DETAILED ACTION
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Applicant’s arguments filed on May 11, 2026 have been receive and entered. Claims 2-5, 7-10, 12, 14-24 26-30, 32-33 have been canceled. Claims 1, 6, 11, 13, 25, 31, 34-41 and 42 are pending in the instant application.
Election/Restrictions
Applicant’s election without traverse of claims 1-13 (group I) in the reply filed on March 4, 2020 was acknowledged. Applicant’s election without traverse of species C1E1, AAVrh10 and constitutively active promoter for species of nucleic acid, vector and promoter respectively is acknowledged. However, upon further consideration, election of species requirements was withdrawn and all the non-elected species of nucleic acid, vectors and promoter were rejoined with the elected species.
Claims 1, 6, 11, 13, 25, 31, 34-41 and 42 are under consideration.
Priority
This application is a divisional of US application no 15/167,729 05/27/2016, now US patent no 10214731, which claims priority from US provisional application 62/324,183 filed on 04/18/2016 that claims priority from US provisional application no 62/167,603 filed on 05/28/2015.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 11/13/2025 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement has been considered by the examiner.
Interview Summary
Applicant’s representative contacted the office on May 8, 2026 to discuss rejection of record. Applicant’s representative argued that functional requirement is not required in the claim. Examiner in part agreed but pointed out the breadth of the claims are directed to a rAAV intended to treat deficiency in plasma C1 estrase inhibitor in mammal. It was Examiner’s position that instant specification and declaration of record both assert clinically relevant levels of C1EI continued through at least 24 weeks. However, claims as such do not require persistent expression of human C1E1 in mammal with minimal side effect that was deemed unexpected. Examiner further pointed out the teaching of Adhi, Hu, Sondhi/ Ballantyne in view of MPEP716.02 (c). Applicant will consider amending the claims and/or rebut the rejection of record. No agreement was reached.
Maintained- 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.
Claims 1, 6, 13, 25, 32, are rejected under 35 U.S.C. 103 as being unpatentable over Adhi et al (Investigative Ophthalmology & Visual Science, 2012, ARVO annual meeting abstract. 53; 1888, art of record), Hu et al (J Gene Med. 2010, 12(9): 766–778, IDS) and Sondhi (Human Gene therapy methods, 2012, 23, 324-335)/ Ballantyne et al (PLoS One, 2015, 1-20, art of record).
Claims are directed to a recombinant adeno-associated virus (AAV) vector, comprising a chicken beta-actin promoter operably linked to a nucleic acid sequence which encodes human C1 esterase inhibitor (C1EI) and a rabbit beta globin polyadenylation signal, wherein the vector is an AAVrh.10 or AAV9 vector.
Claim interpretation: Instant rejection is applied to address both vector alternatives recited in the claim with intended use of expressing hC1E1 in treating a disorder.
With respect to claim 1, Adhi et al teach an adeno-associated virus serotype 8 (AAV8) vector comprising a nucleic acid encoding human c-esterase inhibitor, wherein intravitreal injection result in sustained expression of hC1E1 (se abstract). The vector disclosed in Adhi is capable of producing hC1E1 because results show significant reduction in the leakage (see abstract) suggesting alleviating the deficiency of C1E1 that causes vascular leakage.
Adhi differs from claimed invention by not disclosing (i) use of chicken beta active promoter operably linked to a nucleic acid sequence which encodes human C1 esterase inhibitor and a rabbit beta globin poly A sequence and (ii) use of another adeno-associated virus such as rh10 or AAV9.
However, use of constitutively active promoter with different AAV serotype to express gene of interest was routine in art before the effective filing date of the instant invention., Hu et al teach comparing recombinant AAV vectors expressing firefly luciferase driven by the cytomegalovirus-enhanced chicken β-actin promoter (AAV.CB.LUC) and a poly A signal that were packaged with viral capsids AAV 8, 9, and rh10 (see page 2, under material and method, para. 3). Regarding claims 13, Hu et al teach a composition comprising the AAV8, 9 and rh10 vector in a pharmaceutical acceptable carrier (phosphate buffered saline) (see 768, col. 1, para. 1). It is disclosed that AAV rh10 injected intravenously (see page 768, col. 1, para. 2) to the subject provided the greatest level of expression followed by AAV9 and AAV8 as compared to all other serotypes (see page 770, last para. page 771, col. 1, past para.).
