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 .
Response to Arguments
Applicants' arguments, filed August 10, 2026, have been fully considered. The following rejections and/or objections constitute the complete set presently being applied to the instant application.
The failure of the previously applied references to teach 1-methyl-pseudouridine is remedied by the new grounds of rejection set forth below. No other arguments regarding the previously applied references that are still used in the new grounds of rejection set forth below were set forth for the Examiner to address herein.
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.
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.
Claim(s) 20, 22 – 33 and 36 are rejected under 35 U.S.C. 103 as being unpatentable over Lee et al. (US 2018/0148719) in view of Hjortsvang et al. (US 2006/0269542) and Barth et al. (ACSNano, 2011) further in view of Vaidyanathan et al. (Mol Ther Nucl Acids, 2018) and Dombrowski et al. (WO 2019/067910).
Lee et al. discloses lipid nanoparticles comprising therapeutic nucleic acids such as gRNA that target gene expression (whole document, e.g., abstract). The particles enable effective delivery of a nucleic acid drug into target tissues and cells within the body while protecting the nucleic acid from degradation in the blood stream (¶ [0015]). The nucleic acid-lipid particles can comprise one or more of the molecules described herein, such as a combination of gRNA and an mRNA encoding a Cas9, a cationic lipid, a non-cationic lipid and optionally a conjugated lipid that inhibits particle aggregation (¶¶ [0004] and [0005]). These particles enable the effective delivery of a nucleic acid drug to target tissues and cells within the body (¶ [0015]). The non-cationic lipid can be cholesterol or a phospholipid (¶¶ [0022] and [0023]) and a preferred embodiment is a mixture of phospholipid and cholesterol or a derivative thereof (¶ [0108]). The phospholipid in mixture with cholesterol can be DSPC (¶ [0228]). The conjugated lipid that inhibits particle aggregation can be a PEG-lipid conjugate such as PEG-DAG or PEG-phospholipid (¶ [0026]), which reads on the non-activated pegylated lipid c) of instant claim 20, and can be present in combination with a mixture of phospholipid and cholesterol or a derivative thereof (e.g., ¶ [0116]) and can comprise about 0.5 mol% to about 3 mol% of the total lipids present in the particle (¶ [0035]). Phosphatidylethanolamines having a variety of chain lengths and degrees of saturation can be conjugated to PEG (¶ [0243]). Targeting ligands such as proteins or antibodies can be attached to the cationic lipid and preferably that positive charge is maintained after ligand attachment (¶ [0264]).
The presence of targeting ligand such as an antibody against CD117 on the particles attached via a PEGylated lipid such as phosphatidylethanolamine is not disclosed.
Hjortsvang et al. discloses an immunoliposome composition comprising liposomes bearing a ligand for targeting cells expressing a growth factor receptor such as HER2 that are internalized by cells for cytoplasmic delivery of an entrapped drug (whole document, e.g., abstract). A surface coating of hydrophilic polymers provides long blood circulation times and the extended lifetime is often necessary for the liposome to reach their desired target region or cell from the site of injection (¶ [0003]). Targeting ligands or affinity moieties are present on the surface of targeted liposomes result in healthy tissue not being exposed to the therapeutic agent (¶ [0004]). While the targeting ligands can be directly attached to the surface, this approach is suitable primarily for liposomes that lack surface-bound polymer chains that interfere with the interaction between the targeting ligand and its intended target (¶ [0004]). Alternatively, the targeting ligands can be attached to the free ends of the polymer chains forming the surface coating of the liposome and therefore are readily available for interaction with the intended target (¶ [0005]). As shown in Figure 1A and 1B, activation with maleimide is carried out to prepare the lipid-polymer-antibody conjugate (¶ [0031]). The amount of anti-HER2 receptor antibody conjugates provides more than about 2 and less than about 25 antibodies per liposome on average (¶ [0011]). The liposomes are comprised of vesicle forming lipids, a lipopolymer and conjugate comprised of a hydrophobic moiety, a hydrophilic polymer and an antibody for the extracellular domain of HER2 and the entrapped drug (e.g., claim 1). The hydrophilic polymer can be PEG with a molecular weight in the range of 20,000 – 50,000 Daltons (claim 2). Phospholipids such as phosphatidylcholine or phosphatidylethanolamine with two hydrocarbon chains typically 14 – 22 carbon atoms in length and cholesterol are disclosed as suitable lipids (¶ [0072]). Cationic lipids are also suitable (¶ [0073]).
