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 .
DETAILED ACTION
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 11/18/2025 has been entered.
Claims 11-15 are now pending. Claims 11-15 are amended and currently being examined.
Maintained Rejection
(Arguments and Amendments Addressed)
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 11-15 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
This is a WRITTEN DESCRIPTION rejection.
The claims are drawn to a method of treating cerebral-reperfusion injury in a subject that has experienced a cerebral ischemic event, the method comprising the step of administering to the subject a pharmaceutical composition comprising a pharmaceutically acceptable carrier and a neutralizing interleukin-1α (IL-1α) antibody which comprises a means for binding and neutralizing interleukin-1α (IL-1α) without binding and neutralizing interleukin-1ß (IL-1ß) and a constant region after the subject develops cerebral ischemia; wherein administering the method: (1) reduces the volume of the cerebral infarct compared to the volume of the cerebral infarct, (2) reduces the volume of the cerebral infarct by at least 20%, (2) reduces the magnitude of a neurological deficit, and (3) reduces the number of activated macrophages present in the ischemic penumbra of the brain lesion. Thus, the claims broadly encompass any antibody that neutralizes IL-1α without neutralizing IL-1ß. Thus, the claims identify the antibody by function only, wherein the function to neutralize IL-1α, without neutralizing IL-1ß, and as noted above in (1)-(3). No antibody structure is recited.
The instant specification does not disclose or provide for the full scope of any agent, including antibodies, that inhibits or “neutralizes” IL-1α but not IL-1ß.
State of the Art: Agents that neutralize or “inhibit” IL-1α alpha, are known to have effects on both IL-1α and IL-1ß. Dinarello et al (Nat Rev Drug Discov. 2012 Aug;11(8):633-52) demonstrates that so far, there are only three IL-1 targeted agents, with two that have both IL-1α and IL-1ß inhibition function. Dinarello also demonstrates that the IL-1 receptor is expressed in all tissues and antagonism prevents receptor binding of either IL-1α and IL-1ß, and although Anakinra, is a well-known, and the first selective IL-1Rα approved drug, it has blocking effects of both IL-1α and IL-1ß. (Cao et al., (Int Immunophamcol 13(1):28-36 (abstract), 2014)
Therefore, the teachings in the art do not support broad teachings for any antibody, or compound, that neutralizes IL-1α, without neutralizing, IL-1ß.
To provide adequate written description and evidence of possession of the claimed antibody genus, the instant specification can structurally describe representative antibodies that function to neutralize IL-1α, IL-1α, without neutralizing IL-1ß, and (1) reduce the volume of the cerebral infarct by at least 20%, (2) reduce the magnitude of a neurological deficit, and (3) reduce the number of activated macrophages present in the ischemic penumbra of the brain lesion, or describe structural features common to the members of the genus, which features constitute a substantial portion of the genus. Alternatively, the specification can show that the claimed invention is complete by disclosure of sufficiently detailed, relevant identifying characteristics, functional characteristics when coupled with a known or disclosed correlation between function and structure, or some combination of such characteristics (see University of California v. Eli Lilly and Co., 119 F.3d 1559, 43 USPQ2d 1398 (Fed. Cir. 1997) and Enzo Biochem, Inc. V. Gen-Probe Inc.).
Although Applicants may argue that it is possible to screen for antibodies that neutralize IL-1α and function as claimed, the court found in (Rochester v. Searle, 358 F.3d 916, Fed Cir., 2004) that screening assays are not sufficient to provide adequate written description for an invention because they are merely a wish or plan for obtaining the claimed chemical invention. “As we held in Lilly, “[a]n adequate written description of a DNA … ‘requires a precise definition, such as by structure, formula, chemical name, or physical properties,’ not a mere wish or plan for obtaining the claimed chemical invention.” 119 F.3d at 1566 (quoting Fiers, 984 F.2d at 1171). For reasons stated above, that requirement applies just as well to non-DNA (or RNA) chemical inventions.” Knowledge of screening methods provides no information about the structure of any future antibodies yet to be discovered that may function as claimed. The IL-1α antigen provides no information about the structure of an antibody that binds to it.