The combination of references differs from claimed invention by not disclosing use of modular elements (CB promoter and poly A signal comprises a rabbit beta globulin poly A.
Sondhi et al provided the motivation to use AAVrh.10, an AAV isolated from rhesus monkeys, with the added advantage that it is nonhuman in origin, allowing it to bypass the anti-human AAV immunity that is common in the population (se page 325). Sondhi teaches AAVrh10 comprising an expression cassette consist of chicken beta actin promoter, gene of interest and a rabbit beta globin polyA (see page 325, col. 1, para. 3) has a good safety profile. Likewise, Ballantyne teach generating AAVrh10 comprising chicken beta actin promoter operably linked to a coding sequence of gene of interest and rabbit-beta globin poly A to express higher level of gene of interest as compared to AAV8 (see page 5, para. 4, fig. 7).
Therefore, it would have been prima facie obvious for a person of ordinary skill in the art to combine the teachings of prior art to modify the AAV8 vector comprising a nucleic acid sequence which encodes human C1 esterase inhibitor (C1EI) as disclosed in Adhi to select rAAV vector from serotype, rh10 or AAV 9 with modulator elements (promoter and polyA) as suggested in Hu in view of Sondh/ Ballantyne, in order to improve sustained expression of transgene in humans, as instantly claimed, with a reasonable expectation of success, before the effective filing date of the instant invention. Said modification amounting to combining prior art elements according to known methods to yield predictable results. One of ordinary skill in the art would be motivated to use chicken beta actin promoter with rh.10 or AAV9 vector because this combination explicitly reported (i) the higher levels of transgene expression as compared to the commonly used other AAV capsid including AAV8 and (ii) the use of non-human primate (rhesus macaque)-derived AAV gene transfer vector such as rh.10 in humans would reduce pre-existing anti-vector immunity and (iii) combination of modular elements (CAG promoter and rabbit beta globin polyA) are reported to work well with AAVrh.10 (supra). One of skill in the art would have been expected to have a reasonable expectation of success because (i) all the recited elements were known in the art, and hence "the combination of familiar elements according to known methods is likely to be obvious when it does no more than yield predictable results as evident from the teaching of Adhi and (ii) prior art had successfully reported AAV rh10 or AAV9 provided the greatest level of expression as compared to AAV8 and all other serotypes following intravenous injection (see page 776, col. 1, para. , last para.).
Claims 1, 11, 13, 25, 31, 34-41 and 42 are rejected under 35 U.S.C. 103 as being unpatentable over Adhi et al (Investigative Ophthalmology & Visual Science, 2012, ARVO annual meeting abstract. 53; 1888), Hu et al (J Gene Med. 2010, 12(9): 766–778), Sondhi (Human Gene therapy methods, 2012, 23, 324-335)/ Ballantyne et al (PLoS One, 2015, 1-20) and further in view of Roeth et al (WO/2012/122025, dated 09/13/2012).
The teaching of Adhi, Hu, Sodhi et/ Ballantyne have been described above and relied in same manner here. The combination of reference differs from claimed invention by not disclosing (i) C1E1 encodes a polypeptide comprising SEQ ID NO: 1 or C1E1 comprises a codon optimized sequence.
Roeth cure the deficiency by disclosing vector encodes proteins comprising the amino acid sequence as set forth in SEQ ID NO: 10 (human Cl esterase inhibitor) that has 100% sequence homology with SEQ ID NO 1).
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Regarding Claim 13, 32, 37-42, Roeth et al teach comprising pharmaceutically acceptable carrier and a vector containing human C1E1. (see para. 416, 417, 439). It is further disclosed that vector comprising a polynucleotide sequence encoding a human Cl esterase inhibitor (see para. 391-392, 468) to treat to treat angioedema, wherein said vector is an AAV vector (see para. 171-172, 475-478). Regarding claims 34-36, Roeth teaches contemplated using codon optimized coding sequence for expression in human (see para. 329, 331-337).
