Appeal No. 2007-0531 Page 13
Application No. 10/341,679
the site of damaged cardiac muscle. In addition, Tischer teaches that VEGF121
has advantages over VEGF165, which include an increased half-life. Therefore,
Tischer adds to the teachings of Isner by teaching that VEGF, or more preferably
the therapeutically advantageous VEGF121, can be introduced directly to the site
of the damaged cardiac muscle.
Taken together French, Isner and Tischer teach the use of an adenoviral
vector comprising a nucleic acid capable of expressing VEGF121, with or without
another gene expressing a different angiogenic protein, to treat a damaged heart
by administering multiple injections into different points on the internal surface of
the heart to program recombinant gene expression in cardiomyocytes and
thereby treat a damaged heart by inducing collateral blood vessel formation in
the heart. Following the teachings of the combined references, each injection
would take approximately 5 seconds, resulting in 10 different injections in less
than one minute.
Therefore, we conclude that a person of ordinary skill in the art at the time
the invention was made who was seeking to treat a damaged heart would have
found it prima facie obvious to induce collateral blood vessel formation in a heart
by administering a dose of a pharmaceutical composition comprising a
pharmaceutically acceptable carrier and a replication-deficient adenoviral vector
comprising a DNA encoding VEGF121 at multiple injections to different points on
the internal surface of the heart. In addition, a person of ordinary skill in the art
would have found it prima facie obvious to administer at least 2 of the multiple
injections within about 10 minutes. Based on the combined teachings of French,
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