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 .
Application Status
Claims 1-24 are pending and examined on the merits herein.
Grounds of Rejection Withdrawn
Previous rejections of claims 1-24 under 35 U.S.C. 103 are withdrawn in view of claim amendments.
Claim Objections
Claim 1 is objected to because of the following informalities:
Claim 1 recites “comprises an ABA block triblock polymer” in line 5, but should read “comprises an ABA triblock polymer”;
Appropriate correction is required.
Claim Rejections - 35 USC § 112(b)
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claim 2 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 2 recites the limitation "the one or more DLNs" in line 1. Claim 2 depends from amended claim 1 which does not have a limitation of one or more DLNs but is drawn to a cervical draining lymph node.
There is insufficient antecedent basis for this limitation in the claim.
Claim Rejections - 35 USC § 112(d)
New Rejection Necessitated by Amendment
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claims 2-5 and 8 are rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
Amended claim 1 recites a thermosensitive hydrogel comprising an ABA triblock polymer having a PEG mid-block and hydrophobic end block and wherein the composition is locally placed adjacent to the cervical draining lymph node to form a sustained release depot.
Claim 2-3 and 8 depend directly from claim 1.
Claim 2 is drawn to the draining lymph node comprising a cervical lymph node which is already recited in amended claim 1;
Claim 3 is drawn to the hydrogel comprising an ABA triblock polymer, which is already recited in amended claim 1;
Claim 4 depends from claim 3 and is drawn to the B block of the ABA block comprising PEG, which is already recited in amended claim 1;
Claim 5 depends from claim 3 and is drawn to the A block of the ABA tripolymer comprising one or more hydrophobic polymers, which is already recited in amended claim 1;
Claim 8 is drawn to the hydrogel comprising a thermosensitive hydrogel, which is already recited in amended claim 1;
therefore these claims are not further limiting to the claims from which they depend.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
Claim Rejections - 35 USC § 103New Rejection Necessitated by Amendment
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.
Claims 1-12, 15-16, 19 and 24 are rejected under 35 U.S.C. 103 as being unpatentable over Latik (International Journal of Molecular Sciences. 2019; 20(21):5347; cited in OA 12/09/2025), Fransen ( Int. J. Cancer, 132: 1971-1976; PTO-892), Wainwright (Front Immunol. 2013 May 15;4:116), and Dutta (ACS Omega. 2020 Jul 9;5(28):17531-17542; cited in OA 12/09/2025) as evidenced by Cirillo ( Pharmaceutics, 2019, 11(9):486; IDS entered 10/11/2024).
Regarding claims 1 and 10, Latik teaches that glioblastoma (GBM) is the most common primary central nervous system cancer and has an extremely expansive course where aggressive tumor growth correlates with short median overall survival (abstract). Latik further teaches that the interaction of the proteins programmed death-1 (PD-1) and programmed cell death ligand (PD-L1) creates an immunoregulatory axis promoting invasion of glioblastoma multiforme cells in the brain tissue and PD-L1 expression on glioblastoma surface promotes PD-1 receptor activation in microglia, resulting in the negative regulation of T cell responses (abstract). Latik further teaches that studies demonstrated that the expression of PD-L1 in glioma correlates with WHO grading and could be considered as a tumor biomarker and further that studies in preclinical GBM mouse models confirmed the safety and efficacy of monoclonal antibodies targeting the PD-1/PD-L1 axis including significant regression of tumor mass and longer animal survival time were observed (abstract). Latik further teaches that the CNS was believed to be an immune privileged organ based on the blood brain barrier (BBB) and lack of a typical lymphatic system but several studies have shown that the CNS has a specific connection with the deep cervical lymph nodes (page 2, para 2). Latik further teaches that the BBB is dysfunctional in patients with GBM and that the concomitant inflammation enhances the CNS interplay with the lymphatic system (page 2, para 3). Latik further teaches that monoclonal antibodies (mAbs) have produced a turning point in the immunotherapy of cancer that has been FDA approved in a number of cancers and are currently under investigation for treatment of GBM including nivolumab and pembrolizumab (section 8, page 7-8; Table 1). Latik further teaches that recent clinical studies on PD-1L/PD-1 inhibitors have presented effective responses, even though the trials do not confirm critical extension of OS, these inhibitors may confer different benefits if combined with standard therapies (summary).
Latik does not teach that the anti-PD-1 antibody is in a composition comprising a thermosensitive ABA triblock hydrogel with a PEG midblock administered adjacent to the cervical draining lymph nodes.
