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 .
Amendments
The supplemental response of 3/24/2026 has been considered and is made of record. In the supplemental reply filed 3/24/2026, Applicant has amended Claims 1, 5, 13, 20, and 32, and cancelled Claims 3, 4, 16, 17, 108-111, 132-134.
Claims 13, 15, 20, 32, 38, 45, 93, and 135 are pending but withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a non-elected invention, there being no allowable generic or linking claim.
Claims 1, 2, and 5 are under consideration.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 2/11/2026 was filed after the mailing date of the non-final Office action on 11/18/2025. The submission is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Withdrawn Claim Objections
The objection to Claim 5 has been withdrawn due to Applicant’s amendment to spell-out the abbreviations.
Withdrawn 35 USC § 102
The prior rejection of Claims 1 and 2 under 35 U.S.C. 102(a)(1)(a)(2) as being anticipated by Rodino-Klapac et al., (WO2018/170408, filed 3/16/2018, published 9/20/2018, see IDS filed 9/15/2022) is withdrawn in light of Applicant’s amendment of Claim 1 to limit the polynucleotide encoding the sarcoglycan as SEQ ID NO: 7 or 19, which is a limitation Rodino-Klapac does not teach.
Withdrawn 35 USC § 103
The prior rejection of Claims 1 and 5 under 35 U.S.C. 103 as being unpatentable over Campbell et al., (US 6,262,035, see IDS filed 9/15/2022), in view of Nigro et al. (Nat Genet, 1996, 2:195-198) and NCBI Reference Sequence NM_172244 (1993, pgs. 1-4) is withdrawn in light of Applicant’s amendment of Claim 1 to limit the polynucleotide encoding the sarcoglycan as SEQ ID NO: 7 or 19, which is a limitation neither Campbell nor Nigro teach.
The prior rejection of Claim 1 under 35 U.S.C. 103 as being unpatentable over Campbell et al., (US 6,262,035, see IDS filed 9/15/2022), in view of Nigro et al. (Nat Genet, 1996, 2:195-198) and NCBI Reference Sequence NM_172244 (1993, pgs. 1-4), in further view of Rodino-Klapac et al., (WO2018/170408, see IDS filed 9/15/2022) and Vitale et al. (J Cell Sci, 2012, 125(Pt 7):1807-1813) is withdrawn in light of Applicant’s amendment of Claim 1 to limit the polynucleotide encoding the sarcoglycan as SEQ ID NO: 7 or 19, which is a limitation neither Campbell, Nigro, Rodino-Klapac (WO2018), nor Vitale teach.
New Claim Rejections - 35 USC § 112(a)
(Scope of Enablement)
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 1 and 2 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for a method of restoring or stabilizing a dystrophin-associated protein complex (DAPC) in a subject suffering from Duchenne muscular dystrophy (DMD) or Becker muscular dystrophy (BMD) comprising administering a polynucleotide encoding a beta or gamma sarcoglycan of SEQ ID NOs: 7 or 19, respectively, and a polynucleotide encoding a dystrophin protein, does not reasonably provide enablement for a method without a dystrophin gene. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to practice the invention commensurate in scope with these claims.
SCOPE OF THE INVENTION
The breadth of the claims encompasses a genus of methods of restoring or stabilizing a DAPC in a subject suffering from DMD or BMD. As discussed supra, the specification fails to describe the genus of methods and would require undue experimentation to discover these methods. The specification only discloses and provides guidance for restoring or stabilizing a DAPC in a subject suffering from monogenic LGMDE or LGMD2C muscular dystrophy comprising administering a polynucleotide encoding a beta or gamma sarcoglycan of SEQ ID NOs: 7 or 19, respectively.
Independent claim 1 encompasses a genus of methods of restoring or stabilizing a DAPC in a subject by beta or gamma sarcoglycan gene therapy in a subject suffering from a muscular dystrophy.
Dependent claim 2, limits the muscular dystrophy to DMD or BMD.
The factors to be considered in determining whether undue experimentation is required are summarized In re Wands 858 F.2d 731, 8 USPQ2nd 1400 (Fed. Cir, 1988). The Court in Wands states: “Enablement is not precluded by the necessity for some 'experimentation.'” Clearly, enablement of a claimed invention cannot be predicated on the basis of quantity of experimentation required to make or use the invention. “Whether undue experimentation is needed is not a single simple factual determination, but rather is a conclusion reached by weighing many factual considerations.” (Wands, 8 USPQ2d 1404). The factors to be considered in determining whether undue experimentation is required include: (1) the quantity of experimentation necessary, (2) the amount or direction or guidance presented, (3) the presence or absence of working examples, (4) the nature of the invention, (5) the state of the prior art, (6) the relative skill of those in the art, (7) the predictability or unpredictability of the art, and (8) the breadth of the claims. While all of these factors are considered, a sufficient amount for a prima facie case is discussed below.
