DETAILED ACTION
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 amendment and remarks, filed 5/27/26, are acknowledged.
Claims 1, 6, 27, 33, 64, 72 have been amended.
Claims 1, 6-7, 9, 12 23, 27, 33, 38, 64, 72, 76-78 80, and 90-91 are pending.
Claims 12 and 77-78 and 80 are withdrawn from further consideration by the examiner, 37 CFR 1.142(b), as being drawn to a non-elected invention. Claims 27, 33, and 90-91 are withdrawn from further consideration by the examiner, 37 CFR 1.142(b), as being drawn to non-elected species.
Claims 1, 6-7, 9, 23, 38, 64, 72, and 76 are being acted upon.
In view of Applicant’s claim amendments, the previous grounds of rejection are withdrawn.
The following are new grounds of rejection necessitated by Applicant’s claim amendments. Applicant’s arguments relevant to the new prior art rejections will be addressed below.
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.
Claims 1, 38, 64, 72 and 76 is/are rejected under 35 U.S.C. 103 as being unpatentable over Cheng, 2013, in view of Zhang, 2010 (both of record), US 20100092524 and US2019/0060483 (of record).
Cheng teaches a method of inducing an immune response against M. tuberculosis in a subject in need thereof comprising administering exosomes (i.e. an EV) carrying M. tuberculosis antigens which induces antigen specific CD4 and CD8 T cell response to the antigens. Cheng teaches that induction of Th1 responses and IFN-gamma is important for controlling M. Tuberculosis infection. Cheng teaches administering multiple doses of said exosomes by an intranasal route, wherein the administration can prime an immune response (see materials and methods).
The reference differs from the claimed invention in that it does not explicitly teach that the exosomes comprises IL-12 linked to PTGFRN or intratracheal instillation.
Zhang teaches exosomes comprising IL-12, wherein the IL-12 is anchored to the exosome surface by GPI. Zhang teach that the exosomes also comprise an antigen, and that the IL-12 exosomes induce antigen specific T cell responses (see page 139, in particular). Zhang teaches that the IL-12 exosomes increases antigen specific T cell responses at least two fold compared to IL-12 alone (i.e. without an EV, see Fig. 7, in particular). Zhang teaches that exosomes contain antigens that trigger antigen specific T cells responses (see page 133-134). Zhang explains that IL-12 is a critical cytokine that plays an essential role in induction of T cell response driving induction of CTL (i.e. CD8) T cells and driving differentiation of TH1 cells (i.e. CD4 T cells), see page 133 and 139, in particular. Zhang teaches that anchoring IL-12 to exosomes is a good way to enhance the immunogenicity of exosome based immunotherapy (See page 134, in particular). Zhang also teaches that the IL-12 exosomes increase IFN-gamma production of T cells to higher levels than conventional exosomes or IL-12 alone (i.e. without an EV, see Fig. 6, in particular).
The ‘524 publication teaches the use of exosomes as a vaccine to induce an immune response against one or more antigens in a subject (see paragraph 27, in particular). The ‘524 publication teaches that cytokines can act as adjuvants to enhance the immune response to the antigens in the exosomes and also teaches that exogenous polypeptides can also be in included in the exosomes, such as GPI-linked IL-12 (See paragraph 49 and 62, in particular). The ‘524 publication teaches that exosomes can be administered by a variety of routes, including by intratracheal installation (See paragraph 99, in particular).
The ‘483 publication teaches surface engineered exosomes comprising a fusion protein between a therapeutic peptide ligand and a protein such as PTGFRN that is expressed from an exogenous sequence (see pages 8-9, in particular). The ‘483 publication teaches that the exosomes are advantageous since the proteins are more highly enriched on the cell surface with more controlled biological activity as compared to using a GPI anchor (see page 9, in particular). The ‘483 publication teaches attaching proteins by a linker (see paragraph 30 and 104, in particular). The ‘483 publication also teaches said scaffold protein having SEQ ID NO: 33, which is identical to SEQ ID NO: 33 of the instant application (see page 13, in particular).
