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 .
Priority Claim
This instant application, filed on 09 August, 2023, claims domestic benefit to US provisional application no. 63/371,077, filed on 11 August, 2022.
Status of Application
The response filed on 13 July, 2026 has been entered in full. The response is an amendment to a Non-Final Rejection to the claim set filed on 09 August, 2024. In the amendment no amendments or withdrawals to the claims have been made. Therefore, claims 1-20 are pending and are the subject of this office action.
Status of Objections and Rejections
In the office action of 02/11/2026
Claims 1, 2, 5, 7, 16, 17, and 19 were rejected under 35 U.S.C. 103 over Hean et al. in view of Ferrer et al. The rejections of the claims still stand with expanded clarification on how to art teaches the claim supported by evidenced by Sun et al. which is the source relied upon in the original prior art.
Claims 3 and 4 were rejected under 35 U.S.C. 103 over Hean et al. in view of Ferrer as applied to claim 1 and further in view of Lee et al. as evidenced by Uniprot. The rejections of the claims still stand.
Claims 8, 13, 15, and 18 were rejected under 35 U.S.C. 103 over Hean et al. in view of Ferrer as applied to claim 1, 7, and 17 and further in view of Lee and Choi. The rejections of the claims still stand.
Claims 9, 10, and 20 were rejected under 35 U.S.C. 103 over Hean et al. in view of Ferrer as applied to claim 1 and further in view of Yang et al. The rejections of the claims still stand.
Claim 11 was rejected under 35 U.S.C. 103 over Hean et al. in view of Ferrer as applied to claim 1 and further in view of Ma et al. The rejection of the claim still stands.
Claim 12 was rejected under 35 U.S.C. 103 over Hean et al. in view of Ferrer as applied to claims 1, 4, and 11 and further in view of Veltman et al., Oren et al., Li et al., and Dooley et al. The rejection of the claim still stands.
Claim 14 was rejected under 35 U.S.C. 103 over Hean et al. in view of Ferrer as applied to claim 1 and further in view of Crane et al. The rejection of the claim still stands.
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.
Claims 1, 2, 5, 7, 16, 17, and 19 are rejected under 35 U.S.C. 103 as being unpatentable over Hean et al. (WO2017203260) in view of Ferrer et al. (2021) HIF-Overexpression and Pro-Inflammatory Priming in Human Mesenchymal Stromal Cells Improves the Healing Properties of Extracellular Vesicles in Experimental Crohn’s Disease Int. J. Mol. Sci. (22) 11269 (hereafter Ferrer) as evidenced by Sun et al. (2020) HIF-1α overexpression in mesenchymal stem cell-derived exosomes mediates cardioprotection in myocardial infarction by enhanced angiogenesis Stem Cell Research and Therapy 11:373.
In regards to claims 1, 16, and 17, Hean teaches an extracellular vesicle (EV) comprising one or more polypeptide which can include one or more polynucleotides of interest (POI) (pg.4, lines 19-20), a cis cleaving polypeptide (intein) (pg.5, lines 14-17) and one or more exosomal polypeptide (pg.4, lines 21-22).
In regards to claim 5, Hean teaches the list of potential exosomal polypeptides which include, CD9, CD53, CD63, CD81, CD54, CD50, FLOT1, FLOT2, CD49d, CD71, CD133, CD138, CD235a, ALIX, Syntenin-1, Syntenin-2, Lamp2b, TSPAN8, TSPAN14, CD37, CD82, CD151, CD231, CD102, NOTCH1, NOTCH2, NOTCH3, NOTCH4, DLL1, DLL4, JAG1, JAG2, CD49d/ITGA4, ITGB5, ITGB6, ITGB7, CD11a, CD11b, CD11c, CD18/ITGB2, CD41, CD49b, CD49c, CD49e, CD51, CD61, CD104, Fe receptors, interleukin receptors, immunoglobulins, MFIC-I or MFIC-II components, CD2, CD3 epsilon, CD3 zeta, CD13, CD18, CD19, CD30, CD34, CD36, CD40, CD40L, CD44, CD45, CD45RA, CD47, CD86, CD110, CD111, CD115, CD117, CD125, CD135, CD184, CD200, CD279, CD273, CD274, CD362, COL6A1, AGRN, EGFR, GAPDH, GLUR2, GLUR3, HLA-DM, HSPG2, LI CAM, LAMB1, LAMC1, LFA-1, LGALS3BP, Mac-1 alpha, Mac-1 beta, MFGE8, SLIT2, STX3, TC RA, TCRB, TCRD, TCRG, VTI1A, VTM B, and any combinations thereof (pg.12, lines 14-26).
