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 .
Election/Restrictions
Applicant’s election without traverse of Group (I) with the addition of infection by SARS-Cov-2-virus (Covid-19) as the elected condition that causes a cytokine storm, and MK-8931 as the elected BACE1 inhibitor species in the reply filed on 10/06/2025 is acknowledged.
Priority
This application is a filing under 35 U.S.C. § 371 of International Application No. PCT/US21/45215, filed August 09, 2021, which claims priority to U.S. Provisional application serial number 63/064,753 filed August 12, 2020.
Status of Claims
Acknowledgement is made of the receipt and entry of the amendment to the claims filed on March 13, 2026. Claims 1-13 and 15-18 are pending. Claims 14 and 19-20 are canceled. Claims 5-7 and 13 are withdrawn. Claims 1-4, 8-12, and 15-18 are examined in accordance to the elected species.
Action Summary
Claim 8 rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite, is withdrawn in light of the claim amendment.
Claims 1-4, 8-12, 14-16 and 18 are rejected under 35 U.S.C. 103 as being unpatentable over Trzaska et al (WO2016/053767 A1) in view of Newcombe et al (Journal of Neuroinflammation (2018) 15: 276), Naughton et al (Journal of Alzheimer’s Disease 76 (June 12, 2020) 21–25), and NCT01739348 (Merck Sharp & Dohme LLC, 10/24/2018), are withdrawn in light of the claim amendment.
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1-4, 8-12, and 15-18 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for treating cytokine Covid-19 as an infection that causes cytokine storm from macrophages by administering orally as the route of administrations MK-8931 at a dose of 50 mg/kg as the BACE1 inhibitor in an animal model (mice) a dose of 50 mg/kg, does not reasonably provide enablement for all conditions that cause cytokine storm that include cancer and every BACE-1 inhibitor and every route of administration in a human patient. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to use the invention commensurate in scope with these claims.
There are several guidelines when determining if the specification of an application allows the skilled artisan to practice the invention without undue experimentation. The factors to be considered in determining what constitutes undue experimentation were affirmed by the court in re Wands (8 USPQ2d 1400 (CAFC 1986)). These factors are (1) nature of the invention; (2) state of the prior art; (3) level of one of ordinary skill in the art; (4) level of predictability in the art; (5) amount of direction and guidance provided by the inventor; (6) existence of working examples; (7) breadth of claims; and (8) quantity of experimentation needed to make or use the invention based on the content of the disclosure.
The claims encompass (1) treatment of subject having a condition that causes cytokine storm from macrophage, (ii) multiple disease contexts, including viral infection and other conditions, (iii) multiple routes of administration, including oral, intravenous, and airway delivery, and (iv) use of a BACE1 inhibitors, which encompasses a genus of structurally and functionally diverse compounds. However, the specification only provided limited guidance directed to primarily oral administration of MK-8931 at a doe of 50 mg/kg in specific experimental models, and does not enable for the full scope of these claims.
(1) Nature of the invention
The claims are directed to methods of treating cytokine storm from macrophages in a subject by administering a BACE1 inhibitor, including MK-8931, wherein the cytokine storm is recited as being from macrophages, and wherein the method encompasses multiple administration routes/doses and disease contexts. The invention therefore resides in the clinical therapeutic application of a compound or class of compounds across heterogenous diseases states and biological mechanisms, requiring reliable pharmacological activity under varying physiological conditions.
(2) State of the prior art
The state of the art establishes that:
MK-8931 (verubecestat) has been primarily developed for Alzheimer’s disease
and administered orally in human patients. (See clinical trials NCT01739348 and NCT01496170).
Shideng Bao (2020-111 - Novel utilization of BACE1 inhibitors for suppression of cytokine storm and reduced COVID mortality) suggests the potential repurposing of BACE1 inhibitor for cytokine storm associated with COVID-19.
Trzaska et al. (WO2016053767A1) disclose oral and inhalation formulation of MK-8931.
However, the art further teaches that:
BACE1 inhibitors represent a diverse class of compounds with varying
Pharmacokinetics and pharmacodynamic properties (May et al. (J Neurosci. 2011 Nov 16;31(46):16507–16516), including poor bioavailability and CNS penetration issues,
Certain BACE1 inhibitors (e.g., LY2811376) were discontinued due to toxicity
unrelated to target inhibition, and
Cytokine storm syndromes are heterogenous and dependent on underlying
etiology, with treatment varying across conditions (Hickman (What Is Cytokine Storm Syndrome? An Exaggerated and Dangerous Immune Response, October 21, 2025).
