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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 July 16, 2026 has been entered.
Status of Claims
This action is written in response to applicant’s Remarks received June 16, 2026. Claims 1, 12-16, and 18-25 are currently pending. Claims 13-16, and 18-23 are withdrawn from prosecution as being drawn to non-elected subjection matter on Response to Restriction/Election received on 2 August 2024. Claims 2-11, 17 are cancelled. Accordingly, claims 1, 12, 24, and 25 are examined herein.
Any rejection or objection not reiterated herein has been overcome by amendment. Applicant’s amendments and arguments have been thoroughly reviewed, but are not persuasive to place the claims in condition for allowance for the reasons that follow.
Priority
Acknowledgment is made of applicant’s claim for priority on Provisional Application No. 62/682,772, filed on 08 June 2018. Support for instantly amended claim 1 can be found on pg. 4, para. 4, and originally filed claims.
Nucleotide and/or Amino Acid Sequence Disclosures
REQUIREMENTS FOR PATENT APPLICATIONS CONTAINING NUCLEOTIDE AND/OR AMINO ACID SEQUENCE DISCLOSURES
Items 1) and 2) provide general guidance related to requirements for sequence disclosures.
37 CFR 1.821(c) requires that patent applications which contain disclosures of nucleotide and/or amino acid sequences that fall within the definitions of 37 CFR 1.821(a) must contain a "Sequence Listing," as a separate part of the disclosure, which presents the nucleotide and/or amino acid sequences and associated information using the symbols and format in accordance with the requirements of 37 CFR 1.821 - 1.825. This "Sequence Listing" part of the disclosure may be submitted:
In accordance with 37 CFR 1.821(c)(1) via the USPTO patent electronic filing system (see Section I.1 of the Legal Framework for Patent Electronic System (https://www.uspto.gov/PatentLegalFramework), hereinafter "Legal Framework") as an ASCII text file, together with an incorporation-by-reference of the material in the ASCII text file in a separate paragraph of the specification as required by 37 CFR 1.823(b)(1) identifying:
the name of the ASCII text file;
ii) the date of creation; and
iii) the size of the ASCII text file in bytes;
In accordance with 37 CFR 1.821(c)(1) on read-only optical disc(s) as permitted by 37 CFR 1.52(e)(1)(ii), labeled according to 37 CFR 1.52(e)(5), with an incorporation-by-reference of the material in the ASCII text file according to 37 CFR 1.52(e)(8) and 37 CFR 1.823(b)(1) in a separate paragraph of the specification identifying:
the name of the ASCII text file;
the date of creation; and
the size of the ASCII text file in bytes;
In accordance with 37 CFR 1.821(c)(2) via the USPTO patent electronic filing system as a PDF file (not recommended); or
In accordance with 37 CFR 1.821(c)(3) on physical sheets of paper (not recommended).
When a “Sequence Listing” has been submitted as a PDF file as in 1(c) above (37 CFR 1.821(c)(2)) or on physical sheets of paper as in 1(d) above (37 CFR 1.821(c)(3)), 37 CFR 1.821(e)(1) requires a computer readable form (CRF) of the “Sequence Listing” in accordance with the requirements of 37 CFR 1.824.
If the "Sequence Listing" required by 37 CFR 1.821(c) is filed via the USPTO patent electronic filing system as a PDF, then 37 CFR 1.821(e)(1)(ii) or 1.821(e)(2)(ii) requires submission of a statement that the "Sequence Listing" content of the PDF copy and the CRF copy (the ASCII text file copy) are identical.
If the "Sequence Listing" required by 37 CFR 1.821(c) is filed on paper or read-only optical disc, then 37 CFR 1.821(e)(1)(ii) or 1.821(e)(2)(ii) requires submission of a statement that the "Sequence Listing" content of the paper or read-only optical disc copy and the CRF are identical.
Specific deficiencies and the required response to this Office Action are as follows:
Specific deficiency - The Incorporation by Reference paragraph required by 37 CFR 1.821(c)(1) is missing or incomplete. See item 1) a) or 1) b) above.
Required response – Applicant must provide:
A substitute specification in compliance with 37 CFR 1.52, 1.121(b)(3) and 1.125 inserting the required incorporation-by-reference paragraph, consisting of:
A copy of the previously-submitted specification, with deletions shown with strikethrough or brackets and insertions shown with underlining (marked-up version);
A copy of the amended specification without markings (clean version); and
A statement that the substitute specification contains no new matter.
