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 .
Claims 4 and 14 have been canceled. Claims 1-3, 5-13, 15-20 are pending.
Election/Restrictions
Applicants elected Group I, claims 1-14, without traverse in the reply filed on 2-13-26. Claims 15-20 have been withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 2-13-26.
Claims 1-3, 5-13 are under consideration.
Applicant's arguments filed 6-12-26 have been fully considered but they are not persuasive.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Claim Rejections - 35 USC § 103
A) Claims 1-3, 5-12 remain rejected under 35 U.S.C. 103 as being unpatentable over Kerr (RU 2816871), Stanton (WO 2022226008), Riling (WO 2022165027), Esteves (20210381004), Stanton (WO 2021236479), Kerr (CA 3172572), and Kerr (20220119840) in view of Clark (Sci.,2003, Vol. 302, No. 5652, pg 1960-1963), Wang (WO 2018108106), Nagase (DNA Res., 2008, Vol. 15, No. 3, pg 137-149), J5390642 (2011), JS5390508 (2011), JS53090481 (2011), Mehra (WO 20220660911), Ciuffi (Nature Med., 2005, Vol. 11, No. 12, pg 1287-1289), and JS390642.
Kerr (RU 2816871), Stanton (WO 2022226008), Riling (WO 2022165027), Esteves (20210381004), Stanton (WO 2021236479), Kerr (CA 3172572), and Kerr (20220119840) taught AAV vectors encoding a protein of interest operably linked to 5’ and 3’ ITRs, a CAG promoter, a WPRE, and a bGH polyA sequence (See Examples and Figures). See for example Esteves:
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and
Kerr (WO 2020154645) taught:
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Kerr (RU 2816871) taught the protein was INFβ (para 450).
Stanton (WO 2022226008) taught the protein was INFβ (pg 83, line 8):
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Riling (WO 2022165027) taught the protein was INFβ:
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Esteves (20210381004) taught the protein was INFβ (Table 2).
Stanton (WO 2021236479) taught the protein was INFβ:
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Kerr (CA 3172572) taught the protein was INFβ (para 412)
Kerr (20220119840)
Kerr (RU 2816871), Stanton (WO 2022226008), Riling (WO 2022165027), Esteves (20210381004), Stanton (WO 2021236479), Kerr (CA 3172572), and Kerr (20220119840) did not teach the sequence encoding INFβ was at least 95% identical to SEQ ID NO: 4 as required in claim 1.
However, Clark (Sci.,2003, Vol. 302, No. 5652, pg 1960-1963) taught AY414516 which is 98.9% identical to SEQ ID NO: 4:
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Clark (Sci., 2003, Vol. 302, No. 5652, pg 1960-1963) also taught AY414517 which is 96.9% identical to SEQ ID NO: 4:
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Wang (WO 2018108106) taught BFK14568 which is 99.1% identical to SEQ ID NO: 4:
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Nagase (DNA Res., 2008, Vol. 15, No. 3, pg 137-149) taught AB587428 which is 98.9% identical to SEQ ID NO: 4:
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Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to make an AAV vector comprising an ITR, a CAG promoter, a nucleic acid sequence encoding IFNβ, a WPRE, a bGH polyA, and a second ITR as described by Kerr (RU 2816871), Stanton (WO 2022226008), Riling (WO 2022165027), Esteves (20210381004), Stanton (WO 2021236479), Kerr (CA 3172572), and Kerr (20220119840) wherein the nucleic acid sequence encoding IFNβ operably linked to that is at least 95% identical to SEQ ID NO: 4 as described by Clark, Wang, and Nagase. Those of ordinary skill in the art at the time of filing would have been motivated to use the nucleic acid sequence encoding IFNβ described by Clark, Wang, and Nagase because they are functional equivalents and because they lack a stop codon. Those of skill would have wanted to swap coding sequences as a matter of design choice for optimization and for when the stop codon isn’t needed.
