DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claim Status
Claims 26, 34, 36, 41-42, and 46 are pending.
Claim 26 is currently amended. Applicant elected the peptide of SEQ ID NO. 2 (myr-ARRWR) as a therapeutically effective agent.
Claims 1-25, 27-33, 35, 37-40, 43-45, and 47 were cancelled.
Claims 26, 34, 36, 41-42, and 46 have been examined.
Priority
This application is a DIV of 16/468,066 06/10/2019 ABN
16/468,066 is a 371 of PCT/EP2017/081962 12/08/2017
Maintained Rejection
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 26, 34, 36, 41-42, and 46 are 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. This is a New MATTER rejection.
Claim 26 contains a new limitation (b) of selecting a dosage of “the peptide in an amount of about 5 μg or less” is NOT supported by the specification. The closest disclosure described P1 peptide at a concentration of 5 μg/dose in the specification (p30, line 4), but the disclosure does NOT support the limitation of a dosage of about 5 μg or less as claimed.
In addition, the specification further disclosed 1 μM of peptide P1 (p6, Fig 9) as well as 1 μM or 5 μM of peptide P1 (p29, Example 7), the specification failed to provide a volume for unit conversion to weight. Thus, neither 1 μM nor 5 μM of peptide P1 supports the NEW MATTER limitation “the peptide in an amount of about 5 μg or less”.
Claims 27-30, 32-36, 41-42, and 46 are rejected as depending on claim 26.
Applicant’s Arguments
Mas et al. teach the use a commercial cell culture system of OncoCilAirTM (Journal of Biotechnology 205 (2015) 111–119); thus 1 μM P1 peptide is corresponds to 0.191 μg (Remarks, p2, last para).
Huang et al. teach the commercial cell culture system Mucilair™ (Toxicology in Vitro 27 (2013) 1151–1156); thus 1 μM P1 peptide is corresponds to 0.191 μg (Remarks, p2, last para).
Response to Arguments
Applicant's arguments filed 2/12/2026 have been fully considered but they are not persuasive for the reasons as follows.
Applicant’s argument (i) is not persuasive because no statement of Mas et al. is incorporated by reference in the instant SPEC. Furthermore, Mas et al. only teach 2.5 μM for selumetinib, 50 nM for trametinib, 123 μM for erlotinib in cell culture (p112, col 2, anticancer drugs), suggest an effective amount of a therapeutic agent is a result effective variable and different therapeutic agent has different dosage/concentration. Mas et al. did not teach or suggest administration of the instant SEQ ID NO: 2 or 3 in the cell culture. Thus, the NEW MATTER rejection is proper and CANNOT be overcome by merely verbal arguments or citing irrelevant references.
Applicant’s argument (ii) is not persuasive because no statement of Huang et al. is incorporated by reference in the instant SPEC. Furthermore, Huang et al. teach respiratory chemical sensitizers (p1152, col 1, Sec 2.2. Chemicals), irrelevant to the instant SEQ ID NO: 2 or 3 in cell culture. Thus, the NEW MATTER rejection is proper and CANNOT be overcome by merely verbal arguments or irrelevant references.
Examiner’s Note:
Applicant should expect the examiner to maintain this rejection until claim amendment to overcome this rejection as any verbal arguments or citing irrelevant references off record is unlikely to overcome this NEW MATTER rejection.
Maintained Rejection
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.
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.
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.
Claims 26, 34, 36, 41-42, and 46 are rejected under 35 U.S.C. 103 as being unpatentable over Antonetti et al. (US 2008/0021036 A1, previously cited 11/12/2025) in view of Jain et al. (Biochem. J. 2011; 437: 289-299, previously cited 10/25/2023), Deli (Biochimica et Biophysica Acta 1788 (2009) 892–910, previously cited 11/12/2025), and Conde et al. (WO93/20101, previously cited 3/1/2023).
Claim 26 is drawn to a method comprising:
Selecting SEQ ID NO: 2 (myr-ARRWR) or SEQ ID NO: 3;
Selecting the peptide of SEQ ID NO: 2 or SEQ ID NO: 3 in an amount of about 5 μg or less to enhance transient tissue permeabilization of the therapeutically effective agent;
Selecting a dosage of the therapeutically effective agent;
Administering the peptide of SEQ ID NO: 2 or SEQ ID NO: 3 in a combination for enhancing transient tissue permeabilization of the therapeutically effective agent.
