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 .
Applicant’s response filed on 12/12/2025 is acknowledged and has been entered into the application file.
Priority
The present application is a CON of a (35 U.S.C. 371 national stage filing of International Application No.
PCT/US15/62024, filed 11/20/2015), filed on 05/19/2017, which claims the benefit under 35 U.S.C. 119(e) of prior-
filed provisional application 62/082,315, filed on 11/20/2014. Therefore, the earliest effective filing date of this application is 11/20/2014.
Election/Restrictions
Applicants have previously elected without traverse of Group I, previously drawn to a composition, the composition comprising: an isolated cell comprising a modified endogenous gene, wherein an endogenous gene or fragment thereof is replaced with a transgene using a CRISPR/Cas9 system to generate the modified endogenous gene, the modified cell having an altered response to a cell signal or stimulus and species IL-6 for the endogenous gene in the reply filed on 07/11/2025. Claims 8 and 13-20 remain withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 07/11/2025.
Applicants have now amended independent claim 1 (from elected Group I) to recite a composition, the composition comprising: an isolated cell comprising a modified genome having an Interleukin-6 (IL-6) antagonist transgene operably linked to an endogenous C-C Motif Chemokine Ligand 2 (CCL2) promoter at the endogenous gene CCL2 locus, wherein the endogenous gene encoding CCL2 has been replaced with the transgene, wherein IL-6 stimulation drives transcriptional expression of the transgene. Dependent claims 2-4 are also amended. Claims 5-7 and 9-12 are now cancelled. Therefore, claims 1-4 are pending and under examination in the instant application.
Declaration
A declaration by Inventor Dr. Guilak was submitted on 12/12/2025. The declaration tests a genetically engineered cell with a recombinant IL-6 antagonist that inhibits the effects of IL-6-induced CCL2 upregulation in cells (sections 5-7), argues it is unexpected that IL-6 is capable of driving an IL-6 antagonist transgene operably linked to the CCL2 promoter (section 8), and the cited art of Wu nor Schmidt would not arrive at the claimed invention (section 9).
Applicant's Declaration under 37 CFR 1.132 filed on 12/12/2025 has been fully considered.
Status of Prior Objections/Rejections/Response to Arguments
RE: Objection of claim(s) 9 and 12 because of minor informalities:
Applicants have cancelled claims 9 and 12. The objection is therefore moot.
RE: Rejection of claim(s) 1-7 and 9-12 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph:
Applicants have amended claim 1 to remove the relative term “an altered response” and recite “wherein IL-6 stimulation drives transcriptional expression of the transgene”.
Applicants have also amended claim 4 to remove the recitation “the unmodified endogenous gene” to clarify that “the cell is a modified T-cell”.
Applicants have further cancelled both claim 5 that previously recited the unclear term “the unmodified endogenous gene” and claim 6 that previously recited “the coding region” that did not have sufficient antecedent basis in claim 5, from which claim 6 depends.
Applicant’s amendments, filed 12/12/2025, with respect to claims 1, 4, 5, and 6 have been fully considered and are persuasive. The rejection of claims 1-7 and 9-12 has been withdrawn.
RE: Rejection of claim(s) 1-4, and 10-11 under 35 U.S.C. 102(a)(2) as being anticipated by Wu et al (US20140273226A1):
Applicants have argued that claim amendments overcome the rejection, such that at least independent claim 1 is amended to recite "an isolated cell comprising a modified genome having an Interleukin-6 (IL-6) antagonist transgene operably linked to an endogenous C- C Motif Chemokine Ligand 2 (CCL2) promoter at the endogenous CCI2 locus, wherein the endogenous gene encoding CCL2 has been replaced with the transgene, wherein IL-6 stimulation drives transcriptional expression of the transgene." Wu et al. fails to teach or suggest each and every element of the claimed invention. Applicants have further cancelled claims 10-11.
Applicant’s amendments and arguments, filed 12/12/2025, with respect to claims 1-4 have been fully considered and are persuasive. The rejection of claims 1-4 and 10-11 has been withdrawn. However, in view of applicants’ amendments, a new rejection is made in view of Zheng et al. (Please see the rejection below under Claim Rejections - 35 USC § 103).