Kerr (RU 2816871), Stanton (WO 2022226008), Riling (WO 2022165027), Esteves (20210381004), Stanton (WO 2021236479), Kerr (CA 3172572), and Kerr (20220119840) did not teach ITRs that were SEQ ID NO: 40 as required in claim 1. However, ITR’s that are 100% identical to SEQ ID NO: 40 were well-known in the art:
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Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to make an AAV vector comprising an ITR, a CAG promoter, a nucleic acid sequence encoding IFNβ, a WPRE, a bGH polyA, and a second ITR as described by Kerr (RU 2816871), Stanton (WO 2022226008), Riling (WO 2022165027), Esteves (20210381004), Stanton (WO 2021236479), Kerr (CA 3172572), and Kerr (20220119840) wherein the ITRs were SEQ ID NO: 40 as described by J5390642, J5390508, J5390481. Those of ordinary skill in the art at the time of filing would have been motivated to use the ITRs described by J5390642, J5390508, J5390481because they are functional equivalents. Those of skill would have wanted to swap coding sequences as a matter of design choice for optimization.
Kerr (RU 2816871), Stanton (WO 2022226008), Riling (WO 2022165027), Esteves (20210381004), Stanton (WO 2021236479), Kerr (CA 3172572), and Kerr (20220119840) did not teach a CAG promoter that were at least 95% identical to SEQ ID NO: 48 as required in claim 1. However, CAG that is 97.7% identical to SEQ ID NO: 48 were described by Mehra (WO 20220660911):
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Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to make an AAV vector comprising an ITR, a CAG promoter, a nucleic acid sequence encoding IFNβ, a WPRE, a bGH polyA, and a second ITR as described by Kerr (RU 2816871), Stanton (WO 2022226008), Riling (WO 2022165027), Esteves (20210381004), Stanton (WO 2021236479), Kerr (CA 3172572), and Kerr (20220119840) wherein the CAG promoter was 97.7% identical to SEQ ID NO: 48 as described by Mehra (WO 20220660911). Those of ordinary skill in the art at the time of filing would have been motivated to use the CAG described by Mehra (WO 20220660911) because it is functional equivalent. Those of skill would have wanted to swap coding sequences as a matter of design choice for optimization.
Kerr (RU 2816871), Stanton (WO 2022226008), Riling (WO 2022165027), Esteves (20210381004), Stanton (WO 2021236479), Kerr (CA 3172572), and Kerr (20220119840) did not teach a WPRE that was at least 95% identical to SEQ ID NO: 33 as required in claim 1. However, a WPRE that is 98.1% identical to SEQ ID NO: 33 was taught by Cuiffe (DU644248, DU644244):
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Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to make an AAV vector comprising an ITR, a CAG promoter, a nucleic acid sequence encoding IFNβ, a WPRE, a bGH polyA, and a second ITR as described by Kerr (RU 2816871), Stanton (WO 2022226008), Riling (WO 2022165027), Esteves (20210381004), Stanton (WO 2021236479), Kerr (CA 3172572), and Kerr (20220119840) wherein the WPRE was at least 95% identical to SEQ ID NO: 33 as described by Ciuffi. Those of ordinary skill in the art at the time of filing would have been motivated to use the WPRE described by Ciuffi because it is functional equivalent. Those of skill would have wanted to swap coding sequences as a matter of design choice for optimization.
Kerr (RU 2816871), Stanton (WO 2022226008), Riling (WO 2022165027), Esteves (20210381004), Stanton (WO 2021236479), Kerr (CA 3172572), and Kerr (20220119840) did not teach a bGH polyA that was at least 95% identical to SEQ ID NO: 34 as required in claim 1. However, the bGH polyA of SEQ ID NO: 34 was well known as described by JS390642 (2011):
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Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to make an AAV vector comprising an ITR, a CAG promoter, a nucleic acid sequence encoding IFNβ, a WPRE, a bGH polyA, and a second ITR as described by Kerr (RU 2816871), Stanton (WO 2022226008), Riling (WO 2022165027), Esteves (20210381004), Stanton (WO 2021236479), Kerr (CA 3172572), and Kerr (20220119840) wherein the polyA was at least 95% identical to SEQ ID NO: 34 as described by JS390642. Those of ordinary skill in the art at the time of filing would have been motivated to use the polyA described by JS390642 because it is functional equivalent. Those of skill would have wanted to swap coding sequences as a matter of design choice for optimization.
