DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claim Status
Applicant’s amendment filed 3/23/2026 is acknowledged. Claims 65, 73, and 79 are canceled. Claims 60, 61, 62, 63, 64, 68, 69, 70, 72, 76, 77, and 78 are amended. Claims 80 and 81 are new.
Claims 60-64, 66-72, 74-78, 80-81 are under examination.
Regarding the newly amended and added claims, they are rejected under 35 USC § 103 as addressed below.
Withdrawn Objections/ Rejections
All claim rejections under 35 USC § 112a and § 112b are withdrawn in the light of claim amendments. All objections are withdrawn in light of the claim amendments.
Previous rejection of claims 60-70 under 35 U.S.C. 101 is withdrawn in view of claim amendments.
Applicant’s arguments, see section IX pg. 13, filed 03/23/2026, with respect to the rejection(s) of claim(s) 72-75 under 35 USC § 102 have been fully considered and are persuasive. Therefore, the rejection has been withdrawn.
Previous rejection of claims 60-72 and 76 under 35 USC § 103 is withdrawn in view of claim amendments.
New Rejections Necessitated by Claim Amendments
Claim Rejections - 35 USC § 112(a)
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 72, 74- 78, and 80-81 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
Claims 72, 74- 78, and 80-81 are drawn to a method or kit for diagnosing CNS disease comprising a first and second antibody defined only by the target to which they bind. Specifically, the CNS disease-associated marker, which is the target for the second antibody, is phosphorylated tau (p-tau). Accordingly, the claims encompass a vast number of possible antibodies for p-tau.
State of the relevant art:
The state of the art does provide written description for SHISA9 (Englehart et al., 2010, Fig. 1D), GLT1 (Mennerick et al., 1998, abstract), alpha-synuclein (Dhillon et al., 2017, abstract), and CNPase (Sprinkle et al., 1987, abstract) because antibodies known in the art can bind to the full length of these proteins to achieve the claimed function. However, antibodies binding to phosphorylated tau are limited to phosphorylated sites of the peptide. In other words, antibodies for p-tau require additional specificity that the state of the art and instant disclosure must address in order to demonstrate written description. According to Kimura et al., 2018, (see PTO-328), roughly 40 sites, or roughly 10% of the tau protein can be phosphorylated in pathological tau (pg. 2, second paragraph), but typically not all of these sites will be phosphorylated at the same time (pg. 2, right side, middle of first paragraph). For example, p-tau217 is associated with Alzheimer’s disease but has a single phosphorylated site (Janelidze et al., 2020, See PTO-328 ). Therefore, the site specificity for p-tau is extremely high. Furthermore, the state of the art teaches that leading up to the time of filing, although phosphor-tau antibodies were commercially available, few had actually been validated, leading to false positives. Ercan et al., 2017 (see PTO-328) even teaches that this has led to a ”reproducibility crisis” (pg. 14, right side, last two lines; pg. 15, left side, first paragraph). Specifically, it teaches that the pT217 antibody did not detect its specific modification site and suggests it may actually detect the native tau form better (pg. 15, right side, second paragraph). Lastly it states that this study did not evaluate antibodies described in literature that were generated by academic researchers (pg. 15, last line of second paragraph); in other words, many antibodies known to one of ordinary skill in the art were not validated. Altogether these sources teach that the number of effective p-tau antibodies (i.e. those that one of ordinary skill in the art would know could achieve the claimed function) does not constitute the genus of all available p-tau antibodies.
Furthermore, as was well-known in the antibody art at the time of filing, the formation of an intact antigen-binding site in an antibody typically requires the association of the complete heavy and light chain variable regions of a given antibody, each of which comprises three CDRs (or hypervariable regions) which provide the majority of the contact residues for the binding of the antibody to its target epitope (reviewed in Sela-Culang et al. Frontiers in immunology 4 (2013): 302.; PTO-892). Sela-Culang further teaches that antigens lack intrinsic properties that clearly differentiate between epitopic and non-epitopic residues, and any part of the antigen surface may become part of an epitope under some circumstances (“Ab Epitope Prediction”; Pg. 2). In the same vein, Edwards et al. 2003 (Journal of molecular biology 334.1 (2003): 103-118.; PTO-892) endeavored to uncover the breadth of the structural diversity of antibodies a single antigen can give rise to. Edwards employed a phage display library to screen for antibodies that bind a single protein, BLyS, and isolated over 1000 unique anti-BLyS antibodies, each comprising a different amino acid sequence (Abstract). These antibodies were structurally diverse, resulted from nearly all possible Vh, D, and Jh, germlines (Pg. 105; “Vh and Vl germline usage”), and comprised 568 distinct Vh CDR3 sequences, ranging in length from 5 to 25 amino acid residues (Fig. 4; “Vh CDR3 sequence diversity”; Pg. 105). Together, these works highlight that neither knowledge of the antigen sequence nor the antibody sequence is necessarily predictive of its function.
