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 .
Status of the Claims
Claims 1, 3-4, 12-18, 32-35, 48-50, 54-55, and 59 are pending.
Claims 1, 34-35 and 55 are newly amended.
Claims 1, 3-4, 12-18, 32-35, 48-50, 54-55, and 59 have been examined on their merits.
Withdrawn Objections & Rejections
The objections and rejections presented herein represent the full set of objections and rejections currently pending in the application. Any objections or rejections not specifically reiterated are hereby withdrawn.
The rejection of claims 1, 3-4, 12-18, 32-35, 48-50, and 54-59 under 35 U.S.C. 103 as being unpatentable over Costa Fejoz et al. (WO2017182585 A1, 2017, previously cited) in view of Kingsman et al. (WO2008071959, 2008, on IDS 07/12/2021, previously cited) and Follenzi et al. (Human Gene Therapy, 2002, previously cited) as evidenced by Transfiguracion et al. (Molecular Therapy: Methods & Clinical Development, 2020, previously cited) is withdrawn in order to address the claimed as amended and in order to incorporate Chapel-Fernandes et al. (Cancer Gene Therapy, 2006 and Circosta et al. (Human Gene Therapy, 2009).
Claim Rejections - 35 USC § 103
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 1, 3-4, 12-18, 32-35, 48-50, 54, and 59 are rejected under 35 U.S.C. 103 as being unpatentable over Costa Fejoz et al. (WO2017182585 A1, 2017, previously cited) in view of Kingsman et al. (WO2008071959, 2008, on IDS 07/12/2021, previously cited) and of Chapel-Fernandes et al. (Cancer Gene Therapy, 2006) as evidenced by Transfiguracion et al. (Molecular Therapy: Methods & Clinical Development, 2020, previously cited).
In regards to claims 1, 3, 12-15, and 48, in regards to a “fusosome”, the specification defines this term as a ”bilayer of amphipathic lipids enclosing a lumen or cavity and a fusogen that interacts with the amphipathic lipid bilayer” (specification, paragraph [0154]).
In regards to a “fusogen” the specification defines this term as “an agent or molecule that creates an interaction between two membrane enclosed lumen” (specification, paragraph [0156]).
Turning to the art, Costa Fejos teaches lentiviral vectors (Abstract; claims 1 and 2; Figs. 7 and 8).
As taught by Costa Fejos, these vectors comprise lumina or cavities (Figs. 7 and 8), and as evidenced by Transfiguracion, lentiviral vectors are surrounded by a lipid bilayer (Introduction, p803), which a person of ordinary skill in the art would have recognized is an amphipathic lipid bilayer.
As further taught by Costa Fejos these vectors comprise cell-targeting (a person of ordinary skill in the art would have recognized that cells have amphipathic lipid bilayers) fusion proteins (claims 1 and 2), which sit in the lipid bilayer (Figs. 7 and 8), and therefore, interacts with it.
Therefore, because the lentiviral vectors as taught by Costa Fejos are bilayer of amphipathic lipids enclosing a lumen or cavity and a fusogen that interacts with the amphipathic lipid bilayer, as defined above, they are fusosomes.
It is also noted that the instant specification explicitly states that fusosomes can include lentiviral vectors or particles (paragraph [0006]).
In regards to part (a), as discussed above, the lentiviral vector (fusosome) as taught by Costa Fejos above, comprises a lipid bilayer and a fusogen.
As further taught by Costa Fejos, the fusosome vector is pseudo-typed and comprises targeting fusion proteins (moieties) derived from Paramyxoviridae (Abstract; claims 1 and 2). It is well-understood in the art that pseudo-typing refers to replacing surface proteins with the surface proteins of another type of virus, and thus the pseudo-typed fusosome vectors as disclosed by Costa Fejos are “re-targeted” (see instant specification, paragraph [0166]).
In regards to the property of whether the fusosome vector of Costa Fejos leads to increased delivery of an exogenous agent compared to a non-target cell, Costa Fejos teaches that the fusosome vector selectively modulate the activity of specific subsets of cells (Abstract; p2, lines 26-36, p3, lines 1-3), and demonstrates that particles selectively activate and targeted T cells (by introducing transgenes, which are exogenous agents) over other cells (in which exogenous transgenes are not introduced) (Brief description of the figures, p41-42; Figs. 1 and 6).
Therefore, the composition of Costa Fejos has the property of increased delivery of an exogenous agent compared to a non-target cell.
In regards to part (b)(i), Costa Fejos teaches that the fusosome vector can comprise nucleic acids, including plasmids (which are exogenous agents), comprising at least promoters (p25, lines 20-35), which the instant specification indicates is a “positive target cell-specific regulatory element” (see instant paragraph [0162]).
