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 .
Election/Restrictions
Applicant’s election with traverse of Group II, claims 5-6, 11-12, and 18-20, drawn to dehydroepiandrosterone sulphate-acridinium ester conjugate immunoassay reagents and corresponding kits and methods, in the reply filed 08/12/2026, is acknowledged. The traversal is on the ground that the claimed inventions are linked by a common inventive concept and that restriction is therefore improper. This is not found persuasive because the requirement under 37 CFR 1.475 and PCT Rule 13 is based on whether the claimed inventions are linked by the same or corresponding special technical feature defining a contribution over the prior art, rather than merely whether the inventions share a general technical relationship.
As explained in the restriction requirement, Groups I and II share the general feature of employing a DHEAS-related analyte analog conjugate and an anti-DHEAS antibody in a competitive immunoassay for determining DHEAS. However, that common feature does not constitute a special technical feature because Sun et al. teaches a competitive DHEAS immunoassay employing a DHEAS derivative, an anti-DHEAS antibody, magnetic particles, and chemiluminescent detection. Accordingly, the shared feature does not define a contribution over the prior art. The remaining technical features differ between the groups: Group I places fluorescein on the DHEAS conjugate and acridinium ester on the anti-DHEAS antibody, whereas Group II places acridinium ester on the DHEAS conjugate and fluorescein on the anti-DHEAS antibody associated with the paramagnetic solid phase. Applicant has not identified a deficiency in the Office’s reliance on Sun or otherwise established that Groups I and II share the same or corresponding special technical feature constituting a contribution over the prior art. Accordingly, the requirement for restriction based on lack of unity of invention is maintained. The requirement is still deemed proper and is therefore made FINAL. Hence, claims 1-4, 7-10, 13-17, and 21-23 are withdrawn from further consideration as being drawn to the nonelected invention, there being no allowable generic or linking claim.
Status of the Claims
Claims 1-23 are pending. Claims 1-4, 7-10, 13-17, and 21-23 are withdrawn. Claims 5-6, 11-12, and 18-20 are examined herein in view of the restriction.
Priority
The present application, filed 04/10/2024, is a 371 of PCT/US2022/076904, filed 09/23/2022, which claims benefit of U.S. Provisional Patent Application 63/262,472, filed 10/13/2021. The benefit is acknowledged and the claims examined herein are treated as having an effective filing date of 10/13/2021.
Information Disclosure Statement
The Information Disclosure Statement(s) filed 04/10/2024, 02/04/2025, 10/20/2025, and 08/19/2026 are acknowledged and have been considered.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 6 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Regarding claim 6, the limitation the DHEAS-AE conjugate lacks sufficient antecedent basis. Claim 5, from which claim 6 depends, recites a dehydroepiandrosterone sulphate-carboxymethoxylamino-dimethyl acridinium ester (DHEAS-CMO-DMAE) conjugate, but does not previously introduce or define a DHEAS-AE conjugate. Claim 6 subsequently recites the DHEAS-AE conjugate, thereby introducing different terminology with the definite article the without a corresponding antecedent in claim 5.
Regarding claim 12, the limitation the DHEAS-AE conjugate lacks sufficient antecedent basis. Claim 11 recites a dehydroepiandrosterone sulphate-carboxymethoxylamino-dimethyl acridinium ester (DHEAS-CMO-DMAE) conjugate, but does not previously introduce or define a DHEAS-AE conjugate. Claim 12 therefore introduces the DHEAS-AE conjugate without clear antecedent basis in claim 11.
Regarding claim 19, the limitation the DHEAS-AE conjugate likewise lacks sufficient antecedent basis. Claim 18 recites a dehydroepiandrosterone sulphate-carboxymethoxylamino-dimethyl acridinium ester (DHEAS-CMO-DMAE) conjugate, but does not introduce or define that conjugate as a DHEAS-AE conjugate. Accordingly, the subsequent recitation of the DHEAS-AE conjugate in claim 19 renders the scope of the claim unclear.
For purposes of compact prosecution, the DHEAS-AE conjugate recited in claims 6, 12, and 19 will be interpreted as referring to the DHEAS acridinium-ester conjugate associated with the DHEAS-CMO-DMAE conjugate recited in respective parent claims 5, 11, and 18, with claims 6, 12, and 19 further specifying the recited conjugate as comprising DHEAS-CMO-EDA-DMAE or DHEAS-CMO-Z-NSP-DMAE, as applicable. These interpretations are adopted solely for purposes of examination and compact prosecution and do not cure either §112(b) deficiency. Appropriate correction is required. Additionally, for purposes of compact prosecution, the nomenclature DHEAS-CMO-EDA-DMAE recited in claims 6, 12, and 19 is interpreted in light of the specification and Figure 7 as referring to the chemical structure depicted therein. In particular, Figure 7 depicts DHEAS-CMO coupled through the recited EDA moiety to DMAE, with DMAE-EDA containing the aminoethyl/two-carbon diamine liner shown therein.
