Ex Parte Singh et al

Patent Trial and Appeal Board

Feb 28, 2017

14466697 (P.T.A.B. Feb. 28, 2017)

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.
14/466,697 08/22/2014 Rajinder Singh 7946-87766-08 4133
74839 7590
Klarquist Sparkman, LLP
121 SW Salmon St
Suite 1600
Portland, OR 97204
EXAMINER
BALASUBRAMANIAN, VENKATARAMAN
ART UNIT PAPER NUMBER
1624
NOTIFICATION DATE DELIVERY MODE
03/02/2017 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):
tanya.harding@klarquist.com
docketing @klarquist.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte RAJINDER SINGH,
SOMASEKHAR BHAMIDIPATI, and VADIM MARKOVTSOV
Appeal 2016-002562
Application 14/466,697
Technology Center 1600
Before ERIC B. GRIMES, JEFFREY N. FREDMAN, and
RYAN H. FLAX, Administrative Patent Judges.
FREDMAN, Administrative Patent Judge.
DECISION ON APPEAL
This is an appeal1 under 35 U.S.C. § 134 involving claims to a method
for inhibiting JAK activity in a cell with a therapeutically effective amount
of a compound. The Examiner rejected the claims as failing to comply with
the enablement requirement. We have jurisdiction under 35 U.S.C. § 6(b).
We affirm.
Statement of the Case
Background
“Protein kinases constitute a large family of structurally related
enzymes that are responsible for the control of a variety of signal
1 Appellants identify the Real Party in Interest as Rigel Pharmaceuticals, Inc.
(see App. Br. 2).
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Application 14/466,697
transduction processes within cells” (Spec. 12). “JAK kinases (JAnus
Kinases) are a family of cytoplasmic protein tyrosine kinases” that “bind
various STAT (Signal Transducer and Activator of Transcription) proteins”
(Spec. 3—4). “JAK/STAT signaling has been implicated in the mediation
of many abnormal immune responses such as allergies, asthma, autoimmune
diseases such as transplant (allograft) rejection, rheumatoid arthritis,
amyotrophic lateral sclerosis and multiple sclerosis, as well as in solid and
hematologic malignancies such as leukemia and lymphomas” (Spec. 14).
“This invention is directed to 2,4-pyrimidinediamines substituted at
N2 with tricyclic carbamates, tautomers, N-oxides, salts thereof, and
methods of using these in the treatment of conditions in which modulation of
the JAK pathway or inhibition of JAK kinases, particularly JAK2, will be
therapeutically useful” (Spec. 16).
The Claims
Claims 1—20, 22, and 23 are on appeal. The claims subject to the
scope of enablement rejection have not been argued separately and therefore
stand or fall together. Claim 1 is representative and reads as follows:
1. A method for inhibiting JAK activity in a cell, comprising
contacting the cell with a therapeutically effective amount of a
compound having a formula I
I
2
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Application 14/466,697
a tautomer, N-oxide, or salt thereof, wherein:
ring A is aryl or heteroaryl;
n is 0 or 1;
p is 0, 1, 2 or 3 when ring A is monocyclic aryl or heteroaryl or
p is 0, 1, 2, 3, 4, or 5 when ring A is bicyclic or tricyclic
aryl or heteroaryl;
X is selected from the group consisting of alkyl, substituted
alkyl, hydroxy, alkoxy, substituted alkoxy, amino,
substituted amino, carboxyl, carboxyl ester, cyano, halo,
nitro, alkenyl, substituted alkenyl, alkynyl, and
substituted alkynyl;
Y is O or S;
Z is O;
W is hydrogen, -S02N(R4)R5, -alk-S02N(R4)R5, -N(R4)S02R5,
or -alk-N(R4) S 02R5;
-alk- is selected from the group consisting of straight or
branched chain Ci_6 alkylene group, and straight or
branched chain substituted Ci_6 alkylene group;
R1 is hydrogen or C1-3 alkyl;
each R2 independently is selected from the group consisting of
alkyl, substituted alkyl, alkoxy, substituted alkoxy,
alkenyl, substituted alkenyl, alkynyl, substituted alkynyl,
cycloalkenyl, substituted cycloalkenyl, alkynyloxy,
amino, substituted amino, aryl, substituted aryl, aryloxy,
substituted aryloxy, cyano, cycloalkyl, substituted
cycloalkyl, cycloalkoxy, substituted cycloalkoxy,
heteroaryl, substituted heteroaryl, heteroaryloxy,
