Ex Parte Ward

Patent Trial and Appeal Board

Oct 22, 2012

12120322 (P.T.A.B. Oct. 22, 2012)

UNITED STATES PATENT AND TRADEMARK OFFICE
__________

BEFORE THE PATENT TRIAL AND APPEAL BOARD
__________

Ex parte KENNETH WARD
__________

Appeal 2011-012653
Application 12/120,322
Technology Center 1600
__________

Before DONALD E. ADAMS, FRANCISCO C. PRATS, and
JEFFREY N. FREDMAN, Administrative Patent Judges.

FREDMAN, Administrative Patent Judge.

DECISION ON REQUEST FOR REHEARING
Appellant has requested rehearing of the decision entered July 24,
2012. That decision affirmed the Examiner‟s rejection of claims 1-5, 8-14,
17-52, 55-62, and 65-77 under 35 U.S.C. § 103(a).
Appellant‟s request has been granted to the extent that the decision
has been reconsidered, but such request is denied with respect to making any
modifications to the decision affirming the Examiner‟s rejection under 35
U.S.C. § 103(a).
Appeal 2011-012653
Application 12/120,322

2
DISCUSSION
We begin by noting that Appellant‟s arguments were already
addressed by both the Examiner and our Decision. However, in the interests
of clarity, we further specifically address the arguments.
Argument 1
Appellant first argues that Antor represents a change in law and that
“appellant rebutted the presumption of enablement” for Treloar
1
and
Viganò
2
(Req. Reh‟g 2). Appellant contends that “the prior art is not
enabled for a test to „assess a predisposition for endometriosis in a subject
that does not exhibit an endometriosis symptom‟” (id. at 3).
We have reviewed our Decision in light of this argument. However,
we are not persuaded that our Decision was in error. In Antor, the Court
held that as “long as an examiner makes a proper prima facie case of
anticipation by giving adequate notice under § 132, the burden shifts to the
applicant to submit rebuttal evidence of nonenablement.” In re Antor Media
Corp., 689 F.3d 1282, 1289 (Fed. Cir. 2012).
Antor explains that “[e]nablement of prior art requires that the
reference teach a skilled artisan to make or carry out what it discloses in
relation to the claimed invention.” Id. at 1290. Antor further teaches that the
Appellant must show “that undue experimentation would be required to

1
Treloar et al., Genomewide Linkage Study in 1,176 Affected Sister Pair
Families Identifies a Significant Susceptibility Locus for Endometriosis, 77
AM. J. HUM. GENET. 365-376 (2005).
2
Viganò et al., Intercellular adhesion molecule-1 (ICAM-1) gene
polymorphisms in endometriosis, 9 MOL. HUM. REPRODUCTION 47-52
(2003).
Appeal 2011-012653
Application 12/120,322

3
perform the claimed invention based on the teaching” in the prior art. Id. at
1289.
Appellant has made no clear or specific evidentiary showing as to
undue experimentation. In particular, Appellant has provided no specific
evidence that undue experimentation would have been required to replicate
the genotyping methods of either Treloar or Viganò, or to apply these
genotyping methods for identification of genomic regions associated with
increased risk of endometriosis to the method of claim 13 of Foster,
3
“A
method of preventing endometriosis in a woman at higher than normal risk
of developing endometriosis, comprising: administering to the woman at
higher than normal risk of developing endometriosis a pharmaceutically
acceptable composition . . . to inhibit the growth or thickening of
endometriotic tissue in the woman” (FF 5, Dec. 5).
We also note that absolute predictability is not required to
demonstrate enablement of the prior art. As Kubin commented,
“[r]esponding to concerns about uncertainty in the prior art influencing the
purported success of the claimed combination, this court [in O’Farrell]
stated: „[o]bviousness does not require absolute predictability of success …
all that is required is a reasonable expectation of success.”‟ In re Kubin,
561 F.3d 1351, 1360 (Fed. Cir. 2009) (citing In re O’Farrell, 853 F.2d 894,
903-904 (Fed. Cir. 1988)). Appellant‟s additional arguments relating to the
applicability of Treloar and Viganò to Foster‟s method were already
addressed by the Decision, which found that “both Treloar and Vigano
disclose genetic markers that correlate with endometriosis” (Dec. 12).

