Ex Parte Kwong

Patent Trials and Appeals Board

Jun 25, 2019

11871057 - (D) (P.T.A.B. Jun. 25, 2019)

UNITED STA TES p A TENT AND TRADEMARK OFFICE
APPLICATION NO. FILING DATE
11/871,057 10/11/2007
23579 7590 06/25/2019
Pabst Patent Group LLP
1545 PEACHTREE STREET NE
SUITE 320
ATLANTA, GA 30309
FIRST NAMED INVENTOR
Yok-LamKwong
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.
UHK00230 6065
EXAMINER
CHOI, FRANK I
ART UNIT PAPER NUMBER
1616
MAIL DATE DELIVERY MODE
06/25/2019 PAPER
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.
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte YOK-LAM KWONG
Appeal2018-001094
Application 11/871,057 1
Technology Center 1600
Before DONALD E. ADAMS, ERIC B. GRIMES, and
FRANCISCO C. PRATS, Administrative Patent Judges.
ADAMS, Administrative Patent Judge.
DECISION ON APPEAL
This Appeal2 under 35 U.S.C. § 134(a) involves claims 1, 3, 5, 7, and
11-13 (App. Br. 3). Examiner entered a rejection under 35 U.S.C. § 103(a).
We have jurisdiction under 35 U.S.C. § 6(b).
We AFFIRM.
1 Appellant identifies "The University of Hong Kong" as the real party in
interest (Appellant's May 1, 2017 Appeal Brief (App. Br.) 2).
2 This Appeal is related to Appeal 2012-005618 (Application 11/871,068),
Decision on Appeal reversing the rejections of record entered May 12, 2014
and Appeal 2012-008942 (Application 11/549,347), Decision on Appeal
affirming the rejection of record entered May 9, 2014.
Appeal2018-001094
Application 11/871,057
STATEMENT OF THE CASE
Appellant's disclosure "relates to methods of inhibiting certain
cancers by affecting expression, translation, and biological activity of
cancers expressing receptor tyrosine kinases using arsenic trioxide" (Spec.
1:8-10). Appellant's claims 1, 3, and 11 are representative and reproduced
below:
1. A method for promoting cytokine receptor or receptor
tyrosine kinase degradation in cancer cells comprising
orally administering to a patient with epidermal growth
factor or cytokine dependent cancer cells that have been tested
for dependency on tyrosine kinase receptors for signaling,
proliferation, survival, metastasis and differentiation, wherein
the cancer cells are not head and neck squamous cell
carcinoma, acute promyelocytic leukemia, and multiple
myeloma,
an amount of arsenic trioxide in a pharmaceutically
acceptable carrier for enteral administration which is effective
to inhibit proliferation of the cancer cells.
(App. Br. 26.)
(Id.)
(Id.)
3. The method of claim 1, wherein the cancer is an epithelial
growth factor receptor dependent cancer.
11. The method of claim 1 wherein the arsenic trioxide is
present in an amount from 5 to 10 mg.
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Claims 1, 3, 5, 7, and 11-13 stand rejected under 35 U.S.C. § 103(a)
as unpatentable over the combination of Warrell, 3 Kwong, 4 Rojewski, 5
Appellant's Admission, Cui, 6 Soresi, 7 and Cheung. 8
ISSUE
Does the preponderance of evidence relied upon by Examiner support
a conclusion of obviousness?
FACTUAL FINDINGS (FF)
FF 1. We adopt Examiner's findings concerning the scope and content of
the prior art (Final Act. 9 2---6), and provide the following findings for
emphasis.
3 Warrell, Jr. et al., US 6,723,351 B2, issued Apr. 20, 2004.
4 Yok-Lam Kwong, Arsenic trioxide in the treatment of haematological
malignancies, 3 EXPERT OPIN. DRUG SAF. 589-597 (2004).
5 Rojewski et al., Dual effects of arsenic trioxide (As203) on non-acute
promyelocytic leukaemia myeloid cell lines: induction of apoptosis and
inhibition of proliferation, 116 BRITISH JOURNAL OF HAEMATOLOGY 555-
563 (2002).
