DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 11/06/2025 has been entered. Applicant also entered a request for suspension of action for three months. Since the 3 months have passed, this action is submitted in response to the RCE of 11/06/2025.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 02/06/2021 was considered by the examiner.
Response to Amendment
In the amendment filed on 11/06/2025, Applicant argued against the rejection of
record without amending any of the claims. Claims 3, 5 and 10-25 are pending and are
examined.
Maintained claim rejections
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 3, 5 and 10-25 remain rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claims contain subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventors, at the time the application was filed, had possession of the claimed invention.
"[T]he purpose of the written description requirement is to 'ensure that the scope of the
right to exclude, as set forth in the claims, does not overreach the scope of the inventor's contribution to the field of art as described in the patent specification."' Ariad Pharm., Inc. v. Eli Lilly & Co., 598 F.3d 1336, 1353-54 (Fed. Cir. 2010) (en banc) (quoting Univ. of Rochester v. G.D. Searle & Co., 358 F.3d 916,920 (Fed. Cir. 2004)). To satisfy the written description requirement, the specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. Vas-Cath, Inc. v. Mahurkar, 935 F.2d 1555, 1562-63, 19 USPQ2d 1111 (Fed. Cir. 1991). See also MPEP 2163.04. (emphasis added).
As indicated in the previous Office actions, to provide this precise definition" for a
claim to a genus, a patentee must disclose "a representative number of species within
the scope of the genus of structural features common to the members of the genus so
that one of skill in the art can visualize or recognize the member of the genus" (see Amgen at page 1358). Also, it is not enough for the specification to show how to make and use the invention, i.e., to enable it (see Amgen at page 1361).
In the instant case, the specification disclose three instances in which the antimouse CCR8 antibody (SA214G2-from Biolegend), in combination with a mouse anti-PD- 1 (clone RMP1-14, Bio X Cell), is used to treat mouse xenografts of CT26 cells (colon cancer cells), EMT6 cells (breast cancer cells), and Mouse Kidney Cancer-Derived Cell Line RAG (Examples 131, 261 and 271 -respectively).
However, the claims encompass a genus of methods of treatment of breast cancer, colorectal cancer and kidney cancer with any lgG antibody against CCR8 having antibody-dependent cell-mediated cytotoxicity (ADCC). By providing only one method using one single antib-CCR8 antibody, it is considered that this Application does not provide a representative number of species of the claimed genus of methods. Therefore, considering the Specification, a skilled artisan would conclude that Applicant was not in possession of the full scope of the claims but only using SA214G2 and for the breast, colon and kidney cancers.
On page 5 of the Remarks, Applicant argues that: “… based on what was known in the art at the time of filing, one of ordinary skill in the art would conclude that inventors were in possession of using the recited lgG antibody against CCR8 having ADCC for specific cancers as set forth in the pending claims. … As previously submitted, there have been other CCR8 antibodies known in the art at the time of filing. Accordingly, in view of what was known at the time of filing, one of ordinary skill in the art would have been able to extrapolate the working example data using SA214G2 to the recited genus of lgG antibody against CCR8 having ADCC for specific cancers
as set forth in the pending claims.”
The arguments were carefully considered but not found persuasive because, as
repeatedly presented in the previous Office actions, the issue is not that other anti-CCR8 are not known in the art. Indeed, if Applicant had been claiming the anti-CCR8 used in the method, SA214G2, indeed the mere fact that the antibody was commercially available would have been an anticipatory reference. The issue is that the claims encompass a genus of methods of treatment of breast cancer, colorectal cancer and kidney cancer with any lgG antibody against CCR8 having antibody-dependent cell-mediated cytotoxicity (ADCC). This fact need to be really understood by Applicant. Therefore, considering the Specification, a skilled artisan would conclude that Applicant was not in possession of the full scope of the claims but only of a method that uses SA214G2 for treatment of breast, colon and kidney cancers.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
Claims 3, 5, 10-21 and 23-25 remain rejected under 35 U.S.C. 103 as being unpatentable over Skobe (Skobe'010) in view of Charo et al. and Vargas et al. (all cited previously), for reasons of record.