In regards to whether this has the property of increasing expression of the exogenous agent in a target cell or tissue relative to an otherwise similar fusosome lacking the positive target cell-specific regulatory element, similarly to as above, Costa Fejos demonstrates that particles selectively activate and targeted T cells (by introducing transgenes, which are exogenous agents) over other cells (in which exogenous transgenes are not introduced) (Brief description of the figures, p41-42; Figs. 1 and 6).
Therefore, the composition of Costa Fejos has the property of increased expression of the exogenous agent in a target cell or tissue relative to an otherwise similar fusosome lacking the positive target cell-specific regulatory element.
While Costa Fejos teaches that the fusosome particle may modulate the activity of specific subsets of cells (positive targets), and in particular immune cell (Abstract; Abstract; Description of the invention, p2-3), and teaches that these cells can be targeted with nucleic acid regulatory elements such as promoter (p25, lines 20-35), Costa Fejos does not explicitly teach that the regulatory element comprises a tissue-specific enhancer.
However, a person of ordinary skill in the art would have been motivated to include a tissue-specific enhancer in order to ensure that correct targets are hit, while avoiding off-target effects, and therefore increasing efficacy in gene therapy uses.
They would also have been motivated to include a tissue-specific enhancer because Chapel-Fernandes teaches that tissue-specific enhancers, including prostate-specific enhancers (which are not liver), restricts transgene expression to specific cells (e.g., PSA-secreting cells) and improves tissue-specific expression in these tissues in a lentiviral vector context (Abstract, p919; Introduction, p919-920; Fig. 1, p921). Furthermore, because Chapel-Fernandes demonstrates that lentiviral vectors can be constructed with tissue-specific promoters which are not liver (Fig. 1, p921) and because Costa Fejos and Chapel-Fernandes are in the same technical field of using lentiviral vectors to deliver exogenous DNA to target-cells for cell therapy for gene therapy, it could have been done with predictable results and a reasonable expectation of success.
In regards to part (b)(ii), Costa Fejos does not explicitly teach that the fusosome vector also comprises a non-target cell-specific regulatory element linked to the nucleic acid encoding the exogenous agent.
However, a person of ordinary skill in the arts would have been predictably motivated to include non-target specific regulatory elements because as taught by Kingsman, one concern with vectors as potential therapeutic agents is background expression in non-target cells (p5, last sentence). To this end, Kingsman teaches a method for silencing transgene expression in non-target cells (specifically muscle cells, which are non-cancerous) using tissue-specific miRNA, and that this restricts expression of transgenes (such as therapeutic genes) in non-target cells (p6, top paragraph; p36, miRNA). Kingsman also teaches that miRNAs can be encoded into vectors of interest (the exogenous agent) (p36, miRNA), which may comprise regulatory sequences (p16, middle paragraph) and in a UTR (p6, second paragraph). A person of ordinary skill in the art would have been motivated to include these elements, because Kingsman indicates that they restrict transgene (an exogenous agent) to target cells (p1, Field of the Invention).
In regards to the property of decreased expression of the exogenous agent in a non-target cell or tissue relative to an otherwise similar fusosome lacking the non-target cell-specific regulatory element, since Kingsman teaches that it is known in the art that transfection systems can be used to down-regulate (decrease) gene expression, without affecting other cell types (p6, second paragraph) and that the promoter can be specifically engineered to decrease levels of expression of a nucleotide sequence (p15, first paragraph), it would be expected that the non-target cell-specific regulatory element would in fact decrease expression of an exogenous agent.
In regards to claim 4, in regards to the property of fusing at a higher rate with a target than a non-target, Costa Fejos demonstrates that particles (fusosomes) not only selectively activate and transduce (gene transfer, an exogenous agent) targeted T cell subsets, but that after 3 days (72 hours) about 39% (which overlaps with the ranges as in claim 4) had been transfected (Brief description of the figures, p41-42; Figs. 1 and 6). Therefore, the composition of Costa Fejos in fact fuses with a target cell as in claim 4.
In regards to claim 16, Costa Fejos teaches that fusosome (a retroviral vector, of which the lentiviral vector as taught by Costa Fejos is a type) can comprise an RNA that is not derived from the virus (Pseudotyped retrovirus-like particle or retroviral vector, p6) and is thus an exogenous RNA.
In regards to claim 17, it is noted that claim 17 allows for “a first immunostimulatory protein that is absent . . . and a second immunostimulatory protein that is absent”. Thus, claim 17 does not require either a first or secondary immunostimulatory protein. Costa Fejos does not necessarily require immunostimulatory proteins on the fusosome which reads on the claim.
In regards to claim 18, the use of the fusosome (“to be administered to a subject”) is an intended uses of the composition, and the claim does not require steps of administering the fusosome to patient.