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.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 1, 12, and 24-25 are rejected under 35 U.S.C. 103 as being unpatentable over Pleger (Science Translational Medicine., 2011, 3, 92, 92ra64-74), as evidenced by Mueller (Cardiovascular Research., 2006, 70, 70-78), in view of Chatterjee (J Thorac Cardiovasc Surg., 2003, 125, 1461-9), Jazwa (Vascular Cell., 2013, 5, 13, 1-11), Prasad (J Gene Med., 2011, 13, 333-341), and Kotin (WO 2017/075335 A1; Published Date: May 04, 2017).
Regarding claim 1, Pleger teaches a recombinant adeno-associated virus (rAAV) particle comprising nucleic acid vector for delivering transgenes as gene therapy to treat heart failure in a subject, wherein said vector (AAV9-S100A1) comprises the human S100A1 cDNA under the control of a cardiomyocyte-specific promoter (section "Retrograde coronary venous AAV9-S100A1 gene delivery enhances S100A1 expression levels in failing hearts"; pg 4, left-column; abstract). Pleger teaches S100A1 is a positive inotropic regulator of myocardial contractility and becomes depleted in failing cardiomyocytes; thus, S100A1 gene transfer rescues cardiac contractile function and could potentially complement current strategies to treat end-stage heart failure (abstract). Pleger further teaches S100A1 gene therapy reverse progressive deterioration of cardiac performance and left ventricular remodeling (abstract). Pleger further teaches said vector is constructed as designed by Muller (section "AAV9 vector production"; pg. 8, left-column). Muller teaches the promoters include a MLC-2v promoter and a series of MLC promoters as evidenced by Muller (“Introduction”, pg. 71, left-column and Fig. 1). Muller also teaches that AAV vectors are designed to have a SV40 late poly (A) signal and are flanked by the AAV inverted terminal repeats (ITR) (Figure 1, caption). Thus, the vector used by Pleger contained from 5' to 3' in order, a first AAV ITR, a transgene (S100A1) and a promoter operably linked to it, and a second AAV ITR.
However, Pleger does not teach a rAAV vector comprising two or more transgenes, wherein the two or more transgenes comprise an S100 family protein and an apoptotic inhibitor, wherein the apoptotic inhibitor is a cardiac Apoptosis Repressor with Caspase Recruitment Domain (cARC) protein.
Chatterjee teaches an adenoviral vector containing the transgene encoding Apoptosis Repressor with Caspase Recruiting Domain (cARC) protein (section "Adenoviral Vector Construction/Viral Delivery", pg. 1463, left-column) and its usage in vivo to preserve left ventricular function after ischemia by mediating reduction in apoptosis and ventricular remodeling.
It would have been obvious to one of ordinary skill in the art before the effective filling date of the invention to have modified the rAAV vector of Pleger to include an apoptotic inhibitor, specifically cARC protein, because it would have merely amounted to a simple combination of known genes whose functions in gene therapy are known to be associated to treat heart failures. One would have been motivated to have done so for the known advantage of cARC protein that reduces apoptosis and preserve ventricular geometry and function. Moreover, Chatterjee teaches that cARC protein “offers a potential strategy after myocardial ischemia to protect the heart from late postischemic cardiomyopathy” (subsection “Conclusions”, pg. 1461).
In addition, Jazwa teaches rAAV bicistronic vectors carrying two angiogenic genes (AAV-FGF4-IRES-VEGF-A) for treatment of peripheral and myocardial ischemia in mice (Abstract). Jazwa further teaches “blood flow in ischemic hindlimbs of AAV-FGF4-IRES-VEGF-A-treated mice showed significantly better perfusion” than mice treated with rAAV vectors carrying individual angiogenic genes (Figure 5A and B; pg. 7).
Therefore, it would have been obvious for one to have modified the rAAV vector of Pleger as discussed above and incorporate an Internal Ribosome Entry Site (IRES) between the S100 family protein transgene and the apoptotic inhibitor transgene as taught by Jazwa’s bicistronic rAAV vector. One would have had a reasonable expectation of success in doing so because constructions and applications of bicistronic rAAV vectors are known in the art, in particular, Jazwa’s teachings on bicistronic rAAV vectors and their therapeutic uses in cardiovascular diseases in vivo.
