DETAILED ACTION
Claims 1, 7, 12, 16, 18-19, 23, 47-48, 63, 65, 71, 73, 75-79, 194-196 are pending.
Information Disclosure Statement
The information disclosure statements (IDS) filed on 01/18/2025 have been considered by the examiner.
Claim Objections
Claims 1 and 12 are objected to because of the following informalities: grammatical clarity.
Claim 1 recites “…of the cells”. Prior to the recitation of “of the cells” the claim teaches CD8+ cells. Examiner suggests amending to recite “of the CD8+ cells” or a variant thereof.
Claim 12 recites “…of the cells”. Prior to the recitation of “of the cells” the claim teaches early memory CD8 T cells. Examiner suggests amending to recite “of the early memory CD8 T cells” or a variant thereof.
Appropriate correction is required.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 1 and 196 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claims 1 recite “(a) detecting the presence in a biological sample from the cancer patient one or more cellular components selected from the group consisting of:(i) TSCM, TRM, naive, exhausted, cycling, and effector CD8 positive T cells, that express PVRIG; and/or (ii) activated DC cells, DC 1, and/or DC2 that express PVRL2, (b) quantitating the measurement of the level of components selected from the group consisting of:(i) TSCM, TRM, naive, exhausted, cycling, and effector CD8 positive T cells, that express PVRIG; and/or (ii) activated DC cells, DC1, and/or DC2 that express PVRL2”. Claim 1 recites improper Markush grouping. The recitation of “and/or” improper for a Markush grouping.
It appears that the claim should recite one Markush group reciting. Examiner suggests amending to recite “(a) detecting the presence in a biological sample from the cancer patient one or more cellular components selected from the group consisting of:(i) TSCM, TRM, naive, exhausted, cycling, and effector CD8 positive T cells, that express PVRIG, activated DC cells, DC 1, and DC2 that express PVRL2” and “(b) quantitating the measurement of the level of components selected from the group consisting of:(i) TSCM, TRM, naive, exhausted, cycling, and effector CD8 positive T cells, that express PVRIG, activated DC cells, DC1, and DC2 that express PVRL2”.
Claim 196 recites “wherein the cancer selected from the group consisting of prostate cancer, liver cancer (HCC), colorectal cancer (CRC), colorectal cancer MSS (MSS-CRC; including refractory MSS colorectal), CRC (MSS unknown),ovarian cancer (including ovarian carcinoma), endometrial cancer (including endometrial carcinoma), breast cancer, pancreatic cancer, stomach cancer, cervical cancer, head and neck cancer, thyroid cancer, testis cancer, urothelial cancer, lung cancer, melanoma, non- melanoma skin cancer (squamous and basal cell carcinoma), glioma, renal cell cancer (RCC), renal cell carcinoma (RCC), lymphoma (non-Hodgkins' lymphoma (NHL) and Hodgkin's lymphoma (HD)), Acute myeloid leukemia (AML), T cell Acute Lymphoblastic Leukemia (T-ALL), Diffuse Large B cell lymphoma, testicular germ cell tumors, mesothelioma, esophageal cancer, triple negative breast cancer, Merkel Cells cancer, MSI-high cancer, KRAS mutant tumors, adult T-cell leukemia/lymphoma, pleural mesothelioma, anal SCC, neuroendocrine lung cancer (including neuroendocrine lung carcinoma), NSCLC, NSCL (large cell), NSCLC large cell, NSCLC squamous cell, cervical SCC, malignant melanoma, pancreatic cancer, pancreatic adenocarcinoma, adenoid cystic cancer (including adenoid cystic carcinoma), primary peritoneal cancer, microsatellite stable primary peritoneal cancer, platinum resistant microsatellite stable primary peritoneal cancer, Myelodysplastic syndromes (MDS), HNSCC, PD1 refractory or relapsing cancer, gastroesophageal junction cancer, gastric cancer, and/or fallopian tube cancer.” Claim 196 recites improper Markush grouping.