Therefore, it would have been prima facie obvious to one of ordinary skill in the art at the time the invention was made to include IL-12 as taught by Zhang and the 524 publication, in the exosomes of Cheng. The ordinary artisan at the time the invention was made would have been motivated to do so with a reasonable expectation of success, because the references teach that including IL-12 on exosomes increase antigen specific T cells responses. Thus, the ordinary artisan would expect that including IL-12 in the exosomes of the Cheng would function to increase the antigen specific T cell response to the antigens in the exosomes. Additionally, as induction of TH1 immunity and IFN-gamma production was known as a therapeutic for tuberculosis, as taught by Cheng, the ordinary artisan would also be motivated to include IL-12 in the exosome of to enhance treatment outcomes by inducing essential IFN-gamma. Furthermore, it would have been obvious to a person of ordinary skill in the art at the time the invention was made to apply the teachings of the ‘483 publication regarding the use of PTGFRN as a scaffold moiety, in place of the GPI anchor in the exosomes made obvious by the Zhang and the ‘524 publication. One of ordinary skill in the art at the time the invention was made would have been motivated to substitute the GPI anchor with the PTGFRN scaffold moiety, since the ‘483 publication teaches that it allows for more highly enriched cell surface expression with more controlled biological activity as compared to using a GPI anchor. Furthermore, selecting from known routes for exosome administration to induce an antigen specific immune response would involve choosing among a finite number of predictable options which could be pursued with a reasonable expectation of success. A person of ordinary skill has good reason to pursue the known options within his or her technical grasp. If this leads to the anticipated success, it is likely the product not of innovation but of ordinary skill and common sense (see KSR International Co. V. Telefex Inc 82 USPQ2d 1385).
Regarding the limitation that the EV is administrated after priming, as noted above, the Cheng reference teaches administration of more than one dose of the exosomes to induce an antigen specific immune response. Therefore, the second dose of the IL-12/antigen exosomes made obvious above would be administered after the subject is primed ty administration of the first dose of the IL-12/antigen exosomes, thus meeting the limitation of the instant claims.
Claims 1, 38, 64, 72 and 76 is/are rejected under 35 U.S.C. 103 as being unpatentable over Cheng, 2013, in view of Zhang, 2010, US 20100092524 and Dooley, April 1, 2019.
Cheng teaches a method of inducing an immune response against M. tuberculosis in a subject in need thereof comprising administering exosomes (i.e. an EV) carrying M. tuberculosis antigens which induces antigen specific CD4 and CD8 T cell response to the antigens and that induction of Th1 responses and IFN-gamma is important for controlling M. Tuberculosis infection. Cheng teaches administering multiple doses of said exosomes by an intranasal route, wherein the first administration is a priming administration. In other words, the subsequence administrations of the exosomes in the method of Cheng have been administered to subject that is primed by administration of M. tuberculosis antigen.
The reference differs from the claimed invention in that it does not explicitly teach that the exosomes comprises IL-12 linked to PTGFRN.
Zhang teaches exosomes comprising IL-12, wherein the IL-12 is anchored to the exosome surface by GPI. Zhang teach that the exosomes also comprise an antigen, and that the IL-12 exosomes induce antigen specific T cell responses (see page 139, in particular). Zhang teaches that the IL-12 exosomes increases antigen specific T cell responses at least two fold compared to IL-12 alone (i.e. without an EV, see Fig. 7, in particular). Zhang teaches that exosomes contain antigens that trigger antigen specific T cells responses (see page 133-134). Zhang explains that IL-12 is a critical cytokine that plays an essential role in induction of T cell response driving induction of CTL (i.e. CD8) T cells and driving differentiation of TH1 cells (i.e. CD4 T cells), see page 133 and 139, in particular. Zhang teaches that anchoring IL-12 to exosomes is a good way to enhance the immunogenicity of exosome based immunotherapy (See page 134, in particular). Zhang also teaches that the IL-12 exosomes increase IFN-gamma production of T cells to higher levels than conventional exosomes or IL-12 alone (i.e. without an EV, see Fig. 6, in particular).
The ‘524 publication teaches the use of exosomes as a vaccine to induce an immune response against one or more antigens in a subject (see paragraph 27, in particular). The ‘524 publication teaches that cytokines can act as adjuvants to enhance the immune response to the antigens in the exosomes and also teaches that exogenous polypeptides can also be in included in the exosomes, such as GPI-linked IL-12 (See paragraph 49 and 62, in particular). The ‘524 publication teaches that exosomes can be administered by a variety of routes, including by intratracheal installation (See paragraph 99, in partiuclar0.
Dooley teaches that PTGFRN can be used to display IL-12 in exosomes by linking (via a linker) IL-12 to PTGFRN scaffold protein (see Fig. 8A). Dooley teaches that said IL-12 exosomes induce durable IFN-gamma responses in vivo, inducing more than a two-fold increase in IFN-gamma immune response as compared to IL-12 not in exosomes (see Fig. 9 C). Dooley teach that the use of PTGFRN in surface display of therapeutic proteins is advantageous since it results in a high density surface display of bioactive molecules that enables production of potent exosomes.