According to MPEP 2114, if the prior art structure is capable of performing the intended use, then it meets the claim.
To this end, Costa Fejos teaches that the fusosome vectors can be administered to patients (Pharmaceutical composition, p32) and is therefore suitable for this intended purpose.
In regards to properties of as in claim 18, in regards to a detectable antibody response, in specific embodiments, Costa Fejos also taches that vectors can be pseudotyped with glycoproteins from Nipah virus of which there are low pre-existing antibodies in human beings (p3, lines 20-36, p4, lines 1-9]), which suggests that the fusosome would not produce, or produce only a low level innate immune response, and appear at least close to the percentages as in claim 18.
In regards to claim 32, Costa Fejos teaches that the targeting domain (moiety) comprises a scFv (claim 5).
In regards to claims 33-35, it is noted that these are properties of fusosome, and claims do not require a step of contacting cells. However, in regards to the properties as in claim 33-35, Costa Fejos teaches that the particles can be at least contacted with CD34+ HSCs for activation of those cells (example 8, p51).
In regards to claim 49, Costa Fejos teaches that the exogenous agent can be therapeutic genes (agents) (p41, lines 6-16).
In regards to claim 50, Costa Fejos teaches that the fusosome vector is a retroviral vector (claim 1).
In regards to claim 54, Costa Fejos teaches that the fusosome vector transfers an Erb2-CAR gene (p47, Example 2), which is a gene that encodes a membrane protein.
In regards to claim 59, Costa Fejos teaches that the re-targeted fusogen (pseudotyped targeting fusion proteins can be derived from Nipah virus F and G proteins (p40, lines25-30).
Therefore, the combined teachings of Costa Fejos, Kingsman, and Chapel-Fernandes render obvious Applicant’s invention as claimed.
Claim 55 is rejected under 35 U.S.C. 103 as being unpatentable over Costa Fejoz et al. (WO2017182585 A1, 2017, previously cited) in view of Kingsman et al. (WO2008071959, 2008, on IDS 07/12/2021, previously cited) and of Chapel-Fernandes et al. (Cancer Gene Therapy, 2006) as evidenced by Transfiguracion et al. (Molecular Therapy: Methods & Clinical Development, 2020, previously cited) as applied to claims 1, 3, and 54 above, and in further view of Circosta et al. (Human Gene Therapy, 2009).
In regards to claim 55, while as above, Costa Fejos teaches that the fusosome vector transfers an Erb2-CAR gene (p47, Example 2), which is a gene that encodes a membrane protein, this is not one of the membrane proteins as in claim 55.
However, it was known in the art before the effective filing date that vectors could be used to introduce exogenous membrane proteins such as TCRs.
Specifically, a person of ordinary skill in the art would have been motivated to introduce a TCR because Circosta teaches that TCE gene transfer with lentiviral vectors allows for efficient redirection of tumor specificity in naïve and memory T cells without prior stimulation of endogenous TCR and preserves proliferative potential and differentiation stage (Title, Abstract, p1576). Furthermore, because Circosta teaches that vectors can be constructed comprising TCR genes (Materials and Methods, p1577-1579) and because as above, Costa Fejos teaches that the fusosome vector can transfer membrane proteins, it could have been done with predictable results and a reasonable expectation of success.
Therefore, the combined teachings of Costa Fejos, Kingsman, Chapel-Fernandes, and Circosta render obvious Applicant’s invention as claimed.
Double Patenting
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.
Claims 1, 3-4, 12-18, 33, 48-50, 54-55, and 59 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-4, 6-9, 16-17, 19-20, 23, 27, 33, 37, 39-40, and 43-53, and 62 of copending Application No. 17/293,842 (reference application).
Although the claims at issue are not identical, they are not patentably distinct from each other because both inventions are drawn to a re-targeted paramyxoviral fusogen, a positive target cell-specific regulatory element, a non-target cell regulatory element, and a nucleic acids, wherein the fusosome comprises Nipah F or G proteins.
While copending Application No. 17/293,842 does not explicitly teach a that the tissue-specific regulatory sequence is an enhancer, copending Application No. 17/293,842 discloses payload genes such as synapsinI (SYN) which is known to comprise a neuron-specific promoter (and also, thus directed to a liver cell/tissue). A person of ordinary skill in the art would have been motivated to include a tissue-specific enhancer in order to better express genes in specific tissues while limiting off-target effects. Furthermore, because copending Application No. 17/293,842 teaches genes (such as the Syn gene) which are known to comprise tissue-specific enhancers, it could have been done with predictable results and a reasonable expectation of success.
