DETAILED ACTION
Applicant’s amendment and Arguments/Remarks received on 12 June 2026 have been entered. Claims 1-20 and 28-31 were previously pending in the application. Claims 2, 3, and 29 have been cancelled by Applicant. Claims 1, 4-20, 28, and 30-31 are currently pending in the application. Claims 1, 20, and 28 are independent claims.
The election of Group II, drawn to a method for treating or alleviating a tumor in a subject, remains in effect in the instant application.
The following election of species remains in effect in the instant application:
Immunostimulatory agents: b. IL-12;
Immunotherapeutic agents: a. anti-PD-1;
Brain tumors: a. glioma.
Claims 1 and 20 remain withdrawn from consideration as being directed to a nonelected invention, there being no allowable generic or linking claim.
Claims 4-19, 28, and 30-31 are currently pending and under examination in the instant application. An action on the merits follows.
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA . The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Priority
The present application is a 35 U.S.C. 371 national stage filing of International Application No. PCT/CN2021/135336, filed 03 December 2021, which claims priority to PCT/CN2020/133943, filed 04 December 2020. Filing of a certified copy of PCT/CN2020/133943, filed 04 December 2020, is acknowledged.
Thus, the earliest possible priority for the instant application is 04 December 2020.
Claim Objections
The objection to amended, previously presented, and cancelled claims 3, 5-6, 8-19, and 28 for reciting abbreviations without first writing out the terms for which they stand is withdrawn in view of the amendment to claims.
The objection to amended claim 31 for the misspelling “glioblastoma multiform” is withdrawn in view of the amendment to claim 31 correcting the error.
Claim Rejections - 35 USC § 112(b)
The rejection of amended, previously presented, and cancelled claims 2-19 and 28-31 under 35 U.S.C. 112(b) as failing to particularly point out and distinctly claim the subject matter which the inventor(s) regards as the invention for multiple issues of indefiniteness is withdrawn over amended, previously presented, cancelled claims 2-7, 11-19, and 28-31 and maintained in part over amended and previously presented claims 8-10. Applicant's amendments to the claims and arguments have been fully considered but have not been found persuasive in overcoming the rejection for reasons of record as discussed in detail below.
Applicant amended the claims to address most of the issues of indefiniteness, but has insufficiently addressed the following issues identified in the prior action:
Claim 8 recites, “wherein the deletion of an internal inverted repeat region starts from the stop codon of the last gene in the UL component to the promoter of the first gene in the US component”, which is indefinite because it is unclear whether the stop codon and/or promoter are included in the deleted sequences.
Additionally, claims 8-10 are further indefinite by claim 8 reciting that “the deletion of an internal inverted repeat region starts from the stop codon of the last gene in the UL component to the promoter of the first gene in the US component”, claim 9 reciting that the last gene is UL56, and claim 10 reciting that the first gene is US1; such that claims 8-10 conflicts with the limitation of independent claim 28, upon which it depends (claim 8 depends on claim 6, which depends on claim 28), in that the final UL gene (e.g., UL56 gene) is in the reverse orientation relative to the direction of a prototype (P) standard gene arrangement for UL1-UL56, as diagram depicted in instant Figure 1 [as evidenced by ViralZone, 2017, retrieved on 06 March 2026 from: <web.archive.org/web/20170523041329/https://viralzone.expasy.org/5756>, archived on 23 May 2017], and is oriented such that the promoter is the closest part of the gene to the internal repeat region. Therefore, by claiming to delete from the stop codon of the UL56 gene to the promoter of the US1 gene, Applicant is claiming to delete at least the full coding sequence of the UL56 gene, thereby reciting a limitation which conflicts with the limitation of claim 28 which recites, “wherein all single-copy genes in both UL and US components of the genome are intact such that they are capable of expressing respective functional proteins.”
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Regarding issue 1), claim 8 was amended to recite, “wherein the deletion of an internal inverted repeat region starts from the end of the stop codon of the last gene in the UL component to the start of the promoter of the first gene in the US component”, which is still indefinite because it is unclear whether “from the end of the stop codon” is meant to include the nucleotide(s) of the stop codon or whether the deletion is meant to start immediately before after the stop codon. Likewise, “to the start of the promoter” is still indefinite because it is unclear whether the start of the promoter is meant to be included in the deletion or whether the deletion is meant to end immediately before or after the “start” of the promoter. As such, Applicant’s amendments do not overcome the finding of indefiniteness and the metes and bounds of the claim still cannot be determined.