Therefore, it would have been prima facie obvious to one of ordinary skill in the art at the time the invention was made to include IL-12 as taught by Zhang, the 524 publication, and Dooley, in the exosomes of Cheng. The ordinary artisan at the time the invention was made would have been motivated to do so with a reasonable expectation of success, because the references teach that the IL-12 on exosomes increase antigen specific T cells responses. Thus, the ordinary artisan would expect that including IL-12 in the exosomes of the ‘Cheng would function to increase the antigen specific T cell response to the antigens in the exosomes. Additionally, as induction of TH1 immunity and IFN-gamma production was known as a therapeutic for tuberculosis, as taught by Cheng, the ordinary artisan would also be motivated to include IL-12 in the exosome of to enhance treatment outcomes by inducing essential IFN-gamma. Furthermore, it would have been obvious to a person of ordinary skill in the art at the time the invention was made to use the PTGRN linked IL-12 exosomes of Dooley in particular, since Dooley teaches the use of PTGFRN in surface display of therapeutic proteins is advantageous since it results in a high density surface display of bioactive molecules that enables production of potent exosomes. Regarding claim 38, it would be obvious to use a human PTGFRN for compatibility with humans, and having a sequence of SEQ ID NO: 33 or having 80% identity to SEQ ID NO: 1 would be latent property thereof.
Furthermore, selecting from known routes for exosome administration to induce an antigen specific immune response would involve choosing among a finite number of predictable options which could be pursued with a reasonable expectation of success. A person of ordinary skill has good reason to pursue the known options within his or her technical grasp. If this leads to the anticipated success, it is likely the product not of innovation but of ordinary skill and common sense (see KSR International Co. V. Telefex Inc 82 USPQ2d 1385).
Regarding the limitation that the EV is administrated after priming, as noted above, the Cheng reference teaches administration of more than one dose of the exosomes to induce an antigen specific immune response. Therefore, the second dose of the IL-12/antigen exosomes made obvious above would be administered after the subject is primed ty administration of the first dose of the IL-12/antigen exosomes, thus meeting the limitation of the instant claims.
Claims 6-7, 9, and 23 is/are rejected under 35 U.S.C. 103 as being unpatentable over Cheng, 2013, Zhang, 2010, US 20100092524 and US2019/0060483 OR Cheng, 2013, Zhang, 2010, US 2010092524 and Dooley, as applied to claim 1, and further in view of JP 2017-101012 (as evidenced by an attached translation).
The teachings of Cheng, 2013, Zhang, 2010, US 2010092524 and US2019/0060483 OR Cheng, 2013, Zhang, 2010, US 2010092524 and Dooley are descried above.
They do not teach explicitly teach that the M. tuberculosis antigen is ESAT6.
The ‘012 publication teaches exosome formulations for treating and preventing Mycobacteria tuberculosis infection comprising an M. tuberculosis antigen (see claims and disclosure). The ‘012 publication teaches that the antigen can be ESAT-6 from Mycobacterium tuberculosis, which inherently would have at least 3 amino acids from SEQ ID NO: 370. The ‘012 publication teaches that the exosomes induce a T cell immune response against the ESAT-6 antigen (see page 4 of the translation and Fig. 4, in particular).
Therefore, it would have been obvious to a person of ordinary skill in the art at the time the invention was made to apply the teachings of the ‘012 publication regarding the use of ESAT-6 as a M. tuberculosis antigen, to the exosomes made obvious by the other cited references. One of ordinary skill in the art at the time the invention was made would have been motivated to do since the ‘012 publication teaches that ESAT-6 can be included in exosomes and functions to treat and prevent tuberculosis.
Claims 1, 6-7, 9, 23, 38, 64, 72, and 76 is/are rejected under 35 U.S.C. 103 as being unpatentable over 5,928,636, in view of Zhang, 2010, US2019/0060483 and US 20180193270.
The ‘636 patent teaches a method of treating a patient infected with tuberculosis (i.e. patients primed to M. tuberculosis antigens) comprising administering to the patient a composition comprising IL-12 (see columns 1-4 and claims). The ‘636 patent teaches intratracheal administration (i.e. intratracheal installation, see column 5, in particular).