3
Foster et al. US 2002/0147155 A1, issued Oct. 10, 2002.
Appeal 2011-012653
Application 12/120,322

4
We continue to conclude that there would have been a “reasonable
expectation of success” to modify Foster‟s method using known risk factors
to treat and prevent endometriosis and to incorporate the newly identified
genetic risk factors of Treloar and Viganò for endometriosis since these
present additional information for the ordinary artisan in the identification of
patients for whom Foster‟s therapy would have been appropriate.

Argument 2
Appellant contends that “FF #10 does not render the rejected claims
obvious and that FF #10 cannot be used for instance in „assessing a
predisposition for endometriosis in a subject that does not exhibit an
endometriosis symptom‟” (Req. Reh‟g 3). Appellant then creates a
hypothetical analogy which fundamentally results in an argument requiring
Treloar alone to anticipate the invention. Appellant contends that “Treolar
[sic] does not render the rejected claims obvious” (id. at 4).
We have reviewed our Decision in light of this argument. However,
we are not persuaded that our Decision was in error. We can agree with
Appellant that Treloar alone does not render the claimed invention obvious.
It is the combination of Treloar with Foster (as well as Viganò and De
Koning
4
), which renders claim 2 obvious.
5
Foster teaches “[a] method of
preventing endometriosis in a woman at higher than normal risk of
developing endometriosis, comprising: administering to the woman at higher

4
De Koning, WO 00/21511, published Apr. 20, 2000.
5
As we noted in the decision, Treloar and Viganò were not required for the
obviousness of claim 1 (see Dec. 8).
Appeal 2011-012653
Application 12/120,322

5
than normal risk of developing endometriosis a pharmaceutically acceptable
composition ... to inhibit the growth or thickening of endometriotic tissue in
the woman” (Foster 9, claim 13; Dec. 5; FF 5). As extensively discussed in
the Decision, it is Foster who teaches the “assessing” step, that is, the
association of a higher than normal risk of endometriosis in an asymptomatic
woman with treatment for that increased risk (Dec. 5-6, FF 2-9).
Treloar is solely relied upon in the Decision and by the Examiner to
demonstrate that the prior art was aware of genetic markers that were
correlated with endometriosis related conditions, as required by claim 2 (see,
e.g., Dec. 8). In that vein, FF10 of the Decision simply established the fact
that Treloar teaches the linkage of some alleles in a specific genetic locus,
10q26, with endometriosis. Treloar‟s title demonstrates that a “Genomewide
Linkage Study in 1,176 Affected Sister Pair Families Identifies a Significant
Susceptibility Locus for Endometriosis on Chromosome 10q26” (Treloar
365, title). The Examiner‟s obviousness determination then, combines
Foster and Treloar, finding it obvious to
detect if a woman, that does not show any symptoms of
endometriosis, and has genetic markers correlated with
increase susceptibility to endometriosis as taught by Treolar
[sic] . . . to further assess, based on those genetic markers,
the predisposition for that woman to be susceptible to
endometriosis . . . and administer a pharmaceutical
composition known to treat or reduce the conditions
associated with endometriosis as taught by Foster . . . in
order to reduce the risk of these women of developing
endometriosis.

(Ans. 7-8.) Similarly, we noted in the decision that Foster teaches certain
risk factors for endometriosis (Dec. 5; FF 4, 6), and that Treloar teaches
Appeal 2011-012653
Application 12/120,322

6
another risk factor (Dec. 6; FF 10) and agreed with the Examiner that
“selection of other known risk factors simply represents the „mere
substitution of one element for another known in the field‟ to yield a
predictable result” (Dec. 8).
We continue to conclude that it is the combination of all of the
references, including not only Treloar, but Foster, Viganò, and De Koning
that renders the claimed invention obvious, and Appellant‟s focus solely on
Treloar fails to properly capture the obviousness analysis.

