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 .
Claim Status
Claims 1-6, 8-10, 14-23 are canceled. Claims 7, 12 and 24 are amended.
Claims 7, 11-13, and 24-25 are being examined on the merits in this office action.
Claim Objections and Rejections- Withdrawn
The objection of claim 11 is withdrawn in view of the claim amendment.
The rejection of claim 12 under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, is withdrawn in view of the claim amendment.
Claim Rejections - 35 USC § 112 – New Necessitated by Amendment
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.
Claims 7, 11-13, and 24-25 are 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.
Regarding claim 7, the phrase "such as" renders the claim indefinite because it is unclear whether the limitations following the phrase are part of the claimed invention. See MPEP § 2173.05(d). Claims 11-13, and 24-25 depend on an indefinite claim and are similarly rejected.
Response to Amendment
The Declaration under 37 CFR 1.132 filed 01/15/2026 is insufficient to overcome the rejection of claims 7, 11-13, and 24-25 based upon 35 U.S.C. 103 as set forth in the last Office action because the invention is rendered obvious by the cited references.
Applicant Arguments
Applicant argues that claim 7 requires a method in which administration of specific AVP fragments, NC1900, AVP metabolites, or VlaR agonists increases AQP4 expression in astrocytic endfeet and thereby enhances glymphatic clearance of brain waste (Declaration Page 2).
Applicant further argues unexpected results and that Alzheimer's patients exhibited an average 36.37% reduction in CB values after two weeks of treatment, which was statistically significant, that this rapid and substantial reduction was unexpected and not suggested by the prior art and that the results are consistent with enhanced glymphatic clearance mediated by increased AQP4 expression (Declaration Page 2-3).
Applicant argues that neither Koupilova, Pietrowsky, nor Szczgielski, alone or in any combination, teaches or suggests that arginine vasopressin (AVP) fragments or vasopressin la receptor (VlaR) agonists would increase aquaporin-4 (AQP4) expression in astrocytic endfeet so as to enhance glymphatic clearance. Applicant argues that a person of ordinary skill in the art would not have had a reasonable expectation of success in achieving enhanced glymphatic clearance through administration of AVP fragments or VlaR agonists. Applicant argues that the skilled person would have been dissuaded from intentionally activating VlaR signaling or increasing AQP4 expression, and would not reasonably have expected that A VP fragment administration, particularly via intranasal delivery, could safely and selectively enhance glymphatic clearance without inducing pathological edema or other adverse effects and that the combination of Koupilova, Pietrowsky, and Szczgielski relies on impermissible hindsight. Applicant argues that the references address different scientific questions, operate at different biological levels, and point in divergent therapeutic directions-namely behavioral cognition, peptide delivery routes, and pathological versus homeostatic roles of AQP4 (Page 3-4 of Declaration).
Examiner’s Response
The arguments presented above have been fully considered but are unpersuasive. Examiner notes that administering AVP fragments such as the instant fragment AVP(4-9) to treat cognitive impairment conditions such as dementia is known in the art as taught by Koupilova. Koupilova teaches that the method reversed memory impairment (Abstract) and that the peptides facilitated memory retrieval processes (Page 34, line 6-7). Koupilova does not teach administering the peptide intranasally. However, administering the instant peptide intranasally is known in the art as taught by Pietrowsky and the reference teaches the motivation to administer the peptides intranasally. Pietrowsky teaches that intranasal (IN) administration of 20 IU arginine-AVP and that the passage from nose to brain appears to offer a chance to directly influence CNS functioning in humans by peptide molecules, also for therapeutic purposes (Page 339, right col. Last paragraph). Thus, one of ordinary skill in the art is motivated to administer the instant peptides intranasally, to subjects with Dementia. Examiner notes that that limitation of enhancing the function of the glymphatic system, augmenting clearance and increasing AQP4 expression are all expected results of administering the instant peptide, in the instant method of administration (intranasally e.t.c.) to the instant patient population (i.e. subjects with dementia). Examiner notes that even if the limitation was not an expected result, it is known in the art (as taught by Szczgielski ), that vasopressin activates aquaporin-4 (AQP4) and impact the density and function of AQP4 (Page 6, right col., 2nd paragraph, line 18-24) and aquaporin-4 (AQP4) plays the central role in cerebral fluid homeostasis, acting as a water channel protein and that AQP4 not only enables water permeability through the blood-brain barrier but also regulates water exchange between perivascular spaces and the rest of the glymphatic system, described as pan-cerebral fluid pathway interlacing macroscopic cerebrospinal fluid (CSF) spaces with the interstitial fluid of brain tissue (Abstract). Szczgielski teaches that AQP4 is a regulator of the glymphatic flow (Title page 6). Szczgielski further teaches that the main physiological functions of AQP4 a direct impact on the clearance of water and cellular metabolites, altering extracellular fluid dynamics, and (most probably indirect and less precisely described) regulation of neuronal and synaptic activity including plasticity (thus impacting memory and behavior) (Page 5, right col. 1st paragraph). Examiner notes that all the cited references teach vasopressin and analogs and hail from the same field of study and further, Pietrowsky teach other modes of administration of the instant peptides such as intranasal administration to circumvent the blood-brain barrier and the primary references teaches the instant peptide administration to the instant patient population. Examiner notes that Applicants’ assertion that the three cited references come from divergent fields and do not constitute analogous art is unpersuasive. Thus, in response to applicant's argument that the cited references is nonanalogous art, it has been held that a prior art reference must either be in the field of the inventor’s endeavor or, if not, then be reasonably pertinent to the particular problem with which the inventor was concerned, in order to be relied upon as a basis for rejection of the claimed invention. See In re Oetiker, 977 F.2d 1443, 24 USPQ2d 1443 (Fed. Cir. 1992). This argument is unpersuasive.