The instant specification fails to describe structural features common to the members of the genus, which features constitute a substantial portion of the genus because the instant specification does not disclose a single exemplary agent that functions as claimed. A definition by function does not suffice to define the genus because it is only an indication of what the agent does, rather than what it is. The specification fails to provide any structural features coupled to the claimed functional characteristics. The instant specification fails to describe a representative number of antibody sequences for the genus of agents that function as claimed. Accordingly, in the absence of sufficient recitation of distinguishing identifying characteristics, the specification does not provide adequate written description of the claimed genus required to perform the claimed method.
Given the lack of representative examples to support the full scope of the claimed agents used in the claimed method, and lack of reasonable structure-function correlation with regards to the unknown sequences in the variable domains or CDRs that provide IL-1α neutralizing function, the present claims lack adequate written description. Thus, the specification does not provide an adequate written description of an antibody that neutralize IL-1α, without neutralizing IL-1ß, or (1) reduces the volume of the cerebral infarct by at least 20%, (2) reduces the magnitude of a neurological deficit, and (3) reduces the number of activated macrophages present in the ischemic penumbra of the brain lesion that is required to practice the claimed invention. Since the specification fails to adequately describe the product to which the claimed method uses, it also fails to adequately describe the method.
Response to Relevant Arguments
Applicant amended claim 11 to recite “a neutralizing interleukin-1α (IL-1α) antibody which comprises a means for binding and neutralizing interleukin-1α (IL-1α) without binding and neutralizing interleukin-1ß and a constant region”. Applicant argues that 35 USC 112(f) does not require a description of equivalents.
Applicant’s arguments have been considered but are not persuasive. Although the claims have been amended to recite “means plus function”, the structure disclosed in the written description of the specification must clearly link or associate that structure to the function under 35 U.S.C. 112(f). see MPEP 2181 below. The Applicant did not reference or point to a specific antibody in the instant application that performs the indicated function. There is no definition of what the structure of the antibody is that functions as listed above.
2181 Identifying and Interpreting a 35 U.S.C. 112(f) or Pre-AIA 35 U.S.C. 112, Sixth Paragraph Limitation [R-07.2022]
C. The Supporting Disclosure Clearly Links or Associates the Disclosed Structure, Material, or Acts to the Claimed Function
The structure disclosed in the written description of the specification is the corresponding structure only if the written description of the specification or the prosecution history clearly links or associates that structure to the function recited in a means- (or step-) plus-function claim limitation under 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph. See B. Braun Medical Inc., v. Abbott Laboratories, 124 F.3d 1419, 1424, 43 USPQ2d 1896, 1900 (Fed. Cir. 1997). The requirement that a particular structure be clearly linked with the claimed function in order to qualify as corresponding structure is the quid pro quo for the convenience of employing 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph, and is also supported by the requirement of 35 U.S.C. 112(b) or pre-AIA 35 U.S.C. 112, second paragraph, that an invention must be particularly pointed out and distinctly claimed. See Medical Instrumentation & Diagnostics Corp. v. Elekta AB, 344 F.3d 1205, 1211, 68 USPQ2d 1263, 1268 (Fed. Cir. 2003). For a means- (or step-) plus- function claim limitation that invokes 35 U.S.C. 112(f) or pre-AIA 35 U.S.C. 112, sixth paragraph, a rejection under 35 U.S.C. 112(b) or pre-AIA 35 U.S.C. 112, second paragraph, is appropriate if one of ordinary skill in the art cannot identify what structure, material, or acts disclosed in the written description of the specification perform the claimed function.
Maintained Rejection
(Necessitated by amendments)
Claim Rejections - 35 USC § 103
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.