Therefore, it would have been prima facie obvious for a person of ordinary skill in the art to combine the teachings of prior art to substitute coding sequence of hC1esterase inhibitor disclosed in Adhi, Hu and Sodhi with one gene encoding hC1E1 protein or codon optimized hC1E1 sequence as disclosed in Roeth, as instantly claimed, with a reasonable expectation of success, before the effective filing date of the instant invention. Said modification amounting to combining prior art elements according to known methods to yield predictable results. One of ordinary skill in the art would be motivated to use codon optimized the coding sequence encoding the hC1E1 protein for optimal use in in human as suggested in Roeth. One of skill in the art would have been expected to have a reasonable expectation of success because hC1E1 sequence was known in art and hence "the combination of familiar elements according to known methods is likely to be obvious when it does no more than yield predictable results as evident from the teaching of Adhi and (ii) prior art had successfully reported AAV rh10 provided the greatest level of expression followed by AAV9 as compared to all other serotypes including AAV8 following intravenous injection (see page 776, col. 1, para. , last para.). It should be noted that the KSR case forecloses the argument that a specific teaching, suggestion, or motivation is required to support a finding of obviousness See the recent Board decision Ex parte Smith , --USPQ2d--, slip op. at 20, (Bd. Pat. App. & Interf. June 25, 2007) (citing KSR , 82 USPQ2d at 1396) (available at http: www.uspto.gov/web/offices/dcom/bpai/prec/fd071925.pdf).
Claims 1, 6, 11, 13, 34 and 36 , 37, 39-42, are rejected under 35 U.S.C. 103 as being unpatentable over Sondhi (Human Gene therapy methods, 2012, 23, 324-335)/ Ballantyne et al (PLoS One, 2015, 1-20), Adhi et al (Investigative Ophthalmology & Visual Science, 2012, ARVO annual meeting abstract. 53; 1888), Hu (J Gene Med. 2010, 12(9): 766–778) and Roeth et al (WO/2012/122025, dated 09/13/2012).
Instant rejection is applied to the extent, claim reads on AAVrh10.
With respect to claim 1, 6., Sondhi teaches a recombinant AAVrh10 comprising an expression cassette comprising a chicken beta actin promoter, gene of interest and a rabbit beta globin polyA (see page 325, col. 1, para. 3). Likewise, Ballantyne teach generating AAVrh10 comprising chicken beta actin promoter operably linked to a coding sequence of gene of interest and rabbit-beta globin poly A to express higher level of gene of interest as compared to AAV8 (see page 5, para. 4, fig. 7). Sondhi et al provided the motivation to use AAVrh.10, an AAV isolated from rhesus monkeys, with the added advantage that it is nonhuman in origin, allowing it to bypass the anti-human AAV immunity that is common in the population (se page 325). Sondhi differs from claimed invention by not disclosing ) C1E1 encodes a polypeptide comprising SEQ ID NO: 1 or C1E1 comprises a codon optimized sequence.
Adhi et al teach an adeno-associated virus serotype 8 (AAV8) vector comprising a nucleic acid encoding human c-esterase inhibitor, wherein intravitreal injection result in sustained expression of hC1E1 (se abstract). The vector disclosed in Adhi is capable of producing hC1E1 because results show significant reduction in the leakage (see abstract) suggesting alleviating the deficiency of C1E1 that causes vascular leakage. The combination of references differs invention by not disclosing ) C1E1 encodes a polypeptide comprising SEQ ID NO: 1 or C1E1 comprises a codon optimized sequence. Hu teaches a composition comprising the AAV8, 9 and rh10 vector in a pharmaceutical acceptable carrier (phosphate buffered saline) (see 768, col. 1, para. 1). It is disclosed that AAV rh10 injected intravenously (see page 768, col. 1, para. 2) to the subject provided the greatest level of expression as compared to all other serotypes including AAV8 (see page 770, last para. page 771, col. 1, past para.). The combination of references differs from claimed invention by not disclosing (i) C1E1 encodes a polypeptide comprising SEQ ID NO: 1 or C1E1 comprises a codon optimized sequence.
Roeth cure the deficiency by disclosing a composition comprising a vector encodes proteins comprising the amino acid sequence as set forth in SEQ ID NO: 10 (human Cl esterase inhibitor) that has 100% sequence homology with SEQ ID NO 1) (limitation of claim 11, 40).