The claims are drawn to a method for treating breast, colorectal, and kidney cancer in a patient in need thereof, comprising: administering a therapeutically effective amount of an lgG antibody against CCR8 having antibody-dependent cell-mediated cytotoxicity (ADCC) activity against cells expressing CCR8, further administering a therapeutically effective amount of nivolumab or pembrolizumab, wherein the antibody against CCR8 binds to CCR8 on tumor infiltrating Treg cells or tumor infiltrating macrophage cells, and removes these cells by the ADCC activity of this antibody.
Skobe '010 discloses a method of treating a subject having a solid tumor which
comprises administering to the subject an antagonist of CCR8 receptors in an amount
effective to reduce binding of CCL1 to the CCR8 receptors so as to thereby treat the
subject (abstract). Example 8 shows that blocking CCR8 arrests metastases in the afferent lymphatic vessels and inhibits tumor cell entry into the lymph node. The reference further discloses that the antagonist of the CCR8 receptor is an antibody which binds to the extracellular domain of the CCR8 receptor at a site that prevents binding of a CCL1 ligand to the CCR8 receptor (page 17, lines 23-25), i.e., it is a CCR8-neutralizing antibody. In some embodiments, the monoclonal antibody is 414B, 141C, 141 E, 433H, 459M, 464A, 464B, 433B or 455AL. These monoclonal antibodies, are described in WO/2007/044756 (incorporated by reference in the Skobe ‘010 reference) (p. 18, first paragraph). Claim 9 explicitly discloses "A method of treating a subject who has, or has been treated for, a solid tumor which comprises administering to the subject an antagonist of CCR8 receptors on the surface of tumor cells present in the solid tumor in an amount effective to reduce binding of CCL1 to the CCR8 receptors so as to thereby treat the subject, wherein the anti-CCR8 antibody is the monoclonal antibody 414B, 141C, 141 E, 433H, 459M, 464A, 464B, 433B or 455AL". WO2007/044756, referenced as the source of the antibodies of Skobe '010, is an international patent application ICOS corporation (Raport '756- cited previously). It provides the CCR8-specific monoclonal antibodies 414B, 141 C, 141 E, 433H, 459M, 464A, 464B, 433B and 455AL ([0007]). Example 6 of the reference confirms that the 433H antibody blocks chemotaxis of CCR8 towards CCL1 and is therefore a CCR8-neutralizing antibody. Mutalithas et al. (cited previously) contains further evidence of the 433H antibody as it states that "[t]he 433H is an unconjugated mouse lgG2a mAb directed against human CCR8, and was a gift from ICOS Corporation" (page 1177, first paragraph). As is well-known, lgG2a is a mouse lg isotype that induces significant ADCC activity, indeed, it is even the lg isotype with the highest ADCC activity amongst the different mouse isotypes. See, for example, Kipps et al. (cited previously) at page 1, last paragraph and Figure 3.
The same is also derivable from Vargas et al. (Fc-optimized anti-CD25 depletes
tumor infiltrating regulatory T cells and synergizes with PD-1 blockade to eradicate
established tumors. Immunity, 46, 577-586, 2017), wherein murine lgG2a is referred to
as 'the classical mouse isotype associated with ADCC (p. 578, last paragraph) and wherein it is observed that, as previously described, the mlgG2a isotype binds to all FcγR subtypes with a high activatory to inhibitory ratio (p. 580, first paragraph). Thus, the 433H antibody from Skobe '010 has ADCC activity.
For these reasons, Skobe '010 directly and unambiguously discloses a method of
treating cancer using the monoclonal neutralizing anti-CCR8 antibody 433H that has
ADCC activity. The treatment would necessarily deplete the tumor infiltrating Treg cells
or tumor-infiltrating macrophages because the property is intrinsic to a CCR8-neutralising antibody having ADCC activity (Nota bene: the antibody used by Applicant, lgG2b anti CCR8 SA214G2 antibody is also a neutralizing antibody and has ADCC activity). The Skobe reference disclosed that the administration of CCR8 antagonists described may be by way of compositions containing one of the antagonists and a pharmaceutically acceptable carrier. A "pharmaceutical acceptable carrier" is a pharmaceutically acceptable solvent, suspending agent or vehicle, for delivering an active compound to a mammal, including humans. The carrier may be liquid, aerosol, gel or solid and is selected with the planned manner of administration in mind. In an embodiment, the pharmaceutical carrier is a sterile pharmaceutically acceptable solvent suitable for intravenous or intraperitoneal administration (p. 79-80).