The office has analyzed the specification in direct accordance to the factors outlined in In re Wands. MPEP 2164.04 states: "[W]hile the analysis and conclusion of a lack of enablement are based on factors discussed in MPEP 2164.01(a) and the evidence as whole, it is not necessary to discuss each factor in written enablement rejection." These factors will be analyzed, in turn, to demonstrate that one of ordinary skill in the art would have had to perform "undue experimentation" to make and/or use the invention and therefore, Applicant's claims are not enabled commensurate with the scope of the invention.
ACTUAL REDUCTION TO PRACTICE
The specification does not provide guidance for or a working example for restoring or stabilizing a dystrophin-associated protein complex (DAPC) in a subject suffering from Duchenne muscular dystrophy (DMD) or Becker muscular dystrophy (BMD) comprising administering a polynucleotide encoding a beta or gamma sarcoglycan of SEQ ID NOs: 7 or 19, respectively. The absence of working examples directed to this gene therapy method necessitates further experimentation. Additionally, no working examples were provided that utilize the claimed gene therapy to treat the claimed DMD/BMD patients. Therefore, the specification does not provide sufficient guidance on how to practice the claimed method.
In regard to claim 1 encompassing a genus of methods of restoring or stabilizing a DAPC in a subject suffering from a muscular dystrophy, wherein the muscular dystrophy is DMD or BMD as per claim 2, the specification enables two embodiments for the claimed genus of methods.
Specifically, Applicant discloses that in a SGCB knockout mouse model (i.e., a subject with LGMD2E), the administration of a AAV-hSGCB restores not only beta-sarcoglycan expression, but also dystrophin and alpha-sarcoglycan (Examples 1 & 2, [0249-0283], Figs. 5-9). Applicant’s specification admits that the SGCB -/- mice have been shown to concurrently display loss of additional sarcoglycans (alpha, gamma, and delta) [0257]. Similarly, Applicant demonstrates that in the gamma-sarcoglycan (GSG) knock out mouse (i.e., a subject with LGMD2C), there is also a restoring effect not only on gamma-sarcoglycan, but also on alpha-sarcoglycan and dystroglycan ([0273], Fig. 6). In both the LGMDE and LGMD2C embodiments, Applicant has established that there was a reasonable expectation of predictability in the monogenic muscular dystrophies of LGMD that the unmutated accessory proteins could be restored or stabilized at the DAPC in an otherwise wildtype genetic background.
However, Applicant does NOT demonstrate that beta or gamma sarcoglycan can restore stabilize the DAPC in a DMD or BMD mutant model. Furthermore, Applicant admits DMD and BMD are caused by mutations in the dystrophin gene. Applicant explains that these mutations ultimately lead to “protein deficiency” and loss of stabilization of the dystrophin-associated protein complex [0002]. Importantly, Applicant’s reduction to practice for restoring or stabilizing the DAPC have been conducted in a wildtype dystrophin background, not in a DMD/BMD mutant background. Therefore, although Applicant demonstrates that beta-sarcoglycan can restore the DAPC in a beta-sarcoglycan mutant model and that gamma-sarcoglycan can restore the DAPC in a gamma-sarcoglycan mutant model, there is no evidence nor reasonable expectation that these sarcoglcyan based gene therapies could restore the DAPC in a DMD/BMD mutant model where the dystrophin gene has been mutated and is otherwise unavailable for restoration or stabilization in the dystrophin-associated complex.
STATE OF THE ART & QUANTITY OF EXPERIMENTATION
In fact, the state of the art teaches that beta or gamma sarcoglycan gene therapies to restore or stabilize the DAPC in a DMD/BMD patient is not a highly successful technique or has highly variable results. Specifically, the review of Shimizu-Motohashi (JPMed, 2019 (9):1, “Restoring Dystrophin Expression in Duchenne Muscular Dystrophy: Current Status of Therapeutic Approaches”) explains that to date, the therapeutic approaches to restore the dystrophin-associated complex can be divided into two groups: restoring dystrophin expression or compensating for the lack of dystrophin. The former group includes read-through therapy, exon skipping therapy, gene therapy, and cell therapy, all of which replace the mutated dystrophin gene. The later group compensate for the loss of dystrophin with anti-inflammatories, anti-fibrotics, antioxidants, myostatin pathway inhibitors, nNOS enhancement, and utrophin upregulation therapies (Introduction, p.2). Importantly, none of the current compensatory therapies for patients with a mutated dystrophin gene are directed to sarcoglycan gene therapy. Consequently, there is ample reason to conclude that there would be a high degree of unpredictability in restoring or stabilizing the dystrophin-associated complex in a DMD/BMD patient with a mutated dystrophin gene with sarcoglycan gene therapy.