The concept of “reduced CpG dinucleotides” or “increased methylation of CpG dinucleotides” of the polynucleotide encoding IFNβ as compared to SEQ ID NO: 2 in claim 1, item c) has been included because the metes and bounds are unclear and because some sequences encoding the INFβ inherently MUST be less CpG’d and more methylated than those in SEQ ID NO: 2. The concept has also been included because Kerr (CA 3172572) and Kerr (20220119840) taught reducing the CpGs of the polynucleotide encoding a protein of interest (luciferase). While Kerr and Kerr did not specifically teach reducing the CpGs in a polynucleotide encoding INFβ as claimed it would have been obvious to do so in order to reduce the immunogenicity of the polynucleotide and avoid unwanted immune activation, especially in a therapeutic application of the AAV.
Claim 2 has been included because:
SEQ ID NO: 40 was well-known as described by J5390642, J5390508, J5390481;
SEQ ID NO: 48 was well-known as described by Mehra;
SEQ ID NO: 4 is an obvious variant of the sequences described by Clark, Wang, and Nagase because there is only one indel and one mismatch which do not effectively change the structure or function of the coding sequence or the resultant IFNβ;
SEQ ID NO: 33 is an obvious variant of the WPRE that is 98.1% identical to SEQ ID NO: 33 taught by Cuiffe because there are only 7 mismatches which do not effectively change the structure or function of the WPRE or the resultant WPRE; and
SEQ ID NO: 34 was well-known as described by JS390642.
Claim 3 has been included because the sequences of Clark, Wang, and Nagase encoding SEQ ID NO: 1.
Claims 5-8 have been included because it is indefinite and because some sequences encoding the INFβ inherently MUST have be 100% more methylated and 100% depleted of CpG dinucleotides as compared to SEQ ID NO: 2.
Claims 9-10 have been included because Kerr (RU 2816871), Stanton (WO 2022226008), Riling (WO 2022165027), Esteves (20210381004), Stanton (WO 2021236479), Kerr (CA 3172572), and Kerr (20220119840) taught AAV2 and AAV9.
Claim 11 has been included because Kerr (RU 2816871), Stanton (WO 2022226008), Riling (WO 2022165027), Esteves (20210381004), Stanton (WO 2021236479), Kerr (CA 3172572), and Kerr (20220119840) taught an antibiotic resistance gene (see Materials and Methods).
Claim 12 has been included because Kerr (RU 2816871), Stanton (WO 2022226008), Riling (WO 2022165027), Esteves (20210381004), Stanton (WO 2021236479), Kerr (CA 3172572), and Kerr (20220119840) taught the antibiotic resistance gene was kanamycin, streptomycin, ampicillin, or neomycin (see Materials and Methods).