While the Skobe ‘010 does not specifically disclose the use of nivolumab or
pembrolizumab, the art at the time that the invention was filed indicate the use of
antibodies having ADCC activity with PD-1.
Indeed, Vargas et al. disclose that murine lgG2a, referred to as 'the classical
mouse isotype associated with ADCC (p. 578, last paragraph), binds to all FcγR subtypes with a high activatory to inhibitory ratio (p. 580, first paragraph) in a setting similar to what is claimed instantly, and antibody that depletes tumor infiltrating regulatory T cells in conjunction with anti-PD-1 antibodies or CTLA-4 antibodies (p. 584).
For instance, Charo et al. teaches a method for treating a subject having a solid
tumor cancer by administering to the subject in need thereof a therapeutically effective
amount of a CCR1 chemokine receptor antagonist and a therapeutically effective amount of a PD-1 inhibitor or a PD-L1 inhibitor ([0007]-[0009]). ]). The solid tumor cancer can be breast cancer, colorectal cancer, or kidney cancer ([0079]). The PD-1 inhibitor may be pembrolizumab or nivolumab ([0073]).
The CCR1 is in the same family of chemokine receptors as CCR8 and they even
share some ligands (see evidentiary reference: Singhal et al., Do chemokines have a role in the pathophysiology of depression? Chapter 8 in Inflammation and Immunity in
Depression, 2018, p. 135-159, ISBN 978-0-12-811073-7) (see table 2).
It would have been obvious for a person of ordinary skill in the art at the time that
the invention was filed to have used the method of Skobe ‘010 and the teachings of Charo et al. and Vargas et al. and treat cancer with a CCR8 antibody combined with
pembrolizumab or nivolumab with a reasonable expectation of success. This is because
Skobe ‘010 teaches the treatment method with the CCR8 antibody with the same
properties as the instantly claimed antibody and the art was using CCR antagonists in
combination with pembrolizumab or nivolumab. A person of ordinary skill in the art is
always motivated to pursue the known options within her or his technical grasp. If this
leads to the anticipated success, it is likely the product not of innovation but of ordinary
skill and common sense.
Regarding claim 11, which claims that the antibody used in the method does not
recognize CT26 cell, it is not expected that the antibody would recognize the CT26 cells
since CCR8 is not expressed in this type of cells (see evidentiary reference: Chantry et
al., cited previously).
Regarding claims 13-16, the Vargas et al. reference indicates the use of anti CTLA-4 or PD-L1 antibodies in the context described therein. The specific atezolizumab, avelumab, durvalumab or ipilimumab are known and used therapeutically anti-PD-L1 and anti-CTLA4 antibodies respectively and thus obvious to be used in the methods claimed.
On page 5 of the Remarks argues that: “… a person of ordinary skill in the art would not have been motivated to combine nivolumab or pembrolizumab of Charo with Skobe and would not have expected success in treating the recited cancers from doing so because it is unpredictable whether a particular compound will show a beneficial effect when administered together in vivo for treatment. Additionally, Charo discloses CCR1, not CCR8…”.
The arguments were carefully considered but not found persuasive because Skobe '010 directly and unambiguously discloses a method of treating cancer using the
monoclonal neutralizing anti-CCR8 antibody 433H that has ADCC activity. The treatment would necessarily deplete the tumor infiltrating Treg cells or tumor-infiltrating
macrophages because the property is intrinsic to a CCR8-neutralising antibody having
ADCC activity (Nota bene: the antibody used by Applicant, lgG2b anti CCR8 SA214G2
antibody is also a neutralizing antibody and has ADCC activity). Moreover, Charo et al. teaches a method for treating a subject having a solid tumor cancer by administering to the subject in need thereof a therapeutically effective amount of a CCR1 chemokine receptor antagonist and a therapeutically effective amount of a PD-1 inhibitor or a PD-L1 inhibitor ([0007]-[0009]). The PD-1 inhibitor may be pembrolizumab or nivolumab ([0073]); also, CCR1 is in the same family of chemokine receptors as CCR8 and they even share some ligands.