Examiner suggests amending claim 196 to recite ““wherein the cancer selected from the group consisting of prostate cancer, liver cancer (HCC), colorectal cancer (CRC), colorectal cancer MSS (MSS-CRC; including refractory MSS colorectal), CRC (MSS unknown),ovarian cancer (including ovarian carcinoma), endometrial cancer (including endometrial carcinoma), breast cancer, pancreatic cancer, stomach cancer, cervical cancer, head and neck cancer, thyroid cancer, testis cancer, urothelial cancer, lung cancer, melanoma, non- melanoma skin cancer (squamous and basal cell carcinoma), glioma, renal cell cancer (RCC), renal cell carcinoma (RCC), lymphoma (non-Hodgkins' lymphoma (NHL) and Hodgkin's lymphoma (HD)), Acute myeloid leukemia (AML), T cell Acute Lymphoblastic Leukemia (T-ALL), Diffuse Large B cell lymphoma, testicular germ cell tumors, mesothelioma, esophageal cancer, triple negative breast cancer, Merkel Cells cancer, MSI-high cancer, KRAS mutant tumors, adult T-cell leukemia/lymphoma, pleural mesothelioma, anal SCC, neuroendocrine lung cancer (including neuroendocrine lung carcinoma), NSCLC, NSCL (large cell), NSCLC large cell, NSCLC squamous cell, cervical SCC, malignant melanoma, pancreatic cancer, pancreatic adenocarcinoma, adenoid cystic cancer (including adenoid cystic carcinoma), primary peritoneal cancer, microsatellite stable primary peritoneal cancer, platinum resistant microsatellite stable primary peritoneal cancer, Myelodysplastic syndromes (MDS), HNSCC, PD1 refractory or relapsing cancer, gastroesophageal junction cancer, gastric cancer, and fallopian tube cancer.”
Claim 19 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
A broad range or limitation together with a narrow range or limitation that falls within the broad range or limitation (in the same claim) may be considered indefinite if the resulting claim does not clearly set forth the metes and bounds of the patent protection desired. See MPEP § 2173.05(c). In the present instance, claim 19 recites the broad recitation “flow cytometry” and the claim also recites “e.g., FACS” which is the narrower statement of the range/limitation. The claim(s) are considered indefinite because there is a question or doubt as to whether the feature introduced by such narrower language is (a) merely exemplary of the remainder of the claim, and therefore not required, or (b) a required feature of the claims.
A broad range or limitation together with a narrow range or limitation that falls within the broad range or limitation (in the same claim) may be considered indefinite if the resulting claim does not clearly set forth the metes and bounds of the patent protection desired. See MPEP § 2173.05(c). In the present instance, claim 19 recites the broad recitation “mass cytometry”, and the claim also recites “e.g., CyTOF” which is the narrower statement of the range/limitation. The claim(s) are considered indefinite because there is a question or doubt as to whether the feature introduced by such narrower language is (a) merely exemplary of the remainder of the claim, and therefore not required, or (b) a required feature of the claims.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1, 7, 12, 18-19, 71, 75, 77-78, and 196 are rejected under 35 U.S.C. 102(a)(1) and 102(a)(2) as being anticipated by White et al., (WO2016134333A1) (IDS filed on 01/18/2025).
White teaches a method for determining a cancer patient population for treatment with an anti-PVRIG antibody, the method comprising:
detecting the presence in a biological sample that is a tumor (see claim 16 of White) (instant claim 7) from the cancer patient one or more cellular components selected from the group consisting of:(i) TSCM, TRM, naive, exhausted, cycling, and effector CD8 positive T cells, that express PVRIG (see [00720] teaching measuring effector CD8 T cells, see [00962] teaching CD8 T cells express PVRIG, see [0051] and [00475] teaching exhausted T cells);
quantitating the measurement of the level of components selected from the group consisting of:(i) TSCM, TRM, naive, exhausted, cycling, and effector CD8 positive T cells, that express PVRIG (see figure 5a-5c, see figure 29, see [00559] teaching quantification); and
treating the cancer patient with the anti-PVRIG antibody when one or more cellular components in (a) as quantitated in step (b) are present at an increased level as compared to a control or a patient that does not have detectable levels of the cells (see [00980], see [001012], see claims 7 and 37 of White) (instant claim 1).
