Becker Hewes

Patent Trials and Appeals Board

Oct 27, 2020

2019006474 (P.T.A.B. Oct. 27, 2020)

UNITED STATES PATENT AND TRADEMARK OFFICE
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
APPLICATION NO. FILING DATE FIRST NAMED INVENTOR ATTORNEY DOCKET NO. CONFIRMATION NO.
12/129,935 05/30/2008 Becker Hewes PC69808A 3004
25291 7590 10/27/2020
Pfizer Inc.
Attn:Legal Patent Department, Chief IP Counsel
235 East 42nd Street
New York, NY 10017
EXAMINER
CHONG, YONG SOO
ART UNIT PAPER NUMBER
1627
NOTIFICATION DATE DELIVERY MODE
10/27/2020 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):
PfizerPatentDocketing@pfizer.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
____________

BEFORE THE PATENT TRIAL AND APPEAL BOARD
____________

Ex parte BECKER HEWES
____________

Appeal 2019-006474
Application 12/129,935
Technology Center 1600
____________

Before DONALD E. ADAMS, ERIC B. GRIMES, and
TIMOTHY G. MAJORS, Administrative Patent Judges.

MAJORS, Administrative Patent Judge.

DECISION ON APPEAL
Appellant1 submits this appeal2 under 35 U.S.C. § 134(a) involving
claims to a method for treating a BcrAbl positive leukemia in a subject that
is resistant to imatinib, which claims have been rejected for obviousness
under 35 U.S.C. § 103 and for obviousness-type double patenting. We have
jurisdiction under 35 U.S.C. § 6.
We REVERSE.

1 We use the word “Appellant” to refer to “applicant” as defined in
37 C.F.R. § 1.42(a). Appellant identifies Wyeth LLC as the real party-in-
interest. Appeal Br. 3. We also note that Pfizer Inc., and its Legal
Department, is identified as the addressee of record for this application, and
Pfizer’s counsel appears to be responsible, at least in part, for prosecution of
this application. See, e.g., id. at 12; Ans. (mailing page).
2 This appeal is related to Appeal 2014-007550, decided July 22, 2016.
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STATEMENT OF THE CASE
Patients with chronic myelogenous leukemia (“CML”) are often
treated with imatinib, a drug sold under the name Gleevec (also known as
STI-571). Spec. ¶¶ 2–3. This drug “blocks the tyrosine kinase protein
‘BcrAbl,’ an abnormal protein driving overproduction of abnormal white
blood cells characteristic of leukemia.” Id. ¶ 2. Some patients, however,
develop resistance to imatinib “due to point mutations in the bcr/abl gene.”
Id. ¶ 4.
“[T]he invention is directed to methods of treating imatinib-resistant
BcrAbl positive leukemia.” Id. ¶ 2. According to the Specification, it has
“been discovered that a significant number of patients having known point
mutations associated with resistance to imatinib respond favorably to
treatment with SK-606”—a drug also known as “bosutinib,” with the
chemical name 4-[(2,4-Dichloro-5-methoxy-phenyl)amino]-6-methoxy-7-[3-
(4-methyl-1-piperazinyl)propoxy]-3-quinolinecarbonitrile. Id. ¶ 13; see also
id. ¶ 9. The Specification identifies F317L as such a mutation. Id. ¶ 52.
The amino acid change of F317L corresponds to mutation of the bcr/abl
gene at 949T>C, reflecting the specific nucleotide position and change. Id.
Claims 17–28 are on appeal. Appeal Br. 13–14. Claim 17 is
illustrative and reads:
17. A method for treating a BcrAbl positive leukemia in a
subject that is resistant to imatinib which comprises
administering to the subject a therapeutically effective amount
of 4-[(2,4-Dichloro-5-methoxy-phenyl)amino]-6-methoxy-7-[3-
(4-methyl-1-piperazinyl)propoxy]-3-quinolinecarbonitrile,
wherein the subject has a mutation in BcrAbl protein selected
from F317L.
Id. at 13 (underlining omitted).
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Claim 18, the other independent claim on appeal, is substantially
identical to claim 17, except the corresponding wherein clause reads:
“wherein [the subject3] has a resistance-associated nucleic acid mutation in
the BcrAbl gene selected from the group consisting of: 949T>C.” Id.
Appellant seeks review of the following rejections:
I. Claims 17–20, 23, and 24 under 35 U.S.C. § 103 as obvious over
Manley;4
II. Claims 17–28 under 35 U.S.C. § 103 as obvious over
Boschelli ’7805 in view of Shah.6
III. Claims 17–28 for obviousness-type double patenting over claims
of Boschelli ’1487 in view of Shah.