The reference differs from the claimed invention in that it does not explicitly teach that the IL-12 is linked to PTGFRN on an exosome.
Zhang teaches that IL-12 is critical in inducing cellular immune responses, but that administration IL-12 has a very short half-life and can induce side effects (see page 133, in particular). Zhang teaches an improved method for IL-12 delivery by delivery via exosomes wherein the IL-12 is anchored to the exosome surface by GPI (see pages 133-134, in particular).
The ‘270 publication teaches that exosomes are useful as drug delivery vehicles including for delivery of surface bound proteins, wherein the exosomes exhibit enhanced in vivo stability (See abstract and paragraph 40, in particular). The ‘270 publication teaches that the exosomes can be used for delivery of cytokines, such as interferons and interleukins (see paragraph 135, in particular). The ‘270 publication teaches loaded exosomes can be delivered via an intratracheal route (see paragraph 74, in particular).
The ‘483 publication teaches that exosomes can be used as drug delivery vehicles and have many advantages over traditional drug delivery methods (See paragraph 3, in particular). The ‘483 publication teaches producing surface engineered exosomes comprising a fusion protein between a therapeutic ligand and a protein such as PTGFRN expressed from an exogenous sequence ( see pages 8-9, in particular). The ‘483 publication teaches that the exosomes are advantageous since the proteins are more highly enriched on the cell surface and provide for greater biological activity as compared to using a GPI anchor (see page 9 and paragraph 129, in particular). The ‘483 publication teaches attaching proteins by a linker (see paragraph 30 and 104, in particular). The ‘483 publication also teaches said scaffold protein having SEQ ID NO: 33, which is identical to SEQ ID NO: 33 of the instant application (see page 13, in particular).
Therefore, it would have been prima facie obvious to one of ordinary skill in the art at the time the invention was made to administer the IL-12 in the method of treating tuberculosis of the ‘636 patent, linked to the surface of an exosome as taught by Zhang, the ‘270 publication, and the ‘483 publication. The ordinary artisan at the time the invention was made would have been motivated to do so with a reasonable expectation of success, because the references teach that exosomes are advantageous as delivery vehicle for cytokines. Furthermore, it would have been obvious to a person of ordinary skill in the art at the time the invention was made to apply the teachings of the ‘483 publication regarding the use of PTGFRN as a scaffold moiety, in place of the GPI anchor in the exosomes made obvious by the Zhang. One of ordinary skill in the art at the time the invention was made would have been motivated to substitute the GPI anchor with the PTGFRN scaffold moiety, since the ‘483 publication teaches that it allows for more highly enriched cell surface expression with more controlled biological activity as compared to using a GPI anchor.
Regarding the limitation of the present claims wherein the subject is primed by administration of an M. tuberculosis antigen prior to administering the EV, it is noted that the subjects treated in the ‘636 patent are infected with tuberculosis, i.e. they have been “primed” because they have been infected and contain M. tuberculosis antigens from the infection. It is noted that the claimed method has only a single active method step, administering an EV comprising IL-12. The limitation wherein the subject is primed “by” administration of tuberculosis antigen defines the nature of the treated subjects, i.e. they are primed in response to tuberculosis antigen. Subjects infected with tuberculosis have inherently been administered M. tuberculosis antigen that infects the subjects and also primes the subject to the antigens, thus meeting the claimed limitation. The induction of an immune response to M. tuberculosis antigens present in the infected subjects, which include ESAT-6, would be a latent property of IL-12 administration.
Claims 1, 6-7, 9, 23, 38, 64, 72, and 76 is/are rejected under 35 U.S.C. 103 as being unpatentable over 5,928,636, in view of Zhang, 2010, Dooley, April 1 2019, and US 20180193270
The ‘636 patent teaches a method of treating a patient infected with tuberculosis (i.e. patients primed to M. tuberculosis antigens) comprising administering to the patient a composition comprising IL-12 (see columns 1-4 and claims). The ‘636 patent teaches intratracheal administration (i.e. intratracheal installation, see column 5, in particular).
The reference differs from the claimed invention in that it does not explicitly teach that the IL-12 is linked to PTGFRN on an exosome.
Zhang teaches that IL-12 is critical in inducing cellular immune responses, but that administration IL-12 has a very short half-life and can induce side effects (see page 133, in particular). Zhang teaches an improved method for IL-12 delivery by delivery via exosomes wherein the IL-12 is anchored to the exosome surface by GPI (see pages 133-134, in particular).