substituted heteroaryloxy, heterocyclic, substituted
heterocyclic, heterocyclyloxy, substituted
heterocyclyloxy, aminocarbonyl, aminocarbonyloxy,
carboxyl, carboxyl ester, (carboxyl ester)oxy, nitro, halo,
and oxo, wherein if R2 is oxo, then the oxo substituent is
attached to a nonaromatic portion of ring A; or
R3 is hydrogen or C 1.3 alkyl;
R4 is selected from the group consisting of hydrogen, alkyl,
substituted alkyl, cycloalkyl, substituted cycloalkyl,
heterocyclic, substituted heterocyclic, aryl, substituted
aryl, heteroaryl, substituted heteroaryl, acyl and M+,
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wherein M+ is a counterion selected from the group
consisting of K+, Na+, Li+ and +N(R8)4, wherein each R8
is independently hydrogen or alkyl, and the nitrogen of -
S02N(R4)R5 or -N(R4)S02R5 is N"; and
R5 is selected from the group consisting of hydrogen, alkyl,
substituted alkyl, amino, alkylamino, dialkylamino,
cycloalkylamino, cycloalkyl, substituted cycloalkyl,
heterocyclic, substituted heterocyclic, aryl, substituted
aryl, heteroaryl, substituted heteroaryl, and acyl; or
R4 and R5 together with the intervening atom or atoms bound
thereto form a heterocyclic or a substituted heterocyclic
group.
The issue
The Examiner rejected claims 1—20, 22, and 23 under 35 U.S.C.
§ 112, first paragraph as failing to comply with the enablement requirement
because the Specification, while enabling for treating leukemia does not
reasonably provide enablement for treatment any or all diseases (Ans. 2—20).
The issue with respect to this rejection is: Does the evidence of
record support the Examiner’s conclusion that the claims fail to comply with
the enablement requirement?
Findings of Fact
Breadth of Claims
1. Claim 1 is drawn to the use of a “therapeutically effective
amount” of a JAK inhibitor of formula I that encompasses an immense
number of different chemical entitites (see Claim 1).
2. The Specification explains that the term ‘“therapeutically
effective amount’ refer[s] to an amount of a compound sufficient to treat a
specified disorder or disease or one or more of its symptoms and/or to
prevent the occurrence of the disease or disorder” (Spec. 1 59).
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3. The Specification and claim 5 provide a detailed and extensive
list of specific “disease[s] associated with JAK2 activity” (claim 5)
encompassed by the “therapeutically effective amount” language of claim 1,
which include:
but are not limited to allergies, asthma, autoimmune diseases
such as transplant rejection (e.g., kidney, heart, lung, liver,
pancreas, skin; host versus graft reaction (HVGR), graft versus
host reaction (GVHR) etc.), rheumatoid arthritis, and
amyotrophic lateral sclerosis, T-cell mediated autoimmune
diseases such as multiple sclerosis, psoriasis and Sjogren’s
syndrome, Type II inflammatory diseases such as vascular
inflammation (including vasculitis, arteritis, atherosclerosis and
coronary artery disease), diseases of the central nervous system
such as stroke, pulmonary diseases such as bronchitis obliteraus
and primary pulmonary hypertension, and solid, delayed Type
IV hypersensitivity reactions, and hematologic malignancies
such as leukemia and lymphomas
(Spec. 1120);
essential thrombocythemia (ET), polycythemia vera (PV) or
primary myelofibrosis (PMF). . . nonclassic
myeloproliferative neoplasms (MPNs), such as atypical
chronic myelogenous leukemia (aCML), chronic
myelomonocytic leukemia (CMML), juvenile
myelomonocytic leukemia (JMML), myelodysplastic
syndrome (MDS), systemic mastocytosis and refractory
anemia with ringed sideroblasts and associated with marked
thrombocytosis (RARS-T). . . acute myeloid leukemia
(AML) and acute lymphoid leukemia (ALL). . . rejection in
organ and/or tissue transplant recipients (i.e., treat and/or
prevent allo[]graft rejection).
(Spec. 11 126-129);
a T-cell mediated autoimmune disease ... In certain
embodiments of the methods the autoimmune disease is
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multiple sclerosis (MS), psoriasis, or Sjogran’s [sic] syndrome .
