Ex Parte Hewes

Patent Trial and Appeal Board

Jul 20, 2016

12129935 (P.T.A.B. Jul. 20, 2016)

UNITED STA TES p A TENT AND TRADEMARK OFFICE
APPLICATION NO. FILING DATE
12/129,935 05/30/2008
25291 7590 07/22/2016
Pfizer Inc,
Attn:Legal Patent Department, Chief IP Counsel
235 East 42nd Street
NEW YORK, NY 10017
FIRST NAMED INVENTOR
Becker Hewes
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.
PC69808A 3004
EXAMINER
CHONG,YONGSOO
ART UNIT PAPER NUMBER
1627
NOTIFICATION DATE DELIVERY MODE
07/22/2016 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):
-IPGSMadisonDocketing@pfizer.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte BECKER HEWES 1
Appeal2014-007550
Application 12/129,935
Technology Center 1600
Before ERIC B. GRIMES, MELANIE L. McCOLLUM,
and TIMOTHY G. MAJORS, Administrative Patent Judges.
MAJORS, Administrative Patent Judge.
DECISION ON APPEAL
This is an appeal under 35 U.S.C. § 134 involving claims to methods
of treating imatinib-resistant leukemia, which have been rejected as obvious.
We have jurisdiction under 35 U.S.C. § 6(b ).
We affirm.
STATEMENT OF THE CASE
Patients with chronic myelogenous leukemia ("CML") are often
treated with imatinib, a drug sold under the trade name Gleevec or Glivec
(also known as STI-571). (Spec. i-fi-12-3.) This drug "blocks the tyrosine
1 Appellant identifies the Real Party in Interest as Wyeth LLC. (App. Br. 3.)
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Application 12/129,935
kinase protein 'BcrAbl,' an abnormal protein driving overproduction of
abnormal white blood cells characteristic of leukemia." (Id. at i-f 2.) Some
patients, however, develop resistance to imatinib "due to point mutations in
the bcr/abl gene" of the cancerous cells. (Id. at i-f 4.) 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, and
having the chemical name 4-[(2,4-Dichloro-5-methoxy-phenyl)amino ]-6-
methoxy-7-[3-( 4-methyl-1-piperazinyl)propoxy ]-3-quinolinecarbonitrile.
(Id. at i-f 13; see also id. at i-f 9.)
Claims 17-28 are on appeal. Claim 17 is illustrative:
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, \vherein the subject has
at least one mutation in BcrAbl protein selected from M351 T; H396P;
I432T; F486S; M244V; L248V; G250E; Y253F; K263E; L273M;
F317L; and N331 S.
The claims stand rejected as follows:
I. Claims 17-20, 23, and 24 under 35 U.S.C. § 103(a) over Manley. 2
2 Manley et al., Advances in the structural biology, design and clinical
development of Ber-Ahl kinase inhibitors for the treatment of chronic
myeloid leukaemia, 1754 BIOCHIMICA ET BIOPHYSICA ACTA 3-13 (2005)
("Manley").
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II. Claims 17-28 under 35 U.S.C. § 103(a) over Boschelli3 and
Shah. 4
DISCUSSION - I
Issue
Has the Examiner established by a preponderance of the evidence that
claims 17-20, 23, and 24 would have been obvious under 35 U.S.C. § 103(a)
over Manley?
Findings of Fact
FF 1. The Examiner's findings of fact and statement of the rejection
of claims 17-20, 23, and 24 under 35 U.S.C. § 103(a) over Manley may be
found at pages 4--7 of the Final Action dated July 3, 2013. (See also Ans. 3-
5 and 7-9.) We adopt those findings here unless otherwise stated, and
discuss below various material teachings of the prior art.
FF 2. Manley discloses that "patients who have progressed to
advanced phases of CML frequently fail to respond to imatinib or develop
resistance to therapy and relapse." (Manley Abstract.) Manley teaches this
resistance is "often due to the emergence of clones expressing mutant forms
of Bcr-Abl, which exhibit a decreased sensitivity towards inhibition by
imatinib." (Id.) Manley identifies the "most prevalent imatinib-resistant
3 Boschelli et al. (US 2005/010780 Al, publ. May 12, 2005) ("Boschelli").
4 Shah et al., Multiple BCR-ABL kinase domain mutations confer polyclonal
resistance to the tyrosine kinase inhibitor imatinib (STI57 l) in chronic
phase and blast crisis chronic myeloid leukemia, 2 CANCER CELL 117-125
(2002) ("Shah").