Claims 3, 5, 10-21 and 23-24 remain rejected under 35 U.S.C. 103 as being unpatentable over Benoist et al. (Benoist'032) in view of Charo et al. and Vargas et al. (all cited previously) for reasons of record.
On page 6 of the Remarks Applicant argues that: “ ... a person of ordinary skill in
the art would not have been motivated to combine nivolumab or pembrolizumab of Charo with Benoist and would not have expected success from doing so because Charo discloses CCR1, not CCR8, while Benoist focuses on an antibody for CCR8.”
The arguments were carefully considered but not found persuasive because
Benoist '032 clearly discloses methods of decreasing the number or activity of tumor
infiltrating T regulatory cells (TITR) in a tumor in a subject with cancer by administering
to the subject an antibody specific for a protein product of CCR8. The antibody induces
cytotoxicity in cells that express a product of CCR8 or TNFRSF8. The antibodies may be polyclonal or monoclonal; xenogeneic, allogeneic, or syngeneic; or modified forms thereof (e.g., humanized, chimeric, etc.). Antibodies may also be fully human (p. 14, line 9 to p.15, line 5). The methods use antibodies and antigen binding fragments thereof that bind specifically to a product of CCR8 and inhibit the function of the protein, such as inhibiting the activity of the protein, or interfering with protein-protein interactions (a.k.a. neutralizing antibodies) (p. 15, lines 13-15). The cytotoxicity of the antibodies may be antibody dependent cell-mediated cytotoxicity (ADCC) (p. 2, lines 2-3, claims 1, 2, 4, 12-16, Example 7). The administration may be performed systemically or intravenously and the agent is in a pharmaceutically acceptable formulation (claims 26, 27, and 33). The methods of decreasing the number or activity of tumor infiltrating T regulatory cells (TITR) in a tumor may be effected by conjointly administering to the subject an antibody (e.g., a monoclonal antibody) that inhibits the activity or expression of a product of the CCR8 and an immune checkpoint inhibitor, an antibody against PD-1 or PD-L 1 (example 8, claim 36, 37). The effect of the mAb treatment is tested in example 10 and can be seen in figure 10. The treated cancer comprise a breast tumor, a colorectal tumor, and a kidney tumor (claims 91-96).
While the Benoist '032 does not specifically disclose the use of nivolumab or
pembrolizumab, the art at the time that the invention was filed indicate the use of
antibodies having ADCC activity with PD-1. Indeed, Vargas et al. disclose that murine
lgG2a, referred to as 'the classical mouse isotype associated with ADCC (p. 578, last
paragraph), binds to all FcyR subtypes with a high activatory to inhibitory ratio (p. 580,
first paragraph) in a setting similar to what is claimed instantly, and antibody that
depletes tumor infiltrating regulatory T cells in conjunction with anti-PD-1 antibodies or
CTLA-4 antibodies (p. 584). Moreover, Charo et al. teaches a method for treating a
subject having a solid tumor cancer by administering to the subject in need thereof a
therapeutically effective amount of a CCR1 chemokine receptor antagonist and a
therapeutically effective amount of a PD-1 inhibitor or a PD-L 1 inhibitor ([0007]-[0009]).
The solid tumor cancer can be breast cancer, colorectal cancer, or kidney cancer ([0079]). The PD-1 inhibitor may be pembrolizumab or nivolumab ([0073]). It should be noted that the CCR1 is in the same family of chemokine receptors as CCR8 and they even share some ligands.
Claims 3, 5, 10-21 and 23-25 remain rejected under 35 U.S.C. 103 as being unpatentable over Rudensky in view of Charo and Vargas for reasons of record.
On page 6 of the Remarks Applicant argues that: “…a person of ordinary skill in the art would not have been motivated to combine nivolumab or pembrolizumab of Charo with Rudensky and would not have expected success in treating the recited cancers from doing so because Charo discloses CCR1, not CCR8, as the office action notes while Rudensky focuses on an antibody for CCR8.”
