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Over 750
million people world-wide suffer from chronic respiratory tract diseases such
as asthma and COPD (chronic obstructive bronchitis and emphysema) and together
these conditions drive an annual market in excess of $10 billion worldwide.
There is considerable demand for new therapeutic options that target the
inflammatory components of both of these conditions. In this respect targeting
the adhesion molecules may be of particular use. As described in
our recent analysis of therapeutic targets for the treatment of COPD (click
here for access), preventing the recruitment of neutrophils, monocytes and
cytotoxic T cells into the lungs and respiratory tract may be of benefit to
patients with emphysema or chronic bronchitis. For example, preventing the
interaction of E-selectin on endothelial cells interacts with sialyl-Lewis x
on neutrophils may limit the severity of COPD. Likewise, the expression of
Mac-1 (CD11b/CD18) is increased on neutrophils of patients with COPD,
suggesting that targeting this adhesion molecule, which is also expressed on
monocytes and macrophages, might also be beneficial. In a soon to be
published dossier reviewing emerging therapeutic targets for asthma we
highlight VCAM1. The interaction between VLA-4 and VCAM-1 is important for
eosinophil inflammation, a hallmark of asthma. Humanized antibodies to VLA-4
have been developed as have small molecule peptide inhibitors of VLA-4 which
are effective in inhibiting allergen-induced responses in sensitized sheep.
Small molecule non-peptide inhibitors of VLA-4 are also now in development for
asthma. Merck researchers have recently reported one such molecule which, when
administered intranasally, dose-dependently inhibited eosinophilia and
eosinophil activation in an ovalbumin model of allergic airway disease. Entry date March, 2003 Adapted from Koo et al, Am J Respir Crit Care Med 2003 Jan 31; [epub ahead of print]
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