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Antonetti et al. teach administration of a composition comprising a therapeutically effective amount of a PKC zeta inhibitor to treat cancer or other disease or disorder (Abstract, claim 1). Antonetti et al. teach that the PKC Zeta inhibitor is an inhibitor of phosphorylation of a tight junction protein, such as occludin or other proteins that control cell to cell interactions which regulate vascular permeability [0013] in combination with an antineoplastic therapeutic agent to treat a neoplastic disease or disorder [0015]. Antonetti et al. teach a PKC zeta inhibitor is a myristoylated PKC Zeta (PKC ζ) pseudosubstrate of myr-SIYRRGARRWRKL (SEQ ID No. 1) comprising the active motif of ARRWR [0048]. Jain et al. is cited to show inhibition of PKC Zeta (PKC ζ) with a pseudosubstrate (p290, col 1, Chemicals) disrupting tight junction formation (p292, Fig 1; p293, Fig 3), preventing assembly of tight junction (p293, Fig 2), and disrupting adherent junction (p294, Fig 4) known in the art. Deli is further cited to show the use of tight junction modulators to reversibly open membranous barriers and improve drug delivery known in the art (Title and Abstract; p895) shown in figure 1 as follows, consistent with applicant’s admission in the Background of the invention (p1, last para to p3, para 1).
Antonetti et al. in view of Jain et al. and Deli did not specify a pseudosubstrate peptide inhibitor of PKC ζ as SEQ ID NO. 2 (myr-ARRWR) or SEQ ID NO: 3 (myr-AKRWR).
Similarly, Conde et al. teach specific inhibitors of protein kinase C isotype zeta, ζ-PKC, (p3, line 23-25) to treat tumours, hyperproliferative disorders and viral infections (p8, para 2; claim 10), consistent with Antonetti et al. described above. Conde et al. show a preferred peptide inhibitor consisting of the peptide of Ala-Arg-Arg-Trp-Arg, SEQ ID NO: 3/ARRWR) (p4, line 3; claim 4) and suggest a pseudosubstrate peptide inhibitor of PKC ζ further modified by myristoylation (p3, line 13), reading on the elected species of myr-ARRWR. Conde et al. suggest the peptide can be easily made by appropriate adaptation of conventional methods for peptide synthesis (p4, line 19-20). Conde et al. teach PKC zeta peptide inhibitor consisting of the active motif of ARRWR as a result effective variable optimized in a composition ranged from 0.1%-99% of a protein kinase C zeta inhibitor [0079] used for both human and non-human animals (p8, line 12-15). Because Conde et al. teach myr-ARRWR is a preferred inhibitor of protein kinase C isotype zeta (PKC-ζ) and it can be easily made by conventional methods for peptide synthesis, one of ordinary skill in the art would have found it obvious to substitute and/or combine Antonetti’s myr-SIYRRGARRWRKL with Conde’s myr-ARRWR comprising the same functional motif (Fig 6) for the same function as an inhibitor of protein kinase C isotype zeta (PKC-ζ) to treat various diseases including serving as a tight junction modulator to reversibly open membranous barriers and improve anticancer drug delivery as taught by Jain et al. and Deli. Conde et al. a peptide of formula (I) in combination with other therapeutic ingredients (p11, line16-19).
With respect to the limitation (a), Conde et al. teach myr-ARRWR (the instant SEQ ID NO: 2) is a preferred inhibitor of protein kinase C isotype zeta (PKC-ζ) and it can be easily made by conventional methods for peptide synthesis.
With respect to the limitation (b), Conde et al. teach a composition includes 0.1%-99% of a protein kinase C zeta inhibitor [0079]. Conde et al. suggest in general a therapeutically effective amount of a protein kinase C Zeta inhibitor in a composition is in the range of about 0.001 mg/kg (1 µg/kg) -100 mg/kg body weight [0117] and PKC zeta peptide inhibitor is a result effective variable optimized in a composition ranged from 0.1%-99% of a protein kinase C zeta inhibitor as taught by Conde et al. [0079]. Antonetti et al. suggest the use of 500 g rat to conduct animal tests [0181]. Using a 500 g rat for a cancer model, the amount of a protein kinase C Zeta inhibitor comprising the functional motif of ARRWR (e.g., myr-SIYRRGARRWRKL or Conde’s myr-ARRWR) is estimated to be about 0.5 µg calculated as 1 µg/kg x (500g/1 kg).
With respect to the limitation (c), Antonetti et al. teach one of skill in the art could determine a therapeutically effective amount and route of administration in view of these and other considerations typical in medical practice [0116], such as antineoplastic therapeutic agents listed in [0119]. Therefore, one of ordinary skill in the art would have found it obvious to select an optimized dosage of an antineoplastic therapeutic agent suggested by Antonetti et al. [0119].