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 5 and 6 are rejected under 35 U.S.C. 103 as being unpatentable over Barlow et al. (US 6146836 A) in view of Law et al. (US 5241070 A).
Regarding claim 5, for an immunoassay reagent comprising a dehydroepiandrosterone sulphate-carboxymethoxylamino-dimethyl acridinium ester (DHEAS-CMO-DMAE) conjugate, Barlow teaches a DHEA-S immunoassay employing a primary antiDHEA-S monoclonal antibody, DHEA-S standards, and a tracer-Dimethylacridinium ester conjugated to DHEA-S (Example 3, p. 11). Thus, Barlow expressly teaches a DHEAS-DMAE immunoassay tracer.
Barlow additionally provides an express direction to the particular acridinium-ester chemistry relevant to modifying its DHEA-S tracer. Barlow teaches that the detectable label may be a chemiluminescent compound, a fluorescent compound, an enzyme or a radioisotope and, for its preferred acridinium-ester labels, expressly identifies U.S. Pat. Nos. 4,745,181; 5,227,489; 5,241,070 (Law); and 5,395,752 (col. 5, p. 7).
However, Barlow does not expressly teach that the DHEA-S-DMAE tracer contains the claimed CMO linkage.
Law teaches the missing CMO-linked steroid/DMAE architecture. Law identifies cortisol-3-carboxylmethyloxime and estradiol-6-carboxymethyloxime as suitable carboxylate-containing steroid compounds for conjugation to its acridinium esters (col. 3, p. 18). Law further teaches that a derivative of cortisol is 3-carboxymethyloxime cortisol, and that the conjugate is preferably prepared by activating the carboxylic group of the 3-carboxymethyloxime cortisol and then reacting the activated cortisol derivative with an appropriate acridinium ester, with the resulting tracer being usable in an assay for cortisol (cols. 8–9, pp. 20–21). Law then actually prepares cortisol-3-CMO-ED-DMAE conjugate by reacting 3-carboxylmethyloxime-cortisol (Cortisol-3-CMO) with DMAE-ED (Example 9, p. 24), and similarly prepares estradiol-6-CMO-ED-DMAE conjugate from 6-carboxymethyloxime-17-beta estradiol (Estradiol-6-CMO) and DMAE-ED (Example 10, p. 24). The CMO structural motif taught by Law corresponds to the relevant CMO motif depicted by Applicant for DHEAS-CMO in Figure 7, notwithstanding the differing textual nomenclature used by Applicant. Applicant’s Figure 7 expressly depicts DHEAS-CMO as the precursor to DHEAS-CMO-EDA-DMAE.
Law also supplies a concrete technical reason for employing its conjugation chemistry. Law explains that prior acridinium esters often cannot effectively form conjugates with certain analytes and that conjugation may have a deleterious effect on the immunoactivity of the analyte, resulting in loss of or reduction of the immunoactivity of the resulting conjugate (col. 1, p. 17). Law further explains that selection of the conjugating functional group depends on compatibility with the desired immunoassay system, the stability of conjugate prepared, and the ease of preparation (col. 8, p. 20).
Therefore, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify Barlow’s DHEA-S-DMAE immunoassay tracer to employ Law’s demonstrated CMO-linked steroid/DMAE conjugation architecture, thereby providing a DHEAS-CMO-DMAE conjugate. The modification is specifically suggested by Barlow itself because Barlow expressly directs the skilled artisan to Law for acridinium-ester label chemistry, while Law specifically teaches CMO-functionalized steroid hormones as suitable substrates for its acridinium conjugation chemistry and identifies immunoassay compatibility and conjugate stability as considerations for selecting the conjugation functionality. A skilled artisan would have had a reasonable expectation of success because Law actually prepares CMO-linked DMAE conjugates of multiple steroid hormones, including cortisol and estradiol, and uses the resulting cortisol conjugate in a competitive steroid assay, while Barlow independently demonstrates that DHEA-S functions successfully as a DMAE-labeled tracer in a quantitative DHEA-S immunoassay.
