Appeal 2007-1152
Application 10/660,924
Tufveson (Immun. Reviews, 1993, No. 136, pages 101-107), Feldman
(Transplant. Proc., 1998, vol. 30, pages 4126-4127), and Cochlovius
(Modern Drug Discovery, October 2003, pages 33-38), and discusses their
relevance to the enablement issue (Answer 4-7).
We have considered the Examiner’s arguments and the supporting
documents, but do not find that the evidence is sufficient to sustain the
rejection.
In beginning our analysis, we note that the Examiner did not correctly
characterize the disclosure in the Specification. Example 1 describes the
treatment of streptozotocin-induced diabetes in C57B6 mice (Spec. 19: 30 to
20: 3), not NOD mice as stated on page 4 of the Answer. The Specification
provides experimental evidence in this example that a tolerizing first dose of
encapsulated insulin-producing cells induced immunological tolerance to a
subsequent curative dose of cells.
Turning to the references cited by the Examiner in support of his
position, we first address Mestas (supra.). The Examiner states that Mestas
provides evidence of the inadequacy of mouse models in predicting the
efficacy of therapies for human disease (Answer 5). Mestas – as noted by
the Examiner – describes the differences between mouse and human
immunology, concluding that “[s]uch differences should be taken into
account when using mice as preclinical models of human disease” (Mestas,
Abstract). Mestas describes its purpose as “to understand the potential
limitations of extrapolating data from mice to humans” (Mestas, at 2731,
col. 2). After extensively characterizing the immunological differences,
Mestas concludes:
4
Page: Previous 1 2 3 4 5 6 7 8 9 10 11 12 Next
Last modified: September 9, 2013