In regards to claim 7, Hean teaches attaching targeting moieties to the polypeptide to enhance the therapeutic potential by targeting tissue or cell types of interest (pg.17, lines 15-18).
In regards to claim 19, Hean teaches using the polypeptide constructs for therapeutic purposes depending on the POI to treat various diseases which include Crohn’s disease, ulcerative colitis, rheumatoid arthritis, multiple sclerosis, lupus, psoriasis, ARDS, sepsis, GVDH, and neurodegenerative diseases (pg.29, lines 3-17).
Hean fails to teach the HIF-1α polypeptide construct and the method for inducing resolutive macrophages of claims 1, 16, and 17. Further Hean fails to teach the modified polarization of macrophages to favor resolutive macrophages and/or the modified balance of macrophage subtypes and/or the indued differentiation of monocytes to resolutive macrophages and/or induced phenotype switching of macrophages of claim 2.
Ferrer, however, teaches in regards to claims 1, 16, and 17 an EV with the overexpression of HIF-1α which is capable of repolarization of M1 macrophages to M2-like macrophages (resolutive macrophages) (abstract). The EVs are derived from MSCs genetically engineered to overexpress HIF-1α using lentivirus which subsequently overexpresses HIF-1α in the EVs (pg.13, lines 39-42 /pg.2, lines 17-19), which is further evidenced by the source relied upon in Ferrer, Sun et al. (source 15), which uses the same technique and demonstrates this method overexpresses HIF-1α on EVs (pg.3, col 1, lines 9-36/ pg.3, col 2, lines 1-31 / Supplemental Figure 2).
In regards to claim 2, Ferrer teaches the EVs with overexpressed HIF-1α had significant greater repolarization capacity on macrophages (pg.4, lines 15-16), as well as demonstrated their ability to significantly increase M2-like macrophages (pg.4, lines 12-15).
It is also noted that Ferrer further supports the teachings of Hean in regards to claim 19 by showing the effectiveness of an EV with overexpressed HIF-1α in the treatment of Chron’s disease (pg.13, lines 25-26).
Thus, Hean discloses an EV therapeutic which consists of a polypeptide which comprises, one or more EV polypeptide, a Cis cleaving Intein, and one or more polypeptide of interest. Further Hean discloses the utilization of a targeting moiety and highlights the different inflammatory conditions this therapeutic would be useful for. Ferrer teaches that HIF-1α overexpression on the surface of EVs can induce a M2-like phenotype in macrophages from a M1-like phenotype. Therefore, a person of ordinary skill in the art before the effective filing date of the claimed invention would have found it obvious to combine the teachings of Hean with the teachings of Ferrer with a reasonable expectation of success to develop a polypeptide which expresses HIF-1α, one or more EV polypeptide, and an Intein on an EV to induce resolutive macrophages for the treatment of various inflammatory conditions.
Claims 3 and 4 are rejected under 35 U.S.C. 103 as being unpatentable over Hean in view of Ferrer as applied to claim 1 above, and further in view of Lee et al. (2006) Differential responses of two degradation domains of HIF-1α to hypoxia and iron deficiency Biochimie (88) 163-169 (hereafter Lee) as evidenced by Uniport Accession B2R617(2008).
Hean in view of Ferrer fails to teach a HIF-1α fragment which defects the oxygen-dependent degradation domain, however, In regards to claim 3 Lee teaches that HIF-1α mutations in the ODD stabilized HIF-1 expression in normoxic conditions when compared to its wild type counter parts (pg.166 col 1, lines 1-21/ Figure 1).