The arguments were carefully considered but not found persuasive because as
indicated previously, the CCR1 is in the same family of chemokine receptors as CCR8 and they even share some ligands.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 3, 5, 10-13 and 21-25 remain rejected on the ground of nonstatutory double patenting as being unpatentable over claims 7-16 of U.S. Patent No. 10,550,191 in view of Charo et al. (cited previously) for reasons of record.
On page 6 of the Remarks Applicant argues that: “… a person of ordinary skill in the art would not have been motivated to combine nivolumab or pembrolizumab of Charo and the claims of the ‘191 patent and would not have expected success from doing so because it is unpredictable whether a particular compound will show a beneficial effect when administered in vivo for treatment.”
The arguments were carefully considered but not found persuasive because ‘191
Patent teaches the treatment method with the CCR8 antibody with the same properties
as the instantly claimed antibody and the art was using CCR antagonists in combination
with pembrolizumab or nivolumab (as indicated by Charo et al.).
The arguments were carefully considered but not found persuasive because the
Patent claims mention administration of the anti-CCR8 antibody with anti-PD-1 or anti-
PD-L 1 antibody but does not specifically name the pembrolizumab or nivolumab. Charo
et al. teaches a method for treating a subject having a solid tumor cancer by administering to the subject in need thereof a therapeutically effective amount of a CCR1 chemokine receptor antagonist and a therapeutically effective amount of a PD-1 inhibitor or a PD-L 1 inhibitor ([0007]-[0009]). The solid tumor cancer can be breast cancer, colorectal cancer, or kidney cancer ([0079]). The PD-1 inhibitor may be pembrolizumab or nivolumab ([0073]). Therefore, it would have been obvious for a person of ordinary skill in the art to have used the method of the Patent and the teachings of Charo et al. and treat cancer with a CCR8 antibody combined with pembrolizumab or nivolumab with a reasonable expectation of success. This is because the patent teaches the treatment method with the CCR8 antibody with the same properties as the instantly claimed antibody and the art was using CCR antagonists in combination with pembrolizumab or nivolumab. Thus, a skilled artisan would have used known and tested methods using similar reagents to solve an existent problem. A person of ordinary skill in the art is always motivated to pursue the known options within her or his technical grasp. If this leads to the anticipated success, it is likely the product not of innovation but of ordinary skill and common sense.
Claims 3, 5, 10-13 and 21-25 remain rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1-7 of U.S. Patent No. 11,932,696 view of Charo et al. for reasons of record.
On page 7 of the Remarks Applicant argues that: “… the claims of the ‘696 patent are silent regarding any nivolumab or pembrolizumab. Accordingly, the claims of the 696 patent fail to teach or suggest each and every element of the pending claims”.
The arguments were carefully considered but not found persuasive because the
Patent claims mention administration of the anti-CCR8 antibody with anti-PD-1 or anti-
PD-L 1 antibody but does not specifically name the pembrolizumab or nivolumab. Charo
et al. teaches a method for treating a subject having a solid tumor cancer by administering to the subject in need thereof a therapeutically effective amount of a CCR1 chemokine receptor antagonist and a therapeutically effective amount of a PD-1 inhibitor or a PD-L 1 inhibitor ([0007]-[0009]). The solid tumor cancer can be breast cancer, colorectal cancer, or kidney cancer ([0079]). The PD-1 inhibitor may be pembrolizumab or nivolumab ([0073]). Therefore, it would have been obvious for a person of ordinary skill in the art to have used the method of the Patent and the teachings of Charo et al. and treat cancer with a CCR8 antibody combined with pembrolizumab or nivolumab with a reasonable expectation of success. This is because the patent teaches the treatment method with the CCR8 antibody with the same properties as the instantly claimed antibody and the art was using CCR antagonists in combination with pembrolizumab or nivolumab. Thus, a skilled artisan would have used known and tested methods using similar reagents to solve an existent problem. A person of ordinary skill in the art is always motivated to pursue the known options within her or his technical grasp. If this leads to the anticipated success, it is likely the product not of innovation but of ordinary skill and common sense.
Conclusion
No claims are allowed.
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ELLY-GERALD STOICA
Primary Examiner
Art Unit 1647
/Elly-Gerald Stoica/Primary Examiner, Art Unit 1647