Ex Parte Kang et al

Patent Trial and Appeal Board

Jul 5, 2016

12698732 (P.T.A.B. Jul. 5, 2016)

UNITED STA TES p A TENT AND TRADEMARK OFFICE
APPLICATION NO. FILING DATE
12/698,732 02/02/2010
38473 7590 07/07/2016
ELMORE PATENT LAW GROUP, PC
484 Groton Road
Westford, MA 01886
FIRST NAMED INVENTOR
Hyun Kang
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.
4043.3000 US2 4583
EXAMINER
ALLEN, MARIANNE P
ART UNIT PAPER NUMBER
1647
NOTIFICATION DATE DELIVERY MODE
07/07/2016 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):
docketing@elmorepatents.com
pair_elmore@firsttofile.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte HYUN KANG, SCOTT SACANE,
JONATHAN L. MOON, ERICA B. GOODHEW, LOPA BHATT,
STACEY L. ROSE, and MILTON H. WERNER
Appeal2013-008803
Application 12/698,732
Technology Center 1600
Before DONALD E. ADAMS, ERIC B. GRIMES, and
ROBERT A. POLLOCK, Administrative Patent Judges.
ADAMS, Administrative Patent Judge.
DECISION ON APPEAL 1
This appeal under 35 U.S.C. § 134(a) involves claims 1, 24, 26, 27,
32, and 33 (App. Br. 2). 2 Examiner entered rejections under 35 U.S.C.
§ 112, second paragraph, the enablement provision of 35 U.S.C. § 112, first
paragraph, and 35 U.S.C. § 102(e). We have jurisdiction under 35 U.S.C.
§ 6(b ).
We AFFIRM-IN-PART.
1 Appellants identify the Real Party in Interest as Celtaxsys, Inc. (App. Br.
1.)
2 Pending "[ c ]laim 31 is objected to as being dependent upon a rejected base
claim, but would be allowable if rewritten in independent form including all
of the limitations of the base claim and any intervening claims" (Ans. 3).
Appeal2013-008803
Application 12/698,732
STATEMENT OF THE CASE
Claims 1 and 24 are representative and reproduced below:
1. A method of inducing negative chemotaxis in human neutrophils
comprising contacting said human neutrophils with a chemorepellent in an
amount sufficient to induce negative chemotaxis along a concentration
gradient wherein the chemorepellent is galectin-1 or galectin-3 and wherein
negative chemotaxis is induced.
24. A method of ameliorating an inflammatory response in a human
subject comprising:
administering a chemorepellent to a site of inflammation in said
subject, wherein said chemorepellent is administered in an amount effective
to induce negative chemotaxis of at least a portion of a population of
neutrophils from the site of inflammation, wherein the chemorepellent is
galectin-1 or galectin-3.
Claim 33 stands rejected under 35 U.S.C. § 112, second paragraph as
indefinite in the recitation of the phrase "tissue-injury induced inflammation,
crystal-induced inflammation, and immune-complex induced inflammation"
(i\.ns. 12).
Claims 1, 24, 26, 27, 32, and 33 stand rejected under the enablement
provision of 35 U.S.C. § 112, first paragraph.
Claims 1, 24, 26, 32, and 33 stand rejected under 35 U.S.C. § 102(e)
as anticipated by Groen. 3
Claims 1, 24, 27, 32, and 33 stand rejected under 35 U.S.C. § 102(e)
as anticipated by Liu. 4
3 Groen et al., US 7,919,097 B2, issued Apr. 5, 2011.
4 Liu et al., US 7,186,681 B2, issued Mar. 6, 2007.
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Definiteness:
ISSUE
Does the preponderance of evidence support Examiner's conclusion
that the phrase "tissue-injury induced inflammation, crystal-induced
inflammation, and immune-complex induced inflammation," as set forth in
Appellants' claim 33, is indefinite?
FACTUAL FINDINGS (FF)
FF 1. Examiner finds that Appellants' "[S]pecification does not provide a
limiting definition for [tissue-induced inflammation, crystal-induced
inflammation, and immune-complex induced] inflammation and the metes
and bounds of the claim cannot be determined" (Ans. 12).
