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 .
Application Status
This action is written in response to applicant’s correspondence received 2/10/2026. Claims 1-2 and 6-15 are currently pending. Claims 3-5 were cancelled. Claims 13-15 are new.
Any rejection or objection not reiterated herein has been overcome by amendment. Applicant’s amendments and arguments have been thoroughly reviewed, but are not persuasive to place the claims in condition for allowance for the reasons that follow.
Objections to the specification are withdrawn in view of Applicant’s amendment filed 2/10/2026.
Rejection of claim 12 under 101 is withdrawn in view of Applicant’s amendment to add “in vitro”. Rejection of claims 1, 6, and 8-12 is withdrawn in view of Applicant’s amendment to incorporate the limitations of claims 3-5 and new limitation “said peptide is coupled to a molecular scaffold or carrier” into claim 1.
Rejection of claims 7-9 on the basis that they contain an improper Markush grouping of alternatives is withdrawn in view of Applicant’s amendment to remove “binding, detecting and/or obtaining”.
Rejection of claim 2 under 112(b) is withdrawn in view of Applicant’s amendment to remove “for instance”.
Rejection of claims 7-9 under 112(b) as being incomplete for omitting essential steps is withdrawn in view of Applicant’s amendment to add “introduced to a non-human animal”.
Drawings
The drawings were received on 2/10/2026. These drawings are not acceptable because Figure 13 has color drawings.
Color photographs and color drawings are not accepted in utility applications unless a petition filed under 37 CFR 1.84(a)(2) is granted. Any such petition must be accompanied by the appropriate fee set forth in 37 CFR 1.17(h), one set of color drawings or color photographs, as appropriate, if submitted via the USPTO patent electronic filing system or three sets of color drawings or color photographs, as appropriate, if not submitted via the via USPTO patent electronic filing system, and, unless already present, an amendment to include the following language as the first paragraph of the brief description of the drawings section of the specification:
The patent or application file contains at least one drawing executed in color. Copies of this patent or patent application publication with color drawing(s) will be provided by the Office upon request and payment of the necessary fee.
Color photographs will be accepted if the conditions for accepting color drawings and black and white photographs have been satisfied. See 37 CFR 1.84(b)(2).
Claim Objections – new necessitated by amendment
Claim 2 is objected to because of the following informalities: claim 2, lines 2-3 recites “for” twice and one of them should be removed. Appropriate correction is required.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 7-10 and 13-15 are 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.
Claim 7 recites the limitation "a nucleic acid molecule or functional equivalent of claim 1" in line 3. There is insufficient antecedent basis for this limitation in the claim. Claims 8-10 depend from claim 7, and are therefore included in this rejection.
Claim 13 recites the limitation "a nucleic acid molecule or functional equivalent of claim 1" in lines 2-3. There is insufficient antecedent basis for this limitation in the claim. Claims 14-15 depend from claim 13, and are therefore included in this rejection.
Claim Rejections - 35 USC § 102 and 103 - withdrawn
Rejection of claims 1, 5-7, and 11-12 under 35 U.S.C. 102(a)(1) as being anticipated by Kudo and Fukuda referred to as “Kudo” herein (A short, novel promoter sequence confers the expression of human leukosialin, a major sialoglycoprotein on leukocytes. JOURNAL J Biol Chem. 1991; as cited in the PTO-892) is withdrawn in view of Applicant’s amendment filed 2/10/2026 to incorporate the limitations of claims 3-5 and new limitation “said peptide is coupled to a molecular scaffold or carrier” into independent claim 1 and to add new limitations “or inducing” and “introduced into a non-human animal” to claim 7.
Rejection of claims 2-4 and 8-10 under 35 U.S.C. 103 as being unpatentable over Kudo as applied to claims 1, 5-7, and 11-12 above, and further in view of Spits et al. referred to as “Spits” herein (WO2015093949A2; published 6/25/2015; with priority to 12/7/2013; cited in IDS filed 10/2/2022) is withdrawn in view of Applicant’s amendment filed 2/10/2026 to incorporate the limitations of claims 3-5 and new limitation “said peptide is coupled to a molecular scaffold or carrier” into independent claim 1, to add new limitations “or inducing” and “introduced into a non-human animal” to claim 7, to amend claim 8, and to add new claims 13-15.
