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 was filed in this application after appeal to the Patent Trial and Appeal Board, but prior to a decision on the appeal. 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examination under 37 CFR 1.114 and the fee set forth in 37 CFR 1.17(e) has been timely paid, the appeal has been withdrawn pursuant to 37 CFR 1.114 and prosecution in this application has been reopened pursuant to 37 CFR 1.114. Applicant’s submission filed on September 29, 2025 has been entered.
Status of Claims/Rejections
Claims 199 and 258-263 are currently pending and under examination on the merits in the instant application.
Any rejections not repeated in this Office action are withdrawn, and the following rejections are the only rejections applied in this application.
Response to Arguments
Applicant’s arguments filed on September 29, 2025 with respect to the previous rejections of record have been considered but are moot because they do not pertain to the new rejections set forth hereinbelow.
Claim Objections
Claim 261 is objected to because of the following informalities: “and” in line 4 should be deleted in view of the fact that “and” is recited in line 6. Appropriate correction is required.
Claim 263 is objected to because of the following informalities: “mutation of or” in line 9 should be “mutation of one or”. 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 261-262 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.
Claim 261 is drawn to a composition comprising (a) a modified human TIL comprising modified nucleotides in SCOS1 and ZC3H12A genes, (b) a gRNA comprising SEQ ID NO:25, and (c) a gRNA comprising SEQ ID NO:400.
It is unclear whether the already “modified” human TIL in (a) should have been “modified” without the gRNAs in (b) and (c) or whether the already “modified” human TIL in (a) comprises the gRNAs in (b) and (c). If the “modified” human TIL in (a) is meant to comprise (b) and (c), the claim is incomplete as it omits the essential element that is required to provide the “modified” human TIL because the gRNAs in (b) and (c) do require an endonuclease, a Cas9 protein, in order to result in the “modified” human TIL as evidenced by the use of gRNA/Cas9 RNP complexes disclosed in the instant specification and as further evidenced by prior art knowledge such as Figure 1 of Wang et al. (The Annual Review of Biochemistry, 2016, 85:227-264, applicant’s citation). Hence, claim 261 is incomplete for omitting essential elements, such omission amounting to a gap between the elements. See MPEP § 2172.01.
Claim 262 recites “The composition of claim 260 further comprising a Cas protein”. It is noted that the TIL included in the composition of claim 260 already comprises a Cas protein as evidenced by claim 199 (a). Hence, it is unclear whether “a Cas protein” recited in claim 262 is added to the composition after producing the human TIL of claim 260. If so, it is unclear whether the additional “a Cas protein” in claim 262 is same as or different from the “Cas protein” of claim 199 (a).
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 199 and 258-263 are 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 claim(s) contains 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 inventor(s), at the time the application was filed, had possession of the claimed invention.
The instant claims are drawn to a human TIL that is modified in endogenous SOCS1 gene and ZC3H12A gene, wherein the ZC3H12A gene is modified by a gRNA comprising SEQ ID NO:400.
It is noted that the instant specification merely lists SEQ ID NO:400 as one gRNA species among a total of 452 gRNA sequences (see Table 16) targeting a human ZC3H12A sequence, which is identified as SEQ ID NO:5 (see Table 2), which is 9,860 nucleotides in length. That is, the mere inclusion of SEQ ID NO:400 in Table 16 is the extent of the disclosure of SEQ ID NO:400 in the instant specification. As such, the specification does not describe the requisite structure-function correlation for the structure of SEQ ID NO:400 having the actual function of providing “an insertion, deletion, or mutation of one or more nucleotides” in the endogenous human ZC3H12A sequence. Further, there is no prior art of record submitted by applicant or searched by the examiner that teaches the required structure-function correlation for SEQ ID NO:400, which is merely listed in Table 16 as one of 452 gRNAs targeting a 9,860-nt target sequence. In fact, regarding TILs modified with the combination of gRNAs targeting SOCS1 and ZC3H12A, the instant specification at best adequately describes the combined use of SEQ ID NO:211 targeting murine Zc3h12a and SEQ ID NO:9 targeting murine Socs1. See Example 10. It is noted that SEQ ID NO:211 that is exemplified in the instant specification has no sequence homology with SEQ ID NO:400 claimed in the instant case. Hence, the function of SEQ ID NO:211 described in Example 10 is not indicative of that of SEQ ID NO:400 thus cannot represent SEQ ID NO:400.