RE: Rejection of claim(s) 1-6 and 9-12 under 35 U.S.C. 103 as being unpatentable over Wu et al. (US20140273226A1), in view of Schmidt et al. (US20100255572A1):
Applicants have argued that claim amendments overcome the rejection, such that at least independent claim 1 is amended to recite "an isolated cell comprising a modified genome having an Interleukin-6 (IL-6) antagonist transgene operably linked to an endogenous C- C Motif Chemokine Ligand 2 (CCL2) promoter at the endogenous CCI2 locus, wherein the endogenous gene encoding CCL2 has been replaced with the transgene, wherein IL-6 stimulation drives transcriptional expression of the transgene." Wu et al. fails to teach or suggest each and every element of the claimed invention. Applicants have further cancelled claims 5-6 and 9-12.
Applicant’s amendments and the Declaration under 37 CFR 1.132, filed 12/12/2025, with respect to claims 1-4 have been fully considered and are not fully persuasive. Applicant’s amendments to the claims are sufficient to overcome the rejections of record. Thus, the rejection of claims 1-6 and 9-12 has been withdrawn..
Applicant’s arguments with regard to alleged unexpected results, in light of the Declaration, have been fully considered but are not persuasive. The Declaration argues it was unexpected that IL-6 is capable of driving an IL-6 antagonist transgene operably linked to the CCL2 promoter. When considering evidence of non-obviousness, “the applicant should establish a nexus between the rebuttal evidence and the claimed invention, i.e., objective evidence of nonobviousness must be attributable to the claimed invention. Additionally, the evidence must be reasonably commensurate in scope with the claimed invention. MPEP 2145. Any differences between the claimed invention and the prior art may be expected to result in some differences in properties. The issue is whether the properties differ to such an extent that the difference is really unexpected. MPEP 716.02. Further, the burden is on Applicant to establish that the evidence provided are unexpected and significant. The evidence relied upon should establish "that the differences in results are in fact unexpected and unobvious and of both statistical and practical significance." MPEP 716.02(b).
Initially, it is noted that amended claim 1 is drawn to a composition, not a method of using the composition. Structurally, the claim requires a recombinant cell, comprising an IL-6 antagonist transgene operably linked to the endogenous CCL2 promoter, and wherein the CCL2 endogenous gene is knocked out. Applicant’s arguments that it is unexpected that IL-6 is capable of driving expression of the transgene is not relevant to the patentability of the claimed composition, as this claimed feature is a continent clause within a composition claim (MPEP 2111.04).
Further, even if Applicant’s argument regarding the mechanism/methodology regarding the ability of IL-6 to drive expression of the transgene operably linked to the endogenous CCL2 promoter bears weight on the patentability of the claimed composition -which the examiner does not concede- the relationship between IL-6 and CCL2 expression was known in the art at the time of the invention, and such results were not unexpected. For example, Roca, 2009 shows recombinant IL-6 is capable of upregulating endogenous CCL2/MCP1 expression in CD11b+ cells (page 34344, FIG 1B). Scheller, 2011 discloses recombinant IL6 upregulates endogenous CCL2/MCP1 in endothelial cells (pages 881,883, FIG 2). Thus, Applicant’s assertion that it is unexpected that IL-6 is capable of driving expression of the IL-6 antagonist transgene operably linked to the endogenous CCL2 promoter is not unexpected, and therefore not persuasive.
And, the evidence provided in the declaration is significantly narrower in scope than that which is presently claimed.
However, in view of applicants’ amendments, a new rejection is made in view of Zheng et al. (Please see the rejection below under Claim Rejections - 35 USC § 103).
RE: Rejection of claim(s) 1, 3, 4-7 and 9 under 35 U.S.C. 103 as being unpatentable over Wu et al. (US20140273226A1), in view of Schmidt et al. (US20100255572A1) as applied to claims 1, 3, 4-6 above, and further in view of Zagury et al. (Zagury et al., “Toward a new generation of vaccines: the anti-cytokine therapeutic vaccines”. Proc Natl Acad Sci U S A. 2001 Jul 3;98(14):8024-9):
The rejection is moot in view of applicants’ cancellation of claim 7.
RE: Rejection of claim(s) 1-6, 9, 11-12 on the ground of nonstatutory double patenting as being unpatentable over claims 1 and 3 of US Patent No. 11,319,555 B2 (issued patent of Application No. 15/528296):
Applicants have argued that the pending claims are patentably distinct from the claims of US Patent No. 11, 319, 555 B2 because at least claim 1 is amended to recite "an isolated cell comprising a modified genome having an Interleukin-6 (IL-6) antagonist transgene operably linked to an endogenous C- C Motif Chemokine Ligand 2 (CCL2) promoter at the endogenous CCI2 locus, wherein the endogenous gene encoding CCL2 has been replaced with the transgene, wherein IL-6 stimulation drives transcriptional expression of the transgene."