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). Examiner notes that the instant invention requires that the instant peptides are administered to the patient population (i.e. subjects with Dementia). These limitations are taught by both Koupilova and Pietrowsky. Examiner insists the limitations of enhancing the glymphatic system and augmenting brain clearance constitute expected results of the method steps. MPEP 2111.04 states: claim scope is not limited by claim language that suggests or makes optional but does not require steps to be performed, or by claim language that does not limit a claim to a particular structure. In the instant case, the limitation expresses the intended result of the method step of claim 7 and is given little patentable weight.
Further, it is known in the art as taught by Imamura (JP2022104448A – reference cited to rebut Applicants arguments) that the instant vasopressin peptides (AVP (4-8), AVP (4-9), AVP (5-8), AVP (5-9) and NC1900) induce AQP4 expression via V1aR, thereby inducing GLS activation, facilitating water flow in the brain, and further, extracellular voids in brain tissue. In combination with the expansion of the brain, the excretion and purification of waste products in the brain can be achieved [0019-0020]. Thus Applicant assertion that the instant peptides do not promote AQP4 expression, which in turn enhances the function of the glymphatic pathway and that the mechanistic chain, i.e., VlaR agonism [Wingdings font/0xE0]AQP4 induction[Wingdings font/0xE0] enhanced glymphatic function[Wingdings font/0xE0]improved clearance of causative brain waste, is unpersuasive. Examiner notes that when the cited references are combined, the instant invention is rendered obvious.
Regarding Applicants arguments of unexpected results, Examiner acknowledges the data of the experimental study. Examiner further notes that the instant invention contains no data showing the effect of the recited peptides. However, Examiner notes that the administration of the instant peptide intranasally to the instant patient population is known in the art as taught by the cited references and Koupilova teaches that the method reversed memory impairment (Abstract) and that the peptides facilitated memory retrieval processes (Page 34, line 6-7). Further, Imamura teaches intranasal administration of the instant vasopressin peptides (AVP (4-8), AVP (4-9), AVP (5-8), AVP (5-9) and NC1900) to dementia patients and that the peptides prevent the accumulation of waste products (for example, amyloid including Aβ, tau protein, α-synuclein, TCD-43, etc.) in the brain [0019]. Further, Tanaka et al. (reference cited to rebut Applicants arguments – Europ. J. of Pharm. 352 (1998):135–142) teaches that NC-1900 improve β-amyloid protein-induced learning and memory deficits and protects against the β-amyloid protein-induced toxicity (Page 141, left col. Last paragraph). Given what was already known before the effective filing date of the claimed invention, Examiner notes that the results argued by Applicant were indeed expected and known in the art. This argument is unpersuasive.
Claim Rejections - 35 USC § 103 - Maintained
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.
Claims 7, 11-13, and 24-25 remain rejected under 35 U.S.C. 103 as being unpatentable over Koupilova et al. (Collection Symposium Series 1999, 3, 34-36 – cited and enclosed in the previous office action) in view of Pietrowsky et al. (Biol. Psychiatry 1996; 39: 332-340– cited and enclosed in the previous office action) and Szczgielski et al. (Front Neurol. 2021; 12: 767470– cited and enclosed in the previous office action).