Regarding claim 6, and consistent with the interpretation set forth under §112(b), the DHEAS-AE conjugate is interpreted as referring to the DHEAS acridinium-ester conjugate of claim 5, and the DHEAS-CMO-EDA-DMAE alternative is interpreted consistently with the aminoethyl/two-carbon diamine linker structure depicted by Applicant in Figure 7. Figure 7 expressly depicts DMAE-EDA and the resulting DHEAS-CMO-EDA-DMAE (15). Law teaches that a most preferred acridinium ester contains the aminoethyl substituent, –CONH–CH₂CH₂–NH₂ (col. 3, p. 18), the same relevant aminoethyl/two-carbon linker structure depicted by Applicant for DMAE-EDA. Law further identifies this compound as 2’,6’-Dimethyl-4’-[N-(2-aminoethyl)carbomoylphenyl 10-methylacridinium-9-carboxylate bromide (DMAE-ED) and teaches in Example 1 that DMAE-ED is prepared by reacting DMAE with ethylenediamine (Example 1, p. 21). Law’s Example 1 prepares DMAE-ED, which is subsequently used in Example 9 to react with cortisol-3-CMO to produce cortisol-3-CMO-ED-DMAE, and in Example 10 with estradiol-6-CMO to produce the corresponding estradiol-6-CMO-ED-DMAE conjugate (Examples 9-10, p. 24).
Therefore, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to further modify Barlow’s DHEA-S tracer according to Law’s demonstrated CMO–aminoethyl-linker–DMAE steroid architecture so as to provide the DHEAS-CMO-EDA-DMAE alternative of claim 6. Law specifically demonstrates that this linker joins CMO-functionalized steroid hormones to DMAE, rather than merely identifying an unrelated diamine reagent. The skilled artisan would have reasonably expected success because Law successfully prepares this architecture with multiple steroid hormones, including cortisol and estradiol, while Barlow already establishes DHEA-S as an operative DMAE tracer in the same field of competitive steroid immunoassays.
Claims 11 and 12 are rejected under 35 U.S.C. 103 as being unpatentable over Barlow et al. in view of Law et al., and Antonelli et al. (The Pathway for Introducing Novel Examination Procedures in Routine Practice in Accordance with ISO 15189:2012: 17-Hydroxy Progesterone, Dehydroepiandrosterone Sulphate and Vitamin D as Examples. Annals of Clinical Biochemistry. Vol. 56, No. 5, September 2019).
Regarding claim 11, with respect to the teachings of Barlow and Law, see the discussion above, which applies equally here. Regarding an immunoassay kit, Barlow teaches reagents expressly used together to conduct its DHEA-S immunoassay, including primary antiDHEA-S monoclonal antibody, tracer-Dimethylacridinium ester conjugated to DHEA-S, and a solid phase Monoclonal anti-allotype Igh4b coupled to paramagnetic particles (Example 3, p. 11). Barlow additionally states that its invention comprises reagents for carrying out the method and teaches that several reagents can be premixed (col. 3, p. 6). Regarding paramagnetic solid phase particles labeled with fluoresceinated anti-DHEAS monoclonal antibody, Barlow teaches the relevant DHEAS antibody and magnetic-solid-phase components. Barlow specifically teaches primary antiDHEA-S monoclonal antibody and an anti-allotype solid phase coupled to paramagnetic particles (Example 3, p. 11). Barlow also expressly teaches that a detectable label can be a fluorescent compound (col. 5, p. 7). Regarding a DHEAS-CMO-DMAE conjugate, Barlow teaches tracer-Dimethylacridinium ester conjugated to DHEA-S, while Law teaches the CMO-linked steroid/DMAE architecture for the reasons discussed above for claim 5.
However, Barlow and Law do not expressly teach or specify paramagnetic solid phase particles labeled with fluoresceinated anti-DHEAS monoclonal antibody.
Antonelli directly supplies the missing DHEAS-specific fluorescent-antibody/magnetic-particle assay architecture. Antonelli describes serum DHEA-S measurement using a one-step competitive chemiluminescence immunoassay (CLIA), in which magnetic microbeads are coated with sheep polyclonal antifluorescein isothiocyanate (FITC), FITC-labelled monoclonal antibodies anti-DHEAS and antigen conjugated to ABEI (p. 549). Antonelli therefore demonstrates the fluoresceinated anti-DHEAS monoclonal antibody/magnetic solid-phase arrangement in an operative competitive DHEAS assay.