Response to arguments
Applicants argue the references did not teach “reduced CpG dinucleotides” or “increased methylation of CpG dinucleotides” of the polynucleotide encoding IFNβ as compared to SEQ ID NO: 2 in claim 1, item c). Applicants’ argument is not persuasive The concept of “reduced CpG dinucleotides” or “increased methylation of CpG dinucleotides” of the polynucleotide encoding IFNβ as compared to SEQ ID NO: 2 in claim 1, item c) has been included because the metes and bounds are unclear and because some sequences encoding the INFβ MUST be less CpG’d and more methylated than those in SEQ ID NO: 2. The concept has also been included because Kerr (CA 3172572) and Kerr (20220119840) taught reducing the CpGs of the polynucleotide encoding a protein of interest (luciferase). While Kerr and Kerr did not specifically teach reducing the CpGs in a polynucleotide encoding INFβ as claimed it would have been obvious to do so in order to reduce the immunogenicity of the polynucleotide and avoid unwanted immune activation, especially in a therapeutic application of the AAV. Next, reducing CpGs in a coding sequence in a vector encoding INFβ was well-established as described by Ullman (WO 2019/200013; para 58-59); reducing CpGs in a coding sequence in an AAV vector encoding a protein of interest was described by Wright (Mol. Therapy, 2020, Vol. 28, No. 8, pg 1756-1758), Faust (J. Clin. Invest., 2013, Vol. 123, No. 7, pg 2994-3001), Konkle (Blood, 2021, Vol. 137, No. 6, pg 763-774), Bertolini (Frontiers in Immunol., 2021, Vol. 12, pg 1-11), and Xiang (Mol. Therapy, 2020, Vol. 28, No. 3, pg 771-783). Finally, claim 1 is not limited to a polynucleotide encoding INFβ that has reduced CpG dinucleotides as compared to SEQ ID NO: 2 because the concept is in the alternative to “increased methylation of CpGs”.
Applicants argue the references fail to provide a reasonable expectation of successfully make the coding sequence for INFβ have reduced CpGs as claimed. Applicants’ argument is not persuasive because it is unfounded. The argument is also not persuasive because the metes and bounds are unclear, because some sequences encoding the INFβ are less CpG’d and more methylated than those in SEQ ID NO: 2, and because reducing the CpGs in a polynucleotide encoding a protein of interest was well-known as described by Kerr and Kerr. There is nothing on record saying those of skill would have had an unreasonable expectation of applying the technique of decreasing CpGs in a model sequence described by Kerr and Kerr (encoding luciferase) to any polynucleotide (encoding INFβ as claimed). Furthermore, some sequences encoding the INFβ MUST be inherently less CpG’d than those in SEQ ID NO: 2 which is all that is required to meet the limitation in claim 1. Next, reducing CpGs in a coding sequence in a vector encoding INFβ was well-established as described by Ullman (WO 2019/200013; para 58-59); reducing CpGs in a coding sequence in an AAV vector encoding a protein of interest was described by Wright (Mol. Therapy, 2020, Vol. 28, No. 8, pg 1756-1758), Faust (J. Clin. Invest., 2013, Vol. 123, No. 7, pg 2994-3001), Konkle (Blood, 2021, Vol. 137, No. 6, pg 763-774), Bertolini (Frontiers in Immunol., 2021, Vol. 12, pg 1-11), and Xiang (Mol. Therapy, 2020, Vol. 28, No. 3, pg 771-783). Finally, claim 1 is not limited to a polynucleotide encoding INFβ that has reduced CpG dinucleotides as compared to SEQ ID NO: 2 because the concept is in the alternative to “increased methylation of CpGs”.
Applicants argue Kerr says the results using a sequence encoding luciferase cannot be extrapolated to other coding sequences because Kerr says "These results provide alternative methods for tailoring the duration of the response to the desired level by selecting a tissue-restricted promoter and/or changing the CpG content of the cDNA vector in the event of an observed host immune response, a potentially transgene-specific response" (Kerr RU2816871, para 558). Applicants’ argument is not persuasive. Kerr is clearly saying that the method can handily be applied to any sequence as necessary. Kerr is not saying that the technique of reducing CpGs in a coding sequence would be unexpected in other polynucleotides, e.g. those encoding INFβ. Furthermore, reducing CpGs in a coding sequence in a vector encoding INFβ was well-established as described by Ullman (WO 2019/200013; para 58-59); reducing CpGs in a coding sequence in an AAV vector encoding a protein of interest was described by Wright (Mol. Therapy, 2020, Vol. 28, No. 8, pg 1756-1758), Faust (J. Clin. Invest., 2013, Vol. 123, No. 7, pg 2994-3001), Konkle (Blood, 2021, Vol. 137, No. 6, pg 763-774), Bertolini (Frontiers in Immunol., 2021, Vol. 12, pg 1-11), and Xiang (Mol. Therapy, 2020, Vol. 28, No. 3, pg 771-783). Finally, claim 1 is not limited to a polynucleotide encoding INFβ that has reduced CpG dinucleotides as compared to SEQ ID NO: 2 because the concept is in the alternative to “increased methylation of CpGs”.