Regarding claims 1, 11, and 24, Fransen teaches that Tumor-draining LNs (TDLNs) have a dubious position as they can induce antitumor T-cell responses but are at the same time under the direct influence of the often immunity-dampening tumor microenvironment (page 1971). Fransen further teaches that the APCs in the tumor mass and TDLNs frequently display a certain level of maturation owing to the presence of endogenous danger signals from the growing tumor but still yield inadequate T cell priming without costimulation (page 1971). Fransen further teaches that Immune suppression within the tumor microenvironment and TDLNs is characterized by an unfavorable mixture of immunosuppressive cytokines, growth factors and various
immunosuppressive cell populations including Treg suppression of effector T cells (page 1972, col 1, para 2). Fransen further teaches that increased presence of Tregs in TDLNs compared to nondraining LNs has been well established in both animal
models and cancer patients and that Treg accumulation in tumor bearing animals can result from either proliferation of natural, thymic-differentiated Tregs or conversion of naive CD4þ T cells into Tregs (page 1973, col 1, para 3). Fransen further teaches that there are toxic side effects from systemic administration of immune activating targets (page 1972, col 2, para 2) and that one way of reducing side effects is to exclusively target the tumor lymphoid drainage area (page 1973, col 1, para 3). Fransen further teaches an important role for slow-release formulations in targeting immune-stimulating agents to the TDLNs, because they keep the tumor-draining area, or regional basin,
in a proinflammatory status for a prolonged period of time, allowing the T-cell response to fully develop and the immune suppression to remain blocked while keeping the concentration of an immune stimulatory agent remains high only locally and not systemically, thereby preventing undesirable side effects and unspecific overstimulation (page 1974, col 1, para 2). Fransen further teaches that the discovery of several new sustained release systems, such as PLGA opens up possibilities for targeted treatments and further that the targeted approach for delivery of immunotherapy lends itself without
difficulty for combined use with other cancer treatments, like adoptive T-cell transfers and chemotherapy which has been described to have immune-enhancing properties (page 1974, col 1, para 3). Fransen further teaches that the TDLNs are the key locations for important antitumor immunological processes, and therefore the quintessential targets for immune-modulating therapies in solid tumor-bearing subjects because both priming of tumor-specific T-cell responses and immune suppression occur in this area, local therapies designed to balance this equilibrium toward more effective
antitumor T-cell responses will be most efficient (page 1974, col 2, para 3).
Regarding claims 1 and 24, Wainwright teaches that one of the hallmark features of GBM is the accumulation of regulatory T cells which are associated with the promotion of pathological outcomes and immunotherapeutic failure (abstract). Wainwright further teaches that tumors recruit Tregs which is associated with an impaired immune response and further that elimination of the CD25+ Treg population in preclinical studies resulted in a CD8+ mediated tumor rejection in various models (Page 3, col 1, para 3). Wainwright further teaches that most Treg within the tumor in glioma are thymus derived, which travel through the cervical lymph node (Figure 1). Wainwright further teaches that targeting these Treg could be therapeutically beneficial with fewer side effects than systemic treatment in line with the dogma that Treg depletion is associated with more effective anti-glioma response and survival (Page 4, col 1, para 1). Wainwright further teaches that given the pathogenic role that Treg mediate in the context of malignant brain tumors, an obvious therapeutic direction is their selective depletion from both the tumor microenvironment and/or secondary lymphoid tissues, wherein GBM drains to the cervical draining lymph node (Fig 3). (page 7, col 1, para 4; Fig 3).
Regarding claims 11-12, 15-16, and 19, Wainwright teaches that Treg accumulation in brain tumors is dependent on the expression of IDO and that IDO is an attractive target for therapeutic consideration given its minimal expression in normal CNS-resident neurons and glia, versus its high expression in GBM (page 11, col 2, para 2). Wainwright further teaches that IDO promotes glioma genesis by increasing the recruitment of Treg to brain tumors (page 11, col 2, para 2) as well as numerous clinical studies targeting inhibition of IDO as adjuvant immunotherapy in GBM (Table 2). Wainwright further teaches that tenzolomide is a second generation DNA alkylating agent, methylates the O6 position of guanine causing double stranded DNA cross-linking (page 7, last para). Wainwright further teaches that although TMZ is well-tolerated and has an overall beneficial impact on patient survival and is the current standard of car for glioma patients (page 8).