Regarding Claim 13, Roeth et al teach comprising pharmaceutically acceptable carrier and a vector containing human C1E1 (see para. 416, 417, 439). It is further disclosed that vector comprising a polynucleotide sequence encoding a human Cl esterase inhibitor (see para. 391-392, 468) to treat to treat angioedema, wherein said vector is an AAV vector (see para. 171-172, 475-478). Regarding claims 34, 36, 41, Roeth teaches contemplated using codon optimized coding sequence for expression in human (see para. 329, 331-337).
Therefore, it would have been prima facie obvious for a person of ordinary skill in the art to combine the teachings of Sondhi/ Ballantyne by substituting the coding sequence of gene of interest with gene encoding hC1E1 protein or codon optimized hC1E1 sequence as disclosed in Adhi or Roeth, as instantly claimed, with a reasonable expectation of success, before the effective filing date of the instant invention. Said modification amounting to combining prior art elements according to known methods to yield predictable results. One of ordinary skill in the art would be motivated to incorporate the coding sequence of hC1E1 in rAAVrh10 because prior art explicitly reported AAVrh10 provided the higher level of expression as compared to all other AAV serotype including AAV8 following intravenous injection. One of skill in the art would have been expected to have a reasonable expectation of success because hC1E1 sequence was known in art and hence (i) "the combination of familiar elements according to known methods is likely to be obvious when it does no more than yield predictable results as evident from the teaching of Sondhi/ Ballantyne and (ii) prior art had successfully reported use of AAV rh10 achieve greatest level of expression compared to all other serotypes including AAV8 following intravenous injection (see page 776, col. 1, para. , last para. Hu.). It should be noted that the KSR case forecloses the argument that a specific teaching, suggestion, or motivation is required to support a finding of obviousness See the recent Board decision Ex parte Smith , --USPQ2d--, slip op. at 20, (Bd. Pat. App. & Interf. June 25, 2007) (citing KSR , 82 USPQ2d at 1396) (available at http: www.uspto.gov/web/offices/dcom/bpai/prec/fd071925.pdf).
Claims 1, 6, 11, 13, 25, 31-32, 35, 37, 38, 40-41 and 42 are rejected under 35 U.S.C. 103 as being unpatentable over Bosch et al (WO2015/173308, dated 11/19/2015, FD05/13/2015), Adhi et al (Investigative Ophthalmology & Visual Science, 2012, ARVO annual meeting abstract. 53; 1888), Roeth et al (WO/2012/122025, dated 09/13/2012) and Hu (J Gene Med. 2010, 12(9): 766–778).
Instant rejection is applied to the extent, claim reads on only AAV9.
With respect to claim 1, 6., Bosch teaches a recombinant AAV9 vector comprising an expression cassette comprising a CAG promoter comprising chicken beta actin, gene of interest (Naglu) and a rabbit beta globin polyA (see page 3, lines 21-25, example 2). Bosch further teaches using an optimized version of the coding sequence to produce protein in human subject (see example 3). Bosch further teaches a pharmaceutical composition comprising the recombinant AA V9 vectors in a pharmaceutically acceptable carrier (see page 26, lines 6-7).
Bosch differs from claimed invention by not disclosing C1E1 encodes a polypeptide comprising SEQ ID NO: 1 or C1E1 comprises a codon optimized sequence.
Adhi et al teach an adeno-associated virus serotype 8 (AAV8) vector comprising a nucleic acid encoding human c-esterase inhibitor, wherein intravitreal injection result in sustained expression of hC1E1 (se abstract). The vector disclosed in Adhi is capable of producing hC1E1 because results show significant reduction in the leakage (see abstract) suggesting alleviating the deficiency of C1E1 that causes vascular leakage. The combination of references differs invention by not disclosing ) C1E1 encodes a polypeptide comprising SEQ ID NO: 1 or C1E1 comprises a codon optimized sequence.
Roeth cure the deficiency by disclosing vector encodes proteins comprising the amino acid sequence as set forth in SEQ ID NO: 10 (human Cl esterase inhibitor) that has 100% sequence homology with SEQ ID NO 1) (limitation of claim 11, 31).
