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 .
The Non-Final Office action filed 08/12/2025 is hereby vacated. This Non-Final Office action replaces the vacated Non-Final Office action dated 08/12/2025.
DETAILED ACTION
Priority
This application is the U.S. National Stage of PCT/KR2020/008364, filed June 26, 2020 that is hereby acknowledged by the Examiner. The Office acknowledges the Declarations under 37 C.F.R. § 1.130(a) by Drs. Lee, Jo, Kim and Park filed November 12, 2025.
Status of the Claims
The amendment dated 11/12/2025 is acknowledged. Claims 1-7 are pending and under examination.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 11/12/2025 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement(s) is/are being considered by the Examiner.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
(Withdrawn) Claims 1-6 rejected under 35 U.S.C. 102(a)(1) as being anticipated by Wong et al. “Wong” (WO2016/040369) are hereby withdrawn in view of Applicant’s amendment to the claims. Noted: the new rejections made below are necessitated by Applicant’s amendment to claim 1 omitting iNKT cell agonist in the claims dated 11/12/2025.
(New Rejection- necessitated by amendment to claims) Claims 1-7 rejected under 35 U.S.C. 102(a)(1) as being anticipated by Patch et al. “Patch” (Clinical and Vaccine Immunology, 2011, 18(2):280-288).
The claims are directed to an immunogenic adjuvant composition comprising any one or more selected from the group consisting of γδ T cell agonist, MAIT cell agonist and T cell agonist, as an active ingredient.
Regarding claims 1-7, Patch discloses “recombinant human adenovirus vectors as a means of delivering FMDV antigens in a T cell-directed vaccine in pigs. We tested the hypothesis that impaired processing of the FMDV capsid would enhance cytolytic activity, presumably by targeting all proteins for degradation and effectively increasing the class I major histocompatibility complex (MHC)/FMDV peptide concentration for stimulation of a CTL response. We compared such a T cell-targeting vaccine with the parental vaccine, previously shown to effectively induce a neutralizing antibody response. Our results show induction of FMDV-specific CD8+ CTL killing of MHC-matched target cells in an antigen-specific manner. Further, we confirm these results by MHC tetramer staining. This work presents the first demonstration of FMDV-specific CTL killing and confirmation by MHC tetramer staining in response to vaccination against FMDV” (Abstract and pages 281-282 Materials and Methods). Patch discloses “the ability of two nonreplicating adenovirus vectors to generate a CTL cytolytic response in swine to FMDV epitopes. The ability of this vaccine platform to induce the production of neutralizing antibodies to empty FMDV capsids in both swine and cattle (page 286 first column first para.); and “doses of a P1-based vaccine in swine resulted in partial protection in the absence of FMDV-specific antibodies. Similar results were obtained in cattle by the same investigators. In vitro, FMDV inhibition of MHC class I surface expression begins in as little as 30 min postinfection. Thus, even under ideal conditions where anti-FMDV CTLs are primed and expanded, control of infection by CTLs depends on host cells infected by wild-type virus in vivo processing and displaying FMDV peptides leading to the CTL response before inhibition of new MHC class I protein expression is blocked by viral proteases. Although neutralizing antibodies are likely to remain the principal focus of FMDV vaccination, CTLs may be able to contribute to cross-serotype and subtype immunity because potential T cell epitopes are not limited to the structural proteins” (page 287 second and third para.). Therefore, the cited prior art anticipates the claimed invention.
(New Rejection- necessitated by amendment to claims) Claims 1-6 rejected under 35 U.S.C. 102(a)(1) as being anticipated by Emerson et al. “Emerson” (BioDrugs, 2018, 32:221-231).
The claims are directed to an immunogenic adjuvant composition comprising any one or more selected from the group consisting of γδ T cell agonist, MAIT cell agonist and T cell agonist, as an active ingredient.