Applicants argue the results were unexpected (pg 12). Applicants point to Preps 1 (AAV encoding wild-type INFβ), and 9-11 (AAV encoding CpG-depleted variants of INFβ) in Fig. 9B. Applicants’ argument is not persuasive. A search for decreasing CpGs in vectors encoding INF prior to 2023 revealed more than a dozen references, so this argument is untenable. CpG manipulation reduces the number of CpGs without changing the encoded amino acids. 9B shows expression levels were the same which was expected. Furthermore, some sequences encoding the INFβ MUST be inherently less CpG’d than those in SEQ ID NO: 2 which is all that is required to meet the limitation in claim 1. Finally, claim 1 is not limited to a polynucleotide encoding INFβ that has reduced CpG dinucleotides as compared to SEQ ID NO: 2 because the concept is in the alternative to “increased methylation of CpGs”.
Applicants point to Fig. 11 which relates to antitumor effects using AAV comprising a CpG depleted INFβ coding sequence; however, claim 1 is not so limited. Moreover, just pointing to Fig. 11 has nothing to do with an unexpected results analysis because the argument does not start with what was expected related to antitumor effects using AAV comprising a CpG depleted INFβ coding sequence, it does not take secondary considerations into account, and it fails to compare what was expected to applicants results.
Claim 1 is not limited to modifying the number of CpGs in the IFNβ coding sequence, but the concept was obvious for reasons of record. The other elements in claim 1 are also obvious for reasons of record. The rejection stands.
The combined teachings of Kerr, Stanton, Riling, Esteves, Stanton, Kerr, and Kerr, Clark, Wang, Nagase, J5390642, JS5390508, JS53090481, Mehra, Ciuffi, and JS390642 did not teach the vector encoded kanamycin having a nucleic acid sequence that is at least 95% identical to SEQ ID NO: 21 as required in claim 13. The sequence was NOT well known. The closest sequence was described by GQ258349 which is 89.18% identical:
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Claim Rejections - 35 USC § 112
Written Description
Claims 1-3, 5-13 remain 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.
A) The specification lacks written description for any sequence encoding an ITR that is at least 95% identical to SEQ ID NO: 40 other than SEQ ID NO: 40, any sequence encoding a CAG promoter that is at least 95% identical to SEQ ID NO: 48 other than SEQ ID NO: 48, any sequence encoding IFNβ that is at least 95% identical to SEQ ID NO: 4 other than SEQ ID NO: 4, any sequence encoding a WPRE that is at least 95% identical to SEQ ID NO: 33 other than SEQ ID NO: 33, or any sequence encoding a bGH polyA that is at least 95% identical to SEQ ID NO: 34 other than SEQ ID NO: 34 as required in claim 1 or at least 90% identical to SEQ ID NO: 21 in claim 13. The specification contemplates the genuses but does not provide a reasonable number of species within the genuses. The specification does not teach any species that have the same function within the genuses. Accordingly, the concepts lack written description.
Response to arguments
Applicants point to case law which is not persuasive because the fact pattern in this case is not the same as those. More importantly, applicants do not show any variants of SEQ ID NO: 40 that have the same ITR function as SEQ ID NO: 40, any variants of SEQ ID NO: 48 that have the same CAG promoter function as SEQ ID NO: 48, any variants of SEQ ID NO: 4 that have the same function as SEQ ID NO: 4, any variants of SEQ ID NO: 33 that have the same WPRE function as SEQ ID NO: 33, or any variants of SEQ ID NO: 34 that have the same polyA function as SEQ ID NO: 34.
Applicants point to para 148 for ITRs. Applicants argument is not persuasive because it does not teach any specific variants of SEQ ID NO: 40 that are 95% identical and have ITR function.