White teaches a method for determining a cancer patient population for treatment with an anti-PVRIG antibody, the method comprising: (a) detecting the presence in a biological sample from the cancer patient early memory CD8 T cells (see [00561], [00565] and [00943] teaching the detection of CD28. The instant application teaches that early memory CD8 T cells are CD28 cells (see instant application [0271]));
quantitating the measurement of the level of early memory CD8 T cells (see [00943]);
treating the cancer patient with the anti-PVRIG antibody when the level of early memory CD8 T cells are present at an increased level as compared to a control or a patient that does not have detectable levels of the cells (see [00569] teaching increased levels for CD28. See [00651], see [00943] teaching the use of anti-PVRIG antibodies with CD28) (instant claim 12).
White teaches the single-cell resolution analysis being flow cytometry (FACs) (see [0045], see [0047], see [00105]) (instant claims 18-19). White teaches anti-PVRIG treatment antibody is administered at a dose of about 0.1-10 mg/kg (See [00293]) (instant claim 71) and the anti-PVRIG antibody is administered in combination with an anti-PD-1 antibody (see [00307]) (instant claim 75) or in combination with anti-TIGIT (see [00926]) (instant claim 77), or in combination with both anti-PD-1 and anti-TIGIT (see example 15, see [00941]) (instant claim 78). White further teaches the cancer is selected from the group consisting of prostate cancer, liver cancer (HCC), colorectal cancer, ovarian cancer, endometrial cancer, breast cancer, pancreatic cancer, stomach cancer, cervical cancer, head and neck cancer, thyroid cancer, testis cancer, urothelial cancer, lung cancer, melanoma, non melanoma skin cancer (squamous and basal cell carcinoma), glioma, renal cancer (RCC), lymphoma (NHL or HL), Acute myeloid leukemia (AML), ), T cell Acute Lymphoblastic Leukemia (T-ALL), Diffuse Large B cell lymphoma, testicular germ cell tumors, mesothelioma and esophageal cancer (see claim 10 of White) (instant claim 196).
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 16, 47-48, 63, 65, 73, 76, and 79 are rejected under 35 U.S.C. 103 as being unpatentable over White et al., as applied to claims 1, 7, 12, 18-19, 71, 75, 77-78, and 196, in view of Adewoye et al., (US20220280643A1) (effectively filed on 07/28/2020) (IDS filed on 01/18/2025).
The teachings of White as it pertains to claims 1, 7, 12, 18-19, 71, 75, 77-78, and 196 are discussed in the 35 USC 102 rejection above. White does not teach the use of CHA.7.518.1.H4(S241P), a pharmaceutical formulation, the anti-PVRIG treatment antibody being administered 20 mg/kg every 4 weeks, and anti-PVRIG, anti-PD-L1, and anti-TIGIT being administered together.
