Appeal No. 2001-1905 Page 4
Application No. 08/245,827
discussed in the application for those aspects which act to
oxidize the NMDA receptor.”
[Alteration original].
With regard to the “state of the art,” the examiner finds (id.) that “neuronal
injury results in neuronal cell death” and that according to Jackowski “CNS
neurons do not regenerate.” However, as appellant points out (Reply Brief,
bridging sentence, pages 9-10) regenerating dead neurons is irrelevant to the
claimed methods. We agree. Therefore we are not persuaded by the
examiner’s position (Answer, page 10) that the claimed invention encompasses
regeneration. As appellant explains (Brief, page 10) “the present invention is not
directed to regenerating dead neurons in the CNS; it is directed to limiting
neuronal injuries, e.g., providing live neurons a better chance of surviving an
insult.”
Addressing the “predictability of the art” the examiner concludes (Answer,
pages 5-6) that since Lehninger teaches “glutathione is well known in the art to
be already present in high concentrations (approximately 5mM) in all animal
tissues … the objective truth of being able to treat stroke with 0.5-10mM
glutathione is questionable, because the human population still suffers from
stroke.” However, as appellant points out (Brief, bridging sentence, pages 10-
11) the examiner’s argument is flawed in that it does not take into consideration
that the administration of glutathione according to the claimed invention will
“involve raising the level of glutathione in vivo [sic].”
The examiner finds (Answer, page 6) that “[n]o assays are disclosed, nor
is any guidance provided for determining when, or if, a patient is ‘effectively
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