DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Priority
This application is a National Stage application under 35 U.S.C. Q 371 of International Application No. PCT/US2021/025939 having an International Filing Date of April 6, 2021, which claims benefit of priority from U.S. Provisional Application Serial No. 63/010,376, filed on April 15, 2020, and U.S. Provisional Application Serial No. 63/005,937, filed on April 6, 2020.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 10/06/2025 has been considered by the examiner.
Claim status
Acknowledgement is made of the receipt and entry of the amendment to the claims filed on October 06, 2025. Claims 27-29, 31, 45, 49-51, 53-65 are pending and under examination. Claims 1-26, 30, 32-44, 36-37, 46-48, and 52 are canceled.
Action Summary
Claims 27-29, 31 45, and 50 rejected under 35 U.S.C. 103 as being unpatentable over Jackson et al (British Journal of Pharmacology (2017) 174 4738–475) in view of McGonagle et al (Autoimmunity Reviews 19, April 03, 2020, 102537, pages 1-8) and Li et al (Drug Design, Development and Therapy 2014:8 315–323), are withdrawn in light of the claim amendment.
Claims 27-29, 31-32, 33-35, 38, 39, 42, 45, and 50-52 are rejected under 35 U.S.C. 103 as being unpatentable over Jackson et al (British Journal of Pharmacology (2017) 174 4738–475) in view of McGonagle et al (Autoimmunity Reviews 19, April 03, 2020, 102537, pages 1-8) and Li et al (Drug Design, Development and Therapy 2014:8 315–323) as applied to claims 1, 27-29, 31-32, 42, 45, and 50-52, in further view of Elder Jr. et al (US9,308,167 B2), are withdrawn in light of the cancelation of claims 33-35, 38-39, and 52.
Claims 27-29, 31-35, 38-39, 42, and 45-53 provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 25-33, 36- and 42-47 of copending Application No. 18/271,125 (reference application) in view of McGonagle et al (Autoimmunity Reviews 19, April 03, 2020, 102537, pages 1-8) and Li et al (Drug Design, Development and Therapy 2014:8 315–323), are withdrawn in light of the cancelation of claims 33-35, 38-39, and 52.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 27-29, 31, 45, 49-51, 53-65 are rejected under 35 U.S.C. 103 as being unpatentable over Harvey et al (WO2018/156946 A1) in view of Jackson et al (British Journal of Pharmacology (2017) 174 4738–475), McGonagle et al (Autoimmunity Reviews 19, April 03, 2020, 102537, pages 1-8), Li et al (Drug Design, Development and Therapy 2014:8 315–323), and Pan et al (Radiology. 2020 Feb 13:200370).
Harvey teaches a method for preventing, reducing, or mitigating, in a subject in need thereof, one or more effects of exposure to proton radiation, comprising administering to the subject a composition comprising nanoparticulate genistein, wherein the subject is identified as having been exposed to proton radiation or as being at risk of exposure to proton radiation, and wherein the composition has a nanoparticulate genistein concentration between about 250 mg/mL and about 500 mg/ml.(See claim 28.) The composition is formulated for oral, intramuscular, subcutaneous, or intravenous use. (See claim 18.) Moreover, Harvey teaches the subject is human and the composition at a dose of about 0.5 g to about 2.5 g. (See claims 29 and 50.) Harvey also teaches because of radiation's ionizing effects on cells, exposure to radiation can have detrimental consequences, posing health risks to exposed individuals. The risks of terrestrial exposure to ionizing radiation include, for example, ARS, and DEARE, such as carcinogenesis, damage to the central nervous system, and degenerative effects on tissue, such as fibrosis. Ionizing radiation encountered during space missions also can present potential health problems for astronauts, with a significant risk of ARS. (See lines 31-33 of page 8 bridging lines 1-5 of page 9.) Harvey teaches protective effect of genistein against proton irradiation where mice were prophylactically administered genistein (200 mg/kg) via s.c. injection 24 hours prior to radiation exposure. DNA damage in tissues — Lungs and heart were surgically removed and subjected to thin-slice sectioning, followed by western blot analysis for the DNA damage markers p53 and YH2AX (an effective measure of proton radiation-induced biological damage, as well as tubulin control. Genistein ameliorated