Description of representative species in the specification:
MPEP § 2163 states that a “representative number of species” means that the species which are adequately described are representative of the entire genus. Thus, when there is substantial variation within the genus, one must describe a sufficient variety of species to reflect the variation within the genus. With respect to p-tau, there is substantial variation regarding the structure and function of p-tau specific antibodies. As addressed above, due to the lack of written description support for species provided in the art, the written description turns to the species described in the disclosure. The p-tau antibodies taught in the specification are simply described by their target, such as such as a “… a disease-associated marker antibody p-tau217” (pg. 34, lines 15-17). The specification does not provide the VH/VL sequences for any p-tau antibody or provide details on antibody format. Therefore, given the breadth of the claims and the depth and diversity of the antibody repertoire as described above, the current disclosure is not representative of the p-tau antibody genus described only by its binding target.
Identifying characteristics and structure/function correlation:
In the absence of a representative number of species, the written description requirement for a claimed genus may be satisfied by disclosure of relevant, identifying characteristics; i.e., structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the applicant was in possession of the claimed genus. To meet this requirement in the instant case for each recited genus, the specification must describe structural features that the skilled artisan, as of the effective filing date, would have expected to convey the claimed p-tau binding activity. Effective binding of the disclosed antibodies is demonstrated in Figs. 1A and 2A. However, there is no disclosure in the specification of formation of these antibodies. The specification does disclose that the p-tau antibody was polyclonal (pg.34 lines 1-2); however, the specification provides no further disclosure regarding antibody structure or other details regarding the antigen-binding sequences of disclosed antibody (or any other p-tau antibody). No amount of epitope mapping is disclosed, and there is no functional relationship established between the claimed antigens in the instant claims and the structure of an antibody capable of binding these targets. Accordingly, in view of the instant disclosure, one of ordinary skill in the art would be unable to envisage the necessary structure of the full genus of antibodies comprising immunological reactivity with p-tau.
Claim Rejections - 35 USC § 101
35 U.S.C. 101 reads as follows:
Whoever invents or discovers any new and useful process, machine, manufacture, or composition of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title.
Claims 60-71 are rejected under 35 U.S.C. 101 because the claimed invention is directed to a natural phenomenon judicial exception without significantly more.
The claims recite the natural phenomenon whereby -a central nervous system disease is associated with the levels of system-derived markers (such as SHISA9) and disease-associated markers (such p-protein) over control levels. This judicial exception is not integrated into a practical application because the method does not set forth any of the considerations outlined in MPEP 2106.05(a-c), (e) and (h). The additional steps do not constitute an improvement in technological field; and the steps recited in addition to the judicial exception do not integrate detection of the natural phenomenon into a particular treatment/prophylaxis according to MPEP 2106.04(d)(2). The claim(s) does/do not include additional elements that are sufficient to amount to significantly more than the judicial exception because the additional elements fail to provide either an inventive concept or impose meaningful limits upon the method such that the invention does not preempt every observance of the natural phenomenon itself.
Claims 60-71 are directed to a method for diagnosis for a central nervous system disease in a subject comprising acquiring, pretreating, and detecting level and/or size of extracellular vesicles in a peripheral body fluid as compared to that of a control. Methods are one of the statutory categories of invention (STEP 1:YES).