. . this invention provides a method of treating or preventing a
Type IV hypersensitivity reaction
(Spec. 11 137, 149);
the hematopoietic neoplasm treated is a lymphoid neoplasm,
where the abnormal cells are derived from and/or display the
characteristic phenotype of cells of the lymphoid lineage.
Lymphoid neoplasms can be subdivided into B-cell neoplasms,
T and NK-cell neoplasms, and Hodgkin's lymphoma. B-cell
neoplasms can be further subdivided into precursor B-cell
neoplasm and mature/peripheral B-cell neoplasm. Exemplary
B-cell neoplasms are precursor B-lymphoblastic
leukemia/lymphoma (precursor B-cell acute lymphoblastic
leukemia) while exemplary mature/peripheral B-cell neoplasms
are B-cell chronic lymphocytic leukemia/small lymphocytic
lymphoma, B-cell prolymphocytic leukemia,
lymphoplasmacytic lymphoma, splenic marginal zone B-cell
lymphoma, hairy cell leukemia, plasma cell
myeloma/plasmacytoma, extranodal marginal zone B-cell
lymphoma of MALT type, nodal marginal zone B-cell
lymphoma, follicular lymphoma, mantle-cell lymphoma,
diffuse large B-cell lymphoma, mediastinal large B-cell
lymphoma, primary effusion lymphoma, and Burkitt’s
lymphoma/Burkitt cell leukemia. T-cell and Nk-cell neoplasms
are further subdivided into precursor T-cell neoplasm and
mature (peripheral) T-cell neoplasms. Exemplary precursor T-
cell neoplasm is precursor T-lymphoblastic
lymphoma/leukemia (precursor T-cell acute lymphoblastic
leukemia) while exemplary mature (peripheral) T-cell
neoplasms are T-cell prolymphocytic leukemia T-cell granular
lymphocytic leukemia, aggressive NK-cell leukemia, adult T-
cell lymphoma/leukemia (HTLV-1), extranodal NK/T-cell
lymphoma, nasal type, enteropathy-type T-cell lymphoma,
hepatosplenic gamma-delta T-cell lymphoma, subcutaneous
panniculitis-like T-cell lymphoma, Mycosis fungoides/Sezary
syndrome, Anaplastic large-cell lymphoma, T/null cell, primary
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cutaneous type, Peripheral T-cell lymphoma, not otherwise
characterized, Angioimmunoblastic T-cell lymphoma,
Anaplastic large-cell lymphoma, T/null cell, primary systemic
type. The third member of lymphoid neoplasms is Hodgkin’s
lymphoma, also referred to as Hodgkin’s disease. Exemplary
diagnosis of this class that can be treated with the compounds
include, among others, nodular lymphocyte-predominant
Hodgkin’s lymphoma, and various classical forms of Hodgkin’s
disease, exemplary members of which are Nodular sclerosis
Hodgkin’s lymphoma (grades 1 and 2), Lymphocyte-rich
classical Hodgkin’s lymphoma, Mixed cellularity Hodgkin’s
lymphoma, and Lymphocyte depletion Hodgkin’s lymphoma.
(Spec. 1165).
Presence of Working Examples
4. Example 2 of the Specification is the only working example
identified therein, and Example 2 tested 40 compounds of the invention for
inhibition of proliferation of BaF3 V617F cells, a mouse cell line. This
Example determined ranges of IC50 values for each compound, with 10
compounds having an “A” value with IC50 < 0.25 pM; 14 compounds
having a “B” value with IC50 > 0.25 pM and < 0.5 pM; 4 compounds
having a “C” value with IC50 > 0.5 pM and < 1 pM; 9 compounds having a
“D” value with IC50 > 1 pM and < 5 pM; and 3 compounds having an “E”
value with IC50 > 5 pM (see Spec. 271—275).
5. There are no working examples described in the Specification
for any of the specific diseases listed at FF 3, supra (see Ans. 17).
Amount of Direction or Guidance Presented
6. The Specification teaches “exemplary synthetic methods for the
2,4-substituted pyrimidinediamines” encompassed by claim 1 (Spec. 1 84)
and teaches “2,4-pyrimidinediamine compounds disclosed herein may be
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synthesized via a variety of different synthetic routes using commercially
available starting materials and/or starting materials prepared by
conventional synthetic methods” (Spec. 1 83).