6 Cui et al., Effects of Arsenic Trioxide on the Expression of Gene Protein
Related to Vascular Endothelium Induced by Liver Cancer, SmnE HUAREN
XIAOHUAZAZHI (2005) (as translated in PT02010-4450 (July 9, 2010)).
7 Soresi et al., Interleukin-6 and its soluble receptor in patients with liver
cirrhosis and hepatocellular carcinoma, 12 WORLD J. GASTROENTEROLOGY
2563-2568 (2006).
8 Cheung et al., Arsenic Trioxide Targets the Interleukin-6 Cascade in
Multiple Myeloma by Promoting Lysosomal Degradation of the Interleukin-
6 Receptor Complex, 106 BLOOD, Abstract 5159 (2005).
9 Examiner's November 1, 2016 Final Office Action.
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FF 2. Warrell "relates to methods and compositions for the treatment of
leukemia, lymphoma, and certain other cancers" (Warrell 1: 12-14; see
generally Final Act. 3).
FF 3. Warrell
provides a method for treatment of solid tumors, including
metastasises [sic], in humans comprising the administration of a
therapeutically effective and non-lethal amount of arsenic
trioxide ... to the human. Solid tumors that can be treated by
the methods of [Warrell' s] invention include but are not limited
to: cancer of the digestive tract, oesophagus, liver, stomach, and
colon; skin; brain; bone; breast; lung; and soft tissues, including
but not limited to various sarcomas, and preferably prostate
cancer.
(Warrell 6: 58---67; see id. at 4: 41--42 (Warrell's use of the term "'arsenic
compound' refers to a pharmaceutically acceptable form of arsenic trioxide
(As203)"); see Final Act. 3.)
FF 4. Warrell's disclosure "encompasses a composition suitable for oral
delivery; comprising arsenic trioxide ... and a pharmaceutically acceptable
excipient or carrier" (Warrell 4: 7-10; see also id. at 5: 18-22 (describing
oral administration as a suitable mode of administering Warrell' s arsenic
compound); id. at 9: 20--44 (describing oral formulations ofWarrell's
arsenic compound); id. at 11: 3-52 (describing oral administration of
Warrell's arsenic compound, including, inter alia, powder, capsule, and
tablet formulations); see Final Act. 3).
FF 5. Warrell discloses, "[i]n general, the daily dose ranges of arsenic
trioxide for the conditions described [by Warrell] are generally from about
0.05 to about 5 mg per kg body weight administered in divided doses
administered parenterally or orally or topically," wherein "[a] preferred total
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daily dose is from about 2.5 to about 40 mg of arsenic trioxide" (Warrell 10:
25-31; see Final Act. 3).
FF 6. Kwong discloses that a standard oral dose of arsenic trioxide is 10
mg/day, wherein, "current practice is to use half the standard dose (5
mg/day) for patients with impaired renal function," because "[r]enal
excretion is a major route of elimination of arsenic" and "[i]n patients with
impaired renal function, the dose of arsenic trioxide should be adjusted"
(Kwong 593; see Final Act. 3; Ans. 10 6; cf Spec. 15: 3-5 (Appellant
discloses that the "dose of oral As203 is typically adjusted according to age
and kidney function. In one embodiment, the dose range of As203 varies
from 1 to 10 mg, typically about 5 to 10 mg")).
FF 7. Kwong discloses that although arsenic trioxide "is a well-known
poison ... at therapeutic doses, arsenic trioxide has much fewer side effects .
. . than standard chemotherapy" (Kwong 591; see id. at 591-593; see Final
Act. 3).
FF 8. Kwong discloses "that oral arsenic trioxide is comparable with
intravenous arsenic trioxide in its clinical profile and efficacy" (Kwong 591;
see Final Act. 3).
FF 9. Cui discloses that
As203 has an inhibiting effect on the EGFR expression in
liver cancer cells. EGFR plays an important part in the process
of the emergence and development of human liver cancer. ...