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Application 12/129,935
mutant forms of the enzymes identified in patients" as including G250E,
Y253H, F317L, M351 T, and F486S, among others. (Id. at 6, Table I.)
FF 3. Manley discloses drugs designed for treatment of imatinib-
resistant CML. (Manley Abstract.) In particular, Manley teaches "two
classes of drug candidates are being evaluated as monotherapies in early
clinical trials for the treatment of CML. These are the second generation
selective Bcr-Abl kinase inhibitor, AMN107 and the dual Abl-Src inhibitors,
BMS-354825, AZD05340, and SKI-606." (Id. at 5.) Manley teaches:
Since Src family kinases regulate downstream elements of the
Bcr-Abl signalling [sic] cascade, inhibition of these enzymes
could therefore provide synergy with Bcr-Abl inhibition and
potentially counteracting the availability of alternative survival
pathways which CML cells could utilise in the face of Bcr-Abl
inhibition .... Therapy with combined Bcr-Abl and Src-family
kinase inhibitors might also counteract the oncogenic potential
of drug-resistant mutant forms of Bcr-Abl in CML and/or ALL.
(Id. at 7.) Table 1 of Manley discloses therapeutic activity (e.g., effect on
autophosphorylation and cell proliferation) for the dual Abl-Src inhibitor,
BMS-354825, relative to the most prevalent imatinib-resistant mutants. (Id.
at 6.) Manley further describes testing of SKI-606, which demonstrated
"induced GI arrest and enhanced apoptosis in CD34+ cells isolated from
blast crisis CML patients, including those harbouring Y253H, E255K or
F359V mutant BCR-ABL." (Id. at 9.)
Analysis
Appellant argues the patentability of claims 17-20, 23, and 24 as a
group. (App. Br. 4---6.) So, in this discussion, we focus on the rejection of
claim 1 7, which is representative.
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The Examiner concludes that claim 17 would have been obvious over
Manley. (Ans. 3-5.) The Examiner finds that Manley teaches "imatinib
resistance is due to emergence of clones expressing mutant forms of Bcr-
Abl, which exhibit decreased sensitivity towards inhibition of imatinib." (Id.
at 5.) According to the Examiner, "Manley et al. teach that a promising
class of new chronic myeloid leukaemia (CML) drugs for patients with
imatinib resistance is the dual Bcr-Abl/Src inhibitor, SKI-606." (Id.) With
respect to another of the "promising" dual Abl-Src inhibitors -BMS-
3 54825 - the Examiner finds that "In Table 1, BMS-3 54825 is shown to
have activity for not only the four mentioned mutants,
F317V>T315A>T315I>F317L, but also other mutant forms of Bcr-Abl."
(Id. at 8.) The Examiner finds that "[i]n the same manner, SKI-606 or
bosutinib, is expected to have activity towards the mutant forms listed in that
section, but also other mutant forms that are mentioned in Manley and that
are instantly claimed." (Id.) The Examiner thus concludes that it would
have been obvious to administer SKI-606 to the imatinib-resistant subject
expressing the most prevalent mutant forms of Bcr-Abl, which overlap with
mutant forms recited in claim 17, and that the skilled artisan would have
done so with a reasonable expectation of success. (Id. at 5, 8.)
Appellant raises several arguments in response. First, Appellant
argues the Examiner "inappropriately conflates unrelated sections of the
Manley review article" to arrive at the claimed invention. (App. Br. 4.) In
particular, Appellant argues the Examiner improperly combined teachings
concerning Section 2.2.1 (related to dasatinib/BMS-354825) with teachings
in Section 2.2.3 (related to bosutinib/SKI-606). (Id.) Second, Appellant
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argues the Examiner's rejection invokes an unsupported "obvious to try"
rationale that is inappropriate because cancer treatments are unpredictable.
(Id. at 5.) Third, Appellant argues the Examiner should have provided
"crystal structure data comparing and contrasting bosutinib' s and imatinib' s
respective interactions with Bcr-Abl" or other evidence to properly support
the rejection. (Id. at 6.)
