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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 10 Nov 2025 has been entered.
Status of Claims
This action is written in response to applicant’s Remarks received March 23, 2026. Claims 1, 9-10, 12, and 24-25 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 Claims 13-16, and 18-23 are withdrawn from prosecution as being drawn to non-elected subjection matter on Response to Restriction/Election received on 2 August 2024.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 2-8 11, 17 are cancelled. Accordingly, claims 1, 9-10, 12, and 24-25 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.
Declaration Filed under 37 CFR 1.132
The Declaration of Sweeney under 37 CFR 1.132 filed 10 Nov 2025 has been considered but it is insufficient to overcome the rejection of claim 1, 9-10, 12, and 24-25 based upon 35 U.S.C. 103 as set forth in this Office action, and Examiner’s discussion included in section 11 “Response to Arguments”, reason ii.
Priority
Acknowledgment is made of applicant’s claim for priority on Provisional Application No. 62/682,772, filed on 08 June 2018.
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, 9-10, 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), and Prasad (J Gene Med., 2011, 13, 333-341). This is a new rejection necessitated by Applicant's amendments to the claims in the response filed on March 23, 2026.
Regarding claim 1, Pleger teaches a recombinant adeno-associated virus (rAAV) 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). 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.
Regarding claim 9, 10, and 12, Pleger further teaches the rAAV vector of claim 1 is encapsidated in an AAV capsid, wherein the AAV capsid comprises capsid proteins derived from AAV9 serotype (Abstract).
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 arguments (Remarks received on March 23, 2026) have been fully considered but are not persuasive for the reasons set forth below.
i) “one of skill in the art would not have been motivated to combine two transgenes, including one previously tested in an adenoviral vector, (emphasis added) into a single rAAV vector under the control of a cTnT promoter as claimed because each of those changes from the teachings of the prior art carry the risk of reducing expression of the transgenes.” (pg. 6 of Remarks)
As previously explained in Office Action 12/22/2025, the rejection does not rely on the adenoviral backbone taught by Chatterjee, but rather on the cARC protein’s function and therapeutic use in cardia tissues. 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). The fact that Chatterjee uses an adenoviral vector backbone or delivery system does not teach away the function and therapeutic use of the cARC protein itself, which is the basis of the proposed combination. Thus, 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. Inventor’s Declaration supports, rather than undermines, this rationale for combining the teachings of Pleger and Chatterjee with the statement that “adenovirus vectors, which result in transient gene expression and significant morbidity in vivo, limit the usefulness of these vectors in human gene therapy; whereas AAV vectors demonstrate long-term gene expression in vivo, a broad host range, and the ability to infect growth-arrested cells” (Declaration on received 10 Nov 2025, paragraph 12). Accordingly, one of ordinary skill in the art would have been motivated to utilize the AAV vector taught by Pleger deliver the two therapeutic transgenes, rather than the adenoviral vector taught by Chatterjee, with a reasonable expectation of success as demonstrated by Jazwa with rAAV vectors comprising two transgenes.
In addition, as previously explained in Office Action 12/22/2025, Applicant has not provided any teachings in the prior art that would have discouraged one of ordinary skilled in the art from co-expressing two or more transgenes in an rAAV vector. On the other hand, construction and in vivo delivery of single recombinant AAV vectors comprising two transgenes are known in the art (see section 10 for teachings of Jazwa on rAAV vectors carrying two angiogenic genes (AAV-FGF4-IRES-VEGF-A) for treatment of peripheral and myocardial ischemia in mice). In addition, Renaud-Gabardos (World J Exp Med., 2015, 5, 1, 11-20) further supports the disadvantages of using two different vectors for multiple transgene expression, including ratio of the therapeutic molecules cannot be controlled and the cost of two therapeutic vectors in a clinical perspective in higher than a single one (pg. 15, left-column, second paragraph). In fact, co-expressing two transgenes in a single vector (multicistronic) allows stable transgene expression with a constant ratio of the proteins (Figure 2). Further, Table 2 teaches the use of multicistronic AAV vectors in clinical trials for various pathologies, including cardiovascular diseases.
With respect to cTnT promoter, 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.
ii) Applicant argues that “while lower expression is beneficial for VEGF-A expression in Jazwa’s experiments, it may not be beneficial for every transgene. There is no teaching or suggestion in Chatterjee, for example, that levels of cARC, which was expressed in an adenoviral vector, should be limited or titrated for beneficial effects” (pg. 6 of Remarks).