Regarding claims 1-6, Emerson discloses advancements in T-cell biology and antibody engineering have opened doors to significant improvement in cancer immunotherapy. Emerson discloses ligand-immunoglobulin fusion proteins that target costimulatory immune receptors are being developed and tested in clinical trials to further enhance the anti-tumor immune response (Abstract), whereby one approach is to enhance T-cell recognition of tumor-associated antigens (TAAs) presented on MHC molecules through the provision of exogenous tumor-specific vaccines, known as therapeutic vaccination” (page 222 first column second para.). Emerson discloses T-cell-targeted immunotherapies and the discovery of immune checkpoints that regulate activation and inhibition following TCR stimulation (page 222 first column last para., Table 1 and Table 2); and the development of blocking-antibodies utilized to block cytotoxic T lymphocyte antigen 4 (CTLA-4) to boost anti-tumor immunity by inhibiting Tregs and enhancing T-cell effector function (instant claims 1-6, T cell agonists adjuvant composition, oil or non-oil preparation, vaccine composition comprising adjuvant )(page 222 second column first and second para.). Therefore, the cited prior art anticipates the claimed invention.
Claims 1-6 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Dantzler et al. “Dantzler” (Clinical & Translational Immunology, 2019, (8):1-16, IDS of record dated 12/16/2022).
The claims are directed to an immunogenic adjuvant composition comprising any one or more selected from the group consisting of γδ T cell agonist, MAIT cell agonist and T cell agonist, as an active ingredient.
Regarding claims 1-6, Dantzler teaches the evidence for a role for γδ T cells in vaccine-induced protection against various bacterial, protozoan and viral infections…results suggesting potential mechanisms for protection and “building on current efforts to integrate strategies targeting γδ T cells into immunotherapies for cancer, we discuss potential approaches to improve vaccines for infectious diseases by inducing γδ T-cell activation and cytotoxicity” (Abstract). Dantzler teaches that “a number of studies have not only demonstrated γδ T-cell expansion in various bacterial infections, but also possible mechanisms of protection provided by this cell population, including both direct killing and recruitment of other cell types via production of pro-inflammatory cytokines. Although clear that γδ T cells respond differently based on infectious agent, specific proliferation of the Vγ9Vδ2 subset in response to a number of bacterial pathogens correlates with protection from symptomatic disease. Consequently, upregulating activation and/or functional responses of this subset by vaccination may enhance protection against the agent targeted by immunization” (instant claims 1-6) (page 4 first column first full para.). Therefore, the cited prior art anticipates the claimed invention.
Claims 1-6 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Downey et al. “Downey” (FEBS Letters, 2019:1627-1640).
The claims are directed to an immunogenic adjuvant composition comprising any one or more selected from the group consisting of γδ T cell agonist, MAIT cell agonist and T cell agonist, as an active ingredient.
Regarding claims 1-6, Downey discloses MAIT cell agonists and the possible role in MAIT cell agonist in the treatment of viral and bacterial infections and roles in vaccine development by stating “Some functions of MAIT cells can be activated by innate inflammatory and antiviral cytokines, most commonly IL-12 and IL-18, but also IL-15, IFN-a/b, in an MR1-independent mechanism and can concurrently augment MAIT cell’s TCR-dependent activation. TCR-independent activation is the primary mode of action for MAIT cells in combating viral infection mainly through secretion of cytokine IFN-ᵧ and serine protease granzyme B. The implications of MR1-independent MAIT cell activation are tremendous as this response provides utility for MAIT cells beyond antimicrobial effects and into viral infection, including influenza, HIV, and hepatitis B and C” (page 1630 second column first para.). Downey discloses that “it appears easier to target MAIT cells in an antimicrobial vaccine, either therapeutic or preventative and believe that their ability to serve primarily as adjuvant is the greatest…In viral infection, we believe that the current data most strongly support the exploitation of MAIT cells in a therapeutic vaccine and could serve as both the antiviral agent and offer concurrent prevention against bacterial co-infection. As discussed, MAIT cell levels are severely depleted and can show a compromised MR1-dependent response in viral infections. The ability to reconstitute their numbers somehow during administration of a therapeutic vaccine would be highly beneficial. In HIV-1, the administration of recombinant IL-7 has been shown to restore MAIT cells levels in peripheral blood as part of ART” (instant claims 1-6) (page 1635 second column first para.). Further, Downey discloses that “It would certainly be worth determining if the addition of IL-7 to a vaccine serum could possibly induce the same effect. In malignancies, research implicating MAIT cells is still in its preliminary stages, but a very encouraging fact is that MAIT cells found in the blood and liver, common places for metastasis, produce insignificant amounts of the pro-tumorigenic cytokine IL-17A [12]. An artificial method to increase MAIT cell numbers as part of a therapeutic vaccine is worth investigating. MAIT cells could have the potential to reduce or abate metastasis and should protect against bacterial co-infection in the cancerous patient” (page 1635 second column first para.). Therefore, the cited prior art anticipates the claimed invention.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103(a) which forms the basis for all obviousness rejections set forth in this Office action:
(a) A patent may not be obtained though the invention is not identically disclosed or described as set forth in section 102 of this title, if the differences between the subject matter sought to be patented and the prior art are such that the subject matter as a whole would have been obvious at the time the invention was made to a person having ordinary skill in the art to which said subject matter pertains. Patentability shall not be negatived by the manner in which the invention was made.