Additionally, the prior art does not establish intravenous administration of MK-8931, further reflecting limitations in known delivery methods. Thus, the state of the art reflects uncertainty and lack of predictability in applying BACE1 inhibitors broadly across different disease conditions and clinical settings.
Further, the prior art demonstrates that the development of BACE1 inhibitors has been largely unsuccessful in clinical settings. For example, Bazzari et al. (molecules 2022, 27, 8823, pages 1-15) report that although numerous BACE1 inhibitors progressed through early development, nearly all BACE1 inhibitors failed in later phases of clinical trials due to safety and/or efficacy issues. (See Abstract.) The evidence indicates even when BACE1 inhibition shows promise in early experimental models, such results do not translate into effective and safe therapeutic outcomes in humans. This also demonstrates that the relationship between BACE1 inhibition and therapeutic benefit is not reliably predictable, particularly when extended across different disease conditions and biological contexts. The widespread clinical failure of BACE1 inhibitors further confirms that the claimed invention, which broadly encompass the use of BACE1 inhibitors for treating cytokine storm conditions from macrophages, cannot be practiced across its full scope without undue experimentation.
(3) Level of one of ordinary skill in the art
The level of skill in the art is deemed to be high, typically that of a physician or Ph.D. scientists specializing in immunology, pharmacology, or clinical therapeutics. However, even a skilled artisan would require substantial guidance to apply a compound across multiple disease etiologies, compound variants, and administration routes.
(4) Level of predictability in the art
The art is highly unpredictable. Cytokine storm arise from diverse and complex immune responses, depending on the underlying condition (e.g., viral infection, malignancy, or immune dysregulation). As noted in the cited references, the optimal treatment varies depending on the specific cause, and no single therapeutic approach is universally effective.
Further, BACE1 inhibitors exhibit variable pharmacological behavior, including:
Inconsistent pharmacokinetics.
Limitations in tissue distribution, and
Potential toxicity concerns.
The lack of established intravenous administration of MK-8931 and uncertainty
regarding macrophages-specific mechanisms across diseases further underscore the unpredictability of the claimed invention.
(5) Amount of direction and/or Guidance provided
The specification provides limited guidance, primarily directed to oral administration of MK-8931 at a dose of 50 mg/kg, a viral cytokine response context, and specific experimental systems. In particular, the specification includes:
in vitro experiments using U937-derived macrophages stimulated with SARS-CoV-2 spikes protein, and
an in vivo LPS-induced cytokine response model in mice.
However, such disclosures are confined to narrow experimental conditions and do not
reasonably guide one of ordinary skill in the art to treat other cytokine storm-inducing conditions, administer the compound via intravenous or airway routes, or practice the invention across the full genus of BACE1 inhibitors recited in the claims.
Additionally, the claims recite the cytokine storm is “from macrophages” and that
the BACE1 inhibitor inhibits such macrophage-associated cytokine storm. While the specification demonstrates cytokine suppression in macrophages-related experimental systems, it does not provide sufficient guidance demonstrating that such effects are consistently attributable to macrophage modulation across different disease contexts. Cytokine storm syndrome involve multiple immune cell types and pathways, and the specification does not teach how to achieve macrophage-specific modulation across the full scope of the claimed invention.
(6) Existence of working examples
The specification provides limited working examples, restricted to a single compound (MK-8931 at a dose of 50 mg/kg), a single administration route (oral), and a limited number of experimental model (in vitro macrophage system, and LPS-induced mouse models). There are no working examples demonstrating treatment of multiple disease etiologies, use of other BACE1 inhibitor with the claimed genus, or administration via intravenous or airways routes.
(7) Breadth of claims
The claims are extremely broad encompassing multiple conditions that cause cytokine storm from macrophages, multiple routes of administration, doses, and a genus of BACE1 inhibitors. The breadth is not commensurate in scope with the limited disclosure in the specification. Although MK-8931 is exemplified, the claims are not limited to the specific experimental contexts disclosed, and the specification does not enable the full range of claimed embodiments.
(8) Quantity of experimentation Required
A person of ordinary skill in the art would be required to engage in undue experimentation to determine which BACE1 inhibitors within the claimed genus are effective, evaluate efficacy across different cytokine storm etiologies, develop and validate intravenous and airway formulations, and establish safe and effective dosing regimen for such uses. Such experimentation would require extensive clinical investigation and unpredictable trial-and-error, exceeding routine optimization.