Barth et al. discloses that small populations of cells within solid and nonsolid tumors have stem cell-like characteristics including exhibiting markers resembling embryonic and adult stem cells and are fully capable of initiating tumor growth in vivo (p 5325, col 1). Leukemia stem cells (LSCs) reside with a lineage-Sca-1+CD117+ cellular population in patients with chronic myeloid leukemia (CML; p 5325, col 2, ¶ 1). LSCs have also been identified in both acute and chronic lymphoblastic leukemia (p 5329, col 1, ¶ 1). Indocyanine green (ICG)-loaded CPSNPs (calcium phosphosilicate nanoparticles) functionalized with PEG effectively accumulated within tissues such as breast and pancreatic cancer tumors (p 5326, col 2, ¶ 1). ICG can be used as a therapeutic agent with targeting to the specific leukemic cell population responsible for the maintenance and progression of the disease (p 5326, col 2, ¶ 2). CPSNPs were functionalized with specific antibodies targeting CD96 or CD117 (p 5327, col 2, ¶ 2 and figure 1). CD177 targeted CPSNPs entered via receptor-mediated endocytosis with CD117 normally being internalized by ligand binding (p 5330, col 1, ¶ 2). CD117-targeted ICG-CPSNPs dramatically enhanced the in vivo efficacy of the photodynamic therapy using ICG in a murine leukemia model (e.g., abstract).
It would have been obvious to the person of ordinary skill in the art before the effective filing date of the claimed invention to use a targeting ligand such as an antibody against CD117 attached to a PEGylated lipid of the LNPs of Lee et al. The person of ordinary skill in the art would have been motivated to make those modifications and reasonably would have expected success because the therapeutic lipid nanoparticles of Lee et al. can be targeted but specific targeting ligands such as antibodies attached to the hydrophilic coating of the liposome as disclosed by Hjortsvang et al. is not disclosed. Some cells with solid and nonsolid tumors exhibit markers resembling embryonic and adult stem cells and such cells can be targeted using an antibody for targeting CD117, improving the in vivo efficacy of the anti-cancer therapeutic present in the labeled nanoparticles as disclosed by Barth et al. The placement of the antibody on the free end of the PEG on the liposomes of Lee et al. allows the targeting ligand to be readily exposed for interaction with the intended target and will result in more efficient delivery of the nucleic acids targeting gene expression of Lee et al. to cells such as the cancer stem cells that express CD117 such as hematopoietic stem cells. The particular lipids used to prepare the lipid particles and the selection of the PEG-lipid to which the antibody is conjugated from those that are disclosed by Lee et al. as suitable for lipid particles targeting gene expression using therapeutic nucleic acids is within the skill of the person of ordinary skill in the art and there is no evidence as to the criticality of the claimed lipid nanoparticle composition and structure. The selection of the target and therefore the appropriate targeting ligand is also within the skill of the art depending on the indication to be treated and the characteristics of the target cells and/or tissues. Such lipid particles can be used to edit the gene expression of these cells to treat the cancer. Barth et al. discloses that cancer stem cells can be targeted using anti-CD117 antibodies and can replace the anti-HER2 antibody disclosed by Hjortsvang et al. to target a different population of cells.
Modification of the nucleic acid cargo with nucleosides such as 1-methyl-pseudouridine is not disclosed.
Vaidyanathan et al. discloses that the Cas9/gRNA system consists of an RNA-guided nuclease (Cas9) and a single short gRNA and is a powerful tool for manipulating genomes (p 530, col 1). An ideal Cas9 mRNA should mimic a fully processed mRNA and not activate innate immune pathways (p 520, col 2, ¶ 3). Cas9 mRNAs were modified with pseudouridine (Ψ) and 5-methyl-cytosine to reduce innate immune response (abstract). The immune response was studied using encapsulated Cas9 mRNAs (p 535, col 1, ¶ 1). Full substitution of mRNA with Ψ also increased in vivo activity (p 533, col 1, ¶ 1).