In regards to claim 4, Lee teaches that the ODD domain is between amino acid (aa) residues 390 and 582 (Figure 1). Further Lee teaches deletions of the ODD domain in various ways impacts HIF-1α stability in normoxic and hypoxic conditions (pg.166 col 1, lines 1-21/ Figure 1). When SEQ ID NO 3 of instant claim is aligned to the aa sequence for Human HIF-1α (Uniport ID: B2R617, released in 2008) the variant of the HIF-1α contains a deletion of the ODD (see Examiner Figure 1, below).
Thus, Hean in view of Ferrer discloses an EV expressing one or more polypeptide comprising HIF-1α, one or more EV polypeptide, and an Intein for the purpose of inducing resolutive macrophages and Lee teaches ODD defects (including deletion) in HIF-1α to increase their stability in normoxic conditions. Therefore, a person of ordinary skill in the art before the effective filing date of the claimed invention would have found it obvious to combine the teachings of Hean in view of Ferrer and Lee with a reasonable expectation of success to get the expected results of an EV expressing a polypeptide comprising a HIF-1α variant in which the ODD is defected (such as the deletion of instant application SEQ ID NO: 3) for increased stability in normoxic conditions.
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Examiner Figure 1: Alignment of instant application SEQ ID NO: 3 to Human HIF-1α.
Claim 6 is rejected under 35 U.S.C. 103 as being unpatentable over Hean in view of Ferrer as applied to claim 1 above, and further in view of Green et al. (2018) The dynamic intein landscape of eukaryotes Mobile DNA (9) 4 (hereafter Green) .
Hean in view of Ferrer fails to teach the monomeric cis-cleaving intein originating from the protein selected from the group consisting of Prp8, VMA1, DdRP, ThrRs, GLT, CHS, IF2, e1F5B, DnaB, ClpP, RIR, Helicase, and MutS-like. Green however teaches that these inteins are the most common inteins in nuclear (nDNA), chloroplast (cpDNA), and eukaryotic virus (vDNA) genomes (Table 1).
Thus, Hean in view of Ferrer discloses an EV expressing one or more polypeptide comprising HIF-1α, one or more EV polypeptide, and an Intein for the purpose of inducing resolutive macrophages and Green teaches the most common inteins for self-excision. Therefore, a person of ordinary skill in the art before the effective filing date of the claimed invention would have found it obvious to combine the teachings of Hean in view of Ferrer with the teachings in Green with a reasonable expectation of success to get an EV expressing one or more polypeptide comprising HIF-1α, one or more EV polypeptide, and an Intein wherein the intein is well known and functional.
Claims 8, 13, 15, and 18 are rejected under 35 U.S.C. 103 as being unpatentable over Hean in view of Ferrer as applied to claims 1, 7, and 17 above, and further in view of Lee and Choi (2018) Macrophages and Inflammation J Rheum Dis (25) 1 (hereafter Lee and Choi).
Hean in view of Ferrer fails to teach the targeting moieties targeting one or more monocytes and/or monocyte-derived macrophage of claim 8. Hean in view of Ferrer also fails to teach the subject is in a status of (a) increased M1 and/or M1- like macrophages compared to normal conditions and/or (b) inflammatory condition accompanying increased proportion and/or increased number of monocytes-derived macrophage compared to normal conditions of claims 13 and 18. Further Hean in view of Ferrer fails to teach the resolutive macrophage selected from the group consisting of a pro-efferocytic and an anti-oxidant macrophage of claim 15.
However, Lee and Choi in regards to claim 8 states that monocytes differentiate and into tissue resident macrophages when stimulated (pg.13, col 1, lines 1-3), and further teaches the heterogeneity in function of macrophages is important for successful resolution of inflammation (pg.17, col 1, lines 37-39). Lee and Choi also teach that targeting specific macrophage subsets presents a novel treatment strategy for rheumatoid arthritis (pg.16. col 1, lines 23-24).
In regards to claims 13 and 18, Lee and Choi teach when the stress or malfunction of a tissue is extreme, local macrophages may be insufficient to resolve the situation in which case additional macrophages might be recruited (pg.15, col 1, line 46). Lee and Choi also teach that in M1- macrophages drive pro-inflammatory conditions (pg.13, col 1, lines 13-22) and are increased in inflammatory diseases such as in rheumatoid arthritis (pg.15, col 2, lines 45-46), and systemic lupus erythematosus (pg.16, col 2, lines 21-22).