Furthermore, according to MPEP 2112.01, “Where the claimed and prior art products are identical or substantially identical in structure or composition or a are produced by identical or substantially identical processes, a prima facie case of either anticipation or obviousness has been established. In re Spada, F.2d 1252, 1255, 195 USPQ 430, 433 (CCPA 1977)”. Furthermore, “Products of identical chemical composition cannot have mutually exclusive properties”. In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990). Continuing, “When the PTO shows a sound basis for believing that the products of the applicant and the prior art are the same, the applicant has the burden of showing that they are not” Id.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Response to Arguments
Applicant argues that Kingsman does not teach the use of tissue-specific enhancers as a positive cell target regulatory element (Remarks, p8-9). Instead, Applicant argues that Kingsman only uses non-specific enhancers (Remarks, p9).
Applicant also argues that Kingsman does not teach a tissue-specific enhancer that “increases expression of the exogenous agent in a target cell or tissue relative to an otherwise similar fusosome lacking the positive target cell-specific regulatory element” or that , “the target cell or tissue is not a liver cell or a liver tissue,” as recited in amended claim 1 (Remarks, p9).
Applicant argues that Follenzi fails to teach or suggest a tissue-specific enhancer of amended claim 1 as Follenzi targets hepatocytes (Remarks, p9).
Therefore, Applicant concludes that the rejections under 35 USC 103 should be withdrawn (Remarks, p8-9).
In regards to Follenzi, Applicant’s arguments filed 06/12/2026 have been fully considered and are found persuasive, therefore, the rejection of the claims under 35 U.S.C. 103 as being unpatentable over Costa Fejoz et al. (WO2017182585 A1, 2017, previously cited) in view of Kingsman et al. (WO2008071959, 2008, on IDS 07/12/2021, previously cited) and Follenzi et al. (Human Gene Therapy, 2002, previously cited) as evidenced by Transfiguracion et al. (Molecular Therapy: Methods & Clinical Development, 2020, previously cited) has been withdrawn as discussed above.
However, in view of Applicant’s amendment to the claims, specifically disallowing the target cell to be a liver cell/tissue, a new grounds of rejection incorporating Chapel-Fernandes et al. (Cancer Gene Therapy, 2006) is made as discussed above.
Specifically, in regards to a cell/tissue-specific enhancer that is not a liver cell/tissue, it would still have prima facie obvious to modify the fusosome of Kingsman and incorporate this feature as discussed above.
Therefore, in regards to Applicant’s arguments against the rejections under 35 USC 103 generally, Applicant’s arguments filed 06/12/2026 have been fully considered but are not found persuasive.
Specifically, as discussed above, a person of ordinary skill in the art would have been motivated to include a tissue-specific enhancer in order to ensure that correct targets are hit, while avoiding off-target effects, and therefore increasing efficacy in gene therapy uses.
They would also have been motivated to include a tissue-specific enhancer because Chapel-Fernandes teaches that tissue-specific enhancers, including prostate-specific enhancers (which are not liver), restricts transgene expression to specific cells (e.g., PSA-secreting cells) and improves tissue-specific expression in these tissues in a lentiviral vector context (Abstract, p919; Introduction, p919-920; Fig. 1, p921). Furthermore, because Chapel-Fernandes demonstrates that lentiviral vectors can be constructed with tissue-specific promoters which are not liver (Fig. 1, p921) and because Costa Fejos and Chapel-Fernandes are in the same technical field of using lentiviral vectors to deliver exogenous DNA to target-cells for cell therapy for gene therapy, it could have been done with predictable results and a reasonable expectation of success.
In regards to whether this has the property of increasing expression of the exogenous agent in a target cell or tissue relative to an otherwise similar fusosome lacking the positive target cell-specific regulatory element, similarly to as above, Costa Fejos demonstrates that particles selectively activate and targeted T cells (by introducing transgenes, which are exogenous agents) over other cells (in which exogenous transgenes are not introduced) (Brief description of the figures, p41-42; Figs. 1 and 6).
Therefore, the composition of Costa Fejos has the property of increased expression of the exogenous agent in a target cell or tissue relative to an otherwise similar fusosome lacking the positive target cell-specific regulatory element.
Applicant argues that the provisional double-patenting rejection over Co-pending Application No. 17/293,842 be withdrawn because the claims are allowable (Remarks, p10).
Applicant’s arguments filed 06/12/2026 have been fully considered but are not persuasive because the claims are still prima facie obvious as discussed above and therefore, withdrawal of the double-patenting rejection over Co-pending Application No. 17/293,842 is premature.
Conclusion
No claims are 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 JOSEPH (PAUL) MIANO whose telephone number is (571)272-0341. The examiner can normally be reached Mon-Fri from 8:30am to 5:30pm.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, James (Doug) Schultz can be reached at (571) 272-0763. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/JOSEPH PAUL MIANO/Examiner, Art Unit 1631
Prosecution Insights