Claim Rejections - 35 USC § 103 – new necessitated by amendment
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.
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 1-2 and 6-15 are rejected under 35 U.S.C. 103 as being unpatentable over Kudo and Fukuda referred to as “Kudo” herein (A short, novel promoter sequence confers the expression of human leukosialin, a major sialoglycoprotein on leukocytes. JOURNAL J Biol Chem. 1991; as cited in the PTO-892), in view of in view of Spits et al. referred to as “Spits” herein (WO2015093949A2; published 6/25/2015; with priority to 12/7/2013; cited in IDS filed 10/2/2022). This is a new rejection in view of Applicant’s amendment to incorporate the limitations of claims 3-5 and new limitation “said peptide is coupled to a molecular scaffold or carrier” into independent claim 1, to add new limitations “or inducing” and “introduced into a non-human animal” to claim 7 and to add new claims 13-15.
Regarding claims 1, 2, and 12, Kudo teaches isolating CD43 (referred to as leukosialin) from in vitro host human leukemia cell lines having specific O-glycosylation patterns (entire document). Kudo further teaches that there is a change in the structures of about 80 O-linked oligosaccharide chains depending on different cell lineages as well as at discrete stages of cell differentiation in a given cell lineage (p. 8483, left column). Kudo teaches expressing CD43 from K562 cells (CML cells) (p. 8488, right column, para 4). The limitation “for AT14-013 antibody binding” does not add any additional structural limitations beyond the sequence itself, therefore the CD43 nucleic acid can inherently be used for AT14-013 antibody binding (see entire document). Kudo teaches the CD43 nucleic acid molecule comprising cDNA (abstract). Kudo teaches a nucleic acid molecule, or a functional equivalent thereof, encoding a CD43 peptide said peptide comprising the amino acid sequence of SEQ ID NO: 3 (see sequence alignment below).
(Query is Applicant SEQ ID NO: 3.)
Query 1 GTITTNSPETSSRTSGAPVTTAASSLETSRGTS 33
Sbjct 133 GTITTNSPETSSRTSGAPVTTAASSLETSRGTS 165
(Sbjct is Kudo disclosed sequence.)
However, Kudo does not specifically teach that CD43 peptide having acute myeloid leukemia (AML)-specific or myelodysplastic syndrome (MDS)-specific glycosylation patterns, that the nucleic acid molecule is codon-optimized for a non-human cell, that the nucleic acid molecule comprises a chain comprising non- natural nucleotides, modified nucleotides and/or non-nucleotide building blocks which exhibit the same function as natural nucleotides, that the nucleic acid molecule comprises a DNA/RNA helix, peptide nucleic acid (PNA), locked nucleic acid (LNA) and/or a ribozyme, or that the peptide is coupled to a molecular scaffold or carrier.
Spits teaches human AML-specific binding compounds that are able to bind a cell surface component of AML cells. Therapeutic uses of binding compounds such as antibodies against AML are also provided (entire document).