3 This bracketed text reflects what, in context, appears to be the missing
language. Claim 23 also depends from “claim 1,” which is not pending.
Appeal Br. 13. For this appeal, we treat claim 23 as depending from
claim 17. If prosecution continues, corrections should be made.
4 Manley et al., Advances in the structural biology, design and clinical
development of Bcr-Abl kinase inhibitors for the treatment of chronic
myeloid leukaemia, 1754 BIOCHIMICA ET BIOPHYSICA ACTA 3–13 (2005)
(“Manley”).
5 Boschelli et al., US 2005/0101780 A1, publ. May 12, 2005 (“Boschelli”).
6 Shah et al., Multiple BCR-ABL kinase domain mutations confer polyclonal
resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic
phase and blast crisis chronic myeloid leukemia, 2 CANCER CELL 117–125
(2002) (“Shah”).
7 Boschelli et al., US 7,417,148 B2, issued Aug. 26, 2008 (“Boschelli
’148”). Boschelli ’148 issued from the application that published as
Boschelli ’780. Boschelli ’148, code (65). The Examiner indicates that the
double patenting rejection is over claims 1–10, 21, and 22 of Boschelli ’148.
Final Act. 3–4. There are, however, no claims numbered 21 or 22 in that
patent. Boschelli ’148, 18:28–31 (ending at claim 12).
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I. Obviousness Over Manley
The issue on appeal is whether a preponderance of the evidence
supports the Examiner’s conclusion that claims 17–20, 23, and 24 would
have been obvious over Manley. The Examiner’s and Appellant’s positions
are addressed to the claims as a group. Appeal Br. 4–8; Final Act. 4–6. We
focus on claim 17 as illustrative, which claim relates to the treatment of
imatinib-resistant leukemia in a subject having a “mutation in BcrAbl
protein selected from F317L.” Appeal Br. 13 (emphasis added).8 That
treatment involves administering a therapeutically effective amount of a
drug known as bosutinib (with the chemical name recited in claim 17). Id.;
Spec. ¶ 9 (describing bosutinib (also known as SKI-606)). The Examiner’s
determinations and Appellant’s arguments are summarized below, followed
by our analysis.
The Examiner finds that claim 17 would have been obvious over
Manley. Final Act. 4–10. According to the Examiner, Manley teaches “a
promising class of new chronic myeloid leukaemia (CML) drugs for patients
with imatinib resistance.” Id. at 5. Also, the Examiner finds, Manley
teaches “[t]his resistance is often due to the emergence of clones expressing
mutant forms of Bcr-Abl, which exhibit decreased sensitivity towards
inhibition by imatinib.” Id. (citing Manley’s Abstract and Introduction).
The Examiner interprets Manley as teaching that “[t]he most frequently
occurring mutants are F317V>T315A>T315I>F317L.” Id. (citing Manley 8