Since the prior art at the effective filing date of the present application did not provide guidance for a beta or gamma sacroglycan gene therapy method to restore or stabilized the DAPC in a DMD/BMD patient, it is incumbent upon the instant specification to do so. The physiological art is recognized as unpredictable (MPEP 2164.03). As set forth in In re Fisher, 166 USPQ 18 (CCPA 1970), compliance with 35 USC 112, first paragraph requires: “That scope of claims must bear a reasonable correlation to scope of enablement provided by specification to persons of ordinary skill in the art; in cases involving predictable factors, such as mechanical or electrical elements, a single embodiment provides broad enablement in the sense that, once imagined, other embodiments can be made without difficulty and their performance characteristics predicted by resort to known scientific laws; in cases involving unpredictable factors, such as most chemical reactions and physiological activity, scope of enablement varies inversely with degree of unpredictability of factors involved.” Moreover, the courts have also stated that reasonable correlation must exist between scope of exclusive right to patent application and scope of enablement set forth in the patent application (27 USPQ2d 1662 Ex parte Maize!.). In view of the foregoing, due to the lack of sufficient guidance provided by the specification regarding the issues set forth above, the state of the relevant art, and the breadth of the claims, it would have required undue experimentation for one skilled in the art to practice the instant broadly claimed invention.
CONCLUSION
In conclusion, since the art teaches that success of said method is prone to influence by multiple factors, and is highly unpredictable with respect to restoring or stabilizing the DAPC in a DMD/BMD patient with a mutated dystrophin gene by sarcoglycan gene therapy, and the specification does not provide ample guidance with respect to achieving the unexpected results, one would be burdened with undue experimentation to practice the claimed invention.
In conclusion, given the breadth of the claims and the limited scope of the specification, there is an undue quantity of experimentation is require to practice the invention beyond the scope of restoring or stabilizing a dystrophin-associated protein complex (DAPC) in a subject suffering from Duchenne muscular dystrophy (DMD) or Becker muscular dystrophy (BMD) comprising administering a polynucleotide encoding a beta or gamma sarcoglycan of SEQ ID NOs: 7 or 19, respectively, and a polynucleotide encoding dystrophin.
Withdrawn Double Patenting
The prior rejection of Claims 1 and 5 on the grounds of nonstatutory double patenting over claims 1-13 of U.S. Patent No. 12,258,573 (Rodino-Klapac et al., Patented 03/25/2025) is withdrawn in light of Applicant’s amendment of Claim 1 to limit the polynucleotide encoding the beta or gamma sarcoglycans as SEQ ID NO: 7 or 19, respectively, which is a limitation not claimed by cited patent that is directed to alpha sarcoglycan.
The prior rejection of Claims 1 and 2 on the grounds of nonstatutory double patenting over claims 1-16 of U.S. Patent No. 11,534,501 (Rodino-Klapac et al., Patented 12/27/2022) is withdrawn in light of Applicant’s amendment of Claim 1 to limit the polynucleotide encoding the beta or gamma sarcoglycans as SEQ ID NO: 7 or 19, respectively, which is a limitation not claimed by cited patent that id directed to microdystrophin.
Withdrawn Provisional Double Patenting
The prior provisional rejection of Claims 1 and 2 on the grounds of nonstatutory double patenting as being unpatentable over claims 1, 15 and 17 of copending Application No. 17/832,325 is withdrawn in light of Applicant’s amendment of Claim 1 to limit the polynucleotide encoding the beta or gamma sarcoglycans as SEQ ID NO: 7 or 19, respectively, which is a limitation not claimed by application that is directed to microdystrophin.
The prior provisional rejection of Claims 1 and 2 on the grounds of nonstatutory double patenting as being unpatentable over claims 1-3, 5, 10, 12, 13, 18, 20, 23, 26, 29 of copending allowed Application No. 17/253,956 is withdrawn in light of Applicant’s amendment of Claim 1 to limit the polynucleotide encoding the the beta or gamma sarcoglycans as SEQ ID NO: 7 or 19, respectively, which is a limitation not claimed by cited application that is directed to microdystrophin.