Claims 60-71 recite diagnosis/prognosis/monitoring or comparing, all of which are abstract mental concepts that belong to enumerated group (c) of the Abstract Idea Groupings described in MPEP § 2106.04(a)(2): Mental processes — concepts performed in the human mind (including an observation, evaluation, judgment, opinion). But more importantly, the claims recite a natural correlation/phenomenon/law of nature whereby -condition pathology, ex. Parkinson’s disease, is correlated with changes in the level of extracellular vesicles in a peripheral body fluid that have both CNS-derived and disease-associated markers. Therefore, the claims recite at least one judicial exception (STEP 2A, Prong One: YES).
According to Step 2A, Prong Two, as set forth in set forth in MPEP 2106.04 II A (2), the claims are next evaluated with respect to whether the judicial exception is integrated into a practical application. This analysis turns to the additional steps/elements recited within the claim. In Claims 60-62 the additional steps include acquiring and pretreating the peripheral body fluid, detecting a CNS-marker and a CN disease-associated marker simultaneously, and counting/measuring the extracellular vesicles that express both markers. Dependent claims 63-71 do not include any additional steps that would amount to significantly more than the judicial exception recited in the claims from which they depend.
To determine whether the additional elements individually and in combination integrate the judicial exception into a practical application, they must be evaluated based on the considerations set forth in MPEP 2106.05 (a) through (c), (e), and (h).There are no additional elements that reflect an improvement within the technical field; there are no additional elements that apply the natural correlation/phenomena judicial exception to a particular treatment or which utilize a particular machine; there are no additional elements that effect a transformation; and, there are no additional elements that apply the judicial exception in some other meaningful way beyond generally linking it to a field, namely, central nervous system diseases. Therefore, the additional elements fail to integrate the judicial exception into a practical application.
The next part of the Alice/Mayo test is the search for inventive concept to determine whether the additional elements amount to significantly more than the judicial exception itself. In this case, the additional elements when considered individually and in combination do not amount to significantly more than the judicial exception because they are well-known, routine and, conventional in the art. When considered in combination, Lucien, of record, teaches the steps of acquiring a sample (pg. 1052, left side, first line), pretreating it (pg. 1052, right side, first 6 lines of second paragraph), and counting exosomes that have both a disease and system associated marker using nanoscale flow cytometry (pg. 1053, left side, third paragraph). Furthermore, Biggs, of record, teaches that nanoscale flow cytometry was the known method able to “provide quantitative information of multiple biomarkers expressed on EV’s” (pg. 8840, third paragraph). Together, these sources teach that the additional elements recited in the claim when considered in combination were well-known, routine, and conventional at the time of filing. In other words, one of ordinary skill in the art would know how to detect biomarkers on exosomes and how to use that information for disease diagnosis. When considered alone, Applicant admits in the specification that the acquiring and pretreating steps could be achieved by any method known by those skilled in the art (pg. 21, lines 5-10; pg. 22 lines 1-3) and Hornung, of record, teaches one method of exosome biomarker detection and counting (pg.10, first and second paragraph, and Table 2).
Therefore, the steps/elements recited in addition to the judicial exception (detecting, counting, and measuring both disease-associated and system-derived biomarkers from a biological sample) were all well understood, routine, conventional activities in the field of biomarker disease detection prior to filing the application at hand (STEP 2B: NO). The claimed steps/elements recited in addition to the judicial exception(s), alone or in combination, do not make an inventive contribution over the methods that were known in the art prior to filing, and they amount to mere observation of the natural phenomenon itself, by any means known, with the words “apply it” in order to append it to the field biomarker disease detection. Therefore, in accordance with MPEP 2106.07(a)(III)(C), the examiner has cited publications within the field of technical expertise, that demonstrate the well-understood, routine, conventional nature of the additional element(s).