the effects of proton radiation on expression of these markers (FIGS. 2, 3A, and 3B), indicating its ability to mitigate the toxicity of proton radiation. Cytokine response — Peripheral blood was taken from the treated and irradiated mice 3, 6, and 12 days after radiation exposure, and assessed using a multi- cytokine LUMINEX® panel to evaluate the global inflammatory cytokine response. As shown in FIGS. 4A, 4B, and 4C, specific cytokine responses were reduced by genistein treatment. In particular genistein mitigated the effects of proton radiation on expression of CXCL1 cytokine (FIG. 4A), G-CSF (FIG. 4B), and TNFα. (FIG. 4C). (See lines 10-28.) Lastly, Harvey teaches the in vivo studies include analysis of any or all of the following parameters including, but not limited to DNA damage in tissues such as lungs, liver and bowel from sacrificed animals (4 hours and 16 days post radiation exposure) are surgically removed and subjected to thin-slice sectioning, followed by immune-histological analysis for YH2AX, which has been demonstrated to be an effective measure of proton radiation-induced biological damage. Additionally. pathological parameters such as fibrosis and evidence of inflammation are qualitatively assessed. Tissue analysis is performed on sections from groups of animals demonstrating therapeutic efficacy by CBC measures. (See lines 26-33 of page 23.) A person of ordinary skill in the art can reasonably infer the fibrosis is lung fibrosis. Furthermore, Harvey teaches the genistein-containing composition can be administered one or more times daily, every other day, biweekly. weekly. bimonthly, monthly, or less often, for any suitable length of time after exposure to the radiation has occurred (e.g., for about a week, about two weeks, about three weeks, about a month, about six weeks, about two months, about three months, about six months, about a year, or more than a year after exposure). (See lines 21-26.)
Harvey does not teach the human patient is identified as being infected or having been infected with a coronavirus in this case SARS-Cov-2. Moreover, Harvey does not teach the composition is administered to the mammal beginning about 4 to 8 weeks after the mammal was diagnosed with a coronavirus infection or beginning about 4 to 8 weeks after the onset of one or more symptoms of coronavirus infection.
Jackson teaches a method of mitigating pneumonitis/fibrosis in a mammal subject that has been exposed to high dose of radiation, the method comprising administering orally an effective amount of BIO 300 daily in the range of 200 or 400 mg/kg to said mammal subject, the BIO 300 is a nanoparticulate genistein (See Abstract and the second paragraph of the left column of page 4739.) Moreover, Jackson teaches the C57L/J mouse strain was chosen based on extensive model development that has shown this strain reacts over a time period and dose range that covers the responses seen in non-human primates and humans, with the pneumonitis reaction progressing to a pathology of fibrosis. (See last paragraph of the left column of page 4739.) Furthermore, Jackson teaches BIO 300, a patent-protected nanosuspension formulation that contains synthetic genistein nanoparticles, is being developed to mitigate and/or treat DEARE in the lung (radiation pneumonitis/pulmonary fibrosis). (See second paragraph of the left column of page 4739.)
McGonagle teaches severe Covid-19 associated pneumonia patients may exhibit features of systemic hyper-inflammation designated under the umbrella term of macrophage activation syndrome (MAS) or cytokine storm, also known as secondary haemophagocytic lymphohistocytosis (sHLH). Covid-19 infection with MAS (macrophage activation syndrome) typically occurs in human patients with adult respiratory distress syndrome (ARDS) and historically, non-survival in ARDS was linked to sustained IL-6 and IL-1 elevation. (See Abstract.) Moreover, McGonagle teaches cytokine profile, resembling MAS/sHLH has also been noted in COVID-19 patients, notably increased IL-1β, IL-2, IL-6, IL-17, IL-8, TNF and CCL2. The apparent recognition of MAS/sHLH complicating COVID-19 pneumonia forms the backdrop for cytokine suppression strategy. (See first paragraph of the left column of page 2.) McGonagle also teaches pneumonitis and lung injury can occur in Covid-19. (Table 1.)
