Ex Parte Dillin et al

Patent Trial and Appeal Board

Aug 11, 2016

12218976 (P.T.A.B. Aug. 11, 2016)

UNITED STA TES p A TENT AND TRADEMARK OFFICE
APPLICATION NO. FILING DATE FIRST NAMED INVENTOR
12/218,976 07/17/2008 Andrew Dillin
54244 7590 08/15/2016
KLARQUIST SPARKMAN, LLP
121 S.W. SALMON STREET
SUITE 1600
PORTLAND, OR 97204
UNITED STATES DEPARTMENT OF COMMERCE
United States Patent and Trademark Office
Address: COMMISSIONER FOR PATENTS
P.O. Box 1450
Alexandria, Virginia 22313-1450
www .uspto.gov
ATTORNEY DOCKET NO. CONFIRMATION NO.
7158-91089-04 4996
EXAMINER
WILSON, MICHAEL C
ART UNIT PAPER NUMBER
1632
NOTIFICATION DATE DELIVERY MODE
08/15/2016 ELECTRONIC
Please find below and/or attached an Office communication concerning this application or proceeding.
The time period for reply, if any, is set in the attached communication.
Notice of the Office communication was sent electronically on above-indicated "Notification Date" to the
following e-mail address( es):
tanya.harding@klarquist.com
docketing@klarquist.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte ANDREW DILLIN, HUGO AGUILANIU,
SILER P ANOWSKI, and SUZANNE C. WOLFF 1
Appeal2013-005665
Application 12/218,976
Technology Center 1600
Before MELANIE L. MCCOLLUM, ULRIKE W. JENKS, and
TA WEN CHANG, Administrative Patent Judges.
CHANG, Administrative Patent Judge.
DECISION ON APPEAL
This is an appeal under 35 U.S.C. § 134(a) involving claims to
methods of increasing longevity or delaying onset of age-related disease in
an animal, which have been rejected as non-enabled and/or anticipated. We
have jurisdiction under 35 U.S.C. § 6(b ).
We AFFIRM-IN-PART.
STATEMENT OF THE CASE
According to the Specification, "reduced food intake as a result of
dietary restrictions increases the lifespan ... and delays the onset of multiple
1 Appellants identify the Real Party in Interest as The Salk Institute for
Biological Sciences. (Appeal Br. 1.)
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age-related pathologies ... in a number of species." (Spec. if 4.) Likewise,
"[t]he insulin/IGF-1 signaling (IIS) pathway is a key regulator of the aging
process in worms, flies and mice." (Id. at if 5.) The Specification states that
"there is a continuing need ... to determine what genes are involved in
regulating dietary restriction induced longevity and ... the pathways and
possible connections between ... insulin/IGF-1 signaling and dietary
restrictions." (Id. at if 8.)
According to the Specification, the mammalian family of Foxa
transcription factors "regulate[s] glucagon production and glucose
homeostasis, particularly in response to fasting." (Id. at if 7.) The
Specification further states that nematode worm transcription factor pha-4,
which is orthologous to the family of Foxa transcription factors, as well as
nematode transcription factor daf-16, are shown in the Specification to
mediate diet-restriction induced longevity. (Id. at iii! 7, 9.)
Claims 10, 11, 16-18, and 22-33 2 are on appeal. Claim 10 is
illustrative and reproduced below:
2 The Examiner rejected claims 33 and 34 in the Feb. 7, 2012 Advisory
Action but did not specify a basis for the rejection of claim 34 and did not
indicate whether claim 33 is rejected as non-enabled as well as anticipated.
(Feb. 7, 2012 Advisory Act. 1-2.) The Examiner addressed claim 34 as part
of the non-enablement rejection in the Answer, but failed to designate the
non-enablement rejection of claim 34 as a new ground. (Ans. 17.) Thus, we
address claim 33 only in the context of the anticipation rejection and do not
address claim 34 in our opinion. We note that claims 33 and 34 depend
respectively from claims 10 and 16 (Appeal Br. 22 (Claims App'x)), and
below we affirm the rejection of claims 10 and 16 as non-enabled. Thus,
claims 33 and 34 currently depend from claims found to be invalid. In the
event of further prosecution, we leave it to the Examiner to consider whether
claims 33 and 34 should also be rejected as non-enabled.