Response to Arguments
Applicant’s arguments filed on 3/23/2026, page 12 section VIII, with respect to the rejection of claims 60-70 under 35 USC § 101 have been considered, but are not persuasive. On page 12, section VIII, of Applicant’s response, applicant argues that that the simultaneous detection of the specifically recited CNS-derived marker and specifically recited CNS-disease associated marker was not a well-understood, routine, or conventional activity in the field at the time of filing. Here, Applicant is effectively arguing against the whether the claims amount to significantly more than the judicial exception (natural phenomenon). Specifically, the applicant argues against the “well-understood, routine, conventional activity” consideration of Step 2B, by stating that the additional elements in the claims, namely the recited disease-associated and system-derived biomarker combinations, is a specific limitation other than what is well-understood, routine and conventional in the field. Applicant argues that these specific biomarkers are more effective for disease diagnosis, which is a technological improvement over the prior art that amounts to significantly more than the judicial exception. However, the correlation of the recited biomarkers to CNS disease is the natural phenomenon judicial exception, so it cannot be an element in addition to the judicial exception. MPEP 2106.05 clearly states: “… an ‘inventive concept’ is furnished by an element or combination of elements that is recited in the claim in addition to (beyond) the judicial exception, and is sufficient to ensure that the claim as a whole amounts to significantly more than the judicial exception itself. Alice Corp., 573 U.S. at 27-18, 110 USPQ2d at 1981 (citing Mayo, 566 U.S. at 72-73, 101 USPQ2d at 1966). Therefore, Applicant’s statement about the technical effect of these biomarkers is moot.
Furthermore, regardless of the identity of the biomarkers, the acts of acquiring a sample, simultaneous detection and counting of biomarkers were well-understood, routine, or conventional activities in the field of biomarker disease detection at the time of filing, as outlined above and in the previous action. As discussed above, the claims do not contain additional active method steps that add significantly more to the judicial exception. In conclusion, the substance of these claims do not contain an element beyond the judicial exception that amounts to significantly more than the judicial exception itself. Thus, claims 60-71 are rejected under 101.
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.
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 60-64, 66-72, 74-78, 80-81 are rejected under 35 U.S.C. 103 as being over Hornung (CNS-Derived Blood Exosomes as a Promising Source of Biomarkers: Opportunities and Challenges. 2020/03/19 Front. Mol. Neurosci, of record) in view of Lucien (Glypican-1 and glycoprotein 2 bearing extracellular vesicles of not discern pancreatic cancer from benign pancreatic diseases, 2019/02/01, Oncotarget, Vol. 10, pg. 1045-1055, of record), Engelhardt (CKAMP44: A Brain-specific protein Attenuating Short-Term Synaptic Plasticity in the Dentate Gyrus, 2010, Science, Vol 327, pgs.1518-1522 , of record), and Chauhan (Surface Glycoproteins of Exosomes Shed by Myeloid-Derived Suppressor Cells Contribute to Function, 2017/01/06, J Proteome Res., pgs.1-22), as evidenced by Fiandaca (Identification of pre-clinical Alzheimer’s disease by a profile of pathogenic proteins in neurally-derived blood exosomes: a case-control study, 2015/06 Alzheimer’s Dement. 2011(6): 600–607.e1., of record).
Hornung teaches detecting a CNS-derived marker and a CNS disease-associated marker expressed on an exosome, but in two separate steps rather than at the same time. Regarding Claims 60 and 61 Hornung teaches acquiring a blood sample and pretreating it using centrifugation to isolate exosomes, which are a type of extracellular vesicle (pg. 8, right side, lines 20-30); regarding claims 60-64, 66-72, 74, 77, and 81 it further teaches detection of a CNS-derived marker using biotinylated antibodies to isolate exosomes with L1CAM, which is cell adhesion molecule (Table 2, caption) mainly expressed in the CNS (pg. 11, left side lines 1-4) and used as a marker for neuronal exosomes (pg. 7, left side, third paragraph); it also teaches detection of a CNS-disease associated marker, namely human P-S396 tau (which is a type of phosphorylated tau), from the L1CAM positive exosomes (pg. 7, left side paragraphs 3, 4); it also teaches that using this method, Fiandaca found that pT181-tau is increased in Alzheimer’s disease (pg. 7, left side paragraphs 4). Regarding claims 70 and 71, as evidenced by Fiandaca, the disease-associated marker pT181-tau is detected and quantified based on the intensity of the signal of an antibody that is fluorescently labeled (pg. 3,4, Methods). Lastly, Hornung teaches that this method successfully diagnosed individuals with Alzheimer’s disease and even predicted its onset (pg. 7, left side, 12 lines from bottom). Regarding claim 62, Hornung teaches using a nanoparticle tracking system to measure exosome number and size (pg.10, first and second paragraph, and Table 2). Regarding claim 78, Hornung teaches a reagent, namely Dulbecco’s balanced Salt solution (DBS-2) with a protease and phosphatase inhibitor, and an apparatus, namely a centrifuge, for acquiring the extracellular vesicles (Fig. 3). Regarding claims 67 and 75, Hornung teaches the system-derived marker L1CAM cell adhesion molecule which, as evidenced by Chauhan, is located on the surface of the extracellular vesicles because the surface of exosomes exhibit the surface proteins of their origin cell (pg. 8, paragraph 4).