Claim(s) 11-15 are rejected under 35 U.S.C. 103 as being unpatentable over Simard et al (US8187817 B2, Published 05/14/2009), in view of Murray et al. (“Interleukin-1 and acute brain injury.” Frontiers in cellular neuroscience vol. 9 18. 6 Feb. 2015; of record), Furuichi et al. (“Interleukin-1-dependent sequential chemokine expression and inflammatory cell infiltration in ischemia-reperfusion injury.” Critical care medicine vol. 34,9 (2006): 2447-55; of record), Parry-Jones et al (Inflammation and reperfusion injury within the penumbra. In The Ischaemic Penumbra (1 ed., pp. 125-137), 2007; of record), Luheshi et al (Interleukin-1α expression precedes IL-1β after ischemic brain injury and is localised to areas of focal neuronal loss and penumbral tissues. J Neuroinflammation. 2011 Dec 29;8:186).
Simard teaches a method of treating cerebrovascular disease, including stroke, comprising administering to a subject an antibody that binds to IL-1α and neutralizes IL-1α bioactivity. Simard teaches the use of IL-1α antibody reduces risk, progression, or symptoms of vascular disease. [Background of Invention]
However, Simard does not explicitly teach: (1) that the IL-1α antibody does not neutralize IL-1ß, (2) treating cerebral ischemia-reperfusion injury comprising administering an IL-1α antibody after the subject develops cerebral ischemia, (3) administering the IL-1α antibody reduces the volume of the cerebral infarct by 20% compared to the volume of the cerebral infarct that would have developed if the subject was not administered the antibody, (4) the IL-1α antibody reduces the magnitude of a neurological deficit compared to the magnitude of the neurological deficit that would have been developed if the subject was not administered the antibody and (4) the IL-1α antibody reduces the number of activated macrophages present in the ischemic penumbra of the brain lesion compared to the number of the activated macrophages that would have been present in the ischemic penumbra of the brain lesion if the subject was not administered the antibody.
Murray teaches the role of interleukin-1 in acute brain injury, including cerebral ischemia. Murray teaches that IL-1 is a key proinflammatory mediator, and one of the main ligands are IL-1α. Murray also teaches a third ligand, which is IL-1 receptor, which when antagonized, blocks all function actions of IL-1. [pg 2, 2nd column: Interleukin -1 and Acute Brain Damage] Murray teaches that high levels of pre-existing IL-1 exacerbates post-stroke damage, and that treatment with IL-1 receptor antagonist reduced infarct volumes by 60%. [pg 5, 1st column, 2nd paragraph] Murray teaches that IL-1 induced hypoperfusion, and that acute administration of IL-1 prior to ischemia resulted in a significant perfusion deficit and larger infarct volumes. [pg 6, 2nd paragraph] Murray further teaches that targeting the IL-1 system is an attractive therapeutic target for acute CNS injuries. Murray teaches therapeutic interventions include direct targeting of IL-1 and use of neutralizing antibodies. [pg 9, 2nd column, last paragraph; Figure 3]
Furuichi teaches that histopathology has shown that inflammatory processes are primarily responsible for tissue destruction in ischemia-reperfusion injury. Furuichi teaches that proinflammatory cytokines, such as interleukin-1 (IL-1) play a major role in escalating the inflammatory state. Furuichi teaches that IL-1α is a member of the IL-1 family and stimulates numerous types of cells to synthesize abundant inflammatory cytokines and chemokines. Furuichi teaches that understanding of the inflammatory process would allow for effective therapeutic interventions. [pg 2447]
Parry-Jones focuses on inflammation and reperfusion injury within the penumbra. Parry-Jones teaches that key mediators of inflammation are cytokines and they have provided targets for therapeutic interventions in CNS disorders, including stroke. Parry-Jones teaches that pro-inflammatory cytokine, IL-1, is the most prominent in these disorders. [pg 125, Introduction] Parry-Jones teaches that inflammation is involved in the pathogenesis of cerebral ischemia following ischemic stroke. [pg 125 last paragraph, Figure 2] Parry-Jones also teaches that glia plays an important role causing acquisition of macrophage differentiation markers, and activated microglia are the primary endogenous brain macrophages that secrete inflammatory molecules, including IL-1. [pg 127-128] Parry-Jones teaches that IL-1 has central neurotoxic roles in acute ischemia, and that when administered centrally or peripherally it increases infarct volumes and cerebral edema. Parry-Jones that when blocking the actions of IL-1 with antibodies this reduces infarct volumes. Parry-Jones further teaches that when IL-1α genes are blocked, there’s a 70% reduction in damage observed in in vivo studies. [pg 129, 1st paragraph] Parry Jones teaches promising targets include inhibition of IL-1, and teaches that inhibition of IL-1 in animal models have been comprehensively shown to reduce damage from focal or global ischemia.