[B]y regulating down the expression of EGFR protein in liver
cancer cells, As203 injections may affect the EGFR mediated
signal transduction paths, thereby inhibiting the proliferation
and migration of the tumor, inhibiting the formation of newly
10 Examiner's September 11, 2017 Answer.
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generated vessels in the tumor, and achieving the goal of curing
the tumor and preventing it from metastasizing and recurring.
Since there is a relatedness among the expressions of EGFR
and its ligands those of E-CD, integrin and other factors, as
soon as a change occurs in the expression of a certain factor, or
a common change in their interaction, this can have a major
impact on the emergence, development, and metastasizing of
tumors. The results of [Cui's] study have demonstrated that
As203 injections have a certain regulating effect on the
expression of all of these factors; however, it remains to be
studied how they are interrelated.
(Cui § 3.4 ( endnotes and emphasis omitted); see Final Act. 4 ( citing Spec. 1:
12-14; 2: 1-2, and 3: 1-2) (the "epidermal growth factor receptor (EGFR) is
[a] tyrosine kinase receptor"); Ans. 7-9.)
FF 10. Warrell discloses:
It should be noted that the attending physician would know how
to and when to terminate, interrupt or adjust therapy to lower
dosage due to toxicity, or bone marrow, liver or kidney
dysfunctions. Conversely, the attending physician would also
know how to and when to adjust treatment to higher levels if
the clinical response is not adequate (precluding toxic side
effects).
(Warrell 10: 63 - 11: 2; see Final Act. 3.)
FF 11. Kwong discloses that, because "oral arsenic trioxide achieves a
lower peak plasma arsenic level, the prolongation of QT interval, which
depends on the plasma arsenic, might be expected to be less serious. This
has in fact been found when oral arsenic trioxide is used clinically" (Kwong
592; see Final Act. 3; Ans. 6).
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ANALYSIS
The combination of prior art relied upon by Examiner makes obvious
a method of treating, inter alia, liver cancer, in a human, by orally
administering "a therapeutically effective and non-lethal amount of arsenic
trioxide ... to the human" (FF 1--4). The evidence of record establishes that
liver cancer is an EGFR dependent cancer, wherein arsenic trioxide
injections have a regulating effect on "EGFR mediated signal transduction
paths, thereby inhibiting the proliferation and migration of the tumor,
inhibiting the formation of newly generated vessels in the tumor, and,"
thereby resulting in "achieving the goal of curing the tumor and preventing it
from metastasizing and recurring" (FF 9).
With regard to arsenic trioxide injections, the evidence of record
establishes "that oral arsenic trioxide is comparable with intravenous arsenic
trioxide in its clinical profile and efficacy" (FF 8). In this regard, the
evidence of record establishes that although arsenic trioxide "is a well-
known poison ... at therapeutic doses, arsenic trioxide has much fewer side
effects ... than standard chemotherapy" (FF 7).
In addition, the combination of prior art relied upon by Examiner
suggests that a therapeutically effective and non-lethal amount of arsenic
trioxide for oral administration to a human for the treatment of, inter alia,
liver cancer is "generally from about 0.05 to about 5 mg per kg body weight
administered in divided doses administered parenterally or orally or
topically" and, more specifically, the oral administration of arsenic trioxide
at a dose of 10 mg/day to patients without impaired renal function (FF 5---6).
Thus, we find no error in Examiner's conclusion that the combination
of Warrell, Kwong, Rojewski, Appellant's Admission, Cui, Soresi, and
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Cheung, make obvious Appellant's claimed invention (see Final Act. 6; FF
1-9).
Claim 1:
Initially, we note that argument by counsel cannot take the place of
evidence. In re Cole, 326 F.2d 769, 773 (CCPA 1964). Therefore, we are
not persuaded by counsel's unsupported assertions (see generally App. Br.
7-9).