However, Hornung, as evidenced by Fiandaca, regarding claims 60-64, 66-71, does not teach detection of the CNS-derived marker and CNS disease-associated marker at the same time. Regarding claims 60-64, 66-72, 74-78, an 80-81, it also does not teach that the CNS-derived marker and disease-associated biomarker must be, respectively, SHISA9 and phosphorylated tau (p-tau). Regarding claims 69, 70, 72, and 76, Hornung does not teach reacting the peripheral body fluid with a labeled antibody and detecting the CNS-derived marker by measuring the intensity of the labeled signal, where the labeling is fluorescent. is nt. Lastly, regarding claims 60 and 62, Hornung does not teach counting and/or measuring samples in which both markers are detected, because the step at which Hornung teaches exosome measurement occurs before the CNS disease-associated marker is detected.
Lucien teaches using Apogee nanoparticle flow cytometry (pg. 1046, right side, middle paragraph) to simultaneously detect a disease related marker and a system specific marker on extracellular vesicles (pg. 1046, left side, 9 lines from bottom) using antibodies conjugated to fluorescent labels (pg. 1052, ride side first paragraph). Lucien further teaches counting extracellular vesicles in which both markers are present (pg. 1052, Table 3) as well as measuring their size, (pg. 1047, Table 3, Figure B).
Engelhardt teaches that SHISA9, also called CKAMP44, is a brain-specific transmembrane protein (abstract) expressed on neurons in the majority of brain regions including the hippocampus (pg. 1518, right column, second paragraph).
Chauhan et al. teaches that the proteins expressed on the surface of exosomes reflect that of the origin cell (pg. 8, paragraph 4).
It would be obvious to one of ordinary skill in the art to substitute the CNS-derived marker from L1CAM, as taught by Hornung, to SHISA9, as taught by Engelhardt, because they both can function as CNS exosome markers. Because exosome surface proteins are based on those of the parent cell, one of ordinary skill in the art would have a reasonable expectation of success using SHISA9 as a surface marker for neuron-derived exosomes because it is expressed across neuronal cell types. Furthermore, one of ordinary skill in the art would be motivated to choose SHISA9, which is brain specific, over L1CAM, which is not restricted to the CNS, to enhance the accuracy of the diagnostic method. Hornung specifically states “…the field should continue searching for, and testing, more specific markers that will allow isolation of purer exosome populations of CNS neurons…” (pg. 11, left side, 8 lines from bottom). In order to detect SHISA9 and p-tau simultaneously on the surface of extracellular vesicles, it would have been obvious to one of ordinary skill in the art to change from Hornung’s method which required sequential steps (pg.7, right side, lines 17-20), to the simultaneous detection method using flow cytometry, as described by Lucien, in order to improve efficiency. One would have been motivated to use flow cytometry because traditional methods of marker detection described in Hornung are time-consuming and tedious. Furthermore, using fluorescently labeled antibodies to detect the aforementioned markers would have been obvious, since that is a conventional implementation of flow cytometry. Regarding kit claims, patentability is determined as an assembly of interrelated parts and whether said assembly distinguishes over the prior art; together, Hornung, as evidenced by Fiandaca, Lucien, and Engelhardt teach all the elements of the recited claims, as addressed previously. It would have been obvious to package all of the elements into a kit for commercial exploitation of the claimed invention.
Conclusion
No claims 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 MICHELLE C BUCCINI whose telephone number is (571)272-1352. The examiner can normally be reached M-F 7:30-5 EST.
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, Jeffrey Stucker can be reached at 5712720911. 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.
/MICHELLE CALLAHAN BUCCINI/Examiner, Art Unit 1675
/JULIE WU/Supervisory Patent Examiner, Art Unit 1643
Prosecution Insights