Regarding issue 2), Applicant did not amend any of claims 28 or 8-10 in a way to clarify the conflict of amended and previously presented claims 8-10 with amended independent claim 28. Therefore, Applicant’s amendments do not overcome the finding of indefiniteness and the metes and bounds of the claim still cannot be determined.
Applicant argues that:
Claim 8 to 10 refers to claim 6 in which the oHSV-1 is specifically defined to have a prototype P genome. Therefore, the limitations of claims 8 to 10 should apply to prototype P only. Paragraph [0051] of the WO publication provides detailed description of the four different genome isomers, i.e., isomers P, IS, IL, and ISL, of HSV-1 virus, and each of the isomers IS, IL, and ISL has one or two components in reverse orientation compared to isomer P. Further, paragraph [0052] gives examples of how the deletion is carried out in isomers P and IL, respectively. A more detailed review of the different isomers of HSV-1 is provided in Shen et al. 2006 (Appendix I).
However, this is not agreed.
As discussed in the prior action, the prototype P orientation, which, as asserted by Applicant and taught by Shen [figure 1], comprises an orientation of UL genes from 1 to 56 such that UL56 is the closest gene to the IRL genes (depicted below as the b’a’ box):
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However, although the UL56 gene is proximal to the IRL gene cluster (b’a’ in the Shen Figure 1 diagram), UL56 itself is oriented in a reverse orientation relative to the orientation of the UL cluster, as taught by the reverse arrow in the ViralZone figure above. As such, the UL56 promoter is proximal to the IRL gene cluster and the stop codon is distal from the IRL gene cluster (proximal to the TRL as shown in the ViralZone figure above). Accordingly, a deletion starting from the end of the UL56 stop codon is starting at the end of the UL56 gene distal from the ILR gene cluster. A deletion of a region starting from the end of the UL56 gene stop codon to the start of the US1 gene promoter therefore comprises the UL56 gene promoter and coding sequence, wherein only the stop codon or a part of the stop codon remains intact. Therefore, the limitations of claims 8-10 conflict with the limitation of independent claim 28, upon which they depend, which states “wherein all single-copy genes in both unique long (UL) and unique short (US) components of the genome are intact” in lines 14-15.
As such, Applicant’s arguments do not overcome a finding of indefiniteness under 35 U.S.C. 112(b), and the rejection is maintained.
**The following new rejection is necessitated by Applicant’s amendments to the claims.
Amended and previously presented claims 4-19, 28, and 30-31 are newly 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. Claims 4-19 and 30-31 are included due to their dependence on amended independent claim 28.
Amended independent claim 28 newly recites, “wherein the oHSV-1 is absence of ICP34.5 protein expression”, which is indefinite because it is unclear how the oHSV-1 can be “absence of ICP34.5” in that the oHSV-1 is an oncolytic virus which can comprise a gene incapable of expressing the ICP34.5 protein but cannot itself be the absence of an ICP34.5 protein.
As such, the metes and bounds of the claim cannot be determined.