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10. A method for increasing longevity of an animal, the method
comprising: increasing expression of pha-4 or a homo log thereof
in the animal, wherein the method comprises administering a
modulator to the animal, wherein the modulator increases
expression of pha-4 or the homolog thereof in the animal, and
wherein the increase in pha-4 expression results in an increase in
longevity in the animal.
The Examiner rejects claims 10, 11, 16-18, and 22-32 under 35
U.S.C. § 112, first paragraph as non-enabled. (Ans. 2.)
The Examiner rejects claims 10, 18, 22-24, and 31-33 3 under 35
U.S.C. § 102(b) as being anticipated by Whitsett. 4 (Id.)
I.
Issue
The Examiner has rejected claims 10, 11, 16-18, and 22-32 under 35
U.S.C. § 112, first paragraph as non-enabled. (Ans. 2; Appeal Br. 16.)
The Examiner finds that the Specification would be enabling "for a
method of increasing the longevity of a nematode comprising administering
a nucleic acid sequence encoding pha[ -]4 to a nematode embryo, making a
transgenic nematode whose genome comprises a nucleic acid sequence
encoding pha4, and disrupting the daf-16 gene in the nematode." (Ans. 2.)
However, the Examiner finds that the Specification does not enable
the method for animals other than nematodes, because it is unclear whether
pha-4 or its homologues function in non-nematode species in the same way
3 Although the Examiner did not include claim 33 under the anticipation
rejection in the Answer, the Examiner rejected claim 33 as anticipated in the
Feb. 7, 2012 Advisory Action and has not withdrawn the rejection. (Feb. 7,
2012 Advisory Act. 2; Ans. 2, 17, 19.)
4 Jeffrey A. Whitsett, WO 2005/046720 A2, published May 26, 2005.
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that pha-4 does in nematodes, particularly as it relates to increasing
longevity or delaying onset of age-related disease. (Id. at 11-13.)
The Examiner also finds that, while the claims encompass
overexpression the pha-4 gene using gene therapy, the state of art of gene
therapy was unpredictable, and "it would have required those of skill undue
experimentation to determine how to administer a nucleic acid sequence
encoding pha-4 in an animal such that increased longevity occur[s]" other
than by making a transgenic nematode as described in the Specification. (Id.
at 13-15.)
The Examiner further finds that the Specification does not enable
methods of increasing the longevity or delaying onset of an age-related
disease in an animal that is not "daf-16 null," and finds that the Specification
does not enable the breadth of claims with respect to the amount of pha-4
overexpression or length of increased longevity. (Id. at 15-16.)
Finally, the Examiner finds that the Specification does not enable a
method of delaying onset of age-related disease by increasing expression of
pha-4. (Id. at 17.) For claims 11, 16, and 25, the Examiner further finds that
the Specification does not enable using homologs of daf-16 to increase
longevity in any animal as claimed. (Id.)
In response, Appellants argue that the Specification enables a method
of increasing longevity for animals other than nematodes, since the
Specification teaches how to determine the homo logs of pha-4 and correlates
the function of nematode pha-4 with the pha-4 genes of other species as well
as with its homologs, in particular the mammalian Foxa family of
transcription factors. (Appeal Br. 10-11, 14.) Appellants argue that the
Specification teaches that pha-4, daf-16, and their homologs such as
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mammalian Foxa all have similar post-development roles in "metabolic
homeostasis, namely, function in response to fasting." (Id. at 10-11.)
Appellants argue that the disclosed function of pha-4 and Foxa relating to
metabolic homeostasis supports enablement of the claims, since the
Specification teaches that "dietary restriction (e.g., fasting) has been shown
to prolong longevity in a number of species" and response to fasting is an
example of metabolic homeostasis. (Id. at 11-12.)
Appellants further contend that the Specification enables a method of
increasing longevity through pha-4 overexpression in nematodes that are not
daf-16 null, because pha-4 overexpression in wild type nematodes still
increased longevity, even though the increase was not found to be
statistically significant. (Id. at 12-13, 15-16.) Appellants cite as additional
supporting evidence the increased expression of pha-4 in mutant nematodes
that are not daf-16 null but that exhibited increased longevity as a result of
dietary restriction. (Id. at 13, 15-16.)