8 As noted above, claim 18 recites the mutation, not as the expressed mutant
protein F317L, but based on the corresponding nucleic acid mutation
(949T>C). Appeal Br. 13. The other challenged claims depend, directly or
indirectly, from either claim 17 or claim 18. Id. at 13–14.
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(left col., first para.)). Further, the Examiner finds, Manley teaches “[o]ne
promising class of CML drugs is the dual Bcr-Abl/Src inhibitor, SKI-606
[i.e., bosutinib].” Id. (citing Manley 9).
The Examiner finds that Manley “fail[s] to disclose a single
embodiment regarding administration of SKI-606 to a patient suffering from
imatinib resistant BCrAbl positive leukemia, which has one of the claimed
mutations,” but the Examiner nevertheless concludes the method of claim 17
would have been obvious over Manley. Id. More specifically, the Examiner
determines “it would have been prima facie obvious . . . to administer the
dual Bcr-Abl/Src inhibitor, SKI-606, to a patient suffering from imatinib
resistant BcrAbl positive leukemia having one of the following mutations,
F317V>T315A>T315I>F317L”—the F317L mutation being the one recited
in claim 17. Id. The Examiner reasons that the ordinarily skilled person
would have been motivated to practice the claimed method based on
Manley’s teaching that bosutinib is one of a class of promising new inhibitor
compounds for treating imatinib-resistant CML, that imatinib resistance is
due to emergence of clones expressing mutant proteins, and that F317L is
alleged to be among the “most frequently occurring mutants.” Id. at 5–6.
Invoking this same reasoning, the Examiner concludes “[t]herefore, one of
ordinary skill in the art would have had a reasonable expectation of success
in treating imatinib resistant BcrAbl positive leukemia” by administering
bosutinib to a subject with the F317L mutation. Id.; see also Ans. 4–13.
Appellant raises five responsive arguments. Appeal Br. 5–8. In
support, Appellant relies on, among other evidence, testimony from Brion
W. Murray, Ph.D., submitted in an affidavit dated October 3, 2016 (“Murray
Affidavit”). Id.; Murray Affidavit pp. 1–6.
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First, Appellant argues “Manley does not suggest that any promising
new CML drug, including bosutinib, could treat imatinib-resistant CML
associated with F317L.” Id. at 5. Indeed, Appellant contends, “none of the
second generation drugs are described in Manley as effectively treating
imatinib-resistant CML associated with F317L.” Id. (citing Manley’s
teaching that “[o]f the patients expressing imatinib-resistant mutants,
complete haematological remissions have been observed in most cases
[treated with another second generation drug, dasatinib], with the exception
of those expressing T315I . . . F317L and D276G.” Id. (citing Manley 8
(with Appellant’s emphasis)).
Appellant’s second, third, and fourth arguments relate, in general, to
alleged unpredictability in treatment of imatinib-resistant leukemia in
subjects with the F317L mutation. Id. at 5–7. According to Appellant,
subjects expressing mutant proteins with mutations in the Bcr-Abl protein’s
hinge region, like the F317L and T315I mutants, had been shown to be
especially resistant to treatment, even with second generation drugs like
dasatinib and nilotinib. Id. (citing, among other evidence, Murray Affidavit
¶¶ 8, 9, 11); see Murray Affidavit ¶ 11 (testifying that “mutations in the
ABL hinge region (T315I, F317L) were shown to confer resistance to both
imatinib and dasatinib in clinical models . . . as well as in patients” (citing
several references)). Appellant further contends, citing Dr. Murray’s
testimony and other references, that imatinib resistance arising from
mutations of the Bcr-Abl gene was, in fact, poorly understood at the time of
the invention. Appeal Br. 6; Murray Affidavit ¶ 12 (explaining that different
patients, even with the same mutations, were known to display different
clinical responses upon treatment). And, Appellant argues, preclinical
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models in this area were poor predictors of clinical efficacy and success.
Appeal Br. 6; Murray Affidavit ¶ 13 (testifying that preclinical models may
have predicted drug potency even against F317L mutants, but “clinical
findings show F317L to be a[n] imatinib/dasatinib-resistant mutation”).
Finally, Appellant contends that the F317L is actually a rare mutation,
which would have detracted from the motivation of treating subjects with
that mutation. Appeal Br. 7 (“[T]he F317L mutation is uncommon [and
thus] there would be a diminished motivation to seek a treatment.”).
Appellant cites evidence that, in one study, “only one of the 20” imatinib-
resistant subjects had a F317L point mutation. Id. (citing Manley Table 1).
Similarly, citing Shah, Appellant contends that in “mutation data for 37
patients having 51 mutations,” evidence shows “only three of the 51
mutations being F317L.” Id.
The Examiner “bears the initial burden . . . of presenting a prima facie
case of unpatentability.” In re Oetiker, 977 F.2d 1443, 1445 (Fed. Cir.
1992). “The Patent Office has the initial duty of supplying the factual basis
for its rejection. It may not . . . resort to speculation, unfounded assumptions
or hindsight reconstruction to supply deficiencies” in the rejection. In re
Warner, 379 F.2d 1011, 1017 (CCPA 1967). And, “[a]fter evidence or
argument is submitted by the applicant in response, patentability is
determined on the totality of the record, by a preponderance of evidence
with due consideration to persuasiveness of argument.” In re Oetiker, 977
F.2d at 1445. Upon considering the prior art, and the argument and evidence
of record for and against the rejection, we conclude that the preponderance
of the evidence on this record does not support the Examiner’s rejection for
obviousness. We explain below.
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As an initial matter, we agree with the Examiner that Manley
discloses bosutinib as among a promising new class of drugs under
investigation for the treatment of imatinib-resistant CML. Manley describes
a drug known as “BMS-354825” (also known as dasatinib) and “AMN107”
(a drug under development by Novartis) and Manley teaches that “both of
these promise a breakthrough in the treatment of imatinib-resistant CML.”
Manley, Abstr., 4 (depicting structures for selective Abl and dual Src-Abl
kinase inhibitors, including dasatinib, AMN107, and SKI-606 (bosutinib),
among others). On bosutinib, Manley teaches that it, like dasatinib, is a dual
Bcr-Abl/Src inhibitor being studied for treatment of CML. Id. at 7, 9.
Indeed, Manley teaches that, “[i]n imatinib-resistant K-562 cells . . ., SKI-
606 [bosutinib] has been shown to inhibit both Bcr-Abl and Lyn
phosphorylation,” and had shown “enhanced apoptosis in CD34+ cells
isolated from blast crisis CML patients, including those harbouring Y253,
E255V, E255K or F359V mutants.” Id. at 9.
We also agree with the Examiner that Manley teaches imatinib-
resistance is “often due to the emergence of clones expressing mutant forms
of Bcr-Abl.” Manley 3–4 (noting that “over 35 such mutant forms of the
enzyme have been observed in CML patients,” prompting “a need for
improved therapies”). Manley identifies many of those mutants. See, e.g.,
Manley 6 (Table 1). The Examiner, however, misinterprets Manley in
finding that “F317V>T315A>T315I>F317L” are the “most frequently
occurring mutants” in imatinib-resistant subjects. Final Act. 5 (citing
Manley 8). The Examiner’s citation to those four identified mutants arises
from a section of Manley describing the most frequent mutants emerging in
dasatinib-resistant clones—not imatinib-resistant subjects. Manley 8 (“For
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BMS-356825 . . ., resistant clones emerged expressing 10 mutant forms of
Bcr-Abl, with the most frequently occurring mutants being
F317V>T315A>T315I>F317L”). The misinterpretation aside, Manley
elsewhere identifies F317L in a listing of “some of the most prevalent
imatinib-resistant mutant forms of the enzymes identified in patients.” Id. at
6 (Table 1); Ans. 9 (citing Table 1).9
Although we agree with many of the Examiner’s findings, and even if
the Examiner’s reasoning provided some motivation to attempt treating
subjects with the F317L mutation with bosutinib, considering the totality of
the evidence, the rejection fails on the issue of reasonable expectation of
success. Intelligent Bio-Systems, Inc. v. Illumina Cambridge Ltd., 821 F.3d
1359, 1367 (Fed. Cir. 2016) (explaining that the motivation and reasonable
expectation inquiries are different, and the latter refers to likelihood of
success in modifying the prior art to reach the claimed invention). As
discussed in more detail below, Appellant’s argument and supporting
evidence shows a lack of predictability in treating imatinib-resistant subjects
with the F317L mutation, in particular. See, e.g., Appeal Br. 5–7; Murray
Affidavit. In the face of this argument and evidence from Appellant, the
Examiner provides no persuasive rebuttal. Ans. 9–13.