This application currently names joint inventors. In considering patentability of the claims under 35 U.S.C. 103(a), the examiner presumes that the subject matter of the various claims was commonly owned at the time any inventions covered therein were made absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and invention dates of each claim that was not commonly owned at the time a later invention was made in order for the examiner to consider the applicability of 35 U.S.C. 103(c) and potential 35 U.S.C. 102(e), (f) or (g) prior art under 35 U.S.C. 103(a).
(Withdrawn) Claim 7 rejected under 35 U.S.C. 103(a) as being unpatentable over Wong et al. “Wong” (WO2016/040369) in view of Lee et al. “Lee” (Frontiers in Immunology, 10:2509):1-14) are hereby withdrawn in view of Applicant’s amendment to claims and acknowledgment of Applicant’s declaration filed 11/12/2025.
The Office acknowledges the Declaration under 37 C.F.R. § 1.130(a) by Drs. Lee, Jo, S. Kim, B. Kim and Park. The Lee et al. cited prior art is hereby withdrawn in the 35 U.S.C. 103(a) rejection made in the Non-Final Office action dated 08/12/2025.
Claim 7 is rejected under 35 U.S.C. 103(a) as being unpatentable over Emerson et al. “Emerson” (BioDrugs, 2018, 32:221-231) as applied to claims 1 and 5 above, in view of Patch et al. “Patch” (Clinical and Vaccine Immunology, 2011, 18(2):280-288).
The claims are directed to an immunogenic adjuvant composition comprising any one or more selected from the group consisting of γδ T cell agonist, MAIT cell agonist and T cell agonist, as an active ingredient.
Regarding claim 7, Emerson discloses advancements in T-cell biology and antibody engineering have opened doors to significant improvement in cancer immunotherapy. Emerson discloses ligand-immunoglobulin fusion proteins that target costimulatory immune receptors are being developed and tested in clinical trials to further enhance the anti-tumor immune response (Abstract), whereby one approach is to enhance T-cell recognition of tumor-associated antigens (TAAs) presented on MHC molecules through the provision of exogenous tumor-specific vaccines, known as therapeutic vaccination” (page 222 first column second para.). Emerson discloses T-cell-targeted immunotherapies and the discovery of immune checkpoints that regulate activation and inhibition following TCR stimulation (page 222 first column last para., Table 1 and Table 2); and the development of blocking-antibodies utilized to block cytotoxic T lymphocyte antigen 4 (CTLA-4) to boost anti-tumor immunity by inhibiting Tregs and enhancing T-cell effector function (instant claims 1-6, T cell agonists adjuvant composition, oil or non-oil preparation, vaccine composition comprising adjuvant )(page 222 second column first and second para.).
Emerson discloses an adjuvant composition comprising a T cell agonist as part of a therapeutic vaccine but does not explicitly state whereby the virus is foot-mouth-disease.