Claim Rejections - 35 USC § 103
The rejection of amended, previously presented, and cancelled claims 2-19 and 28-31 under 35 U.S.C. 103 as being unpatentable over Zhou [US20190083555A1, published 21 March 2019]; in view of Nakashima [US20180133269A1, published 17 May 2018]; and ViralZone [2017, retrieved on 06 March 2026 from: <web.archive.org/web/20170523041329/https://viralzone.expasy.org/5756>, archived on 23 May 2017]; is withdrawn in view of Applicant’s amendment to independent claim 28 to recite, “wherein the oHSV-1 is absence of ICP34.5 protein expression” which has been interpreted to limit the oHSV-1 such that no ICP34.5 protein is expressed from the oHSV-1 genome. This interpretation is supported by the instant specification [0136], cited by Applicant as support for the limitation, which recites, “the recombinant viruses C5252, C8282, and C1212 were confirmed by IL-12, anti-PD-1 antibody expression and absence of ICP34.5 protein expression”, such that the oHSV-1 viruses were confirmed by the absence of IPC34.5 protein expression but are not themselves the absence of IPC34.5 expression. Additionally, Applicant’s arguments support an interpretation of the newly introduced limitation as limiting the oHSV-1 such that no ICP34.5 protein is expressed from the oHSV-1 genome. Applicant argues that:
“Nakashima does not teach that a modified oHSV-1 that is absence of ICP34.5 protein expression is effective to kill brain tumor cell. It is respectfully noted that Nakashima constructed viruses rHSVQ1 and rQNestin34v.2, the former being a virus with both y34.5 gene deleted, while the latter being constructed based on rHSVQ1 with a y34.5 gene expression cassette incorporated into the ICP6 locus (see Figure 1 and para. [0017]). The data in Nakashima shows that rHSVQ1 is not at all effective in killing glioma cells and its effect is not significant than PBS, while the insertion of the y34.5 gene expression cassette (rQNestin34v.2) result in robust tumor killing effect (see Figures 7A and 7B, para. [0151]). These results clearly demonstrated that ICP34.5 protein is essential for glioma tumor killing. Therefore, Nakashima teaches away from modification of the other copy of y34.5 gene. To distinguish the claimed invention more specifically, claim 28 is amended to define that the oHSV-1 is absence of ICP34.5 protein expression. Applicant believes that amended claim 28 is non-obvious over Zhou and Nakashima.” [Remarks pg 8 ¶ 2].
**The following new rejection is necessitated by Applicant’s amendments to the claims.
Amended and previously presented claims 4-19, 28, and 30-31 are newly rejected under 35 U.S.C. 103 as being unpatentable over Zhou [US20190083555A1, published 21 March 2019]; in view of Peters et al. [2018, Journal of Virology, 92(15), e00246-18, 1-17]; and ViralZone [2017, retrieved on 06 March 2026 from: <web.archive.org/web/20170523041329/https://viralzone.expasy.org/5756>, archived on 23 May 2017].
Regarding independent claim 28, Zhou teaches a method for treating or alleviating a glioblastoma by administering to a subject in need thereof an effective amount of an oncolytic HSV-1 (oHSV-1), or a pharmaceutical composition comprising the oHSV-1, wherein the oHSV-1 comprises a deletion of an internal inverted repeat region of the genome which deletes one copy of each of the double-copy genes (i.e., ICP0, ICP4, ICP34.5, ORF P, and ORF O) and one copy of all of the duplicated non-coding sequences within the internal inverted repeat region (i.e., all sequences between the promoter of UL56 and the promoter of US1, including introns of ICP0, LAT domain, and “a” sequences) within the internal inverted repeat region, and wherein all single-copy genes in both UL and US components of the genome are intact such that they are capable of expressing the encoded functional proteins [0002, 0005, 0008, 0013-0014, 0017-0018, 0041-0045, 0047, 0065, Figure 1].
Zhou also teaches prior oHSV-1 constructs which comprise the deletion of both copies of the ɣ34.5 gene, leading to an absence of ICP34.5 protein [0006-0007].
Zhou does not teach wherein the modified oHSV-1 comprises a modification of a copy of the ɣ34.5 gene that is in a terminal repeat of the genome, wherein the modification renders that copy of the ɣ34.5 gene incapable of expressing functional ICP34.5 protein in combination with the deletion of the internal inverted repeat region described above.
However, Peters teaches that to ensure that oHSV is safe in the brain, all oHSVs in clinical trial for glioma lack the ɣ34.5 genes responsible for neurovirulence, wherein loss of ɣ34.5 expression greatly reduced neurovirulence and contributes to selective replication in cancer cells [abstract, pg 2 ¶ 3]. Peters further teaches that oncolytic viruses are replication competent, and so there is potential for normal tissue toxicity, which is why ɣ34.5 was deleted in many oHSVs [pg 13 ¶ 2].