Regarding Claim 13, 32, Roeth et al teach comprising pharmaceutically acceptable carrier and a vector containing human C1E1. (see para. 416, 417, 439). It is further disclosed that vector comprising a polynucleotide sequence encoding a human Cl esterase inhibitor (see para. 391-392, 468) to treat to treat angioedema, wherein said vector is an AAV vector (see para. 171-172, 475-478). Regarding claims 34, 35, Roeth teaches contemplated using codon optimized coding sequence for expression in human (see para. 329, 331-337).
Therefore, it would have been prima facie obvious for a person of ordinary skill in the art to combine the teachings of Bosch by substituting the coding sequence of gene of interest with gene encoding hC1E1 protein or codon optimized hC1E1 sequence as disclosed in Adhi or Roeth, as instantly claimed, with a reasonable expectation of success, before the effective filing date of the instant invention. Said modification amounting to combining prior art elements according to known methods to yield predictable results. One of ordinary skill in the art would be motivated to use coding sequence encoding the hC1E1 protein in an AAV9 vector because prior art explicitly reported AAV9 provided the higher level of expression as compared to AAV8 following intravenous injection. One of skill in the art would have been expected to have a reasonable expectation of success because hC1E1 sequence was known in art and hence (i) "the combination of familiar elements according to known methods is likely to be obvious when it does no more than yield predictable results as evident from the teaching of Bosch and (ii) prior art had successfully reported use of AAV9 to provide higher level of expression as compared to AAV8 (see page 776, col. 1, para. , last para. of Hu.). It should be noted that the KSR case forecloses the argument that a specific teaching, suggestion, or motivation is required to support a finding of obviousness See the recent Board decision Ex parte Smith , --USPQ2d--, slip op. at 20, (Bd. Pat. App. & Interf. June 25, 2007) (citing KSR , 82 USPQ2d at 1396) (available at http: www.uspto.gov/web/offices/dcom/bpai/prec/fd071925.pdf).
Response to arguments
Applicants disagree with the rejection arguing that claim 36 differs from the Office's proposed allowable claim primarily by omitting the proposed functional elements of the claimed vector. These functional elements result from the administration of the vector having the claimed elements, and are therefore inherent to the claimed composition itself. Applicant in part emphasizes that these are capabilities inherent in the claimed vector and do not need to be recited in the claims. Applicant assert that this effect is a consequence of administering a vector having the elements recited in the claims and is, therefore, a capability inherent to the composition as presently claimed. A positive correlation between dose and expression level is a hallmark of a functional gene therapy vector, demonstrating both that the expression is attributed to the expression of the vector and that increasing levels of gene product can be achieved by increasing dose. The fact that the vector can be administered at subclinical levels does not detract from the surprising or unexpected result that the vector itself is capable of long-term expression at clinically relevant levels. Thus, nothing in the submitted data or other parts of the disclosure suggests that dose is an essential feature or otherwise required to make the claims commensurate in scope with the evidence of surprising or unexpected results. Applicants’ arguments have been fully considered, but are not found persuasive.
In response, it is noted that independent claims simply recite the structure of AAV vector. As discussed in previous office action (see final office action of 04/10/2025, pages 9 and 10), Adhi teaches a rAAV of serotype 8 vector comprising a nucleic acid encoding human C1 esterase inhibitor (a complement and kallikrein -kinin system inhibitor). The results in Adhi teaches hC1E1 could be expressed to reduce leakage and therefore capable of producing hC1E1 protein. The teaching of Adhi is limited to only one serotype of AAV8. A variety of constitutively active promoter linking transgene and use of rabbit beta globin polyA for the purpose of increasing expression are well-known in the art. Further, before the effective filing date of instant application art provided explicit motivation to use rh10, AAV9 or AAV8 by comparing the recombinant AAV vectors expressing gene of interest (firefly luciferase) driven by the CAG promoter to show AAV rh10, AAV9 followed by AAV8 provide the greater level of expression as compared to all other serotypes following intravenous injection of the vectors. In view of foregoing, it is apparent that the prior art taught that applicant's preferred AAVrh10, CAG promoter is very efficient, function well and provides better results compared with other prior art AAV serotype like AAV9 or AAV8, and there would have been a reasonable expectation of success to achieve superior expression as compared to all other serotype including AAV8.