Patch, however, Patch discloses recombinant human adenovirus vectors as a means of delivering FMDV antigens in a T cell-directed vaccine in pigs. We tested the hypothesis that impaired processing of the FMDV capsid would enhance cytolytic activity, presumably by targeting all proteins for degradation and effectively increasing the class I major histocompatibility complex (MHC)/FMDV peptide concentration for stimulation of a CTL response. We compared such a T cell-targeting vaccine with the parental vaccine, previously shown to effectively induce a neutralizing antibody response. Our results show induction of FMDV-specific CD8+ CTL killing of MHC-matched target cells in an antigen-specific manner (Abstract). Patch discloses “the ability of two nonreplicating adenovirus vectors to generate a CTL cytolytic response in swine to FMDV epitopes. The ability of this vaccine platform to induce the production of neutralizing antibodies to empty FMDV capsids in both swine and cattle (page 286 first column first para.); and “doses of a P1-based vaccine in swine resulted in partial protection in the absence of FMDV-specific antibodies. Similar results were obtained in cattle by the same investigators. In vitro, FMDV inhibition of MHC class I surface expression begins in as little as 30 min postinfection. Thus, even under ideal conditions where anti-FMDV CTLs are primed and expanded, control of infection by CTLs depends on host cells infected by wild-type virus in vivo processing and displaying FMDV peptides leading to the CTL response before inhibition of new MHC class I protein expression is blocked by viral proteases. Although neutralizing antibodies are likely to remain the principal focus of FMDV vaccination, CTLs may be able to contribute to cross-serotype and subtype immunity because potential T cell epitopes are not limited to the structural proteins” (page 287 second and third para.).
Accordingly, it would have been obvious to one of ordinary skill in the art to generate an adjuvant composition comprising an adjuvant composition comprising a T cell agonist as an active ingredient in a therapeutic vaccine as taught by Emerson, whereby, the vaccine composition is to foot-and-mouth-disease as taught by Patch. One of ordinary skill in the art would have been motivated to do so with a reasonable expectation of success given the knowledge by Patch demonstrating that using T cell agonists whereby their results show induction of FMDV-specific CD8+ CTL killing of MHC-matched target cells in an antigen-specific manner (Abstract); and “the ability of two nonreplicating adenovirus vectors to generate a CTL cytolytic response in swine to FMDV epitopes, the ability of this vaccine platform to induce the production of neutralizing antibodies to empty FMDV capsids in both swine and cattle (page 286 first column first para.); and “doses of a P1-based vaccine in swine resulted in partial protection in the absence of FMDV-specific antibodies (page 287 second and third para.). Therefore, the claimed invention would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention.
(New Rejection- necessitated by amendment) Claim 7 is rejected under 35 U.S.C. 103(a) as being unpatentable over Dantzler et al. “Dantzler” (Clinical & Translational Immunology, 2019, (8):1-16,) as applied to claims 1 and 5 above, in view of Patch et al. “Patch” (Clinical and Vaccine Immunology, 2011, 18(2):280-288).
The claims are directed to an immunogenic adjuvant composition comprising any one or more selected from the group consisting of γδ T cell agonist, MAIT cell agonist and T cell agonist, as an active ingredient.
Regarding claim 1, Dantzler teaches the evidence for a role for γδ T cells in vaccine-induced protection against various bacterial, protozoan and viral infections…results suggesting potential mechanisms for protection and “building on current efforts to integrate strategies targeting γδ T cells into immunotherapies for cancer, we discuss potential approaches to improve vaccines for infectious diseases by inducing γδ T-cell activation and cytotoxicity” (Abstract). Dantzler teaches that “a number of studies have not only demonstrated γδ T-cell expansion in various bacterial infections, but also possible mechanisms of protection provided by this cell population, including both direct killing and recruitment of other cell types via production of pro-inflammatory cytokines. Although clear that γδ T cells respond differently based on infectious agent, specific proliferation of the Vγ9Vδ2 subset in response to a number of bacterial pathogens correlates with protection from symptomatic disease. Consequently, upregulating activation and/or functional responses of this subset by vaccination may enhance protection against the agent targeted by immunization” (page 4 first column first full para.).