The proper inquiry is not whether the prior art teaches that reduced expression is beneficial, but whether the prior art would have discouraged this modification. There is no teaching or suggestion in Chatterjee or other prior art references that expression of cARC in an rAAV vector, or under the control of cTnT promoter, would be inoperable or undesirable.
iii) Applicant asserts that “there was no statistical significance between the monocistronic rAAV vector and the bicistronic rAAV vector” (pg. 7 of Remarks, first paragraph).
This argument is not persuasive because the absence of a statistically significance does not negate the teaching that expression of a bicistronic vector is functional and operable. Rather, this demonstrates that co-expression of two transgenes in a single rAAV vector yields comparable performance, further supporting a reasonable expectation of success when combining S100A1 and cARC into a single rAAV vector. In addition, as mentioned in reason i) Renaud-Gabardos teaches motivations of combining more than one transgene in a single rAAV vector.
iv) Applicant argues that “even small changes in gene expression can affect the efficacy of gene therapy, especially in combination with two untested transgenes in combination, as claimed” (pg. 6 of Remarks) and “the combination of the claimed features yields rAAV vectors having more than a predictable functions in view of the cited references.” (pg. 7 of Remarks, last sentence).
This argument is not persuasive because “[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; however, combination of these two known elements merely results in their co-expression, which 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, which is another reasonable expected outcome (see MPEP 2143 (I)(B)). In addition, applicant’s argument that “there was no statistical significance between the monocistronic rAAV vector and the bicistronic rAAV vector” (pg. 7 of the Remarks, first paragraph) further supports that combining more than one transgenes into a single rAAV vector does not produce unexpected results but rather predictable ones.
v) Applicant argues that “these findings are further illustrated in Hammers et al…bioRxiv [Preprint]. 2025…”.
As previously explained in Office Action 12/22/2025, the cited article provides later validation and optimization of the claimed rAAV vector, and such evidence is not commensurate in scope and does not demonstrate that combination of prior art teachings is not obvious or one of ordinary skill in the art would have had unpredictable success.
vi) Applicant contends that “Examiner’s assertion of obviousness in view of the cited references stems from an improper application of hindsight reasoning starting from the teachings of the present application rather than starting from the teachings in the prior art” (pg. 9 of Remarks, second paragraph).
It must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971). Pleger teaches S100A1 gene therapy reversed progressive deterioration of cardiac performance and left ventricular remodeling (abstract) and Chatterjee teaches cARC gene therapy in vivo preserves left ventricular function after ischemia by mediating reduction in apoptosis and ventricular remodeling (pg. 1463, left-column). Thus, both references are directed to ventricular remodeling and improving cardiac performance via gene therapy. A person ordinary skill in the art would have been motivated to have combine these teachings to achieve additive benefits. Further, neither Pleger or Chatterjee teaches away from this combination of transgenes or discourages usage of additional cardioprotective genes including S100A1 or cARC because the proposed modification would not render the prior art invention being modified unsatisfactory for its intended purpose (see MPEP 2143.01 (V)) and the proposed combination of the prior art would not change of the principle of operation of the prior art invention (see MPEP 2143.01 (VI))
Applicant’s response is not sufficient to rebut the prima facie case of obviousness, and the rationale to combine prior art elements according to known methods to yield predictable results is strengthened with Inventor’s reference cited in the Declaration and teachings of Jazwa and Renaud-Gabardos. Further, the prima facie case of obviousness is not based on hindsight, rather it is based on a reasoned combination and substitution of prior art elements. Accordingly, the rejection under 35 U.S.C. 103 is maintained.
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 7 and 8 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1, 7, 12, 21, 22, 24, 38, and 39 of copending Application No. 18/269,089 (Claims amended on 08 March 2024) in view of Prasad (J Gene Med., 2011, 13, 333-341).
Regarding claims 7 and 8, the teachings of ‘089 are discussed above and applied to claim 1.
However, ‘089 does not teach wherein the promoter is a cardiac-restricted promoter, which is selected from the group of genes listed in the instant claim 8.