Koupilova teaches the effect of six analogs of AVP fragment 4-9 on cognitive impairment and that a single administration of the peptides reversed impairment of the retention of memory and that the results suggest that the peptides tested have therapeutic potential for the treatment of dementia caused by cholinergic dysfunction (Abstract). Therefore, Koupilova teaches vasopressin analogs (AVP fragments) to treat cognitive impairment such as dementia. Koupilova teaches that the method reversed memory impairment (Abstract) and that the peptides facilitated memory retrieval processes (Page 34, line 6-7).
Koupilova does not teach that the AVP is administered intranasally or the other routes recited and does not teach the method of enhancing function of glymphatic system and clearance of brain wastes.
However, one of ordinary skill who has read Pietrowsky et al. would be motivated to administer AVP intranasally. Specifically, Pietrowsky teaches that intranasal application of peptides is a way to circumvent the blood-brain barrier (Abstract). Pietrowsky teaches that intranasal (IN) administration of 20 IU arginine-AVP markedly increased the amplitude of the P3 component of the ERP recorded during the subject's performance on an oddball task (Discussion section, Page 337, left col.). Pietrowsky further teaches that P3 is viewed as a manifestation of context updating in immediate memory, modified by the attention allocation requirements of the task, the P3 enhancement after intranasal vasopressin could well reflect an increase in attentional abilities (Discussion section, Page 337, right col.). Pietrowsky concludes that the passage from nose to brain appears to offer a chance to directly influence CNS functioning in humans by peptide molecules, also for therapeutic purposes (Page 339, right col. Last paragraph).
With regards to “enhancing the function of the glymphatic system and subsequently augmenting brain waste clearance”, Szczgielski teaches that vasopressin activates aquaporin-4 (AQP4) and impact the density and function of AQP4 (Page 6, right col., 2nd paragraph, line 18-24). Szczgielski teaches that aquaporin-4 (AQP4) plays the central role in cerebral fluid homeostasis, acting as a water channel protein and that AQP4 not only enables water permeability through the blood-brain barrier but also regulates water exchange between perivascular spaces and the rest of the glymphatic system, described as pan-cerebral fluid pathway interlacing macroscopic cerebrospinal fluid (CSF) spaces with the interstitial fluid of brain tissue (Abstract). Szczgielski teaches that AQP4 is a regulator of the glymphatic flow (Title page 6). Szczgielski further teaches that the main physiological functions of AQP4 a direct impact on the clearance of water and cellular metabolites, altering extracellular fluid dynamics, and (most probably indirect and less precisely described) regulation of neuronal and synaptic activity including plasticity (thus impacting memory and behavior) (Page 5, right col. 1st paragraph). Examiner notes that Szczgielski teaches that vasopressin activates AQP4, which in turn regulates the glymphatic system, which has a direct impact on the clearance of water and cellular metabolites, altering extracellular fluid dynamics.
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to combine the teachings of Koupilova, Pietrowsky, and Szczgielski and prepare a method of enhancing glymphatic system and augment clearance or excretion of brain wastes involved in neurocognitive disorders including dementia, since Szczgielski teaches that vasopressin activates aquaporin-4 (AQP4) and impact the density and function of AQP4 (Page 6, right col., 2nd paragraph, line 18-24). Szczgielski teaches that aquaporin-4 (AQP4) is a regulator of the glymphatic system and impacts the clearance of water and cellular metabolites in brain ) (Page 5, right col. 1st paragraph). Further, it would have been obvious to administer AVP intranasally since Pietrowsky teaches the advantage of administering AVP intranasally that Pietrowsky teaches that intranasal application of peptides is a way to circumvent the blood-brain barrier (Abstract). One of ordinary skill in the art would be motivated and would have had a reasonable expectation of success in preparing such a method since vasopressin is known in the art to treat neurocognitive disorders such as dementia as taught by Koupilova, and further, vasopressin is taught to activate AQP4 which augments the glymphatic system thus aiding the clearance of brain wastes as taught by Szczgielski AQP4 (Page 6, right col., 2nd paragraph, line 18-24). One of ordinary skill who has read the cited references would indeed arrive at the instant invention rendering obvious claim 7.
Regarding claim 11, Koupilova teaches the effect of six analogs of AVP fragment 4-9 on cognitive impairment and that a single administration of the peptides reversed impairment of the retention of memory and that the results suggest that the peptides tested have therapeutic potential for the treatment of dementia caused by cholinergic dysfunction (Abstract). Koupilova reads on the claim because it teaches vasopressin analogs (AVP fragments) to treat cognitive impairment such as dementia. Koupilova teaches the effect of pyroglutamic fragments of vasopressin and oxytocin on the retention of memory (Abstract; Page 34, last 2 lines).