Dombrowski et al. discloses compositions and methods for genetic editing such as polynucleotides encoding Cas9 that can provide one or more of improved editing efficiency, reduced immunogenicity or other benefits (whole document, e.g. abstract). The disclosed mRNAs can comprise a modified uridine at some or all uridine positions with disclosed modified uridines being pseudouridine and N1-methyl-pseudourdine (¶ [00241]), another name for 1-methyl-pseudourdine. The bases of the polynucleotide or nucleic acid can also include pyrimidine bases with substituent groups at the 5 or 6 position such as 5-methylcytosine (¶ [00150]).
It would have been obvious to the person of ordinary skill in the art before the effective filing date of the claimed invention to include 1-methyl-pseudourdine nucleoside-modified Cas9 RNA in the lipid nanoparticles of Lee et al., Hjortsvang et al. and Barth et al. The person of ordinary skill in the art would have been motivated to make those modifications and reasonably would have expected success because Lee et al. uses the Cas9 system and Vaidyanathan et al. and Dombrowski et al. discloses that nucleoside modifications such pseudouridine, 5-methyl-cytosine or 1-methyl-pseudouridine can increase the Cas9 activity and alter the immunogenicity even when encapsulated. Dombrowski et al. discloses the known functional equivalence in the art of 1-methyl-pseudourdine and pseudouridine as modified bases for inclusion in genetic editing nucleic acids encoding Cas9. The person of ordinary skill in the art would reasonably expect that such modifications would bring about similar effects when the nucleic acids are encapsulated in the lipid nanoparticle system of Lee et al., Hjortsvang et al. and Barth et al. as even when the mRNA is encapsulated as taught by Vaidyanathan et al. and there was an immune response.
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.
Regarding the provisional nonstatutory double patenting rejections set forth below, Applicants request that the rejections be held in abeyance until such time as claims are deemed allowable in this or the copending Application.
The amended claims remain unpatentable in based on the claims of each application as detailed below.
Claims 20, 22 – 33 and 36 were provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 - 19 of copending Application No. 18/558,014 in view of Lee et al. (US 2018/0148719) in view of Hjortsvang et al. (US 2006/0269542) and Barth et al. (ACSNano, 2011). This rejection is MAINTAINED for the reasons of record set forth in the Office Action mailed February 10, 2026 and those set forth herein.
Claims 5 and 6 of US’014 recite RNA molecules such as a Cas9 mRNA and a guide RNA which can be isolated nucleoside-modified RNA modified with pseudouridine or 1-methyl-pseudouridine as required by the amended claims of the instant application.
This is a provisional nonstatutory double patenting rejection.
Claims 20, 22 – 33 and 36 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 2, 4, 5, 8, 11, 16, 25, 32, 34, 35, 43, 44, 50, 57, 58, 60, 61, 63 and 66 of copending Application No. 18/865,098 in view of Lee et al. (US 2018/0148719) in view of Hjortsvang et al. (US 2006/0269542) and Barth et al. (ACSNano, 2011) further in view of Vaidyanathan et al. (Mol Ther Nucl Acids, 2018) and Dombrowski et al. (WO 2019/067910).
The claims of US’098 recite compounds and lipid nanoparticles (LNPs) comprising such compounds (e.g., claim 1). The LNPs also comprise at least one neutral phospholipid, at least one cholesterol lipid such as cholesterol and at least one polymer conjugated lipid such as with PEG (claim 1). The neutral phospholipid can be DSPC (claim 11). The LNP can selectively bind to at least one target cell of interest such as a stem cell and/or can comprise or encapsulate at least one agent (claim 16). The agent can be modified RNA or CRISPR-Cas9 (claim 25). Methods of delivering an agent by administering the LNP are also present (e.g., claim 34). Claimed administration routes include intravenous, intramuscular, intradermal, subcutaneous, intranasal or inhalation (claim 35).