In regards to claim 15, Lee and Choi teach that M2 macrophages can fall within different subsets (Table 1). Further Lee and Choi teach that M2a macrophages high levels of Arginase, a pro efferocytosis cytokine (Specification, pg.18, lines 9-11), and plays a significant role in debris removal (Table 1). Lee and Choi also teach the M2b macrophages secrete high levels of IL-1β, an anti-oxidative cytokine (Specification, pg.18 lines 18-21) and further are regulatory macrophages (Table 1).
Thus, Hean in view of Ferrer discloses an EV expressing one or more polypeptide comprising HIF-1α, one or more EV polypeptide, and an Intein for the purpose of inducing resolutive macrophages. Hean in view of Ferrer also discloses adding a targeting moiety to the polypeptide. Lee and Choi teach targeting macrophages for the treatment of inflammatory conditions, the increased infiltration of macrophages and the skewed M1 phenotype of macrophages in inflammatory conditions, and further the different M2 macrophage subsets which include pro-efferocytic and anti-oxidative. Therefore, a person of ordinary skill in the art before the effective filing date of the claimed invention would have found it obvious to use the teachings of Hean in view of Ferrer informed by the teachings of Lee and Choi with a reasonable expectation of success to an EV expressing one or more polypeptide comprising HIF-1α, one or more EV polypeptide, and an Intein with the addition of a targeting moiety and further to treat subjects with skewed M1 macrophage phenotypes with macrophages selected for their pro-efferocytic or anti-oxidative properties.
Claims 9, 10, and 20 are rejected under 35 U.S.C. 103 as being unpatentable over Hean in view of Ferrer as applied to claim 1 above, and further in view of Yang et al. (2018) Extracellular vesicles as a platform for membrane-associated therapeutic protein delivery Journal of Extracellular Vesicles (7) 1440131 (hereafter Yang).
Hean in view of Ferrer fails to teach the polypeptide construct further comprising a fusogenic peptide in which the fusogenic peptide is selected from the group consisting of (GALA)n (n is integer from 1 to 10), (KALA)n (n is integer from 1 to 10), INF7, influenza virus HA2, melittin, octa-arginine (R8) peptide, vesicular stomatitis virus glycoprotein (VSV-G), tat protein of HIV, HSV-1 gB, EBV gB, thgoto virus G protein, and AcMNPV gp64.
Yang, however, teaches the use of fusogenic proteins (peptides) on exosomes (EVs) to control the function of membrane proteins and developing therapeutic vehicles for membrane protein delivery (pg.7 , col 2, lines 9-12). Yang also teaches a fusogenic exosome harboring the viral fusogen, vascular stomatitis virus (VSV)-G protein, which can fuse with and modify plasma membranes which further effectively transferred GFP-tagged CD63 to plasma membranes (pg.7, col 2, lines 21-31).
Thus, Hean in view of Ferrer discloses an EV expressing one or more polypeptide comprising HIF-1α, one or more EV polypeptide, and an Intein for the purpose of inducing resolutive macrophages. Further, Yang teaches the addition of a fusogenic peptide to deliver proteins to the membrane and control the function of the membrane proteins and further demonstrates the success of VSV-G. Therefore, a person of ordinary skill in the art before the effective filing date of the claimed invention would have found it obvious to combine the teachings of Hean in view of Ferrer and Yang with a reasonable expectation of success to get a polypeptide with increased therapeutic ability through membrane protein delivery and membrane protein function control.
Claim 11 is rejected under 35 U.S.C. 103 as being unpatentable over Hean in view of Ferrer as applied to claim 1 above, and further in view of Ma et al. (2017) (US Pat No. 9,796,9567).
Hean in view of Ferrer fails to teach the monomeric cis-cleaving intein comprised of SEQ ID NO: 2, however, Ma teaches a cis-cleaving intein comprised of the sequence (SEQ ID NO: 17/ col 77/79) and further shows it attached to a zinc binding motif to demonstrate is functionality (Fig 17.)