Acknowledgement is made of the receipt and entry of Applicant’s remarks/arguments filed on March 13, 2026.
Applicant’s arguments have been full considered by are not persuasive.
Applicant contends that the claims are enabled because the specification demonstrates inhibition of cytokine storm from macrophages using MK-8931, and that such mechanism is generalizable across different cytokine storm conditions. However, the evidence provided in the specification is limited to specific experimental systems, including an in vitro macrophage model (U937-derived macrophages stimulated with SARS-CoV-2 spike protein and an in vivo LPS-induced cytokine response model in mice.
While these models demonstrate cytokine storm suppression under particular conditions, they do not reasonably establish that the claimed invention can be practiced across the full scope of the claims without undue experimentation.
Applicant argues the cytokine storm conditions share a common feature of macrophage-driven cytokine release, and therefore the claimed invention is enabled across such conditions.
This argument is not persuasive. Although macrophages are one source of pro-inflammatory cytokines, cytokine storm syndromes are complex and heterogenous, involving multiple immune cell types and signaling pathways that vary depending on the underlying condition (e.g., viral infection, cancer, CAR-T therapy, autoimmune disease). The specification does not provide sufficient guidance demonstrating BACE1 inhibition in macrophages alone is sufficient to treat cytokine storm across all such conditions. Accordingly, the recitation of “macrophages” does not meaningfully narrow the scope of the claims to a commensurate level of enablement, but instead continues to encompass a wide range of biological contexts not adequately supported by the disclosure.
Applicant further asserts that the LPS-induced cytokine storm model is an art-recognized surrogate that supports utility across cytokine storm conditions.
This argument is not persuasive. While LPC-induced models used to study aspects of inflammatory response, such models do not replicate the full complexity of cytokine storm across different disease etiologies, particularly in human clinical settings. The use of a single surrogate model does not provide sufficient guidance to enable treatment of diverse cytokine storm conditions arising from distinct pathological mechanisms. Thus, reliance on the LPS-driven model does not demonstrate that the claimed invention can be practiced across the full scope of the claims without undue experimentation.
Applicant asserts that MK-8931 exhibits a generalized mechanism of action across stimuli and cell types.
However, the specification does not provide sufficient evidence to support such a broad conclusion. The data is limited to specific experimental conditions, and does not establish that the observed effects extend to different disease etiologies, different immune environments, or different administration routes (e.g., intravenous or airways). Moreover, as discussed in the rejection, the prior art demonstrates that BACE1 inhibitors have exhibited inconsistent efficacy and safety profiles in clinical development, further indicating that such mechanisms are not reliably predictive across different contexts.
Given the breadth of the claims, the limited number of working examples, and the unpredictability nature of cytokine storm biology and BACE1 inhibitor pharmacology, a person of ordinary skill in the art would be required to perform undue experimentation to determine efficacy across different cytokine storm conditions, validate macrophage-specific mechanism in each condition, and establish appropriate dosing and administration parameters.
As such, Applicant’s arguments do not overcome the deficiencies identified in the rejection. The specification does not enable the full scope of the claimed invention without undue experimentation.
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 1-4, 8-12, 14-16 and 18 are rejected under 35 U.S.C. 103 as being unpatentable over Trzaska et al (WO2016/053767 A1) in view of Newcombe et al (Journal of Neuroinflammation (2018) 15: 276), Naughton et al (Journal of Alzheimer’s Disease 76 (June 12, 2020) 21–25), and NCT01739348 (Merck Sharp & Dohme LLC, 10/24/2018, https://clinicaltrials.gov/study/NCT01739348?tab=history).
Neucombe et al has been cited in the Restriction Requirement and copy of it can be in the attached 892 form dated 07/08/2025.
