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 .
Election/Restrictions
Claims 5-8, 11-12, 15, 18-19, 21, 25-27, 28-29, 31-33, 34-35 are pending.
Claims 5-8, 11-12, 15, 18-19, 21, 25-27, 34-35 are examined here. Claims 28-29, 31-33 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim.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 for the group election in the reply filed on 10/24/2025.
Priority
The application claims benefit to US Provisional 62/929,602, filed on 11/01/2019, via its PCT/US2020/058309, filed on 10/30/2020.
The later-filed application must be an application for a patent for an invention which is also disclosed in the prior application (the parent or original nonprovisional application or provisional application). The disclosure of the invention in the parent application and in the later-filed application must be sufficient to comply with the requirements of 35 U.S.C. 112(a) or the first paragraph of pre-AIA 35 U.S.C. 112, except for the best mode requirement. See Transco Products, Inc. v. Performance Contracting, Inc., 38 F.3d 551, 32 USPQ2d 1077 (Fed. Cir. 1994).
The disclosure of the prior-filed application, Application No. ‘602, fails to provide adequate support or enablement in the manner provided by 35 U.S.C. 112(a) or pre-AIA 35 U.S.C. 112, first paragraph for one or more claims of this application. ‘602 does not disclose the SEQ ID NO: 934, but SEQ ID NO: 75 is disclosed in ‘602. Remarks point out that SEQ ID NO: 934 is not identical as instant SEQ ID NO: 74.
Thus, claim 5 and its dependents enjoy the benefit of filing date of its PCT submission, which discloses the recited SEQ ID NOs, 10/30/2020.
Claim Rejections - 35 USC § 112
Rejection of cl. 35 is withdrawn, the claim is amended.
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claim 21 is rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends. Claim 21 recites “(d) each strand has 19-30 nucleotides.” Claim 21, which has lower limit of a strand with 19 nt., does not limit cl. 5, which requires “at least 20 contiguous nucleotides.” Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
In the interest of compact prosecution, claim 21 will be interpreted as “(d) each strand has 20-30 nucleotides.”
Claim Rejections - 35 USC § 101
Rejection of cl. 26 is withdrawn, the claim is amended as an “isolated cell.”
Claim Rejections - 35 USC § 102
Rejection of claims 5, 6, 7, 8, 11, 21, 25, 26, 27 is withdrawn, the claim is amended to and recites “at least 20 contiguous nucleotides” of recited SEQ ID NOs. Khvorova does not teach the elements of the amended independent claim.
Claim Rejections - 35 USC § 103
Rejection of cl. 12, 15, 18, and 19 rejected under 103 rendered obvious over Khvorova and Nair is withdrawn, due to claim amendment; however, upon further search and consideration the claims are rejected as noted below. The rejection of claims 5 and 34, 35 are maintained, and cl. 6-8, 11, 21, 25-27 are rejected as noted below.
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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 5, 6, 21, 26 and 34 are rejected under 35 U.S.C. 103 as being unpatentable over Graham et al. (2015, Modern Pathology, 28, 822-829), Kasashima et al. (2004, Biochimie, 86, 713-721) and Khvorova et al. (US Pat. 8090542, Issued 01/03/2012, referred as Khvorova).
The dsRNA agent comprises the antisense strand and sense strand, SEQ ID NO: 934, with the sequence, aaagaauucu uucacuuccu ccc (23 nt.) and SEQ ID NO: 928, with the sequence gaggaaguga aagaauucuu u (21 nt.), respectively. siRNA of SEQ ID NO: 928 and 934, comprises 2 nt. overhang of CC at the 3’ end of the longer antisense strand. Antisense strand SEQ ID NO: 75 is auaagaauuc uuucacuucc ucc and its complementary sense strand is SEQ ID NO: 74 is aggaagugaa agaauucuua u (21 nt.).
Graham demonstrates that DNAJB1-PRKACA (DP) fusion transcript was found in all fibrolamellar carcinomas, a subtype of hepatocellular carcinoma that predominantly affects young patients, but not in other tumor types (abstract). Further Graham discloses that the fusion transcript DNAJB1 exon 1 followed by PRKACA exon 2 and PRKACA exons at the 3’ end forming the novel chimera (pg. 823). Fig. 1c provides the contiguous 19 nt. fusion point sequence between the DNAJB1 exon 1 and PRKACA exon 2 (see below, the sequence is 5’-GGGAGGAAGtgaaagaatt, the upper case letters represent the DNAJB1 exon1, while lower case letters represent PRKACA exon 2).