Finally, Appellants contend that the Specification enables the use of
gene therapy with the nucleic acids of pha-4 and its homo logs, including by
teaching methods of delivering the nucleic acids, and also enables a method
of delaying the onset of age-related disease. (Id. at 12, 14.)
The issue with respect to this rejection is whether the evidence of
record supports the Examiner's conclusion that the claims fail to comply
with the enablement requirement.
Findings of Fact
Breadth of Claims
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1. Claims 10 and 22 are drawn broadly to increasing longevity or
delaying onset of an age-related disease in an animal by administering to the
animal a compound that increases expression of pha-4 or a homo log.
2. The Specification states that "'increase' or 'modulation' of
longevity also optionally includes a delay in the onset of age-related diseases
and/or conditions and/or a delay and/or stabilization of the aging process."
(Specification i-f 70.)
3. The Specification broadly defines "age-related disease" as
"diseases, conditions and symptoms that are predominantly found or
manifested in older animals, e.g., in humans, people over 50 or more
preferably people over 65." (Id. at i-f 90.) The Specification states that "age-
related diseases" include some types of cancer, such as prostate cancer and
colon cancer, atherosclerosis, diabetes, osteoporosis, hypertension,
depression, neurodegenerative diseases such as Alzheimer's and
Parkinson's, glaucoma, certain immune system defects, kidney failure, liver
steatosis, and others. (Id. at i-fi-189-90.)
Presence of Working Examples
4. The Specification provides examples showing that pha-4
overexpression slightly increased longevity in nine out of eleven lines of
wild-type nematodes and that overexpression of pha-4 in daf-16-null mutant
nematodes resulted in statistically significant increase in lifespan (id. at i-f
229).
Direction or Guidance Presented and Amount of Experimentation Required
5. The Specification states that
reduced food intake as a result of dietary restriction increases the
lifespan of a wide variety of metazoans and delays the onset of
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multiple age-related pathologies. This is a conserved phenomenon in
a number of species, e.g., yeast, worms, flies, mice, waterstriders,
guppies, chickens, labradors, and rats.
(Id. at i-f 4; see also id. at i-f 92.)
6. The Specification teaches that pha-4 is required for and specific
to dietary restriction-induced longevity in nematodes. (Id. at i-fi-17, 96.) The
Specification further states that "expression of pha-4 increased by more than
80% in response to dietary restriction." (Id. at i-f 228.)
7. The Specification states that pha-4 is orthologous to the human
Foxa family of transcription factors. (Id. at i-f 66.) The Specification further
states that "foxal, foxa2, and foxa3 are homologous, e.g., 91 % similar and
85% identical, to pha-4." (Id. at i-f 178.)
8. The Specification states that the foxa gene is involved with
"regulat[ing] glucagon production and glucose homeostasis, particularly in
response to fasting." (Id. at i-fi-1 7, 82.) In particular, the Specification states
that
Foxal homozygous mutant mice die shortly after birth, do not gain
weight and are hypoglycaemic, suggesting an important role for Foxal
in pancreatic cell function and a central role in metabolic homeostasis.
Foxa2 is also required for glucagon expression in the pancreas and
induction of gluconeogenic genes during fasting in the liver. Foxa3
mutant mice become hypoglycaemic after a prolonged fasting.
(Id. at i-f 66 (citations omitted).)
9. The Specification states that
[i]n worms, pha-4 ... regulat[ es] the response to dietary restriction.
DAF-16 ... regulate[ s] the response of ageing to IIS. In mammals, a
parallel regulation of insulin levels by FOXO proteins and glucagon
levels by F oxal and F oxa2 supports a model in which, under
continually low nutrient signaling, PHA-4/Foxa may mediate levels of
glucagon or other changes in hormones ultimately capable of
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regulating the ageing process. In contrast, in times of severe stress or
starvation, DAF-16/FOXO will mediate the response to decreased
insulin signaling. Although C. elegans does not contain an obvious
glucagon orthologue, it does contain a full complement of insulin-like
peptides, suggesting ... conserved functional regulation of glucose
homeostasis .... The finding that some insulin-like peptides work as
agonists, whereas others are antagonists, to insulin signaling in worms
indicates that glucose homeostasis could be more directly regulated by
expression of insulin-like peptides in response to dietary restriction.