With respect to the limitation (d), Conde et al. suggest in general a therapeutically effective amount of a protein kinase C Zeta inhibitor in a composition is in the range of about 0.001 mg/kg (1 µg/kg) -100 mg/kg body weight [0117]. Using a 500 g rat for a cancer model, the amount of a protein kinase C Zeta inhibitor (e.g., myr-ARRWR) is estimated to be 0.5 µg calculated as 1 µg/kg x (500g/1 kg). Since a protein kinase C Zeta inhibitor of myr-ARRWR at a dosage of 0.5 µg is expected to inhibit a protein kinase C Zeta, it is further expected the inhibition of protein kinase C Zeta leading to disrupting tight junction formation (p292, Fig 1; p293, Fig 3), preventing assembly of tight junction (p293, Fig 2), and disrupting adherent junction formation (p292, Fig 1; p293, Fig 3) as demonstrated by Jain et al. Antonetti et al. teach that the PKC Zeta inhibitor regulates vascular permeability [0013] in combination with an antineoplastic therapeutic agent to treat a neoplastic disease or disorder [0015] and, consistently, Conde et al. teach the peptide (e.g., myr-ARRWR) in combination with other therapeutic ingredients (p11, line16-19).
With respect to claims 34 and 36, Antonetti et al. teach the treated cancer disease include various types of carcinoma [0115]. Antonetti et al. teach that the PKC Zeta inhibitor regulates vascular permeability [0013] in combination with an antineoplastic therapeutic agent to treat a neoplastic disease or disorder [0015] and, consistently, Conde et al. teach the peptide (e.g., myr-ARRWR) in combination with other therapeutic ingredients (p11, line16-19).
With respect to claims 41-42, Jain et al. teach a protein kinase C Zeta inhibitor causing redistribution of occludin and zonula occludens-1 (ZO-1) from intercellular junctions into the intracellular compartments (p294, col 1, para 2) indicating a delayed assembly of tight junctions in the absence of optimal levels of PKC ζ (p294, col 1, para 2), reading on a transient opening of a tight junction between adjacent cells of the subject.
With respect to claim 46, Conde et al. teach the therapeutic composition generally includes about 0.1-99% of a protein kinase C Zeta inhibitor [0079]. Antonetti et al. teach the composition comprising a PKC Zeta inhibitor and a second therapeutic agent in a liquid formulation [0087-0088, 0096]. Conde et al. show a preferred peptide inhibitor consisting of the peptide of Ala-Arg-Arg-Trp-Arg, SEQ ID NO: 3/ARRWR) (p4, line 3; claim 4) and suggest a pseudosubstrate peptide inhibitor of PKC ζ further modified by myristoylation (p3, line 13), reading on the elected species of myr-ARRWR. Conde et al. suggest the peptide can be easily made by appropriate adaptation of conventional methods for peptide synthesis (p4, line 19-20). A weight to volume ratio of a therapeutic agent in a liquid formulation is a result effective variable can be optimized within prior art conditions or through routine experimentation. See MPEP. 2144.05 (II).
Applicant’s Arguments
Antonetti et al. teach PKC zeta inhibition reduces VEGF induced permeability; thus, PKC zeta inhibition teaches away increasing transient tissue permeability (Remarks, p3, Sec 2.2.1).
Jain of the cited combination discloses that PKC zeta phosphorylates occludin and promotes tight junction assembly. However, Jain is silent about transient tissue permeabilization and the use of a peptide of SEQ ID NO: 2 or 3 at a dose of about 5 μg or less for enhancing the transient tissue permeabilization of a therapeutically effective agent (Remarks, p3-p4, Sec 2.2.2).
Deli does not address PKC zeta or its inhibition and thus provides no motivation or teaching relevant to the present claims. As such, the skilled person would not be motivated to combine Deli with Antonetti, Jain, and Conde and the combined references do not teach, suggest, or hint at the methods of the present claims (Remarks, p4, Sec 2.2.3).
Conde discloses peptides corresponding to SEQ ID NO: 2 of the present application for use in the treatment of tumors and infections. Conde, like Antonetti, Jain, and Deli, is silent about a method for enhancing transient tissue permeabilization of a therapeutically effective agent using a peptide of SEQ ID NO: 2 or 3 at a dose of about 5 μg or less (Remarks, p4, Sec 2.2.4).