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Kasashima discloses a chimeric/fusion transcript AML1-MTG8 that causes acute myeloid leukemia (AML). Kasashima tested if the fusion transcript knock-down could be used for therapeutic purposes by designing siRNAs to specifically target the region that represents a fusion point between AML1 and MTG8b, see Fig. 1A below from Kasashima.
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In the hopes of knocking down the expression of fusion transcript (AML1-MTG8), Kasashima prepared several kinds of siRNAs targeting a 25-nucleotide region spanning the fusion point of AML1 and MTG8; siRNAs that consisted of double-stranded RNAs with 21-24 nucleotides in length, containing two nt. 3’ overhangs (dT) on each strand (pg. 716). Kasashima also disclosed designing siRNAs with a single or double mismatches and with various 2 nt. overhangs, dTdT, CT, GG (see Fig. 1B, relevant to instant cl. 21). Kasashima demonstrated knock-down of fusion AML1-MTG8 transcript (Fig. 1B, pg. 715) along with knocking-down protein expression in vitro (Fig. 1C/1D, pg. 715, relevant to instant cl. 26). Except for 1 siRNA (AM3s2), nine siRNAs, including the ones with mismatches, reduced expression of transcript levels at various potencies (see Fig. 1B).
The KSR’s “obvious to try” rationale for supporting conclusion of obviousness requires the following three findings:
(1) a finding that at the relevant time, there had been a recognized problem or need in the art, which may include a design need or market pressure to solve a problem; (2) a finding that there had been a finite number of identified, predictable potential solutions to the recognized need or problem; (3) a finding that one of ordinary skill in the art could have pursued the known potential solutions with a reasonable expectation of success.
Here, the recognized problem disclosed by Graham is that DP chimeric transcript was found in all fibrolamellar carcinoma, a carcinoma that predominantly affects young patients. Kasashima provides a method to design a finite number of identified, predictable siRNAs to target a chimeric transcript along its fusion point. Based on the observation of Graham and methodology of Kasashima, a skilled artisan could have a pursued designing reasonable number of siRNAs of various lengths (21-24 nt.) and targeting various sequences of the fusion point region of DP chimeric transcript to combat fibrolamellar carcinoma or attempt to understand its role in fibrolamellar carcinoma.
Here, Graham discloses that the sequence in the fusion point region of DP transcript comprises GGGAGGAAGtgaaagaatt, the upper case letters as DNAJB1 portion of the DP fusion transcript, while the lower case letters representing the PRKACA portion. The sequence is 19 nt. in length. Thus, a canonical antisense strand of 19 nt. would be aauucuuucacuuccuccc (see alignment between instant SEQ ID NO: 934 and Graham sequence, showing 19 nt. that are ) and its sense strand is gggaggaagugaaagaauu; thus representing a contiguous 19 nt. with 0 mismatches or, alternatively, a contiguous 20-21 nt. with 1 mismatch at either or both 5’ or 3’ ends (relevant to instant cl. 5, 6).
SEQ ID NO: 934 5 AAUUCUUUCACUUCCUCCC 23
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Graham-based 1 AAUUCUUUCACUUCCUCCC 19
Further, based on the GenbankTM accession numbers of DNAJB1 (NM_006145.1) and PRKACA (NM_002730.3), a skilled artisan can make siRNAs comprising 21-24 nt. strands along with 2 nt. overhang; thus a 24 nt. or 23 nt. in length would comprise the 23 nt. of instant SEQ ID NOs: 934 and 928 (relevant to instant cl. 5, 6, 34).
Here, the instant siRNA has a blunt end at one end, and a 2 nt. (CC) overhang at the 3’ end of the antisense strand. Khvorova discloses siRNAs of 19-mers, which were blunt ended, and discloses that Dicer enzyme processes the dsRNA into 19-23 base pair short interfering RNAs with characteristic two base 3’ overhangs (Col. 2, line 26-28). Thus, as provided in Kasashima the 2 nt. content of an overhang bases can vary, siRNA designated “AM4” comprises an antisense strand with two guanine bases overhangs at the 3’ end, while others had the canonical dTs overhang, yet siRNA AM4 was potent in inhibiting the target transcript (Fig. 1B, 715). Thus, blunt ends or varying bases of the overhangs do not appear to affect the overall inhibition of the transcript, and therefore variance in the overhang nucleotides is not a patentable distinction.
