Here is a recent press release (sounds great to me):
ISIS AND COLLABORATORS DEMONSTRATE DECREASE IN INFLAMMATORY RESPONSE
VIA ICAM-1 INHIBITION IN MOUSE MODEL OF PNEUMONIA
CARLSBAD, Calif., May 28 /PRNewswire/ -- Isis Pharmaceuticals (Nasdaq: ISIP), in collaboration with Claire Doerschuk at the Harvard School of Public Health and collaborators at several academic research laboratories, have demonstrated inhibition of intercellular adhesion molecule-1 (ICAM-1) with an antisense oligonucleotide in a mouse model of pneumonia, preventing the migration of a type of white blood cell (neutrophils) into the lung and reducing lung inflammation. This paper, published in the May 1996 issue of Journal of Clinical Investigation, describes the first demonstration of inhibition of ICAM-1 expression in normal tissue following systemic dosing with antisense compounds. These experimental results strongly support the therapeutic potential of antisense drugs to treat respiratory disorders where white blood cells play a role in the disease process, through the inhibition of ICAM-1.
The paper describes a study that examined the effectiveness of antisense compounds to inhibit over-production of ICAM-1 (induced via endotoxin administration) and the effect of such ICAM-1 inhibition on the subsequent white blood cell migration into the mouse lung. The antisense compound used in these studies was ISIS 3082, a mouse analog of ISIS 2302. ISIS 2302 is an antisense compound designed to inhibit human ICAM-1 over-production, and is currently in Phase II clinical trials as a treatment for five different inflammatory diseases.
The study showed that E. coli endotoxin, when administered to mice intratracheally, caused an increase in production of ICAM-1 messenger RNA (mRNA) and, subsequently, an increase in the number of neutrophils in the lung and an increase in lung tissue injury. ISIS 3082 prevented this increase of ICAM-1 mRNA in a dose-dependent, specific manner without having any effect on the levels of VCAM-1 (a closely related cell adhesion molecule) mRNA. A control oligonucleotide had no effect on ICAM-1 mRNA levels. A mouse ICAM-1 monoclonal antibody also prevented neutrophil migration into the lungs in this model, supporting the conclusion that inhibition of ICAM-1 levels can result in the reduction of neutrophil invasion and the resultant inflammatory response.
"This paper by Isis and its collaborators provides significant data demonstrating the potentially important role that antisense drugs that inhibit ICAM-1 can play in respiratory disease and supports the large and growing body of data proving that antisense drugs work by their intended mechanism," said Stanley T. Crooke, M.D., Ph.D., Isis Chairman and Chief Executive Officer. "We are encouraged by these data as they underscore the therapeutic and commercial potential of our collaboration in cell adhesion with Boehringer Ingelheim, and support the development of ISIS 2302, the lead compound in that collaboration, in a broad range of inflammatory diseases where ICAM-1 plays a role."
The article, entitled, "The Role of ICAM-1 in Endotoxin-induced Pneumonia Evaluated Using ICAM-1 Antisense Oligonucleotides, anti-ICAM-1 Monoclonal Antibodies, and ICAM-1 Mutant Mice," was authored by Toshio Kumasaka, William M. Quinlan, Nicholas A. Doyle (Herman B. Wells Center for Pediatric Research and the Section of Pulmonology, Department of Pediatrics, Indiana University), Thomas P. Condon (Isis Pharmaceuticals), James Sligh (Department of Molecular and Human Genetics, Baylor College of Medicine), Fumio Takei (Terry Fox Laboratory, British Columbia and the Department of Pathology, University of British Columbia), Arthur L. Beaudet (Department of Molecular and Human Genetics, Baylor College of Medicine), C. Frank Bennett (Isis Pharmaceuticals) and Claire M. Doerschuk (Harvard School of Public Health).
This press release contains forward-looking statements concerning the therapeutic and commercial potential of ISIS 2302, a compound in clinical development, and Isis' collaboration with Boehringer Ingelheim in cell adhesion. Such statements are subject to certain risks and uncertainties, particularly those inherent in the process of discovering, developing and commercializing drugs that are safe and effective for use as human therapeutics. Actual results could differ materially from those projected in this release. As a result, the reader is cautioned not to rely on these forward-looking statements. These and other risks are described in additional detail in Isis' Annual Report on Form 10-K for the year ended December 31, 1995 and in the company's most recent quarterly report on Form 10-Q, which are on file with the U.S. Securities Exchange Commission, copies of which are available from the company.
Isis Pharmaceuticals, based in northern San Diego County, is engaged in the discovery and development of novel human therapeutic compounds. Isis has four compounds in human clinical trials: ISIS 2922, to treat CMV-induced retinitis in AIDS patients, is in Phase III clinical trials; ISIS 2302, an inhibitor of ICAM-1, is in Phase II clinical trials for renal transplant rejection, rheumatoid arthritis, psoriasis, Crohn's disease and ulcerative colitis; and ISIS 3521/CGP 64128A and ISIS 5132/CGP69846A, both anticancer compounds, are in Phase I clinical trials. The company also has several additional compounds in preclinical development. Isis' broad medicinal chemistry and biology research programs support efforts in both antisense and combinatorial drug discovery.
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/CONTACT: Jane Green, Sr. Director Investor Relations of Isis Pharmaceuticals, 619-603-3880/
(ISIP)
CO: Isis Pharmaceuticals ST: California IN: MTC SU: PDT |
