Appeal No. 2001-1905 Page 6
Application No. 08/245,827
Furthermore, as appellant explains (Reply Brief, fn. 5) “[t]here are sound
medical reasons that undercut the [e]xaminer’s assumptions. There is a specific
uptake system for glutathione which renders general experience with charged
amino acids irrelevant. Finally, during stroke, the blood brain barrier is
somewhat disrupted, making experience with a healthy subject irrelevant.” The
examiner provides no response to appellant’s argument.
Finally, the examiner finds (Answer, page 7), with reference to Sucher,
“that ‘[e]xtracellular application of oxidized glutathione (GSSG), but not reduced
glutathione (GSH), inhibited responses mediated by activation of the NMDA
subtype of glutamate receptor in cultures of rat cortical and retinal ganglion cell
neurons’…” [alteration original]. The examiner then contrasts this with the
claimed invention finding (id.) that “the instant specification states that
‘[a]pplicants have also discovered that both reduced and oxidized glutathione …
can protect against toxicity mediated at NMDA receptors…’” [alteration original].
We are not persuaded by the examiner’s position. First, it appears that
the examiner concedes that “oxidized glutathione” can be used according to the
claimed invention. Further, as appellant points out (Brief, bridging paragraph,
pages 11-12) “[i]t is generally believed that no matter which form of glutathione is
administered to a patient, an equilibrium between the oxidized and the reduced
forms of glutathione will be readily established in vivo [sic].” We note that
appellant’s specification (bridging paragraph, pages 3-4) supports this position in
that it discloses that “[u]seful agents need not be oxidizing agents in their own
right, and include those agents which will be acted upon in vivo to produce
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