Regarding claim 1, Spits teaches AML-specific antibodies for binding a cell surface component of AML cells (p. 10, lines 4-24). Spits teaches the AT14-013 antibody derived from AML patients (p. 11, lines 26-30; p. 14, lines 8-34; p. 34; lines 13-26; p.38, lines 27-33). Spits further teaches different AML-specific antibodies that bind different AML subtypes, including MonoMac6, THP-1, and Molm13 cells (Table 3; p. 92, lines 10-14; Example 2). Spits teaches binding compounds suitable for use against acute myeloid leukemia (AML) cells, myelodysplastic syndrome (MDS) cells, chronic myeloid leukemia (CML) cells (abstract; p. 66, lines 19-32). Spits further teaches codon optimization for non-human cells such as E. coli cells, CHO cells, NSA cells or 293T cells, enabling high scale production of binding compounds (p. 48, para 1 and p. 62, para 3). Spits teaches nucleic acid molecules comprising a chain comprising non-natural nucleotides, modified nucleotides and/or non-nucleotide building blocks which exhibit the same function as natural nucleotides (p. 47, lines 23-32). Spits teaches a nucleic acid molecule or functional equivalent comprises a DNA/RNA helix, peptide nucleic acid (PNA), locked nucleic acid (LNA) and/or a ribozyme (p. 47, lines 23-32). Spits teaches pharmaceutical compositions comprising keyhole limpet haemocyanin (KLH), serum albumin, and ovalbumin as carriers (p. 69, lines 8-14).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have isloated the CD43 nucleic acid molecule of Kudo encoding a CD43 peptide from AML and MDS patients, as taught in Spits, with the further modifications and limitations to arrive at the claimed invention. One would have been motivated to do so in order isolate CD43 peptides with AML-specific and MDS-specific glycosylation patterns. Kudo teaches that the CD43 glycosylation patterns differ depending on different cell lineages as well as at discrete stages of cell differentiation in a given cell lineage (p. 8483, left column). Spits teaches different AML-specific antibodies that bind different AML subtypes, including MonoMac6, THP-1, and Molm13 cells (Table 3; p. 92, lines 10-14; Example 2) and further teaches binding compounds suitable for use against AML cells, MDS cells, and CML cells (abstract; p. 66, lines 19-32). Spits further teaches codon optimization for non-human cells, chain modifications, and peptide scaffolds and carriers, see details in the 103 above. One would have had a reasonable expectation of success because Kudo and Spits are directed to CD43 nucleic acids, their isolation, and their use, especially in leukemia cells. Thus, the claimed invention as a whole is prima facie obvious.
Regarding claim 2, Spits teaches codon optimization for a non-human producer cell such as E. coli cells, CHO cells, NSA cells or 293T cells, enabling high scale production of binding compounds (p. 48, para 1 and p. 62, para 3).
Regarding claims 6 and 11, Kudo teaches cloning CD43 nucleic acid molecule into a phage vector, which is also a gene delivery vehicle (see pp. 8483-8484 – Experimental Procedures).
Regarding claim 7, Spits teaches a method for producing or inducing an immune cell and/or an antibody by introduction into a non-human animal for commercial production of antibodies or functional equivalents (p. 62, lines 19-24).
Regarding claim 8, Spits teaches producing immune cells or antibodies able to specifically bind myeloproliferative or lymphoproliferative cells (p. 64, para 1).
Regarding claim 9, Spits teaches that the cells produced or induced are acute myeloid leukemia (AML) cells or myelodysplastic syndrome (MDS) cells or chronic myeloid leukemia (CML) cells (abstract; p. 66, lines 19-32).
Regarding claim 10, Spits teaches that the antibody has antibody-dependent cell-mediated inducing activity or CDC (p. 3, para 3; p. 97, para 1; claims 1 and 3).
Regarding claim 12, Kudo teaches expressing CD43 from K562 in vitro host cells (CML cells) (p. 8488, right column, para 4).
Regarding claims 13-15, Spits teaches methods for binding, detecting, and/or obtaining immune cells or antibodies comprising incubating immune cells or antibodies with acute myeloid leukemia (AML) cells or myelodysplastic syndrome (MDS) cells or chronic myeloid leukemia (CML) cells (abstract; p. 66, lines 19-32; p. 87, lines 19-32; Example 2).
Therefore the invention as a whole would have been prima facie obvious to one of ordinary skill in the art before the effective filing date.
Response to Arguments
Applicant's arguments filed 2/10/2026 have been fully considered but they are not persuasive. Applicant argues that Kudo does not specifically teach that the nucleic acid molecule or functional equivalent has at least one additional feature, comprising of codon optimized for a non-human cell, a chain comprising non-natural nucleotides, modified nucleotides and/or non-nucleotide building blocks which exhibit the same function as natural nucleotides, a DNA/RNA helix, peptide nucleic acid (PNA), locked nucleic acid (LNA) and/or a ribozyme, cDNA, or the peptide is coupled to a molecular scaffold or carrier and therefore, claim 1, and dependent claims thereon, cannot be anticipated by Kudo. The 102 rejection of record has been withdrawn. Accordingly, the arguments are moot.