Argument 3
Appellant contends that “FF #11 is in-fact factually incorrect” (Req.
Reh‟g 4). Appellant contends that “Vigano does not teach „two
polymorphisms (or any polymorphisms) corresponding to an increased risk
of endometriosis‟, but rather what Vigano teaches is perhaps a singular
polymorphism (R241) corresponding to an increased risk of severe
endometriosis but only in those subjects that are otherwise predisposed to
endometriosis” (id. at 5).
Appellant then creates another hypothetical analogy which results in
the contention that “Vigano merely disclosed a biomarker (R241) which is
just as common in women who are not predisposed to endometriosis as it is
in women who are predisposed to endometriosis” (id. at 6). Appellant also
contends that “there is no disease-associated chromosomal location
disclosed - only a potential location and markers that are indeterminate for
an association with endometriosis” (id. at 7).
Appeal 2011-012653
Application 12/120,322

7
We have reviewed our Decision in light of these arguments. We
cannot agree, however, that Viganò is solely interested in increased risk of
severe endometriosis and not endometriosis itself. As the Examiner noted
“Vigano clearly states that, „While the functional correlate of the G/R241
polymorphism remains unclear, this finding indicates that a genetic
polymorphism in the ICAM-1 gene domain may contribute to the
susceptibility to endometriosis‟ (see Vigano abstract)” (Ans. 19). Thus,
consistent with the Examiner‟s position and the Decision, Viganò directly
associates the susceptibility, i.e., risk, of endometriosis itself with the
presence or absence of the G/R241 polymorphism (see Viganò abstract, Ans.
19).
In order to respond to Appellant‟s hypothetical and resulting
conclusion, we need to unpack what Viganò actually did as compared to
Appellant‟s hypothetical. In Appellant‟s hypothetical, two inventors
perform a linkage study without using any controls and, as a result, obtain
data lacking value. However, in contrast, the Examiner finds that:
Vigano teaches: “we have studied two polymorphic sites
located in codons 241 (G/R241) and 469 (E/K469) of the
ICAM-1 gene. Three hundred and sixty three Italian
Caucasian women of reproductive age who underwent
laparoscopy for benign pelvic conditions were enrolled in
the study. Endometriosis was documented and staged in 188
women while 175 subjects, in whom endometriosis was
laparoscopically ruled out, served as the control group. The
frequency of the R241 allele was only marginally higher in
endometriosis patients than in controls. However, a
strikingly high frequency of this allele was found in patients
with stage IV endometriosis vs. controls.”

Appeal 2011-012653
Application 12/120,322

8
(Ans. 20.) Thus, unlike Appellant‟s inventor alpha, Viganò studied two sets
of women, a group with endometriosis and a control group without
endometriosis. Viganò looked at a particular allele, the G/R241 allele, and
found that an R at position 241 in ICAM was found more frequently in
women with endometriosis, and particularly women with severe
endometriosis relative to controls i.e., women without endometriosis than
was the alternate possibility of a G at position 241 in ICAM (see Ans. 20).
This is significantly different than Appellant‟s hypothetical in which neither
hypothetical inventor includes a proper control group, and due to that
scientific failure, cannot obtain a meaningful conclusion.
Consequently, Viganò finds that a woman who has an R241 allele,
that is an R at position 241 of her ICAM gene, has an increased likelihood of
endometriosis relative to a woman who has the G241 allele, and further has
an increased risk of severe endometriosis (see Ans. 20). This R241 allele is
therefore reasonably interpreted in light of Foster‟s definition as a risk
factor, where Foster teaches “[a] woman at higher than normal risk of
developing endometriosis is a woman at greater risk than the general
population of women of developing endometriosis for the first time” (Foster
4 ¶ 0034; Dec. 5; FF 2). Viganò‟s results are not indeterminate, but instead
teaches that the R241 allele is more frequent in endometriosis patients than
in control patients who did not have endometriosis, and in patients with
severe endometriosis more than control patients, would have reasonably
been understood as a risk factor for endometriosis by the ordinary artisan
familiar with Foster (Dec. 5; FF 2).
Appeal 2011-012653
Application 12/120,322