(Id. at i-f 231 (citations omitted).)
10. Using nematode as the preferred animal model (id. at i-fi-1 121,
177), the Specification makes otherwise generic disclosures regarding
screening for compounds that modulate "an activity or expression level of a
pha-4 gene or polypeptide" (id. at i-fi-1100-146), creating cells expressing
pha-4 and/or daf-16 (id. at i-fi-1147-155), regulating expression ofpha-4 or
daf-16 (id. at i-fi-1156-168), and making knock-out and transgenic animals
(id. at i-fi-1 170-177).
11. The Specification makes generic disclosures regarding
administering pha-4 modulators to a subject for purposes of modulating
longevity, including generic disclosures of "gene therapy to extend
longevity, e.g., in human or veterinary subjects." (Id. at i-fi-1196-221.)
12. The Examiner finds that Appellants have not provided
"adequate guidance for those of skill to overcome the unpredictability in the
art so that nematode pha4 [or its orthologs] could be used in any animal as
broadly claimed to increase longevity as claimed." (Ans. 12-13.)
13. The Examiner finds that, "because of the divergent functions of
the nematode pha-4 gene and mammalian FoxA genes, it [is] unpredictable
that overexpression of any of the mammalian FoxA genes would increase
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Application 12/218,976
longevity as exemplified by applicants in nematodes with the nematode pha-
4 gene or any animal as broadly claimed .... " (Id. at 13.)
14. The Examiner finds that "[i]t would have required those of skill
undue experimentation to [use pha-4 in any animal as broadly claimed to
increase longevity as claimed,] because ... pha4 [and mammalian Foxa
genes] may never be able to increase longevity in any animal as broadly
claimed." (Id. at 12-13.)
15. The Examiner finds that
The specification does not teach how to target a vector encoding pha-
4 to the tissue of interest in nematodes or any other species using gene
therapy so that increased longevity or delayed onset of age related
disease would be obtained. The specification fails to teach the target
tissue required to overexpress pha4 or homolog thereof such that
increased longevity occurs. The specification does not correlate
making transgenic nematodes overexpressing pha-4 to using gene
therapy in nematodes to increase longevity or delaying onset of age
related disease. It is not readily apparent that gene therapy can
provide adequate amounts of pha-4 expression or target the desired
tissue of interest so that increased longevity or delayed onset of age-
related disease would be expected to be obtained. Without such
guidance, it would have required those of skill undue experimentation
to determine how to administer a nucleic acid sequence encoding pha-
4 in an animal such that increased longevity occurred other than by
making a nematode whose genome comprises a nucleic acid sequence
encoding pha-4.
(Id. at 14.)
State of the Prior Art and Unpredictability of the Art
16. Antebi5 teaches that there is "a role for a pair of evolutionarily
conserved proteins-PHA-4 and SKN-1-in conferring extended survival
under dietary restrictions in the small roundworm Caenorhabditis elegans."
5 Adam Antebi, When Less is More, 447 NATURE 536 (2007).
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(Antebi 536.) Antebi further teaches that PHA-4 protein is very similar to
mammalian FOXA proteins, which regulate glucose metabolism in
mammals. (Id.) Antebi teaches that findings regarding PHA-4 and SKN-1
"raise a host of other questions":
Although both PHA-4 and SKN-1 are required for dietary-restriction-
induced longevity, neither is truly sufficient. Are other factors
involved? Must PHA-4 and SKN-1 work together? Moreover, what
is the nature of the hormonal pathway that coordinates the effects of
dietary restriction? Do the vertebrate counterparts of these
transcription factors also have a role in regulating survival?
Potentially, the answers to these questions may illuminate the path to
increased human health and longevity.
(Id. at 537.)
17. Brenkman6 teaches that "only in the background of daf-16 null
mutants did pha-4 overexpression induce longevity .... " (Brenkman 408.)
18. The Examiner finds that "Antebi establishe[ s] that it was
unpredictable at the time of filing whether targeting pha4 alone was able to
increase longevity in C. elegans (or invertebrates in general) and whether
homo logs of pha4 in vertebrates would have the same effect." (Ans. 12.)