Applicant’s amendments and arguments, filed 12/12/2025, with respect to claims 1-4 have been fully considered and are persuasive. The rejection of claims 1--6, 9, 11-12 has been withdrawn. However, in view of applicants’ amendments, a modified rejection is made in view of Roca et al. (Please see the rejection below under Double Patenting).
CLAIM INTERPRETATION
As noted above, claim 1 has been amended to recite:
A composition, the composition comprising: an isolated cell comprising a modified genome having an Interleukin-6 (IL-6) antagonist transgene operably linked to an endogenous
C-C Motif Chemokine Ligand 2 (CCL2) promoter at the endogenous gene CCL2 locus, wherein the endogenous gene encoding CCL2 has been replaced with the transgene, wherein IL-6 stimulation drives transcriptional expression of the transgene.
Claim scope is not limited by claim language that suggests or makes optional but does not require steps to be performed, or by claim language that does not limit a claim to a particular structure. However, examples of claim language, although not exhaustive, that may raise a question as to the limiting effect of the language in a claim are:
(A) "adapted to" or "adapted for" clauses;
(B) "wherein" clauses; and
(C) "whereby" clauses
The broadest reasonable interpretation of a system (or apparatus or product) claim having structure that performs a function, which only needs to occur if a condition precedent is met, requires structure for performing the function should the condition occur. The system claim interpretation differs from a method claim interpretation because the claimed structure must be present in the system regardless of whether the condition is met and the function is actually performed. MPEP 2111.04.
The addition of the phrase, “wherein IL-6 stimulation drives transcriptional expression of the transgene” is a contingent limitation that is not required for patentability of the composition claim.
Thus, for the purposes of prosecution, claim 1 is limited to the claimed structure of the cell:
A composition, the composition comprising: an isolated cell comprising a modified genome having an Interleukin-6 (IL-6) antagonist transgene operably linked to an endogenous
C-C Motif Chemokine Ligand 2 (CCL2) promoter at the endogenous gene CCL2 locus, wherein the endogenous gene encoding CCL2 has been replaced with the transgene.
New/Maintained Grounds of Objections/Rejections
Specification
The disclosure is objected to because of the following informalities:
The specification uses both terms CCL2 and Cc12. However, Applicants have not defined anywhere in the instant specification that both CC12 CCL2 are the same. Applicants have amended independent claim 1 to recite an endogenous C- C Motif Chemokine Ligand 2 (CCL2) promoter at the endogenous CCL2 locus; however, applicants use Cc12 locus many times in the instant Specification to refer to the CCL2 locus. See for example, paragraph 0018 of the instant specification that discloses “FIG. 9B shows that a CRISPR/Cas9 RNA-guided nuclease (not depicted) generates a double strand break in the endogenous chromosomal locus near the start codon for Cc12. Provision of a targeting vector with a transgene flanked by regions homologous to the Cc12 locus promotes the use of this template for repair of the damaged allele in a subset of cells.” However, FIG 9B itself mentions “CCL2” as claimed (See applicants’ drawings filed on 03/16/2022, page 17). Applicants further refer to FIG. 9 where support for the current amendments can be found (See applicants’ Remarks filed on 12/12/2025, page 5, second paragraph of Status of the Claims).
Appropriate correction is required.
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.
Claim(s) 1-4 are rejected under 35 U.S.C. 103 as being unpatentable over Zheng et al. (Zheng et al. “Precise Gene Deletion and Replacement Using the CRISPR/Cas9 System in Human Cells. BioTechniques, 57(3), 2014, pages 115–124), in view of Scheller et al. (Scheller et al. “The pro- and anti-inflammatory properties of the cytokine interleukin-6”. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 1813(5), 2011, pages 878-888).
As noted above, the instant claim is directed to an isolated cell wherein an IL-6 antagonist transgene is operably linked to the CCL2 endogenous promoter, and wherein the endogenous CCL2 gene has been replaced by the transgene.
Regarding claim 1, Zheng et al. teaches gene replacement in the human CCL2 gene using a CRISPR/ Cas9 system in human cells. Zheng et al. specifically teaches using CRISPR/ Cas9-mediated replacement by HDR to target the CCL2 locus with a pair of gRNAs and a donor bearing the enhanced green fluorescent protein (EGFP) coding sequence and SV40 poly(A) site (page 121, column 2, lines 9-15). Zheng shows expression of GFP in modified cells following administration of TNFα (FIG 4D), thus demonstrating the GFP transgene is operably linked to the endogenous CCL2 promoter. This reads on an isolated cell comprising a modified genome having a transgene operably linked to an endogenous C-C Motif Chemokine Ligand 2 (CCL2) promoter at the endogenous gene CCL2 locus, wherein the endogenous gene encoding CCL2 has been replaced with the transgene.