Regarding claims 1 and 3-8, Dutta teaches that due to their relatively large molecular sizes and delicate nature, biologic drugs such as peptides, proteins, and antibodies often require high and repeated dosing, which can cause undesired side effects and physical discomfort in patients and render many therapies inordinately expensive but to enhance the efficacy of biologic drugs, they could be encapsulated into polymeric hydrogel formulations to preserve their stability and help tune their release in the body to their most favorable profile of action for a given therapy (abstract). Dutta further teaches formulation of thermoresponsive PLGA-PEG-PLGA hydrogel with IgG as a controlled delivery system for sustained drug release (abstract). Dutta demonstrates that PLGA-Peg-PLGA triblock hydrogels were able to encapsulate and release IgG without significant aggregation or conformational change (page 17537, col 1, para 2) in a controlled manner over a period of approximately 20 days (fig 7). This is interpreted to be a sustained release depot.
Regarding claim 9, as evidenced by Cirillo, drug loaded particles entrapped in a PLGA-PEG-PLGA hydrogel have been proposed as dual stimuli responsive drug delivery systems combining the pH-responsivity of the nanoparticles with the temperature response of the PEGylated polyester gels (page 8, para 1).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application to treat GBM with an anti-PD-1 antibody as taught by Latik in a composition with a PLGA-PEG-PLGA hydrogel as taught by Dutta administered to a draining lymph node as taught Fransen which is the cervical draining lymph node for GBM also treated with chemotherapy as taught by Wainwright. The ordinary artisan would have been motivated to do so because Latik teaches that PD-1/ PD-L1 creates an immunoregulatory axis promoting invasion of glioblastoma multiforme cells in the brain tissue and negative regulation of T cell responses. Latik further teaches that preclinical mouse studies demonstrated safety and efficacy of PD-1 targeting antibodies as well as recent clinical studies on PD-1L/PD-1 inhibitors that have presented effective responses. Fransen teaches that the TDLNs are the key locations for important antitumor immunological processes, and therefore the quintessential targets for immune-modulating therapies in solid tumor-bearing subjects because both priming of tumor-specific T-cell responses and immune suppression occur in this area, and that local therapies designed to balance this equilibrium toward more effective antitumor T-cell responses will be most efficient. Fransen further teaches that the targeted approach for delivery of immunotherapy lends itself without difficulty for combined use with other cancer treatments, like chemotherapy which has been described to have immune-enhancing properties. Wainwright teaches that one of the hallmark features of GBM is the accumulation of regulatory T cells which are associated with the promotion of pathological outcomes and immunotherapeutic failure and that given the pathogenic role that Treg mediate in the context of malignant brain tumors, an obvious therapeutic direction is their selective depletion from both the tumor microenvironment and/or secondary lymphoid tissues. Dutta teaches that the PLGA-PEG-PLGA hydrogel is thermoresponsive to body temperature and has demonstrated that this triblock polymer can be used to encapsulate biologics including antibodies to maintain the conformation as well as prevent aggregation, while also sustaining local release over a period of time. The ordinary artisan has a reasonable expectation of success to substitute PLGA-PEG PLGA for Pluronic F-127 hydrogel in the method of treating a GBM with a composition of a hydrogel and an anti-PD-1 antibody administered to a draining lymph node to enhance efficacy, lower cost, lower toxic side effects, and increase patient comfort during treatment. Therefore the ordinary artisan has a reasonable expectation of success to administer a composition comprising a thermosensitive PLGA-PEG-PLGA hydrogel, an anti-PD-1 antibody (nivolumab) and chemotherapy to the cervical draining lymph node for a subject with GBM to enhance efficacy, lower cost, lower toxic side effects, and increase patient comfort in the treatment for this difficult to access tumor location.
Claims 13-14, 18, 20-21, and 23 are rejected under 35 U.S.C. 103 as being unpatentable over Latik (International Journal of Molecular Sciences. 2019; 20(21):5347; cited in OA 12/09/2025), Fransen ( Int. J. Cancer, 132: 1971-1976; PTO-892), Wainwright (Front Immunol. 2013 May 15;4:116), and Dutta (ACS Omega. 2020 Jul 9;5(28):17531-17542; cited in OA 12/09/2025) as evidenced by Cirillo (Pharmaceutics, 2019, 11(9):486; IDS entered 10/11/2024) as applied to claims 1-12, 15-16, 19 and 24 above and further in view of Khasraw (Clinical Cancer Research 26.20 (2020): 5287-5296; cited in OA 12/09/2025).