One of the KSR rationale that may be used to support a conclusion of obviousness is obvious to try. Therefore, it would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to have modified the teaching of Graham in view of Kasashima and Khvorova and arrive at the claimed invention with a reasonable expectation of success. Based on the observation of Graham that all fibrolamellar carcinoma have DP fusion transcript and methodology of Kasashima and Khvorova in designing siRNAs to target the fusion point region of the DP fusion transcript, a skilled artisan could have pursued designing a reasonable number of siRNAs of various lengths (21-24 nt.), comprising two bases overhangs, and targeting various fusion point regions of DP chimeric transcript to combat fibrolamellar carcinoma or attempt to understand its role in fibrolamellar carcinoma. Thus, SEQ ID NOs: 934/928 are obvious and cl. 5, 6, 21, 26 and 34 are obvious.
Claims 7, 8, 11, 12, 15, 18-19, 25, 27 are rejected under 35 U.S.C. 103 as being unpatentable over Graham et al. (2015, Modern Pathology, 28, 822-829), Kasashima et al. (2004, Biochimie, 86, 713-721) and Khvorova et al. (US Pat. 8090542, Issued 01/03/2012, referred as Khvorova), as applied to claims 5, 6, 21, 26 and 34 above, and further in view of Nair et al. (2014, J. of Am. Chem. Soc., 136, 16958-16961).
The disclosure of rejection of cl. 5, 6, 21, 26 and 34 is noted above.
Graham, Kasashima, and Khvorova do not disclose the triantennary GalNAc ligand modified at the 3’ sense strand of the siRNA, including as shown in claim 19.
Nair discloses a N-acetylgalactosamine (GalNAc)-conjugated siRNA localizes in hepatocytes and elicits robust RNAi mediated gene silencing (title). Nair synthesized GalNAc-conjugated siRNAs that had nucleotide comprising 2’-deoxy-2’-fluoro (2F) and 2’-O-methyl (2OMe) sugar modifications along with phosphorothioate (PS)-internucleotide modifications (see Table 1, pg. 16959, relevant to instant cl. 7, 8, 25). Nair notes that nucleotide modifications provide “systemic stability against nucleases and improved pharmacokinetics relative to the unconjugated siRNAs” (pg. 16959, relevant to instant cl. 7, 8, 25). Nair conjugated the triantennary-GalNAc at the 3’ end of the sense strand (pg. 16959, Table 1; relevant to instant cl. 12, 15). Nair discloses the conjugation as diagrammed below (relevant to instant cl. 18, 19):
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Fig. 2 of Nair discloses that the siRNA conjugated to triantennary-GalNAc ligand (GalNAc3) was robust in its uptake compared to other types of ligands tested when incubated with isolated primary mouse hepatocytes, which have the asialoglycoprotein receptors (ASGPRs) for the efficient GalNAc binding (pg. 16959, 16960). Nair discloses that solubility of conjugates in water and aqueous buffers were comparable to those of unmodified siRNAs (pg. 16959, relevant to instant cl. 27).
One of the KSR rationale that may be used to support a conclusion of obviousness is that there is some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to modify the prior art reference or to combine prior art reference teachings to arrive at the claimed invention. Therefore, it would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to have modified siRNAs of Graham, Kasashima and Khvorova in view of Nair and arrive at the claimed invention with a reasonable expectation of success. Based on improved uptake of siRNAs with triantennary GalNAc that is modified with 2OMe, 2F and PS-internucleotide linkage into hepatocytes of Nair, a skilled artisan would modify a siRNA as taught by Graham, Kasashima, and Khvorova by modifying it with 2OMe, 2F and PS-internucleotide linkage and incorporating a GalNac conjugate at a terminal end in a buffer as taught by Nair for improved uptake into hepatocytes. Thus, cl. 7, 8, 11, 12, 15, 18-19, 25, 27 are obvious.
Claim 35 is rejected under 35 U.S.C. 103 as being unpatentable over Graham et al. (2015, Modern Pathology, 28, 822-829), Kasashima et al. (2004, Biochimie, 86, 713-721) and Khvorova et al. (US Pat. 8090542, Issued 01/03/2012, referred as Khvorova) as applied to claims 5, 6, 7, 8, 11, 12, 15, 18-19, 21, 25, 26, 27, 34 above, and further in view of Foster et al. (2018, Molecular Therapy, 26, pg. 708-717), and as evidenced by Nair et al. (2014, J. of Am. Chem. Soc., 136, 16958-16961).