We recognize Appellant's contention that "Appellant discovered that
arsenic trioxide suppresses cancer cell growth by targeting receptor tyrosine
kinases and cytokine receptors for degradation" and "that oral administration
of arsenic trioxide [was] effective in treating cancer characterized by their
dependency on tyrosine kinase receptors for signaling, proliferation,
survival, metastasis and differentiation" (App. Br. 12; see id. (Appellant
discloses that "the common mechanism linking the activity of arsenic
trioxide in different cell types was not known prior to Appellant's filing,
showing that this had been determined by extensive experimentation"); see
Reply Br. 2-3; cf FF 1-9)). It is, however, "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." In re Swinehart, 439 F.2d 210, 212-13
(CCPA 1971); Atlas Powder Co. v. Ireco Inc., 190 F.3d 1342, 1347 (Fed.
Cir. 1999) ("[T]he discovery of a previously unappreciated property of a
prior art composition, or of a scientific explanation for the prior art's
functioning, does not render the old composition patentably new to the
discoverer.").
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A reference disclosure is not limited only to its preferred
embodiments, but is available for all that it discloses and suggests to one of
ordinary skill in the art. In re Lamberti, 545 F.2d 747, 750 (CCPA 1976);
see also In re Susi, 440 F.2d 442,446 n.3 (CCPA 1971) (disclosed examples
and preferred embodiments do not constitute a teaching away from a broader
disclosure or non-preferred embodiments). Therefore, we are not persuaded
by Appellant's contention that despite Warrell's extensive disclosure of oral
arsenic trioxide formulations for use in the treatment of cancer, including
liver cancer, a "person of ordinary skill in the art reading the disclosure of
Warrell would not have reasonably expected an oral formulation to be both
safe and effective for treating solid tumors" (see App. Br. 9; see also id. at
17 (Appellant contends that "even though Warrell states that arsenic trioxide
can be administered orally, this statement is not supported by the
examples."); Reply Br. 4; cf FF 5). Appellant's contention also fails to
account for Kwong's disclosure of the oral administration of arsenic trioxide
for the treatment of cancer (FF 6).
Notwithstanding Appellant's unsupported assertion that "arsenic
trioxide has been administered systemically (i.v.) to treat cancer, but with
such debilitating side effects that it was a drug of last resort," the evidence
on this record makes clear that although arsenic trioxide "is a well-known
poison," the administration of arsenic trioxide "at therapeutic doses ... has
much fewer side effects ... than standard chemotherapy" and "that oral
arsenic trioxide is comparable with intravenous arsenic trioxide in its clinical
profile and efficacy" (see App. Br. 7; see also id. at 9-10 and 12; Reply Br.
3--4; cf FF 7-8). For the same reasons we are not persuaded by Appellant's
contention that the combination of Warrell, Kwong, Rojewski, Appellant's
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Admission, Cui, Soresi, and Cheung does not make obvious the oral
administration of arsenic trioxide for the treatment of cancer (see FF 1-10;
cf App. Br. 16-17).
The evidence of record establishes that liver cancer is an EGFR
dependent cancer, wherein arsenic trioxide injections have a regulating
effect on "EGFR mediated signal transduction paths, thereby inhibiting the
proliferation and migration of the tumor, inhibiting the formation of newly
generated vessels in the tumor, and," thereby result in "achieving the goal of
curing the tumor and preventing it from metastasizing and recurring" (FF 9).
Appellant does not dispute that EGFR is a tyrosine kinase receptor (see FF
11-12; cf FF 9). For the reasons set forth above, we are not persuaded by
Appellant's contention that "[n]one of the cited art leads one to arsenic
trioxide for the selective killing of cells expressing tyrosine kinases
associated with cancer cells" (App. Br. 14 (emphasis omitted); see also id. at
18; Reply Br. 7-9; cf FF 1-10). Therefore, we are not persuaded by
Appellant's unsupported assertion that:
[S]afe and effective use of an oral formulation of arsenic
trioxide in treating epidermal growth factor ... dependent
cancer cells that have been tested for dependency on tyrosine
kinase receptors for signaling, proliferation, survival, metastasis
and differentiation, wherein the cancer cells are not head and
neck squamous cell carcinoma, acute promyelocytic leukemia,
and multiple myeloma ... is unexpected.