Thus, Hean in view of Ferrer discloses an EV expressing one or more polypeptide comprising HIF-1α, one or more EV polypeptide, and an Intein for the purpose of inducing resolutive macrophages. Further, Ma teaches an intein comprising the sequence of SEQ ID NO 2. Therefore, a person of ordinary skill in the art before the effective filing date of the claimed invention would have found it obvious to combine the teachings of Hean in view of Ferrer and Ma with a reasonable expectation of success to get an EV expressing one or more polypeptide comprising HIF-1α, one or more EV polypeptide, and an Intein of SEQ ID NO: 2.
Claim 12 is rejected under 35 U.S.C. 103 as being unpatentable over Hean in view of Ferrer, Lee, and Ma as applied to claims 1, 4, and 11 above, and further in view of Veltman et al. (2009) A new set of small, extrachromosomal expression vectors for Dictyostelium discoideum Plasmids (61) 110-118 (hereafter Veltman), Oren et al. (1990) TAPA-1, the Target of an Antiproliferative Antibody, Defines a New Family of Transmembrane Proteins Molecular and Cellular Biology (10) 8 4007 – 4015 (hereafter Oren), Li et al. (2004) GALA: a designed synthetic pH-responsive amphipathic peptide with applications in drug and gene delivery Advanced Drug Delivery Reviews (56) 967-985 (hereafter Li), and Dooley at al. (2021) A versatile platform for generating engineered extracellular vesicles with defined therapeutic properties Molecular Therapy (29) 5 (hereafter Dooley).
Hean in view of Ferrer, Lee, and Ma fails to teach the HIF-1α variant of instant application as well as the Intein of instant application SEQ ID NO: 2. Both of these sequences are encompassed in the polypeptide constructs of instant claim 12’s SEQ ID NOs: 4, 8, 9, and 10.
Hean in view of Ferrer, Lee, and Ma fail to teach the other components of the polypeptide sequences (See Examiner Figure 2, below).
However, In regards to instant application SEQ ID NOs: 4, 8, 9, and 10 Veltman teaches the partial FLAG tag from vector pDM320 (Table 1 and Table 2) (aa residues 1-9 of the instant application) for the use in modifiable expression vectors for the purpose of immune blotting (pg.111 col 1, lines 16-18). Veltman fails to teach the CD-81 sequence of SEQ ID NOs: 4 and 8, the GALA sequence of SEQ ID NOs: 8 and 10, and the Fragmented PTGFRN (ESM) sequence of SEQ ID NOs: 9 and 10.
However, Oren in regards to instant application SEQ ID NOs: 4 and 8 teaches the amino acid sequence of TAPA-1 (CD-81) (Figure 3). Oren fails to teach , the GALA sequence of SEQ ID NOs: 8 and 10, and the Fragmented PTGFRN (ESM) sequence of SEQ ID NOs: 9 and 10
However, Li teaches in regards to SEQ ID NOs: 8 and 9 the sequence of the fusogenic protein GALA (pg.970 col 2, lines 5-8) and further its benefit as a viral fusion binding protein (abstract). Li fails to teach the ESM sequence of SEQ ID NOs: 9 and 10.
Dooley however, teaches generating extracellular vesicles with truncated PTGFRN (abstract) as scaffolds to display proteins of interest on the surface (pg.1735 col 1, lines 2-4) with similar functionality to the full-length protein (pg.1732 col 2, lines 11-12).
Thus, Hean in view of Ferrer, Lee, and Ma disclose the HIF-1α variant and the Intein of the claimed sequences in the instant application, Veltman teaches the FLAG Tag of the instant application sequences, Oren teaches the CD-81 sequence of instant application SEQ ID NOs: 4 and 8, Li teaches the GALA of instant application SEQ ID NOs: 8 and 9, and Dooley teaches the functionality of ESM. Therefore, a person of ordinary skill in the art before the effective filing date of the claimed invention would have found it obvious to combine the teachings of Hean in view of Ferrer, Lee, and Ma with the different taught protein sequences of Veltman, Oren, Li, and Dooley with a reasonable expectation of success to construct all of the polypeptide constructs claimed in instant claim 12.