Adewoye teaches wherein the anti-PVRIG treatment antibody comprises a heavy chain variable domain from the heavy chain of CHA.7.518.1.H4(S241P) (SEQ ID NO:8) and a light chain variable domain from the light chain of CHA.7.518.1.H4(S241P) (SEQ ID NO:13) (see [0022] – [0023]) (instant claim 16). Adewoye further teaches the anti-PVRIG treatment antibody is administered as a stable liquid pharmaceutical formulation of the anti-PVRIG antibody comprising:(a) an anti-PVRIG antibody, wherein the anti-PVRIG antibody comprises: i) a heavy chain variable domain comprising the vhCDR1,vhCDR2, and vhCDR3 from the heavy chain of CHA.7.518.1.H4(S241P) (SEQ ID NO:8), and ii) a light chain variable domain comprising the vlCDR1, vlCDR2, and vlCDR3 from the light chain of CHA.7.518.1.H4(S241P) (SEQ ID NO:13); (b) from 10 mM to 100 mM histidine; (c) from 30 mM to 100 mM NaCl;(d) from 20 mM to 150 mM L-Arginine; and (e) from 0.005% to 0.1% w/v polysorbate 80, wherein the formulation has a pH from 5.5 to 7.0. (see claim 1 of Adewoya) (instant claim 47). Adewoye teaches wherein the anti-PVRIG treatment antibody comprises a CH1-hinge-CH2-CH3 sequence of IgG4 (SEQ ID NO:657 or SEQ ID NO:658), wherein the hinge region optionally comprises mutations (see [0023], see claim 2 of Adewoya) (instant claim 48). Adewoye teaches wherein the anti-PVRIG antibody is at a concentration of from 10 mg/mL to 40 mg/mL, 15 mg/mL to 40 mg/mL, 15 mg/mL to 30 mg/mL, 10 mg/mL to 25 mg/mL, or 15 mg/mL to 25 mg/mL (see claim 17 of Adewoya) (instant claim 63). Adewoye teaches wherein the anti-PVRIG antibody formulation comprises: a) a heavy chain comprising: i) a VH-CH1-hinge-CH2-CH3, wherein the VH is from CHA.7.518.1.H4(S241P) (SEQ ID NO:4) and wherein the CH1- hinge-CH2-CH3 region is from IgG4; and b) a light chain comprising: i) a VL-CL, wherein the VL is from CHA.7.518.1.H4(S241P) (SEQ ID NO:9) and wherein the CL region is from human kappa 2 light chain (see claim 22 of Adewoya) (instant claim 65). Adewoye teaches wherein the anti-PVRIG treatment antibody is administered 20 mg/kg every 4 weeks (see claim 30 of Adewoya) (instant claim 73). Adewoye further teaches anti-PVRIG and anti-PD-L1 being administered together and anti-PVRIG, anti-PD-L1, and anti-TIGIT being administered together (see [1018]) (instant claims 76 and 79).
It would have been obvious to one of ordinary skill in the art to combine the method of determining candidates for anti-PVRIG treatment as taught by White with the anti-PVRIG treatment antibody composition taught by Adewoye. Adewoye provides motivation by teaching that CHA.7.518.1.H4(S241P) demonstrates antitumor activity (see [0907], see [0915], see [0919]). Adewoye further teaches that CHA.7.518.1.H4(S241P) inhibits the binding of PVRIG with its ligand, PVRL2 (see [0911]). The artisan would have reasonable expectation of success based on the cumulative disclosure of these prior art references at the time the instant application was filed.
Claim 194-195 are rejected under 35 U.S.C. 103 as being unpatentable over White et al., (WO2016134333A1) as applied to claims 1, 7, 12, 18-19, 71, 75, 77-78, and 196, in view of Fujita et al. “Effective immunotherapy against murine gliomas using type 1 polarizing dendritic cells--significant roles of CXCL10.” Cancer research vol. 69,4 (2009): 1587-95. doi:10.1158/0008-5472.CAN-08-2915
The teachings of White as it pertains to claims 1, 7, 12, 18-19, 71, 75, 77-78, and 196 are discussed in the 35 USC 102 rejection above. White does not teach the expression of CXCL10 and CXCR3.
Fujita teaches the expression of CXCL10 from D cells and the expression of CXCR3 from CD8+ cells (see page 1587 “Moreover, we show that the anti-CNS glioma effects by DC1-based therapy depend on CXCL10 production by DC1s. This novel mouse DC1 system allows us to address how DC1-based therapy can be applied for glioma patients and points to the significance of CXCL10 production as a critical release criterion for patients’ autologous DC1s in vaccine trials.”, see page 1590 “DC1s, control sDCs, or iDCs were loaded with hgp10025-33 peptide and cocultured with Pmel-I mouse-derived, gp10025-33- specific CD8+ T cells. DC1s induced superior levels of intracellular IFN-g, granzyme B, and CXCR3 in responder CD8+ T cells when compared with sDCs or iDCs, whereas the expression levels of IL-4 and CCR5 were comparable in DC1-stimulated versus sDC stimulated CD8+ T cells (Fig. 2A).”) (instant claims 194-195).