(App. Br. 9-10; see also id. at 16-17; cf FF 1-9.) For the reasons set for the
above, we are not persuaded by Appellant's contention that:
Without Appellant's teaching of the route of administration,
and the common mechanism linking the activity of arsenic
trioxide in different cell types, it would not have been
predictable to one of ordinary skill in the art at the time the
application was filed, based on the prior art, that arsenic
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trioxide could be administered orally, to produce a level that
would be effective to treat cancers in patients, wherein the
cancer cells are dependent on receptor tyrosine kinases and/ or
cytokine receptors for signaling, proliferation, survival,
metastasis and differentiation, and wherein the cancer cells are
not head and neck squamous cell carcinoma, acute
promyelocytic leukemia, and multiple myeloma.
(App. Br. 13.)
Warrell "provides a method for treatment of solid tumors, including
[hematological and non-hematological malignancies] ... , in humans
comprising the administration of a therapeutically effective and non-lethal
amount of arsenic trioxide ... to the human" (see FF 3). Warrell discloses,
"[i]n general, the daily dose ranges of arsenic trioxide for the conditions
described [by Warrell] are generally from about 0.05 to about 5 mg per kg
body weight administered in divided doses administered parenterally or
orally or topically," wherein "[a] preferred total daily dose is from about 2.5
to about 40 mg of arsenic trioxide" (FF 5). In this regard, we note that
Kwong discloses that a standard oral dose of arsenic trioxide is 10 mg/ day
(FF 6). Therefore, we are not persuaded by Appellant's contention that
Kwong's disclosure of the treatment of hematological malignancies is
unrelated and fails to support Warrell' s disclosure of the treatment of
hematological and non-hematological malignancies, which include those,
such as liver cancer, that are epidermal growth factor dependent, by orally
administering arsenic trioxide at dosages that encompass Kwong's standard
oral arsenic trioxide dosage (see App. Br. 10; see also id. at 13 (Appellant
contends that "[p]rior to Appellant's discovery, it was not known that
arsenic trioxide targets receptor tyrosine kinases and cytokine receptors in
non-hematological cancer cells, or that an oral dose would be effective to
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treat these non-hematological cancer cells"); Reply Br. 4--7; cf FF 5---6; see
generally FF 1-9). For the foregoing reasons, we are not persuaded by
Appellant's contentions relating to arsenic toxicity (App. Br. 14 (citing
ATSDR Guide 11 and Ratnaike 12); see also App. Br. 15 and 19; cf FF IO
(Warrell discloses that those of ordinary skill in this art understand how to
minimize toxic side effects)).
As discussed above, Warrell in combination with Kwong, Rojewski,
Appellant's Admission, Cui, Soresi, and Cheung "provides a method for
treatment of solid tumors, including [hematological and non-hematological
malignancies, such as liver cancer] ... , in humans comprising the [oral]
administration of a therapeutically effective and non-lethal amount of
arsenic trioxide ... to the human" (see FF 3). The evidence of record also
supports a conclusion that liver cancer is an EGFR dependent cancer,
wherein arsenic trioxide injections have a regulating effect on "EGFR
mediated signal transduction paths, thereby inhibiting the proliferation and
migration of the tumor, inhibiting the formation of newly generated vessels
in the tumor, and," thereby result in "achieving the goal of curing the tumor
and preventing it from metastasizing and recurring" (FF 9). Therefore, we
are not persuaded by Appellant's contentions relating to whether "tyrosine
11 Medical Management Guidelines for Arsenic Trioxide (As203), in Agency
for Toxic Substances & Disease Registry, CAS#: 1327-53-3, UN#: 1561
(2014), available at
https://www.atsdr.cdc.gov/MMG/MMG.asp?id=1200&tid=279.
12 Ratnaike, Acute and chronic arsenic toxicity, 79 POSTGRAD MED. J. 391---6
(2003).