The teachings of Latik, Fransen, Wainwright and Dutta regarding claims 1-12, 15-16, 19 and 24 are detailed above.
Latik, Fransen, Wainwright and Dutta do not teach the specific combination therapy in addition to the anti-PD-1 antibody and hydrogel composition.
Regarding claim 11, Khasraw teaches that glioblastoma (WHO grade IV glioma) is the most common malignant primary brain tumor in adults and while immunotherapy and especially immune checkpoint inhibitors and programmed cell death (PD)-1/PD-L1 inhibitors have transformed the landscape of cancer treatment and improved patient survival in a number of different cancer types, there is still no evidence that PD-1 blockade can lead to meaningful clinical benefit in glioblastoma (abstract). Khasraw further teaches that several phase I/II trials in recurrent and newly diagnosed glioblastoma are evaluating anti-PD-1 agents such as nivolumab, pembrolizumab, cemiplimab, or anti-PD-L1 antibodies including atezolizumab, avelumab, durvalumab, alone or in combination with other therapies (page 5287, col 2, para 3; Table 1), although phase II and phase III trials have yet to prove efficacy (table 2). Khasraw further teaches that although single agent PD-1 blockade has not yielded efficacious results there are a number of new strategies being considered including combination therapy and targeting therapy (page 5293, col 2, para 2) and that combination therapy with two or more therapeutic agents is a cornerstone of cancer therapy (page 529, col 2, para 3).
Regarding claims 13-14, 18, and 20-21, Khasraw teaches hypo fractionated stereotactic irradiation with nivolumab, ipilimumab, and bevacizumab in patients with recurrent high-grade gliomas (table 2).
Regarding claim 23, Khasraw teaches nivolumab with radiotherapy and bevacizumab for recurrent MGMT-methylated glioblastoma (table 2).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application to add an additional therapeutic as taught by Khasraw to the method of treating GBM with a composition of PLGA-PEG-PLGA hydrogel and anti-PD-1 antibody administered to a draining lymph node as taught by Latik, Fransen, Wainwright, and Dutta. The ordinary artisan would have been motivated to do so because Khasraw teaches that combination therapy with two or more therapeutic agents is a cornerstone of cancer therapy and that several phase I/II trials in recurrent and newly diagnosed glioblastoma are evaluating anti-PD-1 agents such as nivolumab, pembrolizumab, cemiplimab, alone or in combination with other therapies. The ordinary artisan has a reasonable expectation of success to add an additional therapeutic in the method of treating a GBM with a composition of a hydrogel and an anti-PD-1 antibody administered to a draining lymph node to enhance efficacy.
Claim 17 is rejected under 35 U.S.C. 103 as being unpatentable over Latik (International Journal of Molecular Sciences. 2019; 20(21):5347; cited in OA 12/09/2025), Fransen ( Int. J. Cancer, 132: 1971-1976; PTO-892), Wainwright (Front Immunol. 2013 May 15;4:116), and Dutta (ACS Omega. 2020 Jul 9;5(28):17531-17542; cited in OA 12/09/2025) as evidenced by Cirillo (Pharmaceutics, 2019, 11(9):486; IDS entered 10/11/2024) as applied to claims 1-12, 15-16, 19 and 24 above, and further in view of Maxwell (Oncoimmunology. 2018 Sep 6;7(12):e1500108; cited in OA 12/25/2025).
The teachings of Latik, Fransen, Wainwright, Dutta, and Khasraw regarding claims 1-3, 8, 10-16, 18-21, and 23-24 are detailed above.
Latik, Fransen, Wainwright, Dutta, and Khasraw do not teach that combination therapy in addition to the anti-PD-1 antibody comprises dexamethasone or prednisone.