Neither Pleger or Chatterjee teaches wherein the promoter is a cardiac troponin T (cTNT) promoter.
Prasad teaches rAAV vector comprising a transgene and a cardiac troponin T (cTnT) promoter operably linked thereto (Abstract, “Methods” subsection). Prasad further teaches expression from the cTnT promoter is only 2.4 fold lower compared to strong viral promoters such as the CMV immediate-early promoter in cardiac myocytes, and expression of transgene under the control of cTnT promoter “confer significant and long-term protection against myocardial infarction in mice” (pg. 339, right-column, first paragraph).
It would have been obvious to one of ordinary skill in the art before the effective filling date of the invention to have modified Pleger’s rAAV vector, comprising a cARC apoptotic inhibitor taught by Chatterjee, with cardiac-restricted cTnT promoter as taught by Prasad because it would have merely amounted to a simple substitution of a cardiomyocyte-specific promoter in Pleger’s rAAV vector with another cardiomyocyte-specific promoter cTnT from Prasad which function was known in the art. One would have been motivated to have done so for the recognized therapeutic benefit of cardioprotective gene expression by the cTnT promoter in rAAV vectors. One would have had a reasonable expectation of success in doing so because Prasad and Pleger teach rAAV vectors comprising cardiomyocyte-specific promoters and their delivery into cardio myocytes to express transgenes, and Jazwa also teach successful construction and delivery of rAAV vectors carrying two transgenes in vivo.
However, Pleger teaches the rAAV particle comprises an AAV capsid comprising capsid proteins from AAV9 serotype and wherein the rAAV nucleic acid vector is encapsidated in the AAV capside from AAV9 serotype (Abstract). Pleger does not teach wherein the capsid proteins are from an AAVrh.10 serotype.
Kotin teaches a rAAV particle comprising an AAV capsid that comprises capsid proteins from an AAV9 or AAVrh.10 serotype ([00117], claim 2) and the AAV capsid encapsidates a payload (i.e., nucleic acid vector) comprising bicistronic or multicistronic reporters (i.e., two or more transgenes) ([0089]). Kotin further teaches the payload comprises an IRES element allowing translation initiation in the middle of the transcript ([0089]), at least one tissue-specific promoter ([0090]), particularly, cardiac troponin T promoter ([00285]), and two inverted terminal repeat sequences ([00293]).
Thus, it would have been obvious to one of ordinary skill in the art before the effective filling date of the invention to have modified Pleger’s rAAV capsid protein serotype to AAVrh.10 as taught by Kotin because it would have merely amounted to a simple substitution of rAAV capsid protein serotypes which functions were known in the art. One would have had a reasonable expectation of success in doing so because Kotin teaches rAAV particles comprising capsid protein from AAVrh.10 serotype and delivery of these rAAV particles in cardiac tissues. In addition, Kotin teaches these rAAV particles comprise nucleic acid vectors of similar architecture required in instant claims, including, (i) a bicistronic payload construct (i.e., nucleic acid vector for delivering two or more transgenes), (ii) two ITR sequences, (iii) a cTnT promoter, (iv) a polyadenylation signal, and (v) an IRES in the middle of the transcript.
Regarding claim 12, the obviousness to modify the rAAV serotype of Pleger to rAAV.rh10 as taught by Kotin is discussed above as applied to claim 1. Further, Kotin teaches the rAAV particles are formulated into a pharmaceutical composition for intracardiac delivery ([00534], [00499], claim 1).
Regarding claims 24 and 25, the teachings of Pleger and Chatterjee and the obviousness of combining Pleger’s rAAV vector with a cARC transgene as taught by Chatterjee are discussed and applied to claim 1. Once motivated to include more than one transgene in the same rAAV vector, it would have been an obvious routine vector design to arrange transgene 1 (S100A1 protein) and transgene 2 (apoptotic inhibitor) under the control of a common promoter (e.g., positioning cS1000A1 5’ to apoptotic inhibitor or positioning apoptotic inhibitor 5’ to S100A1). This arrangement represents a predictable vector design within the level of ordinary skill with reasonable expectation of success, as evidenced by Jazwa’s teachings.
Response to Arguments
Applicant’s remarks filed on June 16, 2026 have been fully considered but they are not persuasive for the following reasons.