FF 2. Examiner refers to page 14 of Appellants' Specification and finds
that "it is unclear if tissue injury-induced inflammation is limited to
ischemia-reperfusion injury and immune complex-induced inflammation is
limited to antibody-mediated glomerunephritis or if these[, examples as
recited in Appellants' Specification,] are non-limiting examples" (Ans. 12-
13).
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Application 12/698,732
FF 3. Witko-Sarsat's5 Table 3 is reproduced below:
Table 3. Clinital C!l:n~:ihmls A.S,~l)l;iilled w'itil
N1mlr:i;il in~ectl\::JI~ r~m3'1 WM~
C ryst~: d~po~:~fo~
A~-t~~~u b3r ~·:t::~:nr3:tx:~~k'!r1t~:.is
S~3k1;~~~s
Sett tissu~ calc~um depos~s jg patients ·#it'i '-~ro1~:c
reMI fa!lmf
Gomp~emen~
C~assi;;:;a~ pathv:.:a:{:
M;mr:~~-~-bimling ::edin path;,->'»v:
Pcsts~reptot:"·Ot~~~ g}ome:rn bn~p~ :itl:s
S;$;r~~ena:: t~~fecttor:-k~~~tH:e{~ :!nn~~ m m~tio~1
A~S:rnat~"-ig; p~Ltl'1··~~-a·y":
!bcte-riai !nf~(;tkm-~:icurnJ :info111matio;1
Tt~ue s:njufy-induG.~~i ;~thn~rr:~~~m
C:yst1i dBpusition-rnt'!urnd mfl~mmJ!icr;
tmrnime ccrnpie.>;
Her.oc~-Sd1i.\1 I~ in p:;iri>~:ui
[c;;~ffitio:I C!YCGlDtui:mm1it ';''1.W.iHtls
Sen1n~-:;;~c~,;i~~~ ~-r~st:tillth
Drug er 3ffi"t?ct:.~:::~'.:r:iduce~ ir:~mu:1e ~:;ump}e;: va~cuH~s
Cytok!n~s
11h·BUrr:ato~d tHit1ritis
;nfl:)nlt::1-at0:-y tm:..~"e1 dl::l>5&s.Rs.
AM:GA (m1ti-neutfnp~ril cyt.::~p~;::~:.n~~c; ;3nf3bc~iV}
~',/~gene(& gn.l~lu~om:atosf5.
Pas.1i:;~ ... ~mn~m1~ necrotizing .crn~csnhe:
\jbm~ruiori~mhrl1'~
~~~nf1i~~ d~~.tJ:rd:ers nf ne:;,;itft.'tpf1ll re-gutati·or:s
fam!li,)I M»di!>;:·;,"ne:m fev~;
F~.mili.~I Hibernti\'" f~l!~f
Witko-Sarsat explains that "neutrophils are activated by a great variety of
stimuli and are involved in diseases that may be classified, as shown in
5 Witko-Sarsat et al., Biology of Disease; Neutrophils: Molecules, Functions
and Pathophysiological Aspects, 80 Laboratory Investigation 617--653
(2000).
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Application 12/698,732
Table 3, according to the major neutrophil-activating event" (Witko-Sarsat
640; see also id. at 638).
ANALYSIS
With reference to Witko-Sarsat Appellants make clear that the terms
in dispute are "utilized in the prior art and have known meanings" (App. Br.
40). Therefore, we are not persuaded by Examiner's rationale that the art
recognized terms are indefinite because, they "embrace conditions broader
than the examples disclosed in [Appellants'] [S]pecification" (Ans. 25).
CONCLUSION OF LAW
The preponderance of evidence fails to support Examiner's conclusion
that the phrase "tissue-injury induced inflammation, crystal-induced
inflammation, and immune-complex induced inflammation," as set forth in
Appellants' claim 33 is indefinite. The rejection of claim 33 under
35 U.S.C. § 112, second paragraph is reversed.
Enablement:
ISSUE
Does the evidence of record support Examiner's conclusion that
undue experimentation would be required to practice the claimed invention?