Appellant's first argument fails to persuade us the Examiner erred in
combining Manley's disclosures. Rather than consider any one disclosure of
Manley in isolation, in a Section 103 inquiry, we consider the prior art for all
that it teaches and suggests to the skilled artisan. In re Lamberti, 545 F.2d
747, 750 (CCPA 1976) ("[A]ll disclosures of the prior art, including
unpreferred embodiments, must be considered.")
Here, the Examiner has drawn from Manley's teachings concerning
two "promising" Abl-Src inhibitors - dasatinib and bosutinib - designed
to treat imatinib-resistant CML subjects, along with Manley's teachings
concerning the "most prevalent mutant forms" expressed in these subjects.
(FF 1, 3.) We agree with the Examiner that the skilled artisan would have
had reason to use the Abl-Src inhibitor, bosutinib, for treatment of imatinib-
resistant cells expressing the most prevalent mutant forms. (FF 3.) And,
absent persuasive evidence to the contrary, we agree with the Examiner that
the person of ordinary skill in the art would have reasonably expected
bosutinib to exhibit treatment of these mutations similar to dasatinib.
(Manley p. 6, Table 1 (describing effects for dasatinib/BMS-354825 against
most prevalent mutant forms).) This would have included the mutant forms
G250E, F317L, M351 T, and F486S-each of which is recited in claim 17.
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Insofar as Appellant argues the "implication" from Section 2.2.3 of
Manley is that bosutinib is "ineffective" against any mutant form beyond the
four listed in that section, we disagree. (App. Br. 4--5.) There is nothing to
suggest the listing in Section 2.2.3 represents a closed set, or that would
indicate bosutinib was tested against other mutations and did not work.
Section 2.2.3 instead reflects that bosutinib was at an earlier stage of clinical
testing compared to dasatinib. But we find nothing in that section- or
elsewhere in Manley- that would have discouraged the skilled artisan from
using bosutinib to treat other mutations as discussed above.
Appellant's argument that the Examiner misinterprets portions of
Section 2.2.1 also fails to persuade us the rejection is flawed. (Id. at 5
("Manley mere[ly] states [in Section 2.2.1] that F317V, T315A, T315I and
F317 are frequently-occurring in the limited universe of dasatinib-resistant
[not imatinib-resistant] patients.").) The Examiner cited four mutations in
Section 2.2.1 as examples only, and further pointed to Table 1 of Manley,
which discloses a more comprehensive listing of the "most prevalent
imatinib-resistant mutant forms" against which the Abl-Src inhibitor
dasatinib was shown to have effect. (Ans. 8; FF 3.) Appellant provides no
persuasive argument or evidence in response showing why the skilled artisan
would not predictably treat these mutant forms with another Abl-Src
inhibitor - bosutinib, as in claim 1 7.
Appellant's second and third arguments are also unpersuasive.
Contrary to Appellant's characterization of the rejection, the Examiner has
not advanced an "obvious to try" rationale. Rather, the Examiner reasons
that bosutinib would have been expected to exhibit similar activity and
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treatment against mutant forms of Bcr-Abl as compared to dasatinib. (Ans.
8.) Manley discloses a handful of promising Abl-Src inhibitors (including
bosutinib and dasatinib) and a finite number of the most prevalent mutant
forms. (FF 2-3.) Also, Manley teaches that bosutinib had shown effect in
preliminary testing against four of these mutations, and that dasatinib, which
Manley discloses was further along in clinical development (Manley
Abstract), had shown effect against almost all of the prevalent mutations (id.
at Table 1 ), including the same four identified with respect to testing of
bosutinib. Manley thus suggests a greater degree of predictability in treating
the commonly-occurring mutant forms with dual Abl-Src inhibitors than
Appellant's arguments suggest - even if the precise effect of bosutinib
against the mutations in claim 17 is not expressly stated in Manley. Pfizer,
Inc. v. Apotex, Inc., 480 F.3d 1348, 1364 (Fed. Cir. 2007) ("obviousness
cannot be avoided simply by a showing of some degree of unpredictability
in the art so long as there was a reasonable probability of success.")