The Examiner alleged that Antonetti discloses the combination of PKC zeta inhibitors with other therapeutic agents. However, claim 26 is directed to a method of enhancing transient tissue permeabilization of a therapeutically effective agent. The present disclosure further specifies that the peptides have no anti-tumoral effect per se less (Remarks, p4-5, Sec 2.3).
The Examiner has not provided any specific reasoning as to why a skilled person would replace Antonetti's peptide with that of Conde. Even if the skilled person were to replace the peptide of Antonetti with that of Conde, he/she would not arrive at the subject-matter of the present disclosure, as neither reference discloses a method for enhancing transient tissue permeabilization of a therapeutically effective agent using a peptide of SEQ ID NO: 2 or 3 at a dose of about 5 μg or less (Remarks, p5-6, Sec 2.4).
Regarding the claimed dose of about 5 ug or less of a peptide of SEQ ID NO: 2 or 3 of
pending claim 26, the Examiner alleged that such a dose is disclosed in Conde (presumably
mistaken with Antonetti) by combining a dose range of0.001 mg/kg - 100 mg/kg body weight
(paragraph [0117] of Antonetti) with the weight of a 500 g rat (paragraph [0181] of Antonetti) (Remarks, p6, Sec 2.5).
Choosing Antonetti over Conde despite the more relevant subject-matter of Conde for the present claims can only be made with hindsight because neither reference teach the claimed dosage (Remarks, p6, Sec 2.5.1).
To arrive at a dose of 5 μg the Examiner relies on reconstructing said dose via selective calculation and not through an explicit disclosure (Remarks, p7, Sec 2.5.2).
Reconstruction of PKC zeta inhibitor doses by combining two isolated disclosures (Remarks, p7-8, Sec 2.5.3).
Claiming obviousness of a dose despite the lack of such disclosure in the cited references (Remarks, p8-9, Sec 2.5.4).
The Examiner further alleged that the feature of pending claim 26(c) which is directed to
selecting a dosage of the therapeutically effective agent is anticipated by paragraph [0116] of Antonetti (Remarks, p9, Sec 2.6). Even if the skilled person managed to combine the references, the combination does not teach, suggest, or hint at all the claimed limitations and furthermore teaches away from the present claims (Remarks, p9, Sec 2.7).
Response to Arguments
Applicant's arguments filed 1/14/2025 have been fully considered but they are not persuasive for the reasons as follows.
Applicant’s argument 1 is not persuasive because the rejection is based on inhibition of PKC Zeta (PKC ζ) with a pseudosubstrate (p290, col 1, Chemicals) disrupting tight junction formation known in the art as evidenced by Jain et al. described above (p292, Fig 1; p293, Fig 3), not VEGF as argued by applicant.
Applicant’s argument 2 is not persuasive because the rejection is based on Antonetti et al. in view of Jain et al., Deli, and Conde et al., not a single reference of Jain et al. as argued by applicant. Antonetti et al. suggest the use of 500 g rat to conduct animal tests [0181]. Using a 500 g rat for a cancer model, the amount of a protein kinase C Zeta inhibitor (e.g., myr-SIYRRGARRWRKL or its homologous compound of myr-ARRWR taught by Conde et al.) is estimated to be 0.5 µg calculated as 1 µg/kg x (500g/1 kg). In the case where the claimed ranges "overlap or lie inside ranges disclosed by the prior art" a prima facie case of obviousness exists. In re Wertheim, 541 F.2d 257, 191 USPQ 90 (CCPA 1976). See MPEP 2144.05. Furthermore, Conde et al. teach PKC zeta peptide inhibitor consisting of the active motif of ARRWR as a result effective variable optimized in a composition ranged from 0.1%-99% of a protein kinase C zeta inhibitor [0079] used for both human and non-human animals (p8, line 12-15). See MPEP 2144.05 (II).
Applicant’s argument 3 is not persuasive because Deli is further cited to show the use of tight junction modulators to reversibly open membranous barriers and improve drug delivery known in the art (Title and Abstract; p895) shown in figure 1, consistent with applicant’s admission in the Background of the invention (p1, last para to p3, para 1). The rationale to modify or combine the prior art does not have to be expressly stated in the prior art; the rationale may be expressly or impliedly contained in the prior art or it may be reasoned from knowledge generally available to one of ordinary skill in the art, established scientific principles, or legal precedent established by prior case law. In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988); In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992). See MPEP 2144(I).