FACTUAL FINDINGS (FF)
FF 4. Examiner finds that Appellants' claimed invention reads on in vivo
methods, but fails to provide an enabling disclosure of an in vivo method to
induce "negative chemotaxis [of] human neutrophils" (Ans. 7).
FF 5. Examiner finds that galectins, as disclosed by Appellants, fail to
"meet the definition of a validated chemorepellent at all concentrations
used" in Appellants' Specification (Ans. 8).
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Application 12/698,732
FF 6. Examiner finds that Appellants' Specification fails to disclose an
assay for negative chemotaxis of neutrophils in vivo and "[ n ]one of
[Appellants'] examples ... discloses administering galectin-1 or galectin-3
to a human subject to induce negative chemotaxis of human neutrophils
(claim 1) or ameliorate an inflammatory response in a subject (claim 24)"
(Ans. 8).
FF 7. Examiner finds that Appellants' Specification fails to disclose how a
person of skill in this art would create a concentration gradient in a human
subject (Ans. 9).
FF 8. Examiner finds that Appellants' claimed invention reads on intact
galectin-1 or -3 proteins or fragments thereof and that variants of the native
galectin-1 or -3 proteins may produce results contrary to Appellants'
claimed invention (Ans. 10-12).
ANALYSIS
Examiner finds that Appellants' Specification fails to enable
Appellants' claimed invention as it relates to in vivo methods (Ans. 7-12).
We are not persuaded.
Initially, we note that Appellants' claimed invention does not require
a "validated chemorepellent" (cf FF 5).
In addition, we recognize Appellants' contention that their claimed
invention is not directed to an assay for the induction of negative chemotaxis
of human neutrophils in vivo (App. Br. 12 ("The claims do not recite or
require assaying or determining negative chemotaxis in vivo"); cf FF 6).
Further, Appellants' Specification discloses a dosage of galectin-1 or -3 that
induces negative chemotaxis (see App. Br. 12-13; Reply Br. 5-7; cf Ans.
6). Further, Appellants' Specification does not require the presence of
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Application 12/698,732
working examples to meet the requirements for the enablement provision of
35 U.S.C. § 112, first paragraph. In re Strahilevitz, 668 F.2d 1229, 1232
(CCPA 1982). Further, we agree with Appellants' contention that Examiner
failed to establish an evidentiary basis on this record to rebut Appellants'
contention that "[ t ]he working examples include in vitro experiments
showing that both galectin-1 and galectin-3 induce negative chemotaxis of
purified neutrophils" and "Examiner has not shown that practicing the
claimed methods in vivo would entail undue experimentation" (Reply Br. 8).
See In re Marzocchi, 439 F.2d 220, 224 (CCPA 1971) (Examiner has the
burden of establishing an evidentiary basis to rebut Appellants'
"presumptively accurate disclosure").
We recognize, but for the reasons provided by Appellants, are not
persuaded by Examiner's assertion that a person of ordinary skill in this art
would not understand how to establish a concentration gradient of galectin-1
or -3 in a human (see FF 7; cf App. Br. 6, 8, and 10-24; Reply Br. 2-7).
We recognize, but for the reasons provided by Appellants, are not
persuaded by Examiner's assertion that Appellants' claimed invention
involves the use of galectin-1 or -3 fragments (FF 8; cf e.g., App. Br. 6).
CONCLUSION OF LAW
The evidence of record fails to support Examiner's conclusion that
undue experimentation would be required to practice the claimed invention.
The rejection of claims 1, 24, 26, 27, 32, and 33 under the enablement
provision of 35 U.S.C. § 112, first paragraph is reversed.
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Anticipation:
ISSUE
Does the preponderance of evidence on this record support
Examiner's finding that Groen or Liu teaches Appellants' claimed
invention?
FACTUAL FINDINGS (FF)
FF 9. Appellants define "[ f]ugetaxis ... as the active movement of a cell
away from a chemokinetic agent," e.g., negative chemotaxis (Spec. 24; see
id. at 1 ("movement away from an agent or stimulus is termed negative
chemotaxis (i.e., the agent or stimulus is chemorepulsive for the cell")).