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Examiner Figure 2: Sequences components of peptide constructs for (A) SEQ ID NO: 4 and (B) SEQ ID NO: 10
Claim 14 is rejected under 35 U.S.C. 103 as being unpatentable over Hean in view of Ferrer as applied to claim 1 above, and further in view of Crane et al. (2014) The Monocyte to Macrophage Transition in the Murine Sterile Wound PLoS ONE 9(1): e86660 (hereafter Crane).
Hean in view of Ferrer fails to teach selecting the resolutive macrophages selected from the group consisting of a Ly6C(low) macrophage and a MerTK-positive macrophage. Crane, however, teaches that the creation of Ly6C(low) macrophages and MerTK-positive macrophages happens on a time dependent manner (abstract). Ly6C(low) macrophages arise first and promote angiogenesis and fibrosis (pg.10, col 1, lines 1-3). MerTK-positive macrophages arise later and possess the ability to clear early apoptotic cells (pg.11, col 2, lines 4-8).
Thus, Hean in view of Ferrer discloses an EV expressing one or more polypeptide comprising HIF-1α, one or more EV polypeptide, and an Intein for the purpose of inducing resolutive macrophages and Crane teaches macrophage subsets Ly6C(low) and MerTK-positive, and their different functions in wound healing. Therefore, a person of ordinary skill in the art before the effective filing date of the claimed invention would have found it obvious to combine the teachings of Hean in view of Ferrer and Crane with a reasonable expectation of success to develop an EV expressing one or more polypeptide comprising HIF-1α, one or more EV polypeptide, and an Intein for the purpose of inducing resolutive macrophages, wherein the macrophages selected are Ly6C(low) or MerTK-positive to promote the desired wound healing effects.
Response to Arguments
Applicant's arguments filed 13 July, 2026 have been fully considered but they are not persuasive.
In response to applicant’s argument that “Ferrer does not disclose that HIF-1α itself is incorporated into the resulting EVs or displayed on their surface” (Applicant Remarks, 07/13/2026, pg.2, lines 14-15), the prior art does teach implicitly overexpression of HIF-1αin EVs by its reference to prior work by themselves and other authors which shows lentiviral transduction of MSCs leading to overexpression in EVs as outlined above in the expanded 103 rejection. Hean further supports this teaching, highlighting there are different methods to load exosomes with polypeptide based therapeutics which includes transfection of the parental cell with a construct and harvesting of exosomes comprising the biotherapeutic polypeptide (pg.1, lines 22-25).
In response to applicant's argument that “Crane does not disclose any therapeutic method, engineered agent, or exogenous mechanism for inducing or increasing macrophage populations” (Applicant Remarks, 07/13/2026, pg.4, lines 13-16). The applicant's argument is against the reference 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). While crane does not supply a method or exogenous mechanism it supplied the teaching that Ly6C(low) and MerTK-positive macrophages play significant roles in wound healing specifically in angiogenesis, fibrosis, and clearance providing a motivation to select the specific macrophage phenotype, while Hean in view of Ferrer provides the teaching of a method of using EVs to induce specific macrophage phenotypes. Further, the test for obviousness is not whether the features of a secondary reference may be bodily incorporated into the structure of the primary reference; nor is it that the claimed invention must be expressly suggested in any one or all of the references. Rather, the test is what the combined teachings of the references would have suggested to those of ordinary skill in the art. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981).
In response to applicant's argument that the examiner's conclusion of obviousness in regards to claim 14’s combination of Hean, Ferrer and Crane is based upon improper hindsight reasoning (Applicant Remarks 07/13/2026, pg.5, lines 1-4), it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
Conclusion
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.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to DASIA A ALDARONDO whose telephone number is (571)272-1977. The examiner can normally be reached on Monday – Friday from 8:30am to 4:30pm.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Joanne Hama, can be reached at telephone number (571)272-1977. The fax phone number for the organization where this application or proceeding is assigned is (571)273-8300.
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/D.A.A/Examiner, Art Unit 1647 /JOANNE HAMA/Supervisory Patent Examiner, Art Unit 1647
Prosecution Insights