Luheshi teaches that inflammation is a major contributor to the worsening of acute brain injury, and that two inflammatory members, IL-1α and IL-1ß, are the major effectors of injury. Luheshi demonstrates that IL-1α is expressed by microglia at sites of brain injury within a relevant window of time at which blocking the effects of I-1 are known to be neuroprotective. Luheshi teaches that during these times IL-1ß is not present and suggesting that IL-1α is the active IL-1 isoform mediating the early inflammatory period following ischemic brain injury. [pg 4, 2nd column]
It would have been prima facie obvious to one of ordinary skill in the art at the time the invention was filed to treat cerebral ischemia reperfusion injury comprising neutralizing IL-1α antibody, without neutralizing IL-1ß, after a subject develops cerebral ischemia. One would have been motivated to, because: (1) Luheshi teaches that IL-1α is expressed alone during the time of brain injury, and mediates the early inflammatory period following ischemic brain injury, (2) Furuichi teaches that IL-1α plays an important role in ischemia-reperfusion injuries, and that understanding these mechanisms will allow for effective therapeutic interventions, (3) Simard teaches a method of treating cerebrovascular disease, including stroke, by administering an antibody that binds to IL-1α, which neutralizes IL-1α, (4) Murray teaches that high levels of pre-existing IL-1 exacerbates post-stroke damage, and (5) Parry-Jones teaches that IL-1 is a key mediator in CNS disorders, including reperfusion injuries and when IL-1 is administered it increases infarct volumes. One would have a reasonable expectation of success, because: (1) Simard teaches that the use of IL-1α antibody reduces risk, progression, or symptoms of vascular disease, (2) Murray teaches that targeting IL-1 system, including the use of antibodies, is an attractive therapeutic target for acute CNS injuries, and (3) Parry-Jones further teaches that when IL-1α genes are blocked, there’s a 70% reduction in damage observed in in vivo studies. Given the recognized need to treat cerebral ischemia-reperfusion injury, and given the mechanism of action of of IL-1α antibody (neutralize IL-1α), and given the known role of IL-1α in cerebral ischemia, one of skill in the art could have pursued neutralizing IL-1α without neutralizing IL-1ß after a subject develops cerebral ischemia, with a reasonable expectation of success.
It is noted that claims 3 and 13 require to reduces the volume of the cerebral infarct by 20% less than the volume of the cerebral infarct that would have resulted from an occlusive stroke if the subject was not administered the antibody that neutralizes IL-1α, without neutralizing IL-1ß. This limitation would have been obvious to those of ordinary skill in the art because: (1) Simard teaches that the use of an IL-1α antibody reduces risk, progression, or symptoms of vascular disease, (2) Murray teaches that IL-1 induced hypoperfusion, and that acute administration of IL-1 prior to ischemia resulted in a significant perfusion deficit and larger infarct volumes. (3) Murray teaches that targeting IL-1 receptor, which blocks all the functions of IL-1 (including IL-1α) reduces infarct volumes by 60% as IL-1 induces hypoperfusion, (4) Parry-Jones teaches that IL-1 is a key mediator in CNS disorders, including reperfusion injuries and when IL-1 is administered it increases infarct volumes, and (5) Luheshi teaches that IL-1α is expressed alone during the time of brain injury, and mediates the early inflammatory period following ischemic brain injury. Given the recognized need to reduce the volume of a cerebral infarct, and given the known role of IL-1α to increase volume of cerebral infarctions, and given the known use of an IL-1α antibody in cerebrovascular disease, one of skill in the art could have pursued administering an IL-1α antibody after a subject develops a cerebral infarct after a cerebral ischemia event to reduce the volume of the cerebral infarct by 20%, with a reasonable expectation of success.