9 According to the Examiner, “[i]n Table 1, BMS-354825 [dasatinib] is
shown to have activity for not only the four mentioned mutants,
F317V>T315A>T315I>F317L, but also other mutant forms of Bcr-Abl.”
Ans. 9. Table 1 does not, however, show that dasatinib has therapeutic
activity for the T315I mutant, and the T315A mutant is not identified in the
table. Manley 6–7 (“In cellular assays, . . . the compound [dasatinib]
maintains high potency against a wide range of Bcr-Abl mutants . . .,
although, again like AMN107, with the exception of T315I (Table 1)”).
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Appellant is correct that none of the second generation drugs in
Manley are disclosed as effectively treating imatinib-resistant CML
associated with the F317L mutation. Appeal Br. 5. Insofar as the Examiner
suggests that Manley teaches the second generation drug dasatinib (BMS-
354825) is “useful for” treating imatinib-resistant CML in subjects with the
F317V, T315A, T315I, and F317L mutations, we are unpersuaded. Ans. 9
(“The key part of this argument [of Examiner] is that each of the active
agents in Manley go through the same mechanism of action, namely
inhibiting Bcr-Abl. For example, in the section drawn to the dual Bcr-Abl
kinase inhibitor, BMS-354825, only 4 mutant forms are listed as being
useful for, F317V>T315A>T315I>F317L.”); see also id. (arguing that “[i]n
the same manner [as BMS-354825], SKI-606 or bosutinib, is expected to
have activity towards the mutant forms listed in that section,” including the
claimed F317L mutation). To the contrary, Appellant persuades us that
Manley teaches that those four cited mutants arose most frequently in
dasatinib-resistant subjects—suggesting, if anything, that dasatinib would
not be useful for effective treatment in subjects expressing F317L. Manley
8; see Murray Affidavit ¶¶ 11, 13.
Although having previously cited Manley’s teachings about the
perceived favorable activity of dasatinib as supporting a conclusion of
obviousness, faced with Appellant’s rebuttal argument and evidence
including the testimony of Dr. Murray, the Examiner responds that
“dasatinib is not bosutinib.” Ans. 10. That is, according to the Examiner,
“nothing can be taken away from the assertion that other next-generation
drugs like dasatinib were shown to be ineffective against F317L.” Id. But it
is the Examiner that bears the ultimate burden of showing unpatentability.
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There is no actual teaching in Manley that bosutinib has activity or would be
therapeutically effective in an imatinib-resistant subject with the F317L
mutation. And Appellant’s evidence, especially Dr. Murray’s testimony,
calls into significant doubt whether the ordinarily skilled person would have
reasonably expected success with bosutinib when other second-generation,
Bcr-Abl/Src inhibitors were known and shown to be ineffective in treating
subjects with the F317L mutation. Manley 8; Murray Affidavit ¶ 11.
The Examiner also responds to Appellant’s arguments and evidence
with an assertion that “none of these lines of argument directly relates to
bosutinib . . . nor anything specific to the teachings of the cited references.”
Final Act. 11; Ans. 10. We find, however, that Dr. Murray’s testimony
about the lack of success with other second generation Bcr-Abl inhibitors is
probative of the skilled person’s reasonable expectations (or lack thereof)
about successful treatment with bosutinib in subjects with the specific
mutation claimed.
The documentary evidence cited by Dr. Murray corroborates his
testimony. For example, to support his opinion that effectively treating
leukemia in subjects expressing F317L was highly unpredictable,
Dr. Murray cites, among other references, a publication describing Phase II
clinical results on five patients treated with dasatinib where resistance to
treatment and relapse coincided with emergence of the F317L mutation. See
Murray Affidavit ¶¶ 9, 11 (citing Simona Soverini et al., Presence or the
Emergence of a F317L BCR-ABL Mutation May Be Associated With
Resistance to Dasatinib in Philadelphia Chromosome-Positive Leukemia,
24:33 JOURNAL OF CLINICAL ONCOLOGY e51–52 (2006)). The Examiner
fails to address directly or persuasively Dr. Murray’s opinions or the
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literature he cites in support of those opinions. The Examiner’s assertions
on the reasonable expectation issue, by comparison, are conclusory and lack
a persuasive evidentiary basis. Moreover, the Examiner’s assertion (Final
Act. 11) that Appellant’s argument and Dr. Murray’s testimony are not
specific to the references cited in the rejection is incorrect. The Murray
Affidavit repeatedly cites Manley and Shah (among other references) in
support of his opinions; both Manley and Shah are asserted by Examiner
here. See, e.g., Murray Affidavit ¶¶ 9, 11, 13.
The Examiner also characterizes Appellant’s evidence as “merely
opinions” on the state of the art, among other issues. Final Act. 10; Ans. 10–
11. We are unpersuaded Dr. Murray’s “opinions” can be summarily swept
aside in this way. As already explained, Dr. Murray cites repeatedly to the
scientific literature in support of his opinions, grounding those opinions in
an adequate factual basis (e.g., explaining, with citation support, that
treatment of subjects expressing the Bcr-Abl protein with hinge-region
mutants (like F317L or T315I) have been described in the literature as
difficult to treat). See, e.g., Murray Affidavit ¶ 11.10 The Examiner does not
grapple persuasively with Dr. Murray’s opinions or the facts on which they
are based.