Therefore, an ordinarily skilled artisan at the time of filing the instant application would have been motivated to delete both copies of the oHSV-1 ɣ34.5 gene, including all or part of the coding or regulator region of the ɣ34.5 gene to ablate ɣ34.5 gene expression, to ensure that the oHSV is safe in the brain by promoting selective replication in cancer cells.
Regarding claims 30-31, Zhou and Peters teach the limitations of independent claim 28. Additionally, Zhou teaches the use of tissue specific promoters specific for expression in glioma brain tumors, as elected, including glioblastoma multiforme (GBM) tumor cells [0033, 0069].
Further, Peters teaches that glioblastoma (GBM) is a lethal brain tumor and that serum-cultured GBM cells are permissive to replication and cell killing by oHSV with deletion of the ɣ34.5 genes [abstract]. Peters also teaches that GBM affects thousands of patients each year and that conventional treatment only extends survival for several months because the tumor ultimately recurs resistant to therapy [pg 1 ¶ 3- pg 2 ¶ 1].
Therefore, an ordinarily skilled artisan at the time of filing the instant application would have been motivated to select a GBM glioma as the cancer to target with the oHSV1 as taught by Zhou and Peters to improve treatment outcomes of GBM.
Regarding claim 4, Zhou teaches wherein the all single-copy genes in both UL and US components include UL1 to UL56 genes in the UL component and US1 to US12 genes in the US component [0047].
Regarding claim 5, Zhou teaches wherein the oHSV-1 is selected from strains F, KOS, and 17 [0046, claim 4].
Regarding claim 6, Zhou teaches wherein the oHSV-1 has a genome isomer of prototype (P) [0103, claim 3].
Regarding claim 7, Zhou teaches wherein the deletion of an internal inverted repeat region causes excision of nucleotide positions 117005 to 132096 in the genome of F strain, in that the homology arms for cloning comprise sequences upstream of nucleotide 11705 and downstream of nucleotide 132096 [0103, Figure 1, 2, SEQ ID NO: 4, 7, 8, 9, claim 5].
Regarding claims 8-10, as discussed above for the 35 U.S.C. 112(b) rejection, the limitations of claims 8-10 conflict with the limitation of claim 28 which recites, “wherein all single-copy genes in both UL and US components of the genome are intact such that they are capable of expressing respective functional proteins” in that ViralZone teaches that the UL56 gene in the standard orientation (wherein the UL genes are arranged such that UL56 is the last UL gene before the internal repeat), is oriented away from the internal repeat such that the promoter is proximal to the internal repeat and the stop codon is further from the internal repeat. Therefore, in the interest of compact prosecution, claim 8 has been interpreted such that the deletion comprises sequences between the UL56 promoter and the US1 promoter. Zhou teaches a deletion between the promoter of UL56 gene and the promoter of US1 gene [0041].
Regarding claims 11-19, Zhou teaches wherein the oSHV-1 comprises a heterologous nucleic acid sequence encoding an immunostimulatory (e.g., the elected IL-12) and an immunotherapeutic agent (e.g., the elected anti-PD-1 agent) which do not interfere with ethe expression of native genes of the HSV-1 genome [0001, 0011, 0022, 0059-0063, 0071-0072, 00109, Figure 1, 2, claim 9, 12, 15]. Zhou also teaches wherein the heterologous nucleic acid sequence encoding IL-12 is incorporated into the internal inverted repeat region and the heterologous nucleic acid sequence encoding the anti-PD-1 agent is incorporated between UL3 and UL4 genes in the UL component [0060-0061].
Given the motivations of Peters to delete both copies of the oHSV-1 ɣ34.5 gene, including all or part of the coding or regulator region of the ɣ34.5 gene to ablate ɣ34.5 gene expression, to ensure that the oHSV is safe in the brain by promoting selective replication in cancer cells and to select a GBM glioma as the cancer to target with the oHSV1 as taught by Zhou and Peters to improve treatment outcomes of GBM, it would have been prima facie obvious to an ordinarily skilled artisan at the time of filing the instant application to modify the method of Zhou to incorporate a deletion of the second ɣ34.5 gene (e.g., the ɣ34.5 gene present in the terminal repeat of the HSV-1 genome) with a reasonable expectation of success.