7. The Specification teaches the
compounds of the invention, or pharmaceutically acceptable
salts thereof, described herein are potent and selective inhibitors
of JAK kinases, and particularly selective for cytokine signaling
pathways containing JAK2. As a consequence of this activity,
the compounds can be used in a variety of in vitro, in vivo and
ex vivo contexts to regulate or inhibit JAK kinase activity,
signaling cascades in which JAK kinases play a role, and the
biological responses effected by such signaling cascades.
(Spec. 1118).
8. The Specification teaches “[ajnimal models useful for testing
the efficacy of compounds to treat or prevent the various diseases or
conditions described above are well known in the art” (Spec. 1168).
State of the Prior Art and Unpredictability of the Art
9. Fabbro2 teaches the “discovery of therapeutic agents, based
upon the principle of inhibiting kinases, is not trivial” (Fabbro 81, col. 1).
10. Fabbro teaches “two major obstacles have to be overcome:
access to the intracellular targets and selectivity of inhibition. Considering
the fact that there are as many as 600 protein kinases, it is not surprising that
selectivity has proven to be the more difficult of the two problems” (Fabbro
81, col. 2).
2 Fabbro et al., Protein Kinases as Targets for Anticancer Agents: from
Inhibitors to Useful Drugs, 93 Pharmacology & Therapeutics 79-98
(2002) (“Fabbro”).
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Application 14/466,697
11. Fabbro teaches “[i]t is also important to recognize that in the
protein kinase area, it will be unlikely to find the ‘holy grail of kinase
inhibitors, ’ a compound that specifically inhibits but one single protein
kinase, leaving the other -600 protein kinases unaffected” (Fabbro 95, col.
2).
12. Fabbro teaches “an effective long-term cancer therapy is still
likely to require [a] cocktails of dmgs, each aimed at a specific target”
(Fabbro 95, col. 2).
13. Cohen3 teaches
The specificities of protein kinase inhibitors are not yet tested
routinely against every human protein kinase. Therefore, lack
of inhibition of 20 or more other protein kinases, while
encouraging, does not exclude the possibility of inhibition of
protein kinases (or other enzymes) that have not been
examined. For example, PD 98059 and SB 203580 are reported
to inhibit cyclooxygenases 1 and 2.
(Cohen 463, col. 2).
14. Cohen teaches: “Even the finding that the most closely related
protein kinase is unaffected by the drug is no guarantee of specificity. For
example, SB 203580 does not inhibit SAPK3/p38y or SAPK4/p386 ... yet
several protein kinases with much less similarity are inhibited, albeit more
weakly” (Cohen 463, col. 2 to 464, col. 1).
3 Cohen, P., The development and therapeutic potential of protein
kinase inhibitors, 3 Current Opinion in Chemical Biology 459-465
(1999) (“Cohen”).
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15. Cohen teaches a “recurring theme throughout this review has
been the potential of many protein kinase inhibitors for the treatment of
more than one disease” (Cohen 464, col. 1).
16. Verstovsek4 teaches
JAK2 inhibitors, by virtue of their near equipotent activity on
wild-type JAK2, which is important for normal hematopoiesis,
should have adverse myelosuppression as an expected side
effect if administered at doses that aim to completely inhibit the
mutant JAK2 enzyme. While they may prove to be effective at
controlling hyperproliferation of hematopoietic cells in PV and
ET, they may not be able to eliminate mutant clones in a
manner similar to BCR-ABL inhibitors.
(Verstovsek 637, col. 2).
17. Verstovsek teaches: “Will the use of JAK2 inhibitors in MF
patients have any influence on the biology of the disease and the
transformation process? It remains to be seen. Thus far, a handful of JAK2
inhibitors have been evaluated in clinical trials with variable though
promising results.” (Verstovsek 640, col. 2),
18. The Examiner finds that there is no “evidence that the instantly
disclosed tests are highly predictive for all the uses disclosed and embraced
by the claim language for the intended host” (Ans. 5).
Quantity of Experimentation
19. Mass5 teaches “[t]here is an extensive, ongoing clinical
development program under way for Tarceva [a kinase inhibitor], with 4
4 Verstovsek, S., Therapeutic Potential of JAK2 Inhibitors, American
Society of Hematology 636-42 (2009) (“Verstovsek”).
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Phase I trials completed” and “[t]wo Phase III trials of Tarceva in
combination with chemotherapy are ongoing” (Mass 935, col. 1—2).