The prior provisional rejection of Claims 1 and 5 on the grounds of nonstatutory double patenting as being unpatentable over claims 3, 12-15, 17, 20, 22, and 26 of copending Application No. 18/060,263 is withdrawn in light of Applicant’s amendment of Claim 1 to limit the polynucleotide encoding the beta or gamma sarcoglycans as SEQ ID NO: 7 or 19, respectively, which is a limitation not claimed by cited application that is directed to alpha sarcoglycan.
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 obviousness-type 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); and 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 a nonstatutory double patenting ground provided the conflicting application or patent either is shown to be commonly owned with this application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement.
Effective January 1, 1994, a registered attorney or agent of record may sign a terminal disclaimer. A terminal disclaimer signed by the assignee must fully comply with 37 CFR 3.73(b).
Claims 1 and 5 stand rejected on the grounds of nonstatutory double patenting over claims 1-10 of U.S. Patent No. 12,377,170 (Rodino-Klapac et al., Patented 08/5/2025).
The subject matter claimed in the instant application is fully disclosed in the referenced patent as follows: the method of treating LGMD2E beta-sarcoglycanopathy in a subject comprising administering an AAV vector comprising flanking AAV ITRs, the MHCK7 promoter, intron, polyA and human sarcoglycan beta gene of SEQ ID NO:19 anticipates the method of instant application comprising the AAV vector comprising flanking AAV ITRs, the MHCK7 promoter, intron, polyA and human sarcoglycan beta gene of SEQ ID NO:7 (See SCORE 11/3/2025, rni.file, result #1).
Since the instant application claims are anticipated by cited patent claims, said claims are not patentably distinct.
RESPONSE TO ARGUMENTS
Applicant's arguments filed on 3/24/2026 are acknowledged.
Applicant argues that although the patented method recites treating a beta-sarcoglycanopathy , the cited patented claims do not recite the restoration or stabilization of the dystrophin-associated complex (DAPC) as claimed. Specifically, Applicant argues that the instant method restores or stabilizes the entire DAPC comprising dystrophin, alpha, beta, and gamma sacroglycans comprising administering only a single beta sarcoglycan based AAV vector (i.e., SEQ ID NO:7).
Applicant's arguments have been fully considered but they are not persuasive.
Contrary to Applicant’s assertion, the patented method would have inherently achieved the restorative or stabilizing effect recited in the preamble of instant claim 1. In other words, both the cited patent and instant claims are directed to the same patient with LGMD muscular dystrophy, the same gene therapy vector encoding human SGCB operably linked to a MCHK7 promoter, and the same routes of administration. Furthermore, the cited patent acknowledges that beta-sarcoglycan is a member of the DAPC, and that beta-sarcoglycan upregulated expression of the entire sarcoglycan complex as indicated by detection of alpha-sarcoglycan (col 44, 3rd para., Fig. 9, see also patented claim 10). MPEP 2145, Section II, states that the mere recognition of latent properties in the prior patent method does not render nonobvious an otherwise known invention. In re Wiseman, 596 F.2d 1019, 201 USPQ 658 (CCPA 1979). The court held that granting a patent on the discovery of an unknown but inherent function (here venting steam or vapor) "would remove from the public that which is in the public domain by virtue of its inclusion in, or obviousness from, the prior art." 596 F.2d at 1022, 201 USPQ at 661.).
Claims 1 and 5 stand rejected on the grounds of nonstatutory double patenting over claims 1-10 of U.S. Patent No. 12,285,497 (Rodino-Klapac et al., Patented 04/29/2025).
The subject matter claimed in the instant application is fully disclosed in the referenced patent as follows: the method of treating LGMD beta-sarcoglycanopathy in a subject comprising administering an AAV vector comprising flanking AAV ITRs, the MHCK7 promoter, intron, polyA and human sarcoglycan beta gene of SEQ ID NO:1 anticipates the method of instant application comprising the AAV vector comprising flanking AAV ITRs, the MHCK7 promoter, intron, polyA and human sarcoglycan beta gene of SEQ ID NO:7 (See SCORE 11/3/2025, rni.file, result #2).
Since the instant application claims are anticipated by cited patent claims, said claims are not patentably distinct.
RESPONSE TO ARGUMENTS
Applicant's arguments filed on 3/24/2026 are acknowledged and have been addressed above. As stated supra, both the cited patent and instant claims are directed to the same patient with LGMD muscular dystrophy, the same gene therapy vector encoding human SGCB operably linked to a MCHK7 promoter, and the same routes of administration.