Applicant’s argument 4 is not persuasive. See response to arguments 1-3 above. In particular, applicant’s admission of the use PKC inhibitor for enhancing transient tissue permeabilization in the Background of the invention (p1, last para to p3, para 1) consistent with Jain et al. and Deli described above not repeated here. Antonetti et al. suggest the use of 500 g rat to conduct animal tests [0181]. Using a 500 g rat for a cancer model, the amount of a protein kinase C Zeta inhibitor (e.g., myr-SIYRRGARRWRKL or its analog of myr-ARRWR taught by Conde et al.) is estimated to be 0.5 µg calculated as 1 µg/kg x (500g/1 kg) for non-human animals. Furthermore, it would be obvious to optimize the dosage of a result variable of PKC zeta peptide inhibitor in a composition ranged from 0.1%-99% of a protein kinase C zeta inhibitor as taught by Conde et al. [0079] for preventing assembly of tight junction to promote drug delivery in humans. See MPEP 2144.05 Optimization Within Prior Art Conditions or Through Routine Experimentation.
Applicant’s argument 5 is not persuasive because the argument of claim 26 is directed to a method “of” enhancing transient tissue permeabilization of a therapeutically effective agent is not commensurate in scope of a method “for” the intended use of enhancing transient tissue permeabilization of a therapeutically effective agent in claim 26. Furthermore, the limitation of peptides with no anti-tumoral effect as argued by applicant is not found in the claims.
Applicant’s argument 6 is not persuasive because a person of ordinary skill in the art is NOT a person requiring explicitly teachings from a specific prior art reference as argued by applicant. A person of ordinary skill in the art is well defined as a person of ordinary creativity able to fit the teachings of multiple patents together like pieces of a puzzle.” Id. Office personnel may also take into account “the inferences and creative steps that a person of ordinary skill in the art would employ.” Id. at ___, 82 USPQ2d at 1396. See MPEP 2141.03 (I). Thus, the examiner concluded one of ordinary skill in the art as defined in MPEP 2141.03 (I) would have found it obvious to fit the teachings of cited references together like pieces of a puzzle under the prior art conditions.
Applicant’s arguments 7-12 are not persuasive because the claims are arguing one of ordinary skill in the art CANNOT select the claimed dosage range of the instant SEQ ID Nos: 2-3 under the prior art conditions. One of ordinary skill in the art as defined in MPEP 2141.03 (I) would have found it obvious to fit the teachings of cited references together like pieces of a puzzle under the prior art conditions. In particular, Antonetti’s PKC Zeta inhibitor comprises the active motif of ARRWR used in an animal model and Conde’s PKC zeta peptide inhibitor consists of the active motif of ARRWR as a result effective variable optimized in a composition ranged from 0.1%-99% of a protein kinase C zeta inhibitor [0079] for the treatment of both human and non-human animals (p8, line 12-15). Jain et al. is further cited to show inhibition of PKC Zeta (PKC ζ) with a pseudosubstrate (p290, col 1, Chemicals) disrupting tight junction formation (p292, Fig 1; p293, Fig 3), preventing assembly of tight junction (p293, Fig 2), and disrupting adherent junction (p294, Fig 4) known in the art. Deli is further cited to show the use of tight junction modulators to reversibly open membranous barriers and improve drug delivery known in the art. The rationale to modify or combine the prior art does not have to be expressly stated in the prior art; the rationale may be expressly or impliedly contained in the prior art or it may be reasoned from knowledge generally available to one of ordinary skill in the art, established scientific principles, or legal precedent established by prior case law. In re Fine, 837 F.2d 1071, 5 USPQ2d 1596 (Fed. Cir. 1988); In re Jones, 958 F.2d 347, 21 USPQ2d 1941 (Fed. Cir. 1992). See MPEP 2144(I).
Applicant’s argument 13 is not persuasive because the rejection is based on Antonetti et al. in view of Jain et al., Deli , and Conde et al. not anticipation by a single reference of Antonetti as argued by applicant. See the rejection and response to arguments above in details not repeated here. The use of patents as references is not limited to what the patentees describe as their own inventions or to the problems with which they are concerned. They are part of the literature of the art, relevant for all they contain." In re Heck, 699 F.2d 1331, 1332-33, 216 USPQ 1038, 1039 (Fed. Cir. 1983). See MPEP 2123 as well as a person of ordinary skill in the art defined in MPEP 2141.03 (I).
Conclusion
No claim is allowed.
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.
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/J.L/Examiner, Art Unit 1658
03-March-2026
/LI N KOMATSU/ Primary Examiner, Art Unit 1658