Li teaches genistein decreased the secretion of IL-1β, IL-6, and IL-8 from TNF-α-stimulated MH7A cells in a dose-dependent manner. Genistein prevented TNF-α-induced NF-κB translocation as well as phosphorylation of IκB kinase-α/β and IκBα, and also suppressed TNFα-induced AMPK inhibition. The production of IL-1β, IL-6, and IL-8 induced by TNF-α was decreased by the phosphatidylinositol-3 kinase inhibitor LY294002, suggesting that inhibition of Akt activation might inhibit IL-1β, IL-6, and IL-8 production induced by TNF-α. (See Abstract.)
Pan teaches in patients who recovered from COVID-19 pneumonia, initial lung findings on chest CT (computed tomography) were small subpleural ground glass opacities (GGO) that grew larger with crazy-paving pattern and consolidation. Lung involvement increased to consolidation up to two weeks after disease onset. After two weeks, the lesions were gradually absorbed leaving extensive GGO and subpleural parenchymal bands. (Key Results Section.) Moreover, Pan teaches chest CT abnormalities increased in number and severity of lesions in the first 10 weeks (peaking at approximately 10 days). Subsequently, there was a short plateau phase and a gradual decrease in abnormalities. (See first paragraph under Discussion Section.)
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to modify the method of Harvey by administering to the human patient beginning about 4 to 8 weeks after the human patient was diagnosed with a coronavirus infection or beginning about 4 to 8 weeks after the onset of one or more symptoms of coronavirus infection in the human patient for treating or reducing pneumonitis, pneumonia or pulmonary fibrosis in a mammalian subject that can include a human that is identified as being infected of Covid-19 (SARS-CoV-2) by suppressing IL-1β, IL-6, IL-8, TNF-α (cytokine storm) to give Applicant’s claimed invention. One would have been motivated to do so, not only because Harvey teaches genistein which can be administered about a month, about six weeks, about two months after exposure to the radiation that can give rise to fibrosis has occurred and is effective for reducing specific cytokine responses such as TNF-α and is effective for treating fibrosis of the lung, but also Jackson teaches genistein is effective for treating pneumonitis/fibrosis, but also because McGonagle teaches cytokine profile, resembling MAS/sHLH has also been noted in COVID-19 patients, notably increased IL-1β, IL-2, IL-6, IL-17, IL-8, TNF and CCL2, and also because Li teaches genistein decreased the secretion of IL-1β, IL-6, and IL-8 from TNF-α-stimulated MH7A cells in a dose-dependent manner, and lastly because Pan teaches chest CT abnormalities in Covid-19 pneumonia increased in number and severity of lesions in the first 10 weeks (peaking at approximately 10 days). One would have a reasonable expectation of success of using the BIO 300 formulation comprising nanoparticulated genistein to reduce or treat pneumonitis, pneumonia, or pulmonary fibrosis in a mammalian subject including a human, that is identified as being infected of Covid-19 (SARS-CoV-2), by suppressing IL-1β, IL-6, IL-8, TNF-α (cytokine storm).
Acknowledgement is made of the receipt and entry of applicant’s arguments/remarks filed on October 06, 2025.
Applicant’s argument
Applicant argues that given the lack of knowledge (see Exhibit A) at the time of Applicant's priority filings that any similarities in the detrimental effects of radiation and COVID-19 in the lung were not appreciated before Applicant's priority filings, a person of ordinary skill in the art would not have been motivated to modify the method of Jackson in order to use genistein to reduce pneumonitis, pulmonary fibrosis, dyspnea, pneumonia, and/or pulmonary edema in a mammal identified as being infected or having been infected with a coronavirus, as required by the present claim.