The modified SEQ ID NO: 916 (sense) and 922 (antisense), and 42 (sense) and 43 (antisense) are as noted below, from spec. Table 9A.
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Disclosure of rejections of claims 5, 6, 7, 8, 11, 12, 15, 18-19, 21, 25, 26, 27, 34 are noted above.
Graham, Kasashima and Khvorova do not disclose the modified pattern of instant SEQ ID NO: 916/922.
Foster discloses that a conjugated “chemically modified, metabolically stable siRNAs to a synthetic triantennary N-acetylgalactosamine (GalNAc) ligand, represents a promising approach for safe and effective targeted delivery of RNAi therapeutics to hepatocytes in vivo” (pg. 708). Foster demonstrates substantial efficacy improvements can be achieved by optimizing the position of 2F and 2OMe modifications across both the strands of the dsRNA siRNA duplex to enhance stability without comprising intrinsic RNAi activity (abstract, relevant to instant cl. 7, 8). Foster highlights that modifying the 2’ position of RNA can significantly enhance the stability of oligonucleotides and that the bulky 2OMe has a greater stabilizing effect than the less bulky 2F modification, however, steric bulk, “if not applied judiciously” results in reduction of RNAi activity (pg. 708, relevant to instant cl. 7, 8). Before conducting bench studies, they conducted an in silico analysis based on a dataset of 1,890 duplexes with varying 2F and 2OMe composition across five targets and 15 target sites. The in silico results describing impact of 2F relative to 2OMe at each position in the antisense strand (AS) and sense strand (SS) was generated (Foster’s fig. 1A, B is provided below, and indicates “Negative numbers indicate activity improvement with inclusion of 2’-F relative to 2’-OMe at that position, positive numbers reflect decreased activity. Asterisks (*) indicate significant differences between 2’-F and 2’-OMe at the noted positions” (pg. 709, 710, Fig. 1).
Foster also reduced the overall numbers of 2F with the rationale that 2OMe significantly enhances nuclease stability thus having a greater stabilizing effect while still maintaining inhibitory activity (pg. 708).
Foster: Fig. 1A, B, pg. 710.
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Reviewing Foster’s sense strand data of Fig. 1B, it appears that although there are significant inhibition differences between 2OMe and 2F at various positions, except for position 11 of sense strand (Fig. 1B), which has a strong (and a significant) preference for 2F, there is not a strong preference for 2OMe or 2F along the sense strand. Here, both instant sense strand has a 2F at position 11. Similarly reviewing the antisense strand data of Fig. 1A, there is a strong (and significant) preference for 2F at pos. 2 and 14, and a strong preference for 2OMe at position 21. Here instant antisense strand has 2F at pos. 2 and 14. Using the in silico data as a starting point, Foster tested various sense and antisense strands pattern modifications in vitro and in vivo with the aim to identify an optimal 2OMe and 2F modification pattern, while maintaining a low 2F content, across a siRNA targeting a murine transthyretin gene (abstract, Fig. 1C, D, and other figures). Thus, it is known in the art to modify the nt. positions of 2OMe and 2F on a siRNA to identify a modification pattern(s) that improves stability and maintains or increases activity.
Regarding PS linkages, Foster introduced PS linkages in the antisense strand between position 1 and 2, 2 and 3, 21 and 22 and 22 and 23 and for sense strands, between position 1 and 2 and 2 and 3 from 5’ end (all nt. positions are from 5’ end unless indicated otherwise). Foster discloses that PS linkages provide additional protection against 3’ and 5’ exonucleases and thus are placed at terminal ends (pg. 708). Thus modifying the PS linkage content is known in the art (relevant to instant cl. 25).
Regarding L96, Foster discloses that GalNAc ligand was introduced at the 3’ end of the sense strand as described in Nair et al. (as illustrated above, L96 is identical the triantennary structure of Nair disclosed above for cl. 11-12, 15, 18-19).
The KSR’s “obvious to try” rationale for supporting conclusion of obviousness requires the following three findings: (1) a finding that at the relevant time, there had been a recognized problem or need in the art, which may include a design need or market pressure to solve a problem; (2) a finding that there had been a finite number of identified, predictable potential solutions to the recognized need or problem; (3) a finding that one of ordinary skill in the art could have pursued the known potential solutions with a reasonable expectation of success. Foster indicates placement of a bulky 2OMe modification provides an improved nuclease stability compared to a less bulky 2F modification, and with the aims of keeping a low level of 2F modification, identifies optimal 2OMe and 2F modification pattern for the genes tested by testing numerous siRNAs with different modification patterns of 2OMe and 2F.