Under these circumstances, we are not persuaded the Examiner erred
in concluding that claim 17 would have been obvious. Nor are we
persuaded the Examiner was required to provide even more detailed
evidence (such as analysis of the crystal structure data) to establish the prima
facie case. Manley's teachings and the Examiner's rationale are sufficient.
Conclusion of Law
We conclude that the Examiner established by a preponderance of the
evidence that claim 17 would have been obvious under 35 U.S.C. § 103(a)
over Manley.
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Claims 18-20, 23, and 24 have not been argued separately and
therefore fall with claim 17. 37 C.F.R. § 41.37(c)(l)(iv).
DISCUSSION - II
Issue
Has the Examiner established by a preponderance of the evidence that
claims 17-28 would have been obvious under 35 U.S.C. § 103(a) over
Boschelli and Shah?
Findings of Fact
FF 4. The Examiner's findings of fact and statement of the rejection
of claims 17-28 under 35 U.S.C. § 103(a) over Boschelli and Shah may be
found at pages 8-13 of the Final Action dated July 3, 2013. (See also Ans.
5-7 and 9-11.) We adopt those findings here unless otherwise stated, and
discuss below various material teachings of the prior art.
FF 5. Boschelli teaches "[i]nhibition of the tyrosine kinase activity of
Bcr-Abl is an effective strategy for targeting CML as demonstrated by the
clinical efficacy of STI-571 [imatinib/Gleevec]." (Boschelli i-f 3.) Boschelli
further teaches:
Although the selective Abl kinase inhibitor STI-571 is
efficacious and well tolerated by most patients in chronic-stage
CML, patients in accelerated and blast crises stages of the
disease tend to be less responsive. Consequently, there is a need
for alternative agents that are effective in late-stage disease.
(Id. at i-f 4.) Boschelli teaches that"[ o ]ther molecules, including Src family
kinases, play a role in downstream signaling from Bcr-Abl, and as such, are
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potential therapeutic targets for the treatment of STI-571-resistant disease."
(Id. at if 3.)
FF 5. Boschelli teaches compounds "for treating, preventing, or
inhibiting CML." (Id. at if 45.) In particular, Boschelli teaches the
compound with the chemical name 4-[(2,4-Dichloro-5-methoxy-
phenyl)amino ]-6-methoxy-7-[3-( 4-methyl-1-piperazinyl)propoxy ]-3-
quinolinecarbonitrile. (Id. at iii! 5, 13-14, 115.) This compound is also
known as SKI-606 or bosutinib. (Spec. if 9.) Boschelli discloses that
bosutinib exhibits dual Abl-Src inhibitory activity. (Boschelli iii! 86, 137-
139; claim 20.) Boschelli discloses that "[c]ompounds of formula I [e.g.,
bosutinib] ... originally identified as a Src inhibitor, are shown here to be a
potent antiproliferative and proapoptotic agent against CML cells in
culture." (Id. at if 139.) Boschelli teaches that bosutinib may be
administered alone or with Gleevec to treat CML. (Id. at claims 21-22.)
FF 6. Shah teaches that experimental results "establish the primary
role of BCR-ABL kinase domain mutations as the cause of imatinib
resistance in CML" and further that "[k ]inase domain mutations are detected
in 90% of CML patients who relapse after responding to imatinib." (Shah
118.) Shah identifies the mutations, including M244V, G250E, Y253F,
E255K, F317L, and M351 T, among others. (Id. at Figs. 1, 3, Tables 1, 2.)
Shah teaches that "E255K, in addition to the mutations T315I and M315T,
accounted for over 60% of the cases." (Id. at 118.) Shah further teaches:
[R ]ecent insights gained from structural analysis of ABL bound
to imatinib versus the dual ABL/SRC inhibitor indicate that two
different inhibitors can bind to the same kinase in different
conformational states. . . . If a significant number of the
mutations that cause imatinib resistance do so by preventing the
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kinase domain from achieving the closed conformation
necessary for imatinib binding ... one can envision that
inhibitors that bind ABL in the open configuration might retain
activity against many of these mutants. Indeed, we have
evidence that the E255K mutant remains sensitive to such a
dual ABL/SRC inhibitor.
(Id. at 123.)
Analysis
Appellant argues the patentability of claims 17-28 over Boschelli and
Shah as a group. (App. Br. 6-10.) We address claim 17 as representative.