Maxwell teaches that corticosteroid are widely used in the course of canner management but can have negative effects on the anti-PD-1 treatment response, however corticosteroid treatment did not abrogate the benefits conferred by ani-PD-1 therapy in a mouse model of intracranial tumors (abstract). Maxwell further teaches that clinically, corticosteroids are routinely used in the management of cancer for fatigue, night sweats, appetite stimulation, antiemesis, and the reduction of side effects associated with certain chemotherapies (platinum-based agents and taxanes) and corticosteroids are especially important in the management of tumors residing in the central nervous system (CNS), since they can effectively palliate neurological deficits and reduce complications caused by cerebral edema through restoring the integrity of the blood-brain barrier (BBB) (introduction; para 2). Maxwell further teaches that cerebral edema is often potentiated by the additive pro-inflammatory effects of brain radiation plus immunotherapy, even when not given concurrently, thus necessitating the use of corticosteroids post-treatment (introduction; para 2). Maxwell further teaches that dexamethasone is the most potent synthetic corticosteroid and demonstrated that dexamethasone treatment disrupted the benefits of PD-1 blockade in mice bearing peripheral colon adenocarcinoma tumors, antitumor immunity and responses mediated by anti-PD-1 therapy remained intact for those bearing intracranial glioma tumors (introduction; para 3).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application to use dexamethasone as the additional therapeutic as taught by Maxwell to the method of treating GBM with a composition of PLGA-PEG-PLGA, anti-PD-1 antibody and an additional therapeutic administered to a draining lymph node as taught by Latik, Fransen, Wainwright, Dutta, and Khasraw. The ordinary artisan would have been motivated to do so because Maxwell teaches that dexamethasone is the most potent synthetic corticosteroid and that corticosteroids are especially important in the management of tumors residing in the central nervous system (CNS), since they can effectively palliate neurological deficits and reduce complications caused by cerebral edema through restoring the integrity of the blood-brain barrier. Maxwell further teaches that cerebral edema is often potentiated by the additive pro-inflammatory effects of brain radiation plus immunotherapy, even when not given concurrently, thus necessitating the use of corticosteroids post-treatment. The ordinary artisan has a reasonable expectation of success to use dexamethasone as the additional therapeutic in the method of treating a GBM with a composition of a hydrogel and an anti-PD-1 antibody administered to a draining lymph node to reduce complications and inflammation caused by immunotherapy in patients.
Claim 22 is rejected under 35 U.S.C. 103 as being unpatentable over Latik (International Journal of Molecular Sciences. 2019; 20(21):5347; cited in OA 12/09/2025), Fransen ( Int. J. Cancer, 132: 1971-1976; PTO-892), Wainwright (Front Immunol. 2013 May 15;4:116), and Dutta (ACS Omega. 2020 Jul 9;5(28):17531-17542; cited in OA 12/09/2025) as evidenced by Cirillo (Pharmaceutics, 2019, 11(9):486; IDS entered 10/11/2024) as applied to claims 1-12, 15-16, 19 and 24 above, and further in view of Polivka (Anticancer Res. 2017 Jan;37(1):21-33; cited in OA 12/09/2025).
The teachings of Latik, Fransen, Wainwright, Dutta, and Khasraw regarding claims 1-3, 8, 10-16, 18-21, and 23-24 are detailed above.
Latik, Fransen, Wainwright, Dutta, and Khasraw do not teach that combination therapy in addition to the anti-PD-1 antibody comprises cediranib.
Polivka teaches that the major role in tumor angiogenesis is played by vascular growth factors, especially vascular endothelial growth factor (VEGF) and excessive microvascular proliferation as well as VEGF overexpression were identified in tumor tissues from patients with GBM (page 24, col 1, para 1). Polivka further teaches the VEGFR tyrosine kinase inhibitor cediranib showed activity in an early phase II clinical trial as a monotherapy in patients with recurrent GBM but showed no PFS benefit as a monotherapy (page 24, col 2, para 2).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application to use dexamethasone as the additional therapeutic as taught by Maxwell to the method of treating GBM with a composition of PLGA-PEG-PLGA hydrogel, an anti-PD-1 antibody and an additional therapeutic administered to the cervical draining lymph node as taught by Latik, Fransen, Wainwright, Dutta, and Khasraw. The ordinary artisan would have been motivated to do so because Polivka teaches that the major role in tumor angiogenesis is played by vascular growth factors, especially vascular endothelial growth factor (VEGF) and excessive microvascular proliferation as well as VEGF overexpression were identified in tumor tissues from patients with GBM and that the VEGFR tyrosine kinase inhibitor cediranib showed activity in an early phase II clinical trial as a monotherapy in patients with recurrent GBM. The ordinary artisan has a reasonable expectation of success to use cediranib as the additional therapeutic in the method of treating a GBM with a composition of a hydrogel and an anti-PD-1 antibody administered to a draining lymph node to reduce tumor angiogenesis.
Response to Arguments
Applicant’s arguments with respect to claim(s) 1-24 have been considered but are moot because the new ground of rejection does not rely on any reference applied in the prior rejection of record for any teaching or matter specifically challenged in the argument.
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 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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/AMBER K FAUST/Examiner, Art Unit 1643
/JULIE WU/Supervisory Patent Examiner, Art Unit 1643
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