Applicant argues that “none of Pleger, Mueller, Chatterjee, Jazwa, and Prasad teach or suggest encapsidating the nucleic acid vector of claim 1 in an AAV capsid comprising capsid proteins from an AAVrh.10 serotype” (pg. 6, para. 3)
Applicant’s arguments have been fully considered but they are not persuasive because, as stated in instant Office Action, Pleger teaches a rAAV particle comprising capsid proteins from AAV9 serotype and Kotin teaches a rAAV particle comprising capsid proteins from AAVrh.10 serotype for delivery into cardiac tissues. Further, Kotin teaches the rAAV particle comprises an rAAV nucleic acid vector comprising an architecture similar to instantly amended claims, including two or more transgenes ([0089]), two inverted terminal repeat sequences ([00293]), a cardiac troponin T promoter ([00285]), and an IRES translation element in the middle of the transcript ([0089]). Thus, it would have been obvious to have modified Pleger’s rAAV capsid protein from AAV9 to AAVrh.10 as taught by Kotin because it would have merely amounted to a simple substitution of prior art elements according to known methods to yield predictable results. One would have had a reasonable expectation of success in doing so because Kotin teaches the rAAV particle carrying the nucleic acid vector could comprise capsid proteins from AAV9 or AAVrh.10 serotypes.
Applicant argues that “the claimed rAAV particles show beneficial effects that could not have been reasonably predicted by one of ordinary skill in the art at the time of filling” (pg. 6, para. 4)
This argument is not persuasive because MPEP § 2145(II) notes that prima facie obviousness is not rebutted by merely recognizing additional advantages or latent properties present but not recognized in the prior art. The combination of instantly cited references teaches the structure and therapeutic benefits of transgenes in the claimed invention, and it is the opinion of the examiner that, as such, any purported advantages that result from the claimed structure would also flow naturally from the prior art combination.
As previous stated in Office Action mailed on April 16, 2026, Pleger already teaches an rAAV vector suitable for delivering therapeutic transgenes (S100A1 protein) into the heart of a subject, and Chatterjee teaches the use of an additional therapeutic transgenes (cARC protein). One of ordinary skill in the art would have been motivated to include cARC transgene in the rAAV vector of Pleger as both teaches the therapeutic functions of S100A1 and cARC proteins in cardiac tissues. Further, Prasad discloses therapeutic advantages of using cTnT promoter where expression of transgene under the control of cTnT promoter “confer significant and long-term protection against myocardial infarction in mice” despite expression levels is 2.4-fold lower than strong viral promoter CMV (pg. 339, right-column, first paragraph). Accordingly, a person ordinary skill in the art would have been motivated to select cTnT promoter to obtain these benefits. Optimization of expression levels through promoter selection represents routine design choice.
Also as previous stated in Office Action mailed on April 16, 2026, “[o]bviousness does not require absolute predictability, but at least some degree of predictability is required. Evidence showing there was no reasonable expectation of success may support a conclusion of nonobviousness” (see MPEP 2143.02 (II)). In this instance, each element, S100A1 gene, cARC gene, rAAV vector, and cTnT promoter, was known in the art and performs the same function in the combination as it does individually. Pleger’s rAAV vector and the claimed invention differs in the combination of S100A1 and cARC into a single rAAV vector and under the control of cTnT promoter, a substitute of Pleger’s cardiomyocyte-specific promoter; combination of these two known elements merely results in their co-expression is a reasonable expected outcome (see MPEP 2143 (I)(A)) and substitution of two known elements merely represents swapping similar features that serve the same purpose to drive expression in cardiac tissues is another reasonable expected outcome (see MPEP 2143 (I)(B)).
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, 12, and 24-25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 4-6, 10-12, 18-19 of U.S. Patent No. 12,667,629 in view of Prasad (J Gene Med., 2011, 13, 333-341).
Regarding instant claims 1, 12, and 24-25, ‘629 recites a rAAV particle comprising a rAAV nucleic acid vector for delivering two or more transgenes into the heart of a subject (claim 10). ‘629 further recites wherein the nucleic acid vector comprises two AAV inverted terminal repeat (ITR) sequences, a transgene encoding an S100 family protein that is at least 95% identical to SEQ ID NO: 25 or SEQ ID NO: 26, which the specification teaches they are S100A1 proteins (pg. 22, line 9), another transgene encoding for a cardiac apoptosis repressor with caspase recruitment domain, a polyadenylation signal, and a cardiac-restricted promoter (claims 1, 5, and 6). ‘629 further recites a composition comprising the rAAV particle (claim 12), and wherein the rAAV particle comprises capsid protein derived from AAVrh.10 (claim 11). ‘629 also recites the same arrangement of transgenes as recited in instant claims 24 and 25 (claims 18 and 19).