Applicants point to SEQ ID NO: 36-41 (see pg 7, 6 lines from the bottom) which are all ITRs. Applicants’ argument is not persuasive. There is nothing that says SEQ ID NO: 36-39 and 41 are 95% identical to SEQ ID NO: 40 as required in claim 1.
Applicants point to para 141 and 178 for CAG promoters. Applicants argument is not persuasive because it does not teach any specific variants of SEQ ID NO: 48 that are 95% identical and have CAG promoter function.
Applicants point to para 147 and 165 for WPRE. Applicants argument is not persuasive because it does not teach any specific variants of SEQ ID NO: 33 that are 95% identical and have WPRE function. Para 147 mentions SEQ ID NO: 30, it does not mention SEQ ID NO: 33.
Applicants point to para 139 for bovine polyA. Applicants argument is not persuasive because it does not teach any specific variants of SEQ ID NO: 34 that are 95% identical and remain “bovine” or have polyA function. Para 139 refers to SEQ ID NO: 19 and lists names of polyAs.
Applicants point to para 103, SEQ ID NO: 1, and UniProt #P01574 which are amino acids for INFβ. Applicants’ argument is not persuasive. Para 103 and the specification do not teach any specific variants of SEQ ID NO: 4 that are 95% identical and have INFβ function and reduced CpGs or increased methylation of CpGs as required in claim 1. Para 103 does not refer to any SEQ ID NOs; it merely lists species and names of INF subtypes.
B) The specification does not teach any variants of SEQ ID NO: 4 with any “reduced CpG dinucleotides” or “increased methylation of CpG dinucleotides” “as compared to SEQ ID NO: 2” as required in claim 1. The specification contemplates the concept on pg 14-15 and throughout the specification. Pg 26-29 discusses “CpG dinucleotide modification” and contemplates how much CpG modification occurs without teaching what it means or how to accomplish it. The specification does not teach any specific variants of SEQ ID NO: 4 with “reduced” CpGs, specifically “at least 50%, “as compared to SEQ ID NO: 2” as required in claims 1 and 7. The specification does not define a nucleic acid wherein the CpGs are “depleted” as required in claim 8. The specification does not teach any variants of SEQ ID NO: 4 that have increased methylation of CpGs “as compared to SEQ ID NO: 2” as broadly encompassed by claim 1, that methylation has increased by 50% as compared to SEQ ID NO: 2 as required as required in claim 5, or completely methylated as required in claim 6. Accordingly, the concepts lack written description.
Response to arguments
Applicants do not address this rejection.
Indefiniteness
Claims 1-3, 5-13 remain 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.
A) The metes and bounds of SEQ ID NO: 4 with any “reduced CpG dinucleotides” or “increased methylation of CpG dinucleotides” “as compared to SEQ ID NO: 2” as required in claims 1 and 5-8 cannot be determined. The specification contemplates the concept on pg 14-15 and throughout the specification. Pg 26-29 discusses “CpG dinucleotide modification” and contemplates how much CpG modification occurs without teaching what it means or how to accomplish it. The specification does not teach any specific variants of SEQ ID NO: 4 with “reduced” CpGs, specifically “at least 50%, “as compared to SEQ ID NO: 2” as required in claims 1 and 7. The specification does not define a nucleic acid wherein the CpGs are “depleted” as required in claim 8. The specification does not teach any variants of SEQ ID NO: 4 that have increased methylation of CpGs “as compared to SEQ ID NO: 2” as broadly encompassed by claim 1, that methylation has increased by 50% as compared to SEQ ID NO: 2 as required as required in claim 5, or completely methylated as required in claim 6. Accordingly, those of skill would not be able to determine when they were infringing on the claim.
Response to arguments
Applicants argue the amendment overcomes the rejection. Applicants’ argument is not persuasive for reasons set forth above.
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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Michael C. Wilson
/MICHAEL C WILSON/
Primary Examiner, Art Unit 1638
Prosecution Insights