Appeal 2007-1152
Application 10/660,924
While caution in interpreting preclinical data obtained in mice
is clearly warranted, we believe that with these caveats in mind,
mice will continue to be the premiere in vivo model for human
immunology and will be absolutely essential for continued
progress in our understanding of immune function in health and
disease.
(Mestas, at 2736, col. 2.) Thus, far from abandoning the mouse as a model
of human disease, Mestas characterizes it as “absolutely essential for
continued progress” in understanding immunological diseases.
The Examiner contends that Tufveson’s statement that “today’s small
animal models seem to be insufficient to produce data for clinical decision-
making” (Tufveson, at 101) raises reasonable doubt about the predictability
of mouse models (Answer 6). However, Tufveson concluded that after “this
airing of problems in the clinical field it is clear that small animal models are
sought” for human disease (Tufveson, at 101). Tufveson reviewed its own
efforts at developing such models and concludes that “it would seem to be
reasonable to test new immunosuppressive drugs . . . in allograft models”
(Tufveson, at 107). Thus, Tufveson does not disavow the use of animal
models nor does it provide any evidence that the particular mouse model
described in the Specification is deficient.
With respect to the NOD mouse model of Type I diabetes, Atkinson
acknowledges that “specific differences . . . restrict their interpretation”
(Atkinson, at 601, col. 2), but also states that “investigations of NOD mice
have enhanced our appreciation of the etiologic complexity of type I
diabetes in humans and provided an example of how promising results
obtained in an animal model can be translated into human clinical trials”
(Atkinson, at 604, col. 1). Thus, contrary to the Examiner’s position,
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