Interestingly, it is found that the sequence alignment between the art-recognized human ZC3H12A sequence represented by NM_025079.1 (of record) and SEQ ID NO:400 claimed in the instant claims reveals no significant sequence complementarity or homology, while the sequence alignment between SEQ ID NO:400 and the disclosed human ZC3H12A sequence of SEQ ID NO:5 reveals that SEQ ID NO:400 is complementary to a 20-mer sequence at positions 5906-5925 of SEQ ID NO:5, wherein the 20-mer sequence appears to be a genomic sequence that is not transcribed as the 20-mer sequence is not found in NM_025079.1. Now, it is noted that SEQ ID NO:211 exemplified as a murine Zc3h12a gRNA appears to be homologous to, not complementary to, a murine Zc3h12a sequence, specifically positions 5473-5492 of SEQ ID NO:6 of the instant application. Hence, as already noted above, the actual function of SEQ ID NO:400 cannot be extrapolated from the exemplified gRNA sequence of SEQ ID NO:211, which shares no structural similarity with the instantly claimed gRNA.
It is also found that SEQ ID NO:400 shares significant levels of sequence homology with a number of art-recognized human sequences such as below.
1. A 15-mer is found in human APOBEC3F mRNA (see positions 775-789 of NM_145298.6) as underlined in SEQ ID NO:400: 5’-AGGCACCACTCACCTGTGAT.
2. A 14-mer is found in human RNF10 mRNA (see positions 2158-2171 of NM_014868.5) and human PLEKHG3 mRNA (see positions 4183-4196 of NM_001308147.2) as underlined in SEQ ID NO:400: 5’-AGGCACCACTCACCTGTGAT.
3. SEQ ID NO:400 (5’-AGGCACCACTCACCTGTGAT) contains underlined nucleotides, which align with 18 nucleotides within the 20-mer sequence of human CYP3A7 mRNA (see positions 1128-1147 of NM_000765.5) and human CYP3A4 mRNA (see positions 1128-1147 of NM_017460.6), thereby rendering a 90% sequence identity with a sequence of a completely unrelated target sequences of human CYP3A7 and CYP3A4.
In view of the above-shown sequence homology levels between the non-ZC3H12A sequences and SEQ ID NO:400, it is highly questionable as to the actual function/activity of SEQ ID NO:400 in modifying ZC3H12A that is endogenous to a human TIL. Even better, SEQ ID NO:400 is not identified by relevant artisans after the filing date as being a candidate gRNA sequence that actually modifies endogenous human ZC3H12A (also known as Regnase-1) as evidenced by Dequeant et al. (US 2022/0016173 A1), who actually tested and validated gRNAs. See Tables 1 and 22. Hence, the functionality of SEQ ID NO:400 in introducing “an insertion, deletion, or mutation of one or more nucleotides” in human ZC3H12A that is endogenously present in a human TIL is not only undescribed in the instant specification as of the filing date, but it still remains unknown after the filing date, which thus suggests a complete lack of prior art knowledge and a high level of unpredictability pertaining to the required structure-function correlation for SEQ ID NO:400. Now, applicant’s attention is directed to the fact that the specificity of the specification’s disclosure is inversely correlated with the level of predictability and knowledge. See MPEP §2163. As such, in view of the non-existent level of predictability and knowledge pertaining to SEQ ID NO:400, the instant specification must describe the required function of SEQ ID NO:400 in sufficient detail in order to comply with the written description requirement, which is not satisfied by the mere listing of SEQ ID NO:400 in Table 16 in view of the ample evidence that suggests non-functionality and/or unpredictability of SEQ ID NO:400 as explained in detail above.