The Examiner concludes that claim 17 would have been obvious over
Boschelli and Shah. The Examiner finds that Boschelli teaches that
bosutinib "play[s] a role in downstream signaling from Bcr-Abl, [and]
therefore [is] useful in the treatment of STI-571 resistant disease." (Ans. 7.)
The Examiner finds that Shah teaches that the majority of subjects with
CML relapse despite treatment with STI-571/imatinib, and that Shah
identifies the mutations in the Bcr-Abl protein responsible for imatinib-
resistance, including F317L, M351 T, M244V, and others that overlap with
the mutations recited in claim 17. (Id.) In further support, the Examiner
finds that both Boschelli and Shah teach or suggest treating imatinib-
resistant CML with Abl-Src kinase inhibitors. (Id. at 11.) Based on these
(and other) teachings of Boschelli and Shah, the Examiner concludes it
would have been obvious to treat the mutations identified in Shah (e.g.,
M351 T) with the second-generation dual Abl-Src inhibitor, bosutinib, as
disclosed in Boschelli - thus satisfying all the elements of claim 1 7.
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Appellant raises three arguments: (i) the Examiner's downstream
signaling argument is unsupported; (ii) use ofbosutinib to treat CML
associated with Shah-listed mutations is not suggested; and (iii) the prior art
teaches away from the proposed combination of Boschelli and Shah. These
arguments are unpersuasive for the reasons discussed below.
Appellant argues that "Boschelli does not teach or suggest that
bosutinib would, or even could, affect signaling downstream from Ber/ Abl."
(App. Br. 7.) According to Appellant, when Boschelli teaches that "other
molecules, including Srcfamily kinases, play a role in downstream signaling
from Bcr-Abl," Boschelli is "referring to other biological proteins, and not to
specific drug compounds that might inhibit activity of such proteins." (Id.)
We are, however, not persuaded. Appellant's argument does not
adequately consider Boschelli's teachings in full context. Boschelli
discusses development of imatinib resistance in late-stage CML subjects.
(Boschelli i-fi-12, 3.) There it expressly discloses Src family kinases play a
role in downstream signaling from Bcr-Abl, and identifies these molecules
as "potential therapeutic targets for the treatment of S TI-5 71-resistant
diseases." (FF 4.) Boschelli states that there "is a need for alternative
agents [to STI-571] that are effective in late-stage disease" (Boschelli i14),
and then immediately introduces its inventive compounds, including the dual
Abl-Src inhibitor bosutinib (id. at i-fi-15, 13, 14). Later, Boschelli expressly
teaches that bosutinib "inhibit[s] src kinase in vitro." (Id. at i-fi-186, 138.)
And Boschelli discloses that bosutinib showed anti-proliferative activity
against Ahl-dependent CML cells. (Id. at i-fi-f 112, 115, 137-139.) We thus
find that Boschelli teaches, or at least reasonably implies, that bosutinib
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inhibits downstream signaling proteins from Bcr-Abl, and that the skilled
artisan would have understood that bosutinib was designed to provide
effective treatment of CML in imatinib-resistant subjects.
Appellant's second argument fails as well. Appellant argues
Boschelli and Shah individually, which does not persuasively show that
claim 17 is nonobvious. In re Merck & Co., 800 F.2d 1091, 1097 (Fed. Cir.
1986) ("Non-obviousness cannot be established by attacking references
individually where the rejection is based upon the teachings of a
combination of references. . . . [The reference] must be read, not in
isolation, but for what it fairly teaches in combination with the prior art as a
whole.") For example, Appellant argues that "Shah mentions specific
mutations ... but does not suggest using bosutinib, or any other specific
compound, to address imatinib resistance." (App. Br. 7.) True, Shah does
not name bosutinib as a treatment for imatinib-resistant CML. That teaching
is supplied in Boschelli. (FF 4--5.) Also, Appellant's contention that Shah
does not suggest using any other compound to address imatinib-resistance is
incorrect. To the contrary, Shah suggests treatment with second generation
dual Abl-Src inhibitors may be beneficial, and cites to early testing against at
least one of the mutations in support. (FF 6.) One such dual Abl-Src
inhibitor is bosutinib, as disclosed in Boschelli. (FF 4--5.) The Examiner's
rejection is based on the combination of Boschelli and Shah. And the
Examiner's reasoning, which draws on the teachings of Boschelli and Shah
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discussed above, is sufficient to establish a prima face case that claim 17
would have been obvious. 5
Appellant's final argument is that Puttini6 and Shah teach away from
the use ofbosutinib to treat the mutations recited in claim 17. (App. Br. 8-
9.) According to Appellant, Puttini shows that "mutants can confer imatinib
resistance in a multitude of different ways" and that for the point mutants
T315I and E255K, Puttini showed that bosutinib was "ineffective" or "only
partially effective." (Id. at 8.)