Regarding the 103 rejection of record, Applicant argues that claims 3-5 are canceled, rendering the rejection moot.
The Office disagrees. The limitations of cancelled claims 3-5 were incorporated into independent claim 1. Additionally, Applicant further incorporated previously unexamined limitation “said peptide is coupled to a molecular scaffold or carrier” into independent claim 1. A new rejection necessitated by all of these amendments is detailed in the 103 rejection above.
Applicant argues that combination of the cited documents fail at least the first and second criterion of the KSR test, because the references fail to provide any suggestion or motivation to arrive at the method recited and the references fail to provide a reasonable expectation of success to arrive at the claimed invention. Applicant further argues that Kudo does not teach isolating CD43 from host human leukemia cells lines having AML-specific glycosylation patterns, but rather expresses their nucleic acid constructs in Jurkat, K562, and CEM cells. Applicant argues that the Kudo reference does not mention AML or MDS, so one of skill in the art would not have been motivated to combine the Kudo and Spits references to arrive at the claimed invention because there is no suggestion that the T-cell leukemia cells, CML cells, and ALL cells function similarly as the AML cells. Applicant argues none of the cited art, either alone or in combination teach or suggest all of the elements of the claims as described, therefore, one of skill in the art would not have a reasonable expectation of success in arriving at the instantly claimed methods.
The Office agrees that the Kudo reference does not specifically mention AML or MDS. However, as detailed in the new 103 rejection above, Kudo teaches that CD43 glycosylation patterns differ depending on different cell lineages as well as at discrete stages of cell differentiation in a given cell lineage (p. 8483, left column). Spits teaches different AML-specific antibodies that bind different AML subtypes, including MonoMac6, THP-1, and Molm13 cells (Table 3; p. 92, lines 10-14; Example 2) and further teaches binding compounds suitable for use against AML cells, MDS cells, and CML cells (abstract; p. 66, lines 19-32). Spits further teaches codon optimization for non-human cells, chain modifications, and peptide scaffolds and carriers, see details in the 103 above. Thus, one would have been motivated to do so in order isolate CD43 peptides with AML-specific and MDS-specific glycosylation patterns. Accordingly, there is (1) a motivation, either in the references themselves or in the knowledge generally available to one of ordinary skill in the art, to modify the reference or to combine the reference teachings and (2) a reasonable expectation of success because both references CD43 nucleic acids, their isolation, and their use, especially in leukemia cells. Therefore the invention as a whole would have been prima facie obvious to one of ordinary skill in the art before the effective filing date.
Double Patenting – new necessitated by amendment
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claim 1 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-9 of U.S. Patent No. 11524989. This rejection is modified to reflect Applicant’s incorporation of limitations from claims 3-5 into claim 1 and amendment of claim 7.
Although the claims at issue are not identical, they are not patentably distinct from each other because there is significant overlap in the claims.
Claims 1-9 of the ‘989 patent encompass a recombinant or purified CD43 peptide for AT14-013 antibody binding, said peptide comprising: the amino acid sequence of SEQ ID NO: 3, wherein said peptide has an AML-specific glycosylation pattern or an MDS-specific glycosylation pattern, and wherein the peptide is coupled to a molecular scaffold or a carrier (instant claim 1).
Therefore, claims 1-9 of the ‘989 patent anticipate instant claim 1 .
Claims 2 and 6-15 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-9 of U.S. Patent No. 11524989 in view of Spits (WO2015093949A2). This rejection is modified to reflect Applicant’s cancellation of claims 3-5, incorporation of limitations from claims 3-5 into claim 1, amendment of claim 7, and addition of new claims 13-15.
Claims 1-9 of the ‘989 patent encompass a recombinant or purified CD43 peptide for AT14-013 antibody binding, said peptide comprising: the amino acid sequence of SEQ ID NO: 3, wherein said peptide has an AML-specific glycosylation pattern or an MDS-specific glycosylation pattern, and wherein the peptide is coupled to a molecular scaffold or a carrier (instant claim 1).