9
We continue to conclude that the combination of all of the references,
including Treloar, Foster, Viganò, and De Koning renders the claimed
invention obvious, and that “Vigano teaches that „genotyping of the patients
could be useful to select subgroups that could develop a more severe form of
the disease,‟” addressing the limitation of claim 2 (Viganò 52; Dec. 6; FF
12).

Argument 4
Appellant contends that “FF #12 does not render the rejected claims
obvious and that FF #12 cannot be used for instance in „assessing a
predisposition for endometriosis in a subject that does not exhibit an
endometriosis symptom‟” (Req. Reh‟g 7). Appellant contends that “such
genotyping is as likely to identify a predisposition in a woman to severe
endometriosis when in fact the woman isn‟t predisposed to endometriosis at
all (i.e. a false positive), as it is to identify a predisposition in a woman to
severe endometriosis wherein the woman is predisposed to developing
endometriosis” (id. at 7-8).
We have reviewed our Decision in light of these arguments. However,
we are not persuaded that our Decision was in error. Appellant again fails to
address the combination of all of the references, focusing only on the
teaching of Viganò alone that “‟genotyping of the patients could be useful to
select subgroups that could develop a more severe form of the disease
(Viganò 52)‟” (Dec. 6; FF 12). It is Foster who teaches the “assessing” step,
that is, the association of a higher than normal risk of endometriosis in an
asymptomatic woman with treatment for that increased risk (Dec. 5-6, FF 2-
Appeal 2011-012653
Application 12/120,322

10
9). Foster teaches “[a] method of preventing endometriosis in a woman at
higher than normal risk of developing endometriosis, comprising:
administering to the woman at higher than normal risk of developing
endometriosis a pharmaceutically acceptable composition ... to inhibit the
growth or thickening of endometriotic tissue in the woman” (Foster 9, claim
13; Dec. 5; FF 5). Viganò (along with Treloar) is relied upon by the
Examiner in the obviousness analysis to establish that the prior art
recognized genetic markers that were correlated with an endometriosis
related condition as required by claim 2 and established at least a small
“higher than normal risk” in the language of Foster (FF 2, 5).
To the extent that the obvious method over Foster, De Koning,
Treloar, and Viganò would have resulted in the treatment false-positives, the
same risk always exists and was evident in Foster, as the Examiner finds that
“Foster teaches the administration of a pharmaceutical composition, which is
known to be effective in the treatment of endometriosis, to women with no
symptoms of endometriosis that have a higher risk to acquire endometriosis,
like for example a women with a close relative (mother, sibling, aunt, etc)
that has already being diagnosed with endometriosis” (Ans. 25). There is no
reasonable expectation that every woman at higher risk will necessarily
develop endometriosis, only that they are at higher risk of endometriosis
than other equivalent women lacking the same risk factors.
We continue to conclude that the combination of all of the references,
including Treloar, Foster, Viganò, and De Koning renders the claimed
invention obvious.

Appeal 2011-012653
Application 12/120,322

11
SUMMARY
We have carefully reviewed the original opinion in light of
Appellant‟s request, but we find no point of law or fact which we
overlooked or misapprehended in arriving at our decision. To the extent
relevant, Appellant‟s request amounts to a reargument of points already
considered by the Board and the Examiner.
Therefore, Appellant‟s request has been granted to the extent that the
decision has been reconsidered, but such request is denied with respect to
making any modifications to the decision affirming the Examiner's rejection
under 35 U.S.C. § 103(a).

DENIED

cdc