Claims 1 and 5 stand rejected on the grounds of nonstatutory double patenting over claims 1 and 10 of U.S. Patent No. 12,263,230 (Rodino-Klapac et al., Patented 04/1/2025).
The subject matter claimed in the instant application is fully disclosed in the referenced patent as follows: the method of treating gamma-sarcoglycanopathy in a subject comprising administering an AAV vector comprising flanking AAV ITRs, the MHCK7 promoter, intron, polyA and human sarcoglycan gamma gene of SEQ ID NO:3 anticipates the method of instant application comprising the AAV vector comprising flanking AAV ITRs, the MHCK7 promoter, intron, polyA and human sarcoglycan gamma gene of SEQ ID NO:19 (See SCORE 11/3/2025, rni.file, result #1).
Since the instant application claims are anticipated by cited patent claims, said claims are not patentably distinct.
RESPONSE TO ARGUMENTS
Applicant's arguments filed on 3/24/2026 are acknowledged.
Applicant argues that although the patented method recites treating a gamma-sarcoglycanopathy , the cited patented claims do not recite the restoration or stabilization of the dystrophin-associated complex (DAPC) as claimed. Again, Applicant argues that the instant method restores or stabilizes the entire DAPC comprising dystrophin, alpha, beta, and gamma sacroglycans comprising administering only a single gamma sarcoglycan based AAV vector (i.e., SEQ ID NO:19).
Applicant's arguments have been fully considered but they are not persuasive.
As stated supra, the patented method would have inherently achieved the restorative or stabilizing effect recited in the preamble of instant claim 1 (see MPEP 2145, Section II). As above, both the cited patent and instant claims are directed to the same patient with muscular dystrophy, the same gene therapy vector encoding human SGCG operably linked to a MCHK7 promoter, and the same routes of administration. Furthermore, the cited patent acknowledges that gamma-sarcoglycan is a member of the DAPC (col 3, 2nd para., col 18, 1st para.).
Maintained Provisional Double Patenting
Claims 1 and 5 stand are provisionally rejected on the grounds of nonstatutory double patenting as being unpatentable over claims 1-20 of copending Application No. 19/086,011. This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented
The subject matter claimed in the instant application is disclosed in the referenced application as follows: the method of treating LGMD2E muscular dystrophy in a subject comprising administering an AAV vector comprising flanking AAV ITRs, the MHCK7 promoter, intron, polyA and beta-sarcoglcyan gene of SEQ ID NO:1 anticipates the method of instant application comprising the AAV vector comprising flanking AAV ITRs, the MHCK promoter, intron, polyA and beta-sarcoglycan gene of SEQ ID NO:7. The difference between the cited application claims and the instant claims lies in the fact that the cited application claims are much more specific to the AAV vector. Thus the invention of said claims of the cited application are in effect “species” of the “generic” invention of the instant claim. It has been held that the generic invention is “anticipated” by the “species”. See In re Goodman, 29 USPQ2d 2010 (Fed. Cir. 1993).
Since the instant application claims are anticipated by cited application claims, said claims are not patentably distinct.
RESPONSE TO ARGUMENTS
Applicant's arguments filed on 3/24/2026 are acknowledged and have been addressed above. As stated supra, both the cited patent and instant claims are directed to the same patient with LGMD muscular dystrophy, the same gene therapy vector encoding human SGCB operably linked to a MCHK7 promoter, and the same routes of administration.
Allowable Subject Matter
The method of restoring or stabilizing the DAPC in a LGMD2E subject comprising administering a polynucleotide encoding SEQ ID NO:7 is free of the prior art, albeit previously patented by the inventor. Specifically, SEQ ID NO:7 is a nucleotide expression cassette comprising flanking AAV ITRs, the MHCK7 promoter, intron, polyA and human sarcoglycan beta gene.
The method of restoring or stabilizing the DAPC in a LGMD2C subject comprising administering a polynucleotide encoding SEQ ID NO:19 is free of the prior art, albeit previously patented by the inventor. Specifically, SEQ ID NO:19 is a nucleotide expression cassette comprising flanking AAV ITRs, the MHCK7 promoter, intron, polyA and human sarcoglycan gamma gene.
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 extension fee 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 date of this final action.
No claims are allowed.
Examiner Contact Information
Any inquiry concerning this communication or earlier communications from the examiner should be directed to ARTHUR S LEONARD whose telephone number is (571)270-3073. The examiner can normally be reached on Mon-Fri 9am-5pm.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, James Doug Schultz can be reached on 571-272-0763. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/ARTHUR S LEONARD/Examiner, Art Unit 1631