It would have been obvious to one of ordinary skill in the art to combine the method of determining candidates for anti-PVRIG treatment as taught by White with teachings of CXCL10 and CXCR3 as taught by Fujita. Fujita provides motivation by teaching that DC1-derived CXCL10 plays a major role in the systemic induction of antigen-specific CTLs and their CNS glioma homing (see page 1592). Fujita provides motivation by teaching that CD1s promote desirable type 1 adaptive immune responses against CNS gliomas, with the effects being significantly dependent on the DC production of CXCL10 (see page 1592). Fujita further teaches that CXCL10 is required in the CNS glioma homing, as well as the induction of effector CTLs because its receptor CXCR3 is expressed on activated T cells at high levels (see page 1592). Lastly, Fujita teaches αDC1s attract natural killer cells (NK cells) in vitro in a manner dependent on CXCR3, which is a receptor for CXCL10, leading to INF-γ production from NK cells (see page 1593).
Double Patenting
A rejection based on double patenting of the “same invention” type finds its support in the language of 35 U.S.C. 101 which states that “whoever invents or discovers any new and useful process... may obtain a patent therefor...” (Emphasis added). Thus, the term “same invention,” in this context, means an invention drawn to identical subject matter. See Miller v. Eagle Mfg. Co., 151 U.S. 186 (1894); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Ockert, 245 F.2d 467, 114 USPQ 330 (CCPA 1957).
A statutory type (35 U.S.C. 101) double patenting rejection can be overcome by canceling or amending the claims that are directed to the same invention so they are no longer coextensive in scope. The filing of a terminal disclaimer cannot overcome a double patenting rejection based upon 35 U.S.C. 101.
Claims 1, 7, and 12 are provisionally rejected under 35 U.S.C. 101 as claiming the same invention as that of claims 1, 7, 10, and 12 of copending Application No. US 18249957 (reference application). This is a provisional statutory double patenting rejection since the claims directed to the same invention have not in fact been patented.
Regarding instant claim 1, ‘957 teaches a method for determining a cancer patient population for treatment with an anti-PVRIG antibody, the method comprising:(a) detecting the presence in a biological sample from the cancer patient one or more cellular components selected from the group consisting of:(i) TSCM, TRM, naive, exhausted, cycling, and effector CD8 positive T cells, that express PVRIG; and/or (ii) activated DC cells, DC 1, and/or DC2 that express PVRL2, (b) quantitating the measurement of the level of components selected from the group consisting of:(i) TSCM, TRM, naive, exhausted, cycling, and effector CD8 positive T cells, that express PVRIG; and/or (ii) activated DC cells, DCl, and/or DC2 that express PVRL2; and (c) treating the cancer patient with the anti-PVRIG antibody when one or more cellular components in (a) as quantitated in step (b) are present at an increased level as compared to a control or a patient that does not have detectable levels of the cells (see claims 1 and 10 of ‘957).
Regarding instant claim 7, ‘957 teaches wherein the biological sample is obtained from a tumor, tumor microenvironment, and/or peripheral blood from the cancer patient (see claim 7 of ‘957).
Regarding instant claim 12, ‘957 teaches a method for determining a cancer patient population for treatment with an anti-PVRIG antibody, the method comprising: (a) detecting the presence in a biological sample from the cancer patient early memory CD8 T cells; (b) quantitating the measurement of the level of early memory CD8 T cells; (c) treating the cancer patient with the anti-PVRIG antibody when the level of early memory CD8 T cells are present at an increased level as compared to a control or a patient that does not have detectable levels of the cells (see claim 12 of ‘957).
Claim 1 is provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 2 and 116 of copending Application No. 18249957 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the instant application and ‘957 teach methods for determining or predicting the efficacy of treatment with anti-PVRIG antibodies.