All of the components of the instant claimed lipid nanoparticles with an CD117 targeting antibody are not claimed.
Lee et al. Hjortsvang et al. and Barth et al. are discussed above.
It would have been obvious to the person of ordinary skill in the art before the effective filing date of the claimed invention to use a targeting ligand such as an antibody against CD117 attached to a PEGylated lipid of liposome such as those taught by Lee et al. as the materials used in the lipid nanoparticles of US’098. The person of ordinary skill in the art would have been motivated to make those modifications and reasonably would have expected success because the composition of the delivery vehicle such as a lipid nanoparticle in US’098 is not particularly specified and those taught by Lee et al. are suitable for the delivery of cargoes such as those claimed in US’098. The therapeutic lipid nanoparticles of Lee et al. can be targeted but specific targeting ligands such as antibodies attached to the hydrophilic coating of the liposome as disclosed by Hjortsvang et al. is not disclosed. Some cells with solid and nonsolid tumors exhibit markers resembling embryonic and adult stem cells and such cells can be targeted using an antibody for targeting CD117, improving the in vivo efficacy of the anti-cancer therapeutic present in the labeled nanoparticles as disclosed by Barth et al. The placement of the antibody on the free end of the PEG on the liposomes of Lee et al. allows the targeting ligand to be readily exposed for interaction with the intended target and will result in more efficient delivery of the nucleic acids targeting gene expression of Lee et al. to cells such as the cancer stem cells that express CD117 disclosed by Barth et al. The particular lipids used to prepare the lipid particles and the selection of the PEG-lipid to which the antibody is conjugated from those that are disclosed as suitable for lipid particle targeting gene expression using therapeutic nucleic acids by Lee et al. is within the skill of the person of ordinary skill in the art and there is no evidence as to the criticality of the claimed lipid nanoparticle. The selection of the target and therefore the appropriate targeting ligand is also within the skill of the art depending on the indication to be treated and the characteristics of the target cells and/or tissues. Such lipid particles can be used to edit the gene expression of these cells to treat the cancer. Barth et al. discloses that cancer stem cells can be targeted using anti-CD117 antibodies and can replace the anti-HER2 antibody disclosed by Hjortsvang et al. to target a different population of cells.
Modification of the nucleic acid cargo with nucleosides such as 1-methyl-pseudouridine is not disclosed.
Vaidyanathan et al. and Dombrowski et al. are discussed above.
It would have been obvious to the person of ordinary skill in the art before the effective filing date of the claimed invention to include 1-methyl-pseudourdine nucleoside-modified Cas9 RNA in the lipid nanoparticles of US’098. The person of ordinary skill in the art would have been motivated to make those modifications and reasonably would have expected success because the Cas9 system can be present in the LNPs of US’098 and Vaidyanathan et al. and Dombrowski et al. discloses that nucleoside modifications such pseudouridine, 5-methyl-cytosine or 1-methyl-pseudouridine can increase the Cas9 activity and alter the immunogenicity even when encapsulated. Dombrowski et al. discloses the known functional equivalence in the art of 1-methyl-pseudourdine and pseudouridine as modified bases for inclusion in genetic editing nucleic acids encoding Cas9. The person of ordinary skill in the art would reasonably expect that such modifications would bring about similar effects when the nucleic acids are encapsulated in the lipid nanoparticle system of US’098, Lee et al. Hjortsvang et al. and Barth et al. as even when the mRNA is encapsulated as taught by Vaidyanathan et al. and there was an immune response.
This is a provisional nonstatutory double patenting rejection.
Claims 20, 22 – 33 and 36 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 - 19 of copending Application No. 19/389,975 in view of Lee et al. (US 2018/0148719), Hjortsvang et al. (US 2006/0269542) and Barth et al. (ACSNano, 2011) further in view of Vaidyanathan et al. (Mol Ther Nucl Acids, 2018) and Dombrowski et al. (WO 2019/067910).