We are unpersuaded. As the Examiner correctly points out, "the
mutant, T315I, that was claimed to be ineffective for bosutinib [in Puttini], is
not even claimed [by applicant]." (Ans. 10.)7 Moreover, as other references
of record show, T315I appears to be an outlier among the mutations, and has
proven difficult to treat with a variety of drugs. (See, e.g., Manley, Table 1;
p. 10 ("Although clinical candidates which address the currently intractable
T315I mutant have not yet been identified, such drugs are likely to be
discovered in the near future.").) Also, Puttini's other teachings do not help
Appellant. Quite the opposite, they reinforce the obviousness of claim 17.
5 For similar reasons, we disagree with Appellant's contention that the
Examiner is invoking an improper "obvious to try" rationale. (App. Br. 7-
8.) The express disclosures of Boschelli and Shah would have reasonably
led to the Examiner's proposed combination.
6 Puttini et al., In vitro and In vivo Activity of SKI-606, a Novel Src-Abl
inhibitor against Imatinib-Resistant Ber-Ahl+ Neoplastic Cells, 66, no. 23
CANCER RES. 11314--11322 (2006) ("Puttini").
7 We agree with Appellant that Puttini may be considered for its evidentiary
value (e.g., whether it "teaches away") even if Puttini "was not a reference
used in the instant rejections." (App. Br. 8, n. 2.)
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Indeed, for three of the four mutants forms tested (all but T315I), Puttini
teaches that bosutinib "induced a statistically significant decrease in the rate
of tumor growth and prolonged event-free survival." (Puttini 11319; see
also id. at Figure 5 incl. caption.) One of those mutant forms is Y253F- a
mutation recited in claim 17. (Id.) On balance, Puttini teaches towards the
subject matter of claim 17, not away from it.
We are likewise unpersuaded that Shah teaches away from the
Examiner's proposed combination. Appellant cites a statement in Shah that
it is "difficult to envision a single second generation ABL kinase inhibitor
that would have activity against all mutants." (App. Br. 9 (quoting Shah
123).) Appellant argues that this statement (and another) in Shah "suggest[]
that alternate kinase inhibitors like bosutinib may not be the best way to treat
imatinib-resistance, and that other approaches [e.g., Hsp90 inhibitors] may
be more productive." (App. Br. 9.) But Appellant misapprehends what it
means to teach away. "The prior art's mere disclosure of more than one
alternative does not constitute a teaching away from ... alternatives because
such disclosure does not criticize, discredit, or otherwise discourage the
solution claimed." In re Fulton, 391F.3d1195, 1200-1201 (Fed. Cir.
2004). ("[T]he question is whether there is something in the prior art as a
whole to suggest the desirability, and thus the obviousness, of making the
combination, not whether there is something in the prior art as a whole to
suggest that the combination is the most desirable combination available.")
(Citation omitted). The portions of Shah cited by Appellant, at most,
suggest that alternative approaches to treating imatinib resistance should be
pursued. They do not rise to the level of a teaching away.
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Conclusion of Law
We conclude that the Examiner established by a preponderance of the
evidence that claim 17 would have been obvious under 35 U.S.C. § 103(a)
over Boschelli and Shah.
Claims 18-28 have not been argued separately and therefore fall with
claim 17. 37 C.F.R. § 41.37(c)(l)(iv).
SUMMARY
We affirm the rejection of claims 17-20, 23, and 24 under 35 U.S.C.
§ 103(a) over Manley.
We affirm the rejections of claims 17-28 under 35 U.S.C. § 103(a)
over Boschelli and Shah.
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
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