Therefore, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify the Barlow/Law DHEAS assay reagent set by employing Antonelli’s DHEAS-specific FITC-labelled anti-DHEAS monoclonal-antibody/magnetic-microbead solid-phase architecture while retaining the Barlow/Law DHEAS-CMO-DMAE tracer, thereby providing the reagent combination of claim 11. Antonelli supplies a direct teaching and motivation because it demonstrates that this particular magnetic/FITC antibody arrangement is suitable for the same analyte, DHEAS, in a one-step competitive quantitative immunoassay; thus, the modification would provide a known DHEAS-specific magnetic capture architecture. A skilled artisan would have reasonably expected success because Antonelli actually uses the FITC-labelled monoclonal anti-DHEAS/magnetic-microbead arrangement to quantify DHEA-S in serum, while Barlow independently demonstrates an operative competitive DHEA-S assay using an anti-DHEA-S monoclonal antibody, paramagnetic solid phase, and DHEA-S-DMAE tracer, and Law demonstrates operative CMO-DMAE steroid tracers.
Regarding claim 12, the combination teaches the kit of claim 11. Consistent with the §112(b) interpretation above, Law further teaches the relevant –CONH–CH2CH2–NH2 aminoethyl linker structure and expressly uses DMAE-ED to produce cortisol-3-CMO-ED-DMAE and estradiol-6-CMO-ED-DMAE. Thus, for the reasons stated for claim 6, the combination renders obvious at least the recited DHEAS-CMO-EDA-DMAE alternative.
Claims 18-20 are rejected under 35 U.S.C. 103 as being unpatentable over Barlow et al. in view of Law et al., Antonelli et al., Nakamura et al. (Detection and Removal of Escherichia Coli Using Fluorescein Isothiocyanate Conjugated Monoclonal Antibody Immobilized on Bacterial Magnetic Particles. Analytical Chemistry. Vol. 65, No. 15, August 1993), and Liu et al. (Label-Free Sensitive Detection of Steroid Hormone Cortisol Based on Target-Induced Fluorescence Quenching of Quantum Dots. Langmuir, Vol. 36, No. 27, June 2020).
Regarding claim 18, with respect to the teachings of Barlow, Law, and Antonelli, see the discussion above, which applies equally here. Regarding a method of determining a concentration of DHEAS in a biological sample, Barlow teaches immunoassays for analytes in patient body-fluid samples and specifically identifies blood serum or plasma, urine, lymphatic fluid or cerebrospinal fluid (col. 2, p. 5). Barlow’s Example 3 specifically teaches a DHEAS Immunoassay using DHEA-S standards (Example 3, p. 11). Barlow further states that the assay was used to quantitate DHEA-S in human plasma (col. 17, p. 13).
Regarding combining, either simultaneously or partially or wholly sequentially, to form a mixture: (1) a biological sample suspected of containing DHEAS; (2) paramagnetic solid phase particles labeled with fluoresceinated anti-DHEAS monoclonal antibody; and (3) a DHEAS-CMO-DMAE conjugate, Barlow expressly combined DHEA-S standard, DHEA-S-DMAE tracer, primary anti-DHEA-S monoclonal antibody, and paramagnetic particles in its DHEA-S assay (Example 3, p. 11). Law supplies the CMO-DMAE steroid tracer modification for the reasons discussed for claim 5, and Antonelli supplies the DHEAS-specific FITC-labelled anti-DHEAS monoclonal antibody/magnetic-microbead arrangement for the reasons discussed for claim 11 (p. 549).
Regarding allowing, in the mixture formed in (a), the binding of (3) to (2) or DHEAS present in the biological sample to (2), Barlow expressly teaches competitive binding: the patient sample is combined with a binding protein specific for the analyte and a known amount of detectably labeled tracer, and the analyte and tracer are permitted to competitively bind to the binding protein; Barlow explains that the greater the concentration of analyte present in the sample, the fewer tracer molecules will bind to the binding protein (col. 2, p. 5). In Example 3, the DHEA-S standard, DHEA-S-DMAE tracer, and primary anti-DHEA-S monoclonal antibody are mixed and incubated before addition of the particles (Example 3, p. 11).
However, Barlow, Law, and Antonelli does not expressly teach or specify measuring a fluorescence signal generated in the mixture and determining DHEAS concentration based upon an amount of decrease in fluorescence signal observed when compared to a fluorescence signal observed in the absence of the biological sample. Barlow measures chemiluminescence, and Antonelli likewise ultimately employs chemiluminescent detection.