However, Zheng et al. fails to teach that the transgene is an IL-6 antagonist transgene.
However, Scheller et al. discloses transgenic mice comprising a transgene encoding sgp130Fc operably linked to the liver specific phosphoenolpyruvate carboxykinase (PEPCK) promoter. Expression of the sgp130Fc protein inhibited IL-6 trans signaling in vivo (page 881, column 1, paragraph 3, last 4 lines and column 2, paragraph 1, lines 1-3). The sgp130Fc transgene reads on the claimed IL-6 antagonist transgene.
Scheller notes IL-6 functions as both a pro-inflammatory cytokine or an anti-inflammatory cytokine, depending upon whether the target cells utilize IL-6 “classic” signaling pathways or IL-6 “trans-signaling” pathways (Abstract, FIG 1, FIG 4). IL-6 stimulation via “classic” signaling pathways result in anti-inflammatory properties in target cells, whereas IL-6 stimulation via “trans-signaling” IL-6 pathways result in pro-inflammatory properties in target cells (FIG. 4), Scheller notes expression of sgp130Fc, the IL-6 antagonist transgene, functions as an anti-inflammatory, allowing for the selective blockage of IL-6 trans-signaling (pages 881-882), without impeding “classic” IL-6 signaling (via cells expressing gp130 and IL6R) in target cells (page 885).
Scheller, further recognizes the relationship between IL-6 stimulation and/or antagonism on endogenous CCL2 expression in cells: Scheller discloses recombinant IL-6 upregulates endogenous CCL2(MCP-1) in endothelial cells via pro-inflammatory IL-6 trans-signaling pathways (pages 881,883, FIG 2). Conversely, expression of the sgp130Fc IL-6 antagonist transgene inhibited the pro-inflammatory trans-signaling pathways, resulting in reduced endogenous CCL2 expression (page 881, column 2, paragraph 1, lines 1-3).
Therefore, it would have been prima facie obvious to one of the ordinary skills in the art before the effective filing date of the claimed invention to have substituted the EGFP transgene operably linked to the endogenous CCL2 promoter of Zheng with the sgp130Fc IL-6 antagonist transgene of Scheller with a reasonable expectation of success. One would have been motivated to have done so because A) Scheller discloses the relationship between IL-6 signaling and CCL2 expression was known: increasing IL-6 signaling increases CCL2 expression and inflammation, whereas the selective inhibition of IL-6 trans-signaling by sgp130Fc reduces CCL2 expression; thus functioning as an anti-inflammatory, without impeding the natural anti-inflammatory properties of IL-6 produced via classic signaling pathways; and B) use of the CCL2 promoter to drive expression of an operably linked transgene, wherein the transgene replaced the CCL2 gene was known. See, MPEP 2143(I)(A) Combining prior art elements according to known methods to yield predictable results supports a prima facie case of obviousness, In the instant case, the prior art included each element claimed, and that in combination, each element merely performs the same function as it does separately; the combination were predictable. MPEP 2143(I)(G). Combining prior art elements according to known methods to yield predictable results supports a prima facie case of obviousness, and Some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to modify the prior art reference or to combine prior art reference teachings to arrive at the claimed invention.
Regarding claim 2: Following discussion of claim 1 above, Scheller et al. further teaches neural cells, neural stem cells, hematopoietic stem cells, liver progenitor cells, and murine embryonic stem cells, which read on adult stem cells, utilize IL-6 trans-signaling pathways (page 881, column 2, paragraph 3). Thus, it would have been obvious to express the scg130Fc transgene in these cells to selectively block IL-6 trans-signaling, for the same reasons as stated above for claim 1.
Regarding claim 3: Following discussion of claim 1 above, claim 3 recites “expression of the IL-6 antagonist protects the subject from inflammation by reducing IL-6 signaling levels”. This is a contingent limitation (MPEP 2111.04), and adds no additional structure to the cells of claim 1. Since the structure of the modified cell of claim 1 is rendered obvious by the cells of Zheng et al. in view of Scheller et al., the combination of Zhen in view of Scheller also render obvious the contingent limitation.