It is noted that claims 5 and 15 require to administer an IL-1α antibody to neutralize IL-1α, without neutralizing IL-1ß, to reduce the number of activated macrophages present in the ischemic penumbra of the brain lesion compared to the number of the activated macrophages that would have been present in the ischemic penumbra of the brain lesion if the subject was not administered the antibody. This limitation would have been obvious to those of ordinary skill in the art because: (1) Simard teaches that the use of an IL-1α antibody reduces risk, progression, or symptoms of vascular disease, (2) Parry-Jones teaches that when IL-1α genes are blocked, there’s a 70% reduction in damage observed in in vivo studies, (3) Parry-Jones teaches that key mediators of inflammation are cytokines and they have provided targets for therapeutic interventions in CNS disorders, including stroke and further teaches that activated microglia are important macrophages that secrete IL-1, and (4) Luheshi teaches that IL-1α is expressed alone during the time of brain injury, and mediates the early inflammatory period following ischemic brain injury. Given the recognized need to reduce the number of activated macrophages in the ischemic penumbra, given the known role relationship between activated macrophages and IL-1 section, and given the known mechanism of treating cerebrovascular events by blocking IL-1α, one of skill in the art could have pursued administering an IL-1α antibody after a subject develops a cerebral infarct after a cerebral ischemia event to reduce the number of macrophages in the ischemic penumbra of a brain lesion, with a reasonable expectation of success.
It is noted that claims 5 and 15 require filed to administer an IL-1α antibody, to neutralize IL-1α, without neutralizing IL-1ß, to reduce the neurological deficit compared to the magnitude of the neurological deficit that would have developed if the subject was not administered the antibody. This limitation would have been obvious to those of ordinary skill in the art because: (1) Simard teaches that the use of an IL-1α antibody reduces risk, progression, or symptoms of vascular disease, (2) Murray teaches that high levels of pre-existing IL-1 exacerbates post-stroke damage, (3) Parry-Jones teaches that when IL-1α genes are blocked, there’s a 70% reduction in damage observed in in vivo studies, and (4) Luheshi teaches that IL-1α is expressed alone during the time of brain injury, and mediates the early inflammatory period following ischemic brain injury. Given the recognized need to reduce the neurological deficit caused by a cerebral ischemic event, and given the known role of pro-inflammation and increase in damage due to IL-1α, and given the known role of IL-1α to reduce damage, one of skill in the art could have pursued administering an IL-1α antibody to reduce the magnitude of a neurological deficient caused by cerebral ischemic event, with a reasonable expectation of success.