Note that Applicant’s arguments against the obviousness rejection under 35 U.S.C. 103 are limited to a discussion of the alleged failures of the Nakashima reference, and so are moot with respect to this new rejection under 35 U.S.C. 103 over Zhou, Peters, and ViralZone. Accordingly, Applicant’s arguments do not overcome a finding of obviousness under 35 U.S.C. 103 over Zhou, Peters, and ViralZone.
Double Patenting
The rejection of amended, previously presented, and cancelled claims 2-19 and 28-31 on the ground of nonstatutory double patenting as being unpatentable over claims 1-29 of U.S. Patent No. 10,821,140, hereafter referred to as the ‘140 patent, in view of Nakashima [US20180133269A1, published 17 May 2018], is withdrawn in view of Applicant’s amendment to independent claim 28 to recite, “wherein the oHSV-1 is absence of ICP34.5 protein expression” in line 19.
The rejection of amended, previously presented, and cancelled claims 2-19 and 28-31 on the ground of nonstatutory double patenting as being unpatentable over claims 1-12 of U.S. Patent No. 11,439,679, hereafter referred to as the ‘679 patent, in view of Nakashima [US20180133269A1, published 17 May 2018], is withdrawn in view of Applicant’s amendment to independent claim 28 to recite, “wherein the oHSV-1 is absence of ICP34.5 protein expression” in line 19.
The rejection of amended, previously presented, and cancelled claims 2-19 and 28-31 on the ground of nonstatutory double patenting as being unpatentable over claims 1-5, 11-16, and 18-24 of copending Application No. 17/635,537, hereafter referred to as the ‘537 application, in view of Nakashima [US20180133269A1, published 17 May 2018], is withdrawn in view of the Notice of Abandonment for Application No. 17/635,537 mailed 18 June 2026, such that the status of Application No. 17/635,537 is now abandoned for failure to respond to an office action.
**The following new rejections are necessitated by amendments to the claims.
Amended and previously presented claims 4-19, 28, and 30-31 are newly rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-29 of U.S. Patent No. 10,821,140, hereafter referred to as the ‘140 patent, in view of Peters et al. [2018, Journal of Virology, 92(15), e00246-18, 1-17].
The ‘140 patent claims are drawn to an HSV-1 vector comprising a deletion modification in a wild-type HSV-1 genome, wherein the vector comprises (i) sequences required for expression of all single-copy open reading frames in the genome, comprising the ORFs themselves and regulating sequences necessary for expression of each ORF, wherein the regulating sequences include promoters which are kept intact; (ii) only one copy of each of all double-copy genes in the genome; and (iii) only one copy of duplicated non-coding sequences in the genome (claim 1). Dependent claims further limit the claims such that the double copy genes comprise genes encoding ICP0, ICP4, ICP34.5, ORF P, and ORF O.
The ‘140 patent claims differ from the instant claims in that the ‘140 patent claims do not recite a deletion of all or part of the coding or regulatory region of a copy of y34.5 gene that is in a terminal repeat of a genome of the oHSV-1, wherein the oHSV-1 is absence of ICP34.5 protein expression.
However, Peters teaches that to ensure that oHSV is safe in the brain, all oHSVs in clinical trial for glioma lack the ɣ34.5 genes responsible for neurovirulence, wherein loss of ɣ34.5 expression greatly reduced neurovirulence and contributes to selective replication in cancer cells [abstract, pg 2 ¶ 3]. Peters further teaches that oncolytic viruses are replication competent, and so there is potential for normal tissue toxicity, which is why ɣ34.5 was deleted in many oHSVs [pg 13 ¶ 2].
Therefore, it would have been obvious to an ordinarily skilled artisan at the time of filing the instant application to delete both copies of the oHSV-1 ɣ34.5 gene, including all or part of the coding or regulator region of the ɣ34.5 gene to ablate ɣ34.5 gene expression, to ensure that the oHSV is safe in the brain by promoting selective replication in cancer cells.