It is noted that the instant claims also broadly recite “a Cas protein”, which encompasses Cas9 protein species (e.g., SpCas9, SaCas9), Cas12 protein species, and Cas13 protein species, which are derived from a myriad different organisms as evidenced by paragraphs 00253 and 00258-00262 of the specification and paragraph 0141 of Moriarity et al. (WO 2018/075664 A1, of record). It is art-recognized knowledge that different Cas proteins recognize different PAM sequences in the target. See pages 234-235 of Wang et al. (The Annual Review of Biochemistry, 2016, 85:227-264, applicant’s citation). See also paragraph 0147 of the Moriarity et al. reference (WO 2018/075664 A1, of record) that discloses “the PAM sequence for SpCas9 (5’ NGG 3’)”. Now, the instant specification expressly discloses that “the Cas9 protein derived from S. pyogenes” was used. See paragraph 00356. As such, one of ordinary skill in the relevant art would not reasonably recognize/predict that the instantly claimed gRNAs would function with Cas proteins other than SpCas9. Therefore, the broad genus of “Cas protein” as currently claimed is not adequately described to be used together with the instantly claimed gRNAs, wherein the single species of Cas protein, SpCas9, is not a representative number of Cas proteins that encompasses a myriad number of species as evidenced by the instant specification’s disclosure and paragraph 0141 of Moriarity et al. (WO 2018/075664 A1, of record).
In view of the foregoing, it is concluded that the instant specification fails to adequately describe the claimed subject matter in the manner to reasonably convey that the instant co-inventors had possession of the claimed subject matter as of the filing date sought in the instant application.
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 199 and 258-263 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-14 of U.S. Patent No. 11,111,493 B2 in view of Moriarity et al. (WO 2018/075664 A1, of record), Hashimoto et al. (Cancer Science, 2009, 100:730-736, of record), Herman et al. (US 7,348,139 B1, of record), and NCBI Reference Sequence: NM_025079.1 (National Center for Biotechnology Information, 2006, of record).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘493 patent claims, which are drawn to a modified human T cell that “is a tumor infiltrating lymphocyte” in which the expression/function of ZC3H12A is reduced with a gRNA, which appears to be claimed to comprise SEQ ID NO:1089, which is 100% identical to SEQ ID NO:400 claimed in the instant case. It would have been obvious so further reduce the expression/function of SOCS1 in the same TIL so as to enhance tumor-killing activity of the human TIL of the ‘493 patent claims because genomic disruption in SOCS1 in a human TIL was reasonably suggested by Moriarity and because SOCS1 deficiency was known to increase tumor-killing activity as taught by Hashimoto, wherein the dual genomic disruption of SOCS1 and ZC3H12A would have been deemed to increase anti-tumor efficacy compared to a single genomic disruption of ZC3H12A alone. The gRNA sequence of SEQ ID NO:25 claimed in the instant case would have been obvious in view of the combined teachings of Moriarity, Herman, and NM_025079.1, which taught selection of the a gRNA sequence by identifying “the PAM sequence for SpCas9 (5’ NGG 3’)” and selecting “about 20 bases immediately 5’ of” the PAM sequence (see paragraphs 0147 and 0168 of Moriarity) using the nucleotide sequence of human SOCS1 as disclosed by Herman’s SEQ ID NO:1, wherein a 20-mer-NGG motif (5’-GACGCCTGCGGATTCTACTG(GGG)) within human SOCS1would have been obtained with a reasonable expectation of success by merely identifying the art-recognized gRNA selection motif, wherein the 20-mer sequence is 100% identical to SEQ ID NO:25 claimed in the instant case.