Response to Relevant Arguments
Applicant argues that the inventors of the current application were the first to show that neutralizing IL-1α without neutralizing IL-1ß could (i) reduce the volume of a cerebral infarct that results from an occlusive stroke in a subject, (ii) reduce the neurological deficit that results from an occlusive stroke in a subject, and (iii) reduce the number of activated macrophages in the ischemic penumbra of a brain lesion that results from an occlusive stroke in a subject. Applicant argues that the combination of prior references above does not provide any evidence that would convince the person having a ordinary skill in the art what these effects may be. Applicant argues that none of the results provided in Luheshi prove that IL-1 contributes in any way to brain damage caused by cerebral ischemia-reperfusion injury. Applicant argues that while this reference showed that IL-1α but not IL-1ß was detectable at 4 hours post reperfusion in microglia-like cells in the ischemic hemisphere, and that both of these cytokines were present at 24 hours post reperfusion, it does not show that either of these cytokines played any causative role in development of brain injury The Applicant provided references of Salmeron I and II, and Boutin. The Applicants argue that the reference of Salmeron concludes that IL-1α IS a potential new therapy to promote post-stroke angiogenesis. And that increased IL-1α promotes the formation of new vasculature that might limit damage caused by occlusive stroke. Applicant also provide the reference of Salmeron II to indicate that administration of IL-1α reduces infarct volume and apoptotic cell death following stroke and that these references teach away from the invention and clarify the results that is reported by Luheshi that blocking IL-1α would exacerbate rather than improve the sequala of an ischemia-reperfusion injury to the brain. Applicant also references Boutin and suggests that IL-1α does not contribute to brain damage caused by cerebral ischemia-reperfusion injury. Applicant argues that the teachings of the prior art would teach away from blocking IL-1α as it would exacerbate rather than improve the sequalae of an ischemia-reperfusion injury to the brain.
Applicant's arguments have been fully considered but they are not persuasive. As noted in the prior rejection, it is the combination of the references that render the invention obvious.
With regards to the references cited by the Applicant, Salmeron I, Salmeron II and Boutin, they fail to teach away from the claimed invention as suggested and taught by references cited by the Examiner: Simard, teaches a method of treating cerebrovascular disease, including stroke, comprising administering an antibody that binds to IL-1α and neutralizes IL-1α bioactivity [see column 2, lines 44-50], and teaches that this antibody reduces risk, progression, or symptoms of vascular disease. Murray and Parry-Jones is to demonstrate high levels of pre-existing IL-1 exacerbates post-stroke damage and that when IL-1α genes are blocked, there’s a 70% reduction in damage observed in in vivo studies, respectively. Luheshi explicitly teaches the following: inflammation is a major contributor to the worsening of acute brain injury, and that two inflammatory members, IL-1α and IL-1ß, are the major effectors of injury and Luheshi teaches that during these times IL-1ß is not present and suggesting that IL-1α is the active IL-1 isoform mediating the early inflammatory period following ischemic brain injury. [pg 4, 2nd column] Thus, taken together, the references do not teach away from the fact that IL-1α IS a major inflammatory marker in vascular disease and blocking IL-1α during ischemic events is beneficial as discussed above.
Taken together, the prior art provides motivation and a reasonable expectation of success, as it demonstrates: (1) a method of treating cerebral-ischemia reperfusion injury comprising administering an anti-interluekin-1α antibody, (2) the known roles of IL-1α in cerebral ischemia, and that (3) that IL-1α is the active isoform mediating early inflammation following an ischemic brain injury. Therefore, given the recognized need to reduce the neurological deficit caused by a cerebral ischemic event, and given the known role of pro-inflammation and increase in damage due to IL-1α, and given the known role of IL-1α to reduce damage, one of skill in the art could have pursued administering an IL-1α antibody to reduce the magnitude of a neurological deficient caused by cerebral ischemic event, with a reasonable expectation of success.
Conclusion
All claims are identical to or patentably indistinct from, or have unity of invention with claims in the application prior to the entry of the submission under 37 CFR 1.114 (that is, restriction (including a lack of unity of invention) would not be proper) and all claims could have been finally rejected on the grounds and art of record in the next Office action if they had been entered in the application prior to entry under 37 CFR 1.114. Accordingly, THIS ACTION IS MADE FINAL even though it is a first action after the filing of a request for continued examination and the submission under 37 CFR 1.114. See MPEP § 706.07(b). 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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/SARAH A ALSOMAIRY/Examiner, Art Unit 1646
/Zachariah Lucas/Supervisory Patent Examiner, Art Unit 1600