Regarding claim 12, Koupilova teaches vasopressin analogs (AVP fragments) to treat cognitive impairment such as dementia. Koupilova teaches that the method reversed memory impairment (Abstract) and that the peptides facilitated memory retrieval processes (Page 34, line 6-7). Further, it is known in the art that AVP has the effect of “maintaining or improving the clearance and excretion activities of brain wastes” as taught by Szczgielski.
Regarding claim 13, Pietrowsky teaches that intranasal (IN) administration of 20 IU AVP markedly increased the amplitude of the P3 component of the ERP recorded during the subject's performance on an oddball task (Discussion section, Page 337, left col.). Pietrowsky teaches a composition including saline solution (Abstract). Pietrowsky further teaches that for IN administration, AVP was dissolved in 10 µl sterile water (Page 333, Right col., “Procedure and Design” section, 2nd paragraph). Further, Koupilova teaches the effect of six analogs of AVP fragment 4-9 on cognitive impairment. It would have been obvious to modify Koupilova and administer AVP with one or more members such as saline solution.
Regarding claims 24-25, Szczgielski teaches that aquaporin-4 (AQP4) plays the central role in cerebral fluid homeostasis, acting as a water channel protein and that AQP4 not only enables water permeability through the blood-brain barrier but also regulates water exchange between perivascular spaces and the rest of the glymphatic system, described as pan-cerebral fluid pathway interlacing macroscopic cerebrospinal fluid (CSF) spaces with the interstitial fluid of brain tissue (Abstract). Szczgielski teaches that vasopressin an activation of its receptors seems to impact the density and function of AQP4 (Page 5, right col.). Szczgielski further teaches that the main physiological functions of AQP4 a direct impact on the clearance of water and cellular metabolites, altering extracellular fluid dynamics, and (most probably indirect and less precisely described) regulation of neuronal and synaptic activity including plasticity (thus impacting memory and behavior) (Page 5, right col. 1st paragraph). It would have been obvious to modify Koupilova and administer AVP to promote AQP4 expression thus enhancing the function of the glymphatic system and augmenting brain waste clearance.
Response to Arguments
Applicant's arguments filed 01/15/2026 have been fully considered but they are not persuasive.
Applicant Arguments
Applicant argues that the three cited references come from divergent fields and do not constitute analogous art. That Koupilova investigates the behavioral effects of AVP( 4-9) and related fragments in a cholinergic impairment model in rats, evaluating memory performance (see Koupilova, Abstract) but providing no discussion of astrocyte biology, AQP4, fluid transport, or brain-waste removal. Pietrowsky examines electrophysiological responses (ERP changes) following intranasal administration of native vasopressin in human subjects (see Pietrowsky, Abstract), and likewise contains no teaching related to AQP4, the glymphatic system, or mechanisms of brain-waste clearance. Szczgielski is a review discussing aquaporin physiology in the context of brain water balance, trauma, and edema; while it notes that vasopressin "seems to impact" AQP4, it does not disclose any upregulation of AQP4 expression by vasopressin fragments.
Applicant argues that the cited art does not contain the mechanistic sequence required by amended claim 7. The present specification explains that the AVP fragments recited in claim 7 (including AVP(4-8), AVP(4-9), AVP(5-8), AVP(5-9), and NC1900) act as VlaR agonists and promote AQP4 expression, which in turn enhances the function of the glymphatic pathway and that the mechanistic chain, i.e., VlaR agonism [Wingdings font/0xE0]AQP4 induction[Wingdings font/0xE0] enhanced glymphatic function[Wingdings font/0xE0]improved clearance of causative brain waste, is described in the specification but is wholly absent from the cited prior art.
Applicant argues that none of the cited references demonstrates that AVP fragments increase AQP4 expression, nor that such an increase leads to improved glymphatic clearance and that inherency requires that the missing limitation be necessarily and inevitably present in the prior art, not merely possible or implied.
Applicant argues that the cited prior art provides no motivation to pursue the claimed therapeutic strategy. The references do not recognize impaired glymphatic clearance as a cause or contributor to neurocognitive disorders, nor do they suggest that enhancing AQP4 expression would be beneficial and argues hindsight reasoning. Applicant argues that the present application uniquely recognizes that VlaR agonists, including specific AVP fragments such as AVP(4-9) and NC1900, promote AQP4 expression and thereby improve glymphatic function. This mechanistic insight is absent from the cited art and is not predictable from the disparate teachings of the references.