19. The Examiner finds that "none of the F oxA genes in mammals
have been ... specifically linked to longevity in non-nematodes." (Id. at
12-13.)
20. The Examiner finds that claims 10 and 22 encompass
overexpressing the pha-4 gene using gene therapy, the state of art of which
was unpredictable. (Id. at 13.)
6 Arjan B. Brenkman et al., Live Longer Through PHAsting, 5 CELL
METABOLISM 407 (2007).
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Principles ofLaw
"In order to satisfy the enablement requirement of section 112, an
applicant must describe the manner of making and using the invention 'in
such ... terms as to enable any person skilled in the art ... to make and use
the same .... ' 35 U.S.C. § 112, para. 1." Rasmusson v. SmithKline Beecham
Corp., 413 F.3d 1318, 1322 (Fed. Cir. 2005).
The Examiner has the initial burden to establish a reasonable basis to
question the enablement provided for the claimed invention. See In re
Wright, 999 F.2d 1557, 1561-62 (Fed. Cir. 1993). Factors to be considered
in determining whether a disclosure would require undue experimentation
include
(1) the quantity of experimentation necessary, (2) the amount of
direction or guidance presented, (3) the presence or absence of
working examples, ( 4) the nature of the invention, ( 5) the state of the
prior art, ( 6) the relative skill of those in the art, (7) the predictability
or unpredictability of the art, and (8) the breadth of the claims.
In re Wands, 858 F.2d 731, 737 (Fed. Cir. 1988).
Mere plausibility is not the test for enablement:
If mere plausibility were the test for enablement under section 112,
applicants could obtain patent rights to "inventions" consisting of
little more than respectable guesses as to the likelihood of their
success. When one of the guesses later proved true, the "inventor"
would be rewarded the spoils instead of the party who demonstrated
that the method actually worked. That scenario is not consistent with
the statutory requirement that the inventor enable an invention rather
than merely proposing an unproved hypothesis.
Rasmusson, 413 F.3d at 1325.
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Analysis
Claims 10, 11, 16-18, 22-26, 31, and 32
Having considered the Wands factors, we find that the evidence of
record supports the Examiner's conclusion that undue experimentation
would have been required to apply the claimed methods to animals other
than nematodes. Claims 10, 11, 16-18, 22-26, 31, and 32 are all drawn
broadly to increasing longevity of or delaying the onset of an age-related
disease in a large variety of animals, by increasing the expression of pha-4
or a homo log in the animal. 7 (FF 1-FF3.) However, the Specification
provide examples of increasing longevity only with respect to nematodes.
(FF4.) Furthermore, as evidenced by Antebi, the state of the art with respect
to increasing longevity is unpredictable. (FF16, FF18-FF20.) Thus, the
breadth of the claims in comparison to the working examples, as well as the
unpredictability of the art, all weigh against the enablement of the claims.
We have considered the portions of the Specification cited by
Appellants as support for the enablement of the claims; however, we agree
with the Examiner that the purported guidance provided therein does not
permit a skilled artisan to practice the claimed inventions without undue
experimentation. (FF 12-FF 15.) The Specification at most teaches that
nematode pha-4 and mammalian foxa are orthologs and that both have roles
in situations of dietary restriction or fasting. (FF5-FF9.) However, in light
of the unpredictability of the art and the breadth of the claims, the
7 Although claims 10 and 18 recite a method of increasing longevity without
explicitly reciting delaying onset of an age-related disease, we note that the
Specification broadly defines increase of longevity to optionally include "a
delay in the onset of age-related diseases and/or conditions and/or a delay
and/or stabilization of the aging process." (FF2.)
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Specification does not sufficiently correlate any such similarity to increased
longevity in animals other than nematodes. Likewise, given the generic
nature of Appellants' disclosures regarding administration of pha-4 or its
homo logs (FF 11 ), we find that Appellants have not enabled a skilled artisan,
without undue experimentation, to increase the longevity of animals other
than nematodes through such administration.
Accordingly, we affirm the Examiner's rejection of claims 10, 11, 16-
18, 22-26, 31, and 32 for lack of enablement.
Claims 27-30
A different enablement analysis applies to claims 27-30 because they
are limited to nematodes.