Regarding instant claim 1, ‘957 teaches (a) detecting the presence in a biological sample from the cancer patient one or more cellular components selected from the group consisting of:(i) TSCM, TRM, naive, exhausted, cycling, and effector CD8 positive T cells, that express PVRIG; and/or (ii) activated DC cells, DC 1, and/or DC2 that express PVRL2, (b) quantitating the measurement of the level of components selected from the group consisting of:(i) TSCM, TRM, naive, exhausted, cycling, and effector CD8 positive T cells, that express PVRIG; and/or (ii) activated DC cells, DCl, and/or DC2 that express PVRL2; and (c) treating the cancer patient with the anti-PVRIG antibody when one or more cellular components in (a) as quantitated in step (b) are present at an increased level as compared to a control or a patient that does not have detectable levels of the cells (see claims 2 and 116 of ‘957).
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Claims 47-48, 63, 65, 71, and 73 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-2, 17, 22, and 29-30 of copending Application No. 17631847 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other for the reasons set forth below.
Regarding instant claim 47, ‘847 teaches the limitations of the pharmaceutical formulation of the anti-PVRIG antibody comprising :(a) an anti-PVRIG antibody, wherein the anti-PVRIG antibody comprises: i) a heavy chain variable domain comprising the vhCDR1,vhCDR2, and vhCDR3 from the heavy chain of CHA.7.518.1.H4(S241P) (SEQ ID NO:8), and ii) a light chain variable domain comprising the vlCDR1, vlCDR2, and vlCDR3 from the light chain of CHA.7.518.1.H4(S241P) (SEQ ID NO:13); (b) from 10 mM to 100 mM histidine; (c) from 30 mM to 100 mM NaCl;(d) from 20 mM to 150 mM L-Arginine; and (e) from 0.005% to 0.1% w/v polysorbate 80, wherein the formulation has a pH from 5.5 to 7.0 (see claim 1 of ‘847). Although the instant application teaches a method for determining a cancer population for treatment with an anti-PVRIG antibody and ‘847 teaches a composition, they are not patentably distinct as they both teach a pharmaceutical composition of anti-PVRIG antibody.
Regarding instant claim 48, ‘847 teaches wherein the anti-PVRIG treatment antibody comprises a CH1-hinge-CH2-CH3 sequence of IgG4 (SEQ ID NO:657 or SEQ ID NO:658), wherein the hinge region optionally comprises mutations (see claim 2 of ‘847).
Regarding instant claim 63, ‘847 teaches wherein the anti-PVRIG antibody is at a concentration of from 10 mg/mL to 40 mg/mL, 15 mg/mL to 40 mg/mL, 15 mg/mL to 30 mg/mL, 10 mg/mL to 25 mg/mL, or 15 mg/mL to 25 mg/mL (see claim 17 of ‘847).
Regarding instant claim 65, ‘847 teaches wherein the anti-PVRIG antibody formulation comprises: a) a heavy chain comprising: i) a VH-CH1-hinge-CH2-CH3, wherein the VH is from CHA.7.518.1.H4(S241P) (SEQ ID NO:4) and wherein the CH1- hinge-CH2-CH3 region is from IgG4; and b) a light chain comprising: i) a VL-CL, wherein the VL is from CHA.7.518.1.H4(S241P) (SEQ ID NO:9) and wherein the CL region is from human kappa 2 light chain (see claim 22 of ‘847).
Regarding instant claim 71, ‘847 teaches wherein the anti-PVRIG treatment antibody is administered at a dosage of about 0.01 mg/kg to about 20 mg/kg of the anti-PVRIG antibody or about 0.01 mg/kg to about 10 mg/kg of the anti-PVRIG antibody (see claim 29 of ‘847).
Regarding instant claim 73, ‘847 teaches wherein the anti-PVRIG treatment antibody is administered 20 mg/kg every 4 weeks (see claim 30 of ‘847).
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Allowable Subject Matter
Claim 23 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.
The closest prior art for claim 23 is White et al., (WO2016134333A1).
White teaches the use of anti-PVRIG antibodies. However, White does not teach the heavy and light chain sequences of claim 23 or the clone of anti-PVRIG.
Conclusion
No claim is allowed.
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/MCKENZIE A DUNN/ Examiner, Art Unit 1678
/GREGORY S EMCH/ Supervisory Patent Examiner, Art Unit 1678