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                                                          CV THERAPEUTICS (CVTX)

                                                    A Potential Breakthrough Drug

       CV Terapeutics investigational drug, CVT-6883, could be a potential breakthrough for the treatment of inflammatory lung diseases, including fibrosis, asthma, injury and complication of treatments.  The Journal of Clinical Investigation (JCI) published a preclinical study suggesting that CVT-6883 significantly reduced elevated markers of inflammation, fibrosis and pulmonary injury in two separate in vivo models.

        CVT-6883 is a selective, potent and orally available A2B-adenosine receptor antagonist, which CV Therapeutics is investigating for the potential treatment of asthma and other conditions related to inflammation and fibrosis.

        We have not heard before about any drugs that deal with lung fibrosis. Yet, in the case of CVT-6883, a preclinical study done with the drug revealed that mice predisposed to elevated adenosine levels and developed pulmonary inflammation, fibrosis and enlargement of air sacs in the lungs called alveolar spaces responded to CVT-6883 with a reduction in these conditions and a significantreduction in elevated proinflammatory cytokines and chemokines. In a separate in vivo model, CVT-6883 also inhibited pulmonary inflammation and fibrosis induced by bleomycin.

        "These in vivo models exhibit many of the characteristics typical of patients with chronic lung disease and asthma, so the results support the scientific rationale for treating asthma and other conditions related to inflammation and fibrosis with a selective A2B-adenosine receptor antagonist," said Michael Blackburn, Ph.D., professor of biochemistry and molecular biology at the University of Texas Medical School at Houston and corresponding author of the study.

        Asthma is a chronic lung disease characterized by recurrent episodes of wheezing, breathlessness, chest tightness and coughing. Pulmonary inflammation contributes to the bronchoconstriction that can precipitate an asthma attack and to the progression of this chronic disease. In asthma, increased levels of adenosine can overactivate the A2B- adenosine receptor leading to mast cell degranulation and the release of inflammatory cytokines associated with bronchoconstriction and chronic lung inflammation. CVT-6883 may provide a potentially novel approach to preventing or reducing this inflammatory process by selectively inhibiting the A2B- adenosine receptor.

Will the drug be the long waited for healer for athma and other lung complications?

                                                  Eye  On

 Antigenics Reports Second Quarter 2006 Financial Results

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