The claims of US’975 recite compounds and lipid nanoparticles (LNPs) comprising such compounds (e.g., claim 1). The LNPs also comprise at least one neutral phospholipid, at least one cholesterol lipid such as cholesterol and at least one polymer conjugated lipid such as with PEG (claim 1). The neutral phospholipid can be DSPC (claim 11). The LNPs can be used in gene editing (claim 8) or nucleic acid delivery (claim 18) so nucleic acid cargoes are encompassed by the clams.
All of the components of the instant claimed lipid nanoparticles with an CD117 targeting antibody are not claimed.
Lee et al., Hjortsvang et al. and Barth et al. are discussed above.
It would have been obvious to the person of ordinary skill in the art before the effective filing date of the claimed invention to use a targeting ligand such as an antibody against CD117 attached to a PEGylated lipid of liposome such as those taught by Lee et al. as the materials used in the lipid nanoparticles of US’975. The person of ordinary skill in the art would have been motivated to make those modifications and reasonably would have expected success because the composition of the delivery vehicle such as a lipid nanoparticle in US’975 is very generally specified and those taught by Lee et al. are suitable for the delivery of cargoes such as nucleic acids. The therapeutic lipid nanoparticles of Lee et al. can be targeted but specific targeting ligands such as antibodies attached to the hydrophilic coating of the liposome as disclosed by Hjortsvang et al. is not disclosed. Some cells with solid and nonsolid tumors exhibit markers resembling embryonic and adult stem cells and such cells can be targeted using an antibody for targeting CD117, improving the in vivo efficacy of the anti-cancer therapeutic present in the labeled nanoparticles as disclosed by Barth et al. The placement of the antibody on the free end of the PEG on the liposomes of Lee et al. allows the targeting ligand to be readily exposed for interaction with the intended target and will result in more efficient delivery of the nucleic acids targeting gene expression of Lee et al. to cells such as the cancer stem cells that express CD117 disclosed by Barth et al. The particular lipids used to prepare the lipid particles and the selection of the PEG-lipid to which the antibody is conjugated from those that are disclosed as suitable for lipid particle targeting gene expression using therapeutic nucleic acids by Lee et al. is within the skill of the person of ordinary skill in the art and there is no evidence as to the criticality of the claimed lipid nanoparticle. The selection of the target and therefore the appropriate targeting ligand is also within the skill of the art depending on the indication to be treated and the characteristics of the target cells and/or tissues. Such lipid particles can be used to edit the gene expression of these cells to treat the cancer. Barth et al. discloses that cancer stem cells can be targeted using anti-CD117 antibodies and can replace the anti-HER2 antibody disclosed by Hjortsvang et al. to target a different population of cells.
Modification of the nucleic acid cargo with nucleosides such as pseudouridine is not disclosed.
Vaidyanathan et al. and Dombrowski et al. are discussed above.
It would have been obvious to the person of ordinary skill in the art before the effective filing date of the claimed invention to include 1-methyl-pseudourdine nucleoside-modified Cas9 RNA in the lipid nanoparticles of US’975. The person of ordinary skill in the art would have been motivated to make those modifications and reasonably would have expected success because the Cas9 system can be present in the LNPs of US’098 and Vaidyanathan et al. and Dombrowski et al. disclose that nucleoside modifications such pseudouridine, 5-methyl-cytosine or 1-methyl-pseudouridine can increase the Cas9 activity and alter the immunogenicity even when encapsulated. Dombrowski et al. discloses the known functional equivalence in the art of 1-methyl-pseudourdine and pseudouridine as modified bases for inclusion in genetic editing nucleic acids encoding Cas9. The person of ordinary skill in the art would reasonably expect that such modifications would bring about similar effects when the nucleic acids are encapsulated in the lipid nanoparticle system of US’975, Lee et al., Hjortsvang et al. and Barth et al. as even when the mRNA is encapsulated as taught by Vaidyanathan et al. and there was an immune response.
This is a provisional nonstatutory double patenting rejection.
Conclusion
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Nissa M Westerberg whose telephone number is (571)270-3532. The examiner can normally be reached M - F 8 am - 4 pm.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Michael Hartley can be reached at 571-272-0616. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/Nissa M Westerberg/Primary Examiner, Art Unit 1618
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