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 before the effective filling date of the invention to have modified the rAAV vector taught by ‘089 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 ‘089 and Prasad teach rAAV vectors and their delivery into cardio myocytes.
This is a provisional nonstatutory double patenting rejection.
Claim 1, 2, 4, 6-10, 12, 24, and 25 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 3, 5, 8, 10, 11, 16, 17, and 19 of copending Application No. 17/628,139 (hereinafter as ‘139) (Claims amended on 21 Oct 2025). Although the claims at issue are not identical, they are not patentably distinct from each other.
Regarding claims 1, 2, 4, 6-10, 12, 24, and 25, ‘139 teaches 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 teaches the two transgenes comprise an apoptotic inhibitor cARC and a S100 family protein (claim 3), wherein the S100 family protein is a S100A1 protein (claim 5), as evidenced by BLAST alignment of SEQ ID NO:8 recited in the claim. ‘139 also teaches 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 serotypes listed in the instant claim 10 (claims 16, 17, and 19). ‘139 does not explicitly teach 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 March 23, 2026) have been fully considered but are not persuasive for the reasons set forth below.
i) Applicant asserts that “the later-filed, later-expiring patent could nor properly serve as reference patent in an ODP rejection with respect to the earlier-filed, earlier-expiring patent” (pg. 10 of Remarks).
This argument is not persuasive because Applicant has not identified and Examiner is not aware of any binding authority (e.g., statute, Federal Circuit precedent, MPEP) that supports Applicant’s assertion. Therefore, the Examiner applies the established principles set forth in the MPEP and relevant Federal Circuit case law governing obviousness-type double patenting.
In addition, Applicant’s assertion regarding relative expiration dates is speculative. The actual expiration date of instant application cannot be definitively determined at this stage as it may be affected by factors including patent term adjustment or patent term extension. Accordingly, the premise that the instant application is an earlier-filed, earlier-expiring patent and the reference application is a later-filed, later-expiring patent has not been established based on the present record.
Further, MPEP 804.02 (VI) discloses terminal disclaimers are required to overcome nonstatutory double patenting rejections in applications filed on or after June 8, 1995:
35 U.S.C. 154(b) includes provisions for patent term adjustment based upon prosecution delays during the application process...As the presence of a terminal disclaimer affects whether the patent is granted an adjustment, it is necessary that the terminal disclaimer be filed in the application in order to accurately determine whether the patent is entitled to a term adjustment...37 CFR 1.321(c)(3) requires that a terminal disclaimer filed to obviate a nonstatutory double patenting rejection based on commonly owned conflicting claims include a provision that any patent granted on that application be enforceable only for and during the period that the patent is commonly owned with the application or patent which formed the basis for the rejection...These requirements serve to avoid the potential for harassment of an accused infringer by multiple parties with patents covering the same patentable invention. See, e.g., In re Van Ornum, 686 F.2d 937, 944-48, 214 USPQ 761, 767-70 (CCPA 1982). Not insisting upon a terminal disclaimer to overcome a nonstatutory double patenting rejection in an application subject to a 20-year term under 35 U.S.C. 154(a)(2) would result in the potential for the problem that 37 CFR 1.321(c)(3) was promulgated to avoid. Further, as a terminal disclaimer is only effective in the application in which it is filed, it is necessary to require that the terminal disclaimer be filed in each application and/or patent that is subject to the common ownership requirement in order to provide complete notice to the public of this obligation. Further, as a terminal disclaimer is only effective in the application in which it is filed, it is necessary to require that the terminal disclaimer be filed in each application and/or patent that is subject to the common ownership requirement in order to provide complete notice to the public of this obligation.
In addition, MPEP 804 (I)(B)(1)(b)(i) states that
“If a provisional nonstatutory double patenting rejection is the only rejection remaining in an application having the earlier patent term filing date, the examiner should withdraw the rejection in the application having the earlier patent term filing date and permit that application to issue as a patent, thereby converting the provisional nonstatutory double patenting rejection in the other application into a nonstatutory double patenting rejection upon issuance of the patent.”
Accordingly, the provisional nonstatutory double patenting rejections are maintained.
Conclusion
No claims are allowable.
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.
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QIWEN SU-TOBON
Examiner
Art Unit 1636
/NEIL P HAMMELL/Supervisory Patent Examiner, Art Unit 1636
Prosecution Insights