FF 10. Appellants disclose that in the context of a neutrophil that "fugetactic
effective dose may occur at least within the ranges ofO.OlµM-0.lµM,
O.lµM-15µM, lµM-15µM, 2µM-10µM, 5µM-8µM or preferably less than
O.lµM" (Spec. 24; cf Ans. 14 ("Page 17 of [Appellants'] [S]pecification
does not provide particular dosage amounts")).
FF 11. Groen "relates to methods of inducing interleukin- I 0 production in a
cell" (Groen 1; see generally Ans. 13).
FF 12. Groen teaches the administration of a multimeric galectin-1
polypeptide to "an inflamed tissue (or a tissue that is at risk of becoming
inflamed)" to inhibit inflammation (Groen 2; see also id. at 10
"[i]nflammation is inhibited by administering to tissue galectin-1
polypeptide ... in an amount sufficient to decrease (e.g., inhibit)
immunosuppressive cytokine production"); Groen 29 ("infiltrating
inflammatory cells" include "neutrophils"); see generally Ans. 13).
FF 13. Groen discloses that "[i]nflammatory disorders include for example,
cardiovascular inflammation, gastrointestinal inflammation, hepatic
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Application 12/698,732
inflammation, pulmonary inflammation, autoimmune disorders, allergy or
skeletal inflammation" (Groen 2; see also id. at 14; see generally Ans. 13;
see also Ans. 28 (Groen teaches "[t]reating inflammatory conditions such as
bacterial hepatitis and endocarditis (i.e. bacterial infection)")).
FF 14. Groen discloses an "amount of the stable multimeric galectin-1
polypeptide to induce apoptosis is ... at a concentration less than 20µM,
15mM, lOµM, 5µM, l[]mM, 0.1 µM, or0.001 µM" (Groen 17; see
generally Ans. 13).
FF 15. Groen discloses that "[a]n effective amount of a therapeutic
compound is preferably from about 0.1 mg/kg to about 150 mg/kg" (Groen
18; see generally Ans. 13).
FF 16. Groen discloses various routes of administration of a galectin-1
composition (Groen 18; see generally Ans. 13).
FF 17. Groen discloses that for "cardiac inflammation," galectin-1 may be
"coated or impregnated on a stent that is placed in a coronary vessel" (Groen
19; see generally Ans. 13-14).
FF 18. Examiner acknowledges that Groen fails to disclose "negative
chemotaxis" of a neutrophil, but nonetheless finds that Groen inherently
discloses this subject matter (Ans. 14).
FF 19. Liu "relates to methods for modulating migration of cells, especially
[] neutrophils ... using galectin-3" (Liu 1, see Ans. 14--15).
FF 20. Liu's methods stimulate or inhibit migration (Liu 2, see Ans. 14--15).
FF 21. Liu' s "invention also provides methods for increasing migration of .
. . neutrophils ... to an inflammatory, infection or tumor site[, which]
compris[ es] contacting the inflammatory, infection or tumor site ... with a
migration-increasing amount of galectin-3" (Liu 2).
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FF 22. Liu discloses the administration of galectin-3 to an inflammatory site
through the use of "a microfabricated device containing galectin-3" (Liu 2;
see Ans. 14--15).
FF 23. Liu defines a "migration modulating-amount" of galectin-3 as "any
amount of galecting-3 ... that produces a statistically significant change in
the migration of a cell" (Liu 5; see Ans. 14--15).
FF 24. Liu distinguishes a chemotactic response (i.e., a response that results
in the movement toward or away from an agent) from a chemokinetic
response (i.e., "a response by a motile cell to a substance that involves an
increase or decrease in speed or frequency of movement or a change in the
frequency or magnitude of turning behavior") and discloses that galectin-3
"is chemotactic at high concentrations ( 1. 0 µM) but chemokinetic at low
concentrations (10-100 nM)" (Liu 6; see Ans. 14--15).
FF 25. Liu discloses that "galectin-3 may be a chemoattractant for
neutrophils" (Liu 8; see also id. at 13 (Liu's "invention also relates to a
method of alleviating or treating a disease, symptom or condition in an
animal in which galectin-3-mediated modulation of cell migration, in
particular modulation of ... neutrophils, has a beneficial effect, by
administering a therapeutically effective amount of a galectin-3")).