However, claims 1-9 of the ‘989 do not specifically teach codon optimization for a non-human producer cell, the nucleic acid molecule or functional equivalent comprises a DNA/RNA helix, peptide nucleic acid (PNA), locked nucleic acid (LNA) and/or a ribozyme, that the nucleic acid molecule comprises cDNA, a vector comprising the nucleic acid molecule (claim 6), a method for producing or inducing an immune cell and/or an antibody characterized in that a nucleic acid molecule or functional equivalent of claim 1 is introduced to a non-human animal (claim 7), producing or inducing immune cells and/or antibodies able to specifically bind myeloproliferative cells, AML, MDS, or CML cells (claims 8-9), the antibody has antibody-dependent cell-mediated inducing activity or CDC (claim 10), a gene delivery vehicle comprising the nucleic acid (claim 11), or a host cell comprising the nucleic acid (claim 12), method for binding, detecting and/or obtaining an immune cell or antibody, or a functional part or functional equivalent thereof, comprising the steps of expressing a nucleic acid molecule or functional equivalent of claim 1, and incubating an immune cell or antibody, or a functional part or functional equivalent thereof, with the expressed CD43 peptide (new claim 13), wherein said immune cell and/or said antibody, or a functional part or functional equivalent thereof, specifically binds myeloproliferative or lymphoproliferative cells (new claim 14), and wherein said myeloproliferative cells are AML cells or MDS cells or CML cells (new claim 15).
The teachings of Spits are applied to claims 2 and 6-15 as discussed in the 103 rejection above. Spits teaches codon optimization for a non-human producer cell (claim 2), producing antibodies able to specifically bind and/or detect AML myeloproliferative cells (claims 8-9), and that the antibody has antibody-dependent cell-mediated inducing activity or CDC (claim 10). Regarding claim 5-6 and 11-12, Spits further teaches generating cDNA and cloning into a vector into host cells (p. 87, para 2). Regarding new claims 13-15, Spits teaches methods for binding, detecting, and/or obtaining immune cells or antibodies comprising incubating immune cells or antibodies with acute myeloid leukemia (AML) cells or myelodysplastic syndrome (MDS) cells or chronic myeloid leukemia (CML) cells (abstract; p. 66, lines 19-32; p. 87, lines 19-32; Example 2).
It would have been obvious to have modified the nucleic acid of the ‘989 patent, especially the codon-optimized CD43 cDNA into a vector and expressing in helper cells. One would have been motivated to clone the codon-optimized CD43 cDNA into a vector because Spits teaches that the codon optimization for helper cells enables high scale production of CD43 antibodies. It would have been further obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have isolated the nucleic acid of the ‘989 patent from AML and MDS patients, as taught in Spits, with the further modifications and limitations to arrive at the claimed invention. One would have been motivated to do so in order isolate CD43 peptides with AML-specific and MDS-specific glycosylation patterns. Spits teaches different AML-specific antibodies that bind different AML subtypes, including MonoMac6, THP-1, and Molm13 cells (Table 3; p. 92, lines 10-14; Example 2) and further teaches binding compounds suitable for use against AML cells, MDS cells, and CML cells (abstract; p. 66, lines 19-32). Spits further teaches codon optimization for non-human cells, chain modifications, and peptide scaffolds and carriers, see details in the 103 above. One would have had a reasonable expectation of success because the ‘989 patent and Spits are directed to CD43 nucleic acids, their isolation, and their use, especially in leukemia cells. Thus, the claimed invention as a whole is prima facie obvious.
Response to Arguments
Applicant's arguments filed 2/10/2026 have been fully considered but they are not persuasive. Applicant requests that the rejection be held in abeyance until allowable subject matter is identified. However, such a response is not a proper reply to the outstanding rejection of record.
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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to KHALEDA B HASAN whose telephone number is (571)272-0239. The examiner can normally be reached IFP, Monday - Friday 7:30am-5pm.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Neil Hammell can be reached at (571) 270-5919. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/KHALEDA B HASAN/Examiner, Art Unit 1636
/BRIAN WHITEMAN/Primary Examiner, Art Unit 1636
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