20. Verstovsek teaches a “number of JAK2 inhibitors have been
discovered and are currently being developed for MPNs [myoproliferative
neoplasms]. These early clinical trials are focused on patients with MF
[myelofibrosis]” (Verstovsek 637, col. 2).
21. The Examiner finds “[o]ne of skill in the art would need to
determine what diseases out of the multitude claimed would be benefited
(i.e. treated) by the administration of the compounds of formula (I) and
would furthermore have to determine which of the claimed compounds
would provide treatment of which disease” (Ans. 18—19).
Skill in the Art
22. The Examiner finds the “level of skill in the art is high” (Ans.
18).
Principles of Law
Factors to be considered in determining whether a disclosure
would require undue experimentation ... include (1) the
quantity of experimentation necessary, (2) the amount of
direction or guidance presented, (3) the presence or absence
of working examples, (4) the nature of the invention, (5) the
state of the prior art, (6) the relative skill of those in the art,
(7) the predictability or unpredictability of the art, and (8)
the breadth of the claims.
In re Wands, 858 F.2d 731, 737 (Fed. Cir. 1988).
5 Mass, R., The HER Receptor Family: A Rich Target For Therapeutic
Development, 58 Int. J. Radiation Oncology Biol. Phys. 932^40 (2004)
(“Mass”).
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Analysis
The analytical framework for determining whether claims fail to
satisfy the enablement requirement balances the Wands factors to determine
if undue experimentation would have been required to perform the
reasonable scope of the claimed method at the time of filing of the
Specification.
Claim 1 is reasonably interpreted as a method broadly encompassing
the treatment of many of the diseases to which humankind is susceptible (FF
3) , using an extremely large genus of 2,4-pyrimidinediamine based
compounds (FF 1). While the Specification has a working example of forty
compounds tested an in vitro inhibition assay in a mouse cell line (FF 4), the
Specification has no working examples in any human disease or even in any
animal model of a human disease (FF 5). The Specification provides
guidance on compound synthesis (FF 6) and suggests use in any JAK related
condition (FF 7) by testing in animal models (FF 8), but provides no specific
guidance on the treatment of any specific disease. The only guidance in the
Specification is either generic or simply shows that the compounds claimed
are, in fact, capable of inhibiting JAK kinase in an in vitro assay system (FF
4) .
The cited prior art is replete with statements that identification of
selective kinase inhibitors for particular targets and diseases is
unpredictable. Fabbro teaches that finding kinase inhibitors “is not trivial”
(FF 9) and that “it will be unlikely to find the ‘holy grail of kinase
inhibitors, ’ a compound that specifically inhibits but one single protein
kinase” (FF 11). Cohen teaches “[e]ven the finding that the most closely
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related protein kinase is unaffected by the drug is no guarantee of
specificity” (FF 14), though Cohen does suggest that inhibitors may be
useful in multiple diseases (FF 15). Verstovsek teaches that JAK2 inhibitors
may have side effects such as myelosuppression (FF 16) and that clinical
trials have produced “variable though promising results” (FF 17).
Regarding quantity of experimentation, Mass and Verstovsek
evidence that in order to demonstrate efficacy of an inhibitor for a single
human disease, clinical trials in large groups of patients are required (FF 19—
20).
The Examiner finds “Appellants have not provided any competent
evidence that the instantly disclosed tests are highly predictive for all the
uses disclosed and embraced by the claim language for the intended host”
(Ans. 5; FF 18).
While we agree with Appellants that the claims “are not reach-through
claims” (App. Br. 5) and “specifically refer to JAK or JAK2-mediated
diseases” (App. Br. 6), we are not persuaded by Appellants that the
Specification provides all “particular and sufficient examples of JAK kinase-
mediated diseases to entitle appellant to claim the genus of JAK kinase-
mediated diseases” (App. Br. 6).
The Examiner has
set forth a reasonable basis for finding that the scope of the
appealed claims is not enabled by the general description and
the single working example in the specification. Consequently,
the burden shifted to [Appellants] to present persuasive
arguments, supported by suitable proofs where necessary, that
the appealed claims are truly enabled.
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In re Wright, 999 F.2d 1557, 1562 (Fed. Cir. 1993). Appellants fail to meet
this burden and provide no evidence for treatment of a single disease using
the claimed inhibitors, but generally allege that any inhibitor sharing a
compound I structure will function to treat a list of diseases that extends over
several pages (FF 3).