Nakamura supplies the direct fluorescence-decrease detection principle in a FITC-monoclonal-antibody/magnetic-particle immunoassay. Nakamura teaches FITC-conjugated monoclonal antibody immobilized on magnetic particles (p. 2036) and directly measures FITC fluorescence (p. 2037). Critically, Nakamura teaches that the extent of the decrease in fluorescence compared to the initial value allows determination of analyte concentration and reports that fluorescence intensity did not decrease in the absence of target antigen (p. 2038). Thus, Nakamura directly teaches quantitative determination from an analyte-dependent fluorescence decrease relative to a no-analyte condition. Nakamura, however, uses E. coli as the antigen, and its operative fluorescence decrease is associated with antigen-antibody-mediated aggregation/sedimentation of the FITC-antibody magnetic particles (pp. 2036, 2038–2039). Nakamura therefore does not itself establish that binding of a small steroid hormone such as DHEAS would predictably provide a quantitatively useful fluorescence decrease.
Liu resolves that remaining steroid-specific predictability issue. Liu teaches fluorescent probes carried by magnetic nanoparticles (pp. 7781-7782) and demonstrates a decrease in fluorescence intensity in response to the capture of cortisol (p. 7782). Liu further teaches that the sensing approach can be extended to detect other steroid hormones that exhibit similar capability of fluorescence quenching (p. 7782) and experimentally evaluates structurally related steroids, including DHEA (pp. 7782-7784, and 7787). Thus, Liu establishes that analyte-dependent fluorescence decrease/quenching is applicable to small steroid hormones and provides the technical bridge from Nakamura’s fluorescence-decrease immunosensor principle to the DHEAS assay architecture already taught by Barlow and Antonelli.
Therefore, it would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify Barlow’s quantitative competitive DHEAS assay, first according to Law’s CMO-DMAE steroid conjugation chemistry and Antonelli’s DHEAS-specific FITC-labelled anti-DHEAS monoclonal-antibody/magnetic-particle architecture, and further according to Nakamura’s direct FITC fluorescence-decrease detection principle, so that binding is detected by measuring the decrease in fluorescence relative to the no-analyte condition, as supported for small steroid analytes by Liu. The modifications are supported by affirmative teachings: Barlow expressly directs the artisan to Law for acridinium chemistry; Antonelli demonstrates the FITC-anti-DHEAS/magnetic-particle architecture in the same competitive DHEAS assay context; Nakamura expressly teaches quantitative analyte determination from decreasing FITC fluorescence in a monoclonal-antibody/magnetic-particle system; and Liu demonstrates that small steroid capture produces measurable fluorescence decrease/quenching and expressly extends that principle to other steroid hormones. The skilled artisan would have had a reasonable expectation of success because each modification had already been experimentally demonstrated in the directly relevant portion of the assay architecture: Barlow demonstrates competitive quantitative DHEAS binding, Law demonstrates functional CMO-DMAE steroid tracers, Antonelli demonstrates FITC-labelled monoclonal anti-DHEAS with magnetic microbeads in an operative DHEAS assay, Nakamura demonstrates direct quantitative fluorescence-decrease detection from FITC-antibody magnetic particles, and Liu demonstrates steroid-dependent fluorescence decrease, including a response to DHEA. The combination therefore provides a technically supported path to the claimed DHEAS fluorescence-decrease assay.
Regarding claim 19, the combination teaches the method of claim 18. Consistent with the §112(b) interpretation, the DHEAS-AE conjugate is interpreted as the DHEAS acridinium-ester conjugate recited in claim 18. Law teaches the relevant –CONH–CH2CH2–NH2 aminoethyl/two-carbon linker and expressly uses DMAE-ED to prepare cortisol-3-CMO-ED-DMAE and estradiol-6-CMO-ED-DMAE. For the reasons stated for claim 6, it would therefore have been obvious to employ Law’s demonstrated CMO–aminoethyl-linker–DMAE architecture for Barlow’s DHEAS tracer, providing at least the DHEAS-CMO-EDA-DMAE alternative recited in claim 19, with a reasonable expectation of success based upon Law’s successful preparation and use of the corresponding steroid CMO-DMAE architecture.
Regarding claim 20, wherein, in step (d), the concentration of DHEAS present in the biological sample is determined by comparing the fluorescence signal to a calibration curve, Barlow expressly teaches that in its competitive immunoassay, the resulting signal is inversely proportional to the amount of analyte in the sample and that the amount of analyte present can be determined by comparing the results obtained to a standard curve (col. 2, p. 5). In the DHEA-S-specific Example 3, Barlow actually generates DHEA-S standard curves (Table 6, p. 11; Fig. 3, p. 4).
Conclusion
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/E.O./Examiner, Art Unit 1677
/BAO-THUY L NGUYEN/Supervisory Patent Examiner, Art Unit 1677
September 18, 2026
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