However, ‘629 does not recite wherein the cardiac-restricted promoter is a cardiac troponin T promoter.
Prasad teaches rAAV vector comprising a transgene and a cardiac troponin T (cTnT) promoter operably linked thereto (Abstract, “Methods” subsection). Prasad further teaches expression from the cTnT promoter is only 2.4 fold lower compared to strong viral promoters such as the CMV immediate-early promoter in cardiac myocytes, and expression of transgene under the control of cTnT promoter “confer significant and long-term protection against myocardial infarction in mice” (pg. 339, right-column, first paragraph).
It would have been be obvious to one of ordinary skill in the art to have modified the rAAV vector taught by ‘629’s rAAV vector with cardiac-restricted cTnT promoter as taught by Prasad because it would have merely amounted to a simple substitution of prior art elements according to known methods to yield predictable results. One would have been motivated to have done so for the recognized therapeutic benefit of cardioprotective gene expression by the cTnT promoter in rAAV vectors. One would have had a reasonable expectation of success in doing so because ‘629 recites and Prasad teaches rAAV vectors comprising cardiomyocyte-specific promoters and their delivery into cardio myocytes to express transgenes.
Claim 1, 12, 24, and 25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 3, 8, 10, 11, 16, 17, and 19 of copending Application No. 17/628,139 (hereinafter as ‘139) (claims filed on 05/01/2026). Although the claims at issue are not identical, they are not patentably distinct from each other.
Regarding instant claims 1, 12, 24, and 25, ‘139 recites a recombinant rAAV nucleic acid vector for delivering two or more transgenes into the heart of a subject, wherein said vector comprises all limitations required in the instant claim 1. ‘139 further recites the two transgenes comprise an apoptotic inhibitor cARC and a S100A1 protein (claim 3). ‘139 also recites the presence of an IRES element between the two transgenes (claim 8), a cardiac-restricted promoter cTnT (claims 10 and 11), an rAAV particle encapsidated in an AAV capsid comprised of capsid proteins derived from AAVrh.10 (claims 16 and 17). ‘139 also recites a composition comprising the rAAV particle (claim 19). ‘139 does not explicitly recite the instant claims 24 and 25 reciting the positions of the two transgenes; however, it would have been an obvious routine vector design to arrange transgene 1 and transgene 2 under the control of a common promoter (e.g., positioning cS1000A1 5’ to apoptotic inhibitor or positioning apoptotic inhibitor 5’ to S100A1). This arrangement represents a predictable vector design within the level of ordinary skill with reasonable expectation of success.
This is a provisional nonstatutory double patenting rejection.
Response to Arguments
Applicant’s arguments (Remarks received on June 16, 2026) have been fully considered but are not persuasive for the following reasons.
Applicant argues that “claims 7 and 8 are not pending in the present application, and, therefore, the rejection is moot” (pg. 5, para. 3).
This argument has been fully considered but it is not persuasive because the instant double patenting rejection is necessitated by amendments to the independent claim. The amendment changes the scope of the independent claim and therefore, requires reevaluation for double patenting. The instantly cited U.S. Patent, previously cited as copending Application No. 18/269,089, recites same structural limitations in the instant claims, particularly specific S100A1 proteins that fall within the instantly recited S100A1 protein genus. As supported by secondary references in the instant Double Patenting rejection above, it would have been obvious to have applied the recited subject matter in ‘629’s claims to instantly recited claims.
Applicant argues that “arguments and amendments submitted herein place the claims in condition for allowance, other than the provisional nonstatutory double patenting rejection. This application has an earlier patent term filing date than the US 17/628,139 applications” (pg. 5, para. 6).
Applicant’s arguments have been fully considered but they are not persuasive because as stated in the instant Office Action 35 U.S.C. 103 rejection and response to arguments regarding prior art rejections, instantly amended claims are not in condition for allowance. Thus, the provisional nonstatutory double patenting rejection of copending Application No. 17/628,139 is maintained.
Conclusion
No claims are allowable.
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/QIWEN SU-TOBON/Examiner, Art Unit 1636
/NEIL P HAMMELL/Supervisory Patent Examiner, Art Unit 1636
Prosecution Insights