10 Regarding the Puttini reference, the Examiner responds “Appellant is
reminded that that the Puttini reference was not a reference used in the
instant rejections.” Ans. 11. As we explained in our prior decision,
secondary references like Puttini may be considered for their evidentiary
value on issues relevant to the obviousness inquiry even if such references
are not applied by the Examiner in a rejection. In re Hewes, Appeal 2014-
007550, 14 n.7 (PTAB July 22, 2016).
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Finally, the Examiner points to the Board’s prior decision in the
related appeal, where we affirmed the rejection of the then-pending claims
for obviousness over the same art asserted by Examiner here. Final Act. 12.
But the circumstances and record have changed. The claims have been
amended and materially narrowed since the earlier appeal. Claim 17
previously recited a list of twelve mutations,11 now only one mutation is
recited. New evidence is also before the Examiner and the Board, including
testimonial evidence that persuades us of an art-recognized difficulty in
effectively treating leukemia in subjects with the F317L mutation now
recited in claim 17. In our prior decision, we agreed with the Examiner’s
prima facie case of obviousness, including on the reasonable expectation of
success issue, “absent persuasive evidence to the contrary” from Appellant.
In re Hewes, Appeal 2014-007550, 16 (PTAB July 22, 2016). Appellant has
since submitted the sort of persuasive rebuttal argument and evidence that
we remarked was missing previously.
For the reasons above, we determine that the preponderance of the
evidence does not support the Examiner’s conclusion that claim 17 (or
claims 18–20, 23, and 24) would have been obvious over Manley.
II. Obviousness Over Boschelli ’780 and Shah
The Examiner concludes that claims 17–28 would have been obvious
over Boschelli ’780 and Shah. Final Act. 8–12. This rejection is similar to