The Examiner argues that claims 27-30 are also non-enabled because
the Specification does not enable methods of increasing the longevity or
delaying onset of an age-related disease in an animal that is not "daf-16
null." (Ans. at 15-16.) In particular, the Examiner argues that the
Specification shows that overexpression of pha-4 in wild-type nematodes did
not result in a statistically significant increase in longevity and cites to
Brenkman, which teaches that "only in the background of daf-16 null
mutants did p ha-4 overexpression induce longevity." (FF 1 7.)
On balance, we find that the weight of the relevant Wands factors
supports a conclusion that claims 27-30 comply with the enablement
requirement. While overexpression of pha-4 in wild-type nematodes did not
result in a statistically significant increase in longevity, some increase was
obtained. (FF4.) Furthermore, the Specification teaches that diet restriction-
induced longevity in nematodes with wild type daf-16 was associated with
substantially heightened expression of pha-4. (FF6.) Finally, we note that
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the claims use the open-ended transitional phrase "comprising"; thus, there
is no requirement that pha-4 alone induce the increase in longevity.
The Examiner further argues that, since overexpression of pha-4 in
wild type nematodes did not result in a statistically significant increase in
longevity, the full breadth of claims is not enabled because the claims
encompass any amount of pha-4 overexpression. (Ans. 16.) We do not find
this argument persuasive for the reasons already discussed.
The Examiner also argues that the Specification and art at the time of
the filing do not enable a skilled artisan to increase longevity in an animal
forever. (Id.) We do not find this argument persuasive; the claims do not
require increasing longevity in an animal forever.
Finally, the Examiner argues that the Specification and art at time of
filing do not teach how to administer a nucleic acid sequence to a nematode
using gene therapy. (Id. at 26.) We are not persuaded. The Examiner does
not dispute that the Specification enables "making a transgenic nematode
whose genome comprises a nucleic acid sequence encoding pha4" (Ans. 2),
and "[t]he enablement requirement is met if the description enables any
mode of making and using the invention." Johns Hopkins Univ. v. Cellpro
Inc., 152 F.3d 1342, 1361 (Fed. Cir. 1998) (quoting Engel Indus., Inc. v.
Lodiformer Co., 946 F.2d 1528, 1533 (Fed. Cir. 1991)).
We likewise do not find persuasive the Examiner's argument that
claims 27-30 are not enabled because the Specification fails to teach that
overexpression of a pha-4 homo log (rather than pha-4 itself) would increase
longevity in nematode. (Ans. 26.) Claims are not necessarily invalid merely
because some of the claimed combinations are inoperative; the question is
whether the number of inoperative combinations is so significant that it in
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effect forces a skilled artisan to unduly experiment in order to practice the
claimed invention. Atlas Powder Co. v. E.I. Du Pont De Nemours & Co.,
750 F.2d 1569, 1576 (Fed. Cir. 1984). We do not find this to be the case
with respect to claims 27-30.
Accordingly, we reverse the Examiner's rejection of claims 27-30.
II.
Issue
The Examiner has rejected claims 10, 18, 22-24, and 31-33 under 35
U.S.C. § 102(b) as being anticipated by Whitsett. The Examiner finds that
Whitsett teaches "administering a nucleic acid sequence encoding FoxA2 to
a mammal, specifically a human." (Ans. 18.) The Examiner finds that
"FoxA2 is a homolog of pha-4" and that "[t]he method of Whitsett has the
same active step claimed, i.e., administering a nucleic acid sequence
encoding FoxA2." (Id.) Accordingly, the Examiner finds that Whitsett
inherently discloses increasing longevity as claimed. (Id.at 18, 27)
Appellants contend that
Whitsett pertains to treatment of pulmonary diseases and does not
teach or suggest increasing longevity or delaying the onset of an age-
related disease in an animal by increasing expression of pha-4 or a
pha-4 homolog, such as a foxa gene. In Whitsett, the amount of
FoxA2 administered to a subject is an amount effective to treat a
respiratory disorder. Whitsett is silent with regard to administration
of FoxA2 to increase longevity or to delay the onset of an age-related
disease. Therefore, it is not at all clear that the administration of
FoxA2 according to Whitsett would inherently increase longevity or
delay the onset of an age-related disease in the subject to which it was
administered.