Claims 259-263 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-16 of U.S. Patent No. 11,421,228 B2 in view of Moriarity et al. (WO 2018/075664 A1, of record), Hashimoto et al. (Cancer Science, 2009, 100:730-736, of record), Herman et al. (US 7,348,139 B1, of record), and NCBI Reference Sequence: NM_025079.1 (National Center for Biotechnology Information, 2006, of record).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘228 patent claims drawn to an engineered TIL cell that is modified in ZC3H12A gene expression by a “gRNA” comprising SEQ ID NO:1089, which is claimed in the ‘228 patent claims and is 100% identical to SEQ ID NO:400 claimed in the instant case. It would have been obvious to further treat that TIL cell of the ‘228 patent claims with a gRNA targeting SOCS1 comprising SEQ ID NO:25 claimed in the instant case so as to enhance tumor-killing activity of the human TIL of the ‘228 patent claims because genomic disruption in SOCS1 in a human TIL was reasonably suggested by Moriarity and because SOCS1 deficiency was known to increase tumor-killing activity as taught by Hashimoto, wherein the dual genomic disruption of SOCS1 and ZC3H12A would have been deemed to increase anti-tumor efficacy compared to a single genomic disruption of ZC3H12A alone. The gRNA sequence of SEQ ID NO:25 claimed in the instant case would have been obvious in view of the combined teachings of Moriarity, Herman, and NM_025079.1, which taught selection of the a gRNA sequence by identifying “the PAM sequence for SpCas9 (5’ NGG 3’)” and selecting “about 20 bases immediately 5’ of” the PAM sequence (see paragraphs 0147 and 0168 of Moriarity) using the nucleotide sequence of human SOCS1 as disclosed by Herman’s SEQ ID NO:1, wherein SEQ ID NO:25-NGG motif (5’-GACGCCTGCGGATTCTACTG(GGG)) within human SOCS1would have been obtained with a reasonable expectation of success by merely identifying the art-recognized gRNA selection motif.
Claims 259-263 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of U.S. Patent No. 11,608,500 B2 in view of Moriarity et al. (WO 2018/075664 A1, of record), Hashimoto et al. (Cancer Science, 2009, 100:730-736, of record), Herman et al. (US 7,348,139 B1, of record), and NCBI Reference Sequence: NM_025079.1 (National Center for Biotechnology Information, 2006, of record).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘500 patent claims that require a population of “at least 1x106” engineered TIL cell that is modified in ZC3H12A gene expression by “insertion and deletion”, which is defined to be provided by a “gene-regulating system” comprising a gRNA comprising SEQ ID NO:1089 for targeting ZC3H12A in the ‘500 patent specification. See columns 53-55, 83, 90-91. It is noted that SEQ ID NO:1089 is 100% identical to SEQ ID NO:400 claimed in the instant case. It would have been obvious to further treat that TIL cell of the ‘500 patent claims with a gRNA targeting SOCS1 comprising SEQ ID NO:25 claimed in the instant case so as to enhance tumor-killing activity of the human TIL of the ‘500 patent claims because genomic disruption in SOCS1 in a human TIL was reasonably suggested by Moriarity and because SOCS1 deficiency was known to increase tumor-killing activity as taught by Hashimoto, wherein the dual genomic disruption of SOCS1 and ZC3H12A would have been deemed to increase anti-tumor efficacy compared to a single genomic disruption of ZC3H12A alone. The gRNA sequence of SEQ ID NO:25 claimed in the instant case would have been obvious in view of the combined teachings of Moriarity, Herman, and NM_025079.1, which taught selection of the a gRNA sequence by identifying “the PAM sequence for SpCas9 (5’ NGG 3’)” and selecting “about 20 bases immediately 5’ of” the PAM sequence (see paragraphs 0147 and 0168 of Moriarity) using the nucleotide sequence of human SOCS1 as disclosed by Herman’s SEQ ID NO:1, wherein SEQ ID NO:25-NGG motif (5’-GACGCCTGCGGATTCTACTG(GGG)) within human SOCS1would have been obtained with a reasonable expectation of success by merely identifying the art-recognized gRNA selection motif.