Examiner’s response
In response, Applicant’s argument is not persuasive. Exhibit A cannot be considered by the Examiner because it is not cited in an IDS. Even assuming the consideration of Exhibit A, a POSA would have a reasonable expectation of success of using the BIO 300 formulation comprising nanoparticulated genistein to reduce or treat pneumonitis and pulmonary fibrosis in a mammalian subject including a human, that is identified as being infected of Covid-19 (SARS-CoV-2), by suppressing IL-1β, IL-6, IL-8, TNF-α (cytokine storm) not only because Harvey teaches genistein which can be administered about a month, about six weeks, about two months after exposure to the radiation that can give rise to fibrosis has occurred and is effective for reducing specific cytokine responses such as TNF-α and is effective for treating fibrosis of the lung, but also Jackson teaches genistein is effective for treating pneumonitis/pneumonia/fibrosis, but also because McGonagle teaches cytokine profile, resembling MAS/sHLH has also been noted in COVID-19 patients, notably increased IL-1β, IL-2, IL-6, IL-17, IL-8, TNF and CCL2, and also because Li teaches genistein decreased the secretion of IL-1β, IL-6, and IL-8 from TNF-α-stimulated MH7A cells in a dose-dependent manner, and lastly because Pan teaches chest CT abnormalities in covid-19 pneumonia increased in number and severity of lesions in the first 10 weeks (peaking at approximately 10 days).
Applicant’s argument
Applicant argues that the cells used by Li were not lung cells, nor were they primary cells of any type. A person having ordinary skill in the art at the time of Applicant's priority filing would have appreciated that it is unclear how immortalized synovial cells would be applicable to the mammalian lung.
Examiner’s response
In response, Applicant’s argument is not persuasive. Just because the cells used by Li were not lung cells, does not mean genistein cannot be expected to inhibit or reduce IL-1β, IL-6, and IL-8 from TNF-α. In fact, Harvey clearly teaches genistein can reduce specific cytokine responses such as TNF-α in lung tissues. Therefore, a POSA can reassembly expect genistein to reduce IL-1β, IL-6, and IL-8 from TNF-α in mammalian lung.
Applicant’s argument
Applicant argues that there is no suggestion in Pan or any of the other cited references, which disclose administering genistein to mice beginning 4 weeks or more after diagnosis or onset of one or more symptoms of coronavirus infection. As such, a person of ordinary skill in the art at the time of Applicant's priority filings would have had no reasonable expectation that administration of genistein beginning weeks after COVID diagnosis or onset would be useful to reduce pneumonitis, pulmonary fibrosis, dyspnea, pneumonia, and/or pulmonary edema.
Examiner’s response
In response, Applicant’s argument is not persuasive. It may well be true that Pan or any of the other cited references, which disclose administering genistein to mice beginning 4 weeks or more after diagnosis or onset of one or more symptoms of coronavirus infection. However, the Examiner contends that Pan teaches chest CT abnormalities in Covid-19 pneumonia increased in number and severity of lesions in the first 10 weeks (peaking at approximately 10 days). Therefore, a person of ordinary skill in the art would have had a reasonable expectation that administration of genistein beginning weeks after COVID diagnosis or onset would be useful to reduce pneumonitis, pulmonary fibrosis, or pneumonia with success.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 27-29, 31, 45, 49-51, 53-65 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 25-33, 36- and 42-47 of copending Application No. 18/271,125 (reference application) in view of McGonagle et al (Autoimmunity Reviews 19, April 03, 2020, 102537, pages 1-8) Li et al (Drug Design, Development and Therapy 2014:8 315–323), and Pan et al (Radiology. 2020 Feb 13:200370). Although the claims at issue are not identical, they are not patentably distinct from each other.
The copending claims teach a method for reducing inflammation and/or an immune response in a mammal identified as having an inflammatory or immunological disorder, the method comprising administering to the mammal a composition comprising genistein in an amount effective to reduce inflammation and/or an immune response in the mammal. (See claim 25.) The copending claims teach the genistein is nanoparticulate genistein and the composition has a nanoparticulate genistein concentration between about 250 mg/mL and about 500 mg/mL. (See claims 26-27.) The subject is human. After all the dependent claims of the copending claims are substantially similar to the instant claims.
The copending claims do not teach treating or reducing pneumonitis pulmonary fibrosis or pneumonia in a mammalian subject that can include a human that is identified as being infected. Moreover, the copending claims do not teach the composition is administered to the mammal beginning about 4 to 8 weeks after the mammal was diagnosed with a coronavirus infection or beginning about 4 to 8 weeks after the onset of one or more symptoms of coronavirus infection.