FF 26. Liu discloses various galectin-3 dosage forms and routes of
administration (Liu 12-13; see Ans. 14--15).
FF 27. Liu discloses that
The daily dosage of the products may be varied over a
wide range, such as from 0. 001 to 100 mg per adult human per
day. For oral administration, the compositions are preferably
provided in the form of tablets containing 0.001, 0.01, 0.05, 0.1,
0.5, 1.0, 2.5, 5.0, 10.0, 15.0, 25.0, 50.0, 100.0, 250.0, or 500.0
mg of the active ingredient for the symptomatic adjustment of
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the dosage to the patient to be treated. A unit dose typically
contains from about 0.001 mg to about 500 mg of the active
ingredient, preferably from about 0 .1 mg to about 100 mg of
active ingredient, more preferably from about 1.0 mg to about
10 mg of active ingredient. An effective amount of the drug is
ordinarily supplied at a dosage level of from about 0.0001
mg/kg to about 25 mg/kg of body weight per day. Preferably,
the range is from about 0.001 to 10 mg/kg of body weight per
day, and especially from about 0.001 mg/kg to 1 mg/kg of body
weight per day. The compounds may be administered on a
regimen of, for example, 1 to 4 or more times per day.
(Liu 14).
FF 28. Examiner finds that "[a]lthough [Liu] does not disclose negative
chemotaxis, this effect would have been inherent to the method of Liu"
(Ans. 15).
ANALYSIS
The rejection over Groen:
Examiner finds that Groen anticipates the subject matter of
Appellants; claims 1 and 33 (Ans. 13-14). 6
Claim 1:
We recognize, but are not persuaded by, Appellants' contention that
Groen "does not disclose or teach that galectin-1 induces negative
chemotaxis of neutrophils" (App. Br. 44). Groen teaches the administration
of multimeric galectin-1 polypeptide to "an inflamed tissue" to inhibit
inflammation (FF 12). Groen teaches that "neutrophils" are "infiltrating
6 We recognize Appellants' separate argument relating to Appellants' claim
27 (App. Br. 45). Examiner, however, withdrew the anticipation rejection of
Appellants' claim 27 over Groen (see Ans. 4). Therefore, we did not include
Appellants' contentions relating to Appellants' claim 27 in our deliberation
of the anticipation rejection over Groen.
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inflammatory cells" (id.). Groen teaches the administration of a
therapeutically effective amount of galectin-1 which is preferably from
about 0 .1 mg/kg to about 150 mg/kg (FF 15). Absent evidence to the
contrary, the administration of an amount of galectin-1 to a site, will, by
diffusion, necessarily result in a concentration gradient. In this regard,
Groen teaches the administration of galectin-1 to a cell, which includes a
human neutrophil, in an amount that Appellants disclose will result in the
induction of negative chemotaxis along a concentration gradient (FF 12, 14,
and 15; cf FF 9--10).
Taken as a whole, while, as Examiner appreciates, Groen does not
expressly teach "negative chemotaxis" of a neutrophil, Groen inherently
teaches the subject matter of Appellants' claim 1 (see FF 18; cf Reply Br.
10). "Under the principles of inherency, if the prior art necessarily functions
in accordance with, or includes, the claimed limitations, it anticipates." In re
Cruciferous Sprout Litig., 301 F.3d 1343, 1349 (Fed. Cir. 2002) (citations
and internal quotation marks omitted). Therefore, we are not persuaded by
Appellants' contention that "nothing in [Groen] ... would establish that the
Groen [] method would have inevitably or necessarily induced negative
chemotaxis of human neutrophils" or that Groen's method administers an
amount of galectin-1 that "would have had an effect on neutrophils, let alone
the effect of inducing negative chemotaxis ofneutrophils" (App. Br. 44).
We appreciate Appellants' contention that the induction of "negative
chemotaxis is dependent on the dose of the chemorepellant [sic]" and Groen
"describes administration of a galectin-1 polypeptide in an amount 'effective
to induce immunosuppressive cytokine production' ... and 'effective to
induce apoptosis"' (App. Br. 44; see Reply Br. 10-11). Nonetheless, as
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discussed above, Groen teaches the administration of galectin-1 to a cell,
which includes a human neutrophil, in an amount that Appellants disclose
will result in the induction of negative chemotaxis along a concentration
gradient (FF 12, 14--15, and 18; cf FF 9-10). Thus, as Examiner explains,
the subject matter of Appellants' claim 1 is inherent in view of Groen (id.).