Regarding claim 4: Following discussion of claim 1 above, Scheller et al. further teaches “IL-6 has been shown to rescue T cells from entering apoptosis, a process that seems to rely on STAT3-dependent upregulation of anti-apoptotic regulators (Bcl-2, Bcl-xL) and modulation of Fas surface expression. This reads on the cell can be a T-cell. Scheller discloses during inflammation, IL-6 trans-signaling inhibits T-cell apoptosis in activated T cells, maintains activated TH17 cells (which have been implicated in the induction of autoimmune diseases), and inhibit Treg differentiation (page 883; FIG 4). Thus, it would have been obvious to express the scg130Fc transgene in these cells to selectively block IL-6 trans-signaling, for the same reasons as stated above for claim 1.
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 1-4 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 4, 7, and 21 of US Patent No. 11,319,555 B2 (issued patent of Application No. 15/528296), in view of Roca et al. (Roca et al. “CCL2 and interleukin-6 promote survival of human CD11b+ peripheral blood mononuclear cells and induce M2-type macrophage polarization”. J Biol Chem. 2009, 284(49), pages 34342-54).
Although the claims at issue are not identical, they are not patentably distinct from each other.
Regarding instant claim 1, issued claim 1 of US Patent No. 11,319,555 B2 is directed to a composition, the composition comprising a modified cell comprising a modified genome having a type I soluble tumor necrosis factor receptor antagonist (sTNFR1) transgene or an interleukin-1 receptor antagonist (IL-1 Ra) transgene under the transcriptional control of the endogenous C-C Motif Chemokine Ligand 2 (CcI2) promoter or A disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS-5) promoter at the endogenous CcI2 or ADAMTS-5 locus wherein the endogenous nucleic acid encoding CcI2 or ADAMTS- 5, or a fragment thereof, have been replaced by the transqene for transcriptional regulation of the transgene by the endogenous promoter.
However, issued claim 1 of US Patent No. 11,319,555 B2 fails to teach that the antagonist transgene that is inserted into the CCL2 locus is IL-6 antagonist transgene.
However, Roca et al. teaches that CCL2 and IL-6 induced expression of each other in CD11b cells isolated from human peripheral blood (page 34342, first paragraph). Roca et al. further teaches “CCL2 and IL-6 Induce Each Other in Human CD11b Cells— Tumor cells produce numerous chemokines that attract inflammatory cells, which are capable of producing an assorted array of cytokines, angiogenic growth factors, and proteases, all of which dictate the fate of a developing tumor. CCL2 is one of the most prevalent cytokines expressed in the tumor microenvironment and is a major chemoattractant of monocytes/macrophages to the sites of inflammation” (page 34344, column 2, Results, first 8 lines).
Therefore, it would have been prima facie obvious to one of the ordinary skills in the art before the effective filing date of the claimed invention to have substituted the type I soluble tumor necrosis factor receptor antagonist (sTNFR1) transgene with an IL-6 antagonist transgene to replace the endogenous gene at the CCL2 locus with a reasonable expectation of success. One would have been motivated to have done so as CCL2 and IL-6 induce each other’s expression and inhibiting IL-6 signaling levels would reduce the levels and production of CCL2 which would protect the cell from inflammation as taught by Roca et al. MPEP 2141 I. states that Substitution of one element for another known in the field, wherein the result of the substitution would have been predictable, is considered to be obvious. See KSR International Co. v Teleflex Inc 82 USPQ2d 1385 (US 2007) at 1395.
Regarding instant claim 2, issued claim 4 of US Patent No. 11,319,555 B2 teaches that the modified cell is an induced pluripotent stem cell or an adult stem cell.
Regarding instant claim 3, issued claim 7 of US Patent No. 11,319,555 B2 teaches that expression of the antagonist protects the subject from inflammation by reducing gene signaling levels.
Regarding instant claim 4, issued claim 21 of US Patent No. 11,319,555 B2 teaches that the modified cell is a modified T-cell.
As such the patented claims represent a species of the instant broader product. It is well established that a species of a claimed invention renders the genus obvious. In re Schaumann, 572 F.2d 312, 197 USPQ 5 (CCPA 1978). Thus, the claims of the patented application render obvious instant pending claims 1-4.
This is a non-provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Conclusion
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to HANAN ISAM ABUZEINEH whose telephone number is (571)272-9596. The examiner can normally be reached Mon- Fri 8:30-5:00.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, CHRISTOPHER BABIC can be reached at (571)272-8507. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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Hanan Isam Abuzeineh
/H.I.A./Examiner, Art Unit 1633
/CHRISTOPHER M BABIC/Supervisory Patent Examiner, Art Unit 1633