Publication Page A483, Poster Board #F34, presented in a poster session titled, "Biologically Based Therapies for Asthma," on Monday, May 21 at 8:15 a.m.)
* "Distribution and Characterization of Lung Mast Cell Subtypes in COPD" (Publication Page A320, Poster Board #303, presented in a poster session titled, "Innate and Immune Mechanisms of Inflammation in Microbial Pathogenesis" on Monday, May 21 at 8:15 a.m.)
— "Occurrence of Mast Cells and Basophils in Central and Peripheral Airways of Patients with Mild Asthma" (Publication Page A455, Poster Board #D18, presented in a poster session titled, "Mast Cells," on Monday, May 21 at 8:15 a.m.)
–"Enzymatically Inactive Chitinase-Like Protein YKL-40 Promotes Macrophage Activation and Lung Inflammation" (Publication Page A471, Poster Board #D63, presented in a poster session titled, "Macrophages and Lymphocytes," on Monday, May 21 at 8:15 a.m.)
— "IL-33 Is a Potent Activator of Mast Cells" (Publication Page A456, Poster Board #D19, presented in a poster session titled, "Mast Cells," on Monday, May 21 at 8:15 a.m.)
— "A Central Role for IL-9 in Regulating Mast Cell Progenitor Trafficking and Lung Inflammation After Allergen Challenge" (Publication Page A798, Poster Board #910, presented in a poster session titled, "Cytokine and Chemokine Regulation of Lung Inflammation," on Tuesday, May 22 at 1:30 p.m.)
— "Central Role of IL-9 in Allergen-Induced Airway Remodeling" (Publication Page A798, Poster Board #913, presented in a poster session titled, "Cytokine and Chemokine Regulation of Lung Inflammation" on Tuesday, May 22 at 1:30 p.m.)
— "Antibody Responses in Primary RSV Bronchiolitis Are T-Lymphocyte Independent" (Publication Page A761, presented in a poster session titled, "Modeling RSV Infection and Host Response," on Tuesday, May 22 at 3 p.m.)
— "Modeling the Interaction Between Aeroallergens and the Immune System In Vivo" (Publication Page A929, Poster Board #G92, presented in a poster session titled, "Modulation of Immunologic Inflammation in Animal Models" on Wednesday, May 23 at 8:15 a.m.)
Preclinical results from several of MedImmune’s inflammation biology programs were also presented at the AAI meeting, including new information about the role High Mobility Group Box Protein 1 (HMGB1) may play in inflammatory disorders.
"As we advance our pipeline of innovative product candidates targeting inflammatory diseases, we are particularly focused on the role of B cells in autoimmunity," said Anthony J. Coyle, Ph.D., vice president, research and development, and head, inflammation and autoimmunity research. "These data provide new insight into the mechanisms by which the pro-inflammatory protein HMGB1, implicated in the activation of B cells, may contribute to the pathology of a range of disorders such as joint inflammation and sepsis."
Data presented at AAI include:
— "Regulation of TLR9 dependent DNA Immune complex mediated cell activation by High Mobility Group Box Protein 1 (HMGB1) and Receptor for Advanced Glycation End products (RAGE)," J. Immunol., Apr 2007; 178: 128.35.
–"Targeting different isoforms of HMGB1 leads to different beneficial effects in preclinical models of sepsis and joint inflammation," J. Immunol., Apr 2007; 178: 100.6.
— Genomic-based high throughput screening and identification of small molecule inhibitors targeting interferon-alpha signaling pathways," J. Immunol., Apr 2007; 178: 131.17.
— "Fc dependent mechanisms are necessary for ADCC and effective depletion of murine B cells by humanized anti-CD19 MAb," J. Immunol., Apr 2007; 178: 131.27.
About IL-9 and Asthma
As mentioned above, IL-9 has been associated with symptoms of asthma. It is one of at least 29 naturally occurring interleukins in the human body. MedImmune is conducting research to evaluate the potential to use MAbs targeting IL-9 to treat or prevent symptomatic, moderate-to-severe, persistent asthma.
Asthma is a chronic disease of the airways that may cause wheezing, breathlessness, chest tightness and coughing. According to the U.S. Centers for Disease Control and Prevention (CDC), more than 20 million Americans reported having asthma in 2001, including more than six million children. In 2000, the CDC reported that there were more than 10 million asthma-related outpatient visits to private physician offices and hospital clinics (nearly 5 million of these involved children under 18). The National Institutes of Health (NIH) have estimated asthma-related healthcare costs in the U.S. at $14 billion annually.
About HMGB1
HMGB1, a pro-inflammatory protein secreted by different cell types, is part of the body’s response to trauma and infection. HMGB1 is expressed at high levels beginning 12 to 72 hours after an injury, which is about the time inflammation-associated tissue damage begins. Because of the timing and duration of expression of HMGB1, it may be an important factor in the sequence of events that result in severe tissue damage following injury or during chronic inflammation.
About MedImmune, Inc.
MedImmune strives to provide better medicines to patients, new medical options for physicians, rewarding careers to employees, and increased value to shareholders. Dedicated to advancing science and medicine to help people live better lives, the company is focused on the areas of infectious diseases, cancer and inflammatory diseases. With more than 2,500 employees worldwide, MedImmune is headquartered in Maryland. For more information, visit the company’s website at http://www.medimmune.com.
This announcement may contain, in addition to historical information, certain forward-looking statements that involve risks and uncertainties, in particular, related to the research and development of antibodies targeting Il-9. Such statements reflect management’s current views and are based on certain assumptions about the success of this program. Actual results could differ materially from those currently anticipated as a result of a number of factors, including risks and uncertainties discussed in MedImmune’s filings with the SEC. MedImmune is developing IL-9-related product candidates for potential future marketing. There can be no assurance that such development efforts will succeed, that such products will receive required regulatory clearance or that, even if such regulatory clearance were received, such products would ultimately achieve commercial success.
Notice to Investors and Stockholders of MedImmune
This release is neither an offer to purchase nor a solicitation of an offer to sell shares of MedImmune. MedImmune stockholders are urged to read the relevant tender offer documents from AstraZeneca PLC that have been filed on May 3, 2007 because they contain important information that stockholders should consider before making any decision regarding tendering their shares. AstraZeneca has filed tender offer materials with the U.S. Securities and Exchange Commission, and MedImmune has also filed a Solicitation/Recommendation Statement on Schedule 14D-9 with respect to the offer. The tender offer materials (including an Offer to Purchase, a related Letter of Transmittal and certain other offer documents) and the Solicitation/Recommendation Statement contain important information, which should be read carefully before any decision is made with respect to the tender offer. The Offer to Purchase, the related Letter of Transmittal and certain other offer documents, as well as the Solicitation/Recommendation Statement, are available for free at the U.S. Securities and Exchange Commission’s web site at http://www.sec.gov, at AstraZeneca’s website at http://www.astrazeneca.com or at MedImmune’s website at http://www.medimmune.com.
SOURCE MedImmune, Inc.
Post Views: 166