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receptors were found in significantly different levels and types depending on
the type of cancer" (App. Br. 19 (citing Miiller-Tidow 13 and Johnson 14)).
Warrell discloses that those of ordinary skill in the art understand how
to minimize the toxic side effects associated with oral arsenic trioxide
administration (FF 10). Nevertheless, Appellant contends that its claimed
invention is not prima facie obvious over the combination of Warrell,
Kwong, Rojewski, Appellant's Admission, Cui, Soresi, and Cheung,
because Weingart 15 suggests that practitioners may not orally administer
chemotherapeutic drugs in a safe and effective manner (see App. Br. 15-16
("Weingart states that safeguards in routine use for infusion chemotherapy
have not been adopted for oral chemotherapy")). Because Examiner
established an evidentiary basis on this record to support a conclusion of
obviousness, we are not persuaded by Appellant's contentions regarding
safety.
The use of drugs in medicine is frequently a matter of balancing
risks to save a life.
And Congress has given the responsibility to the FDA,
not to the Patent Office, to determine in the first instance
whether drugs are sufficiently safe for use that they can be
introduced in the commercial market, under the conditions
13 Miiller-Tidow et al., High-Throughput Analysis of Genome-Wide Receptor
Tyrosine Kinase Expression in Human Cancers Identifies Potential Novel
Drug Targets, 10 CLINICAL CANCER RESEARCH 1241-1249 (2004).
14 Johnson, Screening Methods in Antineoplastic Drug Discovery, 82
JOURNAL OF THE NATIONAL CANCER INSTITUTE 1082-1083 (1990).
15 Weingart et al., Oral chemotherapy safety practices at US cancer centres:
questionnaire survey, BMJ, doi: 10.1136/bmj.39069.489757.55 (published
12 January 2007).
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prescribed, recommended, or suggested in the proposed
labeling thereof ....
In re Anthony, 414 F.2d 1383, 1395 (CCPA 1969).
For the foregoing reasons, we are not persuaded by Appellant's
contentions regarding each ofRojewski, Cui, Soresi, Cheung, and Kwong
individually, which fail to account for the combined disclosures of Warrell,
Kwong, Rojewski, Appellant's Admission, Cui, Soresi, and Cheung (see
App. Br. 20; see also Reply Br. 5---6 and 9-10; cf FF 1-10). See 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."); see also Ans. 5 (citing In re Keller, 642 F.2d 413,
425 (CCPA 1981)).
Unexpected Results:
We are not persuaded by Appellant's contention that "[i]t was not
known prior to Appellant's experimental results that orally administered
arsenic trioxide is effective and significantly safer than intravenously
administered arsenic trioxide" (App. Br. 18 (citing Siu 16); cf FF 7-8 and 11;
Ans. 10).
Warrell "provides a method for treatment of solid tumors, including
metastasises [sic], in humans comprising the [oral] administration of a
therapeutically effective and non-lethal amount of arsenic trioxide ... to the
16 Siu et al., Effects of oral arsenic trioxide therapy on QT intervals in
patients with acute promyelocytic leukemia: implications for long-term
cardiac safety, 108 BLOOD 103-106 (2006).
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human" (FF 3). Kwong, as Appellant recognizes, also discloses the oral
administration of arsenic trioxide for the treatment of cancer (see App. Br.
19 (Appellant expressly states that "Kwong describes oral administration of
arsenic trioxide to treat leukemias"); see also id. at 10). Therefore, we are
not persuaded by Appellant's contention that "Appellant was the first to
develop an oral formulation of arsenic trioxide and demonstrate efficacy of
systemic cancer treatment with this formulation" (App. Br. 21; cf FF 1-5).
Thus, Appellant failed to establish an evidentiary basis on this record to
support Appellant's contention that those in the art tried and failed to solve
the problem addressed by Appellant.