The ‘140 patent claims further differ from the instant claims in that the ‘140 patent claims are drawn to a product and the instant claims are drawn to a method of using the product, but double-patenting rejections of claims to a method of using based on a claimed composition are proper. This rejection is necessitated by the decision of the Court of Appeals for the Federal Circuit in Pfizer Inc. v Teva pharmaceuticals USA Inc., 86 USPQ2d 1001, at page 1008 (March 2008), which indicates that there is no patentable distinction between claims to a product and a method of using that product disclosed in the specification of the application and that the preclusion of such a double patenting rejection under 35 USC 121 does not apply where the present application is other than a divisional application of the patent application containing such patentably indistinct claims.
Accordingly, the ‘140 patent claims encompass and render obvious the claims of the instant application.
Amended and previously presented claims 4-19, 28, and 30-31 are newly rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-12 of U.S. Patent No. 11,439,679, hereafter referred to as the ‘679 patent, in view of Peters et al. [2018, Journal of Virology, 92(15), e00246-18, 1-17].
The ‘679 patent claims are drawn to a pharmaceutical composition for treating or alleviating cancer in a subject, comprising a pharmaceutically acceptable carrier and a recombinant oHSV-1, wherein the oHSV-1 has a deletion modification in a wildtype HSV-1 genome and comprises: (i) sequences required for expression of all single-copy ORFs in the genome, comprising the ORFs themselves and regulating sequences necessary for expression of each ORF, wherein the regulating sequences include promoters which are kept intact, (ii) only one copy of each of all double-copy genes in the genome; (iii) only one copy of duplicated non-coding sequences in the genome; and (iv) a heterologous nucleic acid sequence encoding IL-12 and an anti-PD-1 agent, wherein the heterologous nucleic acid sequence encoding IL-12 is inserted into the deleted region of the modified HSV-1 genome, and the heterologous nucleic acid sequence encoding the anti-PD-1 agent is inserted between UL3 and UL4 genes in the UL component of the modified HSV-1 genome, and wherein the incorporation of the heterologous nucleic acid sequence does not interfere with the expression of the wildtype HSV-1 genes (claim 1).
The ‘679 patent claims differ from the instant claims in that the ‘679 patent claims do not recite a deletion of all or part of the coding or regulatory region of a copy of y34.5 gene that is in a terminal repeat of a genome of the oHSV-1, wherein the oHSV-1 is absence of ICP34.5 protein expression.
However, Peters teaches that to ensure that oHSV is safe in the brain, all oHSVs in clinical trial for glioma lack the ɣ34.5 genes responsible for neurovirulence, wherein loss of ɣ34.5 expression greatly reduced neurovirulence and contributes to selective replication in cancer cells [abstract, pg 2 ¶ 3]. Peters further teaches that oncolytic viruses are replication competent, and so there is potential for normal tissue toxicity, which is why ɣ34.5 was deleted in many oHSVs [pg 13 ¶ 2].
Therefore, it would have been obvious to an ordinarily skilled artisan at the time of filing the instant application to delete both copies of the oHSV-1 ɣ34.5 gene, including all or part of the coding or regulator region of the ɣ34.5 gene to ablate ɣ34.5 gene expression, to ensure that the oHSV is safe in the brain by promoting selective replication in cancer cells.
The ‘697 patent claims further differ from the instant claims in that the ‘697 patent claims are drawn to a product and the instant claims are drawn to a method of using the product, but double-patenting rejections of claims to a method of using based on a claimed composition are proper. This rejection is necessitated by the decision of the Court of Appeals for the Federal Circuit in Pfizer Inc. v Teva pharmaceuticals USA Inc., 86 USPQ2d 1001, at page 1008 (March 2008), which indicates that there is no patentable distinction between claims to a product and a method of using that product disclosed in the specification of the application and that the preclusion of such a double patenting rejection under 35 USC 121 does not apply where the present application is other than a divisional application of the patent application containing such patentably indistinct claims.
Accordingly, the ‘697 patent claims encompass and render obvious the claims of the instant application.
Conclusion
No claim is 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.
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DR. KATIE L. PENNINGTON
Examiner
Art Unit 1634
/KATIE L PENNINGTON/Examiner, Art Unit 1634
Dr. A.M.S. Wehbé
/ANNE MARIE S WEHBE/Primary Examiner, Art Unit 1634
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