(Appeal Br. 17.)
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The issue with respect to this rejection is whether the evidence of
record supports the Examiner's finding that Whitsett discloses the
limitations relating to increasing longevity and/or delaying the onset of an
age-related disease.
Findings of Fact
21. Whitsett discloses methods to protect a subject from an airway
obstructive disease by "administering to a subject in need of such treatment
a therapeutically effective amount of a FoxA2 gene, or pharmaceutically
acceptable composition thereof, for overexpressing the FoxA2 gene."
(Whitsett Abstract.)
22. Whitsett defines "subject" for purposes of treatment as "any
animal classified as a mammal, including humans .... " (Id. at i-f 102; see
also id. at i-f 215.)
23. Whitsett discloses aerosol administration. (Id. at i-f 214--219.)
24. Whitsett discloses that, "based on estimates of nebulizer
efficiency, an effective dose delivered [by aerosol administration] usually
lies in the range of about 1 mg/treatment to about 500 mg/treatment,
although more or less may be found to be effective depending on the subject
and desired result." (Id. at i-f 219.)
25. The Specification discloses that, "[d]epending on the type and
severity of the disease, about 1 µg/kg to 50 mg/kg (e.g., 0.1-20 mg/kg) of
the [compounds of the invention] is an initial candidate dosage for
administration to a patient . . . . A typical daily dosage might range from
about 1 µg/kg to about 100 mg/kg or more .... " (Spec. i-f 206.)
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26. The Specification discloses that compositions of the invention
"can also be made into aerosol formulations (i.e., they can be "nebulized") to
be administered via inhalation." (Id. at i-f 206.)
Principles of Law
[I]t is elementary that the mere recitation of a newly discovered
function or property, inherently possessed by things in the prior art,
does not cause a claim drawn to those things to distinguish over the
prior art. Additionally, where the Patent Office has reason to believe
that a functional limitation asserted to be critical for establishing
novelty in the claimed subject matter may, in fact, be an inherent
characteristic of the prior art, it possesses the authority to require the
applicant to prove that the subject matter shown to be in the prior art
does not possess the characteristic relied on.
In re Best, 562 F.2d 1252, 1254--55, (CCPA 1977) (internal quotation marks
and citation omitted).
Analysis
Whitsett discloses administering to a subject, including a human, an
amount ofFoxA2 gene composition for overexpressing the gene. (FF21,
FF22.) FoxA2 is a homolog of pha-4. (FF7.) Whitsett further discloses
aerosol administration of the gene and teaches that "an effective dose
delivered [by aerosol administration] usually lies in the range of about 1
mg/treatment to about 500 mg/treatment, although more or less may be
found to be effective depending on the subject and desired result." (FF23,
FF24.) The Specification discloses that the longevity modulator (e.g., a
nucleic acid that encodes pha-4 or a homo logs) may be administered via
inhalation through use of an aerosol formulation (FF26), and further
discloses an initial dosage range (1 µg/kg to 50 mg/kg (e.g., 0.1-20 mg/kg))
17
Appeal2013-005665
Application 12/218,976
that overlaps Whitsett's disclosed range for a human subject of average
weight. (FF25.) Thus, we find that the Examiner has established a
reasonable basis that increasing longevity would be inherent to the method
disclosed in Whitsett, which shifts the burden to Appellants to show that the
characteristic is not possessed by the prior art method. In re Best, 562 F.2d
at 1255. Appellants have not provided persuasive evidence to satisfy this
burden.
Accordingly, we affirm the Examiner's rejection of claim 10. Claims
18, 22-24, and 31-33, which are not separately argued, fall with claim 10.
See App. Br. 17; 37 C.F.R. § 41.37(c)(l)(iv).
SUMMARY
For the reasons above, we affirm the Examiner's rejection of claims
10, 11, 16-18, 22-26, 31, and 32 as non-enabled and reverse the rejection of
claims 27-30 on the same basis. We affirm the rejection of claims 10, 18,
22-24, and 31-33 as anticipated by Whitsett.
TIME PERIOD FOR RESPONSE
No time period for taking any subsequent action in connection with
this appeal may be extended under 37 C.F.R. § 1.136(a).
AFFIRMED-IN-PART
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