The ‘270 publication teaches that exosomes are useful as drug delivery vehicles including for delivery of surface bound proteins, wherein the exosomes exhibit enhanced in vivo stability (See abstract and paragraph 40, in particular). The ‘270 publication teaches that the exosomes can be used for delivery of cytokines, such as interferons and interleukins (see paragraph 135, in particular). The ‘270 publication teaches loaded exosomes can be delivered via an intratracheal route (see paragraph 74, in particular).
Dooley teaches that PTGFRN can be used to display IL-12 in exosomes by linking (via a linker) IL-12 to PTGFRN scaffold protein (see Fig. 8A). Dooley teaches that said IL-12 exosomes induce durable IFN-gamma responses in vivo, inducing more than a two-fold increase in IFN-gamma immune response as compared to IL-12 not in exosomes (see Fig. 9 C). Dooley teach that the use of PTGFRN in surface display of therapeutic proteins is advantageous since it results in a high density surface display of bioactive molecules that enables production of potent exosomes.
Therefore, it would have been prima facie obvious to one of ordinary skill in the art at the time the invention was made to administered the IL-12 in the method of treating tuberculosis of the ‘636 patent, linked to the surface of an exosome as taught by Zhang, the ‘270 publication, and Dooley. The ordinary artisan at the time the invention was made would have been motivated to do so with a reasonable expectation of success, because the references teach that exosomes are advantageous as delivery vehicle for cytokines. Furthermore, it would have been obvious to a person of ordinary skill in the art at the time the invention was made to use the PTGFRN linked IL-12 of Dooley in particular, since Dooley teach that the use of PTGFRN in surface display of therapeutic proteins is advantageous since it results in a high density surface display of bioactive molecules that enables production of potent exosomes.
Regarding the limitation of the present claims wherein the subject is primed by administration of an M. tuberculosis antigen prior to administering the EV, it is noted that the subjects treated in the ‘636 patent are infected with tuberculosis, i.e. they have been “primed” because they have been infected and contain M. tuberculosis antigens from the infection. It is noted that the claimed method has only a single active method step, administering an EV comprising IL-12. The limitation wherein the subject is primed “by” administration of tuberculosis antigen defines the nature of the treated subjects, i.e. they are primed in response to tuberculosis antigen. Subjects infected with tuberculosis have inherently been administered M. tuberculosis antigen that infects the subjects and also primes the subject to the antigens, thus meeting the claimed limitation. The induction of an immune response to M. tuberculosis antigens present in the infected subjects, which include ESAT-6, would be a latent property of IL-12 administration.
Applicant’s arguments filed 5/27/26 have been fully considered, but they are not persuasive.
Applicant argues that the present specification demonstrates unexpected results in Example 1 which show that IL-12/PTGRN EVs have a more potent effect on immune response.
Example 1 involves inoculating mice with M. tuberculosis and administering exo-IL-12 intratracheally. The results show increased immune response to M. tuberculosis using exo-IL-12 as comped to rIL-12 or exosomes without IL-12.
The enhanced immune response is an art recognized expected benefit of IL-12 administration in exosomes as compared to recombinant IL-12 or exosomes alone. For example, Zhang teaches that IL-12 exosomes increase antigen specific T cell responses at least 2 fold compared to IL-12 not in an exosome (Fig. 7). See also Dooley, 2019 (of record), which teaches that IL-12 in an exosome is superior to soluble IL-12 in inducing IFN-gamma production. See also the ‘483 publication and the ‘270 publication which teaches that delivery of proteins via exosomes has advantages in that the proteins have greater biological activity and in vivo stability.
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, 6-7, 9, 23, 38, 64, 72, and 76 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-19 of U.S. Patent No. 10,723,782, or over claims 1-18 of US 12,030,924, or over claims 1-20 of US 12,331,100, in view of Zhang, 2010, Cheng, 5,928,636, and US 2010092524.
The patents claim a composition comprising an extracellular vesicle comprising a fusion comprising PTGFRN fused to IL-12 that functions in immunomodulation. The patents claim that the vesicle is an exosome.
It would be obvious to administer the immunomodulating IL-12 exosomes claimed in the patents by intratracheal administration to treat or vaccinate against M. tuberculosis in a subject primed to M. tuberculosis based on the teachings of the cited references for the same reasons set forth above.
No claim is allowed.
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.
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Amy E. Juedes
Patent Examiner
Technology Center 1600
/AMY E JUEDES/Primary Examiner, Art Unit 1644
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