McGonagle teaches severe Covid-19 associated pneumonia patients may exhibit features of systemic hyper-inflammation designated under the umbrella term of macrophage activation syndrome (MAS) or cytokine storm, also known as secondary haemophagocytic lymphohistocytosis (sHLH). Covid-19 infection with MAS (macrophage activation syndrome) typically occurs in human patients with adult respiratory distress syndrome (ARDS) and historically, non-survival in ARDS was linked to sustained IL-6 and IL-1 elevation. (See Abstract.) Moreover, McGonagle teaches cytokine profile, resembling MAS/sHLH has also been noted in COVID-19 patients, notably increased IL-1β, IL-2, IL-6, IL-17, IL-8, TNF and CCL2. The apparent recognition of MAS/sHLH complicating COVID-19 pneumonia forms the backdrop for cytokine suppression strategy. (See first paragraph of the left column of page 2.) McGonagle also teaches pneumonitis and lung injury can occur in Covid-19. (Table 1.)
Li teaches genistein decreased the secretion of IL-1β, IL-6, and IL-8 from TNF-α-stimulated MH7A cells in a dose-dependent manner. Genistein prevented TNF-α-induced NF-κB translocation as well as phosphorylation of IκB kinase-α/β and IκBα, and also suppressed TNFα-induced AMPK inhibition. The production of IL-1β, IL-6, and IL-8 induced by TNF-α was decreased by the phosphatidylinositol-3 kinase inhibitor LY294002, suggesting that inhibition of Akt activation might inhibit IL-1β, IL-6, and IL-8 production induced by TNF-α. (See Abstract.)
Pan teaches in patients who recovered from COVID-19 pneumonia, initial lung findings on chest CT (computed tomography) were small subpleural ground glass opacities (GGO) that grew larger with crazy-paving pattern and consolidation. Lung involvement increased to consolidation up to two weeks after disease onset. After two weeks, the lesions were gradually absorbed leaving extensive GGO and subpleural parenchymal bands. (Key Results Section.) Moreover, Pan teaches chest CT abnormalities increased in number and severity of lesions in the first 10 weeks (peaking at approximately 10 days). Subsequently, there was a short plateau phase and a gradual decrease in abnormalities. (See first paragraph under Discussion Section.)
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to modify the method of the copending claims by administering to the human patient beginning about 4 to 8 weeks after the human patient was diagnosed with a coronavirus infection or beginning about 4 to 8 weeks after the onset of one or more symptoms of coronavirus infection in the human patient for treating or reducing pneumonitis or pulmonary fibrosis in a mammalian subject that can include a human that is identified as being infected of Covid-19 (SARS-CoV-2) by suppressing IL-1β, IL-6, IL-8, TNF-α (cytokine storm) for treating or reducing pneumonitis and pneumonia in a mammalian subject that can include a human that is identified as being infected of Covid-19 (SARS-CoV-2) by suppressing IL-1β, IL-6, IL-8, TNF-α (cytokine storm) to give Applicant’s claimed invention. One would have been motivated to do so, because McGonagle teaches cytokine profile, resembling MAS/sHLH has also been noted in COVID-19 patients, notably increased IL-1β, IL-2, IL-6, IL-17, IL-8, TNF and CCL2, and also because Li teaches genistein decreased the secretion of IL-1β, IL-6, and IL-8 from TNF-α-stimulated MH7A cells in a dose-dependent manner, and lastly because Pan teaches chest CT abnormalities increased in number and severity of lesions in the first 10 weeks (peaking at approximately 10 days). One would have a reasonable expectation of success of using the method of the copending claims to reduce or treat pneumonitis or pulmonary fibrosis in a mammalian subject including a human, that is identified as being infected of Covid-19 (SARS-CoV-2), by suppressing IL-1β, IL-6, IL-8, TNF-α (cytokine storm).
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Applicant argues that this provisional rejection be held in abeyance until the claims of the present application are determined to otherwise be in condition for allowance.
In response, since the claims of the present application are not in condition for allowance, the double patenting rejection is maintained
Conclusion
Claims 27-29, 31, 45, 49-51, 53-65 are not allowed.
THIS ACTION IS MADE FINAL. 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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/JEAN P CORNET/ Primary Examiner, Art Unit 1628
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