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| |  Promising Data on Inhibition of Lung Fibrosis Reported PALO ALTO, Calif.—Dec. 18, 1996 -- Connective Therapeutics Inc. (NASDAQ:CNCT) announced today results from a preclinical study of ConXn(TM) (recombinant human relaxin H2) to inhibit pulmonary (lung) fibrosis. The findings, which were published in the December issue of Journal of Clinical Investigation, indicated that ConXn blocked excessive collagen production in vitro as well as inhibited lung fibrosis and maintained normal lung appearance in vivo in a murine model of pulmonary fibrosis. "These results indicate that ConXn, a natural protein, has the ability to prevent lung fibrosis in an established animal model," said W. Scott Harkonen, M.D., senior vice president of Product Development and Operations at Connective. "These are encouraging data which complement ongoing clinical development in scleroderma and support earlier observations of ConXn's potential use in a variety of fibrotic conditions." Excess collagen production (or scarring) is a pathogenic characteristic of many connective tissue diseases. In the case of lung fibrosis, excessive collagen destroys lung architecture and blocks oxygen exchange, resulting in respiratory impairment. In the present study, ConXn demonstrated an ability to inhibit over-production of collagen by up to 45 percent in a dose dependent manner. In addition, ConXn was evaluated in a chemically (bleomycin)-induced murine lung fibrosis model. ConXn was administered by continuous infusion via an osmotic pump which was implanted subcutaneously seven days after bleomycin or saline injection. Results indicated that ConXn prevented lung fibrosis by inhibiting thickening of alveolar tissue (where oxygen exchange occurs) caused by bleomycin. In comparison, lungs from animals treated with bleomycin alone were composed of large areas of fibrosis, completely lacking in normal structure. In the ConXn treated group, the appearance of lungs remained normal. ConXn, a natural protein, has been shown to inhibit excessive connective tissue formation and promote connective tissue remodeling. In the present and other preclinical studies, ConXn demonstrated a dose-dependent ability to inhibit collagen accumulation in fibrosis models. The product is currently being evaluated in a Phase II clinical trial for the treatment of scleroderma, a severe connective tissue disease which primarily afflicts women. Pulmonary fibrosis, also known as interstitial lung disease, represents a group of diseases associated with chronic inflammation and excessive production of collagen in the walls of the alveolar spaces in the lung. Approximately 140,000 individuals suffer from this disease, which may result from many stimuli including environmental irritants and exposure to toxic drugs as well as a secondary condition of other diseases. Connective Therapeutics Inc., headquartered in Palo Alto, is focused on the acquisition, development and marketing of products in the areas of rheumatology and dermatology. Ridaura(R) (auranofin), a treatment for rheumatoid arthritis that Connective recently agreed to acquire from SmithKline Beecham, is currently being marketed by SmithKline Beecham. Several other products are under development: gamma interferon for the treatment of atopic dermatitis and keloids; betamethasone mousse for the treatment of scalp psoriasis and other scalp dermatoses; ConXn for the treatment of scleroderma and other fibrotic conditions; and TCR vaccines for the treatment of rheumatoid arthritis and multiple sclerosis. Special Note: This news release contains forward-looking statements that involve risks and uncertainties that could cause actual results or events to differ materially from those in such forward-looking statements. Potential risks and uncertainties include, without limitation, those mentioned in Connective's prospectus dated January 31, 1996 under the heading "Risk Factors" and in Connective's Report on Form 10-Q for the quarter ended March 31, 1996 under the heading "Additional Factors That May Affect Future Results."
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