For the foregoing reasons, we are not persuaded by Appellants'
contention that "Examiner has not established that the amount of multimeric
galectin-1 sufficient to decrease immunosuppressive cytokine production or
to induce apoptosis would be the same as or would overlap with an amount
sufficient to induce negative chemotaxis of human neutrophil as required by
the present invention" (App. Br. 45).
Claim 33:
We recognize, but are not persuaded by, Appellants' contention that
"Examiner does not articulate where the reference discloses that galectin-1 is
administered to a human patient suffering from bacterial infection, tissue-
injury induced inflammation, crystal-induced inflammation, and immune-
complex induced inflammation" (App. Br. 45; cf FF 13).
For the reasons discussed above, with respect to Appellants' claim 1,
we recognize, but are not persuaded by, Appellants' contention that
Examiner fails to "provide any indication of where Groen [] teaches that
galectin-1 is administered to a site of inflammation in a patient suffering
from any of these conditions wherein the galectin-1 is administered in an
amount sufficient to induce negative chemotaxis" (App. Br. 45--46).
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The rejection over Liu:
Examiner finds that Liu anticipates Appellants' claimed invention
(Ans. 14--15). We are not persuaded.
Liu "relates to methods for modulating migration of cells, especially
[] neutrophils ... using galectin-3," wherein Liu discloses that "galectin-3
may be a chemoattractant for neutrophils" (FF 19 and 25; see generally App.
Br. 46-48; see Reply Br. 12). In sum, Examiner failed to establish that Liu
teaches, or inherently teaches, the subject matter of Appellants' claims 1 and
24 (see App. Br. 48 (Liu "discloses and teaches an amount of galectin-3
sufficient to induce positive chemotaxis ( chemoattraction) of neutrophils
toward a site of inflammation," which is the opposite of Appellants' claimed
invention); see also id. at 49).
We recognize, but are not persuaded by, Examiner's assertion that Liu
teaches that "[h ]igher concentrations (such as 1 µM) increase migration and
lower concentrations (such as 10 nM or 100 nM) decrease migration" (Ans.
29). Liu teaches that the concentrations relied upon by Examiner relate to
chemotactic and chemokinetic responses, respectively (FF 24). Liu
distinguishes a chemotactic response (i.e., a response that results in the
movement toward or away from an agent) from a chemokinetic response
(i.e., "a response by a motile cell to a substance that involves an increase or
decrease in speed or frequency of movement or a change in the frequency or
magnitude of turning behavior')" (id.; see generally Reply Br. 12
("chemokinesis is not negative chemotaxis")). On this record, Examiner
failed to establish an evidentiary basis to support a finding that Liu discloses
a dosage of galectin-3 sufficient to induce negative chemotaxis. In this
regard, we recognize that Liu's disclosure of a chemokinetic response does
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not anticipate, or inherently anticipate, negative chemotaxis (see App. Br. 48
("Examiner has not established that Liu []necessarily or inevitably
administers galectin-3 in an amount sufficient to induce negative chemotaxis
of human neutrophils as required by" Appellants' claimed invention); see
generally App. Br. 49; Reply Br. 11 ).
CONCLUSION OF LAW
The preponderance of evidence on this record supports Examiner's
finding that Groen teaches Appellants' claimed invention.
The rejection of claims 1and33 under 35 U.S.C. § 102(e) as
anticipated by Groen is affirmed. Because they were not separately argued
claims 24, 26, and 32 fall with 1.
The preponderance of evidence on this record fails to support
Examiner's finding that Liu teaches Appellants' claimed invention.
The rejection of claims 1, 24, 27, 32, and 33 under 35 U.S.C. § 102(e)
as anticipated by Liu is reversed.
TIME PERIOD FOR RESPONSE
No time period for taking any subsequent action in connection with
this appeal may be extended under 37 C.F.R. § 1.136(a).
AFFIRMED-IN-PART
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