Appellants contend that
at the time the present application was filed, the JAK pathway
and its biological implications were well known in the art. A
simple internet search of the JAK pathway illustrates as much.
Appellant’s specification provides numerous literature citations
that discuss and/or detail the JAK pathway and its biological
implications. For example, see paragraphs [0005]-[0008],
which provide numerous references indicating the state of the
prior art. Thus, at the time of the present invention, and at the
time the application was filed, knowledge of the JAK pathway
and its biological implications were well developed in the art.
(App. Br. 7).
We are not persuaded. Knowledge of a general pathway does not
demonstrate enablement of any particular compound (or “a therapeutically
effective amount” thereof) for any particular disease, and the prior art cited
by the Examiner demonstrates substantial unpredictability in the application
of kinase inhibitors for treatment of patients as discussed above (FF 9-14,
16, 17).
We recognize, but find unpersuasive, Appellants’ contention that “the
specification provides ample guidance to a person of ordinary skill in the art
to assay any particular compound’s ability to inhibit an activity of a JAK
kinase (in vivo and/or in vitro). These assays have an accepted correlation
with in vivo results” (App. Br. 7). The issue of undue experimentation over
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the scope of claim 1 is not whether an in vitro assay can be performed to
assay JAK inhibitor activity, but rather whether that in vitro assay correlates
with results in patients, and the quantity of experimentation necessary to
verily that correlation for the large number of compounds and extremely
large number of diseases listed by Appellants. We agree with the Examiner
that a very large quantity of experimentation would be required to practice
the full scope of claim 1. See In re Fisher, 427 F.2d 833, 839 (CCPA 1970)
(the first paragraph of § 112 requires that the scope of the claims must bear a
reasonable correlation to the scope of enablement provided by the
specification).
Appellants contend that “the specification provides sufficient working
examples to show how to make and use the disclosed compounds, and to
demonstrate their activity against JAK kinase-mediated diseases” (App. Br.
8).
We find this argument unpersuasive because the Specification lacks
even a single working example demonstrating that the claimed compounds
are effective against any JAK kinase-mediated disease. The only working
example is an in vitro activity assay (FF 4). An example showing that the
compounds can inhibit JAK in a mouse cell is not a working example that
the compounds will treat disease.
Appellants contend the “scope of compounds covered by claim 1 is
not so broad [so] as to require undue experimentation in order to practice
appellant’s claimed embodiments” (App. Br. 8).
While the scope of claim 1 regarding compounds encompasses an
immense genus of different molecules, the scope of enablement concerns
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substantially focus on the extensive list of diseases encompassed by claims 1
and 5, that, when combined with the large genus of molecules, renders claim
1 extremely broad (see, e.g., FF 3). While Cohen supports some breadth (FF
15), we agree with the Examiner that the overall scope of claim 1 requires a
large quantity of experimentation to “determine what diseases out of the
multitude claimed would be benefited (i.e. treated) by the administration of
the compounds of formula (I) and would furthermore have to determine
which of the claimed compounds would provide treatment of which disease”
(Ans. 18-19).
We acknowledge Appellants’ argument that the “skill in the art is
high”, but are not persuaded that only “minimal searching and testing . . .
may be required” (App. Br. 9) or that only a “minimal amount of
experimentation, if any, would be required” (App. Br. 10). Indeed, Fabbro
teaches the “discovery of therapeutic agents, based upon the principle of
inhibiting kinases, is not trivial” (FF 9). Even the Specification teaches that
different animal models are necessary to test each different compound for
each different disease, a very large quantity of experimentation, not simply
minimal testing (see Spec. 1214).
As we balance the Wands factors, we find the balance of factors,
including a large quantity of necessary experimentation (FF 21), the limited
guidance in the Specification, the isolated working example pertaining to
mouse cell lines, the lack of any nexus for the breadth of disease treatments
and the JAK kinase inhibitors, the unpredictability of the art regarding
disease treatments, and the extreme breadth of the claims, weighed against a
high skill level in the art, support the Examiner’s conclusion that undue
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experimentation would have been required to enable the full scope of the
instantly claimed invention.
Conclusion of Law
The evidence of record supports the Examiner’s conclusion that the
claims fail to comply with the enablement requirement.
SUMMARY
In summary, we affirm the rejection of claim 1 under 35U.S.C. § 112,
first paragraph as failing to comply with the enablement requirement.
Claims 2—20, 22, and 23 fall with claim 1.
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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