Examiner has provided evidence showing the each of the modular elements (promoter and polyA sequences) were known in prior art to function in obvious manner in enhancing gene expression of while designing/ modifying the rAAVrh10 or rAAV9 vector as compared to rAAV8 as evident form the teaching of Hu, Sodhi (1), Sondhi/Ballantyne. Applicant should note that any differences between the claimed invention and the prior art may be expected to result in some differences in properties. The issue is whether the properties differ to such an extent that the difference is really unexpected. In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
It is well documented and made of record that AAV rh10 injected intravenously (see page 768, col. 1, para. 2. Hu) to the subject provided the greatest level of expression followed by AAV9 and AAV8 as compared to all other serotypes (see page 770, last para. page 771, col. 1, past para.). This is further evident from Sodhi et al who reported highest levels of expression of a secreted marker protein with AAVrh.10 (see page 481, col. 2, para. 2 and reference therein). It is further disclosed that AAVrh.10 vector comprising gene of interest under the control of CAG promoter (see page 489, col. 1, para.2) gave the highest levels of transgene expression as compared to the commonly used AAV 2, 5 and 8 capsid (see page 481, col. 2, last para.).
Thus, the relevance of Applicants' arguments with respect to use of rAAV9 or AAVrh10 vector for higher expression is not apparent (emphasis added). Further, beneficial use of AAVrh10 or AAV9 over AAV8 are described in prior art of record (Hu and Sondhi see above). Such methodology for using different vector with modulator element was considered routine in the prior art for optimal level of gene expression.
Therefore, the fact that AAVrh10 or AAV9 may be used over AAV8 for higher gene expression is an expected result, and is the goal behind using AAV9 or AAVrh10 vector. As indicated in MPEP 716.02(c), Where the unexpected properties of a claimed invention are not shown to have a significance equal to or greater than the expected properties, the evidence of unexpected properties may not be sufficient to rebut the evidence of obviousness. In re Nolan, 553 F.2d 1261, 1267, 193 USPQ 641, 645 (CCPA 1977). "Expected beneficial results are evidence of obviousness of a claimed invention, just as unexpected results are evidence of unobviousness thereof." In re Gershon, 372 F.2d 535, 538, 152 USPQ 602, 604 (CCPA 1967). Ex parte Blanc, 13 USPQ2d 1383 (Bd. Pat. App. & Inter. 1989) (Claims at issue were directed to a process of sterilizing a polyolefinic composition which contains an antioxidant with high-energy radiation. Although evidence was presented in appellant’s specification showing that particular antioxidants are effective, the Board concluded that these beneficial results would have been expected because one of the references taught a claimed antioxidant is very efficient and provides better results compared with other prior art antioxidants.).
In view of foregoing, it is apparent that use of AAVrh10 or AAV9 showing higher expression would be an expected benefit of using such vector(s) was already known in prior art as discussed above. Applicant has neither provided evidence nor argument to show how expected benefits known in prior art is different from the benefit of higher expression observed in the instant application. It is re-emphasized that should applicant amend the base claim to recite a feature that distinguishes the claimed vector/composition from the expected benefit of prior art vector/composition, instant obviousness may be overcome, pending further consideration.
Therefore, in view of the fact patterns of the instant case, and the ground of rejection outlined by the examiner, applicants’ arguments are not compelling and do not overcome the rejection of record.
Conclusion
No claims allowed.
Niwa et al. (Gene, 108: 193-199, 1991) reported testing efficiency of different promoter elements for the construction of expression vector that enhances the level of expression of the linked exogenous gene. The results show CAG promoter showed highest activity as compared to CMV and RSV (see table 1). Shin et al (Methods Mol Biol. 2012; 798: 267–284) teaches generic AAV production and purification protocol. Guo teaches higher A1AT transgene expression using AAV8 as compared to other AAV serotypes.
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. Any inquiry concerning this communication or earlier communications from the examiner should be directed to ANOOP K. SINGH whose telephone number is (571)272-3306. The examiner can normally be reached Monday-Friday, 8AM-5PM. 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, Peter Paras can be reached on (571)272-4517. 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.
/ANOOP K SINGH/Primary Examiner, Art Unit 1632
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