Dantzler does not explicitly state the virus is foot-mouth-disease.
Patch, however, Patch discloses recombinant human adenovirus vectors as a means of delivering FMDV antigens in a T cell-directed vaccine in pigs. We tested the hypothesis that impaired processing of the FMDV capsid would enhance cytolytic activity, presumably by targeting all proteins for degradation and effectively increasing the class I major histocompatibility complex (MHC)/FMDV peptide concentration for stimulation of a CTL response. We compared such a T cell-targeting vaccine with the parental vaccine, previously shown to effectively induce a neutralizing antibody response. Our results show induction of FMDV-specific CD8+ CTL killing of MHC-matched target cells in an antigen-specific manner (Abstract). Patch discloses “the ability of two nonreplicating adenovirus vectors to generate a CTL cytolytic response in swine to FMDV epitopes. The ability of this vaccine platform to induce the production of neutralizing antibodies to empty FMDV capsids in both swine and cattle (page 286 first column first para.); and “doses of a P1-based vaccine in swine resulted in partial protection in the absence of FMDV-specific antibodies. Similar results were obtained in cattle by the same investigators. In vitro, FMDV inhibition of MHC class I surface expression begins in as little as 30 min postinfection. Thus, even under ideal conditions where anti-FMDV CTLs are primed and expanded, control of infection by CTLs depends on host cells infected by wild-type virus in vivo processing and displaying FMDV peptides leading to the CTL response before inhibition of new MHC class I protein expression is blocked by viral proteases. Although neutralizing antibodies are likely to remain the principal focus of FMDV vaccination, CTLs may be able to contribute to cross-serotype and subtype immunity because potential T cell epitopes are not limited to the structural proteins” (page 287 second and third para.).
Accordingly, it would have been obvious to one of ordinary skill in the art to generate an adjuvant composition comprising a γδ T-cell agonist as an active ingredient in a viral vaccine as taught by Dantzler, whereby, the viral vaccine composition is to foot-and-mouth-disease as taught by Patch. One of ordinary skill in the art would have been motivated to do so with a reasonable expectation of success given the knowledge by Patch demonstrating that using T cell agonists, whereby their results show induction of FMDV-specific CD8+ CTL killing of MHC-matched target cells in an antigen-specific manner (Abstract); and “the ability of two nonreplicating adenovirus vectors to generate a CTL cytolytic response in swine to FMDV epitopes, the ability of this vaccine platform to induce the production of neutralizing antibodies to empty FMDV capsids in both swine and cattle (page 286 first column first para.); and “doses of a P1-based vaccine in swine resulted in partial protection in the absence of FMDV-specific antibodies (page 287 second and third para.). Therefore, the claimed invention would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention.
Claim 7 is rejected under 35 U.S.C. 103(a) as being unpatentable over Downey et al. “Downey” (FEBS Letters, 2019:1627-1640) as applied to claims 1 and 5 above, in view of Patch et al. “Patch” (Clinical and Vaccine Immunology, 2011, 18(2):280-288).
The claims are directed to an immunogenic adjuvant composition comprising any one or more selected from the group consisting of γδ T cell agonist, MAIT cell agonist and T cell agonist, as an active ingredient.
