Appeal 2007-1614
Application 09/779,447
involved in using the claimed elements. Id. (citing United States v. Adams,
383 U.S. 39, 51-52, 148 USPQ 479, 484 (1966)).
In the instant case, Tiganis discloses that “when guinea pigs and
weanling rats were treated with tunicamycin the permeability of brain
microvessels was increased” (Tiganis 192, citations omitted). Tiganis
concludes that “the damage to brain microvessels in tunicamycin-treated
animals is likely to be due to a direct action of tunicamycin on the
endothelial cells” (id. at 199). Because Tiganis discloses that administration
of tunicamycin to test animals results in damage to brain microvessels, we
agree with Appellants that Tiganis teaches away from using tunicamycin as
a therapeutic agent.
The Examiner argues that Tiganis does not teach away from
administering tunicamycin to patients (Answer 6). Specifically, the
Examiner points out that Tiganis discloses that tunicamycin was cytotoxic to
dividing endothelial cells, but not confluent cells (id.). The Examiner also
points to Tiganis’ statement that “[s]ince a feature of tunicamycin toxicity in
animals is impaired permeability of brain microvessels[,] an important
question is whether tunicamycin has a direct effect on microvessels in vivo”
(id., quoting Tiganis at 199, right column). The Examiner reasons that
“since the prior art has recognized the levels at which tunicamycin toxicity
occurs, one of skill in the art would know what dosage levels would be
inappropriate” (id.).
We are not persuaded by this argument. We note that tunicamycin
was not cytotoxic to non-dividing endothelial cells in vitro. We also note
that Tiganis was not entirely certain as to the mechanism by which
6
Page: Previous 1 2 3 4 5 6 7 8 Next
Last modified: September 9, 2013