For the reasons discussed above, Warrell and Kwong alone or in
combination support a conclusion that the oral administration of arsenic
trioxide for the treatment of cancer was well-known in this art prior to the
date of Appellant's claimed invention (see FF 1-8; see also App. Br. 19
(Appellant expressly states that "Kwong describes oral administration of
arsenic trioxide to treat leukemias")). In addition, Kwong discloses that
"at therapeutic doses, arsenic trioxide has much fewer side effects ... than
standard chemotherapy" (FF 7). Therefore, we are not persuaded by
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Appellant's contention regarding a long-felt but unmet need in this art (see
App. Br. 21-22 (citing Au 2011, 17 Au 2012, 18 and Gill 19; cf Ans. 10).
For the reasons discussed above, we are not persuaded by Appellant's
contention that "[ s ]ince publication of the data described in this application
and that which it claims priority to, the oral route has become a route of
choice for administration of arsenic trioxide, precisely because it's safer and
more efficacious in contrast to intravenous administration" (App. Br. 22; cf
FF 1-8; see also App. Br. 19 (Appellant expressly states that "Kwong
describes oral administration of arsenic trioxide to treat leukemias" prior to
the date of Appellant's claimed invention); Ans. 11).
For the foregoing reasons, we are not persuaded by Appellant's
contention that Examiner's conclusion of obviousness is based on improper
hindsight reasoning (see App. Br. 22; see also Reply Br. 10-11; cf Ans. 11-
12).
Claim 3:
Warrell discloses the oral administration of arsenic trioxide for the
treatment of cancer, including liver cancer (FF 3). In addition, the evidence
of record establishes that liver cancer is an EGFR dependent cancer, wherein
17 Au et al., Oral arsenic trioxide-based maintenance regimens for first
complete remission of acute promyelocytic leukemia: a 10-year follow-up
study, 118 BLOOD 6535-6543 (2011).
18 Au et al., Oral Arsenic Trioxide for relapsed Acute Promyelocytic
Leukemia in Pediatric Patients, 58 PEDIATR BLOOD CANCER 630-632
(2012).
19 Gill et al., Oral arsenic trioxide-based regimen as salvage treatment for
relapsed or refractory mantle cell lymphoma, 25 ANN ONCOL 1391-1397
(2014).
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arsenic trioxide injections have a regulating effect on "EGFR mediated
signal transduction paths, thereby inhibiting the proliferation and migration
of the tumor, inhibiting the formation of newly generated vessels in the
tumor, and," thereby result in "achieving the goal of curing the tumor and
preventing it from metastasizing and recurring" (FF 9).
Therefore, for the reasons set forth above, we are not persuaded by
Appellant's contention that the evidence of record fails to suggest an EGFR
dependent cancer and "[t]here is no reason why one of ordinary skill in the
art would expect success in using an orally administered dose of arsenic
trioxide to treat cancers that is an epithelial growth factor receptor dependent
cancer" (see App. Br. 23; see also Reply Br. 12-13; cf FF 1-11).
Claim 11:
For the reasons set forth above, we are not persuaded by Appellant's
contentions that "none of the cited references disclose or suggest that 5 to 10
mg of arsenic trioxide administered orally would be effective for treating a
patient with epidermal growth factor ... dependent cancer cells" and
"[t]here is no reason why one of ordinary skill in the art would expect
success in using an orally administered dose of arsenic trioxide at 5 to 10 mg
to treat cancer" (see App. Br. 23-24; see also Reply Br. 13; cf FF 1-11).
CONCLUSION
The preponderance of evidence relied upon by Examiner supports a
conclusion of obviousness.
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The rejection of claims 1, 3, and 11 under 35 U.S.C. § 103(a) as
unpatentable over the combination of Warrell, Kwong, Rojewski,
Appellant's Admission, Cui, Soresi, and Cheung is affirmed.
Appellant provides the following claim groupings: (a) claims 1 and 12; (b)
claims 3, 5, and 7; and (c) claims 11 and 13 (App. Br. 5; see also Reply Br.
2). Therefore, Appellant's claims 5, 7, 12, and 13, fall with Appellant's
claims 1, 3, and 11, respectively.
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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