Trzaska teaches a method of treating an Αβ pathology or one or more symptoms thereof, wherein said Αβ pathology is Alzheimer's disease, olfactory impairment associated with Alzheimer's disease, Down's syndrome, olfactory impairment associated with Down's syndrome, Parkinson's disease, olfactory impairment associated with Parkinson's disease, stroke, microgliosis brain inflammation, pre-senile dementia, senile dementia, progressive supranuclear palsy, cortical basal degeneration, β-amyloid angiopathy, cerebral amyloid angiopathy, hereditary cerebral hemorrhage, mild cognitive impairment, glaucoma, amyloidosis, type II diabetes, diabetes-associated amyloidogenesis, scrapie, bovine spongiform encephalitis, traumatic brain injury, or Creutzfeld-Jakob disease, said method comprising administering a pharmaceutical composition comprising a Crystalline Form of Verubecestat. Verubecestat is the same as MK-8931. (See claims 20 and 21.) Trzaska teaches verubecestat is a potent inhibitor of BACE- 1 and BACE-2. (See lines 4-5 of page 1.) The pharmaceutical composition includes an oral dosage form, parenteral injection, and inhalation. (See lines 22-26.) Inhalation is considered an administration via the airway. Moreover, Trzaska teaches the crystalline form of verubecestat can be provided at a dose 1 mg or 100 mg/dose once or twice per day. (See lines 26-28 of page 49 bridging lines 1-5 of page 51.) This amount touches the claimed 0.5-4.0 mg/kg. The overlapping dose of 1-100 mg once per day for at least one day would have been within the level of the skilled artisan to optimize. See in re Aller, 220 F.2d 454 (CCPA) 1955). The term pharmaceutical composition is intended to include tablets and pills. (See lines 9-15.). Furthermore, Trzaska teaches the patient is a human. (See line 20 of page 8.)
Trzaska does not covid-19 (SARS-Cov-2) which is a coronavirus that causes a cytokine storm from macrophage. Moreover, Trzaska does not teach administering or providing the composition to the subject such that said subject administers said composition to themselves. Lastly, Trzaska does not teach repeating administering or providing daily for at least one week or at least three weeks.
Newcombe teaches although neurons account for most BACE-1-mediated Aβ synthesis in AD, it has been demonstrated that inflammatory mediators, such as IFN-ϒ, TNF-α, and IL-1β induce the expression of BACE1 and the release of Aβ in astrocytes, suggesting that these cells also contribute to the amyloidosis in AD. (See first paragraph of the right column of page 6.)
Naughton teaches the “cytokine storm” associated with COVID-19 has been associated with an increase of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), and IL-6 all of which have been identified to be increased in the elderly. The potential for elevations in blood glucose to increase inflammation through IRF5 activity, along with the overlapping pathology of T2D and AD may create a “perfect storm” of excessive immune response after infection with SARS-CoV-2 in AD patients. (See second paragraph of the left column of page 22.) Moreover, Naughton teaches suppression of IFN-ϒ response in both AD and COVID-19 (or comorbidity of the two) may be an advantageous strategy for controlling excessive immune response. Additionally, it is interesting to speculate on how AD therapeutics might interact with SARS-CoV-2 infection. (See first paragraph of the left column of page 23.)
NCT01739348 suggests a method of treating mild to moderate Alzheimer’s disease to a human patient comprising administering 12 mg verubecestat once daily for 78 weeks and 12 gm once daily for an additional 260 weeks to themselves. (See Title and Participant group/Arm.)
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 taught by Trzaska by having the patient taking/administer to themselves verubecestat in the form of a pill at least a period of 78 weeks and repeating said administration for an additional 260 weeks to treat either AD caused by Covid-19 which is a condition of a cytokine storm or by suppressing or inhibiting IFN-ϒ, TNF-α, and IL-1β that is expressed in Covid-19, thereby treating Covid-19. One would have been motivated to do so, because verubecestat is a BACE1 inhibitor that can treat AD as taught by Trzaska, inflammatory mediators, such as IFN-ϒ, TNF-α, and IL-1β induce the expression of BACE1 and the release of Aβ in astrocytes in AD as taught by Newcombe, IL-1, TNF-α, and IFN have been increased in Covid-19 and AD as taught by Naughton, and lastly, NCT01739348 suggests a method of treating AD by administering orally 12 mg verubecestat once daily for 78 weeks and 12 gm once daily for an additional 260 weeks to themselves as taught by NCT01739348. One would have a reasonable expectation that modulation of BACE1 activity would influence cytokine-mediated inflammatory pathways, based on the established relationship between inflammatory cytokines and BACE1 expression as taught by Newcombe.
The recitation of cytokine storm “from macrophages” does not result in a patentable distinction over the cytokine storm condition taught by the prior art. Cytokine storm in COVID-19 is mediated by well-known immune cells, including macrophages, which are a primary source of pro-inflammatory cytokines such as TNF-α, IL-1, and IL-6. Accordingly, specifying macrophages as the source of the cytokine does not alter the nature of the condition being treated, nor does it require a different method of treatment.