Examiner’s Response
The arguments presented above have been fully considered but are unpersuasive. Examiner notes that administering AVP fragments such as the instant fragment AVP(4-9) to treat cognitive impairment conditions such as dementia is known in the art as taught by Koupilova. Koupilova teaches that the method reversed memory impairment (Abstract) and that the peptides facilitated memory retrieval processes (Page 34, line 6-7). Koupilova does not teach administering the peptide intranasally. However, administering the instant peptide intranasally is known in the art as taught by Pietrowsky and the reference teaches the motivation to administer the peptides intranasally. Pietrowsky teaches that intranasal (IN) administration of 20 IU arginine-AVP and that the passage from nose to brain appears to offer a chance to directly influence CNS functioning in humans by peptide molecules, also for therapeutic purposes (Page 339, right col. Last paragraph). Thus, one of ordinary skill in the art is motivated to administer the instant peptides intranasally, to subjects with Dementia. Examiner notes that that limitation of enhancing the function of the glymphatic system, augmenting clearance and increasing AQP4 expression are all expected results of administering the instant peptide, in the instant method of administration (intranasally e.t.c.) to the instant patient population (i.e. subjects with dementia). Examiner notes that even if the limitation was not an expected result, it is known in the art (as taught by Szczgielski ), that vasopressin activates aquaporin-4 (AQP4) and impact the density and function of AQP4 (Page 6, right col., 2nd paragraph, line 18-24) and aquaporin-4 (AQP4) plays the central role in cerebral fluid homeostasis, acting as a water channel protein and that AQP4 not only enables water permeability through the blood-brain barrier but also regulates water exchange between perivascular spaces and the rest of the glymphatic system, described as pan-cerebral fluid pathway interlacing macroscopic cerebrospinal fluid (CSF) spaces with the interstitial fluid of brain tissue (Abstract). Szczgielski teaches that AQP4 is a regulator of the glymphatic flow (Title page 6). Szczgielski further teaches that the main physiological functions of AQP4 a direct impact on the clearance of water and cellular metabolites, altering extracellular fluid dynamics, and (most probably indirect and less precisely described) regulation of neuronal and synaptic activity including plasticity (thus impacting memory and behavior) (Page 5, right col. 1st paragraph). Examiner notes that all the cited references teach vasopressin and analogs and hail from the same field of study and further, Pietrowsky teach other modes of administration of the instant peptides such as intranasal administration to circumvent the blood-brain barrier and the primary references teaches the instant peptide administration to the instant patient population. Examiner notes that Applicants’ assertion that the three cited references come from divergent fields and do not constitute analogous art is unpersuasive. Thus, in response to applicant's argument that the cited references is nonanalogous art, it has been held that a prior art reference must either be in the field of the inventor’s endeavor or, if not, then be reasonably pertinent to the particular problem with which the inventor was concerned, in order to be relied upon as a basis for rejection of the claimed invention. See In re Oetiker, 977 F.2d 1443, 24 USPQ2d 1443 (Fed. Cir. 1992). This argument is unpersuasive.
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). Examiner notes that the instant invention requires that the instant peptides are administered to the patient population (i.e. subjects with Dementia). These limitations are taught by both Koupilova and Pietrowsky. Examiner insists the limitations of enhancing the glymphatic system and augmenting brain clearance constitute expected results of the method steps. MPEP 2111.04 states: claim scope is not limited by claim language that suggests or makes optional but does not require steps to be performed, or by claim language that does not limit a claim to a particular structure. In the instant case, the limitation expresses the intended result of the method step of claim 7 and is given little patentable weight.
Further, it is known in the art as taught by Imamura (JP2022104448A – reference cited to rebut Applicants arguments) that the instant vasopressin peptides (AVP (4-8), AVP (4-9), AVP (5-8), AVP (5-9) and NC1900) induce AQP4 expression via V1aR, thereby inducing GLS activation, facilitating water flow in the brain, and further, extracellular voids in brain tissue. In combination with the expansion of the brain, the excretion and purification of waste products in the brain can be achieved [0019-0020]. Thus Applicant assertion that the instant peptides do not promote AQP4 expression, which in turn enhances the function of the glymphatic pathway and that the mechanistic chain, i.e., VlaR agonism [Wingdings font/0xE0]AQP4 induction[Wingdings font/0xE0] enhanced glymphatic function[Wingdings font/0xE0]improved clearance of causative brain waste, is unpersuasive. Examiner notes that when the cited references are combined, the instant invention is rendered obvious.
Conclusion
No claims are allowed.
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any 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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Mercy H. Sabila whose telephone number is (571)272-2562. The examiner can normally be reached Monday - Friday 5:00 am - 3:00 pm.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Lianko G. Garyu can be reached at (571)270-7367. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/MERCY H SABILA/Examiner, Art Unit 1654
/LIANKO G GARYU/Supervisory Patent Examiner, Art Unit 1654 N