Foster tested the finite number of 2’-sugar modifications using 2OME and 2F to identify the optimal modification pattern comprising 2OMe and 2F modifications.
One of the KSR rationale that may be used to support a conclusion of obviousness is obvious to try. Therefore, it would have been prima facie obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to have tried modifying sequences as taught by Graham, Kasashima, and Khvorova in view of Foster with a reasonable expectation of success. Because Foster discloses that a siRNA that is fully modified and conjugated to a targeting moiety is needed for a safe and effective targeted delivery of a siRNA and demonstrates testing different 2OMe and 2F modifications positions across a siRNA to identify a modification pattern with desired siRNA activity, and because Graham teaches that all fibrolamellar carcinoma have DP fusion transcript and Kasashima teaches a methodology in designing siRNAs to target the fusion point region of the DP fusion transcript, and Khvorova teaches an siRNA with either a blunt or overhang ends, a skilled artisan with these known, finite options would reasonably expect success that these modifications would result in identifying a stable siRNA targeting the DP fusion transcript at its fusion point region comprising sequences of instant SEQ ID NO: 916/922 with an optimal modification pattern comprising 2OMe and 2F and phosphorothioate at either ends. Thus claim 35 is obvious.
Response to Arguments
Applicant's arguments filed 05/01/2026 (“the Remarks”) have been fully considered but they are not persuasive.
First, since the rejection has been edited due the claim amendments, the response will address the references noted in the Remarks that still apply.
The Remarks argue the following:
Regarding rejection of cl. 5 and 34, Graham does not teach “any dsRNA agents for inhibiting expression of a DNAJB1-PRKACA fusion gene” (pg. 12) and the sequence of 5’-GGGAGGAAGtgaagaatt is “used for the detection of the DNAKB1-PRKACA fusion transcript and teachings of Kasashima, which teaches “an entirely different fusion protein associated with a different disease” and Khvorova do not cure the deficiencies of Graham (pg. 13).
Further art of Foster “does not negate the non-obviousness of the component unmodified dsRNA” (pg. 13).
The Remarks note that “claimed dsRNA agents demonstrated efficacy of knockdown of DNAJB1-PRKACA mRNA in vitro, for example, by an average of 44% for duplex 13A (about 40% knockdown in replicate 1, and 48% knockdown in replicate 2) and an average of 50% for duplex 14 . . . at 50 nM in Hep3B cells (see Table 5B)” (pg. 11).
The argument is not persuasive.
Addressing 1), in response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986). Here, it is in view of Kasashima and Graham that renders the claimed invention of cl. 5 and 34 obvious. Kasashima demonstrates designing therapeutic siRNAs against a chimeric protein, specifically at the fusion point of the chimeric protein, that also causes cancer; thus a skilled artisan can apply the teachings of Kasashima to Graham, which teaches the chimeric protein of DNAJB1-PRKACA that also causes a different type of cancer.
Addressing 2, Foster’s teaching still applies because it teaches that although Graham, Kasashima, and Khvorova do not teach the modification pattern of claimed invention, a skilled artisan can modify the positioning of 2OMe and 2F modifications to arrive at the claimed invention with reasonable expectation of success.
Addressing 3, the unmodified siRNAs of Kasashima, which target a different chimeric protein, that were successful at knocking down the target chimeric protein were in the range from ~75% to 20% inhibition in vitro at the concentration at 66.7 nM (see Fig. 1B, only 1 siRNA did not appear to knockdown target protein expression, pg. 715; see Material Methods section 2.3 for Cell culture and transfection, pg. 714). Further Kasashima also discloses that a siRNA targeting a fusion point specifically reduces the target chimeric point as opposed to the non-chimeric proteins. A skilled artisan would reasonably expect similar inhibition levels for siRNAs as taught by Kasashima for targeting DP chimeric protein of Graham. The inhibition levels of Kasashima is similar to instant claimed products, with minor differences based on different types of cells.
Thus, examined claims are rejected under 103.
Allowable Subject Matter
No claim allowed.
Conclusion
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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/KEYUR A VYAS/Examiner, Art Unit 1637
/Jennifer Dunston/Supervisory Patent Examiner, Art Unit 1637
Prosecution Insights