Acknowledgement is made of the receipt and entry of Applicant’s remarks/arguments filed on March 13, 2026.
Applicant’s arguments have been full considered by are not persuasive.
Applicant argues that none of the cited references teach or suggest BACE1 function in macrophage or cytokine storm arising from macrophage.
This argument is not persuasive. Specifically, the claims are directed to treating a condition that causes cytokine storm from macrophages. Condition of cytokine storms is characterized by elevated levels of pro-inflammatory cytokines such as TNF-α, IL-18, and IL-6. As evidenced by Naughton, such cytokines are known to be elevated in COVID-19-associated cytokine storm. Newcombe further teaches that these same inflammatory cytokines induce BACE1 expression in relevant cell types, thereby establishing a relationship between cytokine signaling and BACE1 activity. Accordingly, the cited references collectively establish a functional relationship between inflammatory cytokines and BACE1, regardless of the specific cell type in which such activity occurs. The claims do not require any specific manipulation of macrophage, but rather recite a condition “that cause a cytokine storm from macrophages.” This language describes the biological origine of cytokines, not a distinct method step or structural limitation.
Therefore, the absence of an explicit reference to “macrophages” in the prior art does not constitute a patentable distinction, as the claimed method relies on known inflammatory pathways already described in the art.
Applicant contends that the cited art is limited to neuronal BACE1 activity (e.g., Alzheimer’s disease) and is mechanistically distinct from macrophage-driven cytokine release.
This argument is not persuasive. The rejection does not rely on the specific disease context of Alzheimer’s disease, but rather on the known biological role of BACE1 in inflammatory signaling pathways, as evidenced by Newcombe, which teaches that inflammatory cytokines induce BACE1 expression. Furthermore, Newcombe teaches COVID-19 cytokine storm involves elevated levels of the same inflammatory mediators.
Applicant asserts that the Examiner’s rational requires impermissible hindsight and relies on a chain of unsupported inferences.
In response to applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971). In the present case, the motivation to combine arises from the fact that Trzaska teaches administration of a known BACE1 inhibitor (verubecestat)/MK-8931). Newcombe teaches that inflammatory cytokines induce BACE1 expression, and Naughton teaches that COVID-19 cytokines storm involves elevated inflammatory cytokines. Taken together, these references provide a reason for a person of ordinary skill in the art to apply a known BACE1 inhibitor in a context where BACE1 is implicated in cytokine-associated pathways, such as cytokine storm. The combination does not require undue inference, but rather reflects the application of known therapeutic agents to closely related biological processes, which is a recognized basis for obviousness.
Applicant argues that the cited references do not support a reasonable expectation that BACE1 inhibition would suppress cytokine storm.
This argument is not persuasive. Given that cytokine storm is defined by elevated inflammatory cytokines (Naughton), and BACE1 expression is influenced by such cytokines (Newcombe), a person of ordinary skill in the art would have reasonably expected that modulating BACE1 activity would impact cytokine-associated inflammatory processes. Absolute predictability is not required. Rather, only a reasonable expectation of success, which is present here.
Applicant argues that the specification demonstrates unexpected results: MK-8931 at a dose of 50 mg/lg orally reduce cytokine storm in animals and nearly completely abolished macrophage cytokine release induced by SARS-CoV-2 spike protein. Such results would not have been expected in view of the cited references.
This argument is not persuasive. The Examiner does not dispute the fact that MK-8931 administered orally at a dose of 50 mg/kg in LPS-induced cytokine response model in mice. However, the Examiner contends that the claims encompass (i) treatment of a subject having a condition that causes cytokine storm from macrophages, (ii) multiple disease contexts, including viral infection and other conditions, (iii) multiple routes of administration, including oral/dose, intravenous, and airway delivery, and (iv) use of a BACE1 inhibitors, which encompasses a genus of structurally and functionally diverse compounds. Therefore, the alleged unexpected results are not commensurate in scope with the breadth of the claims and therefore is entitled to limited weight. Even assuming arguendo, that the results are considered, the evidence does not demonstrate that such results are unexpected in view of the prior art. Specifically the cited references teach the involvement of inflammatory cytokines in cytokine storm conditions and the relationship between such cytokines and BACE1 activity. Accordingly, a reduction in cytokine levels upon demonstration of a BACE1 inhibitor would have reasonably expected by one of ordinary skill in the art.
Conclusion
Claims 1-4, 8-12, and 15-18 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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