11 As we noted during the prior appeal, some of the evidence/references
actually indicated that bosutinib was likely to be efficacious in treating
leukemia in subjects with mutations expressly claimed at that time. In re
Hewes, Appeal 2014-007550, 14 (PTAB July 22, 2016) (pointing out that
Puttini disclosed a significant rate of decrease in tumor growth and
prolonged survival related to the then-claimed Y253F mutant form).
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the rejection over Manley, except the Examiner relies on Boschelli ’780’s
teachings about treating CML with inhibitor compounds, including the Brc-
Abl/Src inhibitor compound with the chemical name recited in claim 17.
Final Act. 8 (citing Boschelli ’780, claims 1–10, 21–22).12 The Examiner,
acknowledging that Boschelli ’780 does not disclose treating BcrAbl
positive leukemia in an imatinib-resistant subject due to particular
mutations, much less the F317L mutation, turns to Shah. Id. at 9. The
Examiner finds that Shah describes common mutations that arise in subjects
with imatinib resistance, including F317L, T315I, M244V, and several
others. Id. The Examiner describes the art’s teachings as a “typical
genus/species situation” and concludes it would have been obvious to
provide effective CML treatment by administering SKI-606/bosutinib to
imatinib-resistant subjects with the F317L mutation. Id. at 9–10.
This rejection fails for substantially the same reasons as discussed
above. Appellant has presented persuasive evidence showing that treatment
of leukemia in resistant subjects with the F317L mutation with second
generation Abl-Brc/Src inhibitors (like dasatinib and others) was, for several
reasons, known to be especially difficult and unpredictable. Appeal Br. 8–
11; Murray Affidavit ¶¶ 9–14. Examiner provides no persuasive rebuttal.
On this record, we are unpersuaded the ordinarily skilled person would have
had a reasonable expectation of success in practicing the method claimed.
Accordingly, the preponderance of the evidence does not support the
Examiner’s conclusion of obviousness.

12 Claim 1 of Boschelli ’780 recites a method of inhibiting CML comprising
administering a class of compounds, and dependent claim 6 recites the
compound with the chemical name recited in Appellant’s claim 17.
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III. Obviousness-Type Double Patenting Over Boschelli ’148 and Shah
Both Examiner and Appellant treat the double-patenting rejection as
rising or falling with the obviousness rejection based on Boschelli ’780 and
Shah. Final Act. 4 (“[T]his [double-patenting rejection] is the same rejection
as the 103(a) rejection below, therefore please see below for the full body of
the rejection”); Appeal Br. 12 (“In view of the above, reconsideration and
withdrawal of the 35 USC § 103 rejection (and corresponding obviousness-
type double patenting rejection) based on Boschelli and Shaw is therefore
respectfully requested.”). Because we conclude that the preponderance of
the evidence does not support the conclusion that claims 17–28 would have
been obvious over Boschelli ’780 and Shah, the obviousness-type double
patenting rejection fails for the same reasons. See supra (Sections I and II).
CONCLUSION
In summary:
Claims
Rejected
35 U.S.C. § Reference(s)/Basis Affirmed Reversed
17–20, 23,
24
103 Manley 17–20, 23,
24
17–28 103 Boschelli ’780,
Shah
17–28
17–28 obviousness-
type double
patenting
Boschelli ’148,
Shah
17–28
Overall
Outcome

17–28

REVERSED