Claims 259-263 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 284-286, 288-291, 298, 315, 329-340, and 345-350 of copending Application No. 16/791,273 in view of Moriarity et al. (WO 2018/075664 A1, of record), Hashimoto et al. (Cancer Science, 2009, 100:730-736, of record), Herman et al. (US 7,348,139 B1, of record), and NCBI Reference Sequence: NM_025079.1 (National Center for Biotechnology Information, 2006, of record).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘273 claims drawn to and require an engineered TIL cell that is modified in ZC3H12A gene expression by a “gRNA” comprising SEQ ID NO:1089, which is 100% identical to SEQ ID NO:400 claimed in the instant case. It would have been obvious to further treat that TIL cell of the ‘273 claims with a gRNA targeting SOCS1 comprising SEQ ID NO:25 claimed in the instant case so as to enhance tumor-killing activity of the human TIL of the ‘273 claims because genomic disruption in SOCS1 in a human TIL was reasonably suggested by Moriarity and because SOCS1 deficiency was known to increase tumor-killing activity as taught by Hashimoto, wherein the dual genomic disruption of SOCS1 and ZC3H12A would have been deemed to increase anti-tumor efficacy compared to a single genomic disruption of ZC3H12A alone. The gRNA sequence of SEQ ID NO:25 claimed in the instant case would have been obvious in view of the combined teachings of Moriarity, Herman, and NM_025079.1, which taught selection of the a gRNA sequence by identifying “the PAM sequence for SpCas9 (5’ NGG 3’)” and selecting “about 20 bases immediately 5’ of” the PAM sequence (see paragraphs 0147 and 0168 of Moriarity) using the nucleotide sequence of human SOCS1 as disclosed by Herman’s SEQ ID NO:1, wherein SEQ ID NO:25-NGG motif (5’-GACGCCTGCGGATTCTACTG(GGG)) within human SOCS1would have been obtained with a reasonable expectation of success by merely identifying the art-recognized gRNA selection motif.
Claims 199 and 258-263 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-2, 4, 8, 10-12, 14-15, 18-20, and 26 of copending Application No. 17/802,080.
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims are anticipated by and/or overlap in scope with the ‘080 claims drawn to a method of producing TILs that are engineered to comprise modified SOCS1 gene and modified ZC3H12A gene using “a guide RNA.” It is noted that the “guide RNA” for SOCS1 is defined to read on SEQ ID NO:61 (see Table 26 of the ‘080 specification), which is 100% identical to SEQ ID NO:25 claimed in the instant case and the “guide RNA” for ZC3H12A is defined to read on SEQ ID NO:377 (see Table 30), which is 100% identical to SEQ ID NO:400 claimed in the instant case.
Claims 259-263 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 289-290 and 292-298 of copending Application No. 18/065,464 in view of Moriarity et al. (WO 2018/075664 A1, of record), Hashimoto et al. (Cancer Science, 2009, 100:730-736, of record), Herman et al. (US 7,348,139 B1, of record), and NCBI Reference Sequence: NM_025079.1 (National Center for Biotechnology Information, 2006, of record).
Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims would have been obvious over the ‘464 claims that require a composition comprising engineered TIL cell that is modified in ZC3H12A gene expression by “insertion” or “deletion”, which is defined to be provided by a “gene-regulating system” comprising a gRNA comprising SEQ ID NO:1089 for targeting ZC3H12A in the ‘464 specification. See paragraphs 0034, 0087-0093, 00321, and 00328. It is noted that SEQ ID NO:1089 is 100% identical to SEQ ID NO:400 claimed in the instant case. It would have been obvious to further treat that TIL cell of the ‘464 claims with a gRNA targeting SOCS1 comprising SEQ ID NO:25 claimed in the instant case so as to enhance tumor-killing activity of the human TIL of the ‘464 claims because genomic disruption in SOCS1 in a human TIL was reasonably suggested by Moriarity and because SOCS1 deficiency was known to increase tumor-killing activity as taught by Hashimoto, wherein the dual genomic disruption of SOCS1 and ZC3H12A would have been deemed to increase anti-tumor efficacy compared to a single genomic disruption of ZC3H12A alone. The gRNA sequence of SEQ ID NO:25 claimed in the instant case would have been obvious in view of the combined teachings of Moriarity, Herman, and NM_025079.1, which taught selection of the a gRNA sequence by identifying “the PAM sequence for SpCas9 (5’ NGG 3’)” and selecting “about 20 bases immediately 5’ of” the PAM sequence (see paragraphs 0147 and 0168 of Moriarity) using the nucleotide sequence of human SOCS1 as disclosed by Herman’s SEQ ID NO:1, wherein SEQ ID NO:25-NGG motif (5’-GACGCCTGCGGATTCTACTG(GGG)) within human SOCS1would have been obtained with a reasonable expectation of success by merely identifying the art-recognized gRNA selection motif.
Conclusion
No claim is allowed.
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/DANA H SHIN/Primary Examiner, Art Unit 1635