Regarding claim 7, Downey discloses MAIT cell agonists and the possible role in MAIT cell agonist in the treatment of viral and bacterial infections and roles in vaccine development by stating “Some functions of MAIT cells can be activated by innate inflammatory and antiviral cytokines, most commonly IL-12 and IL-18, but also IL-15, IFN-a/b, in an MR1-independent mechanism and can concurrently augment MAIT cell’s TCR-dependent activation. TCR-independent activation is the primary mode of action for MAIT cells in combating viral infection mainly through secretion of cytokine IFN-ᵧ and serine protease granzyme B. The implications of MR1-independent MAIT cell activation are tremendous as this response provides utility for MAIT cells beyond antimicrobial effects and into viral infection, including influenza, HIV, and hepatitis B and C” (page 1630 second column first para.). Downey discloses that “it appears easier to target MAIT cells in an antimicrobial vaccine, either therapeutic or preventative and believe that their ability to serve primarily as adjuvant is the greatest…In viral infection, we believe that the current data most strongly support the exploitation of MAIT cells in a therapeutic vaccine and could serve as both the antiviral agent and offer concurrent prevention against bacterial co-infection. As discussed, MAIT cell levels are severely depleted and can show a compromised MR1-dependent response in viral infections. The ability to reconstitute their numbers somehow during administration of a therapeutic vaccine would be highly beneficial. In HIV-1, the administration of recombinant IL-7 has been shown to restore MAIT cells levels in peripheral blood as part of ART” (instant claims 1-6) (page 1635 second column first para.). Further, Downey discloses that “It would certainly be worth determining if the addition of IL-7 to a vaccine serum could possibly induce the same effect. In malignancies, research implicating MAIT cells is still in its preliminary stages, but a very encouraging fact is that MAIT cells found in the blood and liver, common places for metastasis, produce insignificant amounts of the pro-tumorigenic cytokine IL-17A [12]. An artificial method to increase MAIT cell numbers as part of a therapeutic vaccine is worth investigating. MAIT cells could have the potential to reduce or abate metastasis and should protect against bacterial co-infection in the cancerous patient” (page 1635 second column first para.).
Downey discloses a composition comprising a MAIT cell agonist as part of a therapeutic vaccine but does not explicitly state whereby the virus is foot-mouth-disease.
Patch, however, Patch discloses recombinant human adenovirus vectors as a means of delivering FMDV antigens in a T cell-directed vaccine in pigs. We tested the hypothesis that impaired processing of the FMDV capsid would enhance cytolytic activity, presumably by targeting all proteins for degradation and effectively increasing the class I major histocompatibility complex (MHC)/FMDV peptide concentration for stimulation of a CTL response. We compared such a T cell-targeting vaccine with the parental vaccine, previously shown to effectively induce a neutralizing antibody response. Our results show induction of FMDV-specific CD8+ CTL killing of MHC-matched target cells in an antigen-specific manner (Abstract). Patch discloses “the ability of two nonreplicating adenovirus vectors to generate a CTL cytolytic response in swine to FMDV epitopes. The ability of this vaccine platform to induce the production of neutralizing antibodies to empty FMDV capsids in both swine and cattle (page 286 first column first para.); and “doses of a P1-based vaccine in swine resulted in partial protection in the absence of FMDV-specific antibodies. Similar results were obtained in cattle by the same investigators. In vitro, FMDV inhibition of MHC class I surface expression begins in as little as 30 min postinfection. Thus, even under ideal conditions where anti-FMDV CTLs are primed and expanded, control of infection by CTLs depends on host cells infected by wild-type virus in vivo processing and displaying FMDV peptides leading to the CTL response before inhibition of new MHC class I protein expression is blocked by viral proteases. Although neutralizing antibodies are likely to remain the principal focus of FMDV vaccination, CTLs may be able to contribute to cross-serotype and subtype immunity because potential T cell epitopes are not limited to the structural proteins” (page 287 second and third para.).
Accordingly, it would have been obvious to one of ordinary skill in the art to generate an adjuvant composition comprising a MAIT cell agonist as an active ingredient in a therapeutic vaccine as taught by Downey, whereby, the vaccine composition is to foot-and-mouth-disease as taught by Patch. One of ordinary skill in the art would have been motivated to do so with a reasonable expectation of success given the knowledge by Patch that their results show induction of FMDV-specific CD8+ CTL killing of MHC-matched target cells in an antigen-specific manner (Abstract); and “the ability of two nonreplicating adenovirus vectors to generate a CTL cytolytic response in swine to FMDV epitopes, the ability of this vaccine platform to induce the production of neutralizing antibodies to empty FMDV capsids in both swine and cattle (page 286 first column first para.); and “doses of a P1-based vaccine in swine resulted in partial protection in the absence of FMDV-specific antibodies (page 287 second and third para.). Therefore, the claimed invention would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention.
Conclusion
No claims are 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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/BARRY A CHESTNUT/Primary Examiner, Art Unit 1672